Cardiogenic shock is characterized by a decreased pumping ability of the heart that causes a shocklike state (ie, global hypoperfusion). It most commonly occurs in association with, and as a direct result of, acute myocardial infarction (AMI).
Similar to other shock states, cardiogenic shock is considered to be a clinical diagnosis characterized by decreased urine output, altered mentation, and hypotension. Other clinical characteristics include jugular venous distension, cardiac gallop, and pulmonary edema. The most recent prospective study of cardiogenic shock defines cardiogenic shock as sustained hypotension (systolic blood pressure [BP] less than 90 mm Hg lasting more than 30 min) with evidence of tissue hypoperfusion with adequate left ventricular (LV) filling pressure (Hochman, 1999). Tissue hypoperfusion was defined as cold peripheries (extremities colder than core), oliguria (<30 mL/h), or both.
Physical: The physical examination findings are consistent with shock. Patients are in frank distress, are profoundly diaphoretic with mottled extremities, and are usually visibly dyspneic. Clinical assessment begins with attention to the ABCs and vital signs.
Although the patient may eventually require endotracheal intubation, the airway usually is patent initially.
Breathing may be labored, with audible coarse crackles or wheezing.
As in any shocklike state, circulation is markedly impaired. Tachycardia, delayed capillary refill, hypotension, diaphoresis, and poor peripheral pulses are frequent findings.
Other signs of end-organ dysfunction (eg, decreased mental function, urinary output) may be present.
Initial vital sign assessment should include BP measurements in both arms to evaluate possible thoracic aortic aneurysm or dissection. Vital signs should be regularly updated with continuous noninvasive physiologic monitoring.
Neck examination may reveal jugular venous distention, which may be prominent. This finding is evidence of RV failure.
LV dysfunction, characterized by florid pulmonary edema, can be auscultated as crackles with or without wheezing.
Careful cardiac examination may reveal mechanical causes of cardiogenic shock.
Loud murmurs may indicate a valvular dysfunction, whereas muffled heart tones with jugular venous distention and pulsus paradoxus may suggest tamponade (Beck triad).
A gallop may also be heard. The presence of an S3 heart sound is pathognomonic of congestive heart failure. The presence of pulmonary edema increases the likelihood of cardiogenic shock in the setting of hypotension.
Causes: The vast majority of cases of cardiogenic shock are due to acute myocardial ischemia.
Mechanisms not related to acute infarction include the following:
Diastolic - Ventricular hypertrophy and restrictive cardiomyopathies
After load - Aortic stenosis, hypertrophic cardiomyopathy, dynamic outflow obstruction, aortic coarctation, and malignant hypertension
Valvular/structural - Mitral stenosis, endocarditis, mitral or aortic regurgitation, atrial myxoma or thrombus, and tamponade
Risk factors for the development of cardiogenic shock include preexisting myocardial damage or disease (eg, diabetes, advanced age, previous AMI), AMI (eg, Q-wave, large or anterior wall AMIs), and dysrhythmia.
Lab Studies:
No one test is completely sensitive or specific for cardiogenic shock. Laboratory studies are directed at the potential underlying cause.
In most cases, the usual workup includes tests of all of the following, which usually are assessed in cases of suspected cardiac ischemia:
Coagulation profile (eg, prothrombin time, activated partial thromboplastin time)
An ABG may be useful to evaluate acid-base balance because acidosis can have a particularly deleterious effect on myocardial function. Elevated serum lactate level is an indicator of shock.
Brain natriuretic peptide (BNP) may be useful as an indicator of congestive heart failure and as an independent prognostic indicator of survival. A low BNP level may effectively rule out cardiogenic shock in the setting of hypotension; however, an elevated BNP level does not rule in the disease.
Imaging Studies:
A portable chest radiograph is helpful because it gives an overall impression of the cardiac size, pulmonary vascularity, and coexistent pulmonary pathology, and it provides a rough estimate of mediastinal and aortic sizes in the event that an aortic etiology is being considered.
Other Tests:
An ECG is helpful if it reveals an acute injury pattern consistent with an AMI. A normal ECG, however, does not rule out the possibility. ECGs are often most helpful when they can be compared with previous tracings.
An echocardiogram obtained in the ED can be extremely useful.
It may be diagnostic and reveal akinetic or dyskinetic areas of ventricular wall motion.
It may reveal surgically correctable causes, such as valvular dysfunction and tamponade.
Procedures:
Placement of a central line may facilitate volume resuscitation, provide vascular access for multiple infusions, and allow invasive monitoring of central venous pressure and pulmonary capillary wedge pressure. Although not necessary for the diagnosis of cardiogenic shock, invasive monitoring with a pulmonary artery catheter may be helpful in guiding fluid resuscitation in situations in which LV preload is difficult to determine. Central venous pressure may also be used to guide fluid resuscitation. Cardiogenic shock may be indicated by a cardiac index of less than 1.8 L/min/m2 with a pulmonary capillary wedge pressure greater than 18 mm Hg.
An intra-aortic balloon pump may be placed in the ED as a bridge to percutaneous coronary intervention (PCI) or coronary artery bypass graft (CABG) to decrease myocardial workload.
Prehospital Care: Prehospital care is aimed at minimizing any further ischemia and shock.
All patients require intravenous access, high-flow oxygen administered by mask, and cardiac monitoring.
Twelve-lead electrocardiography performed in the field by appropriately trained paramedics may be useful in decreasing door to PCI times and/or thrombolytics because acute ST-segment elevation myocardial infarctions can be identified earlier. The ED physician, can thus be alerted, and may mobilize the appropriate resources.
Inotropic medications should be considered in systems with appropriately trained paramedical personnel.
Emergency Department Care: ED care is aimed at making the diagnosis, preventing further ischemia, and treating the underlying cause. Treatment of the underlying cause is directed in the case of acute myocardial infarction (AMI) at coronary artery reperfusion. This is best accomplished with rapid transfer of the patient to a cardiac catheterization laboratory. The ED physician should be alert to the fact that the SHOCK trial demonstrated that PCI or coronary artery bypass are the treatments of choice and that they have been shown to markedly decrease mortality rates at 1 year. PCI should be initiated within 90 minutes of presentation; however, it remains helpful, as an acute intervention, within 12 hours of presentation. If such a facility is not immediately available, thrombolytics should be considered. However, this treatment is second best.
Treatment begins with assessment and management of the ABCs.
The airway should be assessed for patency and breathing evaluated for effectiveness and increased work of breathing. Endotracheal intubation and mechanical ventilation should be considered for patients with excessive work of breathing. Positive pressure ventilation may improve oxygenation but may also compromise venous return, preload, to the heart. In any event, the patient should be treated with high-flow oxygen.
Other interventions are directed at supporting myocardial perfusion and maximizing cardiac output. Intravenous fluids should be provided to maintain adequate preload. The administration of such fluids should be guided by central venous pressure or pulmonary capillary wedge pressure monitoring.
Intravenous vasopressors provide inotropic support increasing perfusion of the ischemic myocardium and all body tissues. However, extreme heart rates should be avoided because they may increase myocardial oxygen consumption, increase infarct size, and further impair the pumping ability of the heart.
Dopamine may provide vasopressor support. With higher doses, it has the disadvantage of increasing the heart rate and myocardial oxygen consumption.
Dobutamine, inamrinone (formerly amrinone), or milrinone may provide inotropic support. In addition to their positive inotropic effects, inamrinone and milrinone have a beneficial vasodilator effect, which reduces preload and afterload.
Natrecor (nesiritide) may be considered. Although nesiritide has been shown to increase mortality and renal dysfunction, it continues to be studied as a treatment for acute congestive heart failure and currently retains Food and Drug Administration (FDA) approval. It should be used with caution in the setting of cardiogenic shock because it has been shown to cause hypotension.
Nitrates and/or morphine are advised for the management of pain; however, they must be used with caution because these patients are in shock, and excessive use of either of these agents can produce profound hypotension. Neither of these options has been shown to improve outcomes in cardiogenic shock.
The use of an intra-aortic balloon pump (IABP) is recommended for cardiogenic shock not quickly reversed with pharmacologic therapy. It is also recommended as a stabilizing measure combined with thrombolytic therapy when angiography and revascularization are not readily available. Counterpulsation of the IABP reduces LV afterload and improves coronary artery blood flow. Although this procedure is generally not performed in the ED, planning is essential, and early consultation with a cardiologist regarding this option is recommended. Although complications may occur in up to 30% of patients, extensive retrospective data support its use.
