Cardiogenic shock (CS) is characterized by systemic hypoperfusion due to severe depression of the cardiac index (<2.2 [L/min]/m2) and sustained systolic arterial hypotension (<90 mmHg) despite an elevated filling pressure (pulmonary capillary wedge pressure [PCWP] >18 mmHg). It is associated with in-hospital mortality rates >50%. The major causes of CS are listed in Table 34-1. Circulatory failure based on cardiac dysfunction may be caused by primary myocardial failure, most commonly secondary to acute myocardial infarction (MI) (Chap. 41), and less frequently by cardiomyopathy or myocarditis (Chap. 27), cardiac tamponade (Chap. 28), or critical valvular heart disease (Chap. 23).
TABLE 34-1ETIOLOGIES OF CARDIOGENIC SHOCK (CS)a AND CARDIOGENIC PULMONARY EDEMA ||Download (.pdf) TABLE 34-1 ETIOLOGIES OF CARDIOGENIC SHOCK (CS)a AND CARDIOGENIC PULMONARY EDEMA
|ETIOLOGIES OF CARDIOGENIC SHOCK OR PULMONARY EDEMA |
|Acute myocardial infarction/ischemia |
| LV failure |
| Ventricular septal rupture |
| Papillary muscle/chordal rupture–severe MR |
| Ventricular free wall rupture with subacute tamponade |
| Other conditions complicating large MIs |
| Infection |
| Excess negative inotropic or vasodilator medications |
| Prior valvular heart disease |
| Hyperglycemia/ketoacidosis |
|Post-cardiac arrest |
|Refractory sustained tachyarrhythmias |
|Acute fulminant myocarditis |
|End-stage cardiomyopathy |
|LV apical ballooning |
|Takotsubo’s cardiomyopathy |
|Hypertrophic cardiomyopathy with severe outflow obstruction |
|Aortic dissection with aortic insufficiency or tamponade |
|Severe valvular heart disease |
| Critical aortic or mitral stenosis |
| Acute severe aortic regurgitation or mitral regurgitation |
| β blocker or calcium channel antagonist overdose |
|Other Etiologies of Cardiogenic Shockb |
|RV failure due to: |
| Acute myocardial infarction |
| Acute cor pulmonale |
|Refractory sustained bradyarrhythmias |
|Pericardial tamponade |
| Severe acidosis, severe hypoxemia |
The rate of CS complicating acute MI was 20% in the 1960s, stayed at ~8% for >20 years, but decreased to 5–7% in the first decade of this millennium largely due to increasing use of early reperfusion therapy for acute MI. Shock is more common with ST elevation MI (STEMI) than with non-ST elevation MI (Chap. 41).
LV failure accounts for ~80% of cases of CS complicating acute MI. Acute severe mitral regurgitation (MR), ventricular septal rupture (VSR), predominant right ventricular (RV) failure, and free wall rupture or tamponade account for the remainder.
CS is characterized by a vicious circle in which depression of myocardial contractility, usually due to ischemia, results in reduced cardiac output and arterial blood pressure (BP), which result in hypoperfusion of the myocardium and further ischemia and depression of cardiac output (Fig. 34-1). Systolic myocardial dysfunction reduces stroke volume and, together with diastolic dysfunction, leads to elevated LV end-diastolic pressure and PCWP as well as to pulmonary congestion. Reduced coronary perfusion leads to worsening ischemia and progressive myocardial dysfunction and a rapid downward spiral, which, if uninterrupted, is often fatal. A systemic inflammatory response syndrome may accompany large infarctions and shock. Inflammatory cytokines, inducible nitric oxide synthase, and excess nitric oxide and peroxynitrite may contribute to the genesis of CS as they do to that of other forms of shock. Lactic acidosis and hypoxemia from CS contribute to the vicious circle by worsening myocardial ischemia and hypotension. Severe acidosis reduces the efficacy of endogenous and exogenously administered catecholamines. Refractory sustained ventricular or atrial tachyarrhythmias can cause or exacerbate CS.
Older age, female sex, prior MI, diabetes, anterior MI location, and extensive coronary artery stenoses are associated with an increased risk of CS complicating MI. Shock associated with a first inferior MI should prompt a search for a mechanical cause. CS may rarely occur in the absence of significant stenosis, as seen in LV apical ballooning/Takotsubo’s cardiomyopathy.
Shock is present on admission in only one-quarter of patients who develop CS complicating MI; one-quarter develop it rapidly thereafter, within 6 h of MI onset. Another quarter develop shock later on the first day. Subsequent onset of CS may be due to reinfarction, marked infarct expansion, or a mechanical complication.
Due to the unstable condition of these patients, supportive therapy must be initiated simultaneously with diagnostic evaluation (Fig. 34-2). A focused history and physical examination should be performed, blood specimens sent to the laboratory, and an electrocardiogram (ECG) and chest x-ray obtained.
Echocardiography is an invaluable diagnostic tool in patients with suspected CS.
The emergency management of patients with cardiogenic shock, acute pulmonary edema, or both is outlined.
*Furosemide: <0.5 mg/kg for new-onset acute pulmonary edema without hypervolemia; 1 mg/kg for acute on chronic volume overload, renal insufficiency.
†For management of bradycardia and tachycardia, see Chaps. 15 and 17. Additional information can also be found in Section 9.5 of the 2013 American College of Cardiology Foundation/American Heart Association Guidelines for Management of ST-Elevation Myocardial Infarction and Figures 3 and 4 of the 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Part 8: Adult Advanced Cardiovascular Life Support.
*Indicates modification from published guidelines. ACE, angiotensin-converting enzyme; BP, blood pressure; MI, myocardial infarction. (Modified from Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Part 7: The era of reperfusion: Section 1: Acute coronary syndromes [acute myocardial infarction]. The American Heart Association in collaboration with the International Liaison Committee on Resuscitation. Circulation 102:I172, 2000.)
Most patients have dyspnea and appear pale, apprehensive, and diaphoretic, and mental status may be altered. The pulse is typically weak and rapid, often in the range of 90–110 beats/min, or severe bradycardia due to high-grade heart block may be present. Systolic BP is reduced (<90 mmHg or ≥30 mmHg below baseline) with a narrow pulse pressure (<30 mmHg), but occasionally BP may be maintained by very high systemic vascular resistance. Tachypnea, Cheyne-Stokes respirations, and jugular venous distention may be present. There is typically a weak apical pulse and soft S1, and an S3 gallop may be audible. Acute, severe MR and VSR usually are associated with characteristic systolic murmurs (Chap. 41). Rales are audible in most patients with LV failure. Oliguria is common.
The white blood cell count is typically elevated with a left shift. Renal function is initially unchanged, but blood urea nitrogen and creatinine rise progressively. Hepatic transaminases may be markedly elevated due to liver hypoperfusion. The lactic acid level is elevated. Arterial blood gases usually demonstrate hypoxemia and anion gap metabolic acidosis, which may be compensated by respiratory alkalosis. Cardiac markers, creatine phosphokinase and its MB fraction, and troponins I and T are typically markedly elevated.
In CS due to acute MI with LV failure, Q waves and/or >2-mm ST elevation in multiple leads or left bundle branch block are usually present. More than one-half of all infarcts associated with shock are anterior. Global ischemia due to severe left main stenosis usually is accompanied by severe (e.g., >3 mm) ST depressions in multiple leads.
The chest x-ray typically shows pulmonary vascular congestion and often pulmonary edema, but these findings may be absent in up to a third of patients. The heart size is usually normal when CS results from a first MI but is enlarged when it occurs in a patient with a previous MI.
A two-dimensional echocardiogram with color-flow Doppler (Chap. 12) should be obtained promptly in patients with suspected CS to help define its etiology. Doppler mapping demonstrates a left-to-right shunt in patients with VSR and the severity of MR when the latter is present. Proximal aortic dissection with aortic regurgitation or tamponade may be visualized, or evidence for pulmonary embolism may be obtained (Chap. 45).
Pulmonary artery catheterization
The use of pulmonary artery (Swan-Ganz) catheters in patients with established or suspected CS is controversial (Chap. 13). Their use is generally recommended for measurement of filling pressures and cardiac output to confirm the diagnosis and to optimize the use of IV fluids, inotropic agents, and vasopressors in persistent shock (Table 34-2). O2 saturation measurement from right atrial, RV, and pulmonary arterial blood samples can rule out a left-to-right shunt. In CS, low mixed venous O2 saturations and elevated arteriovenous (AV) O2 differences reflect low cardiac index and high fractional O2 extraction. However, when sepsis accompanies CS, AV O2 differences may not be elevated. The PCWP is elevated. Use of sympathomimetic amines may return these measurements and the systemic BP to normal. Systemic vascular resistance may be low, normal, or elevated in CS. Equalization of right- and left-sided filling pressures (right atrial and PCWP) suggests cardiac tamponade as the cause of CS (Chap. 28).
TABLE 34-2HEMODYNAMIC PATTERNSa ||Download (.pdf) TABLE 34-2 HEMODYNAMIC PATTERNSa
| ||RA, MMHG ||RVS, MMHG ||RVD, MMHG ||PAS, MMHG ||PAD, MMHG ||PCW, MMHG ||CI, (L/MIN)/M2 ||SVR, (DYN · S)/CM5 |
|Normal values ||<6 ||<25 ||0–12 ||<25 ||0–12 ||<6–12 ||≥2.5 ||(800–1600) |
|MI without pulmonary edemab ||– ||– ||– ||– ||– ||~13 (5–18) ||~2.7 (2.2–4.3) ||– |
|Pulmonary edema ||↔↑ ||↔↑ ||↔↑ ||↑ ||↑ ||↑ ||↔↓ ||↑ |
|Cardiogenic shock || || || || || || || || |
| LV failure ||↔↑ ||↔↑ ||↔↑ ||↔↑ ||↑ ||↑ ||↓ ||↔↑ |
| RV failurec ||↑ ||↓↔↑d ||↑ ||↓↔↑d ||↔↓↑d ||↓↔↑d ||↓ ||↑ |
|Cardiac tamponade ||↑ ||↔↑ ||↑ ||↔↑ ||↔↑ ||↔↑ ||↓ ||↑ |
|Acute mitral regurgitation ||↔↑ ||↑ ||↔↑ ||↑ ||↑ ||↑ ||↔↓ ||↔↑ |
|Ventricular septal rupture ||↑ ||↔↑ ||↑ ||↔↑ ||↔↑ ||↔↑ ||↑PBF ↓SBF ||↔↑ |
|Hypovolemic shock ||↓ ||↔↓ ||↔↓ ||↓ ||↓ ||↓ ||↓ ||↑ |
|Septic shock ||↓ ||↔↓ ||↔↓ ||↓ ||↓ ||↓ ||↑ ||↓ |
Left heart catheterization and coronary angiography
Measurement of LV pressure and definition of the coronary anatomy provide useful information and are indicated in most patients with CS complicating MI. Cardiac catheterization should be performed when there is a plan and capability for immediate coronary intervention (see below) or when a definitive diagnosis has not been made by other tests.
TREATMENT Acute Myocardial Infarction GENERAL MEASURES
(Fig. 34-2) In addition to the usual treatment of acute MI (Chap. 41), initial therapy is aimed at maintaining adequate systemic and coronary perfusion by raising systemic BP with vasopressors and adjusting volume status to a level that ensures optimum LV filling pressure. There is interpatient variability, but the values that generally are associated with adequate perfusion are systolic BP ~90 mmHg or mean BP >60 mmHg and PCWP >20 mmHg. Hypoxemia and acidosis must be corrected; most patients require ventilatory support (see “Pulmonary Edema,” below). Negative inotropic agents should be discontinued and the doses of renally cleared medications adjusted. Hyperglycemia should be controlled with insulin. Bradyarrhythmias may require transvenous pacing. Recurrent ventricular tachycardia or rapid atrial fibrillation may require immediate treatment (Chap. 17). VASOPRESSORS
Various IV drugs may be used to augment BP and cardiac output in patients with CS. All have important disadvantages, and none has been shown to change the outcome in patients with established shock. Norepinephrine is a potent vasoconstrictor and inotropic stimulant that is useful for patients with CS. As first line of therapy norepinephrine was associated with fewer adverse events, including arrhythmias, compared to a dopamine randomized trial of patients with several etiologies of circulatory shock. Although it did not significantly improve survival compared to dopamine, its relative safety suggests that norepinephrine is reasonable as initial vasopressor therapy. Norepinephrine should be started at a dose of 2 to 4 μg/min and titrated upward as necessary. If systemic perfusion or systolic pressure cannot be maintained at >90 mmHg with a dose of 15 μg/min, it is unlikely that a further increase will be beneficial.
Dopamine has varying hemodynamic effects based on the dose; at low doses (≤ 2 μg/kg per min), it dilates the renal vascular bed, although its outcome benefits at this low dose have not been demonstrated conclusively; at moderate doses (2–10 μg/kg per min), it has positive chronotropic and inotropic effects as a consequence of β-adrenergic receptor stimulation. At higher doses, a vasoconstrictor effect results from α-receptor stimulation. It is started at an infusion rate of 2–5 μg/kg per min, and the dose is increased every 2–5 min to a maximum of 20–50 μg/kg per min. Dobutamine is a synthetic sympathomimetic amine with positive inotropic action and minimal positive chronotropic activity at low doses (2.5 μg/kg per min) but moderate chronotropic activity at higher doses. Although the usual dose is up to 10 μg/kg per min, its vasodilating activity precludes its use when a vasoconstrictor effect is required. MECHANICAL CIRCULATORY SUPPORT
Circulatory assist devices can be placed percutaneously or surgically and can be used to support the left, right, or both ventricles. Venoarterial extracorporeal membrane oxygenation (VA ECMO, a pump in combination with an oxygenator) may be used when respiratory failure accompanies biventricular failure. Temporary percutaneous devices can be used as a bridge to surgically implanted devices in community hospital settings or when neurologic status is uncertain. The most commonly used device is an intraaortic balloon pump (IABP), which is inserted into the aorta via the femoral artery and provides temporary hemodynamic support. However, routine IABP use in conjunction with early revascularization (predominantly with percutaneous coronary intervention [PCI]) did not reduce 30-day mortality in the IABP-SHOCK II trial. Although other percutaneous devices, including VA ECMO, result in better hemodynamic support compared to IABP, the effects on clinical outcomes are unknown. Surgically implanted devices can support the circulation as bridging therapy for cardiac transplant candidates or as destination therapy (Chap. 21). Assist devices should be used selectively in suitable patients in consultation with advanced heart failure specialists. REPERFUSION-REVASCULARIZATION
The rapid establishment of blood flow in the infarct-related artery is essential in the management of CS and forms the centerpiece of management. The randomized SHOCK Trial demonstrated that 132 lives were saved per 1000 patients treated with early revascularization with PCI or coronary artery bypass graft (CABG) compared with initial medical therapy including IABP with fibrinolytics followed by delayed revascularization. The benefit is seen across the risk strata and is sustained up to 11 years after an MI. Early revascularization with PCI or CABG is recommended in candidates suitable for aggressive care.
Within this high-risk condition, there is a wide range of expected death rates based on age, severity of hemodynamic abnormalities, severity of the clinical manifestations of hypoperfusion, and the performance of early revascularization.
SHOCK SECONDARY TO RIGHT VENTRICULAR INFARCTION
Although transient hypotension is common in patients with RV infarction and inferior MI (Chap. 41), persistent CS due to RV failure accounts for only 3% of CS complicating MI. The salient features of RV shock are absence of pulmonary congestion, high right atrial pressure (which may be seen only after volume loading), RV dilation and dysfunction, only mildly or moderately depressed LV function, and predominance of single-vessel proximal right coronary artery occlusion. Management includes IV fluid administration to optimize right atrial pressure (10–15 mmHg); avoidance of excess fluids, which cause a shift of the interventricular septum into the LV; sympathomimetic amines; the early reestablishment of infarct-artery flow; and assist devices.
Acute severe MR due to papillary muscle dysfunction and/or rupture may complicate MI and result in CS and/or pulmonary edema (see also Chap. 41). This complication most often occurs on the first day, with a second peak several days later. The diagnosis is confirmed by echo-Doppler. Rapid stabilization with IABP is recommended, with administration of dobutamine as needed to raise cardiac output. Reducing the load against which the LV pumps (afterload) reduces the volume of regurgitant flow of blood into the left atrium. Mitral valve surgery is the definitive therapy and should be performed early in the course in suitable candidates.
VENTRICULAR SEPTAL RUPTURE
Echo-Doppler demonstrates shunting of blood from the left to the right ventricle and may visualize the opening in the interventricular septum (see also Chap. 41). Timing and management are similar to those for MR with IABP support and surgical correction for suitable candidates.
Myocardial rupture is a dramatic complication of STEMI that is most likely to occur during the first week after the onset of symptoms; its frequency increases with the age of the patient. The clinical presentation typically is a sudden loss of pulse, blood pressure, and consciousness but sinus rhythm on ECG (pulseless electrical activity) due to cardiac tamponade (Chap. 28). Free wall rupture may also result in CS due to subacute tamponade when the pericardium temporarily seals the rupture sites. Definitive surgical repair is required.
ACUTE FULMINANT MYOCARDITIS
Myocarditis can mimic acute MI with ST deviation or bundle branch block on the ECG and marked elevation of cardiac markers (see also Chap. 27). Acute myocarditis causes CS in a small proportion of cases. These patients are typically younger than those with CS due to acute MI and often do not have typical ischemic chest pain. Echocardiography usually shows global LV dysfunction. Initial management is the same as for CS complicating acute MI (Fig. 34-2) but does not involve coronary revascularization. Endomyocardial biopsy is recommended to determine the diagnosis and need for immunosuppressives for entities such as giant cell myocarditis. Refractory CS can be managed with assist devices with or without ECMO.
The etiologies and pathophysiology of pulmonary edema are discussed in Chap. 5.
Acute pulmonary edema usually presents with the rapid onset of dyspnea at rest, tachypnea, tachycardia, and severe hypoxemia. Crackles and wheezing due to alveolar flooding and airway compression from peribronchial cuffing may be audible. Release of endogenous catecholamines often causes hypertension.
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. Electrocardiographic ST elevation and evolving Q waves are usually diagnostic of acute MI and should prompt immediate institution of MI protocols and coronary artery reperfusion therapy (Chap. 41). Brain natriuretic peptide levels, when substantially elevated, support heart failure as the etiology of acute dyspnea with pulmonary edema (Chap. 19).
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 edema is refractory to therapy, or when it is accompanied by hypotension. Data derived from use of a catheter often alter the treatment plan, but no impact on mortality rates has been demonstrated.
TREATMENT Pulmonary Edema
The treatment of pulmonary edema depends on the specific etiology. As an acute, life-threatening condition, a number of measures must be applied immediately to support the circulation, gas exchange, and lung mechanics. Simultaneously, conditions that frequently complicate pulmonary edema, such as infection, acidemia, anemia, and acute kidney dysfunction, 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. 19)—that may be rapidly treated, with improvement in gas exchange. In contrast, noncardiogenic edema usually resolves much less quickly, and most patients require mechanical ventilation. Oxygen Therapy
Support of oxygenation is essential to ensure adequate O2 delivery to peripheral tissues, including the heart. Positive-Pressure Ventilation
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 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. REDUCTION OF PRELOAD
In most forms of pulmonary edema, the quantity of extravascular lung water is determined by both the PCWP and the intravascular volume status. Diuretics
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 rapidly reduces preload 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. Nitrates
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. Morphine
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. Physical Methods
In nonhypotensive patients, venous return can be reduced by use of 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. Digitalis Glycosides
Once a mainstay of treatment because of their positive inotropic action (Chap. 19), 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, because they do not have the negative inotropic effects of other drugs that inhibit atrioventricular nodal conduction. Intraaortic Balloon Counterpulsation
IABP or other LV-assist devices (Chap. 21) may help relieve cardiogenic pulmonary edema and are indicated when refractory pulmonary edema results from the etiologies discussed in the CS section, especially in preparation for surgical repair. Treatment of Tachyarrhythmias and Atrial-Ventricular Resynchronization
Sinus tachycardia or atrial fibrillation can result from elevated left atrial pressure and sympathetic stimulation (See also Chap. 18). 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. 15). Stimulation of Alveolar Fluid Clearance
A variety of drugs can stimulate alveolar epithelial ion transport and upregulate the clearance of alveolar solute and water, but this strategy has not been proven beneficial in clinical trials thus far. SPECIAL CONSIDERATIONS Risk of Iatrogenic Cardiogenic Shock
In the treatment of pulmonary edema, vasodilators lower BP, and their use, particularly in combination, may lead to hypotension, coronary artery hypoperfusion, and shock (Fig. 34-1). 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. Acute Coronary Syndromes (See also Chap. 41)
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. Assist devices may be used selectively as noted for refractory pulmonary edema. Extracorporeal Membrane Oxygenation
For patients with acute, severe noncardiogenic edema with a potential rapidly reversible cause, ECMO may be considered as a temporizing supportive measure to achieve adequate gas exchange. Usually venovenous ECMO is used in this setting. Unusual Types of Edema
Specific etiologies of pulmonary edema may require particular therapy. Reexpansion pulmonary edema can develop after removal of longstanding pleural space air or fluid. 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, because treatment then is to relieve or bypass the obstruction.