Acute Heart Failure and Cardiogenic Pulmonary Edema

GENERAL PRINCIPLES

Acute heart failure (AHF) results from a sudden increase in intracardiac pressure or acute myocardial dysfunction leading to decreased peripheral perfusion and cardiogenic pulmonary edema (CPE).

• Increased pulmonary capillary pressure may be caused by LV failure of any cause, obstruction to transmitral flow (e.g., mitral stenosis, atrial myxoma), or rarely, pulmonary veno-occlusive disease.

• Alveolar flooding and impairment of gas exchange follow accumulation of fluid in the pulmonary interstitium.

DIAGNOSIS

Clinical Presentation

• Clinical manifestations of AHF and CPE may occur rapidly and include dyspnea, anxiety, cough, and restlessness.

• The patient may expectorate pink frothy fluid.

• Physical signs of decreased peripheral perfusion, pulmonary congestion, hypoxemia, use of accessory respiratory muscles, and wheezing are often present.

Diagnostic Testing

• Radiographic abnormalities include cardiomegaly, interstitial and perihilar vascular engorgement, Kerley B lines, and pleural effusions.

• The radiographic abnormalities may follow the development of symptoms by several hours, and their resolution may be out of phase with clinical improvement.

TREATMENT

• Placing the patient in a sitting position improves pulmonary function.

• Bed rest, pain control, and relief of anxiety can decrease cardiac workload.

• Noninvasive positive-pressure ventilation is preferred and may have particularly favorable effects in the setting of pulmonary edema.⁶⁸ Mechanical ventilation is indicated if oxygenation is inadequate or hypercapnia occurs.

• Precipitating factors should be identified and corrected because resolution of pulmonary edema can often be accomplished with correction of the underlying process.

O Severe hypertension

î MI or myocardial ischemia (particularly if associated with MR)

î Acute valvular regurgitation

î New-onset tachyarrhythmias or bradyarrhythmias

î Vblume overload in the setting of severe LV dysfunction

Medications

• Furosemide is a venodilator that decreases pulmonary congestion within minutes of IV administration, well before its diuretic action begins. An initial dose of 40-80 mg IV should be given over several minutes and can be increased based on response to a maximum of 200 mg in subsequent doses.

• Nitroglycerin is a venodilator that can potentiate the effect of furosemide. IV administration is preferable to oral and transdermal forms because it can be rapidly titrated.

• Supplemental oxygen should be administered initially to raise the arterial oxygen tension to >60 mm Hg.

• Inotropic agents may be necessary for treatment of AHF and CPE in patients with concomitant hypotension or shock.

î Dobutamine and milrinone are positive inotropes, chronotropes, and arterial vasodilators. Major drawbacks include arrhythmias and hypotension.

î Norepinephrine, rather than dopamine (Table 5-5), should be used for stabilization of the hypotensive HF patient. Although a large randomized trial found no mortality difference between dopamine and norepinephrine in a cohort of undifferentiated shock patients, there were more adverse events (primarily arrhythmic) in the dopamine group, and subgroup analysis of those with cardiogenic shock showed an increased rate of death at 28 days in the dopamine group.⁶⁹

• Parenteral vasodilators such as sodium nitroprusside should be reserved for patients with severe HF not responding to oral medications. Sodium nitroprusside is a direct arterial vasodilator with less potent venodilatory properties. It is particularly effective in patients who have concomitant hypertension or severe aortic/mitral valve insufficiency.

î Sodium nitroprosside should be used carefully in patients with myocardial ischemia because of potential reduction in regional myocardial blood flow (coronary steal).

° Parenteral agents should be started at low doses, titrated to the desired hemodynamic effect, and discontinued slowly to avoid rebound vasoconstriction. Continuous hemodynamic monitoring should be utilized to help guide therapy.

î The initial dose of 0.25 μg∕kg∕min can be titrated (maximum dose of 10 μg∕kg∕min) to the desired hemodynamic effect or until hypotension develops.

î The half-life of nitroprusside is 1-3 minutes, and its metabolism results in the release of cyanide, which is metabolized by the liver to thiocyanate and is then excreted via the kidney.

î Toxic levels of thiocyanate (>10 mg/dL) may develop in patients with renal insufficiency. Thiocyanate toxicity may manifest as nausea, paresthesias, mental status changes, abdominal pain, and seizures.

î Methemoglobinemia is a rare complication of treatment with nitroprusside.

• Epinephrine may be considered in patients with refractory cardiogenic shock; however, its use has been associated with increased mortality. Escalation of therapy to include epinephrine should prompt consideration of MCS.

SPECIAL CONSIDERATIONS

• Right heart catheterization (e.g., Swan-Ganz catheter) may be helpful in cases where a prompt response to therapy does not occur by allowing differentiation between cardiogenic and noncardiogenic causes of pulmonary edema via measurement of central hemodynamics and cardiac output. It may then be used to guide subsequent therapy. The routine use of right heart catheterization in acute HF patients is not beneficial.⁷⁰

• An intra-aortic balloon pump (IABP) can be considered for temporary hemodynamic support in patients who have failed pharmacologic therapies and have transient myocardial dysfunction or are awaiting a definitive procedure such as an LVAD or transplantation. Severe aortoiliac atherosclerosis and moderate to severe aortic valve insufficiency are contraindications to IABP placement.

• Percutaneous LVADs provide short-term hemodynamic support for patients in cardiogenic shock. These devices have been shown to provide superior hemodynamic effects compared with IABP. However, use of percutaneous LVADs compared with IABP did not improve 30-day survival in critically ill patients.⁷¹