on 14-Dec-2023 (Thu)

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

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

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

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.

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-

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.

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.

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.

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.

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.

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

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

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.

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.

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.

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.

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.

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.

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?

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.

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.

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.

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]

Appropriate therapy for ADHF requires identification of the specific HF phenotype as well as the potential causes and precipitants.

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

...

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.

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

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.

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).

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 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 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.

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 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 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.

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, 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 thickening), and alveolar edema (with perihilar and lower-lobe airspace filling, with the periphery generally spared in the mid and upper lung zones) [19].

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 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. Underlying conditions include anemia, obesity, thyrotoxicosis, advanced liver failure, and skeletal conditions such as Paget disease.

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.

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.

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 the European Society of Cardiology [ 12].

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).

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).

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.

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].

A BNP or NT-proBNP level is obtained when the diagnosis of HF is uncertain.

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.

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 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 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.

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 "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 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).

● 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].

● 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.

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 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.

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 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].

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].

Repeated examination may also be helpful since B-lines caused by pulmonary edema vary with volume changes and position (sitting versus supine) [32].

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].

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.

Serum troponin (T or I) levels are obtained in any patient with possible ACS.

A complete blood count may help identify the presence of infection or anemia that may have precipitated the event.

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.

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.

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-proBNP testing must be interpreted with caution, and such testing must support rather than override careful clinical judgment.

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.

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).

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

A pulmonary capillary wedge pressure or its equivalent, pulmonary artery occlusion pressure, of ≥18 mmHg favors cardiogenic pulmonary edema.

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.

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.

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.

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].

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.

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.

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 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.

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".)

Generally, the following parameters should be measured in all critically ill patients: mental status, blood pressure, temperature, respiratory rate, heart rate, and urine output.

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

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.