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Cardiogenic Shock Complicating Acute Myocardial Infarction
Matthew A. Cavender
The overall rates of myocardial infarction and the incidence of cardiogenic shock in patients with myocardial infarction have declined over time owing to advances in medical, surgical, and interventional treatments.1
However, mortality rates in acute myocardial infarction (AMI) complicated by cardiogenic shock remain high. Cardiogenic shock in the setting of myocardial infarction is a heterogeneous clinical entity that most commonly occurs with the sudden onset of left ventricular dysfunction owing to a large area of dysfunctional myocardium because of acute ischemia and ensuing cardiac necrosis. In this setting, the heart attempts to maintain cardiac output despite the marked reduction in stroke volume by increasing the heart rate. When this compensatory mechanism is inadequate, end-organ hypoperfusion and circulatory collapse result.
There is no universally accepted definition of cardiogenic shock as it is a subjective and clinical diagnosis best made by the clinician at the bedside. Its occurrence is characterized by inadequate end-organ tissue perfusion secondary to decreased cardiac output despite adequate or elevated left ventricular filling pressures. The SHOCK (SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK) trial utilized these core principles to create a definition for cardiogenic shock that could be applied objectively in the setting of a randomized clinical trial.3
To be included in the SHOCK trial (Table 11.1
), patients with AMI had to manifest hypotension (systolic blood pressure <90 mm Hg sustained for at least 30 minutes or the use of hemodynamic support measures to maintain blood pressure >90 mm Hg) and have evidence of end-organ hypoperfusion (<30 ml of urine output per hour, heart rate >60 beats per minute, cool extremities). Hemodynamic confirmation was mandatory in this trial and patients had to have a cardiac index of <2.2 L per m2
and pulmonary capillary wedge pressure of ≥15 mm Hg on right heart catheterization unless there was overt evidence of pulmonary congestion on chest radiography.
TABLE 11.1 Criteria for Cardiogenic Shock Complicating AMI
ETIOLOGY OF CARDIOGENIC SHOCK IN THE SETTING OF ACUTE MYOCARDIAL INFARCTION
Most of the patients with cardiogenic shock have left ventricular failure owing to an ongoing or recently completed AMI.4
Prior necropsy studies have found that most of the patients who die from cardiogenic shock have lost >40% of their myocardium.5
In this condition, the culprit artery is almost always either left anterior descending or right coronary artery (RCA). The left circumflex is the culprit artery only 13% of the time.6
Isolated right ventricular involvement in the absence of an overt inferoposterior infarction is rare and occurs in only 2% of cases.4
Patients with non-ST-elevation myocardial infarction (NSTEMI) can also develop cardiogenic shock but represent <20% of overall patients and are typically older with more medical comorbidities.6
In addition to the myocardial dysfunction as a result of ischemia, myocardial infarction can also result in mechanical complications such as acute mitral regurgitation owing to loss of the integrity of the mitral valve, ventricular septal rupture (VSR), or ventricular wall rupture. These complications of myocardial infarction are fairly uncommon resulting in <15% of all cases of cardiogenic shock. Hemodynamic instability resulting from β
-blockers or occult blood loss can also present in a similar manner. Other acute cardiac emergencies such as acute aortic dissection, acute pulmonary embolism, myocarditis, and pneumothorax and cardiac tamponade can also have similar presentations and should to be considered by the astute clinician. Seldom is dynamic left ventricular outflow tract obstruction in the setting of an anterior myocardial infarction or hypertrophic obstructive cardiomyopathy encountered. Critical aortic stenosis and stress-induced cardiomyopathy can also be encountered in patients with circulatory collapse. Recognition
of the causative etiology of shock is pivotal to directing appropriate interventions.
Cardiac myocytes need oxygen to generate energy and maintain integrity of the contractile apparatus. Although the body as a whole extracts between 30% and 50% of the oxygen delivered through arterial blood flow, myocytes extract approximately 70% of oxygen delivered to them. The amount of oxygen required by cardiac myocytes, known as myocardial oxygen demand, is predominately dependent on myocardial wall stress, contractility, and the heart rate.7
Thus, in the setting of an AMI, when blood supply is abruptly diminished there is immediate loss of contractility in the area at risk. When compensatory mechanisms are inadequate, hemodynamic instability and cardiogenic shock can ensue.
Coronary artery blood flow, especially to the left coronary artery occurs primarily during diastole and is dependent on a pressure gradient that exists between mean central aortic pressure and the left ventricular end diastolic pressure.9
Cardiogenic shock results in decreased mean arterial blood pressure and elevations in the left ventricular end diastolic pressure so that the pressure gradient driving coronary perfusion decreases. As a result, coronary blood flow is further diminished and ischemia is worsened in the myocardium supplied by both the culprit and nonculprit blood vessels.
Decreased cardiac output, regardless of the etiology, significant enough to cause end-organ hypoperfusion activates the compensatory mechanisms of the body in an attempt to restore tissue perfusion.10
Catecholamine release through activation of the sympathetic nervous system increases heart rate and causes systemic vasocontriction. The decreased renal perfusion causes activation of the renin-angiotensin system, increased angiotensin II, and further systemic vasocontriction. All of these compensatory mechanisms increase myocardial oxygen demand because vasoconstriction increases wall stress, catecholamines increase heart rate and contractility, and increased left ventricular filling pressure from cardiac dysfunction increases wall stress. This results in a self-perpetuating deterioration in hemodynamic status that can ultimately result in death. Large myocardial infarctions can also result in increased levels of nitric oxide and cytokine-release-mediated vasodilation. These agents also have a negative inotropic impact and may manifest in a shock state that closely resembles sepsis. The clinical presentation of this variant of cardiogenic shock is quite heterogeneous although elderly patients with large anterior myocardial infarction appear to be at greatest risk.10
Cardiogenic shock is an infrequent complication of AMI. Analyses of large national databases, such as the National Registry of Myocardial Infarction (NRMI) have estimated that the incidence of cardiogenic shock is between 5% and 9%.11
Recent data suggest that the incidence has been decreasing in conjunction with the widespread utilization of primary angioplasty.12
Shock on presentation remains unchanged but definitive revascularization and salvage of myocardium appear to have decreased the incidence of shock after presentation.12
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