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known objects exist as the consequences of directed operations, not because of conformity of thought or observation with something antecedent. We may, for reasons which Ihope will appear later, give the name intelligence to these directed operations. Using this term, we may say that the worth of any object that lays claim to being an object of knowledge is dependent upon the intelligence employed in reaching it. In saying this, we must bear in mind that intelligence means operations actually performed in the modification of condi- tions, including all the guidance that is given by means of ideas, both direct and symbolic.
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it is only away of saying that the value of any cognitive conclusion depends upon the method by which it is reached, so that the perfecting of method, the perfecting of intelligence, is the thing of su- preme value. If we judge the work of ascientific inquirer by what he does and not by his speech when he talks about his work (when he is likely to talk in terms of traditional notions that have become habitual) we shall have little difficulty, I think, in accepting the idea that he determines the cognitive claims of anything presented to him on the basis of the method by which it is reached. The import of this doctrine is simple. It becomes complicated, however, the moment we contrast it with the doctrines which have dominated thought. For these all rest on the notion that areality in Being indepen- dently of the operations of inquiry is the standard and meas- ure of anything said to be known. Viewed in this connection, the conception just advanced involves hardly less than arevo- lutionary transformation of many of our most cherished con- victions. The essential difference is that between amind which beholds or grasps objects from outside the world of things, physical and social, and one which is aparticipant, interacting
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Heisen- berg's principle of indeterminancy. The basic philosophy of the Newtonian system of the universe is closely connected with what is termed the principle of canonic conjugates. The fun- damental principle of the mechanical philosophy of nature is that it is possible to determine exactly (in principle if not in actual practice) both the position and the velocity of any body. Knowing this for each particle which enters into any change, as amotion, it is possible to calculate mathematically, that is exactly, just what will happen. The laws or physical equations that express the relations of the particles and bodies under different conditions are then assumed to be a"govern- ing" framework of nature to which all particular phenomena conform. Knowing volumes and momenta in aparticular case we can by the aid of fixed laws predict the subsequent course of events.
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a- place's well-known saying that were there aknowledge (in mechanical terms) of the state of the universe at any one time its whole future could be predicted or deduced
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critics had attacked the Newtonian scheme on the basis of alogical flaw in it. It first postulates that the position and velocity of any particle can be determined in isolation from all others. Then it postulates that there is a complete and continuous interaction of all these particles with one another. Logically, the two postulates nullify each other. But as long as the principles involved gave satisfactory results this objection was brushed aside or ignored. Heisenberg's prin- ciple compels arecognition of the fact that interaction prevents an accurate measurement of velocity and position for any body,
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he change for the un- derlying philosophy and logic of science is, however, very great. In relation to the metaphysics of the Newtonian system it is hardly less than revolutionary. What is known is seen to be aproduct in which the act of observation plays aneces- sary role. Knowing is seen to be aparticipant in what is finally known. Moreover, the metaphysics of existence as something fixed and therefore capable of literally exact mathematical description and prediction is undermined. Knowing is, for philosophical theory, acase of specially directed activity in- stead of something isolated from practice. The quest for cer- tainty by means of exact possession in mind of immutable reality is exchanged for search for security by means of active control of the changing course of events. Intelligence in op- eration, another name for method, becomes the thing most worth winning.
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The principle of indeterminancy thus presents itself as the final step in the dislodgment of the old spectator theory of knowledge. It marks the acknowledgment, within scientific procedure itself, of the fact that knowing is one kind of inter-
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If we persist in the tradi- tional conception, according to which the thing to be known is something which exists prior to and wholly apart from the act of knowing, then discovery of the fact that the act of observa- tion, necessary in existential knowing, modifies that pre- existent something, is proof that the act of knowing gets in its own way, frustrating its own intent. If knowing is aform of doing and is to be judged like other modes by its eventual issue, this tragic conclusion is not forced upon us. Fundamen- tally, the issue is raised whether philosophy is willing to sur- render atheory of mind and its organs of knowing which originated when the practice of knowing was in its infancy.
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In technical statement, laws on the new basis are formulae for the 'prediction of the 'probability of an observable occur- rence. They are designations of relations sufficiently stable to allow of the occurrence of forecasts of individualized situa- tions for every observed phenomenon is individual within limits of specified probability, not aprobability of error, but of probability of actual occurrence.
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like all generalizations which go beyond the range of possible as well as of actual experience, aprice was paid for the sublime and inspiring ideal of areign of uni- versal and exact law: the sacrifice of the individual to the general, of the concrete to the relational. Spinoza's magnifi- cently sweeping dictum that "the order and connection of ideas is the order and connection of things" was in effect, although not avowedly as it was with Spinoza, the current measure of the intelligibility of nature. And auniverse whose essential characteristic is fixed order and connection has no place for unique and individual existences, no place for novelty and genuine change and growth. It is, in the words of William James, ablock universe. The fact that in detailed content it is athoroughly mechanistic world is, one may say, amere incident attending the fact that it is afixed and closed world.
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the child who expressed surprise at the fact that rivers or bodies of water are always located conveniently near great cities. Suppose every one had had engrained in his mind the notion that cities, like rivers, are works of nature. Suppose it was then suddenly ascertained that cities were man made and were located near bodies of water in order that the activities of men in industry and com- merce might be better carried on and human purposes and needs be better served. We can imagine that the discovery would bring with it ashock. It would be upsetting because
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rom the stand- point of traditional notions, it appears that nature, intrin- sically, is Irrational. But the quality of irrationality is imputed only because of conflict with aprior definition of ration- ality. Abandon completely the notion that nature ought to conform to acertain definition, and nature intrinsically is neither rational nor irrational. Apart from the use made of it in knowing, it exists in adimension irrelevant to either attribution, just as rivers inherently are neither located near cities nor are opposed to such location. Nature is intelligible and understand^/*?. There are operations by means of which it becomes an object of knowledge, and is turned to human purposes, just as rivers provide conditions which may be utilized to promote human activities and to satisfy human need.
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The doctrine that nature is inherently rational was acostly one. It entailed the idea that reason in man is an outside spec- tator of arationality already complete in itself. It deprived reason in man of an active and creative office; its business was simply to copy, to re-present symbolically, to view agiven rational structure. Ability to make atranscript of this structure in mathematical formulas gives great delight to those who have the required ability. But it does nothing; it makes no difference in nature. In effect, it limits thought in man to retraversing in cognition apattern fixed and complete in itself. The doctrine was both an effect of the traditional separation between knowledge and action and afactor in perpetuating it. It relegated practical making and doing to asecondary and relatively irrational realm.
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There is thus involved more than averbal shift if we say that the new scientific development effects an exchange of reason for intelligence. In saying this, "reason" has the tech- nical meaning given to it in classic philosophic tradition, the nous of the Greeks, the mtellectus of the scholastics. In this meaning, it designates both an inherent immutable order of nature, superempirical in character, and the organ of mind by which this universal order is grasped. In both respects, reason is with respect to changing things the ultimate fixed standard the law physical phenomena obey, the norm human action should obey. For the marks of "reason" in its traditional sense are necessity, universality, superiority to change, domination of the occurrence and the understanding of change.
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The change does not mean that nature has lost intelligi- bility. It rather signifies that we are in position to realize that the term intelligible is to be understood literally. It expresses apotentiality rather than an actuality. Nature is capable of being understood. But the possibility is realized not by amind thinking about it from without but by operations conducted from within, operations which give it new relations summed up in production of anew individual object. Nature has intel- ligible order as its possession in the degree in which we by our own overt operations realize potentialities contained in it. The change from intrinsic rationality in the traditional sense to an intelligibility to be realized by human action places responsibility upon human beings. The devotion we show to the ideal of intelligence determines the extent in which the actual order of nature is congenial to mind.
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rtificial simplifica- tion or abstraction is anecessary 'precondition of securing ability to deal with affairs which are complex, in which there are many more variables and where strict isolation destroys the special characteristics of the subject-matter. This statement conveys the important distinction which exists between physical and social and moral objects. The distinction is one of methods of operation not of kinds of reality.
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what is meant by "physical" in distinction from other adjectives that are prefixed to subject-matter is precisely an abstraction of alimited range of conditions and relations out of atotal complex. The same principle applies to mathematical objects. The use of symbols designating possible operations makes possible agreater degree of exactness and intellectual organization. There is no disparagement of ab- straction involved. Abstraction is simply an instance of the economy and efficiency involved in all intelligent practice: Deal first with matters that can be effectively handled, and then use the results to go on to cope with more complex affairs. Objection comes in, and comes in with warranted force, when the results of an abstractive operation are given astanding which belongs only to the total situation from which they have been selected. All specialization breeds afamiliarity which tends to create an illusion. Material dealt with by specialized abstractive processes comes to have apsychological independence and completion which is converted hyposta- tized into objective independence and self-sufficiency.
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In arriving at statements which hold for all possible experiencers and observers under all possible varying indi- vidual circumstances we arrive at that which is most remote from any one concrete experience. In this sense, the abstrac- tions of mathematics and physics represent the common de- nominators in all things experienceable. Taken by themselves they seem to present aca$ut mortuum. Erected into complete statements of reality as such, they become hallucinatory obses- sions. But in practice, there is always an accompanying reverse movement. These generalized findings are employed to enrich the meanings of individualized experiences, and to afford, within limits of probability, an increased control of them. It is in this sense that all reflective knowledge as such is instrumental. The beginning and the end is the things of gross everyday experience. But apart from knowledge the things of our ordinary experience are fragmentary, casual, unregulated by purpose, full of frustrations and barriers. In the language previously used, they are problematic, obstructive, and chal- lenges to thought. By ignoring for atime their concrete and qualitative fullness, by making abstractions and generalizations, we ascertain certain basic relations upon which occurrence of the things experienced depend. We treat them as mere events,
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There is no kind of inquiry which has amonopoly of the honorable title of knowledge. The engineer, the artist, the historian, the man of affairs attain knowledge in the degree they employ methods that enable them to solve the problems which develop in the subject-matter they are concerned with. As philosophy framed upon the pattern of experimental in- quiry does away with all wholesale skepticism, so it eliminates all invidious monopolies of the idea of science. By their fruits we shall know them.
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he marking off of certain conclusions as alone truly science, whether mathematical or physical, is an historical incident. It sprang originally from man's desire for acertainty and peace which he could not attain practically in the absence of the arts of management and direction of natural conditions. When modern physical inquiry began, it had ahard time to get ahearing, or even to be permitted to carry on. The temp- tation was practically irresistible to treat it as an exclusive and esoteric undertaking. Moreover, as it progressed, it required more and more specialized technical preparation. The motive of defense from social attack and the motive of glorification
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of aspecialized calling conspired together. All the eulogistic connotations that gather about "truth" were called into play. Thus "science," meaning physical knowledge, became a kind of sanctuary. Areligious atmosphere, not to say an idola- trous one, was created. "Science" was set apart jits findings were supposed to have aprivileged relation to the real. In fact, the painter may know colors as well as the physicist} the poet may know stars, rain and clouds as well as the meteorolo- gist jthe statesman, educator and dramatist may know human nature as truly as the professional psychologist} the farmer may know soils and plants as truly as the botanist and min- erologist. For the criterion of knowledge lies in the method used to secure consequences and not in metaphysical concep- tions of the nature of the real. Nevertheless in the end think- ers in all lines are dependent upon the mathematician and the physical inquirer for perfecting of the tools employed in their respective callings. That "knowledge" has many meanings follows from the operational definition of conceptions. There are as many con- ceptions of knowledge as there are distinctive operations by which problematic situations are resolved.
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Many definitions of mind and thinking have been given. Iknow of but one that goes to the heart of the matter: response to the doubtful as such. No inanimate thing reacts to things as problematic. Its behavior to other things is capable of description in terms of what is determinately there. Under given conditions, it just reacts or does not react. Its reactions merely enstate anew set of conditions, in which reactions con- tinue without regard to the nature of their outcome. It makes no difference, so to say, to astone what are the results of its interactions with other things. It enjoys the advantage that it makes no difference how it reacts, even if the effect is its own pulverization. It requires no argument to show that the case is different with aliving organism. To live signifies that a connected continuity of acts is effected in which preceding ones prepare the conditions under which later ones occur. There is achain of cause and effects, of course, in what happens with inanimate things. But for living creatures, the chain has a particular cumulative continuity, or else death ensues.
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This conception of the mental brings to unity various modes of response jemotional, volitional and intellectual. It is usual to say that there is no fundamental difference among these activities that they are all different phases or aspects of a common action of mind. But Iknow of but one way of making this assertion good: that in which they are seen to be distinctive modes of response to the uncertain. The emotional aspect of responsive behavior is its immediate quality. When we are con- fronted with the precarious, an ebb and flow of emotion marks adisturbance of the even tenor of existence. Emotions are conditioned by the indeterminateness of present situations with respect to their issue. Fear and hope, joy and sorrow, aversion and desire, as perturbations, are qualities of adivided response. They involve concern, solicitude, for what the present situation may become. "Care" signifies two quite different things: fret, worry and anxiety, and cherishing attention to that in whose potentialities we are interested. These two meanings represent different poles of reactive behavior to apresent hav- ing afuture which is ambiguous.
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thinking is the actual transition from the problematic to the secure, as far as that is intentionally guided. There is no separate "mind" gifted in and of itself with afaculty of thought jsuch acon- ception of thought ends in postulating the mystery of apower outside of nature and yet able to intervene within it. Thinking is objectively discoverable as that mode of serial responsive behavior to aproblematic situation in which transition to the relatively settled and clear is effected.
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The concrete pathologies of belief, its failures and perver- sions, whether of defect or excess, spring from failure to ob- serve and adhere to the principle that knowledge is the com- pleted resolution of the inherently indeterminate or doubtful. The commonest fallacy is to suppose that since the state of doubt is accompanied by afeeling of uncertainty, knowledge arises when this feeling gives way to one of assurance. Think- ing then ceases to be an effort to effect change in the objective situation and is replaced by various devices which generate a change in feeling or "consciousness." Tendency to premature judgment, jumping at conclusions, excessive love of simplicity, making over of evidence to suit desire, taking the familiar for the clear, etc., all spring from confusing the feeling of certi- tude with acertified situation. Thought hastens toward the settled and is only too likely to force the pace. The natural man dislikes the dis-ease which accompanies the doubtful and is ready to take almost any means to end it. Uncertainty is got rid of by fair means or foul. Long exposure to danger breeds an overpowering love of security. Love for security, translated into adesire not to be disturbed and unsettled, leads to dogmatism, to acceptance of beliefs upon authority, to in-
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Here is where ordinary thinking and thinking that is scrupu- lous diverge from each other. The natural man is impatient with doubt and suspense: he impatiently hurries to be shut of it. Adisciplined mind takes delight in the problematic, and cherishes it until away out is found that approves itself upon examination. The questionable becomes an active questioning, asearch jdesire for the emotion of certitude gives place to quest for the objects by which the obscure and unsettled may be developed into the stable and clear. The scientific attitude may almost be defined as that which is capable of enjoying the doubtful jscientific method is, in one aspect, atechnique for making aproductive use of doubt by converting it into operations of definite inquiry.
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If it is objected that such an examination itself involves mind and its organs, the rejoinder is that the theory we have advanced is self-applying. Its only "assumption" is that something is done, done in the ordinary external sense of that word, and that this doing has consequences. We define mind and its organs in terms of this doing and its results, just as we define or frame ideas of stars, acids, and digestive tissues in terms of their behavior. If it be urged that we do not know whether the re- sults of the directed operations are really knowledge or not, the answer is the objection assumes that we have some kind
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hile traditional theories regard mind as an intruder from without into the natural development, or evolution, of organic structures, or else in the interest of natural continuity feel compelled to deny that mental behavior has any differential features, the theory that organic responses have mental quality in the degree in which they deal with the uncertain recognizes both continuity and difference. It can, in principle if not as yet in detail, give agenetic account of the development of mental and intellectual processes. There is neither asudden jump from the merely organic to the intellectual, nor is there complete assimilation of the latter to primitive modes of the former.
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According to this doctrine, we are doubtful, puzzled, con- fused, undecided jobjects are complete, assured, fixed. It is not easy to reconcile this notion with the fact that in order to relieve our doubt, to "make up" our minds, we have to modify in some way, in imaginative or overt experimentation, the situation in which uncertainty is experienced.
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there are few if any cases of trouble into which apersonal factor of desire or aversion does not enter as a productive cause. But the idea that this causal factor can be changed by purely direct means, by an exercise of "will" or "thought" is illusory. Achange of desire and purpose can it- self be effected only indirectly, by achange in one's actual relation to environment. This change implies definite acts.
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The occurrence of problematic and unsettled situations is due to the charac- teristic union of the discrete or individual and the continuous or relational.
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There are situations in which self-enclosed, discrete, indi- vidualized characters dominate. They constitute the subject- matter of esthetic experience} and every experience is esthetic in as far as it is final or arouses no search for some other ex- perience. When this complete quality is conspicuous the experi- ence is denominated esthetic
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ll experienced objects have adouble status. They are individualized, consummatory, whether in the way of enjoyment or of suffering. They are also involved in a continuity of interactions and changes, and hence are causes and potential means of later experiences. Because of this dual capacity, they become problematic. Immediately and directly they are just what they are} but as transitions to and possi- bilities of later experiences they are uncertain. There is a divided response} part of the organic activity is directed to them for what they immediately are, and part to them as transitive means of other experienced objects. We react to them both as finalities and in preparatory ways, and the two reactions do not harmonize. This two-fold character of experienced objects is the source of their problematic character.
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"tertiary"qualities (as they have been happily termed by Mr. Santayana), those which, in psychological analysis, we call affectional and emotional, are as much products of the doings of nature as are color, sound, pressure, perceived size and distance.
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If existence were either com- pletely necessary or completely contingent, there would be neither comedy nor tragedy in life, nor need of the will to live. The significance of morals and politics, of the arts both technical and fine, of religion and of science itself as inquiry and discovery, all have their source and meaning in the union in Nature of the settled and the unsettled, the stable and the hazardous. Apart from this union, there are no such things as "ends," either as consummations or as those ends-in-view we call purposes. There is only ablock universe, either something ended and admitting of no change, or else apredestined march of events. There is no such thing as fulfillment where there is no risk of failure, and no defeat where there is no promise of possible achievement. Any philosophy that in its quest for certainty ignores the reality of the uncertain in the ongoing processes of nature denies the conditions out of which it arises. The attempt to include all that is doubtful within the fixed grasp of that which is theoretically certain is committed to insincerity and evasion, and in consequence will have the stigmata of internal contradiction. Every such philosophy is marked at some point by adivision of its subject-matter into the truly real and the merely apparent, asubject and an object, aphysical and a mental, an ideal and an actual, that have nothing to do with one another, save in some mode which is so mysterious as to create an insoluble problem. Action is the means by which aproblematic situation is re- solved. Such is the net outcome of the method of science. There is nothing extraordinary about this conclusion. Interac- tion is auniversal trait of natural existence. "Action" is the name given to one mode of this interaction, namely, that named from the standpoint of an organism.
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The distinction once made between theory and practice has meaning as adistinction between two kinds of action: blind and intelligent. Intelligence is aquality of some acts, those which are directed} and directed action is an achievement not an original endowment. The history of human progress is the story of the transformation of acts which, like the interactions of inanimate things, take place unknowingly to actions qualified by understanding of what they are about} from actions con- trolled by external conditions to actions having guidance through their intent: their insight into their own conse- quences. Instruction, information, knowledge, is the only way in which this property of intelligence comes to qualify acts originally blind
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telligent action is purposive action; if it is anatural oc- currence, coming into being under complex but specifiable con- ditions of organic and social interaction, then purpose like in- telligence is within nature jit is a"category" having objective standing and validity. It has this status in adirect way through the place and operation of human art within the natural scene j for distinctively human conduct can be interpreted and under- stood only in terms of purpose. Purpose is the dominant cate- gory of anything truly denominated history, whether in its enacting or in the writing of it, since action which is distinctively human is marked by intent.
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We are free in the degree* in which we act knowing what we are about. The identification of freedom with "freedom of will" locates contingency in the wrong place. Contingency of will would mean that uncertainty was uncer- tainly dealt with jit would be aresort to chance for adecision. The business of "will" is to be resolute; that is, to resolve, under the guidance of thought, the indeterminateness of un- certain situations. Choice wavers and is brought to ahead arbitrarily only when circumstances compel action and yet we have no intelligent clew as to how to act. The doctrine of "free-will" is adesperate attempt to es- cape from the consequences of the doctrine of fixed and im- mutable objective Being. With dissipation of that dogma, the need for such ameasure of desperation vanishes.
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It is not claimed, therefore, that there is no philosophical problem of the relation of physical science to the things of ordinary experience. It is asserted that the problem in the -form in which it has chiefly occupied modern philosophy is an artifi- cial one, due to the continued assumption of premises formed in an earlier period of history and now having no relevancy to the state of physical inquiry. Clearing the ground of this unreal problem, however, only imposes upon philosophy the consid- eration of aproblem which is urgently practical, growing out of the conditions of contemporary life. What revisions and sur- renders of current beliefs about authoritative ends and values are demanded by the method and conclusions of natural science? What possibilities of controlled transformation of the content of present belief and practice in human institutions and associ
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Formal analogy suggests that we regard our direct and original experience of things liked and enjoyed as only 'possi- bilities of values to be achieved jthat enjoyment becomes a value when we discover the relations upon which its presence depends. Such acausal and operational definition gives only a conception of avalue, not avalue itself. But the utilization of the conception in action results in an object having secure and significant value.
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future in which the thing will continue to serve} it will do. It asserts aconsequence the thing will actively institute; it will do. That it is satisfying is the content of aproposition of fact; that it is satisfactory is ajudgment, an estimate, an appraisal. It denotes an attitude to be taken, that of striving to perpetuate and to make secure.
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ithout the introduction of operational thinking, we oscillate between atheory that, in order to saye the objec- tivity of judgments of values, isolates them from experience and nature, and atheory that, in order to save their concrete and human significance, reduces them to mere statements about our own feelings.
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Judgments about values are judg- ments about the conditions and the results of experienced ob- jects; judgments about that which should regulate the forma- tion of our desires^ affections and enjoyments.
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judgment of the value of an object to be experienced is instrumental to appreciation of it when it is realized. But the notion that every object that happens to satisfy has an equal claim with every other to be avalue is like supposing that every object of perception has the same cognitive force as every other. There is no knowledge without perception} but objects perceived are known only when they are determined as consequences of connective op- erations. There is no value except where there is satisfaction, but there have to be certain conditions fulfilled to transform a satisfaction into avalue.
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Amoral law, like alaw in physics, is not something to swear by and stick to at all hazards; it is a formula of the way to respond when specified conditions pre- sent themselves. Its soundness and pertinence are tested by what happens when it is acted upon. Its claim or authority rests finally upon the imperativeness of the situation that has to be dealt with, not upon its own intrinsic nature as any tool achieves dignity in the measure of needs served by it.
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PostGIS 3.4.0dev Manual (whole document)
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Pulmonary embolism in patients with severe COPD exacerbation (September 2023)

Pulmonary embolism (PE) is an important potential trigger for COPD exacerbation. In a recent multicenter study, 1580 patients with COPD who were admitted to the hospital with acute worsening of respiratory symptoms were all screened for PE with computed tomography pulmonary angiogram within 48 hours of admission [1]. PE was identified in 266 (17 percent), with 166 patients (11 percent) having PE involving the main or lobar pulmonary arteries. Purulent sputum production decreased the odds of PE by 60 percent. We suggest obtaining imaging for PE in patients requiring admission for COPD exacerbation who do not have evidence of other triggers (eg, infection or heart failure).

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All topics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: Nov 2023. This topic last updated: Sep 25, 2023. ●What's New <span>Pulmonary embolism in patients with severe COPD exacerbation (September 2023) Pulmonary embolism (PE) is an important potential trigger for COPD exacerbation. In a recent multicenter study, 1580 patients with COPD who were admitted to the hospital with acute worsening of respiratory symptoms were all screened for PE with computed tomography pulmonary angiogram within 48 hours of admission [1]. PE was identified in 266 (17 percent), with 166 patients (11 percent) having PE involving the main or lobar pulmonary arteries. Purulent sputum production decreased the odds of PE by 60 percent. We suggest obtaining imaging for PE in patients requiring admission for COPD exacerbation who do not have evidence of other triggers (eg, infection or heart failure). (See "COPD exacerbations: Clinical manifestations and evaluation", section on 'Triggers' and "COPD exacerbations: Clinical manifestations and evaluation", section on 'Additional testing




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The Global Initiative for Chronic Obstructive Lung Disease (GOLD), a report produced by the National Heart, Lung, and Blood Institute (NHLBI) and the World Health Organization (WHO), defines an exacerbation of chronic obstructive pulmonary disease (COPD) as "an event characterized by dyspnea and/or cough and sputum that worsens over ≤14 days, which may be accompanied by tachypnea and/or tachycardia, and is often associated with increased local and systemic inflammation caused by airway infection, pollution, or other insult to the airways" [1,2]. This generally includes an acute change in one or more of the following cardinal symptoms:

● Cough increases in frequency and severity

● Sputum production increases in volume and/or changes character

● Dyspnea increases

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ions: Clinical manifestations and evaluation", section on 'Triggers' and "COPD exacerbations: Clinical manifestations and evaluation", section on 'Additional testing'.) Read more INTRODUCTION — <span>The Global Initiative for Chronic Obstructive Lung Disease (GOLD), a report produced by the National Heart, Lung, and Blood Institute (NHLBI) and the World Health Organization (WHO), defines an exacerbation of chronic obstructive pulmonary disease (COPD) as "an event characterized by dyspnea and/or cough and sputum that worsens over ≤14 days, which may be accompanied by tachypnea and/or tachycardia, and is often associated with increased local and systemic inflammation caused by airway infection, pollution, or other insult to the airways" [1,2]. This generally includes an acute change in one or more of the following cardinal symptoms: ●Cough increases in frequency and severity ●Sputum production increases in volume and/or changes character ●Dyspnea increases The clinical manifestations and evaluation of patients with exacerbations of COPD are discussed in detail here. A table to assist with emergency management of severe acute exacerbations




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The clinical manifestations and evaluation of patients with exacerbations of COPD are discussed in detail here. A table to assist with emergency management of severe acute exacerbations of COPD is provided (table 1).
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an acute change in one or more of the following cardinal symptoms: ●Cough increases in frequency and severity ●Sputum production increases in volume and/or changes character ●Dyspnea increases <span>The clinical manifestations and evaluation of patients with exacerbations of COPD are discussed in detail here. A table to assist with emergency management of severe acute exacerbations of COPD is provided (table 1). The diagnosis and treatment of stable COPD and the treatment, risk factors, prognosis, and prevention of exacerbations of COPD are discussed separately. ●(See "Chronic obstructive pulmo




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Pseudomonas infection risk factors: Broad spectrum antibiotic use in the past 3 months; chronic colonization or previous isolation of Pseudomonas aeruginosa from sputum (particularly in past 12 months); very severe underlying COPD (FEV1 <30% predicted); chronic systemic glucocorticoid use.
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are for patients with normal renal function. Some agents require dose adjustment for renal impairment; refer to separate UpToDate algorithms of antibiotic treatment of exacerbations of COPD. ¶ <span>Pseudomonas infection risk factors: Broad spectrum antibiotic use in the past 3 months; chronic colonization or previous isolation of Pseudomonas aeruginosa from sputum (particularly in past 12 months); very severe underlying COPD (FEV1 <30% predicted); chronic systemic glucocorticoid use. Graphic 65420 Version 12.0 © 2023 UpToDate, Inc. and/or its affiliates. All Rights Reserved. Graphics in this topic New diagnosis of COPD Initial emergency management of severe COPD exa




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Among patients with COPD, the frequency of exacerbation varies with the severity of disease, and some patients have more frequent exacerbations than others independent of other measures of disease severity [1,3].
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and staging".) ●(See "Stable COPD: Overview of management".) ●(See "COPD exacerbations: Management".) ●(See "COPD exacerbations: Prognosis, discharge planning, and prevention".) EPIDEMIOLOGY — <span>Among patients with COPD, the frequency of exacerbation varies with the severity of disease, and some patients have more frequent exacerbations than others independent of other measures of disease severity [1,3]. ●Among almost 100,000 patients with COPD, the number of exacerbations in a baseline year of observation predicted the rate over the subsequent 10 years [4]. Approximately, 25 percent di




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In a separate survey of more than 1000 patients, 21 percent of those who reported a COPD exacerbation required hospitalization [7].
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n [5]. ●In a survey that included over 4000 respondents with COPD, approximately 10 to 25 percent needed an emergency room evaluation for COPD and 5 to 10 percent required hospitalization [6]. ●<span>In a separate survey of more than 1000 patients, 21 percent of those who reported a COPD exacerbation required hospitalization [7]. RISK FACTORS AND TRIGGERS Risk factors — According to observational studies, the risk of developing an exacerbation of COPD correlates with the following features [8-13]: ●Advanced age




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Risk factors — According to observational studies, the risk of developing an exacerbation of COPD correlates with the following features [8-13]:

● Advanced age

● Productive cough

● Longer duration of COPD

● History of antibiotic therapy

● COPD-related hospitalization within the previous year

● Chronic mucous hypersecretion

● Peripheral blood eosinophil count >0.34 x 109 cells/L (340 cells/microL)

Theophylline therapy

● Presence of one or more comorbidities (eg, ischemic heart disease, heart failure, or diabetes mellitus)

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cent required hospitalization [6]. ●In a separate survey of more than 1000 patients, 21 percent of those who reported a COPD exacerbation required hospitalization [7]. RISK FACTORS AND TRIGGERS <span>Risk factors — According to observational studies, the risk of developing an exacerbation of COPD correlates with the following features [8-13]: ●Advanced age ●Productive cough ●Longer duration of COPD ●History of antibiotic therapy ●COPD-related hospitalization within the previous year ●Chronic mucous hypersecretion ●Peripheral blood eosinophil count >0.34 x 109 cells/L (340 cells/microL) ●Theophylline therapy ●Presence of one or more comorbidities (eg, ischemic heart disease, heart failure, or diabetes mellitus) Women are slightly more likely to experience a COPD exacerbation than men [13,14]. In general, worsening airflow limitation (lower forced expiratory volume in one second [FEV1]) is asso




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The Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines suggest using primarily history of exacerbations, history of hospitalization for exacerbation, and symptoms to assess the exacerbation risk [1].
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vide a good assessment of exacerbation risk [1]. Other potential contributors to an increased risk of exacerbations include the following: ●Severity of COPD and history of prior exacerbations – <span>The Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines suggest using primarily history of exacerbations, history of hospitalization for exacerbation, and symptoms to assess the exacerbation risk [1]. The number of exacerbations in the previous 12 months is stratified: a history of zero or one exacerbation suggests a low future risk of exacerbations, while two or more suggest a high




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Worsening airflow obstruction remains associated with an increasing prevalence of exacerbations, hospitalization, and death [16]. It is used as a component of the BODE index, a prognostic tool that can also be used to assess therapeutic response to medications, pulmonary rehabilitation therapy, and other interventions [17].
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<80 percent predicted) were followed for three years [15]. The single best predictor of exacerbations was a history of prior exacerbations, regardless of severity of airway obstruction [4]. <span>Worsening airflow obstruction remains associated with an increasing prevalence of exacerbations, hospitalization, and death [16]. It is used as a component of the BODE index, a prognostic tool that can also be used to assess therapeutic response to medications, pulmonary rehabilitation therapy, and other interventions [17]. Different COPD staging systems and severity assessments are discussed in more detail separately. (See "Chronic obstructive pulmonary disease: Diagnosis and staging", section on 'Assessm




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A similar observation was made in a case-control study that assessed the presence of GERD symptoms and frequency of COPD exacerbations in 80 patients with COPD. The presence of GERD symptoms was associated with an increased risk of COPD exacerbations (RR 6.55, 95% CI 1.86-23.11) [18]. However, in an observational study of 638 patients with stable COPD, therapy with proton pump inhibitors did not decrease the risk for severe exacerbations [20].
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onal risk factor for COPD exacerbations [18,19]. In the ECLIPSE study noted above, the occurrence of two or more exacerbations in a year was associated with a history of GERD or heartburn [15]. <span>A similar observation was made in a case-control study that assessed the presence of GERD symptoms and frequency of COPD exacerbations in 80 patients with COPD. The presence of GERD symptoms was associated with an increased risk of COPD exacerbations (RR 6.55, 95% CI 1.86-23.11) [18]. However, in an observational study of 638 patients with stable COPD, therapy with proton pump inhibitors did not decrease the risk for severe exacerbations [20]. Additional studies are needed to determine whether GERD contributes to the development of COPD exacerbations. ●Left ventricular diastolic dysfunction – Left ventricular diastolic dysfun




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Gastroesophageal reflux disease (GERD) may be an additional risk factor for COPD exacerbations [18,19].
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re discussed in more detail separately. (See "Chronic obstructive pulmonary disease: Diagnosis and staging", section on 'Assessment of severity and staging'.) ●Gastroesophageal reflux disease – <span>Gastroesophageal reflux disease (GERD) may be an additional risk factor for COPD exacerbations [18,19]. In the ECLIPSE study noted above, the occurrence of two or more exacerbations in a year was associated with a history of GERD or heartburn [15]. A similar observation was made in a case




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Left ventricular diastolic dysfunction at baseline is associated with a higher frequency of hospitalization for COPD exacerbation [21]. Diastolic dysfunction is common in patients with COPD, likely due to both comorbid vascular mechanisms (eg, hypertension, coronary artery disease, systemic inflammation) as well as metabolic and structural consequences of COPD (eg, lung hyperinflation, chronic hypoxia, and hypercapnia) [22,23]. Many of these contributing factors worsen during an exacerbation and may lead to diastolic decompensation, followed by pulmonary congestion and bronchial hyper-reactivity [24]. High heart rates, whether due to breathlessness, anxiety, or atrial arrhythmias, further exacerbate this pathophysiology.
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e the risk for severe exacerbations [20]. Additional studies are needed to determine whether GERD contributes to the development of COPD exacerbations. ●Left ventricular diastolic dysfunction – <span>Left ventricular diastolic dysfunction at baseline is associated with a higher frequency of hospitalization for COPD exacerbation [21]. Diastolic dysfunction is common in patients with COPD, likely due to both comorbid vascular mechanisms (eg, hypertension, coronary artery disease, systemic inflammation) as well as metabolic and structural consequences of COPD (eg, lung hyperinflation, chronic hypoxia, and hypercapnia) [22,23]. Many of these contributing factors worsen during an exacerbation and may lead to diastolic decompensation, followed by pulmonary congestion and bronchial hyper-reactivity [24]. High heart rates, whether due to breathlessness, anxiety, or atrial arrhythmias, further exacerbate this pathophysiology. ●Pulmonary hypertension – Secondary pulmonary hypertension may be an additional risk factor for COPD exacerbations, possibly as an indicator of disease severity. In a follow-up to the E




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Secondary pulmonary hypertension may be an additional risk factor for COPD exacerbations, possibly as an indicator of disease severity. In a follow-up to the ECLIPSE study, chest computed tomography scans were used to compute the ratio of the diameter of the pulmonary artery to the diameter of the aorta (PA:A ratio) [25]. In the study, a PA:A ratio greater than 1 was an independent risk factor for a future severe exacerbation (OR 3.44, 95% CI 2.78-4.25). Notably, a PA:A ratio >1 suggests the presence of pulmonary hypertension, although it does not clarify the cause of pulmonary hypertension (eg, hypoxemia due to COPD or other lung disease, left heart failure, sleep apnea). The clinical usefulness of this observation in terms of treatment decisions is unclear.
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ngestion and bronchial hyper-reactivity [24]. High heart rates, whether due to breathlessness, anxiety, or atrial arrhythmias, further exacerbate this pathophysiology. ●Pulmonary hypertension – <span>Secondary pulmonary hypertension may be an additional risk factor for COPD exacerbations, possibly as an indicator of disease severity. In a follow-up to the ECLIPSE study, chest computed tomography scans were used to compute the ratio of the diameter of the pulmonary artery to the diameter of the aorta (PA:A ratio) [25]. In the study, a PA:A ratio greater than 1 was an independent risk factor for a future severe exacerbation (OR 3.44, 95% CI 2.78-4.25). Notably, a PA:A ratio >1 suggests the presence of pulmonary hypertension, although it does not clarify the cause of pulmonary hypertension (eg, hypoxemia due to COPD or other lung disease, left heart failure, sleep apnea). The clinical usefulness of this observation in terms of treatment decisions is unclear. Triggers — Respiratory infections, most commonly viral (eg, rhinovirus) or bacterial, are estimated to trigger approximately 70 percent of COPD exacerbations (table 2) [1,26]; atypical




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Triggers — Respiratory infections, most commonly viral (eg, rhinovirus) or bacterial, are estimated to trigger approximately 70 percent of COPD exacerbations (table 2) [1,26]; atypical bacteria are a relatively uncommon cause [27,28]. The remaining 30 percent are due to environmental pollution, pulmonary embolism, or have an unknown etiology [1,29-31].
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ulmonary hypertension (eg, hypoxemia due to COPD or other lung disease, left heart failure, sleep apnea). The clinical usefulness of this observation in terms of treatment decisions is unclear. <span>Triggers — Respiratory infections, most commonly viral (eg, rhinovirus) or bacterial, are estimated to trigger approximately 70 percent of COPD exacerbations (table 2) [1,26]; atypical bacteria are a relatively uncommon cause [27,28]. The remaining 30 percent are due to environmental pollution, pulmonary embolism, or have an unknown etiology [1,29-31]. (See "Management of infection in exacerbations of chronic obstructive pulmonary disease".) COPD exacerbations have been associated with exposure to poor outdoor air quality, such as hig




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COPD exacerbations have been associated with exposure to poor outdoor air quality, such as higher levels of ozone, carbon monoxide, particulate matter (up to 10 microns), and nitrogen dioxide [32,33]. Increased ambient levels of fine particulate matter (≤2.5 microns, aka PM2.5) are associated with an increase in hospitalization and mortality in COPD [34]. In a trial of 116 patients with COPD and exposure to poor air quality at home (PM2.5 >10 mcg/m3), use of indoor air filters versus sham air filters resulted in a dose-dependent improvement in respiratory symptoms and risk of moderate exacerbations [35].
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percent are due to environmental pollution, pulmonary embolism, or have an unknown etiology [1,29-31]. (See "Management of infection in exacerbations of chronic obstructive pulmonary disease".) <span>COPD exacerbations have been associated with exposure to poor outdoor air quality, such as higher levels of ozone, carbon monoxide, particulate matter (up to 10 microns), and nitrogen dioxide [32,33]. Increased ambient levels of fine particulate matter (≤2.5 microns, aka PM2.5) are associated with an increase in hospitalization and mortality in COPD [34]. In a trial of 116 patients with COPD and exposure to poor air quality at home (PM2.5 >10 mcg/m3), use of indoor air filters versus sham air filters resulted in a dose-dependent improvement in respiratory symptoms and risk of moderate exacerbations [35]. As dyspnea and cough are nonspecific symptoms, COPD exacerbations of unknown etiology may be triggered or caused by other medical conditions, such as myocardial ischemia, heart failure,




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As dyspnea and cough are nonspecific symptoms, COPD exacerbations of unknown etiology may be triggered or caused by other medical conditions, such as myocardial ischemia, heart failure, aspiration, or pulmonary embolism [1,36].
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uality at home (PM2.5 >10 mcg/m3), use of indoor air filters versus sham air filters resulted in a dose-dependent improvement in respiratory symptoms and risk of moderate exacerbations [35]. <span>As dyspnea and cough are nonspecific symptoms, COPD exacerbations of unknown etiology may be triggered or caused by other medical conditions, such as myocardial ischemia, heart failure, aspiration, or pulmonary embolism [1,36]. The relationship between COPD exacerbation and pulmonary embolism is illustrated by a prospective multicenter study of 1580 patients with COPD who were admitted to the hospital with acu




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Although the frequency of pulmonary embolism among patients hospitalized with an exacerbation of COPD varies across studies [38-41], a systematic review prior to this multicenter study showed a similar pooled prevalence of 23 percent when all patients were evaluated by CTPA within 48 hours of hospital admission (seven studies, 999 patients) [42]. An important limitation of these studies is their inability to determine whether the pulmonary embolism is the cause of the COPD exacerbation, a result of the COPD exacerbation, or a mere bystander.
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ary arteries (CTPA); 166 patients (11 percent) had pulmonary embolism involving the main or lobar pulmonary arteries. The presence of new purulent sputum reduced the odds of pulmonary embolism. <span>Although the frequency of pulmonary embolism among patients hospitalized with an exacerbation of COPD varies across studies [38-41], a systematic review prior to this multicenter study showed a similar pooled prevalence of 23 percent when all patients were evaluated by CTPA within 48 hours of hospital admission (seven studies, 999 patients) [42]. An important limitation of these studies is their inability to determine whether the pulmonary embolism is the cause of the COPD exacerbation, a result of the COPD exacerbation, or a mere bystander. CLINICAL MANIFESTATIONS — The clinical manifestations of exacerbations of COPD range from a mild increase in dyspnea, cough that is productive or nonproductive to respiratory failure wi




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The clinical manifestations of exacerbations of COPD range from a mild increase in dyspnea, cough that is productive or nonproductive to respiratory failure with acute respiratory acidosis and/or hypoxemia.
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e studies is their inability to determine whether the pulmonary embolism is the cause of the COPD exacerbation, a result of the COPD exacerbation, or a mere bystander. CLINICAL MANIFESTATIONS — <span>The clinical manifestations of exacerbations of COPD range from a mild increase in dyspnea, cough that is productive or nonproductive to respiratory failure with acute respiratory acidosis and/or hypoxemia. Medical history — By definition, patients present with the acute onset or worsening of respiratory symptoms, such as dyspnea, cough, and/or sputum production, over several hours to days




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Medical history — By definition, patients present with the acute onset or worsening of respiratory symptoms, such as dyspnea, cough, and/or sputum production, over several hours to days [1,43]. These symptoms should be characterized further in terms of the following features:

● Time course of the symptoms

● Comparison to baseline level of symptoms

● Severity of respiratory compromise (eg, dyspnea at rest, dyspnea climbing stairs, dyspnea severity using a visual analog [1-10] scale)

● Delineation of sputum characteristics (eg, amount, color, purulence, blood)

● Use of home oxygen now or in the past

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manifestations of exacerbations of COPD range from a mild increase in dyspnea, cough that is productive or nonproductive to respiratory failure with acute respiratory acidosis and/or hypoxemia. <span>Medical history — By definition, patients present with the acute onset or worsening of respiratory symptoms, such as dyspnea, cough, and/or sputum production, over several hours to days [1,43]. These symptoms should be characterized further in terms of the following features: ●Time course of the symptoms ●Comparison to baseline level of symptoms ●Severity of respiratory compromise (eg, dyspnea at rest, dyspnea climbing stairs, dyspnea severity using a visual analog [1-10] scale) ●Delineation of sputum characteristics (eg, amount, color, purulence, blood) ●Use of home oxygen now or in the past Associated features that might suggest an alternate diagnosis or comorbidity include: ●Constitutional symptoms (eg, fever, chills, night sweats) ●Chest pain, chest pressure, peripheral




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Associated features that might suggest an alternate diagnosis or comorbidity include:

● Constitutional symptoms (eg, fever, chills, night sweats)

● Chest pain, chest pressure, peripheral edema, or palpitations

● Risk factors for coronary disease

● Risk factors for thromboembolic disease

● Upper respiratory symptoms that might suggest a viral respiratory infection or exposure to anyone with influenza

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dyspnea climbing stairs, dyspnea severity using a visual analog [1-10] scale) ●Delineation of sputum characteristics (eg, amount, color, purulence, blood) ●Use of home oxygen now or in the past <span>Associated features that might suggest an alternate diagnosis or comorbidity include: ●Constitutional symptoms (eg, fever, chills, night sweats) ●Chest pain, chest pressure, peripheral edema, or palpitations ●Risk factors for coronary disease ●Risk factors for thromboembolic disease ●Upper respiratory symptoms that might suggest a viral respiratory infection or exposure to anyone with influenza Patients should be asked if they currently smoke cigarettes or use vaping products. The past history of exacerbations should be ascertained: number of prior exacerbations, courses of sy




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Patients should be asked if they currently smoke cigarettes or use vaping products. The past history of exacerbations should be ascertained: number of prior exacerbations, courses of systemic glucocorticoids, antibiotic therapy in the preceding three months, prior exacerbations requiring hospitalization or ventilatory support, and response to therapy of previous exacerbations.
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ons ●Risk factors for coronary disease ●Risk factors for thromboembolic disease ●Upper respiratory symptoms that might suggest a viral respiratory infection or exposure to anyone with influenza <span>Patients should be asked if they currently smoke cigarettes or use vaping products. The past history of exacerbations should be ascertained: number of prior exacerbations, courses of systemic glucocorticoids, antibiotic therapy in the preceding three months, prior exacerbations requiring hospitalization or ventilatory support, and response to therapy of previous exacerbations. Physical examination — Physical findings associated with an exacerbation of COPD often include wheezing and tachypnea and may include features of respiratory compromise such as difficul




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Attention should also be paid to other physical findings, such as fever, hypotension, bibasilar fine crackles and peripheral edema, which might suggest a comorbidity or alternate diagnosis.
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abdominal motion with respiration). Tachycardia is also frequently present. If present, decreased mental status could reflect hypercapnia or hypoxemia and asterixis could indicate hypercapnia. <span>Attention should also be paid to other physical findings, such as fever, hypotension, bibasilar fine crackles and peripheral edema, which might suggest a comorbidity or alternate diagnosis. EVALUATION AND DIAGNOSIS — The goals of the evaluation of a suspected exacerbation of COPD are to confirm the diagnosis, identify the cause (when possible), assess the severity of respi




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We do not use procalcitonin or C-reactive protein to determine the need for antibiotics in COPD exacerbations, as study results do not clearly and consistently demonstrate that either assay adds value to clinical judgment alone. (See "Evaluation for infection in exacerbations of chronic obstructive pulmonary disease", section on 'Procalcitonin and C-reactive protein'.)
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arbonate (perhaps reflecting compensation for chronic hypercapnia), or the presence of severe airflow obstruction (eg, forced expiratory volume in one second [FEV1] <50 percent of predicted) <span>We do not use procalcitonin or C-reactive protein to determine the need for antibiotics in COPD exacerbations, as study results do not clearly and consistently demonstrate that either assay adds value to clinical judgment alone. (See "Evaluation for infection in exacerbations of chronic obstructive pulmonary disease", section on 'Procalcitonin and C-reactive protein'.) Additional testing — Additional tests are largely used to exclude processes in the differential diagnosis and are obtained depending on the degree of diagnostic uncertainty following cl




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In one multicenter study of nearly 1600 patients hospitalized for COPD exacerbation who were assessed with CT pulmonary angiogram, the rates of pulmonary embolism based on low, moderate, or high probability Wells criteria scores were 7, 38, and 74 percent, respectively [37].
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gnosis for respiratory symptoms. The frequency of pulmonary embolism in patients with COPD and acute respiratory symptoms in the hospital setting appears to be between 15 to 25 percent [37,42]. <span>In one multicenter study of nearly 1600 patients hospitalized for COPD exacerbation who were assessed with CT pulmonary angiogram, the rates of pulmonary embolism based on low, moderate, or high probability Wells criteria scores were 7, 38, and 74 percent, respectively [37]. Purulent sputum production decreased the odds of venous thromboembolism by approximately 60 percent. Given this prevalence rate, we suggest obtaining imaging for pulmonary embolism (typ




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Purulent sputum production decreased the odds of venous thromboembolism by approximately 60 percent.
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n who were assessed with CT pulmonary angiogram, the rates of pulmonary embolism based on low, moderate, or high probability Wells criteria scores were 7, 38, and 74 percent, respectively [37]. <span>Purulent sputum production decreased the odds of venous thromboembolism by approximately 60 percent. Given this prevalence rate, we suggest obtaining imaging for pulmonary embolism (typically CT pulmonary angiogram) in patients with severe symptoms who do not have evidence of other tri




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Given this prevalence rate, we suggest obtaining imaging for pulmonary embolism (typically CT pulmonary angiogram) in patients with severe symptoms who do not have evidence of other triggers (eg, infection or heart failure).
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te, or high probability Wells criteria scores were 7, 38, and 74 percent, respectively [37]. Purulent sputum production decreased the odds of venous thromboembolism by approximately 60 percent. <span>Given this prevalence rate, we suggest obtaining imaging for pulmonary embolism (typically CT pulmonary angiogram) in patients with severe symptoms who do not have evidence of other triggers (eg, infection or heart failure). (See 'Differential diagnosis' below and "Clinical presentation, evaluation, and diagnosis of the nonpregnant adult with suspected acute pulmonary embolism".) ●Sputum Gram stain and cult




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Risk factors for infection with Pseudomonas aeruginosa in patients with acute COPD exacerbations
  • Chronic colonization or previous isolation of Pseudomonas aeruginosa from sputum (particularly in the past 12 months)
  • Very severe COPD (FEV1 <30% predicted)
  • Bronchiectasis on chest imaging
  • Broad-spectrum antibiotic use within the past 3 months
  • Chronic systemic glucocorticoid use
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ile Access Help & Training Demos Wolters Kluwer Health Emmi® Facts & Comparisons® Lexicomp® Medi-Span® Loading Please wait 5 of 6 Export to Powerpoint Print Share Bookmark Rate Feedback <span>Risk factors for infection with Pseudomonas aeruginosa in patients with acute COPD exacerbations Chronic colonization or previous isolation of Pseudomonas aeruginosa from sputum (particularly in the past 12 months) Very severe COPD (FEV1 <30% predicted) Bronchiectasis on chest imaging Broad-spectrum antibiotic use within the past 3 months Chronic systemic glucocorticoid use COPD: chronic obstructive pulmonary disease; FEV1: forced expiratory volume in 1 second. References: Garcia-Vidal C, Almagro P, Romaní V, et al. Pseudomonas aeruginosa in patients hospi




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Sputum Gram stain and culture are not obtained for most exacerbations of COPD. However, sputum Gram stain and culture can be useful in patients at risk for a poor outcome or increased risk of infection with Pseudomonas (table 3 and table 4).
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(eg, infection or heart failure). (See 'Differential diagnosis' below and "Clinical presentation, evaluation, and diagnosis of the nonpregnant adult with suspected acute pulmonary embolism".) ●<span>Sputum Gram stain and culture are not obtained for most exacerbations of COPD. However, sputum Gram stain and culture can be useful in patients at risk for a poor outcome or increased risk of infection with Pseudomonas (table 3 and table 4). Sputum culture may be helpful in patients who are strongly suspected of having a bacterial infection but fail to respond to initial antibiotic therapy. (See "Evaluation for infection in




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Influenza testing is appropriate during influenza season or in patients with features of influenza (eg, acute onset of fever, myalgias, coryza during an influenza outbreak).
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ction but fail to respond to initial antibiotic therapy. (See "Evaluation for infection in exacerbations of chronic obstructive pulmonary disease", section on 'When to obtain sputum studies'.) ●<span>Influenza testing is appropriate during influenza season or in patients with features of influenza (eg, acute onset of fever, myalgias, coryza during an influenza outbreak). Rapid antigen testing and direct or indirect immunofluorescence antibody staining tests are useful screening tests for influenza infection but have limited sensitivity; polymerase chain




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Respiratory virus panel in selected patients – The majority of COPD exacerbations are caused by viral infections, predominantly adenovirus. While not necessary in most patients, PCR diagnostic panels can detect multiple respiratory viruses simultaneously (eg, influenza, adenovirus, parainfluenza virus, respiratory syncytial virus, human metapneumovirus, coronavirus, and rhinovirus). These studies are more frequently obtained in patients with community-acquired pneumonia, and the exact indications for their use in COPD exacerbations are not clear.
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d diagnosis".) ●COVID-19 – Test for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection during the coronavirus disease 2019 (COVID-19) pandemic. (See "COVID-19: Diagnosis".) ●<span>Respiratory virus panel in selected patients – The majority of COPD exacerbations are caused by viral infections, predominantly adenovirus. While not necessary in most patients, PCR diagnostic panels can detect multiple respiratory viruses simultaneously (eg, influenza, adenovirus, parainfluenza virus, respiratory syncytial virus, human metapneumovirus, coronavirus, and rhinovirus). These studies are more frequently obtained in patients with community-acquired pneumonia, and the exact indications for their use in COPD exacerbations are not clear. Severity of exacerbation — The classification of exacerbation severity proposed by an international commission and adopted by the Global Initiative for Chronic Obstructive Lung Disease




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Severity of exacerbation — The classification of exacerbation severity proposed by an international commission and adopted by the Global Initiative for Chronic Obstructive Lung Disease (GOLD) is based on symptoms, vital signs, and arterial blood gas (ABG) and c-reactive protein values (if obtained) (figure 1) [1,17]:

● Mild – Dyspnea <5 on a visual analog (1-10) scale (VAS); respiratory rate <24 breaths per minute; heart rate <95 beats per minute; resting SaO2 ≥92 percent breathing ambient air or the patient's usual oxygen prescription and change in saturation ≤3 percent from baseline (if known); CRP<10 mg/L (if obtained). Treatment with short-acting bronchodilators is often sufficient for mild exacerbations.

● Moderate – Three out of five of the following: Dyspnea ≥5 on VAS; respiratory rate ≥24 breaths per minute, heart rate ≥95 beats per minute; resting SaO2 <92 percent breathing ambient air or the patient's usual oxygen prescription and/or change in saturation >3 percent from baseline (if known); CRP ≥10 mg/L (if obtained). Treatment of moderate exacerbations generally includes short-acting bronchodilators plus antibiotics and/or oral glucocorticoids.

● Severe – Meets moderate criteria combined with hypercapnia and acidosis on ABG (PaCO2 >45 mmHg and pH <7.35). Treatment of severe exacerbations includes short-acting bronchodilators, antibiotics, and oral or intravenous glucocorticoids. Severe exacerbations may be associated with respiratory failure and require noninvasive or invasive ventilation.

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onavirus, and rhinovirus). These studies are more frequently obtained in patients with community-acquired pneumonia, and the exact indications for their use in COPD exacerbations are not clear. <span>Severity of exacerbation — The classification of exacerbation severity proposed by an international commission and adopted by the Global Initiative for Chronic Obstructive Lung Disease (GOLD) is based on symptoms, vital signs, and arterial blood gas (ABG) and c-reactive protein values (if obtained) (figure 1) [1,17]: ●Mild – Dyspnea <5 on a visual analog (1-10) scale (VAS); respiratory rate <24 breaths per minute; heart rate <95 beats per minute; resting SaO2 ≥92 percent breathing ambient air or the patient's usual oxygen prescription and change in saturation ≤3 percent from baseline (if known); CRP<10 mg/L (if obtained). Treatment with short-acting bronchodilators is often sufficient for mild exacerbations. ●Moderate – Three out of five of the following: Dyspnea ≥5 on VAS; respiratory rate ≥24 breaths per minute, heart rate ≥95 beats per minute; resting SaO2 <92 percent breathing ambient air or the patient's usual oxygen prescription and/or change in saturation >3 percent from baseline (if known); CRP ≥10 mg/L (if obtained). Treatment of moderate exacerbations generally includes short-acting bronchodilators plus antibiotics and/or oral glucocorticoids. ●Severe – Meets moderate criteria combined with hypercapnia and acidosis on ABG (PaCO2 >45 mmHg and pH <7.35). Treatment of severe exacerbations includes short-acting bronchodilators, antibiotics, and oral or intravenous glucocorticoids. Severe exacerbations may be associated with respiratory failure and require noninvasive or invasive ventilation. DIFFERENTIAL DIAGNOSIS — Patients with COPD who present to the hospital with acute worsening of dyspnea should be evaluated for potential alternative diagnoses, such as heart failure, c




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Patients with COPD who present to the hospital with acute worsening of dyspnea should be evaluated for potential alternative diagnoses, such as heart failure, cardiac arrhythmia, pneumonia, pulmonary embolism, and pneumothorax [1,44,45].
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, antibiotics, and oral or intravenous glucocorticoids. Severe exacerbations may be associated with respiratory failure and require noninvasive or invasive ventilation. DIFFERENTIAL DIAGNOSIS — <span>Patients with COPD who present to the hospital with acute worsening of dyspnea should be evaluated for potential alternative diagnoses, such as heart failure, cardiac arrhythmia, pneumonia, pulmonary embolism, and pneumothorax [1,44,45]. A chest radiograph will differentiate among several of these possibilities (eg, heart failure, pneumonia, pneumothorax); a clear chest radiograph may be a clue to pulmonary embolism, es




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A chest radiograph will differentiate among several of these possibilities (eg, heart failure, pneumonia, pneumothorax); a clear chest radiograph may be a clue to pulmonary embolism, especially when dyspnea and hypoxemia are more prominent than cough or sputum production.
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al with acute worsening of dyspnea should be evaluated for potential alternative diagnoses, such as heart failure, cardiac arrhythmia, pneumonia, pulmonary embolism, and pneumothorax [1,44,45]. <span>A chest radiograph will differentiate among several of these possibilities (eg, heart failure, pneumonia, pneumothorax); a clear chest radiograph may be a clue to pulmonary embolism, especially when dyspnea and hypoxemia are more prominent than cough or sputum production. The importance of considering these alternate diagnoses was illustrated in an autopsy study of 43 patients with COPD who died within 24 hours of admission for a COPD exacerbation [44].




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The importance of considering these alternate diagnoses was illustrated in an autopsy study of 43 patients with COPD who died within 24 hours of admission for a COPD exacerbation [44]. The primary causes of death were heart failure, pneumonia, pulmonary thromboembolism, and COPD in 37, 28, 21, and 14 percent, respectively.
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heart failure, pneumonia, pneumothorax); a clear chest radiograph may be a clue to pulmonary embolism, especially when dyspnea and hypoxemia are more prominent than cough or sputum production. <span>The importance of considering these alternate diagnoses was illustrated in an autopsy study of 43 patients with COPD who died within 24 hours of admission for a COPD exacerbation [44]. The primary causes of death were heart failure, pneumonia, pulmonary thromboembolism, and COPD in 37, 28, 21, and 14 percent, respectively. ●Heart failure – Acute decompensated heart failure (ADHF) is characterized by the development of acute dyspnea associated with elevated intracardiac filling pressures with or without pu




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Cardiac arrhythmias – Cardiac arrhythmias, such as atrial fibrillation, are frequent in patients with COPD, and may be a trigger or consequence of COPD exacerbation [1]. A bedside electrocardiogram can be diagnostic.
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t radiograph, echocardiogram) are often supportive, the diagnosis cannot be based on a single test. (See "Approach to diagnosis and evaluation of acute decompensated heart failure in adults".) ●<span>Cardiac arrhythmias – Cardiac arrhythmias, such as atrial fibrillation, are frequent in patients with COPD, and may be a trigger or consequence of COPD exacerbation [1]. A bedside electrocardiogram can be diagnostic. (See "Atrial fibrillation: Overview and management of new-onset atrial fibrillation".) ●Pneumonia – Pneumonia can present with acute shortness of breath, hypoxemia, and an inconclusive




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Pneumothorax – COPD is a risk factor for pneumothorax. Worsening dyspnea can be due to either a COPD exacerbation or pneumothorax, but acute pleuritic chest pain would be more suggestive of pneumothorax while increased volume of sputum and sputum purulence would suggest a COPD exacerbation.
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ribution is not present with pneumonia. Fever and leukocytosis may suggest an infectious process. (See "Clinical evaluation and diagnostic testing for community-acquired pneumonia in adults".) ●<span>Pneumothorax – COPD is a risk factor for pneumothorax. Worsening dyspnea can be due to either a COPD exacerbation or pneumothorax, but acute pleuritic chest pain would be more suggestive of pneumothorax while increased volume of sputum and sputum purulence would suggest a COPD exacerbation. A pneumothorax is usually apparent on conventional chest radiograph or thoracic ultrasound, although bullous emphysema can mimic a pneumothorax and necessitate a chest computed tomograp




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Pulmonary embolism – The sudden onset of symptoms such as dyspnea, pleuritic chest pain, tachypnea, and cough may be caused by a pulmonary embolism. The suspicion for pulmonary embolism rises in the absence of purulent sputum production, history of an upper respiratory infection, or pneumothorax [36-42,46,47].
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und, although bullous emphysema can mimic a pneumothorax and necessitate a chest computed tomography (CT) scan for differentiation. (See "Clinical presentation and diagnosis of pneumothorax".) ●<span>Pulmonary embolism – The sudden onset of symptoms such as dyspnea, pleuritic chest pain, tachypnea, and cough may be caused by a pulmonary embolism. The suspicion for pulmonary embolism rises in the absence of purulent sputum production, history of an upper respiratory infection, or pneumothorax [36-42,46,47]. (See 'Triggers' above and 'Additional testing' above.) Testing may include a blood D-dimer test, lower extremity compression ultrasonography with Doppler, and CT pulmonary angiogram. (S




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Examination of the language of dyspnea suggests that this symptom represents a number of qualitatively distinct sensations, and that the words utilized by patients to describe their breathing discomfort may provide insight into the underlying pathophysiology of the disease.
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illions of patients with pulmonary disease and may be the primary manifestation of lung disease, myocardial ischemia or dysfunction, anemia, neuromuscular disorders, obesity, or deconditioning. <span>Examination of the language of dyspnea suggests that this symptom represents a number of qualitatively distinct sensations, and that the words utilized by patients to describe their breathing discomfort may provide insight into the underlying pathophysiology of the disease. The key elements in the evaluation of the patient with dyspnea will be reviewed here. The basic physiology of dyspnea, the evaluation of acute dyspnea, and dyspnea in pregnancy are disc




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Dyspnea is a term used to characterize a subjective experience of breathing discomfort that is comprised of qualitatively distinct sensations that vary in intensity. The experience derives from interactions among multiple physiological, psychological, social, and environmental factors, and may induce secondary physiological and behavioral responses.
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ions to pregnancy: Dyspnea and other physiologic respiratory changes".) DEFINITION OF DYSPNEA — A consensus statement of the American Thoracic Society defines dyspnea in the following way [1]: "<span>Dyspnea is a term used to characterize a subjective experience of breathing discomfort that is comprised of qualitatively distinct sensations that vary in intensity. The experience derives from interactions among multiple physiological, psychological, social, and environmental factors, and may induce secondary physiological and behavioral responses." Dyspnea is considered acute when it develops over hours to days and chronic when it occurs for more than four to eight weeks. Some patients present with acute worsening of chronic brea




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Dyspnea is considered acute when it develops over hours to days and chronic when it occurs for more than four to eight weeks
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nsity. The experience derives from interactions among multiple physiological, psychological, social, and environmental factors, and may induce secondary physiological and behavioral responses." <span>Dyspnea is considered acute when it develops over hours to days and chronic when it occurs for more than four to eight weeks. Some patients present with acute worsening of chronic breathlessness that may be caused by a new problem or a worsening of the underlying disease (eg, asthma, chronic obstructive pulmo




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Respiratory system dyspnea includes discomfort related to disorders of the central controller, the ventilatory pump, and the gas exchanger (table 1), while cardiovascular system dyspnea includes cardiac diseases (eg, acute ischemia, systolic dysfunction, valvular disorders, pericardial diseases), as well as anemia and deconditioning; the latter two lead to dyspnea via altered delivery and/or utilization of oxygen (figure 1).
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at www.thoracic.org/statements. PATHOPHYSIOLOGY — Most patients with breathing discomfort can be categorized into one of two groups: respiratory system dyspnea or cardiovascular system dyspnea. <span>Respiratory system dyspnea includes discomfort related to disorders of the central controller, the ventilatory pump, and the gas exchanger (table 1), while cardiovascular system dyspnea includes cardiac diseases (eg, acute ischemia, systolic dysfunction, valvular disorders, pericardial diseases), as well as anemia and deconditioning; the latter two lead to dyspnea via altered delivery and/or utilization of oxygen (figure 1). More than one process may be active in a given patient, and the basic physiology of dyspnea does not always adhere to this structure; for example, stimulation of pulmonary receptors can




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The "respiratory controller" determines the rate and depth of breathing via efferent signals sent to the ventilatory muscles. Factors that stimulate the respiratory centers in the brainstem lead to increased ventilation and breathing discomfort in a variety of settings; these often are secondary to derangements in other parts of the system, such as hypoxia or hypercapnia due to ventilation/perfusion mismatching in the gas exchanger, or stimulation of pulmonary receptors as occurs with interstitial inflammation or edema.
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he lungs by bulk transport to the atmosphere. Several components must be functioning smoothly for this process to occur; derangements in any of these elements can lead to dyspnea. ●Controller – <span>The "respiratory controller" determines the rate and depth of breathing via efferent signals sent to the ventilatory muscles. Factors that stimulate the respiratory centers in the brainstem lead to increased ventilation and breathing discomfort in a variety of settings; these often are secondary to derangements in other parts of the system, such as hypoxia or hypercapnia due to ventilation/perfusion mismatching in the gas exchanger, or stimulation of pulmonary receptors as occurs with interstitial inflammation or edema. In addition, drugs such as aspirin (at a toxic dose) or progesterone and conditions such as pregnancy or diabetic ketoacidosis can produce dyspnea through central effects independent of




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In addition, drugs such as aspirin (at a toxic dose) or progesterone and conditions such as pregnancy or diabetic ketoacidosis can produce dyspnea through central effects independent of problems in the ventilatory pump or gas exchanger. Typically, dyspnea associated with stimulation of the respiratory controller is described as a sensation of "air hunger" or an "urge or need to breathe" [2-4].
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he system, such as hypoxia or hypercapnia due to ventilation/perfusion mismatching in the gas exchanger, or stimulation of pulmonary receptors as occurs with interstitial inflammation or edema. <span>In addition, drugs such as aspirin (at a toxic dose) or progesterone and conditions such as pregnancy or diabetic ketoacidosis can produce dyspnea through central effects independent of problems in the ventilatory pump or gas exchanger. Typically, dyspnea associated with stimulation of the respiratory controller is described as a sensation of "air hunger" or an "urge or need to breathe" [2-4]. (See "Control of ventilation" and "Physiology of dyspnea".) To some degree, the breathing pattern may also reflect what are presumed to be attempts by the controller to reduce breathing




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To some degree, the breathing pattern may also reflect what are presumed to be attempts by the controller to reduce breathing discomfort. Thus, patients with severe airflow obstruction generally adapt a relatively slow, deep breathing pattern to minimize the pleural pressures needed to overcome airways resistance to generate adequate flow. Alternatively, patients with interstitial fibrosis or kyphoscoliosis and reduced lung or chest wall compliance have a characteristic rapid, shallow breathing pattern which minimizes the work needed to expand the thorax.
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ted with stimulation of the respiratory controller is described as a sensation of "air hunger" or an "urge or need to breathe" [2-4]. (See "Control of ventilation" and "Physiology of dyspnea".) <span>To some degree, the breathing pattern may also reflect what are presumed to be attempts by the controller to reduce breathing discomfort. Thus, patients with severe airflow obstruction generally adapt a relatively slow, deep breathing pattern to minimize the pleural pressures needed to overcome airways resistance to generate adequate flow. Alternatively, patients with interstitial fibrosis or kyphoscoliosis and reduced lung or chest wall compliance have a characteristic rapid, shallow breathing pattern which minimizes the work needed to expand the thorax. When the respiratory controller is stimulated (eg, by exercise), airflow obstruction may heighten the sensation of air hunger. The increase in respiratory rate during exercise in the se




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When the respiratory controller is stimulated (eg, by exercise), airflow obstruction may heighten the sensation of air hunger. The increase in respiratory rate during exercise in the setting of expiratory flow limitation can lead to exercise-induced air-trapping, a process known as dynamic hyperinflation.
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th interstitial fibrosis or kyphoscoliosis and reduced lung or chest wall compliance have a characteristic rapid, shallow breathing pattern which minimizes the work needed to expand the thorax. <span>When the respiratory controller is stimulated (eg, by exercise), airflow obstruction may heighten the sensation of air hunger. The increase in respiratory rate during exercise in the setting of expiratory flow limitation can lead to exercise-induced air-trapping, a process known as dynamic hyperinflation. Dynamic hyperinflation is associated with a reduced inspiratory reserve and increased dyspnea. For those in whom hyperinflation is substantial, such that inspiratory capacity at rest or




Flashcard 7606795373836

Question
In welche sieben Ebenen kann man ein Rechnersystem einteilen?
  1. Anwendungsebene (Anwendersoftware)
  2. [...]
  3. Betriebssystem (Speichermanagment, Prozesskommunikation)
  4. Instruction Set Architecture (ISA,Adressierungsarten)
  5. Microarchitektur (Risc,Cisc,Branch Prediction..)
  6. Logische Ebene (Register,Schieber, Latches..)
  7. Transistorebene (Transistoren, MOS )
Answer
Assemblerebene (Beschreibung von Algorithmen, Link & Bind)

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In welche sieben Ebenen kann man ein Rechnersystem einteilen? Anwendungsebene (Anwendersoftware) Assemblerebene (Beschreibung von Algorithmen, Link & Bind) Betriebssystem (Speichermanagment, Prozesskommunikation) Instruction Set Architecture (ISA,Adressierungsarten) Microarchitektur (Risc,Cisc,Branch Prediction..) Logische Ebene (Register,

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Grundprinzipien der Rechnerarchitektur
- Parallelrechner Zurück zur Übersicht Rechnerarchitektur Grundprinzipien der Rechnerarchitektur. D.h. Themen wie RISC, Branch Prediction oder Tomasulo. Kapitel 1 - Prinzipien und Architekturen <span>In welche sieben Ebenen kann man ein Rechnersystem einteilen? Anwendungsebene (Anwendersoftware) Assemblerebene (Beschreibung von Algorithmen, Link & Bind) Betriebssystem (Speichermanagment, Prozesskommunikation) Instruction Set Architecture (ISA,Adressierungsarten) Microarchitektur (Risc,Cisc,Branch Prediction..) Logische Ebene (Register,Schieber, Latches..) Transistorebene (Transistoren, MOS ) nach Tanenbaum Computerarchitektur Wie lassen sich Architekturen klassifizieren? Nach ihrem Rechenprinzip Von Neumann (Steuerfluss) Datenfluß (Zündregel) Reduktion (Funktionsaufruf) Obj







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For patients with restrictive lung disease, the adoption of breathing patterns with either an increase or decrease in tidal volume from their average resting tidal volume results in increased dyspnea [5]. Breathing with a rapid, shallow pattern, the patient experiences an increase in the ratio of dead space to tidal volume (since anatomic dead space is relatively fixed), which leads to a need for greater total ventilation (hence, the increase in respiratory rate); this adds to respiratory work-load and may contribute to the development of hypercapnia. In contrast, an increase in tidal volume requires a significant increase in respiratory work due to the stiffness of the lung. Since most patients with restrictive lung disease tend to use a rapid, shallow breathing pattern, we conclude that this pattern, relative to alternatives, must produce less dyspnea.
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ise is limited by total lung capacity, dyspnea is further exacerbated, and patients may also complain of an inability to get a deep breath. (See "Dynamic hyperinflation in patients with COPD".) <span>For patients with restrictive lung disease, the adoption of breathing patterns with either an increase or decrease in tidal volume from their average resting tidal volume results in increased dyspnea [5]. Breathing with a rapid, shallow pattern, the patient experiences an increase in the ratio of dead space to tidal volume (since anatomic dead space is relatively fixed), which leads to a need for greater total ventilation (hence, the increase in respiratory rate); this adds to respiratory work-load and may contribute to the development of hypercapnia. In contrast, an increase in tidal volume requires a significant increase in respiratory work due to the stiffness of the lung. Since most patients with restrictive lung disease tend to use a rapid, shallow breathing pattern, we conclude that this pattern, relative to alternatives, must produce less dyspnea. ●Ventilatory pump – The "ventilatory pump" comprises the ventilatory muscles, the peripheral nerves which transmit signals to them from the controller, the bones of the chest wall which




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The most common derangements of the ventilatory pump result in a sense of increased "work of breathing" [6-10].
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hich transforms movement of the chest wall to negative pressure inside the thorax, and the airways that serve as a conduit for the flow of gas from the atmosphere to the alveoli and back again. <span>The most common derangements of the ventilatory pump result in a sense of increased "work of breathing" [6-10]. Neuromuscular weakness (eg, myasthenia gravis, Guillain-Barré syndrome) leads to a condition in which the patient must exert near maximal inspiratory effort to produce a normal negative




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Neuromuscular weakness (eg, myasthenia gravis, Guillain-Barré syndrome) leads to a condition in which the patient must exert near maximal inspiratory effort to produce a normal negative pleural pressure [11].
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a conduit for the flow of gas from the atmosphere to the alveoli and back again. The most common derangements of the ventilatory pump result in a sense of increased "work of breathing" [6-10]. <span>Neuromuscular weakness (eg, myasthenia gravis, Guillain-Barré syndrome) leads to a condition in which the patient must exert near maximal inspiratory effort to produce a normal negative pleural pressure [11]. Patients with reduced compliance of the chest wall (eg, kyphoscoliosis) or lungs (eg, interstitial fibrosis) must perform more work than normal to move air into the lungs. Obstructive l




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When hyperinflation results in an end-inspiratory volume that approximates total lung capacity, patients often complain of an inability to get a deeper satisfying breath [ 9]. A sensation of chest tightness may also be present in patients in whom acute bronchoconstriction is the cause of airflow obstruction [6,7,12,13].
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ncreased resistance to flow and, in patients with significant hyperinflation, reduced compliance as breathing occurs on the stiff portion of the pressure-volume curve of the respiratory system. <span>When hyperinflation results in an end-inspiratory volume that approximates total lung capacity, patients often complain of an inability to get a deeper satisfying breath [9]. A sensation of chest tightness may also be present in patients in whom acute bronchoconstriction is the cause of airflow obstruction [6,7,12,13]. ●Gas exchanger – The "gas exchanger" consists of the alveoli and the pulmonary capillaries across which oxygen and carbon dioxide diffuse. Most of the common cardiopulmonary disorders l




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Most of the common cardiopulmonary disorders leading to dyspnea are associated with some derangement of the gas exchanger due either to destruction of the diffusing membrane (eg, emphysema, pulmonary fibrosis) or the addition of fluid or inflammatory material into the lungs such that ventilation to alveoli is reduced regionally. To a lesser degree, the distance for diffusion may also contribute in these conditions or in the greatly dilated pulmonary capillaries seen in some patients with hepatopulmonary syndrome.
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ction is the cause of airflow obstruction [6,7,12,13]. ●Gas exchanger – The "gas exchanger" consists of the alveoli and the pulmonary capillaries across which oxygen and carbon dioxide diffuse. <span>Most of the common cardiopulmonary disorders leading to dyspnea are associated with some derangement of the gas exchanger due either to destruction of the diffusing membrane (eg, emphysema, pulmonary fibrosis) or the addition of fluid or inflammatory material into the lungs such that ventilation to alveoli is reduced regionally. To a lesser degree, the distance for diffusion may also contribute in these conditions or in the greatly dilated pulmonary capillaries seen in some patients with hepatopulmonary syndrome. Diseases affecting the gas exchanger are typically characterized by hypoxemia, either at rest or with exercise, and by chronic hypercapnia in more severe cases. These gas exchange abnor




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Diseases affecting the gas exchanger are typically characterized by hypoxemia, either at rest or with exercise, and by chronic hypercapnia in more severe cases. These gas exchange abnormalities stimulate the respiratory centers in the brainstem and lead to a sensation of "air hunger" or an increased urge to breathe.
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ally. To a lesser degree, the distance for diffusion may also contribute in these conditions or in the greatly dilated pulmonary capillaries seen in some patients with hepatopulmonary syndrome. <span>Diseases affecting the gas exchanger are typically characterized by hypoxemia, either at rest or with exercise, and by chronic hypercapnia in more severe cases. These gas exchange abnormalities stimulate the respiratory centers in the brainstem and lead to a sensation of "air hunger" or an increased urge to breathe. Cardiovascular — The cardiovascular system is designed to move oxygenated blood from the lungs to metabolically active tissues, and then transport carbon dioxide from the tissues back t




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When heart failure causes an increase in pulmonary venous pressure, it can lead to dyspnea either by producing hypoxemia or by stimulating pulmonary vascular and/or interstitial receptors (eg, unmyelinated J-receptors, also called C-fibers).
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eakness, and dyspnea on exertion) and those due to increased pulmonary or systemic venous pressure and fluid accumulation (dyspnea at rest and exertion, edema, hepatic congestion, and ascites). <span>When heart failure causes an increase in pulmonary venous pressure, it can lead to dyspnea either by producing hypoxemia or by stimulating pulmonary vascular and/or interstitial receptors (eg, unmyelinated J-receptors, also called C-fibers). Causes of heart failure include ventricular systolic dysfunction, ventricular diastolic dysfunction, and valvular disease. Cardiac tamponade may also lead to dyspnea by increasing pulmo




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Deconditioning – Individuals usually complain of respiratory discomfort when they engage in vigorous physical activity, even in the presence of a normal cardiovascular and respiratory system and normal hematocrit. More fit individuals experience less discomfort for any given workload; cardiovascular fitness is determined by the ability of the heart to increase maximal cardiac output and by the ability of the peripheral muscles to utilize oxygen efficiently for aerobic metabolism.
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ac output, which may necessitate elevated left ventricular volume and pulmonary vascular pressures. However, the quality of dyspnea is usually quite different in these two clinical situations. ●<span>Deconditioning – Individuals usually complain of respiratory discomfort when they engage in vigorous physical activity, even in the presence of a normal cardiovascular and respiratory system and normal hematocrit. More fit individuals experience less discomfort for any given workload; cardiovascular fitness is determined by the ability of the heart to increase maximal cardiac output and by the ability of the peripheral muscles to utilize oxygen efficiently for aerobic metabolism. In contrast, a sedentary existence reduces fitness and leads to dyspnea, often with seemingly trivial tasks. It is common for patients with chronic cardiopulmonary disease to assume a s




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Dyspnea due to deconditioning is typically described as "heavy breathing" or a sense of "breathing more" [8], and with careful questioning, one can determine that the patient is actually limited by fatigue or leg discomfort rather than breathing discomfort.
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density in the muscles, and reduced mitochondrial capacity to sustain aerobic metabolism) and ultimately may be limited more by poor cardiovascular fitness than by the underlying disease [16]. <span>Dyspnea due to deconditioning is typically described as "heavy breathing" or a sense of "breathing more" [8], and with careful questioning, one can determine that the patient is actually limited by fatigue or leg discomfort rather than breathing discomfort. A pathologic variant of this phenomenon has been reported in a subset of patients with post-COVID-19 infections and persistent dyspnea. Cardiopulmonary exercise testing has demonstrated




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While clinical history is often insufficient to make a secure diagnosis, it provides guidance in narrowing the diagnostic possibilities and selecting diagnostic tests. In one study of 85 patients presenting to a pulmonary unit with a complaint of chronic dyspnea, the initial impression of the etiology of dyspnea based upon the patient history alone was correct in 66 percent of cases [19].
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oxygen to support aerobic metabolism [17,18]. (See "Cardiopulmonary exercise testing in the evaluation of unexplained dyspnea", section on 'Peripheral causes of dyspnea'.) CLINICAL ASSESSMENT — <span>While clinical history is often insufficient to make a secure diagnosis, it provides guidance in narrowing the diagnostic possibilities and selecting diagnostic tests. In one study of 85 patients presenting to a pulmonary unit with a complaint of chronic dyspnea, the initial impression of the etiology of dyspnea based upon the patient history alone was correct in 66 percent of cases [19]. Thus, a systematic diagnostic approach to history-taking can be extremely helpful. Temporal pattern and triggers — The temporal pattern of breathlessness and association with certain tr




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The temporal pattern of breathlessness and association with certain triggers can provide important clues. Breathing discomfort arising over the course of minutes to hours is due to a relatively limited number of conditions (table 2).
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based upon the patient history alone was correct in 66 percent of cases [19]. Thus, a systematic diagnostic approach to history-taking can be extremely helpful. Temporal pattern and triggers — <span>The temporal pattern of breathlessness and association with certain triggers can provide important clues. Breathing discomfort arising over the course of minutes to hours is due to a relatively limited number of conditions (table 2). These entities typically have associated symptoms and signs that provide clues to the appropriate diagnosis, eg, substernal chest pain with cardiac ischemia; fever, cough, and sputum wi




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Causes of acute dyspnea
Cardiovascular system
Acute myocardial ischemia
Heart failure
Cardiac tamponade
Respiratory system
Bronchospasm
Pulmonary embolism
Pneumothorax
Pulmonary infection - bronchitis, pneumonia
Upper airway obstruction - aspiration, anaphylaxis
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Mobile Access Help & Training Demos Wolters Kluwer Health Emmi® Facts & Comparisons® Lexicomp® Medi-Span® Loading Please wait 2 of 13 Export to Powerpoint Print Share Bookmark Feedback <span>Causes of acute dyspnea Cardiovascular system Acute myocardial ischemia Heart failure Cardiac tamponade Respiratory system Bronchospasm Pulmonary embolism Pneumothorax Pulmonary infection - bronchitis, pneumonia Upper airway obstruction - aspiration, anaphylaxis Causes_of_acute_dyspnea.htm Graphic 82700 Version 1.0 © 2023 UpToDate, Inc. and/or its affiliates. All Rights Reserved. Cardiovascular system Acute myocardial ischemia Heart failure Car




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Chronic exertional dyspnea and paroxysmal nocturnal dyspnea (PND) are both associated with heart failure, although nocturnal dyspnea is more specific to heart failure. Asthma is also associated with exertional and nocturnal dyspnea, but unlike PND does not usually improve with sitting or standing
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is are important. The approach to acute dyspnea is described separately. (See "Approach to the adult with dyspnea in the emergency department".) ●Exertional, positional, and nocturnal dyspnea – <span>Chronic exertional dyspnea and paroxysmal nocturnal dyspnea (PND) are both associated with heart failure, although nocturnal dyspnea is more specific to heart failure. Asthma is also associated with exertional and nocturnal dyspnea, but unlike PND does not usually improve with sitting or standing. Orthopnea, the development of or worsening of dyspnea in the supine position, is also associated with heart failure and increased pulmonary capillary pressure due to the increased veno




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Orthopnea, the development of or worsening of dyspnea in the supine position, is also associated with heart failure and increased pulmonary capillary pressure due to the increased venous return to the heart in this position. Central obesity, however, with a large protuberant abdomen, may also lead to orthopnea; increased intra-abdominal pressure associated with large abdominal girth impairs movement of the diaphragm during inhalation; in addition, intrapleural pressure increases, which may lead to narrowing or closure of small airways at the bases of the lungs, and can worsen gas exchange and hypoxemia. Finally, patients with inspiratory muscle weakness may also complain of orthopnea due to the increased work of breathing associated with moving the diaphragm against high intra-abdominal pressure.
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although nocturnal dyspnea is more specific to heart failure. Asthma is also associated with exertional and nocturnal dyspnea, but unlike PND does not usually improve with sitting or standing. <span>Orthopnea, the development of or worsening of dyspnea in the supine position, is also associated with heart failure and increased pulmonary capillary pressure due to the increased venous return to the heart in this position. Central obesity, however, with a large protuberant abdomen, may also lead to orthopnea; increased intra-abdominal pressure associated with large abdominal girth impairs movement of the diaphragm during inhalation; in addition, intrapleural pressure increases, which may lead to narrowing or closure of small airways at the bases of the lungs, and can worsen gas exchange and hypoxemia. Finally, patients with inspiratory muscle weakness may also complain of orthopnea due to the increased work of breathing associated with moving the diaphragm against high intra-abdominal pressure. Bendopnea, the worsening of dyspnea when leaning forward, is described in patients with decompensated heart failure [20] but may also be seen in patients with central obesity, particula




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Bendopnea, the worsening of dyspnea when leaning forward, is described in patients with decompensated heart failure [20] but may also be seen in patients with central obesity, particularly when the patient attempts to tie their shoes from the sitting position.
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ally, patients with inspiratory muscle weakness may also complain of orthopnea due to the increased work of breathing associated with moving the diaphragm against high intra-abdominal pressure. <span>Bendopnea, the worsening of dyspnea when leaning forward, is described in patients with decompensated heart failure [20] but may also be seen in patients with central obesity, particularly when the patient attempts to tie their shoes from the sitting position. Dyspnea that is not exacerbated by exertion is more often due to a functional or perceptual problem than to cardiopulmonary disease. ●Intermittent dyspnea – Intermittent dyspnea associa




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Dyspnea that is not exacerbated by exertion is more often due to a functional or perceptual problem than to cardiopulmonary disease.
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bed in patients with decompensated heart failure [20] but may also be seen in patients with central obesity, particularly when the patient attempts to tie their shoes from the sitting position. <span>Dyspnea that is not exacerbated by exertion is more often due to a functional or perceptual problem than to cardiopulmonary disease. ●Intermittent dyspnea – Intermittent dyspnea associated with cold air or animal dander exposure suggests asthma; work-related dyspnea may suggest occupational asthma; and dyspnea follow




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Intermittent dyspnea – Intermittent dyspnea associated with cold air or animal dander exposure suggests asthma; work-related dyspnea may suggest occupational asthma; and dyspnea following upper respiratory infections may be due to asthma or chronic obstructive pulmonary disease (COPD).
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ient attempts to tie their shoes from the sitting position. Dyspnea that is not exacerbated by exertion is more often due to a functional or perceptual problem than to cardiopulmonary disease. ●<span>Intermittent dyspnea – Intermittent dyspnea associated with cold air or animal dander exposure suggests asthma; work-related dyspnea may suggest occupational asthma; and dyspnea following upper respiratory infections may be due to asthma or chronic obstructive pulmonary disease (COPD). In addition to asthma, intermittent symptoms that resolve completely between episodes can be seen with recurrent aspiration; recurrent pulmonary emboli and heart failure can also wax an




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In addition to asthma, intermittent symptoms that resolve completely between episodes can be seen with recurrent aspiration; recurrent pulmonary emboli and heart failure can also wax and wane, but generally are characterized by a baseline level of dysfunction. The presence of specific, reproducible inciting events such as exercise or cold air exposure is common with airways hyperreactivity.
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e suggests asthma; work-related dyspnea may suggest occupational asthma; and dyspnea following upper respiratory infections may be due to asthma or chronic obstructive pulmonary disease (COPD). <span>In addition to asthma, intermittent symptoms that resolve completely between episodes can be seen with recurrent aspiration; recurrent pulmonary emboli and heart failure can also wax and wane, but generally are characterized by a baseline level of dysfunction. The presence of specific, reproducible inciting events such as exercise or cold air exposure is common with airways hyperreactivity. ●Rapidity of symptom onset and progression – The rapidity with which symptoms develop during exercise can also provide useful diagnostic information. For example, patients who develop s




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The rapidity with which symptoms develop during exercise can also provide useful diagnostic information. For example, patients who develop shortness of breath and wheezing after walking 50 to 100 feet often have acute elevations in pulmonary capillary wedge pressure (usually due to cardiac diastolic dysfunction) or pulmonary hypertension. In contrast, symptoms of exercise-induced asthma usually are precipitated by more intense activity, beginning three minutes into exercise, peaking within 10 to 15 minutes, and resolving by 60 minutes. (See "Exercise-induced bronchoconstriction".)
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of dysfunction. The presence of specific, reproducible inciting events such as exercise or cold air exposure is common with airways hyperreactivity. ●Rapidity of symptom onset and progression – <span>The rapidity with which symptoms develop during exercise can also provide useful diagnostic information. For example, patients who develop shortness of breath and wheezing after walking 50 to 100 feet often have acute elevations in pulmonary capillary wedge pressure (usually due to cardiac diastolic dysfunction) or pulmonary hypertension. In contrast, symptoms of exercise-induced asthma usually are precipitated by more intense activity, beginning three minutes into exercise, peaking within 10 to 15 minutes, and resolving by 60 minutes. (See "Exercise-induced bronchoconstriction".) Respiratory muscle weakness generally leads to gradually progressive dyspnea, sometimes with an acute worsening at a time of illness, particularly a respiratory infection. Severity of d




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Respiratory muscle weakness generally leads to gradually progressive dyspnea, sometimes with an acute worsening at a time of illness, particularly a respiratory infection.
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lly are precipitated by more intense activity, beginning three minutes into exercise, peaking within 10 to 15 minutes, and resolving by 60 minutes. (See "Exercise-induced bronchoconstriction".) <span>Respiratory muscle weakness generally leads to gradually progressive dyspnea, sometimes with an acute worsening at a time of illness, particularly a respiratory infection. Severity of dyspnea — For patients with chronic dyspnea, formal assessment of the severity of dyspnea can help create a baseline for future comparisons [21]. A number of instruments are




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It is important to note that scales like the mMRC do not measure dyspnea directly; rather, they assess the intensity of exercise that provokes dyspnea and, indirectly, the degree of disability resulting from dyspnea. Routine assessment of dyspnea in hospitalized patients is feasible [27] and severity of dyspnea on admission to the hospital predicts increased mortality [28].
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lp assess the severity of dyspnea, such as the Baseline Dyspnea Index, the Modified Medical Research Council (mMRC) dyspnea scale (calculator 1) (table 3), and the Borg scale (table 4) [22-26]. <span>It is important to note that scales like the mMRC do not measure dyspnea directly; rather, they assess the intensity of exercise that provokes dyspnea and, indirectly, the degree of disability resulting from dyspnea. Routine assessment of dyspnea in hospitalized patients is feasible [27] and severity of dyspnea on admission to the hospital predicts increased mortality [28]. The Edmonton Dyspnea Inventory (EDI), a clinical instrument to measure dyspnea severity with activities of daily living, exercise, and rest using a numeric rating scale (0 through 10),




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Associated symptoms such as cough, sputum production, nasal congestion, chest pain, peripheral edema, Raynaud phenomenon, joint swelling, and muscle weakness can help identify areas for further investigation.
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0 through 10), has been proposed as a measurement of dyspnea severity in the context of daily activities, particularly in patients with idiopathic pulmonary fibrosis [29]. Associated symptoms — <span>Associated symptoms such as cough, sputum production, nasal congestion, chest pain, peripheral edema, Raynaud phenomenon, joint swelling, and muscle weakness can help identify areas for further investigation. As examples, asymmetric lower extremity edema might suggest venous thromboembolic disease; Raynaud phenomenon is seen in a number of rheumatic diseases that are associated with intersti




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While some clusters of phrases were common to a number of disease categories (eg, increased work or effort of breathing was found with COPD, asthma, and neuromuscular disease), each disease had a relatively unique set of clusters associated with it.
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eathing discomfort from a variety of cardiopulmonary disorders [6-8,31]. Subjects were asked to select the phrases that best described their breathing discomfort, and distinct clusters emerged. <span>While some clusters of phrases were common to a number of disease categories (eg, increased work or effort of breathing was found with COPD, asthma, and neuromuscular disease), each disease had a relatively unique set of clusters associated with it. The combined data from studies that were performed in patients with known cardiopulmonary disorders or in normal subjects made breathless under experimental conditions indicate the foll




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The sensation of "air hunger" has been associated with acute bronchoconstriction and hyperinflation in asthma and COPD, heart failure, pulmonary embolism, and restricted thoracic motion, as well as acute hypercapnia from any cause [3,4,32].
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studies that were performed in patients with known cardiopulmonary disorders or in normal subjects made breathless under experimental conditions indicate the following (table 6) [2,6-8,30,31]: ●<span>The sensation of "air hunger" has been associated with acute bronchoconstriction and hyperinflation in asthma and COPD, heart failure, pulmonary embolism, and restricted thoracic motion, as well as acute hypercapnia from any cause [3,4,32]. ●Acute bronchoconstriction leads to a series of sensations as the degree of obstruction worsens, from "chest tightness" to an increased "effort to breathe" to a sensation of "air hunger




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Acute bronchoconstriction leads to a series of sensations as the degree of obstruction worsens, from "chest tightness" to an increased "effort to breathe" to a sensation of "air hunger" [6-9,12,13]. The sensation of "tightness" appears to be independent of the work of breathing [33]. Attention to the use of verbal descriptors of dyspnea may help the clinician avoid underestimation of the severity of airflow limitation when objective measurements of lung function are not possible.
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d with acute bronchoconstriction and hyperinflation in asthma and COPD, heart failure, pulmonary embolism, and restricted thoracic motion, as well as acute hypercapnia from any cause [3,4,32]. ●<span>Acute bronchoconstriction leads to a series of sensations as the degree of obstruction worsens, from "chest tightness" to an increased "effort to breathe" to a sensation of "air hunger" [6-9,12,13]. The sensation of "tightness" appears to be independent of the work of breathing [33]. Attention to the use of verbal descriptors of dyspnea may help the clinician avoid underestimation of the severity of airflow limitation when objective measurements of lung function are not possible. ●Report of "increased work of breathing" is associated with COPD, moderate to severe asthma, myopathy, and pulmonary fibrosis. ●Patients with COPD and dynamic hyperinflation sometimes c




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Report of "increased work of breathing" is associated with COPD, moderate to severe asthma, myopathy, and pulmonary fibrosis.
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on to the use of verbal descriptors of dyspnea may help the clinician avoid underestimation of the severity of airflow limitation when objective measurements of lung function are not possible. ●<span>Report of "increased work of breathing" is associated with COPD, moderate to severe asthma, myopathy, and pulmonary fibrosis. ●Patients with COPD and dynamic hyperinflation sometimes complain of a sensation of "unsatisfying breaths" or a sense that they "cannot get a deep breath" [9]. ●A sensation of rapid, sh




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Patients with COPD and dynamic hyperinflation sometimes complain of a sensation of "unsatisfying breaths" or a sense that they "cannot get a deep breath" [9].
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on when objective measurements of lung function are not possible. ●Report of "increased work of breathing" is associated with COPD, moderate to severe asthma, myopathy, and pulmonary fibrosis. ●<span>Patients with COPD and dynamic hyperinflation sometimes complain of a sensation of "unsatisfying breaths" or a sense that they "cannot get a deep breath" [9]. ●A sensation of rapid, shallow breathing may correspond to interstitial lung disease or reduced chest wall compliance. ●Heart failure is also associated with a sensation of "suffocation




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A sensation of rapid, shallow breathing may correspond to interstitial lung disease or reduced chest wall compliance.
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yopathy, and pulmonary fibrosis. ●Patients with COPD and dynamic hyperinflation sometimes complain of a sensation of "unsatisfying breaths" or a sense that they "cannot get a deep breath" [9]. ●<span>A sensation of rapid, shallow breathing may correspond to interstitial lung disease or reduced chest wall compliance. ●Heart failure is also associated with a sensation of "suffocation" [6]. ●A sense of heavy breathing is typical of deconditioning. Patient questionnaires have been developed for use in




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Heart failure is also associated with a sensation of "suffocation" [6].
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nsatisfying breaths" or a sense that they "cannot get a deep breath" [9]. ●A sensation of rapid, shallow breathing may correspond to interstitial lung disease or reduced chest wall compliance. ●<span>Heart failure is also associated with a sensation of "suffocation" [6]. ●A sense of heavy breathing is typical of deconditioning. Patient questionnaires have been developed for use in research and clinical settings, and allow the doctor to assess symptom in




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A sense of heavy breathing is typical of deconditioning.
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●A sensation of rapid, shallow breathing may correspond to interstitial lung disease or reduced chest wall compliance. ●Heart failure is also associated with a sensation of "suffocation" [6]. ●<span>A sense of heavy breathing is typical of deconditioning. Patient questionnaires have been developed for use in research and clinical settings, and allow the doctor to assess symptom intensity, quality, and associated affective responses as pa




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The absence of cigarette smoking argues strongly against a diagnosis of COPD, unless the patient has a history of tuberculosis or use of biomass cooking fuels. In one study, a history of smoking cigarettes had a positive predictive value for COPD of 0.4; COPD is uncommon among patients who have never smoked or have smoked less than 10 pack years [42].
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the wording used to describe dyspnea [36-41]. Further research in this area is underway. (See 'Perceptual and psychological factors' below.) Cigarette smoking and exposures to dusts and fumes — <span>The absence of cigarette smoking argues strongly against a diagnosis of COPD, unless the patient has a history of tuberculosis or use of biomass cooking fuels. In one study, a history of smoking cigarettes had a positive predictive value for COPD of 0.4; COPD is uncommon among patients who have never smoked or have smoked less than 10 pack years [42]. Exposure to particulates in the air, particularly for individuals living in proximity to highways, may contribute to airway disease and dyspnea [43]. The occupational history may lead t




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Physical examination — A complete physical examination is essential. In particular, the focus should be directed at the presence or absence of stridor, wheezing, crackles, tachycardia, arrhythmia, heart murmurs, gallop, peripheral edema, muscle weakness, dysphonia, and evidence of rheumatic disease. However, the absence of physical findings tends to have a greater negative predictive value, than the positive predictive value of any identified signs [19].
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nal and environmental exposures' and "Overview of bronchiolar disorders in adults" and "Asbestos-related pleuropulmonary disease" and "Chronic beryllium disease (berylliosis)" and "Silicosis".) <span>Physical examination — A complete physical examination is essential. In particular, the focus should be directed at the presence or absence of stridor, wheezing, crackles, tachycardia, arrhythmia, heart murmurs, gallop, peripheral edema, muscle weakness, dysphonia, and evidence of rheumatic disease. However, the absence of physical findings tends to have a greater negative predictive value, than the positive predictive value of any identified signs [19]. ●Clubbing is associated with several causes of dyspnea, including bronchiectasis, idiopathic pulmonary fibrosis, lung cancer, and pediatric cyanotic heart disease, but not asthma, COPD,




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Clubbing is associated with several causes of dyspnea, including bronchiectasis, idiopathic pulmonary fibrosis, lung cancer, and pediatric cyanotic heart disease, but not asthma, COPD, or adult-onset hypoxemia.
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and evidence of rheumatic disease. However, the absence of physical findings tends to have a greater negative predictive value, than the positive predictive value of any identified signs [19]. ●<span>Clubbing is associated with several causes of dyspnea, including bronchiectasis, idiopathic pulmonary fibrosis, lung cancer, and pediatric cyanotic heart disease, but not asthma, COPD, or adult-onset hypoxemia. ●Jugular venous distention indicates elevated R-sided filling pressures that suggest heart failure, valvular disease, or pulmonary hypertension. ●Decreased or distant heart sounds may s




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Jugular venous distention indicates elevated R-sided filling pressures that suggest heart failure, valvular disease, or pulmonary hypertension.
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ated with several causes of dyspnea, including bronchiectasis, idiopathic pulmonary fibrosis, lung cancer, and pediatric cyanotic heart disease, but not asthma, COPD, or adult-onset hypoxemia. ●<span>Jugular venous distention indicates elevated R-sided filling pressures that suggest heart failure, valvular disease, or pulmonary hypertension. ●Decreased or distant heart sounds may suggest a pericardial effusion but may also be due to obesity or hyperinflation from emphysema. ●Abdominal rounding, the protruding of the central




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Decreased or distant heart sounds may suggest a pericardial effusion but may also be due to obesity or hyperinflation from emphysema.
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but not asthma, COPD, or adult-onset hypoxemia. ●Jugular venous distention indicates elevated R-sided filling pressures that suggest heart failure, valvular disease, or pulmonary hypertension. ●<span>Decreased or distant heart sounds may suggest a pericardial effusion but may also be due to obesity or hyperinflation from emphysema. ●Abdominal rounding, the protruding of the central abdomen with diminished transverse diameter during exhalation, has been associated with acute heart failure [47]. EVALUATION OF ACUTE




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Abdominal rounding, the protruding of the central abdomen with diminished transverse diameter during exhalation, has been associated with acute heart failure [47].
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art failure, valvular disease, or pulmonary hypertension. ●Decreased or distant heart sounds may suggest a pericardial effusion but may also be due to obesity or hyperinflation from emphysema. ●<span>Abdominal rounding, the protruding of the central abdomen with diminished transverse diameter during exhalation, has been associated with acute heart failure [47]. EVALUATION OF ACUTE DYSPNEA — Breathing discomfort arising over the course of minutes to hours is generally due to a limited number of conditions (table 2) and generally involves proces




Zur Verarbeitung der Datenworte beherrschen Prozessoren eine Menge von Maschinenbefehlen, die man Maschinenbefehlssatz nennt. Im Maschinenbefehlssatz sind Maschinenbefehle enthalten, um Datenworte z.B. zu addieren, zu multiplizieren oder bitweise logische Verknüpfungen zwischen Datenworten durchzuführen. Weil Maschinenbefehle nur aus Nullen und Ein- sen bestehen, was für Menschen wenig anschaulich ist, bezeichnet man sie mit einem Buch- stabenkürzel, dem Mnemonic. Für den Addierbefehl nimmt man beispielsweise häufig den Mnemonic ADD. Programme, die man unter Verwendung von Mnemonics darstellt, nennt man Assembler-Programme. Der Prozessor wird mit einem Takt betrieben, der die Dauer eines Verarbeitungsschrittes be- stimmt. Die Taktfrequenz ist einer von mehreren wesentlichen Faktoren, die die Rechenleis- tung oder Performance eines Computers bestimmen, also welche Rechenarbeit er in einer gewissen Zeitspanne erbringen kann. Ein weiterer Einflussfaktor sind Maßnahmen zur Paral- lelisierung der Abläufe, z.B. das Pipelining, so dass während eines Takts an mehreren Opera- tionen gleichzeitig gearbeitet wird. Bei vielen Prozessoren, den so genannten CISC-Prozessoren, steht hinter jedem Maschinen- befehl ein Mikroprogramm aus noch einfacheren Befehlen, den Mikrobefehlen. Es ist fest in den Prozessor einprogrammiert. In diesem Fall benötigt ein Maschinenbefehl mehrere Takte. RISC-Prozessoren dagegen führen idealerweise jeden Maschinenbefehl in nur einem Takt aus und besitzen keine Mikroprogrammierung. Für einen Programmierer sind Maschinenprogramme häufig auf einer zu niedrigen Ebene an- gesiedelt, um damit größere Anwendungen zu entwickeln. Für solche Zwecke eignen sich an- dere Programmiersprachen wie C, C++ oder Java besser. Manche Programmiersprachen sind Allzwecksprachen, andere sind auf bestimmte Einsatzbereiche zugeschnitten, z.B. auf Web- Anwendungen oder Simulationen.
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Clues to the need for an urgent evaluation include heart rate >120 beats/minute, respiratory rate >30 breaths/minute, pulse oxygen saturation (SpO2) <90 percent, use of accessory respiratory muscles, difficulty speaking in full sentences (which may be a sign of reduced vital capacity or very high drive to breathe), stridor, asymmetric breath sounds or percussion, diffuse crackles, diaphoresis, and cyanosis.
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iscomfort arising over the course of minutes to hours is generally due to a limited number of conditions (table 2) and generally involves processes that require prompt evaluation and treatment. <span>Clues to the need for an urgent evaluation include heart rate >120 beats/minute, respiratory rate >30 breaths/minute, pulse oxygen saturation (SpO2) <90 percent, use of accessory respiratory muscles, difficulty speaking in full sentences (which may be a sign of reduced vital capacity or very high drive to breathe), stridor, asymmetric breath sounds or percussion, diffuse crackles, diaphoresis, and cyanosis. The evaluation of dyspnea in the emergency department is described separately. (See "Approach to the adult with dyspnea in the emergency department".) INITIAL TESTING IN CHRONIC DYSPNEA




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The five most common causes of chronic dyspnea are the following:

● Asthma (see 'Respiratory' above)

● Chronic obstructive pulmonary disease (COPD) (see 'Respiratory' above)

● Interstitial lung disease (see 'Respiratory' above)

● Myocardial dysfunction (see 'Cardiovascular' above)

● Obesity/deconditioning (see 'Cardiovascular' above)

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iopulmonary disease does not guarantee that the patient's symptoms or the etiology of their exercise limitation are due to that condition, particularly in patients with coexisting disease [16]. <span>The five most common causes of chronic dyspnea are the following: ●Asthma (see 'Respiratory' above) ●Chronic obstructive pulmonary disease (COPD) (see 'Respiratory' above) ●Interstitial lung disease (see 'Respiratory' above) ●Myocardial dysfunction (see 'Cardiovascular' above) ●Obesity/deconditioning (see 'Cardiovascular' above) Pace of testing — For patients with chronic dyspnea, the severity of dyspnea and rate of worsening are important determinants of the pace and location of diagnostic testing [21]. The op




Einheiten Wie erwähnt, sind grundlegende…
#has-images
1.2 Einheiten
Wie erwähnt, sind grundlegende Einheiten in der Informatik das Bit und das Byte. Bei Grö-
ßenangaben verwendet man nach IEC 60027-2 als Einheitenzeichen „bit“ für das Bit. Man
findet aber auch gelegentlich ein „b“, wie es in IEEE 1541 festgelegt wurde.
Für das Byte findet man nach IEC 60027-2 das Einheitenzeichen „B“. Es wird aber auch öfter
in Form von „Byte“ oder „Bytes“ ausgeschrieben. Somit könnte man Angaben wie die folgen-
den finden:

24 bit = 24 b = 3 B = 3 Byte = 3 Bytes.

Üblicherweise verwendet man zur Angabe physikalischer Größen die so genannten SI-Ein- heiten (Système international d’unités), wie sie u.a. in der Norm ISO/IEC 80000-1 festgelegt sind. Darunter fallen Meter, Kilogramm, Sekunde, usw. Die Einheiten können mit SI-Präfixen wie Milli oder Kilo versehen werden, die Zehnerpotenzen darstellen.

Weil die Informatik und auch die Rechnerarchitektur stark durch die Verwendung des Bits mit
seinen zwei möglichen Werten geprägt sind, verwendet man dort gerne Zweierpotenzen, vor
allem in Verbindung mit Bits und Bytes. Die Unterschiede sind in Tab. 1.1 zusammengefasst.
Wie man sieht, sind die auf Zweierpotenzen basierenden IEC-Präfixe ebenfalls genormt wor-
den, wenngleich sich die
...
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Typical ECG findings

● Stage 1, seen in the first hours to days, is characterized by widespread ST elevation (typically concave up) with reciprocal ST depression in leads aVR and V1 (waveform 1). There is also frequently an atrial current of injury, reflected by elevation of the PR segment in lead aVR and depression of the PR segment in other limb leads and in the left chest leads, primarily V5 and V6. Thus, the PR and ST segments typically change in opposite directions. PR segment deviation, which is highly specific, though less sensitive, is frequently overlooked.

The TP segment is recommended as the baseline for comparison when measuring both PR and ST segment changes in acute pericarditis.

● Stage 2, typically seen in the first week, is characterized by normalization of the ST and PR segments.

● Stage 3 is characterized by the development of diffuse T-wave inversions, generally after the ST segments have become isoelectric. It is typically seen in the subacute phase, and its duration is not well documented and likely highly variable.

● Stage 4 is represented by normalization of the ECG. It can occur directly from stage 1 in self-limited cases or with prompt response to medical therapy.

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may evolve through as many as four stages with highly variable temporal evolution of ECG changes. The four typical stages of ECG changes (figure 1) in patients with acute pericarditis include: <span>Typical ECG findings ●Stage 1, seen in the first hours to days, is characterized by widespread ST elevation (typically concave up) with reciprocal ST depression in leads aVR and V1 (waveform 1). There is also frequently an atrial current of injury, reflected by elevation of the PR segment in lead aVR and depression of the PR segment in other limb leads and in the left chest leads, primarily V5 and V6. Thus, the PR and ST segments typically change in opposite directions. PR segment deviation, which is highly specific, though less sensitive, is frequently overlooked. The TP segment is recommended as the baseline for comparison when measuring both PR and ST segment changes in acute pericarditis. ●Stage 2, typically seen in the first week, is characterized by normalization of the ST and PR segments. ●Stage 3 is characterized by the development of diffuse T-wave inversions, generally after the ST segments have become isoelectric. It is typically seen in the subacute phase, and its duration is not well documented and likely highly variable. ●Stage 4 is represented by normalization of the ECG. It can occur directly from stage 1 in self-limited cases or with prompt response to medical therapy. Atypical ECG findings — Pericarditis does not always result in the typical ECG changes described above. In many patients, the ECG returns to normal without going through the above stage




1.2 Einheiten Wie erwähnt, sind grundlegende Einheiten in der Informatik das Bit und das Byte. Bei Grö- ßenangaben verwendet man nach IEC 60027-2 als Einheitenzeichen „bit“ für das Bit. Man findet aber auch gelegentlich ein „b“, wie es in IEEE 1541 festgelegt wurde. Für das Byte findet man nach IEC 60027-2 das Einheitenzeichen „B“. Es wird aber auch öfter in Form von „Byte“ oder „Bytes“ ausgeschrieben. Somit könnte man Angaben wie die folgen- den finden:
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In patients with a clinically compatible syndrome, the demonstration of an infiltrate on chest imaging is generally sufficient to establish an initial working diagnosis and start empiric therapy. However, this combination of findings is ultimately nonspecific and is shared among many cardiopulmonary disorders. Thus, it is important to remain attentive to the possibility of an alternate diagnosis as a patient's course evolves.
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erized by fever, respiratory distress, and sepsis. Because of the wide spectrum of associated clinical features, CAP is a part of the differential diagnosis of most acute respiratory illnesses. <span>In patients with a clinically compatible syndrome, the demonstration of an infiltrate on chest imaging is generally sufficient to establish an initial working diagnosis and start empiric therapy. However, this combination of findings is ultimately nonspecific and is shared among many cardiopulmonary disorders. Thus, it is important to remain attentive to the possibility of an alternate diagnosis as a patient's course evolves. The clinical manifestations, diagnosis, and microbiologic evaluation of CAP in immunocompetent adults are reviewed here. An general overview of CAP in adults is provided separately (see




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For most patients with suspected CAP, we obtain posteroanterior and lateral chest radiographs. Radiographic findings consistent with the diagnosis of CAP include lobar consolidations (image 1A-B), interstitial infiltrates (image 2A-C), and/or cavitations (image 3). Although certain radiographic features suggest specific causes of pneumonia (eg, lobar consolidations suggest infection with typical bacterial pathogens), radiographic appearance alone cannot reliably differentiate among etiologies.
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diagnosis of CAP generally requires the demonstration of an opacity on chest imaging in a patient with a clinically compatible syndrome (eg, fever, dyspnea, cough, and sputum production) [1]. ●<span>For most patients with suspected CAP, we obtain posteroanterior and lateral chest radiographs. Radiographic findings consistent with the diagnosis of CAP include lobar consolidations (image 1A-B), interstitial infiltrates (image 2A-C), and/or cavitations (image 3). Although certain radiographic features suggest specific causes of pneumonia (eg, lobar consolidations suggest infection with typical bacterial pathogens), radiographic appearance alone cannot reliably differentiate among etiologies. ●In selected cases, it is reasonable to make a clinical diagnosis without chest imaging in otherwise healthy patients with highly compatible syndromes (eg, acute onset, fever, cough, an




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In selected cases, it is reasonable to make a clinical diagnosis without chest imaging in otherwise healthy patients with highly compatible syndromes (eg, acute onset, fever, cough, and signs of consolidation on physical examination) and lack of concern for other causes. However, clinical features alone have limited diagnostic accuracy, thus, we typically reserve this option for circumstances in which chest radiography cannot be easily obtained and the patient can be closely followed.
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uggest specific causes of pneumonia (eg, lobar consolidations suggest infection with typical bacterial pathogens), radiographic appearance alone cannot reliably differentiate among etiologies. ●<span>In selected cases, it is reasonable to make a clinical diagnosis without chest imaging in otherwise healthy patients with highly compatible syndromes (eg, acute onset, fever, cough, and signs of consolidation on physical examination) and lack of concern for other causes. However, clinical features alone have limited diagnostic accuracy, thus, we typically reserve this option for circumstances in which chest radiography cannot be easily obtained and the patient can be closely followed. ●When CAP is suspected based on clinical features despite a negative chest radiograph, we obtain computed tomography (CT) of the chest in selected patients. These patients include immun




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When CAP is suspected based on clinical features despite a negative chest radiograph, we obtain computed tomography (CT) of the chest in selected patients. These patients include immunocompromised patients, who may not mount strong inflammatory responses and thus have negative chest radiographs, as well as patients with known exposures to epidemic pathogens that cause pneumonia (eg, severe acute respiratory syndrome coronavirus 2, Legionella spp).
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s alone have limited diagnostic accuracy, thus, we typically reserve this option for circumstances in which chest radiography cannot be easily obtained and the patient can be closely followed. ●<span>When CAP is suspected based on clinical features despite a negative chest radiograph, we obtain computed tomography (CT) of the chest in selected patients. These patients include immunocompromised patients, who may not mount strong inflammatory responses and thus have negative chest radiographs, as well as patients with known exposures to epidemic pathogens that cause pneumonia (eg, severe acute respiratory syndrome coronavirus 2, Legionella spp). ●Obtaining a CT scan is also reasonable when CAP is suspected but the clinical presentation is atypical or the patient has possible alternative explanations for their syndrome (eg, chro




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Obtaining a CT scan is also reasonable when CAP is suspected but the clinical presentation is atypical or the patient has possible alternative explanations for their syndrome (eg, chronic obstructive pulmonary disease exacerbation, pulmonary edema, atelectasis, etc).
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thus have negative chest radiographs, as well as patients with known exposures to epidemic pathogens that cause pneumonia (eg, severe acute respiratory syndrome coronavirus 2, Legionella spp). ●<span>Obtaining a CT scan is also reasonable when CAP is suspected but the clinical presentation is atypical or the patient has possible alternative explanations for their syndrome (eg, chronic obstructive pulmonary disease exacerbation, pulmonary edema, atelectasis, etc). In such cases, CT scanning can help confirm or exclude the diagnosis of pneumonia [2]. Because there is no direct evidence to suggest that CT scanning improves outcomes for most patient




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Because there is no direct evidence to suggest that CT scanning improves outcomes for most patients and cost is high, we do not routinely obtain CT scans when evaluating patients for CAP.
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heir syndrome (eg, chronic obstructive pulmonary disease exacerbation, pulmonary edema, atelectasis, etc). In such cases, CT scanning can help confirm or exclude the diagnosis of pneumonia [2]. <span>Because there is no direct evidence to suggest that CT scanning improves outcomes for most patients and cost is high, we do not routinely obtain CT scans when evaluating patients for CAP. (See 'Chest imaging findings' below.) All patients with possible CAP should be tested for coronavirus disease 2019 during the pandemic. Microbiologic testing is otherwise generally rese




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In all cases, the initial diagnosis of CAP should be considered a working diagnosis. A substantial portion of patients initially diagnosed with CAP are ultimately found to have alternate diagnoses [4], therefore, findings that further support or refute the initial diagnoses should continue to be sought as the patient’s course progresses.
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racy, availability, and affordability of rapid microbiologic diagnostics tests is growing, and we expect that indications for testing will broaden soon [3]. (See 'Microbiologic testing' below.) <span>In all cases, the initial diagnosis of CAP should be considered a working diagnosis. A substantial portion of patients initially diagnosed with CAP are ultimately found to have alternate diagnoses [4], therefore, findings that further support or refute the initial diagnoses should continue to be sought as the patient’s course progresses. CLINICAL EVALUATION History and physical — The history and physical examination should be directed at recognizing the clinical syndrome of CAP, evaluating its severity, assessing for co




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Classically, CAP is characterized by acute onset fever, cough (with or without sputum production), and shortness of breath [5-7]. In some cases, pleuritic chest pain may also be present
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s severity, assessing for complications, identifying important exposures that may indicate the cause of infection, and assessing for comorbidities that may contribute to the patient’s symptoms. <span>Classically, CAP is characterized by acute onset fever, cough (with or without sputum production), and shortness of breath [5-7]. In some cases, pleuritic chest pain may also be present. Less common symptoms include gastrointestinal complaints (eg, nausea, vomiting, diarrhea, abdominal pain), loss of appetite, and mental status changes. In patients with advanced age or




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Less common symptoms include gastrointestinal complaints (eg, nausea, vomiting, diarrhea, abdominal pain), loss of appetite, and mental status changes.
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ptoms. Classically, CAP is characterized by acute onset fever, cough (with or without sputum production), and shortness of breath [5-7]. In some cases, pleuritic chest pain may also be present. <span>Less common symptoms include gastrointestinal complaints (eg, nausea, vomiting, diarrhea, abdominal pain), loss of appetite, and mental status changes. In patients with advanced age or impaired immune systems, presenting symptoms can be subtle. For example, fever may be absent in older patients and mental status changes may be the sole




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Tachycardia, tachypnea, hypoxemia, or increased work of breathing may be present on physical examination. Crackles (rales) and rhonchi may be heard on chest auscultation, along with other signs of consolidation (eg, tactile fremitus, egophony, dullness to percussion).
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dvanced age or impaired immune systems, presenting symptoms can be subtle. For example, fever may be absent in older patients and mental status changes may be the sole presenting symptom [8,9]. <span>Tachycardia, tachypnea, hypoxemia, or increased work of breathing may be present on physical examination. Crackles (rales) and rhonchi may be heard on chest auscultation, along with other signs of consolidation (eg, tactile fremitus, egophony, dullness to percussion). As infection progresses, the dominant clinical picture may be of sepsis and/or respiratory distress. While the clinical features described above support the diagnosis of pneumonia, no c




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As infection progresses, the dominant clinical picture may be of sepsis and/or respiratory distress.
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esent on physical examination. Crackles (rales) and rhonchi may be heard on chest auscultation, along with other signs of consolidation (eg, tactile fremitus, egophony, dullness to percussion). <span>As infection progresses, the dominant clinical picture may be of sepsis and/or respiratory distress. While the clinical features described above support the diagnosis of pneumonia, no combination of symptoms and signs has been found to accurately predict the presence or absence of pneu




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In patients with advanced age or impaired immune systems, presenting symptoms can be subtle. For example, fever may be absent in older patients and mental status changes may be the sole presenting symptom [ 8,9].
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pleuritic chest pain may also be present. Less common symptoms include gastrointestinal complaints (eg, nausea, vomiting, diarrhea, abdominal pain), loss of appetite, and mental status changes. <span>In patients with advanced age or impaired immune systems, presenting symptoms can be subtle. For example, fever may be absent in older patients and mental status changes may be the sole presenting symptom [8,9]. Tachycardia, tachypnea, hypoxemia, or increased work of breathing may be present on physical examination. Crackles (rales) and rhonchi may be heard on chest auscultation, along with oth




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In another study evaluating >28,000 adults presenting to primary care with an acute cough attributed to a lower respiratory tract infection, independent predictors of radiographic-confirmed pneumonia included fever, tachycardia, crackles on chest auscultation, and oxygen saturation <95 percent [7]. However, the positive predictive value (PPV) of all four variables combined was estimated to be only 67 percent.
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e, the sensitivity of the combination of fever, cough, tachycardia, and crackles was less than 50 percent when chest radiograph was used as a reference standard in one retrospective review [6]. <span>In another study evaluating >28,000 adults presenting to primary care with an acute cough attributed to a lower respiratory tract infection, independent predictors of radiographic-confirmed pneumonia included fever, tachycardia, crackles on chest auscultation, and oxygen saturation <95 percent [7]. However, the positive predictive value (PPV) of all four variables combined was estimated to be only 67 percent. Concordantly, studies comparing clinical judgement with chest radiography for the diagnosis of pneumonia have similar findings [6,11]. One cohort study of >2800 adults with acute cou




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One cohort study of >2800 adults with acute cough estimates the PPV of clinical judgement at 57 percent [11].
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ur variables combined was estimated to be only 67 percent. Concordantly, studies comparing clinical judgement with chest radiography for the diagnosis of pneumonia have similar findings [6,11]. <span>One cohort study of >2800 adults with acute cough estimates the PPV of clinical judgement at 57 percent [11]. Similarly, there are no signs or symptoms that reliably distinguish among the many infectious causes of pneumonia (eg, viral versus bacterial or between different bacterial causes) [12]




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Similarly, there are no signs or symptoms that reliably distinguish among the many infectious causes of pneumonia (eg, viral versus bacterial or between different bacterial causes) [12]. However, the presence of certain features may raise the index of suspicion for particular pathogens (table 2).
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h chest radiography for the diagnosis of pneumonia have similar findings [6,11]. One cohort study of >2800 adults with acute cough estimates the PPV of clinical judgement at 57 percent [11]. <span>Similarly, there are no signs or symptoms that reliably distinguish among the many infectious causes of pneumonia (eg, viral versus bacterial or between different bacterial causes) [12]. However, the presence of certain features may raise the index of suspicion for particular pathogens (table 2). This concept is particularly important during outbreaks, family clusters, and other known/potential exposures, where knowledge of a particular exposure may change the need for testing,




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CAP is a common working diagnosis and is on the differential diagnosis of patients presenting with respiratory tract infections, patients with cough and abnormal chest imaging, and patients with sepsis. Because CAP is common and its symptoms overlap with many other cardiopulmonary disorders, it is frequently overdiagnosed [4]. In one cohort study, approximately 17 percent of patients hospitalized with CAP were ultimately found to have a different diagnosis. The most common alternate diagnoses included heart failure, malignancy, and pulmonary infarct or fibrosis [4].
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with established diagnoses of CAP. (See "Procalcitonin use in lower respiratory tract infections", section on 'Community-acquired pneumonia in hospitalized patients'.) DIFFERENTIAL DIAGNOSIS — <span>CAP is a common working diagnosis and is on the differential diagnosis of patients presenting with respiratory tract infections, patients with cough and abnormal chest imaging, and patients with sepsis. Because CAP is common and its symptoms overlap with many other cardiopulmonary disorders, it is frequently overdiagnosed [4]. In one cohort study, approximately 17 percent of patients hospitalized with CAP were ultimately found to have a different diagnosis. The most common alternate diagnoses included heart failure, malignancy, and pulmonary infarct or fibrosis [4]. Other respiratory tract infections that present similarly to CAP include, but are not limited, to influenza, coronavirus disease 2019 (COVID-19), acute bronchitis, chronic obstructive p




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Acute bronchitis – Acute bronchitis is an infection that primarily involves the large airways (bronchi) but not the alveoli or pulmonary parenchyma. Prolonged cough, typically following an upper respiratory tract infection, is the most common symptom of acute bronchitis. In contrast to pneumonia, acute bronchitis is less likely to present with abnormal vital signs (pulse >100/minute, respiratory rate >24 breaths/minute, temperature >38°C [100.4°F], or oxygen saturation <95 percent) (figure 1). Mental status changes and/or other signs of systemic infection are typically absent. Signs of consolidation (rales, egophony, or tactile fremitus) should be absent on chest auscultation.
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, and other respiratory tract infections. Generally, signs of consolidation on chest auscultation and the presence of an opacity on chest imaging distinguish CAP from the latter two disorders. ●<span>Acute bronchitis – Acute bronchitis is an infection that primarily involves the large airways (bronchi) but not the alveoli or pulmonary parenchyma. Prolonged cough, typically following an upper respiratory tract infection, is the most common symptom of acute bronchitis. In contrast to pneumonia, acute bronchitis is less likely to present with abnormal vital signs (pulse >100/minute, respiratory rate >24 breaths/minute, temperature >38°C [100.4°F], or oxygen saturation <95 percent) (figure 1). Mental status changes and/or other signs of systemic infection are typically absent. Signs of consolidation (rales, egophony, or tactile fremitus) should be absent on chest auscultation. (See "Acute bronchitis in adults".) ●Influenza – Influenza is characterized by acute onset fever and cough, often accompanied by pronounced systemic symptoms including chills, rigors, m




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Influenza – Influenza is characterized by acute onset fever and cough, often accompanied by pronounced systemic symptoms including chills, rigors, myalgias, and/or arthralgias. Pneumonia complicates a minority of cases and may be primary (caused by influenza virus itself) or secondary, caused by bacterial respiratory pathogens (most often streptococci or Staphylococcus aureus).
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ther signs of systemic infection are typically absent. Signs of consolidation (rales, egophony, or tactile fremitus) should be absent on chest auscultation. (See "Acute bronchitis in adults".) ●<span>Influenza – Influenza is characterized by acute onset fever and cough, often accompanied by pronounced systemic symptoms including chills, rigors, myalgias, and/or arthralgias. Pneumonia complicates a minority of cases and may be primary (caused by influenza virus itself) or secondary, caused by bacterial respiratory pathogens (most often streptococci or Staphylococcus aureus). (See "Seasonal influenza in adults: Clinical manifestations and diagnosis".) ●Upper respiratory tract infection (URI) – URIs are commonly characterized by fever and cough, but in contra




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Upper respiratory tract infection (URI) – URIs are commonly characterized by fever and cough, but in contrast to pneumonia lack signs of consolidation on chest auscultation. While the presence of rhinorrhea and pharyngitis favor the diagnosis URI over pneumonia, URIs sometimes precede or co-occur with CAP [11]
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itself) or secondary, caused by bacterial respiratory pathogens (most often streptococci or Staphylococcus aureus). (See "Seasonal influenza in adults: Clinical manifestations and diagnosis".) ●<span>Upper respiratory tract infection (URI) – URIs are commonly characterized by fever and cough, but in contrast to pneumonia lack signs of consolidation on chest auscultation. While the presence of rhinorrhea and pharyngitis favor the diagnosis URI over pneumonia, URIs sometimes precede or co-occur with CAP [11]. (See "The common cold in adults: Diagnosis and clinical features".) ●Coronavirus disease 2019 – The range of presenting symptoms for COVID-19 is wide, ranging from asymptomatic infecti




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Exacerbations of chronic pulmonary diseases are frequently triggered by viral or bacterial infection or colonization of the respiratory tract mucosa. In most cases, infection does not extend beyond the mucosa, however, pneumonia can complicate these disorders. Higher fever, adventitious breath sounds on chest auscultation (eg, focal rales/crackles or rhonchi), and impaired oxygenation suggest pneumonia and generally indicate need for chest imaging.
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us disease 2019 – The range of presenting symptoms for COVID-19 is wide, ranging from asymptomatic infection to CAP with profound acute respiratory failure. (See "COVID-19: Clinical features".) <span>Exacerbations of chronic pulmonary diseases are frequently triggered by viral or bacterial infection or colonization of the respiratory tract mucosa. In most cases, infection does not extend beyond the mucosa, however, pneumonia can complicate these disorders. Higher fever, adventitious breath sounds on chest auscultation (eg, focal rales/crackles or rhonchi), and impaired oxygenation suggest pneumonia and generally indicate need for chest imaging. ●Acute exacerbations of chronic obstructive pulmonary disease (AECOPD) – AECOPD is defined as an acute increase in COPD symptoms that go beyond day-to-day variation, typically character




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Febrile illness and/or sepsis can also be the presenting syndrome in patients with CAP; other common causes of these syndromes include urinary tract infections, intra-abdominal infections, and endocarditis.
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s (eg, granulomatosis with polyangiitis, rheumatoid arthritis, systemic lupus erythematosus, dermatomyositis). (See "Approach to the adult with interstitial lung disease: Clinical evaluation".) <span>Febrile illness and/or sepsis can also be the presenting syndrome in patients with CAP; other common causes of these syndromes include urinary tract infections, intra-abdominal infections, and endocarditis. In all cases, monitoring the patient’s progress over time helps confirm or refute the initial diagnosis. For example, the rapid resolution of pulmonary opacities on chest imaging sugges




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In all cases, monitoring the patient’s progress over time helps confirm or refute the initial diagnosis. For example, the rapid resolution of pulmonary opacities on chest imaging suggests a noninfectious process such as pulmonary edema or atelectasis. Conversely, lack of response to empiric treatment in 48 to 72 hours suggest that initial antibiotic selection was inadequate, there are complications, or that there is an alternate diagnosis. (See 'Follow-up care' below.)
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ss and/or sepsis can also be the presenting syndrome in patients with CAP; other common causes of these syndromes include urinary tract infections, intra-abdominal infections, and endocarditis. <span>In all cases, monitoring the patient’s progress over time helps confirm or refute the initial diagnosis. For example, the rapid resolution of pulmonary opacities on chest imaging suggests a noninfectious process such as pulmonary edema or atelectasis. Conversely, lack of response to empiric treatment in 48 to 72 hours suggest that initial antibiotic selection was inadequate, there are complications, or that there is an alternate diagnosis. (See 'Follow-up care' below.) CHEST IMAGING FINDINGS Imaging techniques — Chest imaging is indicated for the majority of patients with suspected CAP to confirm the diagnosis, assess for complications (eg, parapneumo




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Most patients will show some signs of improvement within 48 to 72 hours of starting treatment. Subjectively, we look for improvement in cough, sputum production, dyspnea, and chest pain. Objectively, we assess for resolution of fever and normalization of heart rate, respiratory rate, oxygenation, and white blood cell count. Generally, patients demonstrate some clinical improvement within 48 to 72 hours.
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rtion of patients initially diagnosed with CAP will ultimately be found to have an alternate diagnosis, close follow-up is important for both outpatient and hospitalized patients (algorithm 3). <span>Most patients will show some signs of improvement within 48 to 72 hours of starting treatment. Subjectively, we look for improvement in cough, sputum production, dyspnea, and chest pain. Objectively, we assess for resolution of fever and normalization of heart rate, respiratory rate, oxygenation, and white blood cell count. Generally, patients demonstrate some clinical improvement within 48 to 72 hours. Both failure to improve and very rapid response should raise suspicion for diagnoses other than CAP. Reasons for clinical failure can generally be categorized as either progression of i




comments can occur in SQL input. They are not tokens, they are effectively equivalent to whitespace.
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The SQL syntax is not very consistent regarding what tokens identify commands and which are operands or parameters. The first few tokens are generally the command name, so in the above exam- ple we would usually speak of a “SELECT”, an “UPDATE”, and an “INSERT” command. But for instance the UPDATE command always requires a SET token to appear in a certain position, and this particular variation of INSERT also requires a VALUES in order to be complete. The precise syntax rules for each command are described in Part VI.
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Tokens such as SELECT, UPDATE, or VALUES in the example above are examples of key words, that is, words that have a fixed meaning in the SQL language. The tokens MY_TABLE and A are examples of identifiers. They identify names of tables, columns, or other database objects, depending on the command they are used in. Therefore they are sometimes simply called “names”. Key words and identifiers have the same lexical structure, meaning that one cannot know whether a token is an identifier or a key word without knowing the language.
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SQL identifiers and key words must begin with a letter (a-z, but also letters with diacritical marks and non-Latin letters) or an underscore (_). Subsequent characters in an identifier or key word can be letters, underscores, digits (0-9), or dollar signs ($). Note that dollar signs are not allowed in identifiers according to the letter of the SQL standard, so their use might render applications less portable. The SQL standard will not define a key word that contains digits or starts or ends with an underscore, so identifiers of this form are safe against possible conflict with future extensions of the standard.
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The system uses no more than NAMEDATALEN-1 bytes of an identifier; longer names can be written in commands, but they will be truncated. By default, NAMEDATALEN is 64 so the maximum identifier length is 63 bytes. If this limit is problematic, it can be raised by changing the NAMEDATALEN constant in src/include/pg_config_manual.h.
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Key words and unquoted identifiers are case-insensitive. Therefore: UPDATE MY_TABLE SET A = 5; can equivalently be written as: uPDaTE my_TabLE SeT a = 5; A convention often used is to write key words in upper case and names in lower case, e.g.: UPDATE my_table SET a = 5;
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createContext lets you define and provide context to the child components. Used with useContext.
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Built-in React APIs – React
Built-in React APIs In addition to Hooks and Components, the react package exports a few other APIs that are useful for defining components. This page lists all the remaining modern React APIs. <span>createContext lets you define and provide context to the child components. Used with useContext. forwardRef lets your component expose a DOM node as a ref to the parent. Used with useRef. lazy lets you defer loading a component’s code until it’s rendered for the first time. memo le




forwardRef lets your component expose a DOM node as a ref to the parent. Used with useRef.
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Built-in React APIs – React
Is that are useful for defining components. This page lists all the remaining modern React APIs. createContext lets you define and provide context to the child components. Used with useContext. <span>forwardRef lets your component expose a DOM node as a ref to the parent. Used with useRef. lazy lets you defer loading a component’s code until it’s rendered for the first time. memo lets your component skip re-renders with same props. Used with useMemo and useCallback. start




lazy lets you defer loading a component’s code until it’s rendered for the first time.
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Built-in React APIs – React
APIs. createContext lets you define and provide context to the child components. Used with useContext. forwardRef lets your component expose a DOM node as a ref to the parent. Used with useRef. <span>lazy lets you defer loading a component’s code until it’s rendered for the first time. memo lets your component skip re-renders with same props. Used with useMemo and useCallback. startTransition lets you mark a state update as non-urgent. Similar to useTransition. How do




memo lets your component skip re-renders with same props. Used with useMemo and useCallback.
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Built-in React APIs – React
ith useContext. forwardRef lets your component expose a DOM node as a ref to the parent. Used with useRef. lazy lets you defer loading a component’s code until it’s rendered for the first time. <span>memo lets your component skip re-renders with same props. Used with useMemo and useCallback. startTransition lets you mark a state update as non-urgent. Similar to useTransition. How do you like these docs? Take our survey! ©2023 Learn React Quick Start Installation Describing




startTransition lets you mark a state update as non-urgent. Similar to useTransition.
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Built-in React APIs – React
with useRef. lazy lets you defer loading a component’s code until it’s rendered for the first time. memo lets your component skip re-renders with same props. Used with useMemo and useCallback. <span>startTransition lets you mark a state update as non-urgent. Similar to useTransition. How do you like these docs? Take our survey! ©2023 Learn React Quick Start Installation Describing the UI Adding Interactivity Managing State Escape Hatches API Reference React APIs Rea




createRoot lets you create a root to display React components inside a browser DOM node.
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Client React DOM APIs – React
hese APIs are typically used at the top level of your app to initialize your React tree. A framework may call them for you. Most of your components don’t need to import or use them. Client APIs <span>createRoot lets you create a root to display React components inside a browser DOM node. hydrateRoot lets you display React components inside a browser DOM node whose HTML content was previously generated by react-dom/server. Browser support React supports all popular brows




hydrateRoot lets you display React components inside a browser DOM node whose HTML content was previously generated by react-dom/server.
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Client React DOM APIs – React
A framework may call them for you. Most of your components don’t need to import or use them. Client APIs createRoot lets you create a root to display React components inside a browser DOM node. <span>hydrateRoot lets you display React components inside a browser DOM node whose HTML content was previously generated by react-dom/server. Browser support React supports all popular browsers, including Internet Explorer 9 and above. Some polyfills are required for older browsers such as IE 9 and IE 10. How do you like thes




React supports all popular browsers, including Internet Explorer 9 and above. Some polyfills are required for older browsers such as IE 9 and IE 10.
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Client React DOM APIs – React
ct components inside a browser DOM node. hydrateRoot lets you display React components inside a browser DOM node whose HTML content was previously generated by react-dom/server. Browser support <span>React supports all popular browsers, including Internet Explorer 9 and above. Some polyfills are required for older browsers such as IE 9 and IE 10. How do you like these docs? Take our survey! ©2023 Learn React Quick Start Installation Describing the UI Adding Interactivity Managing State Escape Hatches API Reference React APIs Rea




Client React DOM APIs

The react-dom/client APIs let you render React components on the client (in the browser). These APIs are typically used at the top level of your app to initialize your React tree. A framework may call them for you. Most of your components don’t need to import or use them.

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Client React DOM APIs – React
e Hatches REACT API Hooks Components APIs Legacy APIs REACT DOM API Components APIs Client APIs Server APIs GET INVOLVED React Community STAY INFORMED React Blog Is this page useful? React Docs <span>Client React DOM APIs The react-dom/client APIs let you render React components on the client (in the browser). These APIs are typically used at the top level of your app to initialize your React tree. A framework may call them for you. Most of your components don’t need to import or use them. Client APIs createRoot lets you create a root to display React components inside a browser DOM node. hydrateRoot lets you display React components inside a browser DOM node whose HTML c




State Hooks

State lets a component “remember” information like user input. For example, a form component can use state to store the input value, while an image gallery component can use state to store the selected image index.

To add state to a component, use one of these Hooks:

 function ImageGallery ( ) { 
const [ index , setIndex ] = useState ( 0 ) ;
// ...
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Built-in React Hooks – React
eact Hooks Hooks let you use different React features from your components. You can either use the built-in Hooks or combine them to build your own. This page lists all built-in Hooks in React. <span>State Hooks State lets a component “remember” information like user input. For example, a form component can use state to store the input value, while an image gallery component can use state to store the selected image index. To add state to a component, use one of these Hooks: useState declares a state variable that you can update directly. useReducer declares a state variable with the update logic inside a reducer function. function ImageGallery() { const [index, setIndex] = useState(0); // ... Context Hooks Context lets a component receive information from distant parents without passing it as props. For example, your app’s top-level component can pass the current UI theme to




Context Hooks

Context lets a component receive information from distant parents without passing it as props. For example, your app’s top-level component can pass the current UI theme to all components below, no matter how deep.

 function Button ( ) { 
const theme = useContext ( ThemeContext ) ;
// ...
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Built-in React Hooks – React
iable that you can update directly. useReducer declares a state variable with the update logic inside a reducer function. function ImageGallery() { const [index, setIndex] = useState(0); // ... <span>Context Hooks Context lets a component receive information from distant parents without passing it as props. For example, your app’s top-level component can pass the current UI theme to all components below, no matter how deep. useContext reads and subscribes to a context. function Button() { const theme = useContext(ThemeContext); // ... Ref Hooks Refs let a component hold some information that isn’t used for rendering, like a DOM node or a timeout ID. Unlike with state, updating a ref does not re-render your component.




Ref Hooks

Refs let a component hold some information that isn’t used for rendering, like a DOM node or a timeout ID. Unlike with state, updating a ref does not re-render your component. Refs are an “escape hatch” from the React paradigm. They are useful when you need to work with non-React systems, such as the built-in browser APIs.

  • useRef declares a ref. You can hold any value in it, but most often it’s used to hold a DOM node.
  • useImperativeHandle lets you customize the ref exposed by your component. This is rarely used.
 function Form ( ) { 
const inputRef = useRef ( null ) ;
// ...
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Built-in React Hooks – React
onent can pass the current UI theme to all components below, no matter how deep. useContext reads and subscribes to a context. function Button() { const theme = useContext(ThemeContext); // ... <span>Ref Hooks Refs let a component hold some information that isn’t used for rendering, like a DOM node or a timeout ID. Unlike with state, updating a ref does not re-render your component. Refs are an “escape hatch” from the React paradigm. They are useful when you need to work with non-React systems, such as the built-in browser APIs. useRef declares a ref. You can hold any value in it, but most often it’s used to hold a DOM node. useImperativeHandle lets you customize the ref exposed by your component. This is rarely used. function Form() { const inputRef = useRef(null); // ... Effect Hooks Effects let a component connect to and synchronize with external systems. This includes dealing with network, browser DOM, animations, widgets written using a different UI




Effect Hooks

Effects let a component connect to and synchronize with external systems. This includes dealing with network, browser DOM, animations, widgets written using a different UI library, and other non-React code.

  • useEffect connects a component to an external system.
 function ChatRoom ( { roomId } ) { 
useEffect ( ( ) => {
const connection = createConnection ( roomId ) ;
connection . connect ( ) ;
return ( ) => connection . disconnect ( ) ;
} , [ roomId ] ) ;
// ...

Effects are an “escape hatch” from the React paradigm. Don’t use Effects to orchestrate the data flow of your application. If you’re not interacting with an external system, you might not need an Effect.

There are two rarely used variations of useEffect with differences in timing:

  • useLayoutEffect fires before the browser repaints the screen. You can measure layout here.
  • useInsertionEffect fires before React makes changes to the DOM. Libraries can insert dynamic CSS here.
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Built-in React Hooks – React
t most often it’s used to hold a DOM node. useImperativeHandle lets you customize the ref exposed by your component. This is rarely used. function Form() { const inputRef = useRef(null); // ... <span>Effect Hooks Effects let a component connect to and synchronize with external systems. This includes dealing with network, browser DOM, animations, widgets written using a different UI library, and other non-React code. useEffect connects a component to an external system. function ChatRoom({ roomId }) { useEffect(() => { const connection = createConnection(roomId); connection.connect(); return () => connection.disconnect(); }, [roomId]); // ... Effects are an “escape hatch” from the React paradigm. Don’t use Effects to orchestrate the data flow of your application. If you’re not interacting with an external system, you might not need an Effect. There are two rarely used variations of useEffect with differences in timing: useLayoutEffect fires before the browser repaints the screen. You can measure layout here. useInsertionEffect fires before React makes changes to the DOM. Libraries can insert dynamic CSS here. Performance Hooks A common way to optimize re-rendering performance is to skip unnecessary work. For example, you can tell React to reuse a cached calculation or to skip a re-render if




Performance Hooks

A common way to optimize re-rendering performance is to skip unnecessary work. For example, you can tell React to reuse a cached calculation or to skip a re-render if the data has not changed since the previous render.

To skip calculations and unnecessary re-rendering, use one of these Hooks:

  • useMemo lets you cache the result of an expensive calculation.
  • useCallback lets you cache a function definition before passing it down to an optimized component.
 function TodoList ( { todos , tab , theme } ) { 
const visibleTodos = useMemo ( ( ) => filterTodos ( todos , tab ) , [ todos , tab ] ) ;
// ...
}

Sometimes, you can’t skip re-rendering because the screen actually needs to update. In that case, you can improve performance by separating blocking updates that must be synchronous (like typing into an input) from non-blocking updates which don’t need to block the user interface (like updating a chart).

To prioritize rendering, use one of these Hooks:

  • useTransition lets you mark a state transition as non-blocking and allow other updates to interrupt it.
  • useDeferredValue lets you defer updating a non-critical part of the UI and let other parts update first.
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Built-in React Hooks – React
useLayoutEffect fires before the browser repaints the screen. You can measure layout here. useInsertionEffect fires before React makes changes to the DOM. Libraries can insert dynamic CSS here. <span>Performance Hooks A common way to optimize re-rendering performance is to skip unnecessary work. For example, you can tell React to reuse a cached calculation or to skip a re-render if the data has not changed since the previous render. To skip calculations and unnecessary re-rendering, use one of these Hooks: useMemo lets you cache the result of an expensive calculation. useCallback lets you cache a function definition before passing it down to an optimized component. function TodoList({ todos, tab, theme }) { const visibleTodos = useMemo(() => filterTodos(todos, tab), [todos, tab]); // ... } Sometimes, you can’t skip re-rendering because the screen actually needs to update. In that case, you can improve performance by separating blocking updates that must be synchronous (like typing into an input) from non-blocking updates which don’t need to block the user interface (like updating a chart). To prioritize rendering, use one of these Hooks: useTransition lets you mark a state transition as non-blocking and allow other updates to interrupt it. useDeferredValue lets you defer updating a non-critical part of the UI and let other parts update first. Resource Hooks Resources can be accessed by a component without having them as part of their state. For example, a component can read a message from a Promise or read styling informatio




Resource Hooks

Resources can be accessed by a component without having them as part of their state. For example, a component can read a message from a Promise or read styling information from a context.

To read a value from a resource, use this Hook:

 function MessageComponent ( { messagePromise } ) { 
const message = use ( messagePromise ) ;
const theme = use ( ThemeContext ) ;
// ...
}
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Built-in React Hooks – React
ets you mark a state transition as non-blocking and allow other updates to interrupt it. useDeferredValue lets you defer updating a non-critical part of the UI and let other parts update first. <span>Resource Hooks Resources can be accessed by a component without having them as part of their state. For example, a component can read a message from a Promise or read styling information from a context. To read a value from a resource, use this Hook: use lets you read the value of a resource like a Promise or context. function MessageComponent({ messagePromise }) { const message = use(messagePromise); const theme = use(ThemeContext); // ... } Other Hooks These Hooks are mostly useful to library authors and aren’t commonly used in the application code. useDebugValue lets you customize the label React DevTools displays for you




Other Hooks

These Hooks are mostly useful to library authors and aren’t commonly used in the application code.

  • useDebugValue lets you customize the label React DevTools displays for your custom Hook.
  • useId lets a component associate a unique ID with itself. Typically used with accessibility APIs.
  • useSyncExternalStore lets a component subscribe to an external store.
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Built-in React Hooks – React
e lets you read the value of a resource like a Promise or context. function MessageComponent({ messagePromise }) { const message = use(messagePromise); const theme = use(ThemeContext); // ... } <span>Other Hooks These Hooks are mostly useful to library authors and aren’t commonly used in the application code. useDebugValue lets you customize the label React DevTools displays for your custom Hook. useId lets a component associate a unique ID with itself. Typically used with accessibility APIs. useSyncExternalStore lets a component subscribe to an external store. Your own Hooks You can also define your own custom Hooks as JavaScript functions. PreviousOverview Nextuse How do you like these docs? Take our survey! © 2023 Learn React Quick Start In




Your own Hooks

You can also define your own custom Hooks as JavaScript functions.

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Built-in React Hooks – React
ays for your custom Hook. useId lets a component associate a unique ID with itself. Typically used with accessibility APIs. useSyncExternalStore lets a component subscribe to an external store. <span>Your own Hooks You can also define your own custom Hooks as JavaScript functions. PreviousOverview Nextuse How do you like these docs? Take our survey! © 2023 Learn React Quick Start Installation Describing the UI Adding Interactivity Managing State Escape Hatches AP




INSERT INTO products VALUES (1, 'Cheese'); This form is a PostgreSQL extension. It fills the columns from the left with as many values as are given, and the rest will be defaulted.
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You can request default values explicitly, for individual columns or for the entire row:

INSERT INTO products (product_no, name, price) VALUES (1, 'Cheese', DEFAULT);

INSERT INTO products DEFAULT VALUES;

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<Fragment>, alternatively written as <>...</>, lets you group multiple JSX nodes together.
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Built-in React Components – React
LVED React Community STAY INFORMED React Blog Is this page useful? React Docs Built-in React Components React exposes a few built-in components that you can use in your JSX. Built-in components <span><Fragment>, alternatively written as <>...</>, lets you group multiple JSX nodes together. <Profiler> lets you measure rendering performance of a React tree programmatically. <Suspense> lets you display a fallback while the child components are loading. <Strict




<Profiler> lets you measure rendering performance of a React tree programmatically.
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Built-in React Components – React
exposes a few built-in components that you can use in your JSX. Built-in components <Fragment>, alternatively written as <>...</>, lets you group multiple JSX nodes together. <span><Profiler> lets you measure rendering performance of a React tree programmatically. <Suspense> lets you display a fallback while the child components are loading. <StrictMode> enables extra development-only checks that help you find bugs early. Your own com




<Suspense> lets you display a fallback while the child components are loading.
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Built-in React Components – React
ragment>, alternatively written as <>...</>, lets you group multiple JSX nodes together. <Profiler> lets you measure rendering performance of a React tree programmatically. <span><Suspense> lets you display a fallback while the child components are loading. <StrictMode> enables extra development-only checks that help you find bugs early. Your own components You can also define your own components as JavaScript functions. How do you l




<StrictMode> enables extra development-only checks that help you find bugs early.
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Built-in React Components – React
SX nodes together. <Profiler> lets you measure rendering performance of a React tree programmatically. <Suspense> lets you display a fallback while the child components are loading. <span><StrictMode> enables extra development-only checks that help you find bugs early. Your own components You can also define your own components as JavaScript functions. How do you like these docs? Take our survey! ©2023 Learn React Quick Start Installation Describing t




You can also define your own components as JavaScript functions.
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Built-in React Components – React
<Suspense> lets you display a fallback while the child components are loading. <StrictMode> enables extra development-only checks that help you find bugs early. Your own components <span>You can also define your own components as JavaScript functions. How do you like these docs? Take our survey! ©2023 Learn React Quick Start Installation Describing the UI Adding Interactivity Managing State Escape Hatches API Reference React APIs Rea




When inserting a lot of data at the same time, consider using the COPY command. It is not as flexible as the INSERT command, but is more efficient. Refer to Section 14.4 for more information on improving bulk loading performance.
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Users can add new types to Post- greSQL using the CREATE TYPE command.
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Table 8.1. Data Types Name Aliases Description bigint int8 signed eight-byte integer bigserial serial8 autoincrementing eight-byte integer bit [ (n) ] fixed-length bit string bit varying [ (n) ] varbit [ (n) ] variable-length bit string boolean bool logical Boolean (true/false) box rectangular box on a plane bytea binary data (“byte array”) character [ (n) ] char [ (n) ] fixed-length character string character varying [ (n) ] varchar [ (n) ] variable-length character string cidr IPv4 or IPv6 network address circle circle on a plane date calendar date (year, month, day) double precision float8 double precision floating-point num- ber (8 bytes) inet IPv4 or IPv6 host address integer int, int4 signed four-byte integer interval [ fields ] [ (p) ] time span json textual JSON data jsonb binary JSON data, decomposed line infinite line on a plane lseg line segment on a plane macaddr MAC (Media Access Control) address macaddr8 MAC (Media Access Control) address (EUI-64 format) money currency amount numeric [ (p, s) ] decimal [ (p, s) ] exact numeric of selectable precision path geometric path on a plane pg_lsn PostgreSQL Log Sequence Number pg_snapshot user-level transaction ID snapshot point geometric point on a plane
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Name Aliases Description polygon closed geometric path on a plane real float4 single precision floating-point number (4 bytes) smallint int2 signed two-byte integer smallserial serial2 autoincrementing two-byte integer serial serial4 autoincrementing four-byte integer text variable-length character string time [ (p) ] [ without time zone ] time of day (no time zone) time [ (p) ] with time zone timetz time of day, including time zone timestamp [ (p) ] [ with- out time zone ] date and time (no time zone) timestamp [ (p) ] with time zone timestamptz date and time, including time zone tsquery text search query tsvector text search document txid_snapshot user-level transaction ID snapshot (deprecated; see pg_snapshot) uuid universally unique identifier xml XML data
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Compatibility The following types (or spellings thereof) are specified by SQL: bigint, bit, bit vary- ing, boolean, char, character varying, character, varchar, date, dou- ble precision, integer, interval, numeric, decimal, real, smallint, time (with or without time zone), timestamp (with or without time zone), xml.
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Some of the input and output functions are not invertible, i.e., the result of an output function might lose accuracy when compared to the original input.
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Each data type has an external representation determined by its input and output functions.
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For more about naming a module with a module path, see Managing dependencies.
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Tutorial: Get started with Go - The Go Programming Language
For example, the module path might be github.com/mymodule. If you plan to publish your module for others to use, the module path must be a location from which Go tools can download your module. <span>For more about naming a module with a module path, see Managing dependencies. For the purposes of this tutorial, just use example/hello. $ go mod init example/hello go: creating new go.mod: module example/hello In your text editor, create a file hello.go in which




Note: For other tutorials, see Tutorials.
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Tutorial: Get started with Go - The Go Programming Language
rite some simple "Hello, world" code. Use the go command to run your code. Use the Go package discovery tool to find packages you can use in your own code. Call functions of an external module. <span>Note: For other tutorials, see Tutorials. Prerequisites Some programming experience. The code here is pretty simple, but it helps to know something about functions. A tool to edit your code. Any text editor you have will work f




fmt package
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Tutorial: Get started with Go - The Go Programming Language
, World!") } This is your Go code. In this code, you: Declare a main package (a package is a way to group functions, and it's made up of all the files in the same directory). Import the popular <span>fmt package, which contains functions for formatting text, including printing to the console. This package is one of the standard library packages you got when you installed Go. Implement a main fu




standard library packages
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Tutorial: Get started with Go - The Go Programming Language
it's made up of all the files in the same directory). Import the popular fmt package, which contains functions for formatting text, including printing to the console. This package is one of the <span>standard library packages you got when you installed Go. Implement a main function to print a message to the console. A main function executes by default when you run the main package. Run your code to see the g




go run command
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Tutorial: Get started with Go - The Go Programming Language
. Implement a main function to print a message to the console. A main function executes by default when you run the main package. Run your code to see the greeting. $ go run . Hello, World! The <span>go run command is one of many go commands you'll use to get things done with Go. Use the following command to get a list of the others: $ go help Call code in an external package When you need your co




Use the following command to get a list of all supported Go commands:

$ go help
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Tutorial: Get started with Go - The Go Programming Language
ecutes by default when you run the main package. Run your code to see the greeting. $ go run . Hello, World! The go run command is one of many go commands you'll use to get things done with Go. <span>Use the following command to get a list of the others: $ go help Call code in an external package When you need your code to do something that might have been implemented by someone else, you can look for a package that has functions you can use in y




Mind is no longer aspectator beholding the world from without and finding its highest satisfaction in the joy of self-sufficing contemplation. The mind is within the world as apart of the latter's own on-going process. It is marked off as mind by the fact that wherever it is found, changes take place in adirected way, so that amovement in adefinite one- way sense from the doubtful and confused to the clear, re- solved and settled takes place. From knowing as an outside beholding to knowing as an active participant in the drama of an on-moving world is the historical transition whose record we have been following. As far as philosophy is concerned, the first direct and im- mediate effect of this shift from knowing which makes adiffer- ence to the knower but none in the world, to knowing which is adirected change within the world, is the complete abandon- ment of what we may term the intellectualist fallacy. By this is meant something which may also be termed the ubiquity of knowledge as a measure of reality. Of the older philosophies, framed before experimental knowing had made any significant progress, it may be said that they made adefinite separation between the world in which man thinks and knows and the
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Since knowledge is the mode of expe- rience that puts in our hands the key to controlling our other dealings with experienced objects, it has acentral position. There is no practical point gained in asserting that athing is what it is experienced to be apart from knowledge. If aman has typhoid fever, he has itj he does not have to search for or pry into it. But to know it, he does have to search: to thought, to intellect, the fever is what it is known to be. For when it is known, the various phenomena of having it, the direct experiences, fall into order jwe have at least that kind of control called understanding, and with this comes the pos- sibility of amore active control. The very fact that other experiences speak, so to say, for themselves makes it uneces- sary to ask what they are. When the nature of an existence is in doubt and we have to seek for it, the idea of reality is consciously present. Hence the thought of existence becomes exclusively associated with knowing. Other ways of experi- encing things exist so obviously that we do not think of existence in connection with them.
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hen if only it can be shown that mathematical rela- tions are themselves alogical construction of thought, the knowing mind is enstated as the constitutive author of the whole scheme. Realistic theories have protested against doc- trines that make the knowing mind the source of the thing known. But they have held to adoctrine of apartial equation of the real and the known jonly they have read the equation from the side of the object instead of the subject. Knowledge must be the grasp or vision of the real as it "is in itself," while emotions and affections deal with it as it is affected with an alien element supplied by the feeling and desiring subject. The postulate of the unique and exclusive relation among experi- enced things of knowledge and the real is shared by epistemo- logical idealist and realist.
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The meaning of aCopernican reversal is that we do not have to go to knowledge to obtain an exclusive hold on reality. The world as we experience it is areal world. But it is not in its primary phases aworld that is known, aworld that is understood, and is intellectually coherent and secure. Knowing consists of operations that give experienced objects aform in which the relations, upon which the onward course of events depends, are securely experienced. It marks atransitional redirection and rearrangement of the real. It is intermediate and instrumental
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In knowledge, causes become means and effects become consequences, and thereby things have meanings. The known object is an antecedent object as that is intentionally rearranged and redisposed, an eventual object whose value is tested by the reconstruction it effects. It emerges, as it were, from the fire of experimental thought as arefined metal issues from operations performed on crude material. It is the same object but the same object with adifference, as aman who has been through conditions which try the temper of his being comes out the same man and adifferent man.
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One may report aquality already sensed in a proposition, as when standing before the fire Iremark upon how hot it is. When seeing something at adistance, Ijudge without sensible contact that it must be hot} "hot" expresses aconsequence which Iinfer would be experienced if Iwere to approach close enough jit designates apossibility of what is actually there in experience. The instance is atrivial one, but it sets forth what happens in every case where any predicate, whether quality or relation, expresses an idea rather than a sensibly perceived characteristic. The difference is not between one mental state called asensation and another called an image. It is between what is experienced as being already there and what marks apossibility of being experienced. If we agree to leave out the eulogistic savor of "ideal" and define it in con- trast with the actual, the possibility denoted by an idea is the ideal phase of the existent.
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Anki Manual (whole site)
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Introduction - Anki Manual
iles 19. Statistics 20. Media 21. Math & Symbols 22. Leeches 23. Add-ons 24. Troubleshooting 25. Sync Server 26. Miscellaneous Contributing FAQs Resources Light (default) Rust Coal Navy Ayu <span>Anki Manual Introduction Quickstart In a hurry? Jump straight to Getting Started. Getting Help Looking for help? Please see Getting Help. Translations Volunteers have contributed translations of th




It is not possible to avqid the impression that the idea of such arealm is simply the hypostatizing in awholesale way of the fact that actual existence has its own possibilities. But in any case devotion to such remote and unattached possibili- ties simply perpetuates the other-worldliness of religious tra- dition, although its other-world is not one supposed to exist. Thought of it is arefuge, not aresource. It becomes effective in relation to the conduct of life only when separation of essence from existence is cancelled jwhen essences are taken to be possibilities to be embodied through action in concrete objects of secure experience. Nothing is gained by reaching the latter through acircuitous course.
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Isuppose that no one can deny that the sense of dependence, insisted upon, for example, by Sohleiermacher, comes close to the heart of the matter
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philosophy committed to rational demonstration of the fixed and antecedent certainty of the ideal, with asharp demarcation of knowledge and higher activity from all forms of practical activity, is aphilosophy which perpetuates the obstacles in the way of realization of the possibility that has been pointed out. It is easy both to minimize the practical effect of philosophic theories and to exaggerate it. Directly, it is not very great. But as an intel- lectual formulation and justification of habits and attitudes already obtaining among men its influence is immense. The vis inertiae of habit is tremendous, and when it is reinforced by aphilosophy which also is embodied in institutions, it is so great as to be afactor in sustaining the present confusion and conflict of authorities and allegiances.
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