CARDIOGENIC SHOCK

Cardiogenic shock is the most common cause of in-hospital mortality from acute myocardial infarction (AMI).

Approximately 6% to 8% of patients with AMI will develop cardiogenic shock.

Cardiogenic shock usually occurs early in the course of AMI, with a median onset time of 8 hours.

Risk factors for developing cardiogenic shock after AMI are related to the likelihood of having widespread myocardial dysfunction, and include advanced age, large or anterior MI, preexisting heart failure, and diabetes mellitus.

With medical treatment alone, mortality from cardiogenic shock is high (70–90%). Mechanical revascu-larization improves mortality to ~50%.

PATHOPHYSIOLOGY

Cardiogenic shock occurs when there is insufficient pumping ability of the heart to support the metabolic needs of the tissues.

Cardiogenic shock most commonly occurs secondary to extensive myocardial infarction.

Reduction in cardiac output leads to diffuse tissue hypoperfusion and organ failure. Further myocardial dysfunction results from the subsequent release of systemic inflammatory mediators.

Cardiogenic shock can occur in a wide variety of presentations of ejection fraction, degree of ventricular involvement, and systemic vascular resistance. Unfortunately, the full mechanism of cardiogenic shock is incompletely understood (see Table 21-1)

CLINICAL FEATURES

Patients may complain of chest pain or anginal equivalent.

Cardiogenic shock usually presents with hypotension (systolic blood pressure <90 mm Hg), although systolic blood pressure may be higher if there is pre-existing hypertension.

Heart rate may be fast (compensatory), slow (right or inferior MI with nodal dysfunction), or normal (tachycardia blunted by beta blocker or calcium channel blocker use).

Skin may be cool, clammy, or mottled.

TABLE 21-1 Causes of Cardiogenic Shock

Acute myocardial infarction

Pump failure

Mechanical complications

Acute mitral regurgitation secondary to papillary muscle rupture

Ventricular septal defect

Free-wall rupture

Right ventricular infarction

Severe depression of cardiac contractility

Sepsis

Myocarditis

Myocardial contusion

Cardiomyopathy

Mechanical obstruction to forward blood flow

Aortic stenosis

Hypertrophic cardiomyopathy

Mitral stenosis

Left atrial myxoma

Pericardial tamponade

Regurgitation of left ventricular output

Chordal rupture

Acute aortic insufficiency

Diminished perfusion may lead to altered mentation and oliguria.

LV failure may result in tachypnea, rales, and frothy sputum.

It is crucial to listen for a murmur that may represent acute valvular dysfunction (eg, chordae rupture) or ventricular septal defects, conditions warranting immediate surgical intervention.

Jugular venous distension and abdominal jugular reflex are usually present.

DIAGNOSIS AND DIFFERENTIAL

The diagnosis of cardiogenic shock should be suspected from the initial history and physical exam. The key task is to differentiate cardiogenic shock from shock due to hypovolemia or distributive causes (sepsis, neurogenic).

Ancillary tests, used to assist with determining the shock etiology and complications, may include:

Electrocardiogram (ECG) to detect ischemia and the need for reperfusion. Right ventricular infarction can be detected using right precordial ECG leads (see Figure 20–3 in Chapter 20 Acute Coronary Syndromes).

Chest radiograph for evidence of pulmonary edema, abnormal mediastinum, and evaluation of the cardiac silhouette.

Lab studies including cardiac biomarkers, coagulation parameters, serum lactate, and serum chemistries (including liver function tests) may also help establish the diagnosis and detect secondary organ damage.

A normal B-type natriuretic peptide (BNP) or N-terminal pro-BNP should suggest a different diagnosis other than cardiogenic shock due to a high negative predictive value.

Transthoracic echocardiography done at the bedside can be helpful when evaluating a patient in shock with an unclear etiology.

Disease processes to be considered in the differential diagnosis include aortic dissection, pulmonary embolism, pericardial tamponade, acute valvular insufficiency, cardiotoxic drugs, hemorrhage, and sepsis.

EMERGENCY DEPARTMENT CARE

ED care is a temporizing measure while arranging for revascularization in the cardiac catheterization laboratory or surgical intervention for mechanical catastrophe.

Airway management, circulatory stabilization, and arrangements for definitive cardiac care must occur simultaneously. Cardiology and cardiac surgery should be consulted early. Transfer should be arranged if indicated.

Percutaneous coronary intervention (PCI) or surgical bypass is preferred over fibrinolysis in the setting of AMI complicated by shock. However, fibrinolysis is preferred over supportive treatment alone and should be delivered should PCI not be available in a timely fashion.

Stabilize the patient; perform endotracheal intubation if necessary, attain intravenous access, provide high-flow oxygen, place the patient on a monitor and pulse oximeter, and obtain an ECG and rhythm strip.

Identify rhythm disturbances, hypovolemia, hypox-emia, and electrolyte abnormalities early and treat accordingly.

Especially with concomitant right ventricular ischemia, anti-anginal therapies may precipitate cardiovascular collapse. For chest pain, titrated intravenous nitroglyc-erin 5 to 100 micrograms/min or morphine sulfate given in 2-milligrams increments may be administered with caution. Do not give β-blockers in cardiogenic shock.

For mild hypotension without pulmonary congestion, a small fluid challenge (250–500 mL) may be considered. For hypotension in the setting of right ventricular ischemia, a more robust fluid resuscitation is warranted.

Norepinephrine may be considered for severe hypotension as a vasopressor and positive inotrope.

For mild to moderate hypotension without hypovolemia, dobutamine may be administered. Dobutamine may cause peripheral vasodilatation, requiring the concomitant use of dopamine titrated to the desired effect with the lowest dose possible.

Milrinone may be considered as a positive inotrope. It is less arrhythmogenic than dobutamine, although a comparative survival advantage has not been demonstrated.

As a temporizing measure, intraaortic balloon pump counter pulsation (if available) should be considered to decrease afterload and to augment coronary perfusion.

In the setting of acute mitral regurgitation, afterload reduction through intravenous sodium nitroprusside 0.5 to 10.0 micrograms/kg/min should be combined with inotropic support via dobutamine 2.5 to 20.0 micrograms/kg/min. An intraaortic balloon pump may also be indicated to augment forward blood flow (contraindicated in severe aortic regurgitation).