The etiologies and pathophysiology of pulmonary edema are discussed in Chap. 33.
Acute pulmonary edema usually presents with the rapid onset of dyspnea at rest, tachypnea, tachycardia, and severe hypoxemia. Rales and wheezing due to airway compression from peribronchial cuffing may be audible. Hypertension is usually present due to release of endogenous catecholamines.
It is often difficult to distinguish between cardiogenic and noncardiogenic causes of acute pulmonary edema. Echocardiography may identify systolic and diastolic ventricular dysfunction and valvular lesions. Pulmonary edema associated with electrocardiographic ST elevation and evolving Q waves is usually diagnostic of acute MI and should prompt immediate institution of MI protocols and coronary artery reperfusion therapy (Chap. 245). Brain natriuretic peptide levels, when substantially elevated, support heart failure as the etiology of acute dyspnea with pulmonary edema (Chap. 234).
The use of a Swan-Ganz catheter permits measurement of PCWP and helps differentiate high-pressure (cardiogenic) from normal-pressure (noncardiogenic) causes of pulmonary edema. Pulmonary artery catheterization is indicated when the etiology of the pulmonary edema is uncertain, when it is refractory to therapy, or when it is accompanied by hypotension. Data derived from use of a catheter often alter the treatment plan, but the impact on mortality rates has not been demonstrated.
Treatment: Pulmonary Edema
The treatment of pulmonary edema depends on the specific etiology. In light of the acute, life-threatening nature of the condition, a number of measures must be applied immediately to support the circulation, gas exchange, and lung mechanics. In addition, conditions that frequently complicate pulmonary edema, such as infection, acidemia, anemia, and renal failure, must be corrected.
Support of Oxygenation and Ventilation
Patients with acute cardiogenic pulmonary edema generally have an identifiable cause of acute LV failure—such as arrhythmia, ischemia/infarction, or myocardial decompensation (Chap. 234)—that can be rapidly treated, with improvement in gas exchange. In contrast, noncardiogenic edema usually resolves much less quickly, and most patients require mechanical ventilation.
Support of oxygenation is essential to ensure adequate O2 delivery to peripheral tissues, including the heart.
Pulmonary edema increases the work of breathing and the O2 requirements of this work, imposing a significant physiologic stress on the heart. When oxygenation or ventilation is not adequate in spite of supplemental O2, positive-pressure ventilation by face or nasal mask or by endotracheal intubation should be initiated. Noninvasive ventilation (Chap. 269) can rest the respiratory muscles, improve oxygenation and cardiac function, and reduce the need for intubation. In refractory cases, mechanical ventilation can relieve the work of breathing more completely than can noninvasive ventilation. Mechanical ventilation with positive end-expiratory pressure can have multiple beneficial effects on pulmonary edema: (1) decreases both preload and afterload, thereby improving cardiac function, (2) redistributes lung water from the intraalveolar to the extraalveolar space, where the fluid interferes less with gas exchange, and (3) increases lung volume to avoid atelectasis.
In most forms of pulmonary edema, the quantity of extravascular lung water is determined by both the PCWP and the intravascular volume status.
The "loop diuretics" furosemide, bumetanide, and torsemide are effective in most forms of pulmonary edema, even in the presence of hypoalbuminemia, hyponatremia, or hypochloremia. Furosemide is also a venodilator that reduces preload rapidly, before any diuresis, and is the diuretic of choice. The initial dose of furosemide should be ≤0.5 mg/kg, but a higher dose (1 mg/kg) is required in patients with renal insufficiency, chronic diuretic use, or hypervolemia or after failure of a lower dose.
Nitroglycerin and isosorbide dinitrate act predominantly as venodilators but have coronary vasodilating properties as well. They are rapid in onset and effective when administered by a variety of routes. Sublingual nitroglycerin (0.4 mg × 3 every 5 min) is first-line therapy for acute cardiogenic pulmonary edema. If pulmonary edema persists in the absence of hypotension, sublingual may be followed by IV nitroglycerin, commencing at 5–10 μg/min. IV nitroprusside (0.1–5 μg/kg per min) is a potent venous and arterial vasodilator. It is useful for patients with pulmonary edema and hypertension but is not recommended in states of reduced coronary artery perfusion. It requires close monitoring and titration using an arterial catheter for continuous BP measurement.
Given in 2- to 4-mg IV boluses, morphine is a transient venodilator that reduces preload while relieving dyspnea and anxiety. These effects can diminish stress, catecholamine levels, tachycardia, and ventricular afterload in patients with pulmonary edema and systemic hypertension.
Angiotensin-Converting Enzyme (ACE) Inhibitors
ACE inhibitors reduce both afterload and preload and are recommended for hypertensive patients. A low dose of a short-acting agent may be initiated and followed by increasing oral doses. In acute MI with heart failure, ACE inhibitors reduce short- and long-term mortality rates.
Other Preload-Reducing Agents
IV recombinant brain natriuretic peptide (nesiritide) is a potent vasodilator with diuretic properties and is effective in the treatment of cardiogenic pulmonary edema. It should be reserved for refractory patients and is not recommended in the setting of ischemia or MI.
Reduction of venous return reduces preload. Patients without hypotension should be maintained in the sitting position with the legs dangling along the side of the bed.
Inotropic and Inodilator Drugs
The sympathomimetic amines dopamine and dobutamine (see above) are potent inotropic agents. The bipyridine phosphodiesterase-3 inhibitors (inodilators), such as milrinone (50 μg/kg followed by 0.25–0.75 μg/kg per min), stimulate myocardial contractility while promoting peripheral and pulmonary vasodilation. Such agents are indicated in patients with cardiogenic pulmonary edema and severe LV dysfunction.
Once a mainstay of treatment because of their positive inotropic action (Chap. 234), digitalis glycosides are rarely used at present. However, they may be useful for control of ventricular rate in patients with rapid atrial fibrillation or flutter and LV dysfunction, since they do not have the negative inotropic effects of other drugs that inhibit atrioventricular nodal conduction.
IABP may help relieve cardiogenic pulmonary edema. It is indicated as a stabilizing measure when acute severe mitral regurgitation or ventricular septal rupture causes refractory pulmonary edema, especially in preparation for surgical repair. IABP or LV-assist devices (Chap. 235) are useful as bridging therapy to cardiac transplantation in patients with refractory pulmonary edema secondary to myocarditis or cardiomyopathy.
Treatment of Tachyarrhythmias and Atrial-Ventricular Resynchronization
(See also Chap. 233) Sinus tachycardia or atrial fibrillation can result from elevated left atrial pressure and sympathetic stimulation. Tachycardia itself can limit LV filling time and raise left atrial pressure further. Although relief of pulmonary congestion will slow the sinus rate or ventricular response in atrial fibrillation, a primary tachyarrhythmia may require cardioversion. In patients with reduced LV function and without atrial contraction or with lack of synchronized atrioventricular contraction, placement of an atrioventricular sequential pacemaker should be considered (Chap. 232).
Stimulation of Alveolar Fluid Clearance
Recent mechanistic studies on alveolar epithelial ion transport have defined a variety of ways to upregulate the clearance of solute and water from the alveolar space. In patients with acute lung injury (noncardiogenic pulmonary edema), IV β-adrenergic agonist treatment decreases extravascular lung water, but the outcome benefit is uncertain.
The Risk of Iatrogenic Cardiogenic Shock
In the treatment of pulmonary edema vasodilators lower BP, and, particularly when used in combination, their use may lead to hypotension, coronary artery hypoperfusion, and shock (Fig. 272-1). In general, patients with a hypertensive response to pulmonary edema tolerate and benefit from these medications. In normotensive patients, low doses of single agents should be instituted sequentially, as needed.
(See also Chap. 245) Acute STEMI complicated by pulmonary edema is associated with in-hospital mortality rates of 20–40%. After immediate stabilization, coronary artery blood flow must be reestablished rapidly. When available, primary PCI is preferable; alternatively, a fibrinolytic agent should be administered. Early coronary angiography and revascularization by PCI or CABG also are indicated for patients with non-ST elevation acute coronary syndrome. IABP use may be required to stabilize patients for coronary angiography if hypotension develops or for refractory pulmonary edema in patients with LV failure who are candidates for revascularization.
Specific etiologies of pulmonary edema may require particular therapy. Reexpansion pulmonary edema can develop after removal of air or fluid that has been in the pleural space for some time. These patients may develop hypotension or oliguria resulting from rapid fluid shifts into the lung. Diuretics and preload reduction are contraindicated, and intravascular volume repletion often is needed while supporting oxygenation and gas exchange.
High-altitude pulmonary edema often can be prevented by use of dexamethasone, calcium channel-blocking drugs, or long-acting inhaled β2-adrenergic agonists. Treatment includes descent from altitude, bed rest, oxygen, and, if feasible, inhaled nitric oxide; nifedipine may also be effective.
For pulmonary edema resulting from upper airway obstruction, recognition of the obstructing cause is key, since treatment then is to relieve or bypass the obstruction.