I. Acute Heart Failure: What every physician needs to know.

Acute heart failure (AHF), also known as acute decompensated heart failure or cardiac failure, is not a single disease entity, but rather a syndrome of the worsening of signs and symptoms reflecting an inability of the heart to pump blood at a rate commensurate to the needs of the body at normal filling pressure. AHF is often not acute in onset, typically developing gradually over the course of days to weeks, where the acuity is a function of the need for urgent or emergent therapy due to the severity of these signs or symptoms.

AHF may be the result of a primary disturbance in the systolic or diastolic function of the heart or of abnormal venous or arterial vasoconstriction, but generally represents an interaction of multiple factors, including volume overload. The majority of patients have decompensation of chronic heart failure (CHF) and consequently much of the discussion of the pathophysiology, presentation, and diagnosis of CHF is directly relevant to an understanding of AHF.

II. Diagnostic Confirmation: Are you sure your patient has Acute Heart Failure?


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A. History Part I: Pattern Recognition:

A patient with AHF typically presents with some combination of increased congestion and, less frequently, decreased peripheral perfusion. In addition to disturbances in oxygenation due to pulmonary edema, renal dysfunction is a frequent manifestation of AHF and reflects the multisystem nature of this disease.

The mean age of patients with AHF is in the mid-70s, with about half of each sex and the majority with normal or elevated blood pressure.

Most frequent symptoms at presentation:

  • Dyspnea (including increasing dyspnea on exertion, dyspnea at rest, orthopnea, and paroxysmal nocturnal dyspnea)

  • Fatigue (including confusion)

  • Cough

  • Abdominal discomfort (including early satiety, bloating, anorexia)

  • Leg pain (secondary to tense peripheral edema)

  • Sleep disturbances

The typical patient presents with signs and symptoms of congestion, usually with some combination of lower extremity edema and pulmonary congestion, normal or elevated blood pressure and heart rate, and compromised oxygenation proportional to the extent of the pulmonary edema. A significant minority of patients may manifest worsening of their heart failure with predominantly abdominal congestion symptoms and signs, rather than lower extremity edema.

Other patients, often elderly with hypertension, can present with rapid, if not fulminant, pulmonary edema with no or mild increase in total body fluid. Patients with recurrent heart failure exacerbations tend to recapitulate their clinical presentations in subsequent episodes, so obtaining a history of the time course, triggers, signs and symptoms, and response to therapy of prior events can increase the sensitivity to early decompensation.

B. History Part 2: Prevalence:

In the United States, there are approximately 1 million admissions for heart failure and 3 million admissions where heart failure is a secondary diagnosis. It is the leading cause of hospitalization in patients over 65 years of age.

In Europe, heart failure (HF) is the cause of 5% of acute hospital admissions, is present in 10% of patients in hospital beds, and accounts for 2% of the national expenditure on health, mostly due to the cost of hospital admissions.

Patients with a substrate of cardiovascular disease are most at risk for developing AHF, including those with decreased systolic function (typically due to either ischemic or nonischemic cardiomyopathy), diastolic dysfunction (usually patients with a history of hypertension and/or left ventricular hypertrophy), other forms of cardiac disease (such as severe valvular heart disease), and patients with abnormal vasculature (typically elderly, hypertensive patients).

Common precipitants of decompensation include one or multiple factors, such as medication noncompliance, dietary indiscretion with salt and/or fluid intake, myocardial ischemia, hypertensive episode, and arrhythmias (e.g., atrial fibrillation). The advent and widespread use of troponin assays has revealed that many patients who present with AHF have evidence of myocardial necrosis, suggesting that this event represents a medical condition with ongoing end organ damage, deserving of emergent treatment.

C. History Part 3: Competing diagnoses that can mimic Acute Heart Failure.

Since acute heart failure is manifest by many nonspecific symptoms, there are multiple competing diagnoses, including:

  • Chronic obstructive pulmonary disease (COPD) exacerbation

  • Pneumonia

  • Pulmonary embolism

  • Venous insufficiency

  • Drug-induced peripheral edema (i.e., calcium channel blockers, thiazolidinediones)

  • Acute coronary syndromes, including acute myocardial infarction

  • Severe cardiac valvular disease, especially acute mitral or tricuspid regurgitation (consider endocarditis) or severe mitral or aortic stenosis

  • Sepsis

  • Other forms of noncardiogenic shock, including pseudosepsis due to excessive therapeutic vasodilator use

  • Noncardiac forms of acute kidney injury/renal insufficiency, including overdiuresis

D. Physical Examination Findings.

Most frequent signs at presentation:

  • Edema (legs, abdomen, sacral)

  • Pulmonary rales, pleural effusion

  • Elevated jugular venous pressure

  • Positive abdominojugular reflux (hepatojugular reflux)

  • Increased body weight

  • Increased abdominal girth

  • Normal or elevated blood pressure

  • Tachypnea

  • Increased heart rate

  • Third heart sound

Less common signs at presentation, suggestive of low cardiac output:

  • Cool extremities

  • Hypotension

  • Narrow pulse pressure

  • Pulsus alternans

  • Impaired end organ function, such as decreased urine output

There are no physical exam findings that individually establish a definitive diagnosis of AHF, but relevant findings may be considered in two main categories. First, there are findings that suggest the presence of underlying cardiac dysfunction that provides the substrate for the AHF episode.

These findings include evidence of left ventricular systolic dysfunction (laterally displaced and/or diffuse PMI, S3, decreased stroke volume on carotid pulse), diastolic dysfunction (S4), or both.

Second, physical exam signs can support the diagnosis of AHF by suggesting the predominant pathophysiologic process involved in the decompensation, such as volume overload (peripheral edema, pleural effusions, rales, ascites, elevated jugular venous pressure, hepatojugular reflux), vascular redistribution (elevated jugular venous pressure, hepatojugular reflux, often elevated blood pressure), or low cardiac output (cool extremities, low blood pressure, often narrow pulse pressure, pulsus alternans).

Note that patients with chronic heart failure may have markedly elevated pulmonary venous pressure causing significant dyspnea with relatively mild rales. Patients with AHF due to vascular redistribution frequently have rapid onset of symptoms that can occur in the absence of signs of marked volume overload.

E. What diagnostic tests should be performed?


1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

As with physical exam findings, laboratory tests can provide insight into the diagnosis of AHF.

BNP/ NT-proBNP: Plasma concentrations of B-type natriuretic peptide (BNP) and its by-product, N-terminal-proBNP (NT-proBNP), are increased in the presence of elevated ventricular (both left and right) pressure and volume, and have been demonstrated to assist in the diagnosis of AHF in patients with dyspnea.

While there is no absolute “diagnostic level” of these biomarkers for AHF, most assays have three ranges. For example, for the typical BNP assay, a BNP less than or equal to 100 pg/mL is strongly suggestive of non–heart failure etiology for the dyspnea, BNP 100 to 400 pg/mL is indeterminate, and BNP greater than 400 pg/mL is strongly supportive of AHF.

As with all laboratory tests, BNP concentrations need to be interpreted in the context of the individual patient, and some assays provide different diagnostic ranges based upon a patient’s gender, age, and renal function. In addition, there are known factors other than CHF that can result in high BNP levels (e.g., age, renal dysfunction, myocardial infarction, acute pulmonary embolism, and high output states such as cirrhosis) and in lower than expected BNP levels (e.g., obesity, within 1 hour of flash pulmonary edema, acute mitral regurgitation, and mitral stenosis).

Note specifically that elevated BNP levels can occur with right-sided heart failure, and may be present in acute pulmonary embolus.

Electrolytes: Measurement of serum electrolytes can also often assist in the diagnosis of AHF and are reflective of the patient’s clinical course prior to presentation. Hyponatremia may be suggestive of neurohormonal imbalance due to advanced or undertreated chronic heart failure or iatrogenic from diuretics (particularly thiazides).

Hyperkalemia often suggests acute renal insufficiency due to worsening heart failure, but may also be due to recent initiation of a mineralocorticoid receptor antagonist (spironolactone or eplerenone), ACE inhibitor, or angiotensin receptor blocker while hypokalemia is frequently seen in the presence of increased diuretics with insufficient potassium repletion.

Hypomagnesemia may accompany hypokalemia, especially if diuretic-related, and should be assessed. Hyperchloremia may be associated with excessive diuresis and volume depletion.

Renal function markers: Blood urea nitrogen (BUN) and creatinine serve as markers of renal function. Chronic renal insufficiency is a frequent comorbidity in patients with heart failure and AHF episodes are often accompanied by acute on chronic renal failure.

This renal insufficiency is usually due to increased central venous pressure (increased “afterload” on the kidney), rather than decreased renal perfusion form decreased cardiac output. Cystatin-C is another marker of renal function with the putative advantage of responding more rapidly to acute changes in renal function. Other markers to assess acute kidney injury are in development and should assist the evaluation and treatment of these patients.

Troponin: Increased troponins above the upper limit of normal occur in 15% to 70% of patients with AHF, depending upon the series and the assay used. Acute coronary syndromes (ACS) may precipitate AHF, but much more frequently, AHF is accompanied by mild-to-moderate troponin elevations, suggestive of myocardial damage from the AHF itself. Distinguishing the “troponinemia” of heart failure from that of ACS or myocardial infarction can often be challenging and requires synthesis of symptoms, clinical context, and other diagnostic tests.

2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

Electrocardiogram (ECG): The ECG can assist in the evaluation of myocardial ischemia, left ventricular hypertrophy, arrhythmias, and electrolyte disorders as contributing factors to AHF.

Chest radiography: The chest x-ray (CXR) is useful in assessing the presence and extent of pulmonary congestion, although it may underestimate the extent of congestion and pulmonary venous hypertension in patients with chronic heart failure. Pleural effusions may be detected, as well as evidence of pneumonia, a common confounding differential diagnosis, comorbidity, or exacerbating factor. Changes in cardiac silhouette, suggestive of pericardial effusion, or aortic contour (e.g., aortic dissection) should also be examined.

Echocardiogram: In patients with no prior echocardiogram, this test is probably the most useful noninvasive imaging study, given that it provides information on size, structure, and function of all cardiac chambers and valves, potential wall motion abnormalities, and estimates of hemodynamics, including central venous and left ventricular filling pressure.

However, most patients do not require an emergent or urgent echo to guide early therapy, and a full, more detailed, higher quality, and clinically relevant echocardiographic examination can be performed after compensation is reestablished. One study demonstrated no significant difference in left ventricular ejection fraction upon presentation with AHF compared to later in the hospitalization.

Pulmonary artery catheterization: The PA catheter is an essential and very useful diagnostic tool in properly selected patients. In patients with evidence of shock in whom it is unclear whether the etiology is cardiogenic or noncardiogenic, invasive assessment of central venous pressure, pulmonary arterial (PAP) and pulmonary capillary wedge pressures (PCWP), cardiac output, and vascular resistances can provide crucial information to guide appropriate selection of and evaluate response to therapy.

A PA catheter should not be routinely used in most patients with AHF, given the small, but finite, risk of infection, vascular injury, and other associated complications. One of the greatest problems with the use of the PA catheter is that members of the medical team may lack familiarity with wave forms and have limited experience in distinguishing artefact and recognizing other problems (e.g., migration of the right atrial port into the RV or into permanent wedge position, setting the pressure transducer to the appropriate height).

Vigilance in assessing data obtained from the PA catheter and interpretation in the context of other data from the patient is essential to ensure that information used to guide clinical decisions is correct. Other diagnostic tests, such as noninvasive cardiac stress testing or cardiac catheterization with coronary angiography, should also be considered in selected patients.

III. Management.


A. Immediate management.

The first step in management of the patient with AHF is to address life-threatening issues, including, but not limited to:

Respiratory failure: The most common presenting symptom of subjects with AHF is dyspnea and respiratory failure is the most frequent life-threatening condition for these patients. Immediate administration of the following is recommended:

Reposition the patient: If it is safe to do so, support the patient in assuming an upright, sitting posture. Many patients will do this on their own to optimize their ventilator efficiency

Oxygen: Although no randomized study has been performed, immediate administration of supplemental oxygen is the most readily available means to increase end organ oxygen delivery.

Ventilatory support: If the above measures remain inadequate, rapid application of noninvasive ventilatory support (CPAP or NIPPV) has been shown to be very effective in rapidly improving symptoms, hemodynamics, and metabolic abnormalities associated with AHF. If noninvasive measures are insufficient, rapid intubation with mechanical positive pressure ventilation should be employed.

Nitrates: Sublingual or intravenous nitrates can be very effective as vasodilators, decreasing pulmonary venous pressure and relieving dyspnea. Rapid administration of intravenous nitrates in patients with severe pulmonary edema decreased the need for mechanical ventilation and myocardial infarction compared to a high-dose furosemide strategy in a randomized study.

Diuretic: Most patients will also have significant volume overload contributing to the respiratory insufficiency, so if there is evidence of volume overload (as opposed to volume redistribution), rapid administration of intravenous loop diuretics is recommended. Although it has remained controversial, one early study suggested that furosemide also directly dilates pulmonary veins.

Opiates (morphine) in the setting of AHF have been associated with increased rates of mechanical intubation, prolonged hospitalization, more frequent ICU admissions, and higher mortality. While this association may be reflective of the greater disease severity of patients receiving morphine, these findings argue against routine use of morphine in patients with dyspnea, as well as for careful monitoring in the select patients who receive opiates.

Circulatory failure: Surprisingly few (approximately 5%) patients present with low output syndromes in the general HF population, but these patients require aggressive management of their shock to mitigate or prevent the related end organ damage.

Positive inotropes: To date, there are no “pure” inotropes, since all of the currently available agents also have some vascular effects, and the selection of the specific agent should account for these differences. All of these agents increase cAMP and intracellular calcium, with the related increases in heart rate, myocardial oxygen consumption, and arrhythmias, potentially resulting in myocardial ischemia, infarction, or death.

Monitoring of response to these therapies depends upon the initial derangements, including blood pressure, peripheral perfusion, respiratory status, urine output, mental status, and other end organ function.

Catecholamines such as dobutamine, epinephrine, and norepinephrine have been used to improve myocardial contractility and increase the heart rate in the setting of AHF. Dobutamine is a predominant beta-1adrenergic receptor agonist with mild vasodilating properties.

Recent practice has used lower doses of dobutamine (2 to 5 µg/kg/min) for positive inotropic effect than previously (10 to 20 µg/kg/min), and due to the potential adverse effects, the lowest effective dose should be used. Low doses of dobutamine are also associated with mild vasodilation, while higher doses can cause vasoconstriction.

Dopamine has multiple dose-related effects with mid-range doses (approximately 3 to 5 µg/kg/min) providing increased contractility and higher doses (approximately >5 µg/kg/min) giving increasing amounts of vasoconstriction in addition to augmenting inotropy.

Phosphodiesterasetype III inhibitors, such as milrinone (in U.S. and Europe) andenoximone (in Europe), increase cardiac contractility, as well as acting as peripheral arterial vasodilators. Many clinicians no longer use a bolus loading dose of these agents, so as to avoid significant hypotension, but a bolus may be used in selected situations. Hypotension, tachycardia, atrial, and ventricular arrhythmias, increased myocardial ischemia, and other adverse effects, including suggestions of increased mortality in patients with ischemic heart disease, may occur and patients should be carefully monitored.

Levosimendan (available in Europe and other non-US countries) is an ATP-dependent potassium channel activator with myocardial calcium sensitizing effects (and possible PDE III inhibitor effects), and acts as a vasodilator and inotrope. Many clinicians no longer use a bolus loading dose, so as to avoid significant hypotension, but a bolus may be used in selected situations. Hypotension, tachycardia, atrial and ventricular arrhythmias, and other adverse effects may occur, and patients should be carefully monitored.

Mechanical support: Intraaortic balloon pumps (IABP) can be used at many centers in the setting of severe cardiac compromise and provide a rapid decrease in ventricular afterload with some augmentation of forward flow. Its use is contraindicated in the setting of moderate-to-severe aortic insufficiency and aortic aneurysms/dissections, as well as limited by vascular access issues and complications.

Other mechanical support devices may be used at specialized centers, including ventricular assist devices (VADs) and extracorporeal membrane oxygenation (ECMO).

Renal failure: Fulminant renal failure requiring emergent treatment is uncommon in patients with AHF, but significant renal insufficiency is quite frequent. Emergent hemodialysis may be used to treat life-threatening electrolyte abnormalities or other severe sequelae of renal failure.

Ultrafiltration has been increasingly used to treat patients with significant volume overload. Some centers will initiate veno-venous ultrafiltration in patients with marked fluid overload (i.e., at least 10 kg), while others reserve this therapy for patients who fail diuretics.

Clinical trials are currently underway to provide evidence regarding these strategies. Careful attention should be given to the filtration rate so as to not exceed the vascular refill rate. Some clinicians will monitor for hemoconcentration, presumably to avoid excessive or too rapid volume removal.

“Renal-dose”dopamine (<3 µg/kg/min) has been controversial, but a recent study suggests that low-dose dopamine with furosemide provides diuresis with improved renal function and potassium homeostasis compared to furosemide alone. Nonetheless, many clinicians do not routinely use dopamine in the setting of mild-to-moderate renal insufficiency, and most reserve it for patients who fail diuretics. This strategy is also being evaluated in ongoing clinical studies.

Diuretics remain the most commonly administered agent for AHF. Intravenous furosemide (or equivalent) can provide rapid symptom relief as well as decrease the underlying volume overload. Diuresis can also frequently improve renal insufficiency, since the most common cause of acute renal insufficiency in AHF patients is increased central venous pressure.

Patients receiving high-dose diuretics appear to have more rapid symptom relief with mild transient worsening of renal function, and there does not appear to be a difference between continuous infusion versus bolus-dosing strategies in a recent clinical study.

These findings suggest that the strategy that is most appropriate to ensure reliable diuresis at the specific clinical setting should be implemented. While most patients present with volume overload, there is agroup of patients with AHF due to volume redistribution, and these patients will generally not benefit from aggressive diuresis. Electrolyte repletion is essential in patients with hypokalemia and hypomagnesemia.

Concomitant medications: Many patients with AHF will present with a history of multiple concomitant medications, including therapies for chronic heart failure. Depending on the severity of the AHF episode, most of these medications can and should be continued during their hospitalization.

Beta-blocker therapy in particular should be continued during the hospital course, unless there is cardiogenic shock, symptomatic bradycardia, or advanced heart block. Patients in whom beta-blocker therapy is discontinued during hospitalization have worse clinical outcomes, even when adjusted for disease severity. ACE inhibitors and angiotensin blockers may be held in the context of acute renal failure, but should be resumed as soon as possible.

B. Physical Examination Tips to Guide Management.

The physical exam may be used to assess the response to therapy and guide management.

Blood pressure should be carefully followed, though with the advent of improved noninvasive monitoring, invasive arterial lines are rarely necessary. Hypotension has been associated with poor outcomes in the setting of AHF, and iatrogenic hypotension should be assiduously avoided. Hypertension can be one of the major precipitants of AHF and should be treated.

Heart rate is often a reflection rather than a cause of the AHF episode, and the initial tachycardia often improves in conjunction with the improvement in dyspnea. However, atrial fibrillation with rapid ventricular response is a well-known precipitant of AHF.

Tachycardia may occur due to the positive chronotropic effects of some drugs (e.g., dobutamine, milrinone), excessive volume depletion, or the onset/ worsening of atrial and ventricular arrhythmias, especially atrial fibrillation. Bradycardia is less common and may be due to excess beta-blocker therapy.

Respiratory rate is often not as carefully assessed clinically, and may not be as reliably sensitive to therapy as other vital signs. Tachypnea may represent inadequate resolution of the initial episode of dyspnea or a new event, such as a pulmonary embolus. Fever is suggestive of underlying infectious process, particularly pneumonia or urinary tract infections, both of which can instigate AHF exacerbations.

Oxygen saturation may be measured noninvasively and is useful to follow in patients with marginal oxygenation.

Body weight is frequently overlooked in the assessment of the patient until later in their hospital course, yet can be a very useful measure to follow the response to therapy. Body weight should be obtained as early as practical in the hospital course. Urine output and daily input and output measures are also useful corroborative measures, but in many clinical practices appear to be less reliable.

Jugular venous pressure (JVP) is by far the most useful, and most challenging, physical examination finding to monitor response to therapy in the AHF patient. Elevation of the JVP suggests that there is persistent volume overload and additional diuresis is indicated, whereas a low JVP suggests that there may be excessive volume depletion.

Significant tricuspid regurgitation can confound interpretation of JVP, while the elicitation of hepatojugular reflux can augment the interpretation. Careful positioning of the patient, optimizing the visualization of the jugular pulsation and its meniscus, is essential.

Cardiac auscultation can be useful to follow the presence and severity of extra heart sounds (S3, S4) and murmurs. The disappearance of an S3 and reduction in the intensity of mitral and tricuspid regurgitation murmurs are supportive of a beneficial response to therapy through reduction of ventricular filling pressure and volume.

Lung field examination can follow the resolution of rales, rhonchi, pleural effusions, and other signs of congestion, and reveal possible emerging zones of consolidation in the presence of an underlying pneumonia.

Peripheral and central edema resolution should also be monitored. Perfusion of extremities may also be followed in patients presenting with a low output syndrome.

C. Laboratory Tests to Monitor Response To, and Adjustments in, Management.

Serial evaluation of electrolytes and renal function is important. Iatrogenic diuretic-induced hypokalemia can result in life-threatening arrhythmias and is best prevented by adequate supplementation, rather than treated once present. Decreases in renal function are common during treatment of AHF. Although initially thought to be associated with poor outcomes, transient decreases do not seem to portend a poor prognosis.

Serial BNP testing is not recommended for the routine inpatient management of patients with AHF. Serial testing with chest radiography is usually not necessary in the absence of new signs or symptoms.

D. Long-term management.

The long-term management of a patient admitted for AHF is directed to three main issues (also see section on chronic heart failure):

  • First, establishing the etiology of the heart failure is important, so that measures may be taken to address potentially reversible causes. Selected patients with ischemic cardiomyopathies may benefit from revascularization; patients with hypertensive cardiomyopathy should have an aggressive antihypertensive regimen. Alcoholic cardiomyopathies may resolve with cessation of alcohol consumption.

  • Second, identification of precipitating factors for the AHF episode and intensive education to avoid future hospitalizations (see later section).

  • Third, optimization of therapies with demonstrated long-term benefits (see section on Chronic heart failure). In patients with heart failure and reduced ejection fraction, these pharmacologic therapies include beta-blockers, ACE inhibitors, possibly angiotensin receptor blockers, mineralocorticoid receptor antagonists (spironolactone, eplerenone), possibly isosorbide dinitrate/hydralazine, and possibly digoxin.

    It is absolutely imperative that these therapies be initiated as much as possible during the hospitalization and not be left to the outpatient setting. In addition, consideration and scheduling of device therapy, such as cardiac resynchronization therapy (CRT)/biventricular pacemaker and implantable defibrillator device (ICD), should be done while the patient is still hospitalized, if appropriate.

The hospitalization for AHF is one of the most potent “teachable moments” and care providers are strongly encouraged to take advantage of the patient as a captive audience.

E. Common Pitfalls and Side-Effects of Management

Management of patients with AHF is complex and highly specific to the individual. However, there are some common pitfalls:

Hypotension: Most therapies for AHF can cause hypotension, and the development of hypotension in a number of studies has been related to poor clinical outcomes. Blood pressure (including orthostatic measurements), central venous pressure (usually by assessment of JVP), body weight, urine output, and renal function should be carefully monitored to avoid hypotension. If hypotension ensues, rapidly remove inciting pharmacologic agents (be especially aware of topical nitrates) and position the patient as necessary to improve perfusion. In many patients, raising the legs will provide sufficient augmentation of venous return to improve symptoms.

Worsening renal function: This problem is the most vexing for clinicians, since worsening renal function can result from inadequate diuresis (persistent elevation of central venous pressure) or be the result of excessive diuresis with volume depletion. In these situations, it is very helpful to have measurements of baseline BUN and creatinine as comparators. Ultimately, the treatment decision will be determined by the extent of volume overload as assessed by the JVP and other clinical factors, as well as the subsequent response to therapy. As noted above, transient decreases in renal function may not portend the poor prognosis, as previously believed, and may just reflect the response to therapy.

Premature discharge: Increasing pressure to decrease hospital length of stay (LOS) has resulted in steady declines of LOS for AHF in U.S. hospitals. Unfortunately, this decreased LOS has also been associated with increased 30-day readmission rates. Many patients are inadequately diuresed prior to discharge with persistent symptoms of dyspnea; some are discharged with the plan to “complete diuresis as an outpatient.” This strategy is not successful in many patients, who are not able to monitor all of the factors that impact the active diuresis of AHF. Many centers are treating patients much more aggressively prior to discharge and ensuring early outpatient follow-up to prevent early readmissions for AHF.

IV. Management with Co-Morbidities

The average age of the patient with AHF is in the 70s; therefore, these patients tend to have multiple comorbidities in addition to the underlying cause of the heart failure. Many of these comorbidities can both cause and exacerbate AHF. Some of the most important comorbidities include:

Atrial fibrillation: Atrial fibrillation (AF) can be both a cause of and exacerbated by AHF. Many patients present in atrial fibrillation (AF) with rapid ventricular response (HR >100 bpm) with AHF, but generally, therapies are initially directed to the AHF, since the ventricular rate often decreases as the adrenergic drive resolves. However, in some patients, the AF assumes a more primary role, often with a very rapid ventricular response (usually >140 bpm). In these patients, rate control is important and can be challenging.

In patients with preserved ejection fraction, beta-blockers and calcium channel blockers are often effective. Calcium channel blockers active on the atrioventricular node, such as diltiazem and verapamil, should be avoided in patients with reduced ejection fraction, due to their acute negative inotropic properties. Digoxin, beta-blockers, and amiodarone are often used in the setting of AHF with reduced ejection fraction. Although one must always consider the risk of thromboembolic events, if the patient is truly hemodynamically unstable due to AF with rapid ventricular rate, electrical cardioversion remains an important option.

Acute coronary syndromes (ACS): From 15% to 50% of patients with AHF have troponin levels above the established upper limit of normal and many patients have underlying coronary artery disease. In most of these patients, the troponins decrease with the treatment of the AHF.

In any patient presenting with AHF, it is important to consider the diagnosis of an ACS with an ECG for the evaluation of myocardial ischemia/infarction. Therapies for ACS and AHF can be complementary, such as nitrates (which can improve dyspnea, reduce myocardial oxygen demand, improve coronary blood flow, and decrease platelet aggregation), or additive, such as heparin or other anticoagulant therapies.

Chronic obstructive pulmonary disease (COPD): COPD exacerbations may present with signs and symptoms very similar to AHF, and may also instigate an AHF episode. Although many patients ultimately receive corticosteroid, antibiotics, and diuretics, the careful use of diagnostic tests, such as physical examination with assessment of JVP, BNP, and chest radiography, can reduce the necessity of such indiscriminate approaches.

Renal insufficiency: In patients who present with renal failure as evidenced by an elevated creatinine (i.e., >3.0 mg/dL), consideration should be given to withholding ACE inhibitors, ARBs, and mineralocorticoid receptor antagonists (spironolactone, eplerenone). Diuretic doses need to be adjusted upward in the setting of renal failure, with doubling of initial doses until a diuretic effect is achieved or until concerns of toxicity arise.

V. Patient Safety and Quality Measures

A. Appropriate Prophylaxis and Other Measures to Prevent Readmission.

An episode of AHF often can be seen as representing a failure of outpatient CHF management. It is imperative that this admission be viewed as an opportunity to prevent future decompensations through active education; handouts and checklists without individual instruction are rarely effective. This education should include, but not be limited to, instruction on:

  • Low-salt and weight loss diets (as appropriate)

  • Daily use of a scale and a mechanism to record body weights, including directions on the specific actions to take in the event of a change in body weight (see below)

  • Self-titration of diuretics, in appropriate patients. For example, if weight increases by 3 to 5 lb above baseline, double the diuretic dose for 3 to 5 days. If body weight returns to baseline, resume prior dose of diuretics. If symptoms of hypotension ensue, hold diuretics, and if the symptoms of hypotension do not resolve, call care provider. If weight does not improve or if increasing symptoms of dyspnea or other symptoms of congestion, call a care provider.

  • Chronic heart failure management programs, if available

  • Exercise or rehabilitation program

  • Other health-related issues such as smoking cessation

B. What's the Evidence for specific management and treatment recommendations?

There are three main guidelines that address the treatment of patients with acute heart failure:

Lindenfeld, J, Albert, NM, Boehmer, JP. “HFSA 2010 comprehensive heart failure practice guideline”. J Card Fail. vol. 16. 2010. pp. e1-194. (The section specifically addressing AHF is available online (http://www.heartfailureguideline.org/12_acute_decompensated_hf/28), and is updated.)

Hunt, SA, Abraham, WT, Chin, MH. “2009 focused update incorporated into the ACC/AHA 2005 guidelines for the diagnosis and management of heart failure in adults: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines developed in collaboration with the International Society for Heart and Lung Transplantation”. J Am Coll Cardiol. vol. 53. 2009. pp. e1-e90. (The AHF section (e47-e52) was a new addition to this set of guidelines.)

McMurray, JJ, Adamopoulos, S, Anker, SD. “ESC guidelines for the diagnosis and treatment of acute and chronic heart failure 2012: The task force for the diagnosis and treatment of acute and chronic heart failure 2012 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association (HFA) of the ESC”. Eur Heart J. 2012. (The ESC had an independent set of guidelines for AHF in 2005, which were incorporated into, and updated in, the 2008 and 2012 documents.

It should be noted that there is very limited clinical trial evidence upon which these guidelines are based. However, there are some central articles that inform current practice and perspectives, a brief selection of which follows with annotations:

Fonarow, GC, Corday, E. “Overview of acutely decompensated congestive heart failure (ADHF): a report from the ADHERE registry”. Heart Fail Rev. vol. 9. 2004. pp. 179-85.

Gheorghiade, M, Pang, PS. “Acute heart failure syndromes”. J Am Coll Cardiol. vol. 53. 2009. pp. 557-73. (The ADHERE registry provided important insights into the epidemiology of acute heart failure in the US, while Gheorghiade and Pang’s article provides a general review of the field.)

Damman, K, van Deursen, VM, Navis, G, Voors, AA, van Veldhuisen, DJ, Hillege, HL. “Increased central venous pressure is associated with impaired renal function and mortality in a broad spectrum of patients with cardiovascular disease”. J Am Coll Cardiol. vol. 53. 2009. pp. 582-8.

Mullens, W, Abrahams, Z, Francis, GS. “Importance of venous congestion for worsening of renal function in advanced decompensated heart failure”. J Am Coll Cardiol. vol. 53. 2009. pp. 589-96. (These two articles demonstrate the important role that increases in central venous pressure have on worsening renal function in cardiovascular disease in general and specifically in acute heart failure. Of note, there is little to no relationship with changes in cardiac output.)

Gelman, S, Mushlin, PS. “Catecholamine-induced changes in the splanchnic circulation affecting systemic hemodynamics”. Anesthesiology. vol. 100. 2004. pp. 434-9.

Cotter, G, Metra, M, Milo-Cotter, O, Dittrich, HC, Gheorghiade, M. “Fluid overload in acute heart failure–re-distribution and other mechanisms beyond fluid accumulation”. Eur J Heart Fail. vol. 10. 2008. pp. 165-9.

Fallick, C, Sobotka, PA, Dunlap, ME. “Sympathetically mediated changes in capacitance: redistribution of the venous reservoir as a cause of decompensation”. Circulation. Heart failure. vol. 4. 2011. pp. 669-75. (These articles summarize the principle and the supporting evidence that neurohormonally- and sympathetically-mediated shifts in intravascular volume from the venous system can contribute to decompensation in acute heart failure.)

Peacock, WF, De Marco, T, Fonarow, GC. “Cardiac troponin and outcome in acute heart failure”. N Engl J Med. vol. 358. 2008. pp. 2117-26.

Kociol, RD, Pang, PS, Gheorghiade, M, Fonarow, GC, O’Connor, CM, Felker, GM. “Troponin elevation in heart failure prevalence, mechanisms, and clinical implications”. J Am Coll Cardiol. vol. 56. 2010. pp. 1071-8.

O’Connor, CM, Fiuzat, M, Lombardi, C. “Impact of serial troponin release on outcomes in patients with acute heart failure: analysis from the PROTECT pilot study”. Circ Heart Fail. vol. 4. 2011. pp. 724-32. (These articles provide some of the evidence suggesting that acute heart failure involves on-going myocardial damage that relates to poor outcomes.)

Maisel, AS, Krishnaswamy, P, Nowak, RM. “Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure”. N Engl J Med. vol. 347. 2002. pp. 161-7.

Mueller, C, Scholer, A, Laule-Kilian, K. “Use of B-type natriuretic peptide in the evaluation and management of acute dyspnea”. N Engl J Med. vol. 350. 2004. pp. 647-54. (These two early studies established the ability of B-type natriuretic peptide assays to assist in the diagnosis of patients presenting with dyspnea. Mueller and colleagues demonstrated that patients treated by physicians who had access to early BNP measurements had shorter lengths of stay without an increase in readmission, suggesting more rapid heart failure treatment. The utility of early measurement of BNP (either via BNP or nt-proBNP) has been well-established, although there is no convincing evidence supporting serial in-hospital measurements.)

Gandhi, SK, Powers, JC, Nomeir, AM. “The pathogenesis of acute pulmonary edema associated with hypertension”. N Engl J Med. vol. 344. 2001. pp. 17-22. (While an echocardiogram may be the most useful single diagnostic test in patients with heart failure, its utility in the acute setting is unclear. In this very small study of 38 patients admitted with acute pulmonary edema and systolic blood pressure greater than 160 mm Hg, there was no significant change in the echocardiogram obtained at presentation and after treatment.)

Current therapeutic approaches: These articles provide some of the evidence base for current therapies for acute heart failure.

Cotter, G, Metzkor, E, Kaluski, E. “Randomised trial of high-dose isosorbide dinitrate plus low-dose furosemide versus high-dose furosemide plus low-dose isosorbide dinitrate in severe pulmonary oedema”. Lancet. vol. 351. 1998. pp. 389-93. (This elegant, small study of 110 patients demonstrated the importance of vasodilators in the treatment of AHF. Patients with congestive heart failure and severe pulmonary edema randomized to receive high-dose nitrates had reduced requirements for mechanical ventilation and decreased myocardial infarction compared to those receiving high dose diuretics.)

Mullens, W, Abrahams, Z, Francis, GS. “Sodium nitroprusside for advanced low-output heart failure”. J Am Coll Cardiol. vol. 52. 2008. pp. 200-7. (An observational study suggesting that nitroprusside can have beneficial effects even in patients with advanced low-output heart failure.)

“Intravenous nesiritide vs nitroglycerin for treatment of decompensated congestive heart failure: a randomized controlled trial”. JAMA. vol. 287. 2002. pp. 1531-40.

O’Connor, CM, Starling, RC, Hernandez, AF. “Effect of nesiritide in patients with acute decompensated heart failure”. N Engl J Med. vol. 365. 2011. pp. 32-43. (The VMAC trial was the first large, randomized trial of nesiritide that demonstrated its efficacy in improving hemodynamics and dyspnea. Due to concerns regarding potential increases in renal dysfunction and mortality, the ASCEND-HF trial enrolled over 7,000 patients and demonstrated no significant increase in renal dysfunction or mortality, although it also did not demonstrate a clinically meaningful improvement in dyspnea.)

Felker, GM, Lee, KL, Bull, DA. “Diuretic strategies in patients with acute decompensated heart failure”. N Engl J Med. vol. 364. 2011. pp. 797-805. (DOSE was a relatively small, innovative factorial design trial investigating the relative benefits of high dose versus low dose and bolus dose versus continuous infusion of intravenous diuretics in patients with AHF. No significant differences emerged between the treatment groups, although the high dose strategy tended to provide greater diuresis, earlier and better symptom relief at the expense of transient worsening of renal function.)

Cuffe, MS, Califf, RM, Adams, KF. “Short-term intravenous milrinone for acute exacerbation of chronic heart failure: a randomized controlled trial”. JAMA. vol. 287. 2002. pp. 1541-7.

Felker, GM, Benza, RL, Chandler, AB. “Heart failure etiology and response to milrinone in decompensated heart failure: results from the OPTIME-CHF study”. J Am Coll Cardiol. vol. 41. 2003. pp. 997-1003. (These two articles are from the randomized, placebo-controlled OPTIME-CHF trial report on the effects of milrinone in patients with AHF. Milrinone did not improve clinical outcomes, but did result in increased symptomatic hypotension and new atrial arrhythmias with a trend toward increased mortality, especially in patients with ischemic etiology of heart failure. This trial, and others, reinforce the concept that inodilators such as milrinone and dobutamine should be reserved for patients with severe low-output syndromes, due to their adverse side effects.)

Gray, A, Goodacre, S, Newby, DE, Masson, M, Sampson, F, Nicholl, J. “Noninvasive ventilation in acute cardiogenic pulmonary edema”. N Engl J Med. vol. 359. 2008. pp. 142-51. (The 3CPO trial demonstrated that early intervention with noninvasive ventilatory support, such as continuous positive airway pressure (CPAP) or noninvasive intermittent positive-pressure ventilation (NIPPV) resulted in more rapid symptomatic and metabolic improvement, but no short-term survival benefit. Noninvasive ventilation is probably underutilized in the U.S. compared to Europe.)

C. DRG Codes and Expected Length of Stay.