Acute Decompensated Heart Failure Case File

Acute Decompensated Heart Failure Case File

Eugene C. Toy, Md, Michael d . Faulx, Md

Case 16

A 54-year-old woman presents to the emergency department complaining of several days of progressive shortness of breath and fatigue. She was in her usual state of health until 2 weeks ago, when she fell and injured her left knee. As a result, she had been taking ibuprofen at home around the clock for pain relief. Since then she has noted a 10-lb weight gain, abdominal bloating, and swelling in her legs. Her symptoms have worsened rapidly over the past day. She was unable to lie comfortably in bed and woke up several times at night gasping for air. She is now short of breath at rest, unable to speak in full sentences, and has an unproductive cough. On physical examination, the patient is afebrile, tachypneic with a respiratory rate of 32 breaths/min, and her heart rate is 110 bpm, blood pressure is 160/110 mmHg, and oygen saturation on room air is 82%. There is elevated jugular venous pressure. Heart exam is notable for an audible S3. Lungs have rales bilaterally. She is using accessory muscles to breathe. Abdominal exam reveals a pulsatile liver. Extremities are warm with good pulses and pitting edema bilaterally to the knees. Laboratory evaluation reveals an elevated creatinine and an elevated brain natriuretic peptide level. An arterial blood gas reveals hypoxia and hypercapnia. A chest x-ray shows cardiomegaly, diffuse bilateral infiltrates, and small bilateral pleural effusions.

• What is the most likely diagnosis?
• What is the best next diagnostic step?
• What is the best next step in therapy ?

Answer to Case 16:

Acute Decompensated Heart Failure

Summary: A 54-year-old woman presents to the ED with progressive respiratory distress, exertional dyspnea, orthopnea, and paroxysmal nocturnal dyspnea in the setting of heavy nonsteroidal anti-inflammatory drug (NSAID) use. She is tachycardiac, hypertensive, and hypoxemic. Her physical exam is notable for elevated jugular venous pressure, an audible S3, bilateral rales, a pulsatile liver, and lower extremity edema. Laboratory evaluation reveals acute kidney injury and elevated brain natriuretic peptide. Arterial blood gas reveals hypoxia and hypercapnia. A chest x-ray shows cardiomegaly, diffuse bilateral infiltrates, and small bilateral pleural effusions.

• Most likely diagnosis: Acute decompensated heart failure.
• Best diagnostic step: Determine hemodynamic profile and identify a precipitant of the acute decompensation.
• Best therapy: Administer an intravenous diuretic and a vasodilator. Start noninvasive positive pressure ventilation.

ANALYSIS

Objectives

1. Know the common presenting signs and symptoms of acute decompensated heart failure.
2. Know the common treatment goals for acute heart failure based on hemodynamic profile.
3. Understand the importance of a systematic search for precipitating causes of recent-onset or worsening heart failure.

Considerations

This 54-year-old woman presents in acutely decompensated heart failure with respiratory distress, volume overload, and pulmonary edema. An important first step in evaluating a patient with suspected heart failure is to determine a patient’s hemodynamic profile based on volume status (wet or dry) and overall perfusion (warm or cold). This patient presents wet and warm, the most common hemodynamic profile in decompensated heart failure. She has no clear evidence of organ hypoperfusion, which could manifest as cool extremities, weak pulses, altered mental status, or liver abnormalities. The most immediate problems are severe congestion and hypoxia, which should be treated by volume reduction with diuretics, the administration of vasodilators, and noninvasive positive-pressure ventilation. Once measures to stabilize the patient’s clinical condition and provide symptom relief have been initiated,

it is important to identify the specific factors that led to this particular acute decompensation. In this particular case, the likely culprit is heavy NSAID use. NSAIDs inhibit renal prostaglandins, and as a result can cause sodium and water retention and diminish the effects of diuretics. It is critically important, however, to rule out other precipitating factors in the initial evaluation of the patient.

Approach To:

Acute Decompensated Heart Failure

DEFINITIONS

HEART FAILURE: A syndrome in which the heart cannot meet the metabolic demands of the body or fails to maintain adequate cardiac output in the setting of rising filling pressures.

ACUTE DECOMPENSATED HEART FAILURE: An episode in which a patient’s heart failure signs and symptoms change, resulting in a need for urgent therapy or hospitalization. This is a possibly life-threatening condition that requires immediate medical attention.

CARDIOMYOPATHY: A disease of the heart muscle that can result in heart failure.

FLASH PULMONARY EDEMA: A feature of decompensated heart failure where acute increases in left ventricular diastolic pressure cause rapid fluid accumulation in the pulmonary interstitium and alveolar spaces.

CLINICAL APPROACH

Etiologies

In heart failure, the heart cannot meet the metabolic demands of the body and fails to maintain adequate cardiac output. There are many medical conditions that can adversely affect myocardial performance and promote heart failure (Table 16.1). Heart failure can be classified as heart failure with low EF (impaired systolic function) or heart failure with preserved EF (impaired diastolic function). Patients with heart failure with preserved EF tend to be older, female, and more likely to have atrial fibrillation and hypertension. In the United States, coronary artery disease is the most common cause of heart failure.

Patients with systolic heart failure experience progressive remodeling of the left ventricle with dilatation and impaired contractility. Clinically, patients develop worsening symptoms, decreased exercise tolerance, and reduced quality of life. The progressive decline is characterized by increasingly frequent episodes of acute decompensation that require hospitalization.

Acute heart failure typically arises as a result of deterioration in patients with a previous diagnosis of heart failure. However, acute heart failure may also be the first presentation of a heart failure syndrome. Acute heart failure is associated with the accumulation of fluid within the lungs’ interstitial and alveolar spaces, as a result of acutely elevated cardiac filling pressures.

Clinical Presentation

Dyspnea is the most common presenting symptom of acutely decompensated heart failure. Other typical symptoms include orthopnea, paroxysmal nocturnal dyspnea, reduced exercise tolerance, fatigue, and ankle swelling. Patients may also describe a nocturnal cough, wheezing, weight gain, bloating, loss of appetite, and confusion. The clinician should attempt to quantify symptoms in order to gauge disease severity and monitor both the degree of acute decompensation and the response to treatment.

A thorough physical exam can secure the diagnosis, and should focus on a careful determination of volume status. Signs of heart failure include hypoxia, pulmonary rales, pleural effusions, an accentuated third heart sound, a pulsatile liver, an elevated jugular venous pressure, sustained hepatojugular reflux, lower extremity edema, and abdominal ascites. Signs of low perfusion include cool skin, a narrow pulse pressure, and faint pulses.

On the basis of presenting signs and symptoms, the clinician can determine a patient’s hemodynamic profile (Figure 16-1). This is an important step in evaluating a patient with suspected heart failure because it will guide treatment.

EVIDENCE OF CONGESTION

Figure 16-1. Hemodynamic profiles in heart failure.

Diagnosis

The identification of a precipitant of acute heart failure (HF) is another important aspect of evaluating an acutely decompensated patient. Patients with preexisting HF often have a clear precipitant for an acute decompensation (Table 16.2). Medical and dietary noncompliance are common precipitants of acute decompensation. Coronary ischemia and uncontrolled hypertension can also contribute to the sudden rise in left-sided intracardiac pressures that can trigger episodes of flash pulmonary edema. NSAIDs, and calcium channel blockers, alcohol, and illicit drugs such as cocaine can also precipitate acute heart failure.

In addition to a thorough history and physical exam, the following workup can facilitate the identification of a precipitant and rule out alternative causes for the presenting signs and symptoms such as chronic lung disease, anemia, or kidney failure. Laboratory evaluation should include complete metabolic panel, complete blood count, thyroid function, cardiac enzymes, and coagulation studies. Measurement of brain natriuretic peptide (BNP) can be useful in a patient presenting with suspected heart failure. A normal BNP in this setting can effectively rule out heart failure. Laboratory abnormalities identified on this initial evaluation can confirm end-organ hypoperfusion consistent with a low output state.

All patients presenting with suspected acute decompensated heart failure should receive an electrocardiogram to identify signs of ischemia, old infarction, conduction abnormalities, arrhythmia, pericarditis, or chamber enlargement. A chest x-ray should be obtained to exclude lung disease and evaluate for cardiomegaly, diffuse bilateral infiltrates, focal consolidations, or pleural effusions.

A repeat echocardiogram is not required for the evaluation of an acute episode in a patient with known HF. However, an echocardiogram is essential in cases of recent-onset heart failure, to evaluate cardiac structure and function.

Newly diagnosed HF patients generally undergo coronary angiography to definitively exclude ischemic heart disease as the cause for their pump dysfunction. A pulmonary artery (right heart) catheterization can provide information about rightand left-sided filling pressures, pulmonary pressures, and cardiac output. In select cases of unexplained heart failure, endomyocardial biopsy can be helpful in providing a diagnosis and guiding management.

Treatment

The immediate goals of treatment of acute decompensated heart failure are to provide rapid symptom relief, improve organ perfusion, and return the patient to a warm and dry hemodynamic profile. Therapy should also be directed at the underlying precipitating cause of the acute decompensation of heart failure, if it is known and can be treated.

Specific therapy should be guided by the patient’s hemodynamic profile. Most acutely decompensated heart failure patients are warm and wet, with elevated filling pressures and volume overload. In these cases, administration of an intravenous loop diuretic is the mainstay of therapy and can provide rapid symptom relief with the removal of fluid and reducing central venous and pulmonary capillary wedge pressures. Patients often need a higher dose of loop diuretics in the acute setting. Studies have shown that a single intravenous bolus regimen and a continuous infusion of diuretic have similar efficacy in acutely decompensated heart failure. In cases where substantial congestion persists, severe kidney injury exists, and adequate diuresis cannot be achieved, ultrafiltration or dialysis may be considered. Several randomized trials have examined the efficacy of ultrafiltration in the setting of acutely decompensated heart failure, and ultrafiltration may be indicated for patients with obvious volume overload who are not responding to medical therapy.

Supplemental oxygen therapy should be provided as needed to treat hypoxia. For patients in respiratory distress or persistent hypoxia, noninvasive positive-pressure ventilation (NPPV) should be utilized. In the absence of contraindications, the use of NPPV in patients with cardiac pulmonary edema can decrease the need for intubation and improve dyspnea, hypoxia, hypercapnia, and heart rate. Morphine can also provide symptomatic relief in cases of acute pulmonary edema

Vasodilators such as nitroglycerin or nitroprusside can be useful if blood pressure tolerates them. These medications reduce preload and afterload, and can provide rapid symptom relief in patients with acute pulmonary edema or severe hypertension when used in combination with diuretics.

It is very important to identify those patients who have a cold and wet hemodynamic profile, since they will require inotropes and vasodilators in a monitored, critical care setting. Beta-blockers should not be started in acute decompensated heart failure. In patients already on beta-blockers, beta-blocker dosages should be reduced or entirely discontinued until the patient becomes clinically euvolemic and hemodynamically stable. Accurate weight, fluid intake, urine output, volume status, electrolyte levels, and vitals should be followed closely once treatment has been initiated. After stabilization of the patient, low doses of ACE inhibitors should be introduced with careful attention to creatinine, blood pressure, and serum electrolytes.

CASE CORRELATION

• See also Case 1 (acute coronary syndrome/STEMI), Case 2 (acute coronary syndrome/NSTEMI), and Case 3 (cardiogenic shock).

COMPREHENSION QUESTIONS

16.1 A 55-year-old man complains of increasing dyspnea on exertion and orthopnea. His physical examination reveals an S3 heart sound, pulmonary rales, jugular venous distension, and lower extremity edema. He is normotensive, and his extremities are warm to touch. An echocardiogram confirms an ejection fraction of 25% and a dilated left ventricle. What is the most appropriate next step in management?

A. Oral furosemide

B. Intravenous furosemide

C. Oral beta blocker

D. Sublingual nitroglycerin

16.2 Signs of low perfusion on physical exam include all of the following except

A. Cool skin

B. Narrow pulse pressure

C. Presence of a third heart sound

D. Faint pulses

16.3 Which of the following medications should not be initiated during an episode of acute decompensated heart failure?

A. Beta-blocker

B. Ace inhibitor

C. Potassium supplementation

D. Digoxin

ANSWERS

16.1 B. Intravenous furosemide is indicated in this patient with warm/wet profile decompensated heart failure. Intravenous dosing results in more rapid drug delivery and effect than oral dosing. Beta-blocker initiation or titration is not advisable in patients with acutely decompensated heart failure. Nitroglycerin may cause some venodilatation, which may reduce preload, but it will not affect this patient’s volume overload.

16.2 C. A third heart sound is a marker of left ventricular volume overload. Cool extremities, narrow pulse pressure, and faint pulses are markers of poor distal perfusion.

16.3 A. Chronic beta-blocker use is associated with significantly improved survival in patients with reduced LV systolic function. However, acutely their negative inotropic effects can worsen stroke volume and therefore worsen heart failure symptoms. Beta-blocker initiation should be deferred until the patient is euvolemic and well compensated on exam after treatment with appropriate diuresis and afterload reduction.

CLINICAL PEARLS

• The vast majority of acute heart failure exacerbations have precipitating factors. It is important to identify the reason for decompensation.
• determination of the hemodynamic profile (volume and perfusion status) of an acutely decompensated HF patient is a helpful first step in management.
• A thorough physical exam can secure a diagnosis of decompensated heart failure.
• Intravenous diuretics are the mainstay of the rapid treatment for acute decompensated heart failure.

References

Bart BA, Boyle A, Bank AJ, et al. Ultrafiltration versus usual care for hospitalized patients with heart failure: the relief from acutely fluid-overloaded patients with decompensated congested heart failure (RAPID-CHF) trial. J Am Coll Cardiol. 2005; 46:2043. 

Bart BA, Goldsmith SR, Lee KL, et al. Ultrafiltration in decompensated heart failure with cardiorenal syndrome. N Engl J Med. 2012;367:2296. 

Costanzo MR, Guglin ME, Saltzberg MT, et al. Ultrafiltration versus intravenous diuretics for patients hospitalized for acute decompensated heart failure. J Am Coll Cardiol. 2007;49:675. 

Felker GM, Lee KL, Bull DA, et al. Diuretic strategies in patients with acute decompensated heart failure. N Engl J Med. 2011;364(8):797–805. 

Lindenfeld J, Albert NM, Boehmer JP, et al. HFSA 2010 Comprehensive Heart Failure Practice Guideline. Heart Failure Society of America. J Card Fail. 2010;16(6):e1–e194. 

McMurray JJ, Anker SD, Auricchio A, et. al., 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 J Heart Fail. 2012;14(8):803–869. 

Weng CL, Zhao YT, Liu QH, et al. Meta-analysis: noninvasive ventilation in acute cardiogenic pulmonary edema. Ann Intern Med. 2010;152(9):590. 

Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2013;128(16):1810–1852.

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