Lori Whelan
EPIDEMIOLOGY
Acute heart failure syndromes are classified by clinical presentation (see Table 24-1).
Heart failure has a poor prognosis with an annual death rate of 18.7%. Only 50% of patients will survive 1 year after the development of pulmonary edema.
The majority of acute heart failure patients have arterial hypertension (53–73%) and ischemic heart disease (46–68%): many have diabetes (27–42%) and atrial fibrillation (21–42%).
One-quarter to one-third of patients with acute heart failure present with new onset of symptoms, most commonly with acute coronary artery syndrome.
TABLE 24-1 Classification of Acute Heart Failure
PATHOPHYSIOLOGY
Three factors, preload, afterload, and contractility, determine ventricular stroke volume. Coupled with heart rate, stroke volume determines cardiac output.
Low-output heart failure is due to an inherent problem in myocardial contraction.
High-output heart failure occurs when functionally intact myocardium cannot meet excess systemic demands. The causes of high-output failure are relatively few and include anemia, thyrotoxicosis, large arteriovenous shunts, beriberi, and Paget’s disease of the bone.
Systolic dysfunction, defined as an ejection fraction of less than 40%, is most commonly due to ischemic heart disease, leads to afterload sensitivity, and manifests as increased cardiac pressures with circulatory stress (eg, during exercise). Mechanically, the ventricle has difficulty ejecting blood. Impaired contractility leads to increased intra-cardiac volumes and pressure and afterload sensitivity.
Diastolic dysfunction represents impaired ventricular relaxation with preserved ejection fraction which results in a left ventricle (LV) that has difficulty in receiving blood. Decreased LV compliance necessitates high atrial pressures to ensure adequate diastolic LV filling and results in preload sensitivity. Chronic hypertension and LV hypertrophy often lead to this condition.
The most common cause of right-sided failure is left-sided failure.
Once heart failure has developed, several neurohormonal compensatory mechanisms occur.
The reduction in cardiac output results in increased stimulation of the renin-angiotensin-aldosterone axis and secretion of antidiuretic hormone. The end result is enhanced sodium and water retention by the kidneys, which leads to fluid overload and the clinical manifestations of congestive heart failure (CHF). The increased adrenergic tone leads to arteriolar vasoconstriction, a significant rise in afterload, and finally, to increased cardiac work.
CLINICAL FEATURES
Acute pulmonary edema or congestion is the cardinal manifestation of left-sided heart failure, and patients usually present with severe respiratory distress, frothy pink or white sputum, moist pulmonary rales, and an S3 or S4.
Patients frequently have tachycardia, cardiac dys-rhythmias such as atrial fibrillation or premature ventricular contractions (PVCs), and are hypertensive.
Symptoms of left-sided heart failure include dyspnea (especially with exertion), paroxysmal nocturnal dyspnea, orthopnea, nocturia, fatigue, and weakness.
Patients with right-sided heart failure commonly have dependent edema of the extremities, and may have jugular venous distention, hepatic enlargement, and a hepatojugular reflex.
DIAGNOSIS AND DIFFERENTIAL
The correct diagnosis of CHF and/or acute pulmonary edema is very challenging because neither history nor physical examination is accurate. The diagnosis is clinically based using multiple data points including x-rays, laboratories, and echocardiography with “clinical gestalt” frequently outperforming diagnostic tests available in the ED.
Chest x-ray may reveal vascular redistribution to the upper lung fields, cardiomegaly (cardiothoracic ratio >0.6 on a posteroanterior [PA] film), interstitial edema, enlarged pulmonary artery, pleural effusions, alveolar edema, prominent superior vena cava, and Kerley B lines (short linear markings at the periphery of the lower lung fields) (see Fig. 24-1). Keep in mind, up to 18% of patients with acute heart failure syndromes have no findings on chest x-ray. Although a chest x-ray cannot exclude abnormal left ventricular function, it can confirm other diagnoses, such as pneumonia.
FIG. 24-1. Chest radiograph with findings of congestive heart failure. Chest radiograph demonstrating cardiomegaly, interstitial edema, and left-sided pleural effusion.
B-type natriuretic peptide (BNP) is synthesized in the ventricular myocardium in response to elevated ventricular pressures or volume stimulus. BNP measurement is recommended to aid in the diagnosis or exclusion of acute heart failure and in patients with acute dyspnea, but it has limitations and it should not be used as a stand-alone test.
If the BNP level is low (BNP <100 picograms/mL or N-terminal pro-BNP of 300 picograms/mL) then an alternative diagnosis should be considered.
If the BNP level is markedly elevated (BNP >500 picograms/mL or N-terminal pro-BNP >1000 pico-grams/mL) then there is strong evidence for the diagnosis of congestive heart failure. Normal ranges increase with age.
Intermediate values should prompt consideration of other confounding diagnoses such as pulmonary embolism, myocardial infarction or primary pulmonary hypertension and additional testing directed by the clinical presentation should be obtained.
Other limitations include: (1) higher levels than clinically predicted in renal failure/insufficiency, (2) lower levels in obesity and in the patient who presents acutely as the release of BNP may lag behind by an hour.
Differential diagnosis for acute pulmonary edema includes the common causes of acute respiratory distress: asthma, chronic obstructive pulmonary disease (COPD), pneumonia, pulmonary embolus, allergenic reactions, and other causes of respiratory failure.
EMERGENCY DEPARTMENT CARE AND DISPOSITION
Administer 100% oxygen by non-rebreather to achieve an oxygen saturation of 95% by pulse oximetry in cases of acute pulmonary edema.
If the patient is in any respiratory distress, consider applying continuous positive airway pressure (CPAP) or biphasic positive airway pressure (BiPAP) through face mask.
Immediate intubation is indicated for patients who are visibly tiring, uncooperative with non-invasive ventilation, unconscious, or hemodynamically unstable.
Administer nitroglycerin sublingually 0.4 milligram (may be repeated up to every 1–5 minutes) to all patients who are hypertensive.
Nitroglycerin should be given as an IV drip, 0.2 to 0.4 micrograms/kg/min (starting dose) if the blood pressure is persistently >150/100 as the IV route will be easier to titrate and will be the only route accessible if the patient is on BiPAP.
Administer a potent intravenous diuretic such as furosem-ide 40 to 80 milligrams IV (after initiation of nitrates), or bumetanide, 1 to 3 milligrams IV. Electrolytes should be monitored, especially serum potassium.
For patients with resistant hypertension, or those who are not responding well to nitroglycerin, nitroprusside may be used, starting at 0.3 microgram/kg/min (starting dose) and titrated for blood pressure and symptom improvement.
For hypotensive patients or patients in need of additional inotropic support, begin dopamine at 5 to 10 micrograms/kg/min and titrate to a systolic BP of 90 to 100.
Assess ECG for ST elevation myocardial infarction (see Chapter 20). Dobutamine can be given in combination with dopamine or as a single agent, provided the patient is not in severe circulatory shock. Start dobutamine at 2.5 micrograms/kg/min and titrate to the desired response (see Chapter 21, Cardiogenic Shock).
Consider thrombolytic agents for heart failure caused by myocardial infarction.
Treat coexisting dysrhythmias (see Chapter 4) or electrolyte disturbances (see Chapter 6), avoiding those therapies that impair the inotropic state of the heart.
Morphine can be given (2–5 milligrams IV) and repeated as needed for pain control. It may cause respiratory depression and adds no benefit to that of oxygen, diuretics, and nitrates for the treatment of the underlying heart failure.
A randomized controlled trial of 7141 patients showed no benefit in the use of nesiritide for its use in acute decompensated heart failure compared to standard therapy.
Digoxin acts too slowly to be of benefit in acute situations.
For anuric (dialysis) patients, emergent dialysis is the treatment of choice in these patients who prove resistant to nitrates.
Long-term treatment of congestive heart failure includes dietary salt reduction, preload reduction through chronic use of diuretics (eg, furosemide) and afterload reduction via β-blockers (eg, metoprolol), angiotensin-converting enzyme (ACE) inhibitors (eg, captopril), and digoxin.
Most patients with heart failure require inpatient management or at least observation to monitor kidney function during diuresis and to rule out AMI as a cause of acute decompensation. Patients requiring IV NTG and/or BiPAP will need ICU admission.
Candidates for outpatient management include those with mild symptoms due to a clearly correctable precipitant that have resolved. These patients must have a normal diagnostic evaluation and a strong social network.
For further reading in Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th edition, see Chap. 57, “Congestive Heart Failure and Acute Pulmonary Edema,” by W. Frank Peacock.