Cardiogenic Shock: Current Concepts and Improving Outcomes
Reynolds HR, Hochman JS
Circulation. 2008;117:686-697
Cardiogenic Shock: Basics and Clinical Considerations
Gowda RM, Fox JT, Khan IA
Int J Cardiol. 2008;123:221-228
Historically, cardiogenic shock (CS) was nearly always fatal after myocardial infarction (MI). Mortality rates were consistently reported at approximately 80% until the 1990s, when the mortality improved but only slightly, to 50% to 60%. Since then, advances in medical therapies, aggressive reperfusion, and the increasing availability of percutaneous coronary intervention (PCI) and cardiac bypass for patients in CS may result in even further decreases in mortality rates. It is therefore critical for emergency physicians to be aware of the incidence, presentation, and potential emergent therapies that can save patient lives.
These 2 review articles from the cardiology literature nicely summarize the current knowledge regarding CS, and the authors discuss therapeutic recommendations. Although CS may stem from many causes (eg, acute valvular disorders, cardiac tamponade), this review focuses solely on post-MI CS and stresses important takeaway points for emergency physicians. The reader is urged to review the actual articles for further details and in-depth discussion of pathophysiology.
Background and Definition
CS is defined as a state of tissue hypoperfusion resulting from cardiac failure. Hypoperfusion may manifest as systemic hypotension, peripheral vasoconstriction and diminished pulses, decreased urine output, decreased mental status, or significantly reduced cardiac indices (cardiac index) despite correction of preload.
CS occurs in 5% to 10% of patients hospitalized with MI (ST-segment elevated MI) and is a common cause of death in this group. An unknown additional number of prehospital patients die from CS, making the exact incidence uncertain.
Risk factors for development of post-MI CS include older age, anterior location of MI, hypertension, diabetes, multivessel occlusions, left bundle branch block, and prior history of cardiac disease or heart failure.
Tachycardia and/or hypotension at admission predict CS in patients with MI.
Pathophysiology
Severe left ventricular (LV) dysfunction is the most common cause of post-MI CS. Right ventricular (RV) MI and acute valvular dysfunction (especially acute mitral insufficiency) can also cause CS after MI.
CS progresses through a vicious cascade of events that link both systolic and diastolic dysfunction:
Systolic dysfunction leads to reductions in cardiac output and stroke volume which then lead to reduced coronary perfusion and ischemia.
Diastolic dysfunction leads to increased LV end-diastolic pressure and pulmonary congestion, which then leads to hypoxia and ischemia.
Ischemia is the common link and leads to further systolic and diastolic dysfunction, which promotes the cascade of events.
The earliest effect of myocardial ischemia is often diastolic dysfunction. With this in mind, clinicians should be aware that pulmonary congestion may develop because of ischemia-induced diastolic dysfunction even in the absence of early systolic dysfunction. Eventually, however, a combination of diastolic and systolic dysfunction will develop in the majority of these patients as the cascade progresses.
Ischemia leads to progressive myocardial dysfunction, which will eventually lead to death if the cascade is not aborted by relieving ischemia. Emergent revascularization is the most important means of relieving ischemia.
CS that is associated with RV dysfunction represents only 5% of cases. Shock is usually caused by reduced LV output caused by inadequate filling by the RV. In these cases, the key to treatment is to ensure adequate RV filling pressures with vigorous fluid hydration to maintain LV preload.
Management
Antithrombotic therapy with aspirin and heparin are recommended just as they usually are with acute MI.
Clopidogrel has received increased support in the early treatment of acute MI. However, current recommendations are to withhold this medication within 5 days of cardiac bypass surgery because of increased bleeding complications. Many patients with CS will require cardiac bypass surgery, so the authors state that the use of clopidogrel may be deferred until after emergency angiography, at which time the need for cardiac bypass will be determined.
Avoid negative inotropes (eg, beta-blockers) and vasodilators (eg, nitroglycerin).
Clinicians should have a low threshold for initiating mechanical ventilation, which reduces the work of breathing and maximizes oxygenation.
The need for pulmonary artery (PA or Swan-Ganz) catheterization should be assessed on an individualized basis. Both PA systolic pressure and pulmonary capillary wedge pressure can be assessed accurately by PA catheter or by Doppler echocardiography.
Pharmacologic treatment for shock focuses on inotropic and vasopressor agents to maintain coronary and systemic perfusion. These medications are usually used as a bridge until an intra-aortic balloon pump (IABP) is placed, and then definitive reperfusion is established. Ideally these should be used in the lowest dosages possible.
Intra-aortic balloon counterpulsation improves coronary and peripheral perfusion and augments LV performance. Placement of an IABP is associated with an increased survival regardless of whether emergent reperfusion is performed.
Emergent reperfusion therapy is indicated for patients with post-MI CS regardless of age and is associated with increased survival. Thrombolytic therapy is less effective than percutaneous or surgical intervention but is still indicated when (1) PCI is not available within 90 minutes, (2) less than 3 hours has passed since the onset of ST-segment elevated MI, and (3) there are no contraindications.
Thrombolytics may have decreased penetration into the thrombus in the setting of severe hypotension. Additionally, passive collapse of the infarct-related artery as well as local acidosis may attenuate the efficacy of the thrombolytics.
The use of vasopressors to increase aortic pressure may improve the efficacy of thrombolytics in patients with severe hypotension.
For patients undergoing PCI, the use of stenting and glycoprotein IIb/IIIa receptor antagonists are independently associated with improved outcomes.
Clinicians should recognize that age alone is not a contraindication to emergent reperfusion in elderly patients with CS.
CS caused by mechanical complications of MI (eg rupture of the ventricular septum, free wall, or papillary muscles) have the highest mortality, estimated to be > 85%.
Survival in patients with CS caused by mechanical complications is dependent on rapid surgical repair.
Conclusion
CS is still relatively common in patients with acute MI. Despite a high baseline mortality, significant improvements in outcome can be achieved through aggressive supportive therapy and prompt reperfusion. Emergency physicians should act promptly when caring for these patients and engage the help of consultants for placement of an IABP and performance of rapid invasive therapy whenever possible.
