# on 14-Dec-2023 (Thu)

#### Annotation 7604741999884

 Definition of the argument of a complex number #has-images The angle between the positive real axis and OP is called the argument of $$z$$, which is usually denoted by $$\arg{z}$$: $$\displaystyle \arg z=\angle z=\theta, \text{where }\tan{\theta}=\frac{y}{x},z\neq 0$$

#### Flashcard 7604747242764

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The angle between the positive real axis and OP is called the argument of $$z$$, which is usually denoted by $$\arg{z}$$: [...]

$$\displaystyle \arg z=\angle z=\theta, \text{where }\tan{\theta}=\frac{y}{x},z\neq 0$$

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The angle between the positive real axis and OP is called the argument of $$z$$, which is usually denoted by $$\arg{z}$$: $$\displaystyle \arg z=\angle z=\theta, \text{where }\tan{\theta}=\frac{y}{x},z\neq 0$$

#### Annotation 7604750388492

 复数向量所在区间与其幅角的关系 复数向量所在区间与其幅角的关系：$$\theta=\tan^{-1}\left(\frac{y}{x}\right)= \begin{cases}\tan^{-1}\left(\frac{y}{x}\right) & \text { if } x>0 \\\pi-\tan^{-1}\left(\frac{y}{-x}\right) & \text { if } x<0 \text { and } y \geq 0 \\-\left(\pi-\tan^{-1}\left(\frac{y}{x}\right)\right) & \text { if } x<0 \text { and } y<0 \\ +\frac{\pi}{2} & \text { if } x=0 \text { and } y>0 \\ -\frac{\pi}{2} & \text { if } x=0 \text { and } y<0 \\ \text { undefined } & \text { if } x=0 \text { and } y=0\end{cases}$$

#### Flashcard 7604752223500

Question

$$\theta=\tan^{-1}\left(\frac{y}{x}\right)= \begin{cases}\tan^{-1}\left(\frac{y}{x}\right) & \text { if } x>0 \\\pi-\tan^{-1}\left(\frac{y}{x}\right) & \text { if } x<0 \text { and } y \geq 0 \\-\left(\pi-\tan^{-1}\left(\frac{y}{x}\right)\right) & \text { if } x<0 \text { and } y<0 \\ +\frac{\pi}{2} & \text { if } x=0 \text { and } y>0 \\ -\frac{\pi}{2} & \text { if } x=0 \text { and } y<0 \\ \text { undefined } & \text { if } x=0 \text { and } y=0\end{cases}$$

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#### Annotation 7604754320652

 the object of knowledge is eventual j that is, it is an outcome of directed experimental operations, instead of something in sufficient existence before the act of knowing. The further point to be presented is that, along with this change, sensible and rational factors cease to be competi- tors for primary rank. They are allies, cooperating to make knowledge possible. Isolation from each other is an expression of the isolation of each from organic connection with action.

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#### Annotation 7604755893516

 Kant's well known saying that perception without conception is blind, conception without perception empty. His doctrine none the less is fundamentally different from that which results from an analysis of experimental knowing. The fundamental difference lies in the fact that, according to the latter, the dis- tinction of sense and thought occurs within the process of re-

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#### Annotation 7604757466380

 From the experimental point of view, the art of knowing demands skill in selecting appropriate sense-data on one side and connecting principles, or conceptual theories, on the other. It requires adeveloped and constantly progressive technique to settle upon both the observational data and the idea that assist inquiry in reaching aconclusion in any particular case. But in Kant's view, the distinction and the connection between the two, while necessary to anything which may be termed cognition, have nothing to do with the validity of any particu- lar enterprise of knowing. Illusion and error exemplify the synthesis of sense and understanding quite as much as does the soundest instance of scientific discovery. In one case, the heart of the whole matter is the exercise of adifferential control which makes the difference between good and bad knowing. In Kant's scheme the blessings of the categories descend upon the material of sense without reference to making adistinction be- tween the true and the false.

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#### Annotation 7604759039244

 Aphysician, for example, is called by apatient. His orig- inal material of experience is thereby provided} it requires a stretch of useless imagination to fancy that the ill man is a mass of sense data organized by categories. This experienced object sets the problem of inquiry. Certain clinical operations are performed, sounding, tapping, getting registrations o pulse, temperature, respiration, etc. These constitute the symp- toms} they supply the evidence to be interpreted. The philoso- pher or logician, looking on, sees they are that part of the original object which is capable of being presented in observa- tion as that is sensibly present. The results are not all that is or can be observed, but are those phases and portions of the experienced whole that are judged to be relevant to making an inference as to the nature of the ailment. The observations mean something not in and of themselves, but are given meaning in the light of the systematized knowledge of medi- cine as far as that is at the command of the practitioner. He calls upon his store of knowledge to suggest ideas that may aid him in reaching ajudgment as to the nature of the trouble and its proper treatment.

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#### Annotation 7604760612108

 may be asserted that the Kantian the- ory went wrong because it took distinctions that are genuine and indispensable out of their setting and function in actual inquiry. It generalized them into fixed and wholesale distinc- tions, losing sight of their special roles in attainment of those tested beliefs which give security. Consequently artificial com- plications were engendered, and insoluble puzzles created. Take for example the fragmentary and isolated character of sense-data. Taken in isolation from acontext in aparticu- lar inquiry they undoubtedly have this character. Hence when they are generalized into acharacter at large, the result is the doctrine of the disconnected "atomicity" of sense-data. This doctrine is common to sensationalism and to some forms of the new realism, along with Kantianism. As amatter of fact, smells, tastes, sounds, pressures, colors, etc., are not iso- lated jthey are bound together by all kinds of interactions or connections, among which are included the habitual responses of the one having the experience. Some connections are organic, flowing from the constitution of the subject. Others have be- come engrained in habit because of education and the cus- tomary state of culture. But these habitual connections are obstacles rather than aids. Some of them are irrelevant and mis- leading. In any case, they fail to provide the clews, the evi- dence, which is wanted in the particular inquiry in hand. Con- sequently, sense qualities are artificially isolated from their ordinary connections so that the inquirer is free to see them in anew light or as constituents of anew object.

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#### Annotation 7604762184972

 f we keep an eye on the actual enterprise of knowing, it is clear that only sense-data can supply evidential subject- matter} ideas of what is not presented in sense interpret evi- dence, but they cannot constitute it. The whole history of science shows, however, that material directly and originally observed does not furnish good evidential material} as we saw, it was the essential mistake of ancient science to suppose that we can base inference upon observed objects without an artificial prior analytic resolution. Hence there is need of a distinctive type of experimental operations which detach some qualities of the object} these form sense-data in the technical meaning of the word.

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#### Annotation 7604763757836

 Observed material is necessary to suggest ideas and it is equally necessary to test them. The senses are, existentially speaking, the organs by which we obtain the material of observation. But, as we have previously noted, this material is significant and effective for purposes of knowing only as it is connected with operations of which it is the product. Merely physical interactions, whether of external things or of the organism, yield observations that form the material of inquiry} aprob- lematic material. Only operations intentionally performed and attentively noted in connection with their products give ob- served material apositive intellectual value, and this condi- tion is satisfied only by thought: ideas are the perception of this connection.

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#### Annotation 7604765330700

 neither mere doing nor mere undergoing, but is an acknowledgment of the connection between something done and something undergone in consequence of the doing.

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#### Annotation 7604766903564

 the distinction between sense- data and objects of rational apprehension is one which occurs within reflective investigation, for the sake of regulating its procedure.

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#### Annotation 7604768476428

 The history of the theory of knowledge or epistemology would have been very different if instead of the word "data" or "givens," it had happened to start with calling the quali- ties in question "takens." Not that the data are not existential and qualities of the ultimately "given" that is, the total subject-matter which is had in non-cognitive experiences. But as data they are selected from this total original subject-mat- ter which gives the impetus to knowing} they are discriminated for apurpose: that, namely, of affording signs or evidence to define and locate aproblem, and thus give aclew to its resolution.

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#### Annotation 7604770049292

 Only the assumption such is made by Kant and is common to the traditional theories that all experience is inherently cognitive leads to the doctrine that perception of the patient is acase of knowledge. In reality the original perception furnishes the problem for knowing j it is something to be known, not an object of knowing. And in knowing, the first thing to be done is to select from the mass of presented qualities those which, in distinction from other qualities, throw light upon the nature of the trouble. As they are deliberately selected, being discriminated by special tech- nical operations, they become data; these are called sensible simply because of the role of sense organs in their generation. They may then be formulated as the subject-matter of primi- tive existential propositions. But even so, there is no class of such propositions In general. Each inquiry yields its own primitive existential propositions, even though they all agree in having for their objects qualities which investigation reveals to be connected with the use of organs of sense. Moreover, these primitive propositions are such only in alogical sense as distinct from being empirically primitive, and they are only hypothetical or conditional. This statement does not imply that their existence is hypothetical jperception, as far as it is properly conducted, warrants their existence. But their status in inquiry is tentative. Many, perhaps most, errors in physical inference arise from taking as data things that are not data for the problem in hand; they undoubtedly exist, but they are not the evidence that is demanded.

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#### Annotation 7604771622156

 genuine clews are usually obscure and have to be searched out. The conditional character of sense-data in inferential inquiry means, then, that they have to be tested by their consequences. They are good clews or evidence when they instigate operations whose effect is to solve the problem in hand.

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#### Annotation 7604773195020

 When, on the other hand, it is seen that the object of knowledge is prospective and eventual, being the result of inferential or reflective operations which redispose what was antecedently existent, the subject-matters called respectively sensible and conceptual are seen to be complementary in effec- tive direction of inquiry to an intelligible conclusion.

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#### Annotation 7604774767884

 In effect, traditional theories treat all reflective or inferential knowing as cases of "explanation," and by explanation is meant making some seemingly new ob- ject or problem plain and clear by identifying its elements with something previously known, ultimately something said to be known immediately and intuitively, or without infer- ence. In traditional theory, "discursive" knowledge, that in- volving reflection, must always be referred for its validation back to what is immediately known. It cannot bring its credentials with it and test its results in the very process of reaching them. There is postulated identity implicit or explicit of the results of inference with things known without infer- ence. Making the identity explicit constitutes proof.

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#### Annotation 7604776865036

 hen it is stated that the conclusions of knowledge involving inference must be sub- ordinated to knowledge which is had directly and immediately, and must be carried to the latter for proof and verification, we are at once struck by the multitude of theories regarding what is immediately and infallibly known. The diversity and con- tradictions give ground for asuspicion that in no case is the "knowledge" in question as self-evident as it is asserted to be. And there is good theoretical ground for the suspicion. Suppose aman "explains" the eclipse of the moon by saying it is due to the attempt of adragon to devour it. To him the devouring dragon is amore evident fact than is the darkening of the moon. To us the existence of an animal capable of such afeat is the doubtful matter. It will be objected that it is unfair to take such an absurd case as an instance: dragons are not the sort of thing which any philosopher has asserted to be the ob- ject of direct and certain non-inferential knowledge. But the illustration still serves apurpose.

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#### Annotation 7604778437900

 The thing to be known is "explained" by identification with something else. What guarantees this something else? If it too has to be guaranteed by identification with something else, there is an infinite regress. To avoid this regress, we stop short and assert that this or that object or truth is directly known, by sense intuition, by rational intuition, as adirect de- liverance of consciousness, or in some other way. But what is such aprocedure except the essence of what Bentham called ipse dixitism? What is it but arbitrary dogmatism?

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#### Annotation 7604780010764

 This act of taking and using objects already known is practically justified} it is like eating afruit without asking how it was grown. But many theories of knowledge take this retrospective use of things known in virtue of earlier opera- tions as typical of the nature of knowledge itself. Being re- minded of something we already know is taken as the pattern of all knowing. When the thing of which we are now retro- spectively aware was in process of being known, it was prospec- tive and eventual to inquiry, not something already "given." And it has cognitive force in anew inquiry whose objective and ultimate object is now prospective. Taking what is already known or pointing to it is no more acase of knowledge than taking achisel out of atool-box is the making of the tool. Because some theories of knowledge have taken the operations that yield the known object to be merely mental or psychical instead of overt redispositions of antecedent subject-matter (and thus have terminated in some form of "idealism") is no reason for denying the mediated character of all known objects.

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#### Annotation 7604781583628

 the basic error of traditional theories of knowledge resides in the isolation and fixation of some phase of the whole process of inquiry in resolving problematic situations. Sometimes sense- data are so taken jsometimes, conceptions} sometimes, objects previously known. An episode in aseries of operational acts is fastened upon, and then in its isolation and consequent frag- mentary character is made the foundation of the theory of knowing in its entirety.

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#### Annotation 7604783156492

 The case stands radically otherwise when it is seen that "mental" states and acts are organs of knowing things not directly but through the overt actions which they evoke and direct. For the consequences of these acts constitute the object said to be known jand these consequences are public and open. Doubt and skepticism attach only to the adequacy of the opera- tions used in achieving the issue which transforms aprob- lematic situation into asettled or resolved one. Instead of being impotent and paralyzing, they are opportunities for bettering concrete methods of inquiry.

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#### Annotation 7604793642252

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D The largest proportion of patients (70 percent) with ADHF are admitted due to worsening chronic HF, up to 15 to 20 percent of patients present with HF for the first time, and approximately 5 percent are admitted for advanced or end-stage HF

UpToDate
h postdischarge readmission rates [1-12]. The onset and severity of symptoms of ADHF vary and depend on the nature of the underlying cardiac disease and the rate at which the syndrome develops. <span>The largest proportion of patients (70 percent) with ADHF are admitted due to worsening chronic HF, up to 15 to 20 percent of patients present with HF for the first time, and approximately 5 percent are admitted for advanced or end-stage HF. Low blood pressure (<8 percent) or shock (<3 percent) are complications of ADHF [1,2,11]. CAUSES AND PRECIPITATING FACTORS — Appropriate therapy for ADHF requires identification

#### Annotation 7604794690828

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D Low blood pressure (<8 percent) or shock (<3 percent) are complications of ADHF [ 1,2,11]

UpToDate
with ADHF are admitted due to worsening chronic HF, up to 15 to 20 percent of patients present with HF for the first time, and approximately 5 percent are admitted for advanced or end-stage HF. <span>Low blood pressure (<8 percent) or shock (<3 percent) are complications of ADHF [1,2,11]. CAUSES AND PRECIPITATING FACTORS — Appropriate therapy for ADHF requires identification of the specific HF phenotype as well as the potential causes and precipitants. Causes are the pr

#### Annotation 7604795739404

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D Appropriate therapy for ADHF requires identification of the specific HF phenotype as well as the potential causes and precipitants.

UpToDate
oximately 5 percent are admitted for advanced or end-stage HF. Low blood pressure (<8 percent) or shock (<3 percent) are complications of ADHF [1,2,11]. CAUSES AND PRECIPITATING FACTORS — <span>Appropriate therapy for ADHF requires identification of the specific HF phenotype as well as the potential causes and precipitants. Causes are the primary condition or disease process leading to the development of HF. Precipitants are triggers or contributing factors for decompensation in patients with established c

#### Annotation 7604796787980

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D The following are the major causes for new onset ADHF: ● Coronary artery disease: - Myocardial infarction (MI)/ischemia. - Ventricular septal rupture. (See "Acute myocardial infarction: Mechanical complications".) ● Arrhythmias: • Atrial fibrillation and atrial flutter. (See "Overview of the acute management of tachyarrhythmias", section on 'Narrow QRS complex tachyarrhythmias'.) • Ventricular tachycardia, ventricular fibrillation, or high-frequency ventricular ectopy. (See "Overview of the acute management of tachyarrhythmias", section on 'Wide QRS complex tachyarrhythmias'.) ● Myocarditis. (See "Clinical manifestations and diagnosis of myocarditis in adults".) ● Acute valve syndromes: • Acute mitral or aortic regurgitation secondary to infective endocarditis, ruptured chordae of a degenerative mitral valve, ischemic papillary muscle rupture, or aortic dissection. (See "Acute mitral regurgitation in adults" and "Acute aortic regurgitation in adults".) • Thrombosed mechanical aortic or mitral valve. (See ...

UpToDate
e primary condition or disease process leading to the development of HF. Precipitants are triggers or contributing factors for decompensation in patients with established chronic heart disease. <span>The following are the major causes for new onset ADHF: ●Coronary artery disease: •Acute coronary syndrome. (See "Initial evaluation and management of suspected acute coronary syndrome (myocardial infarction, unstable angina) in the emergency department" and "Diagnosis of acute myocardial infarction".) -Myocardial infarction (MI)/ischemia. -Ventricular septal rupture. (See "Acute myocardial infarction: Mechanical complications".) ●Arrhythmias: •Atrial fibrillation and atrial flutter. (See "Overview of the acute management of tachyarrhythmias", section on 'Narrow QRS complex tachyarrhythmias'.) •Ventricular tachycardia, ventricular fibrillation, or high-frequency ventricular ectopy. (See "Overview of the acute management of tachyarrhythmias", section on 'Wide QRS complex tachyarrhythmias'.) ●Myocarditis. (See "Clinical manifestations and diagnosis of myocarditis in adults".) ●Acute valve syndromes: •Acute mitral or aortic regurgitation secondary to infective endocarditis, ruptured chordae of a degenerative mitral valve, ischemic papillary muscle rupture, or aortic dissection. (See "Acute mitral regurgitation in adults" and "Acute aortic regurgitation in adults".) •Thrombosed mechanical aortic or mitral valve. (See "Bioprosthetic valve thrombosis, thromboembolism, and obstruction: Clinical manifestations and diagnosis".) •Tear or perforation of a bioprosthetic aortic or mitral valve leaflet. (See "Clinical manifestations and diagnosis of surgical aortic and mitral prosthetic valve regurgitation".) ●Progressive valve disease: •Severe aortic or mitral valve stenosis, including left atrial myxoma. (See "Clinical manifestations and diagnosis of aortic stenosis in adults" and "Rheumatic mitral stenosis: Clinical manifestations and diagnosis".) •Severe aortic or mitral regurgitation. (See "Clinical manifestations and diagnosis of chronic aortic regurgitation in adults" and "Clinical manifestations and diagnosis of chronic mitral regurgitation".) ●Cardiomyopathic states: •Hypertrophic cardiomyopathy. (See "Hypertrophic cardiomyopathy: Clinical manifestations, diagnosis, and evaluation".) •Recent onset dilated cardiomyopathy. (See "Familial dilated cardiomyopathy: Prevalence, diagnosis and treatment" and "Causes of dilated cardiomyopathy".) •Tachycardia mediated cardiomyopathy. (See "Arrhythmia-induced cardiomyopathy".) •Stress (takotsubo) cardiomyopathy. (See "Clinical manifestations and diagnosis of stress (takotsubo) cardiomyopathy".) ●Poorly controlled hypertension: •Bilateral renal artery stenosis. (See "Chronic kidney disease resulting from atherosclerotic renal artery stenosis", section on 'Clinical manifestations'.) ADHF due to decompensation of chronic HF can occur without known precipitant factors but more often occurs with one or more factors, such as infection, uncontrolled hypertension, rhythm

#### Annotation 7604797836556

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D ADHF due to decompensation of chronic HF can occur without known precipitant factors but more often occurs with one or more factors, such as infection, uncontrolled hypertension, rhythm disturbances, and nonadherence with drugs and diet.

UpToDate
".) ●Poorly controlled hypertension: •Bilateral renal artery stenosis. (See "Chronic kidney disease resulting from atherosclerotic renal artery stenosis", section on 'Clinical manifestations'.) <span>ADHF due to decompensation of chronic HF can occur without known precipitant factors but more often occurs with one or more factors, such as infection, uncontrolled hypertension, rhythm disturbances, and nonadherence with drugs and diet. Moreover, the in-hospital course is determined by the interplay between precipitants, underlying structural heart disease, and comorbidities. These factors are listed in the table (tabl

#### Annotation 7604798885132

#Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D
Precipitants of heart failure
 Dietary indiscretion Vigorous fluid administration Noncompliance to medical regimen Worsening renal failure Uncontrolled hypertension Anemia Systemic infection Pulmonary embolism Myocardial ischemia Tachyarrhythmias and bradyarrhythmias Electrolyte disturbances Severe emotional or physical stress Hyperthyroidism and hypothyroidism Cardiodepressant and other drugs Anti-inflammatory drugs Antiarrhythmic drugs Calcium channel blockers Beta adrenergic blocking agents

UpToDate
le Access Help & Training Demos Wolters Kluwer Health Emmi® Facts & Comparisons® Lexicomp® Medi-Span® Loading Please wait 1 of 11 Export to Powerpoint Print Share Bookmark Rate Feedback <span>Precipitants of heart failure Dietary indiscretion Vigorous fluid administration Noncompliance to medical regimen Worsening renal failure Uncontrolled hypertension Anemia Systemic infection Pulmonary embolism Myocardial ischemia Tachyarrhythmias and bradyarrhythmias Electrolyte disturbances Severe emotional or physical stress Hyperthyroidism and hypothyroidism Cardiodepressant and other drugs Anti-inflammatory drugs Antiarrhythmic drugs Calcium channel blockers Beta adrenergic blocking agents Graphic 117289 Version 1.0 © 2023 UpToDate, Inc. and/or its affiliates. All Rights Reserved. Graphics in this topic Precipitants of heart failure Acute decompensated heart failure: Rapi

#### Annotation 7604799933708

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D Patients present with a myriad of chief complaints, symptoms, and physical examination findings. Such heterogeneity prompts an initially broad differential diagnosis, thus securing the correct diagnosis can be challenging.

UpToDate
al course is determined by the interplay between precipitants, underlying structural heart disease, and comorbidities. These factors are listed in the table (table 1). CLINICAL MANIFESTATIONS — <span>Patients present with a myriad of chief complaints, symptoms, and physical examination findings. Such heterogeneity prompts an initially broad differential diagnosis, thus securing the correct diagnosis can be challenging. For practical purposes, it is helpful to view the presentation of ADHF according to the predominant clinical characteristics on admission. As noted above, most patients presenting with

#### Annotation 7604800982284

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D Approximately 50 percent of patients hospitalized for HF have HF with preserved ejection fraction (HFpEF; left ventricular ejection fraction [LVEF] >50 percent); the remainder of patients have HF with reduced ejection fraction (HFrEF; LVEF ≤40 percent) or HF with mid-range ejection fraction (LVEF 41 to 50 percent).

UpToDate
ened over the preceding days and weeks but have not been sufficient for the patient to seek medical attention. In a minority of patients, an episode of ADHF may be the first presentation of HF. <span>Approximately 50 percent of patients hospitalized for HF have HF with preserved ejection fraction (HFpEF; left ventricular ejection fraction [LVEF] >50 percent); the remainder of patients have HF with reduced ejection fraction (HFrEF; LVEF ≤40 percent) or HF with mid-range ejection fraction (LVEF 41 to 50 percent). (See "Epidemiology of heart failure", section on 'Magnitude of the problem'.) The following five clinical and hemodynamic profiles are modified from those described in the 2021 European

#### Annotation 7604802030860

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D The following five clinical and hemodynamic profiles are modified from those described in the 2021 European Society of Cardiology guidelines for the diagnosis and treatment of ADHF [12]: ● ADHF without pulmonary edema ● ADHF with severe pulmonary edema ● Cardiogenic shock ● High-output HF ● Right HFThe above clinical groups are not mutually exclusive (eg, a patient with hypertensive crisis or cardiogenic shock may develop severe pulmonary edema).

UpToDate
reduced ejection fraction (HFrEF; LVEF ≤40 percent) or HF with mid-range ejection fraction (LVEF 41 to 50 percent). (See "Epidemiology of heart failure", section on 'Magnitude of the problem'.) <span>The following five clinical and hemodynamic profiles are modified from those described in the 2021 European Society of Cardiology guidelines for the diagnosis and treatment of ADHF [12]: ●ADHF without pulmonary edema ●ADHF with severe pulmonary edema ●Cardiogenic shock ●High-output HF ●Right HF The above clinical groups are not mutually exclusive (eg, a patient with hypertensive crisis or cardiogenic shock may develop severe pulmonary edema). ADHF — This syndrome is seen in patients with new-onset HF or acute decompensation of chronic HF who develop signs or symptoms of decompensation; in this setting, there is no cardiogeni

#### Annotation 7604803079436

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D ADHF — This syndrome is seen in patients with new-onset HF or acute decompensation of chronic HF who develop signs or symptoms of decompensation; in this setting, there is no cardiogenic shock or hypertensive crisis. There may be no, or mild, pulmonary congestion. This scenario accounts for 50 to 70 percent of all HF admissions [13-16]. In contrast to the other phenotypes, this presentation is characterized by more gradual onset, and the primary alteration is progressive fluid retention and systemic congestion. New-onset HF is seen much less frequently (less than one-third of HF admissions) than decompensation of chronic HF but may present with the same phenotype.

UpToDate
ardiogenic shock ●High-output HF ●Right HF The above clinical groups are not mutually exclusive (eg, a patient with hypertensive crisis or cardiogenic shock may develop severe pulmonary edema). <span>ADHF — This syndrome is seen in patients with new-onset HF or acute decompensation of chronic HF who develop signs or symptoms of decompensation; in this setting, there is no cardiogenic shock or hypertensive crisis. There may be no, or mild, pulmonary congestion. This scenario accounts for 50 to 70 percent of all HF admissions [13-16]. In contrast to the other phenotypes, this presentation is characterized by more gradual onset, and the primary alteration is progressive fluid retention and systemic congestion. New-onset HF is seen much less frequently (less than one-third of HF admissions) than decompensation of chronic HF but may present with the same phenotype. Usual symptoms: ●Progressive dyspnea is the most common complaint of patients presenting with ADHF. ●Symptoms of abdominal and peripheral congestion – Patients may report ankle swelling

#### Annotation 7604804128012

 ADHF #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D Usual symptoms: ● Progressive dyspnea is the most common complaint of patients presenting with ADHF. ● Symptoms of abdominal and peripheral congestion – Patients may report ankle swelling and epigastric tenderness or a sensation of abdominal fullness. Abdominal tenderness is often due to hepatic congestion and distention of the hepatic capsule. With severe hepatic congestion, the patient may also complain of nausea and anorexia. ● Other symptoms include nocturia and neurologic symptoms such as confusion, headaches, insomnia, anxiety, disorientation, and impaired memory.

UpToDate
id retention and systemic congestion. New-onset HF is seen much less frequently (less than one-third of HF admissions) than decompensation of chronic HF but may present with the same phenotype. <span>Usual symptoms: ●Progressive dyspnea is the most common complaint of patients presenting with ADHF. ●Symptoms of abdominal and peripheral congestion – Patients may report ankle swelling and epigastric tenderness or a sensation of abdominal fullness. Abdominal tenderness is often due to hepatic congestion and distention of the hepatic capsule. With severe hepatic congestion, the patient may also complain of nausea and anorexia. ●Other symptoms include nocturia and neurologic symptoms such as confusion, headaches, insomnia, anxiety, disorientation, and impaired memory. Physical signs: ●Vary according to the severity of fluid overload HF. ●Signs of congestion – An elevated jugular venous pressure, positive hepatojugular reflux test, and a tender, enlar

#### Annotation 7604805963020

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D Diminished air entry at the lung bases is usually caused by a pleural effusion, which is often more frequent in the right pleural cavity than in the left.

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erity of fluid overload HF. ●Signs of congestion – An elevated jugular venous pressure, positive hepatojugular reflux test, and a tender, enlarged liver are frequent findings in these patients. <span>Diminished air entry at the lung bases is usually caused by a pleural effusion, which is often more frequent in the right pleural cavity than in the left. Rales (crackles) and wheezing may or may not accompany signs of pleural effusion. An absence of rales does not imply lack of pulmonary venous pressure elevation. Leg edema is frequently

#### Annotation 7604807011596

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D Rales (crackles) and wheezing may or may not accompany signs of pleural effusion. An absence of rales does not imply lack of pulmonary venous pressure elevation.

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e frequent findings in these patients. Diminished air entry at the lung bases is usually caused by a pleural effusion, which is often more frequent in the right pleural cavity than in the left. <span>Rales (crackles) and wheezing may or may not accompany signs of pleural effusion. An absence of rales does not imply lack of pulmonary venous pressure elevation. Leg edema is frequently evident in both legs, particularly in the pretibial region and ankles in ambulatory patients. Sacral and upper thigh edema can be detected in patients who are be

#### Annotation 7604808060172

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D Leg edema is frequently evident in both legs, particularly in the pretibial region and ankles in ambulatory patients. Sacral and upper thigh edema can be detected in patients who are bedridden.

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leural cavity than in the left. Rales (crackles) and wheezing may or may not accompany signs of pleural effusion. An absence of rales does not imply lack of pulmonary venous pressure elevation. <span>Leg edema is frequently evident in both legs, particularly in the pretibial region and ankles in ambulatory patients. Sacral and upper thigh edema can be detected in patients who are bedridden. ●Cardiac examination – This may be entirely normal in patients with HF secondary to diastolic dysfunction, whereas many patients with advanced systolic dysfunction exhibit a third heart

#### Annotation 7604809108748

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D Cardiac examination – This may be entirely normal in patients with HF secondary to diastolic dysfunction, whereas many patients with advanced systolic dysfunction exhibit a third heart sound and a laterally displaced apex beat. A murmur of mitral regurgitation is often audible when the left ventricle (LV) is markedly enlarged, or a tricuspid regurgitation murmur is present when the right ventricle is volume or pressure overloaded.

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eg edema is frequently evident in both legs, particularly in the pretibial region and ankles in ambulatory patients. Sacral and upper thigh edema can be detected in patients who are bedridden. ●<span>Cardiac examination – This may be entirely normal in patients with HF secondary to diastolic dysfunction, whereas many patients with advanced systolic dysfunction exhibit a third heart sound and a laterally displaced apex beat. A murmur of mitral regurgitation is often audible when the left ventricle (LV) is markedly enlarged, or a tricuspid regurgitation murmur is present when the right ventricle is volume or pressure overloaded. ●Chest radiograph in this setting may show cardiomegaly. Some patients have evidence of pleural effusion and redistribution of blood flow from bases to the upper lobes. There may or may

#### Annotation 7604810157324

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D ADHF with severe pulmonary edema — Pulmonary edema has been observed in 15 percent or more of patients admitted with ADHF [13], but severe pulmonary edema is seen in less than 3 percent of these patients [1]. This phenotype is characterized by the rapid onset of symptoms or signs of HF, frequently presenting with a systolic blood pressure >180 mmHg [17]. Patients with this condition frequently have a history of poorly controlled hypertension [18]. There is usually predominant pulmonary rather than systemic congestion, as is manifest by minimal weight gain prior to admission.

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atients have evidence of pleural effusion and redistribution of blood flow from bases to the upper lobes. There may or may not be evidence of interstitial edema. (See 'Chest radiograph' below.) <span>ADHF with severe pulmonary edema — Pulmonary edema has been observed in 15 percent or more of patients admitted with ADHF [13], but severe pulmonary edema is seen in less than 3 percent of these patients [1]. This phenotype is characterized by the rapid onset of symptoms or signs of HF, frequently presenting with a systolic blood pressure >180 mmHg [17]. Patients with this condition frequently have a history of poorly controlled hypertension [18]. There is usually predominant pulmonary rather than systemic congestion, as is manifest by minimal weight gain prior to admission. Clinical findings: ●Patients typically experience a sudden and overwhelming sensation of suffocation and air hunger; this is invariably accompanied by extreme anxiety, cough, expectorat

#### Annotation 7604811205900

 ADHF with severe pulmonary edema #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D Clinical findings: ● Patients typically experience a sudden and overwhelming sensation of suffocation and air hunger; this is invariably accompanied by extreme anxiety, cough, expectoration of a pink frothy liquid, and a sensation of drowning. ● The patient sits bolt upright, is unable to speak in full sentences, and may thrash about. The respiratory rate is increased, the alae nasi are dilated, and there is inspiratory retraction of the intercostal spaces and supraclavicular fossae. ● Respiration is often noisy, and there may be audible inspiratory and expiratory gurgling sounds. An ominous sign is obtundation, which may be a sign of severe hypoxemia. Sweating is profuse, and the skin tends to be cool, ashen, and cyanotic, reflecting increased sympathetic outflow. ● The pulse rate is most often elevated secondary to an increased adrenergic drive. When the blood pressure is found to be markedly elevated, it is more likely to be the cause of, or an important contributing factor to, pulmonary edema rather than the consequence of the condition. ● The oxygen saturation is usually less than 90 percent of room air before treatment. Auscultation of the lungs usually reveals coarse airway sounds bilaterally with rhonchi, wheezes, and moist fine crepitant rales that are detected first at the lung bases but then extend upward to the apices as the lung edema worsens. ● Cardiac auscultation may be difficult in the acute situation, but third and fourth heart sounds may be present. When valvular abnormalities and/or mechanical complications after MI result in ADHF, the murmurs of mitral and aortic regurgitation and ischemic ventricular septal defect are often audible, but detection requires a careful and skillful auscultator. (See "Auscultation of cardiac murmurs in adults".)

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equently have a history of poorly controlled hypertension [18]. There is usually predominant pulmonary rather than systemic congestion, as is manifest by minimal weight gain prior to admission. <span>Clinical findings: ●Patients typically experience a sudden and overwhelming sensation of suffocation and air hunger; this is invariably accompanied by extreme anxiety, cough, expectoration of a pink frothy liquid, and a sensation of drowning. ●The patient sits bolt upright, is unable to speak in full sentences, and may thrash about. The respiratory rate is increased, the alae nasi are dilated, and there is inspiratory retraction of the intercostal spaces and supraclavicular fossae. ●Respiration is often noisy, and there may be audible inspiratory and expiratory gurgling sounds. An ominous sign is obtundation, which may be a sign of severe hypoxemia. Sweating is profuse, and the skin tends to be cool, ashen, and cyanotic, reflecting increased sympathetic outflow. ●The pulse rate is most often elevated secondary to an increased adrenergic drive. When the blood pressure is found to be markedly elevated, it is more likely to be the cause of, or an important contributing factor to, pulmonary edema rather than the consequence of the condition. ●The oxygen saturation is usually less than 90 percent of room air before treatment. Auscultation of the lungs usually reveals coarse airway sounds bilaterally with rhonchi, wheezes, and moist fine crepitant rales that are detected first at the lung bases but then extend upward to the apices as the lung edema worsens. ●Cardiac auscultation may be difficult in the acute situation, but third and fourth heart sounds may be present. When valvular abnormalities and/or mechanical complications after MI result in ADHF, the murmurs of mitral and aortic regurgitation and ischemic ventricular septal defect are often audible, but detection requires a careful and skillful auscultator. (See "Auscultation of cardiac murmurs in adults".) ●The chest radiograph may show cardiomegaly, upper zone redistribution of blood flow, interstitial edema (with ill-defined vessels, peribronchial cuffing, and interlobular septal thicke

#### Annotation 7604813040908

 ADHF with severe pulmonary edema #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D The chest radiograph may show cardiomegaly, upper zone redistribution of blood flow, interstitial edema (with ill-defined vessels, peribronchial cuffing, and interlobular septal thickening), and alveolar edema (with perihilar and lower-lobe airspace filling, with the periphery generally spared in the mid and upper lung zones) [19].

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and aortic regurgitation and ischemic ventricular septal defect are often audible, but detection requires a careful and skillful auscultator. (See "Auscultation of cardiac murmurs in adults".) ●<span>The chest radiograph may show cardiomegaly, upper zone redistribution of blood flow, interstitial edema (with ill-defined vessels, peribronchial cuffing, and interlobular septal thickening), and alveolar edema (with perihilar and lower-lobe airspace filling, with the periphery generally spared in the mid and upper lung zones) [19]. (See 'Chest radiograph' below.) Cardiogenic shock — In one study of patients who presented with acutely decompensated HF, at least one sign of cardiogenic shock (eg, blood pressure <

#### Annotation 7604814875916

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D Cardiogenic shock — In one study of patients who presented with acutely decompensated HF, at least one sign of cardiogenic shock (eg, blood pressure <90 mmHg, cutaneous pallor, mental confusion) was present in 3.6 percent of patients [20].

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eptal thickening), and alveolar edema (with perihilar and lower-lobe airspace filling, with the periphery generally spared in the mid and upper lung zones) [19]. (See 'Chest radiograph' below.) <span>Cardiogenic shock — In one study of patients who presented with acutely decompensated HF, at least one sign of cardiogenic shock (eg, blood pressure <90 mmHg, cutaneous pallor, mental confusion) was present in 3.6 percent of patients [20]. ●Low-output HF is characterized by symptoms and signs that are related to decreased end-organ perfusion. A typical patient with this clinical syndrome has severely impaired LV function

#### Annotation 7604815924492

 Cardiogenic shock #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D ● Low-output HF is characterized by symptoms and signs that are related to decreased end-organ perfusion. A typical patient with this clinical syndrome has severely impaired LV function and usually presents with symptoms of fatigue, altered mental status, or signs of organ hypoperfusion such as prerenal azotemia or abnormal hepatic enzymes. ● The patient may present with tachypnea at rest, tachycardia, and a cold and cyanotic periphery with poor capillary refill. The degree of peripheral hypoperfusion may be so advanced that the skin over the lower extremities is mottled, cool, or diaphoretic. ● A diminished pulse pressure, consistent with a reduced stroke volume, is often found in patients with this syndrome. Occasionally, the clinician may detect pulsus alternans: when a strong or normal pulse alternates with a weak pulse during normal sinus rhythm. This physical finding is rare but, when present, is a sign of severe LV dysfunction. (See "Examination of the arterial pulse" and "Examination of the arterial pulse", section on 'Pulsus alternans'.) ● A subset of patients with decompensated end-stage HF present with occult shock and may be difficult to distinguish from patients with mildly decompensated chronic HF and stable HF [21]. The only parameter differentiating occult shock patients from nonshock patients is a significantly elevated lactic acid level. Therefore, we suggest checking a lactic acid level in patients who present with marked weakness and/or uncertain peripheral perfusion. (See 'Laboratory data' below.) ● It is imperative to rapidly identify the cardiac causes of shock. After an acute coronary syndrome has been excluded, echocardiography should be done as soon as possible to exclude cardiac tamponade and further characterize left and right ventricular function and the integrity of the left-sided valves.

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presented with acutely decompensated HF, at least one sign of cardiogenic shock (eg, blood pressure <90 mmHg, cutaneous pallor, mental confusion) was present in 3.6 percent of patients [20]. <span>●Low-output HF is characterized by symptoms and signs that are related to decreased end-organ perfusion. A typical patient with this clinical syndrome has severely impaired LV function and usually presents with symptoms of fatigue, altered mental status, or signs of organ hypoperfusion such as prerenal azotemia or abnormal hepatic enzymes. ●The patient may present with tachypnea at rest, tachycardia, and a cold and cyanotic periphery with poor capillary refill. The degree of peripheral hypoperfusion may be so advanced that the skin over the lower extremities is mottled, cool, or diaphoretic. ●A diminished pulse pressure, consistent with a reduced stroke volume, is often found in patients with this syndrome. Occasionally, the clinician may detect pulsus alternans: when a strong or normal pulse alternates with a weak pulse during normal sinus rhythm. This physical finding is rare but, when present, is a sign of severe LV dysfunction. (See "Examination of the arterial pulse" and "Examination of the arterial pulse", section on 'Pulsus alternans'.) ●A subset of patients with decompensated end-stage HF present with occult shock and may be difficult to distinguish from patients with mildly decompensated chronic HF and stable HF [21]. The only parameter differentiating occult shock patients from nonshock patients is a significantly elevated lactic acid level. Therefore, we suggest checking a lactic acid level in patients who present with marked weakness and/or uncertain peripheral perfusion. (See 'Laboratory data' below.) ●It is imperative to rapidly identify the cardiac causes of shock. After an acute coronary syndrome has been excluded, echocardiography should be done as soon as possible to exclude cardiac tamponade and further characterize left and right ventricular function and the integrity of the left-sided valves. High-output heart failure — This phenotype is an uncommon cause of ADHF and generally presents with warm extremities, pulmonary congestion, tachycardia, and a wide pulse pressure. Under

#### Annotation 7604817759500

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D High-output heart failure — This phenotype is an uncommon cause of ADHF and generally presents with warm extremities, pulmonary congestion, tachycardia, and a wide pulse pressure. Underlying conditions include anemia, obesity, thyrotoxicosis, advanced liver failure, and skeletal conditions such as Paget disease.

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cluded, echocardiography should be done as soon as possible to exclude cardiac tamponade and further characterize left and right ventricular function and the integrity of the left-sided valves. <span>High-output heart failure — This phenotype is an uncommon cause of ADHF and generally presents with warm extremities, pulmonary congestion, tachycardia, and a wide pulse pressure. Underlying conditions include anemia, obesity, thyrotoxicosis, advanced liver failure, and skeletal conditions such as Paget disease. (See "Causes and pathophysiology of high-output heart failure".) Right-sided heart failure — This syndrome of predominantly right-sided HF occurs commonly in patients with severe isolat

#### Annotation 7604818808076

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D Right-sided heart failure — This syndrome of predominantly right-sided HF occurs commonly in patients with severe isolated tricuspid regurgitation, right ventricular dysfunction, and chronic lung disease, such as those with chronic obstructive lung disease, interstitial lung disease, or long-standing pulmonary hypertension. These patients are often oxygen dependent and present with signs and symptoms of right-sided volume overload. Pulmonary embolism as an acute cause of dyspnea and right HF should be excluded.

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lying conditions include anemia, obesity, thyrotoxicosis, advanced liver failure, and skeletal conditions such as Paget disease. (See "Causes and pathophysiology of high-output heart failure".) <span>Right-sided heart failure — This syndrome of predominantly right-sided HF occurs commonly in patients with severe isolated tricuspid regurgitation, right ventricular dysfunction, and chronic lung disease, such as those with chronic obstructive lung disease, interstitial lung disease, or long-standing pulmonary hypertension. These patients are often oxygen dependent and present with signs and symptoms of right-sided volume overload. Pulmonary embolism as an acute cause of dyspnea and right HF should be excluded. (See 'Differential diagnosis' below.) DIAGNOSTIC EVALUATION — Initial assessment of ADHF should include a brief, focused history and a physical examination to evaluate signs and symptom

#### Annotation 7604819856652

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D Initial evaluation for cardiopulmonary instability — The goal of the initial evaluation of patients with ADHF is to determine the patient’s cardiopulmonary status, including the severity of dyspnea, hemodynamic status (evidence of hypoperfusion including hypotension), and heart rate and rhythm.

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the 2010 Heart Failure Society of America [22], the 2013 American College of Cardiology Foundation/American Heart Association [23], and the 2021 European Society of Cardiology guidelines [12]. <span>Initial evaluation for cardiopulmonary instability — The goal of the initial evaluation of patients with ADHF is to determine the patient’s cardiopulmonary status, including the severity of dyspnea, hemodynamic status (evidence of hypoperfusion including hypotension), and heart rate and rhythm. ADHF is a heterogeneous condition, and successful management often relies on identifying the cause of decompensation. The search for specific causes is an essential first step in the ev

#### Annotation 7604820905228

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D The search for specific causes is an essential first step in the evaluation of these patients. These include acute coronary syndrome (ACS), hypertensive emergency, rapid arrhythmias or severe bradycardia/conduction disturbance, acute mechanical causes such as acute valve regurgitation or acute pulmonary embolism, infection, including myocarditis, and tamponade.

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vidence of hypoperfusion including hypotension), and heart rate and rhythm. ADHF is a heterogeneous condition, and successful management often relies on identifying the cause of decompensation. <span>The search for specific causes is an essential first step in the evaluation of these patients. These include acute coronary syndrome (ACS), hypertensive emergency, rapid arrhythmias or severe bradycardia/conduction disturbance, acute mechanical causes such as acute valve regurgitation or acute pulmonary embolism, infection, including myocarditis, and tamponade. The acronym CHAMPIT (ACS, Hypertension, Arrhythmia, Mechanical causes, Pulmonary embolus, Infection, and Tamponade) was suggested as a useful reminder of the etiologic considerations by

#### Annotation 7604821953804

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D The acronym CHAMPIT (ACS, Hypertension, Arrhythmia, Mechanical causes, Pulmonary embolus, Infection, and Tamponade) was suggested as a useful reminder of the etiologic considerations by the European Society of Cardiology [ 12].

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arrhythmias or severe bradycardia/conduction disturbance, acute mechanical causes such as acute valve regurgitation or acute pulmonary embolism, infection, including myocarditis, and tamponade. <span>The acronym CHAMPIT (ACS, Hypertension, Arrhythmia, Mechanical causes, Pulmonary embolus, Infection, and Tamponade) was suggested as a useful reminder of the etiologic considerations by the European Society of Cardiology [12]. Symptoms of ACS (eg, chest pain) are assessed and an electrocardiogram (ECG) is obtained and assessed for evidence of ischemia. (See "Initial evaluation and management of suspected acut

#### Annotation 7604823002380

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D Patients with respiratory failure and/or shock — Patients with respiratory distress and/or hypotension require immediate treatment, as discussed separately, followed by an expedited diagnostic evaluation (table 2).

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ained and assessed for evidence of ischemia. (See "Initial evaluation and management of suspected acute coronary syndrome (myocardial infarction, unstable angina) in the emergency department".) <span>Patients with respiratory failure and/or shock — Patients with respiratory distress and/or hypotension require immediate treatment, as discussed separately, followed by an expedited diagnostic evaluation (table 2). (See "Treatment of acute decompensated heart failure: Specific therapies", section on 'Supplemental oxygen and assisted ventilation' and "Treatment of acute decompensated heart failure:

#### Annotation 7604824050956

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D Patients with acute coronary syndrome — Patients with ADHF with suspected ACS should be promptly identified by ECG and cardiac troponin testing and referred for consideration of cardiac catheterization with coronary angiography and hemodynamic evaluation as appropriate for the condition and prognosis of the patient. The evaluation and management of patients with symptoms and signs of ACS are discussed separately (table 3).

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therapies", section on 'Supplemental oxygen and assisted ventilation' and "Treatment of acute decompensated heart failure: Specific therapies", section on 'Management of hypotensive patients'.) <span>Patients with acute coronary syndrome — Patients with ADHF with suspected ACS should be promptly identified by ECG and cardiac troponin testing and referred for consideration of cardiac catheterization with coronary angiography and hemodynamic evaluation as appropriate for the condition and prognosis of the patient. The evaluation and management of patients with symptoms and signs of ACS are discussed separately (table 3). (See "Initial evaluation and management of suspected acute coronary syndrome (myocardial infarction, unstable angina) in the emergency department" and "Treatment of acute decompensated

#### Annotation 7604825099532

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D Of note, troponin is often mildly elevated in ADHF as a result of myocardial injury, myocyte apoptosis, inflammatory mediator activation, and increased myocardial oxygen demand in the setting of fixed coronary disease. Therefore, troponin elevation in ADHF does not necessarily indicate the presence of an ACS.

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atment of acute decompensated heart failure in acute coronary syndromes".) If myocardial ischemia or MI is suspected, cardiac enzymes should be measured to evaluate potential myocardial injury. <span>Of note, troponin is often mildly elevated in ADHF as a result of myocardial injury, myocyte apoptosis, inflammatory mediator activation, and increased myocardial oxygen demand in the setting of fixed coronary disease. Therefore, troponin elevation in ADHF does not necessarily indicate the presence of an ACS. (See "Troponin testing: Clinical use" and "Use of creatine kinase to detect myocardial injury".) Diagnostic approach — ADHF is diagnosed based upon finding a constellation of clinical s

#### Annotation 7604826148108

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D The diagnosis of ADHF is based primarily on signs and symptoms and supported by appropriate investigations, such as ECG, chest radiograph, biomarkers (B-type natriuretic peptide [BNP] or N-terminal proBNP [NT-proBNP]), and Doppler echocardiography [12,24].

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of HF as well as potential contributing factors and comorbidities. (See "Heart failure: Clinical manifestations and diagnosis in adults" and "Pathophysiology of cardiogenic pulmonary edema".) ●<span>The diagnosis of ADHF is based primarily on signs and symptoms and supported by appropriate investigations, such as ECG, chest radiograph, biomarkers (B-type natriuretic peptide [BNP] or N-terminal proBNP [NT-proBNP]), and Doppler echocardiography [12,24]. (See 'How to diagnose ADHF' below.) •The diagnosis of decompensated chronic HF is generally straightforward, especially when a patient presents with fluid retention and exertional dyspn

#### Annotation 7604827196684

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D A BNP or NT-proBNP level is obtained when the diagnosis of HF is uncertain.

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lly when a patient presents with fluid retention and exertional dyspnea. It is essential to rule out alternate causes of the patient's symptoms and signs. (See 'Differential diagnosis' below.) •<span>A BNP or NT-proBNP level is obtained when the diagnosis of HF is uncertain. (See 'Initial tests' below.) •An echocardiogram is generally recommended, particularly if this is a first presentation of HF or if there has been abrupt deterioration in the patient’s c

#### Annotation 7604828245260

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D An echocardiogram is generally recommended, particularly if this is a first presentation of HF or if there has been abrupt deterioration in the patient’s condition.

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nate causes of the patient's symptoms and signs. (See 'Differential diagnosis' below.) •A BNP or NT-proBNP level is obtained when the diagnosis of HF is uncertain. (See 'Initial tests' below.) •<span>An echocardiogram is generally recommended, particularly if this is a first presentation of HF or if there has been abrupt deterioration in the patient’s condition. (See 'Echocardiography' below.) ●Swan-Ganz catheterization is not generally required but is helpful when the diagnosis is uncertain and for management of patients with persistent sympto

#### Annotation 7604829293836

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D How to diagnose ADHF — ADHF is a clinical diagnosis based upon the presence of a constellation of symptoms and signs of HF. While test results (eg, natriuretic peptide level, chest radiograph, echocardiogram) are often supportive, the diagnosis cannot be based on a single symptom or sign [25] or test result [26]. The simplest approach is to categorize patients with suspected ADHF into three categories

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ation is not generally required but is helpful when the diagnosis is uncertain and for management of patients with persistent symptoms despite treatment of HF. (See 'Swan-Ganz catheter' below.) <span>How to diagnose ADHF — ADHF is a clinical diagnosis based upon the presence of a constellation of symptoms and signs of HF. While test results (eg, natriuretic peptide level, chest radiograph, echocardiogram) are often supportive, the diagnosis cannot be based on a single symptom or sign [25] or test result [26]. The simplest approach is to categorize patients with suspected ADHF into three categories: High probability — ADHF can be diagnosed with high probability in patients with or without prior history of HF: ●Patients with prior history of HF – When a patient with prior history o

#### Annotation 7604830342412

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D High probability — ADHF can be diagnosed with high probability in patients with or without prior history of HF: ● Patients with prior history of HF – When a patient with prior history of HF presents with exertional dyspnea and evidence of fluid retention (ie, elevated jugular venous pressure [JVP] and/or evidence of pulmonary edema and/or peripheral edema), there is a high probability of ADHF [26]. ● Patients with no prior history of HF – When a patient with no prior history of HF presents with new onset orthopnea, elevated JVP, typical chest radiograph findings of pulmonary edema (see 'Chest radiograph' below), and no fever, there is a high probability of ADHF [26].

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often supportive, the diagnosis cannot be based on a single symptom or sign [25] or test result [26]. The simplest approach is to categorize patients with suspected ADHF into three categories: <span>High probability — ADHF can be diagnosed with high probability in patients with or without prior history of HF: ●Patients with prior history of HF – When a patient with prior history of HF presents with exertional dyspnea and evidence of fluid retention (ie, elevated jugular venous pressure [JVP] and/or evidence of pulmonary edema and/or peripheral edema), there is a high probability of ADHF [26]. ●Patients with no prior history of HF – When a patient with no prior history of HF presents with new onset orthopnea, elevated JVP, typical chest radiograph findings of pulmonary edema (see 'Chest radiograph' below), and no fever, there is a high probability of ADHF [26]. Intermediate probability — For patients presenting with symptoms of dyspnea who have no prior history of HF but have known cardiac disease, cardiac risk factors (eg, known coronary arte

#### Annotation 7604831390988

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D Intermediate probability — For patients presenting with symptoms of dyspnea who have no prior history of HF but have known cardiac disease, cardiac risk factors (eg, known coronary artery disease, valve disease, diabetes mellitus, or hypertension), or have ECG abnormalities (atrial fibrillation, evidence of left ventricular hypertrophy, or ischemia), and have uncertain JVP and no evidence of pulmonary edema, there is an intermediate probability of ADHF. In this group of patients, testing of serum natriuretic peptide levels (BNP or NT-proBNP) [26], and in some cases also echocardiography, may be helpful.

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HF presents with new onset orthopnea, elevated JVP, typical chest radiograph findings of pulmonary edema (see 'Chest radiograph' below), and no fever, there is a high probability of ADHF [26]. <span>Intermediate probability — For patients presenting with symptoms of dyspnea who have no prior history of HF but have known cardiac disease, cardiac risk factors (eg, known coronary artery disease, valve disease, diabetes mellitus, or hypertension), or have ECG abnormalities (atrial fibrillation, evidence of left ventricular hypertrophy, or ischemia), and have uncertain JVP and no evidence of pulmonary edema, there is an intermediate probability of ADHF. In this group of patients, testing of serum natriuretic peptide levels (BNP or NT-proBNP) [26], and in some cases also echocardiography, may be helpful. (See 'Natriuretic peptide levels' below.) Low probability — There is low probability of ADHF in patients who present with dyspnea who lack evidence of cardiac disease (including a norma

#### Annotation 7604832439564

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D Low probability — There is low probability of ADHF in patients who present with dyspnea who lack evidence of cardiac disease (including a normal ECG) and who have another explanation for dyspnea such as chronic lung disease or pneumonia. Other causes of dyspnea should be evaluated and treated. If uncertainty regarding a possible diagnosis of ADHF persists, further testing (eg, natriuretic peptide level) may be indicated.

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n this group of patients, testing of serum natriuretic peptide levels (BNP or NT-proBNP) [26], and in some cases also echocardiography, may be helpful. (See 'Natriuretic peptide levels' below.) <span>Low probability — There is low probability of ADHF in patients who present with dyspnea who lack evidence of cardiac disease (including a normal ECG) and who have another explanation for dyspnea such as chronic lung disease or pneumonia. Other causes of dyspnea should be evaluated and treated. If uncertainty regarding a possible diagnosis of ADHF persists, further testing (eg, natriuretic peptide level) may be indicated. Clinical categories — Clinical presentations of ADHF can be categorized according to adequacy of peripheral perfusion ("warm" versus "cold") and the presence of congestion ("dry" or "we

#### Annotation 7604833488140

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D Clinical categories — Clinical presentations of ADHF can be categorized according to adequacy of peripheral perfusion ("warm" versus "cold") and the presence of congestion ("dry" or "wet") (figure 1) [7,27]. Such categorization predicts prognosis and facilitates attention to specific therapies.

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monia. Other causes of dyspnea should be evaluated and treated. If uncertainty regarding a possible diagnosis of ADHF persists, further testing (eg, natriuretic peptide level) may be indicated. <span>Clinical categories — Clinical presentations of ADHF can be categorized according to adequacy of peripheral perfusion ("warm" versus "cold") and the presence of congestion ("dry" or "wet") (figure 1) [7,27]. Such categorization predicts prognosis and facilitates attention to specific therapies. ●The most common combination of peripheral perfusion and congestion (more than 70 percent of patients with ADHF) is the "warm and wet" clinical profile [1,2]. This group of patients typ

#### Annotation 7604834536716

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D ● The most common combination of peripheral perfusion and congestion (more than 70 percent of patients with ADHF) is the "warm and wet" clinical profile [1,2]. This group of patients typically presents with either normal or markedly elevated systolic blood pressure. • The group with normal blood pressure presents largely with significant volume overload with pulmonary and peripheral congestion (cardiac type). • By contrast, patients with the hypertensive profile manifest with fluid redistribution to the lungs and minimal peripheral fluid accumulation (vascular type). This profile of ADHF is often seen in older adult females with labile hypertension and a preserved left ventricular ejection fraction (LVEF).

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heral perfusion ("warm" versus "cold") and the presence of congestion ("dry" or "wet") (figure 1) [7,27]. Such categorization predicts prognosis and facilitates attention to specific therapies. <span>●The most common combination of peripheral perfusion and congestion (more than 70 percent of patients with ADHF) is the "warm and wet" clinical profile [1,2]. This group of patients typically presents with either normal or markedly elevated systolic blood pressure. •The group with normal blood pressure presents largely with significant volume overload with pulmonary and peripheral congestion (cardiac type). •By contrast, patients with the hypertensive profile manifest with fluid redistribution to the lungs and minimal peripheral fluid accumulation (vascular type). This profile of ADHF is often seen in older adult females with labile hypertension and a preserved left ventricular ejection fraction (LVEF). (See 'ADHF with severe pulmonary edema' above.) ●A minority of patients with ADHF (less than 20 percent) present with a "cold and wet" clinical profile. This includes most patients with

#### Annotation 7604835585292

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D ● A minority of patients with ADHF (less than 20 percent) present with a "cold and wet" clinical profile. This includes most patients with cardiogenic shock and low-output syndrome. Patients in this category are at increased risk of death and cardiac transplantation at one year compared with patients with HF with reduced EF with a "wet and warm" profile [7].

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e). This profile of ADHF is often seen in older adult females with labile hypertension and a preserved left ventricular ejection fraction (LVEF). (See 'ADHF with severe pulmonary edema' above.) <span>●A minority of patients with ADHF (less than 20 percent) present with a "cold and wet" clinical profile. This includes most patients with cardiogenic shock and low-output syndrome. Patients in this category are at increased risk of death and cardiac transplantation at one year compared with patients with HF with reduced EF with a "wet and warm" profile [7]. (See 'Cardiogenic shock' above.) ●Less than 10 percent of patients with ADHF present with a "warm and dry" or "cold and dry" profile. Initial tests — Initial testing in patients with AD

#### Annotation 7604836633868

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D ● Less than 10 percent of patients with ADHF present with a "warm and dry" or "cold and dry" profile.

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ategory are at increased risk of death and cardiac transplantation at one year compared with patients with HF with reduced EF with a "wet and warm" profile [7]. (See 'Cardiogenic shock' above.) <span>●Less than 10 percent of patients with ADHF present with a "warm and dry" or "cold and dry" profile. Initial tests — Initial testing in patients with ADHF includes a 12-lead ECG, chest radiograph, and laboratory tests. Electrocardiogram — A 12-lead ECG is performed soon after the patie

#### Annotation 7604837682444

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D Initial tests — Initial testing in patients with ADHF includes a 12-lead ECG, chest radiograph, and laboratory tests.

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with HF with reduced EF with a "wet and warm" profile [7]. (See 'Cardiogenic shock' above.) ●Less than 10 percent of patients with ADHF present with a "warm and dry" or "cold and dry" profile. <span>Initial tests — Initial testing in patients with ADHF includes a 12-lead ECG, chest radiograph, and laboratory tests. Electrocardiogram — A 12-lead ECG is performed soon after the patient presents with ADHF to assess for evidence of ACS (myocardial ischemia or MI) and arrhythmias (eg, atrial fibrillati

#### Annotation 7604838731020

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D A 12-lead ECG is performed soon after the patient presents with ADHF to assess for evidence of ACS (myocardial ischemia or MI) and arrhythmias (eg, atrial fibrillation). The ECG may also identify other predisposing or precipitating conditions for HF such as left ventricular hypertrophy or left atrial abnormalities (waveform 1).

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resent with a "warm and dry" or "cold and dry" profile. Initial tests — Initial testing in patients with ADHF includes a 12-lead ECG, chest radiograph, and laboratory tests. Electrocardiogram — <span>A 12-lead ECG is performed soon after the patient presents with ADHF to assess for evidence of ACS (myocardial ischemia or MI) and arrhythmias (eg, atrial fibrillation). The ECG may also identify other predisposing or precipitating conditions for HF such as left ventricular hypertrophy or left atrial abnormalities (waveform 1). Additional ECG abnormalities may be seen in a patient during an episode of ADHF. These include nonspecific ST and T wave abnormalities. Transient giant negative T waves, global T wave i

#### Annotation 7604839779596

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D Additional ECG abnormalities may be seen in a patient during an episode of ADHF. These include nonspecific ST and T wave abnormalities. Transient giant negative T waves, global T wave inversions, and marked QT interval prolongation have also been reported [28]. These changes may represent subendocardial ischemia (which can be the cause or the result of the pulmonary edema), increase in cardiac sympathetic tone, or metabolic changes. They can also be seen in patients with pulmonary edema due to noncoronary events such as cerebrovascular disease.

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thmias (eg, atrial fibrillation). The ECG may also identify other predisposing or precipitating conditions for HF such as left ventricular hypertrophy or left atrial abnormalities (waveform 1). <span>Additional ECG abnormalities may be seen in a patient during an episode of ADHF. These include nonspecific ST and T wave abnormalities. Transient giant negative T waves, global T wave inversions, and marked QT interval prolongation have also been reported [28]. These changes may represent subendocardial ischemia (which can be the cause or the result of the pulmonary edema), increase in cardiac sympathetic tone, or metabolic changes. They can also be seen in patients with pulmonary edema due to noncoronary events such as cerebrovascular disease. (See "Neurogenic pulmonary edema".) Chest radiograph — Radiographic findings in ADHF can range from mild pulmonary vascular redistribution to marked cardiomegaly and extensive bilateral

#### Annotation 7604840828172

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D Radiographic findings in ADHF can range from mild pulmonary vascular redistribution to marked cardiomegaly and extensive bilateral interstitial markings (image 1 and image 2 and image 3 and image 4). The presence of bilateral perihilar alveolar edema may give the typical "butterfly" appearance [29].

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e, or metabolic changes. They can also be seen in patients with pulmonary edema due to noncoronary events such as cerebrovascular disease. (See "Neurogenic pulmonary edema".) Chest radiograph — <span>Radiographic findings in ADHF can range from mild pulmonary vascular redistribution to marked cardiomegaly and extensive bilateral interstitial markings (image 1 and image 2 and image 3 and image 4). The presence of bilateral perihilar alveolar edema may give the typical "butterfly" appearance [29]. Unilateral cardiogenic pulmonary edema is infrequent (2 percent of cardiogenic pulmonary edema cases in one study) and is chiefly caused by eccentric mitral regurgitation [30]. Pleural

#### Annotation 7604841876748

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D Unilateral cardiogenic pulmonary edema is infrequent (2 percent of cardiogenic pulmonary edema cases in one study) and is chiefly caused by eccentric mitral regurgitation [ 30].

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and extensive bilateral interstitial markings (image 1 and image 2 and image 3 and image 4). The presence of bilateral perihilar alveolar edema may give the typical "butterfly" appearance [29]. <span>Unilateral cardiogenic pulmonary edema is infrequent (2 percent of cardiogenic pulmonary edema cases in one study) and is chiefly caused by eccentric mitral regurgitation [30]. Pleural effusions are often absent in patients with de novo ADHF but are frequently present in patients with acute decompensation of chronic HF. Up to 20 percent of patients with ADHF m

#### Annotation 7604842925324

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D Pleural effusions are often absent in patients with de novo ADHF but are frequently present in patients with acute decompensation of chronic HF.

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appearance [29]. Unilateral cardiogenic pulmonary edema is infrequent (2 percent of cardiogenic pulmonary edema cases in one study) and is chiefly caused by eccentric mitral regurgitation [30]. <span>Pleural effusions are often absent in patients with de novo ADHF but are frequently present in patients with acute decompensation of chronic HF. Up to 20 percent of patients with ADHF may have normal chest radiographs [31]. Lung ultrasound — In experienced centers, LUS is an adjunctive diagnostic modality that may be helpful in

#### Annotation 7604843973900

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D Up to 20 percent of patients with ADHF may have normal chest radiographs [ 31].

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y caused by eccentric mitral regurgitation [30]. Pleural effusions are often absent in patients with de novo ADHF but are frequently present in patients with acute decompensation of chronic HF. <span>Up to 20 percent of patients with ADHF may have normal chest radiographs [31]. Lung ultrasound — In experienced centers, LUS is an adjunctive diagnostic modality that may be helpful in the evaluation of patients with dyspnea with suspected ADHF [32,33]; it should

#### Annotation 7604845022476

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D The presence of multiple B-lines (generally three or more) per intercostal space on point-of-care ultrasound (LUS) is a sign of lung interstitial syndrome; causes of multiple diffuse bilateral B-lines include pulmonary edema as well as interstitial pneumonia or pneumonitis or diffuse parenchymal lung disease (pulmonary fibrosis) [34]. B-lines are laser-like (also described as comet-like), vertical, hyperechoic artifacts that arise from the pleural line, extend to the bottom of the screen without fading, and move synchronously with lung sliding, as defined by the 2012 International evidence-based recommendations for point-of-care lung ultrasound [34].

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uld not replace standard clinical assessment (including chest radiograph and selective natriuretic peptide level testing). (See 'Chest radiograph' above and 'Natriuretic peptide levels' below.) <span>The presence of multiple B-lines (generally three or more) per intercostal space on point-of-care ultrasound (LUS) is a sign of lung interstitial syndrome; causes of multiple diffuse bilateral B-lines include pulmonary edema as well as interstitial pneumonia or pneumonitis or diffuse parenchymal lung disease (pulmonary fibrosis) [34]. B-lines are laser-like (also described as comet-like), vertical, hyperechoic artifacts that arise from the pleural line, extend to the bottom of the screen without fading, and move synchronously with lung sliding, as defined by the 2012 International evidence-based recommendations for point-of-care lung ultrasound [34]. (See "Indications for bedside ultrasonography in the critically ill adult patient", section on 'Thoracic ultrasonography'.) Limitations of this modality include technique-dependence and

#### Annotation 7604846071052

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D Repeated examination may also be helpful since B-lines caused by pulmonary edema vary with volume changes and position (sitting versus supine) [32].

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ung disease (pulmonary fibrosis) include pleural line abnormalities (irregular, fragmented), subpleural abnormalities (small echo-poor areas), and a nonhomogeneous distribution of B-lines [34]. <span>Repeated examination may also be helpful since B-lines caused by pulmonary edema vary with volume changes and position (sitting versus supine) [32]. Sonographic findings indicative of acute respiratory distress syndrome include anterior subpleural consolidation, absence or reduction of lung sliding, spared areas of normal parenchyma

#### Annotation 7604847119628

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D Pulse oximetry is often used for initial identification of hypoxia. Arterial blood gas analysis is recommended in all patients with hypoxia and/or severe respiratory distress to assess ventilatory and acid-base status [37].

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data are obtained when feasible but are generally not needed to make the diagnosis or guide initial therapy; treatment should NOT be delayed while waiting for the results of laboratory tests. ●<span>Pulse oximetry is often used for initial identification of hypoxia. Arterial blood gas analysis is recommended in all patients with hypoxia and/or severe respiratory distress to assess ventilatory and acid-base status [37]. ●Routine chemistries including serum electrolytes, bicarbonate, blood urea nitrogen (BUN), and serum creatinine are helpful in guiding electrolyte (eg, potassium and magnesium) repletio

#### Annotation 7604848168204

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D A decline in renal function is commonly found in patients with advanced HF (cardiorenal syndrome). This may be due in part to a low-output state and elevated central venous pressures. Increased BUN and serum creatinine may also reflect underlying renal disease and, in some cases, may reflect bilateral renal artery stenosis.

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onate, blood urea nitrogen (BUN), and serum creatinine are helpful in guiding electrolyte (eg, potassium and magnesium) repletion during diuresis and in assessing and monitoring renal function. <span>A decline in renal function is commonly found in patients with advanced HF (cardiorenal syndrome). This may be due in part to a low-output state and elevated central venous pressures. Increased BUN and serum creatinine may also reflect underlying renal disease and, in some cases, may reflect bilateral renal artery stenosis. ●We suggest checking a lactic acid level in patients in shock as well as in those with marked weakness and/or uncertain peripheral perfusion. (See 'Cardiogenic shock' above and "Approac

#### Annotation 7604849216780

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D We suggest checking a lactic acid level in patients in shock as well as in those with marked weakness and/or uncertain peripheral perfusion.

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utput state and elevated central venous pressures. Increased BUN and serum creatinine may also reflect underlying renal disease and, in some cases, may reflect bilateral renal artery stenosis. ●<span>We suggest checking a lactic acid level in patients in shock as well as in those with marked weakness and/or uncertain peripheral perfusion. (See 'Cardiogenic shock' above and "Approach to the adult with metabolic acidosis".) ●Serum troponin (T or I) levels are obtained in any patient with possible ACS. For patients with cri

#### Annotation 7604850265356

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D Serum troponin (T or I) levels are obtained in any patient with possible ACS.

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level in patients in shock as well as in those with marked weakness and/or uncertain peripheral perfusion. (See 'Cardiogenic shock' above and "Approach to the adult with metabolic acidosis".) ●<span>Serum troponin (T or I) levels are obtained in any patient with possible ACS. For patients with criteria for ST elevation MI, reperfusion therapy (percutaneous coronary intervention or thrombolysis) should not be delayed to wait for the results of troponin measur

#### Annotation 7604851313932

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D A complete blood count may help identify the presence of infection or anemia that may have precipitated the event.

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gement of suspected acute coronary syndrome (myocardial infarction, unstable angina) in the emergency department" and "Overview of the acute management of ST-elevation myocardial infarction".) ●<span>A complete blood count may help identify the presence of infection or anemia that may have precipitated the event. (See "Evaluation and management of anemia and iron deficiency in adults with heart failure".) Natriuretic peptide levels — If the diagnosis of HF is uncertain in a patient with dyspnea

#### Annotation 7604852362508

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D Decision analysis suggests that BNP or NT-proBNP testing is generally most useful in patients who have an intermediate probability of HF [38]. The natriuretic peptide concentration should not be interpreted in isolation but in the context of all available clinical data bearing on the diagnosis of ADHF.

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iuretic peptide levels — If the diagnosis of HF is uncertain in a patient with dyspnea and other signs and symptoms suggestive of ADHF, plasma BNP or NT-proBNP concentration should be measured. <span>Decision analysis suggests that BNP or NT-proBNP testing is generally most useful in patients who have an intermediate probability of HF [38]. The natriuretic peptide concentration should not be interpreted in isolation but in the context of all available clinical data bearing on the diagnosis of ADHF. (See 'How to diagnose ADHF' above.) Most dyspneic patients with HF have plasma BNP values above 400 pg/mL. For patients <50, 50 to 75, and >75 years of age, the optimal plasma NT-

#### Annotation 7604853411084

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D Most dyspneic patients with HF have plasma BNP values above 400 pg/mL. For patients <50, 50 to 75, and >75 years of age, the optimal plasma NT-proBNP cutoffs for diagnosing HF are 450, 900, and 1800 pg/mL, respectively.

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natriuretic peptide concentration should not be interpreted in isolation but in the context of all available clinical data bearing on the diagnosis of ADHF. (See 'How to diagnose ADHF' above.) <span>Most dyspneic patients with HF have plasma BNP values above 400 pg/mL. For patients <50, 50 to 75, and >75 years of age, the optimal plasma NT-proBNP cutoffs for diagnosing HF are 450, 900, and 1800 pg/mL, respectively. (See "Natriuretic peptide measurement in heart failure".) There is considerable overlap in BNP and NT-proBNP levels in patients with and without HF, which makes the test less robust in

#### Annotation 7604854459660

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D There is considerable overlap in BNP and NT-proBNP levels in patients with and without HF, which makes the test less robust in an individual patient with intermediate levels of BNP (approximately 200 to 400 pg/mL). Since many conditions increase natriuretic peptide levels, low values of BNP (<100 pg/mL) or NT-proBNP (<300 pg/mL) are most useful because the diagnosis of ADHF is very unlikely as an explanation for dyspnea [39].

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, 50 to 75, and >75 years of age, the optimal plasma NT-proBNP cutoffs for diagnosing HF are 450, 900, and 1800 pg/mL, respectively. (See "Natriuretic peptide measurement in heart failure".) <span>There is considerable overlap in BNP and NT-proBNP levels in patients with and without HF, which makes the test less robust in an individual patient with intermediate levels of BNP (approximately 200 to 400 pg/mL). Since many conditions increase natriuretic peptide levels, low values of BNP (<100 pg/mL) or NT-proBNP (<300 pg/mL) are most useful because the diagnosis of ADHF is very unlikely as an explanation for dyspnea [39]. However, unexpectedly low natriuretic peptide levels are occasionally found in some patients with end-stage HF, acute pulmonary edema, and right-sided HF [12]. Results of BNP or NT-proB

#### Annotation 7604855508236

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D However, unexpectedly low natriuretic peptide levels are occasionally found in some patients with end-stage HF, acute pulmonary edema, and right-sided HF [ 12].

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ase natriuretic peptide levels, low values of BNP (<100 pg/mL) or NT-proBNP (<300 pg/mL) are most useful because the diagnosis of ADHF is very unlikely as an explanation for dyspnea [39]. <span>However, unexpectedly low natriuretic peptide levels are occasionally found in some patients with end-stage HF, acute pulmonary edema, and right-sided HF [12]. Results of BNP or NT-proBNP testing must be interpreted with caution, and such testing must support rather than override careful clinical judgment. (See "Natriuretic peptide measurement

#### Annotation 7604856556812

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D Results of BNP or NT-proBNP testing must be interpreted with caution, and such testing must support rather than override careful clinical judgment.

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an explanation for dyspnea [39]. However, unexpectedly low natriuretic peptide levels are occasionally found in some patients with end-stage HF, acute pulmonary edema, and right-sided HF [12]. <span>Results of BNP or NT-proBNP testing must be interpreted with caution, and such testing must support rather than override careful clinical judgment. (See "Natriuretic peptide measurement in heart failure" and "Natriuretic peptide measurement in heart failure", section on 'BNP and the diagnosis of HF in the patient with dyspnea' and

#### Annotation 7604857605388

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D Echocardiography is recommended for patients with new HF and for patients with prior history of HF with suspected change in cardiac function. The urgency of echocardiography varies with the acuity of presentation. This imaging modality should be utilized early on during the evaluation of patients with cardiogenic shock or low-output syndrome.

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t failure", section on 'BNP and the diagnosis of HF in the patient with dyspnea' and "Natriuretic peptide measurement in heart failure", section on 'Acute decompensated HF'.) Echocardiography — <span>Echocardiography is recommended for patients with new HF and for patients with prior history of HF with suspected change in cardiac function. The urgency of echocardiography varies with the acuity of presentation. This imaging modality should be utilized early on during the evaluation of patients with cardiogenic shock or low-output syndrome. This imaging modality is also critical in the evaluation of patients with known or suspected valvular heart disease. In patients with ST elevation MI and pulmonary congestion, echocardi

#### Annotation 7604858653964

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D When preserved LV systolic function is found, the cause of HF may be diastolic dysfunction, transient systolic dysfunction, other causes of HF with preserved EF including valvular heart disease (table 4), or diagnostic error (no HF with symptoms/signs due to another cause).

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tion. When reduced LVEF (<40 percent) is found, the cause of HF may be ascribed to systolic dysfunction (with or without other causes such as diastolic dysfunction or valvular disease) [37]. <span>When preserved LV systolic function is found, the cause of HF may be diastolic dysfunction, transient systolic dysfunction, other causes of HF with preserved EF including valvular heart disease (table 4), or diagnostic error (no HF with symptoms/signs due to another cause). Additional tests Swan-Ganz catheter — Routine use of invasive hemodynamic monitoring in patients with ADHF is NOT recommended [22,40]. Available evidence on flow-directed pulmonary arte

#### Annotation 7604859702540

#Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D
Differential diagnosis of heart failure with preserved ejection fraction
 Heart failure with preserved ejection fraction (HFpEF) HFpEF (contributing factors include hypertension, aging, coronary heart disease, diabetes mellitus, sleep-disordered breathing, chronic kidney disease, and obesity) Cardiomyopathies with preserved ejection fraction Restrictive cardiomyopathy Familial causes include sarcomeric gene mutations, familial amyloidosis (transthyretin [TTR] or apolipoprotein mutation), unknown gene mutation, familial causes of iron overload (hereditary hemochromatosis, hereditary anemias), Fabry disease, glycogen storage disease, desminopathy, and pseudoxanthoma elasticum Nonfamilial causes include amyloid (immunoglobulin light chain [AL] or wild-type transthyretin [ATTR]), systemic sclerosis, endomyocardial fibrosis (idiopathic, caused by hypereosinophilic syndrome, or reaction to a drug), carcinoid heart disease, metastatic cancer, radiation, nonfamilial iron overload (eg, acquired iron-loading anemia, high-dietary intake), and drug toxicity (anthracycline) Hypertrophic cardiomyopathy Familial causes in addition to sarcomere gene mutations include unknown mutations, glycogen storage disease, lysosomal storage disease (including Fabry disease), syndromic hypertrophic cardiomyopathy (eg, Noonan syndrome, LEOPARD syndrome, Friedreich ataxia), and familial amyloidosis (TTR or apolipoprotein mutation) Nonfamilial causes include nonfamilial amyloidosis (AL or wild-type ATTR) Noncompaction cardiomyopathy Valvular heart disease Valvular stenosis Valvular regurgitation Right heart failure Pulmonary hypertension Right ventricular infarction Arrhythmogenic right ventricular cardiomyopathy Pericardial disease Cardiac tamponade Constrictive pericarditis Effusive-constrictive pericardial disease Obstructive lesion in heart or great vessel Atrial myxoma Pulmonary vein stenosis High-output heart failure Transient left ventricular systolic dysfunction

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#### Annotation 7604860751116

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D A pulmonary capillary wedge pressure or its equivalent, pulmonary artery occlusion pressure, of ≥18 mmHg favors cardiogenic pulmonary edema.

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one or more of the following conditions: ●Renal function is worsening with therapy ●Parenteral vasoactive agents are required ●Advanced device therapy or cardiac transplantation may be required <span>A pulmonary capillary wedge pressure or its equivalent, pulmonary artery occlusion pressure, of ≥18 mmHg favors cardiogenic pulmonary edema. (See "Pulmonary artery catheterization: Indications, contraindications, and complications in adults" and "Pulmonary artery catheterization: Interpretation of hemodynamic values and wave

#### Annotation 7604861799692

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D However, it is important to appreciate that pulmonary artery catheterization measurements can be misleading in certain settings. Most importantly, intermittent myocardial ischemia can cause severe but transient reduction in LV compliance, accompanied by an elevation in the LV filling pressure.

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onary artery catheterization: Indications, contraindications, and complications in adults" and "Pulmonary artery catheterization: Interpretation of hemodynamic values and waveforms in adults".) <span>However, it is important to appreciate that pulmonary artery catheterization measurements can be misleading in certain settings. Most importantly, intermittent myocardial ischemia can cause severe but transient reduction in LV compliance, accompanied by an elevation in the LV filling pressure. Because of the change in ventricular compliance, this elevation in pressure may or may not be accompanied by an elevation in the LV volume. Furthermore, if the pulmonary capillary wedge

#### Annotation 7604862848268

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D On the other hand, an elevated wedge pressure does not exclude the possibility of noncardiogenic pulmonary edema. It is estimated that as many as 20 percent of patients with pulmonary edema due to acute respiratory distress syndrome (ARDS) have concomitant LV dysfunction. The contribution of ARDS to the pulmonary edema requires monitoring the wedge pressure response to treatment. Noncardiogenic factors are probable if the pulmonary infiltrates and hypoxemia do not improve appreciably within 24 to 48 hours after normalization of the wedge pressure.

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resolved (and if LV function has improved), a relatively normal value may be obtained, leading to the erroneous conclusion that the respiratory distress was caused by noncardiogenic mechanisms. <span>On the other hand, an elevated wedge pressure does not exclude the possibility of noncardiogenic pulmonary edema. It is estimated that as many as 20 percent of patients with pulmonary edema due to acute respiratory distress syndrome (ARDS) have concomitant LV dysfunction. The contribution of ARDS to the pulmonary edema requires monitoring the wedge pressure response to treatment. Noncardiogenic factors are probable if the pulmonary infiltrates and hypoxemia do not improve appreciably within 24 to 48 hours after normalization of the wedge pressure. (See "Noncardiogenic pulmonary edema".) In patients with adequate acoustic windows, echocardiography may provide a noninvasive means of estimating filling pressures. (See "Tissue Dopple

#### Annotation 7604863896844

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D Pulmonary embolism – The sudden onset of dyspnea, pleuritic chest pain, and cough may be caused by a pulmonary embolism. Establishing the diagnosis may depend upon the characteristics of the ECG and the differences in appearance of typical chest radiograph findings in the two conditions.

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resents with the sudden onset of respiratory distress that may or may not be associated with chest discomfort or a previous history of heart disease, other medical conditions must be excluded: ●<span>Pulmonary embolism – The sudden onset of dyspnea, pleuritic chest pain, and cough may be caused by a pulmonary embolism. Establishing the diagnosis may depend upon the characteristics of the ECG and the differences in appearance of typical chest radiograph findings in the two conditions. (See "Clinical presentation, evaluation, and diagnosis of the nonpregnant adult with suspected acute pulmonary embolism".) In addition to being part of the differential diagnosis, venou

#### Annotation 7604864945420

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D In addition to being part of the differential diagnosis, venous thromboembolism is more common in patients with HF and, in patients with ADHF, is associated with a worse prognosis [42].

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appearance of typical chest radiograph findings in the two conditions. (See "Clinical presentation, evaluation, and diagnosis of the nonpregnant adult with suspected acute pulmonary embolism".) <span>In addition to being part of the differential diagnosis, venous thromboembolism is more common in patients with HF and, in patients with ADHF, is associated with a worse prognosis [42]. (See "Antithrombotic therapy in patients with heart failure".) ●Pneumonia – Pneumonia can present with acute shortness of breath, hypoxemia, and an inconclusive pulmonary examination. C

#### Annotation 7604865993996

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D Pneumonia – Pneumonia can present with acute shortness of breath, hypoxemia, and an inconclusive pulmonary examination. Chest radiograph findings may differ, but some cases of bibasilar pneumonia may be similar to HF, although evidence of upper zone redistribution is not present with pneumonia. Fever and leukocytosis may suggest an infectious process.

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venous thromboembolism is more common in patients with HF and, in patients with ADHF, is associated with a worse prognosis [42]. (See "Antithrombotic therapy in patients with heart failure".) ●<span>Pneumonia – Pneumonia can present with acute shortness of breath, hypoxemia, and an inconclusive pulmonary examination. Chest radiograph findings may differ, but some cases of bibasilar pneumonia may be similar to HF, although evidence of upper zone redistribution 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".) ●Asthma – Reactive airways disease can cause acute shortness of breath, cough, and fatigue

#### Annotation 7604867042572

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D Asthma – Reactive airways disease can cause acute shortness of breath, cough, and fatigue. In addition, patients with ADHF may present with wheezing that can simulate asthma. The chest radiograph can be helpful in differentiating these conditions.

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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>Asthma – Reactive airways disease can cause acute shortness of breath, cough, and fatigue. In addition, patients with ADHF may present with wheezing that can simulate asthma. The chest radiograph can be helpful in differentiating these conditions. (See "Asthma in adolescents and adults: Evaluation and diagnosis".) ●Noncardiogenic pulmonary edema (NCPE) – NCPE is invariably associated with an underlying disease, which may or may n

#### Annotation 7604868091148

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D Noncardiogenic pulmonary edema (NCPE) – NCPE is invariably associated with an underlying disease, which may or may not be readily apparent. The diagnosis of NCPE often depends on pretest probabilities: acute respiratory distress in a patient with documented sepsis (ie, peritonitis) or pancreatitis should raise the strong possibility that the respiratory failure is due to NCPE. In contrast to cardiogenic pulmonary edema (CPE), NCPE is uncommonly associated with a well-defined acute cardiac event (ie, MI).

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may present with wheezing that can simulate asthma. The chest radiograph can be helpful in differentiating these conditions. (See "Asthma in adolescents and adults: Evaluation and diagnosis".) ●<span>Noncardiogenic pulmonary edema (NCPE) – NCPE is invariably associated with an underlying disease, which may or may not be readily apparent. The diagnosis of NCPE often depends on pretest probabilities: acute respiratory distress in a patient with documented sepsis (ie, peritonitis) or pancreatitis should raise the strong possibility that the respiratory failure is due to NCPE. In contrast to cardiogenic pulmonary edema (CPE), NCPE is uncommonly associated with a well-defined acute cardiac event (ie, MI). Subtle physical signs may also aid in differentiating NCPE from CPE. NCPE is usually a hyperdynamic illness, clinically apparent as a warm, vasodilated periphery, whereas CPE is frequen

#### Annotation 7604869139724

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D Subtle physical signs may also aid in differentiating NCPE from CPE. NCPE is usually a hyperdynamic illness, clinically apparent as a warm, vasodilated periphery, whereas CPE is frequently associated with a cold and sweaty periphery. Tachycardia is frequently present with NCPE or CPE. The findings of a third heart sound or murmurs of aortic and mitral regurgitation and aortic stenosis suggest a cardiogenic cause of pulmonary edema.

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strong possibility that the respiratory failure is due to NCPE. In contrast to cardiogenic pulmonary edema (CPE), NCPE is uncommonly associated with a well-defined acute cardiac event (ie, MI). <span>Subtle physical signs may also aid in differentiating NCPE from CPE. NCPE is usually a hyperdynamic illness, clinically apparent as a warm, vasodilated periphery, whereas CPE is frequently associated with a cold and sweaty periphery. Tachycardia is frequently present with NCPE or CPE. The findings of a third heart sound or murmurs of aortic and mitral regurgitation and aortic stenosis suggest a cardiogenic cause of pulmonary edema. ST segment changes on ECG consistent with MI or myocardial ischemia would suggest an acute cardiac event as the cause of the pulmonary edema. Also, ECG evidence of left ventricular stra

#### Annotation 7604870188300

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D In NCPE and CPE, arterial hypoxemia is due to changes in the ventilation-perfusion ratio and in the extent of intrapulmonary shunting. Patients with NCPE usually have a more pronounced defect in oxygenation than is seen in patients with CPE, largely due to the greater shunt fractions found in these patients. Higher concentrations of inspired oxygen concentrations (FiO2) and larger positive end-expiratory pressures are often required to achieve acceptable oxygenation in NCPE compared with CPE (table 5). (See "Noncardiogenic pulmonary edema".)

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her abnormalities of the QRS complex might indicate an underlying cardiac pathology. By contrast, the ECG is usually normal in patients with NCPE, unless there are major metabolic disturbances. <span>In NCPE and CPE, arterial hypoxemia is due to changes in the ventilation-perfusion ratio and in the extent of intrapulmonary shunting. Patients with NCPE usually have a more pronounced defect in oxygenation than is seen in patients with CPE, largely due to the greater shunt fractions found in these patients. Higher concentrations of inspired oxygen concentrations (FiO2) and larger positive end-expiratory pressures are often required to achieve acceptable oxygenation in NCPE compared with CPE (table 5). (See "Noncardiogenic pulmonary edema".) FOLLOW-UP AND DISPOSITION Monitoring — Monitoring of a patient with ADHF should be initiated as soon as possible after admission to the emergency department. The type and level of monit

#### Annotation 7604871236876

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D Generally, the following parameters should be measured in all critically ill patients: mental status, blood pressure, temperature, respiratory rate, heart rate, and urine output.

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ergency department. The type and level of monitoring required for any individual patient vary widely depending on the severity of the cardiac decompensation and the response to initial therapy. <span>Generally, the following parameters should be measured in all critically ill patients: mental status, blood pressure, temperature, respiratory rate, heart rate, and urine output. Some laboratory tests should be monitored by repeated testing (eg, electrolytes, creatinine, glucose). Liver function tests and lactate levels should be measured when there is evidence

#### Annotation 7604872285452

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D Liver function tests and lactate levels should be measured when there is evidence of hypoperfusion. Arterial blood gas analysis is generally not routinely required but is indicated in patients with hypoxia and/or respiratory failure

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ental status, blood pressure, temperature, respiratory rate, heart rate, and urine output. Some laboratory tests should be monitored by repeated testing (eg, electrolytes, creatinine, glucose). <span>Liver function tests and lactate levels should be measured when there is evidence of hypoperfusion. Arterial blood gas analysis is generally not routinely required but is indicated in patients with hypoxia and/or respiratory failure. After admission to the intensive care unit (ICU) or a step down unit, patients with ADHF should be carefully monitored to ensure that the treatment goals are met and continued progress

#### Annotation 7604873334028

 #Acute-heart-failure #Cardiologie #Cardiology #Clinical #Demarche-diagnostique #Diagnostic-workup #Insuffisance-cardiaque-aigue #Topo-Dyspnee #U2D Although no validated algorithms exist at this time to guide the clinician for triaging patients with decompensated chronic HF to regular floor beds or to the ICU, we agree that presence of one or more of the following conditions is generally a criterion for admission to an ICU as described in the 2021 European Society of Cardiology HF guidelines and by other experts [12,52]: ● Patient is intubated or likely to require respiratory support/intubation. This includes patients with either of the following characteristics: • Arterial oxygen saturation (SpO2 ≤90 percent) despite supplemental oxygen. • Patient is using accessory muscles and respiratory rate is ≥25 breaths/minute. ● Signs and symptoms of hypoperfusion and/or systolic blood pressure <90 mmHg. ● Heart rate <40 or >130 beats/minute.