Acute Heart Failure

Author: Daniel F. Leiva, DO, MS
Baystate Medical Center

Acute heart failure is a common and potentially life-threatening disorder the emergentologist should know well. In 2006 there were 5.1 million people living with heart failure in the United States and an estimated 23 million people worldwide.[1,2] Patients can present to the emergency department as a new, acute failure or an acute-on-chronic exacerbation. They typically complain of dyspnea, fatigue, paroxysmal nocturnal dyspnea, or orthopnea, the latter two of which are highly sensitive and specific.[3] Additional symptoms may include cough, chest pain, palpitations, tachypnea, peripheral edema, weight gain, or decreased exercise tolerance, depending especially on the presence of a precipitant. These can include volume excess, especially in renal or liver failure patients, sudden hypertensive states, acute myocardial infarction, myocarditis, pulmonary embolus, excessive exertion in a deconditioned state, changes to drug therapies, including the addition or removal of drugs or changes in dosages, and substance abuse.[3] The most important piece of history to establish in a patient is a previous diagnosis of heart failure. Consideration should be given to systolic dysfunction/heart failure with reduced ejection fraction (HFrEF) versus diastolic dysfunction/heart failure with preserved ejection fraction (HFpEF); left-sided versus right-sided heart failure; and high-output versus low-output failure, which can change the acute management of the patient.[4] Previous echocardiogram records may be beneficial in making this determination if available.

Physical Exam
Physical exam findings include tachycardia or bradycardia, hypertension or hypotension, hypoxia, tachypnea, diaphoresis, increased weight gain, worsening peripheral edema, abnormal pulmonary auscultatory findings including moist rales or cardiac wheezing, jugular venous distention, and a positive abdominojugular reflex. The presence of an S3 gallop murmur has the highest likelihood ratio for heart failure but may be hard to appreciate in the emergent setting.[3] An irregularly irregular heart rate may also be present, as factors contributing to heart failure predispose patients to atrial fibrillation, and uncontrolled atrial fibrillation can exacerbate heart failure.

Laboratory Findings
The biomarkers associated with heart failure are B-type natriuretic peptides (BNP) and N-terminal pro-B-type natriuretic (NT-proBNP) levels. BNP levels above 500 and NT-proBNP levels above 900 are highly associated with heart failure with the caveat that levels may not yet be elevated in the hyperacute phase.[5] Other causes of elevated natriuretic peptides include pulmonary hypertension, pulmonary embolism, renal failure, sepsis, and pneumonia. Cardiac biomarkers, including troponin T and I, may also be elevated in cases where acute coronary syndromes play a role in the development of heart failure. Further testing should be dictated by the patient’s history. Thyroid imbalance may precipitate atrial fibrillation or arrhythmia which may present as acute heart failure. The same is true of electrolyte or divalent imbalances. Other causes of shortness of breath should also be investigated (Table1). Finally, renal function impairment may lead to acute fluid retention and so blood urea nitrogen (BUN) and creatinine levels are examples of further testing that may be warranted.

Adjunct Findings
Obtaining an electrocardiogram is important to determine the presence of a contributing or causative dysrhythmia (e.g. STEMI, atrial fibrillation). Chest x-ray may show pulmonary congestion, interstitial edema, or an enlarged cardiac silhouette (Figure 1). Bedside ultrasound can be used to evaluate the lungs, heart, and inferior vena cava (IVC). Thoracic views may show B lines or “comet-tail images” in a patient with pulmonary edema, although this can also be seen in conditions like pulmonary fibrosis or pulmonary contusion. Cardiac views can give a rough indication of cardiac ejection fraction (EF) depression if present. IVC views can give an idea of the patient’s volume status and the presence of volume overload as seen by an inferior vena cava > 2 cm or with a collapsibility index <50%.[3]

Figure 1: Pulmonary Edema
Image Credit: Wikimedia

Treatment should begin with airway management and the respiratory assessment. Supplemental oxygen with the patient in a seated position using nasal cannula or nonrebreather mask can improve oxygenation and dyspnea. Further support can be obtained by using noninvasive ventilation with continuous positive airway pressure (CPAP) or bi-level positive airway pressure (BiPAP) to a target saturation above 90%. Respiratory failure may necessitate endotracheal intubation.

Cardiovascular support is achieved by reducing preload and afterload with nitrates, optimizing volume status with diuretics, and improving cardiac contractility. Vasodilating agents like nitroglycerin should be given in patients with adequate perfusion. Sublingual nitroglycerin 0.4 mg can be given at a rate of one tablet per minute. Intravenous (IV) nitroglycerin at 5 to 10 mcg/min can be used in place of sublingual tablets and titrated every three to five minutes. Nitroglycerin should be titrated to effect and to tolerance by the patient’s blood pressure. Transdermal nitroglycerin should only be used after stabilization with the sublingual or IV forms.

Severe hypertension or aortic regurgitation may benefit from both preload and afterload reduction. Nitroprusside is a potent arterial and venous vasodilator and can be started at a dose of 5 to 10 mcg/min and titrated every five minutes. Caution against vasodilation should be taken in cases of right ventricular failure, aortic stenosis, or recent phosphodiesterase-5 (PDE-5) inhibitor use.

In addition, diuretics including IV furosemide, bumetanide (1 to 2 mg), or torsemide (10 to 20 mg) can be given. A typical furosemide dosing strategy is 1 to 2.5 times the patient’s oral dose in one day or 0.5 to 1.0 mg/kg IV, either of which can be doubled at two-hour intervals as needed. Of note, utilizing a higher dosing strategy has been associated with greater symptomatic improvement.

In hypoperfusive states, a small crystalloid bolus should be considered while monitoring respiratory status. In cases of severe systolic dysfunction with a refractory low-output state, as seen in cardiogenic shock, inotropic therapy with norepinephrine, epinephrine, dopamine, or dobutamine can be considered. Inotropes should not be used in cases of diastolic dysfunction or acute infarction in which the definitive treatment is revascularization.[3-5]

Previous retrospective and prospective studies including ESCAPE, COMET, OPTIMIZE-HF, and B-CONVINCED have demonstrated outcome benefits with the continuation of beta-blocker therapy during hospitalization for heart failure exacerbation.[6-9] Beta-blocker usage in the acute or decompensated phase with inotropic failure should not be used, as it has not previously been tested in these patient populations.[10] These patients may require temporary cessation of beta blockers during their initial period of hemodynamic instability.

One-third of patient with severe heart failure will die within the first year of diagnosis with a 50% mortality at five years after the onset of symptoms.[11] The cause of death in patients with heart failure is most often from sudden cardiac death. In fact, 85% of patients with severe heart failure have documented ventricular arrhythmias.[11] Epidemiologic data has shown that patients with preserved ejection fraction did better over time than those with depressed ejection fraction, though benefits have been seen in the latter group.[12] Valvular regurgitation, ventricular arrhythmias, higher New York Heart Association (NYHA) functional classes, lower left ventricular EF, high level of NT-proBNP, or low serum sodium level have traditionally been factors associated with a poor outcome.[12] Disposition should be planned according to physician judgment, physiologic risk assessment, and coordination of outpatient care.


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