Cardiogenic shock, in human anatomy and physiology, is defined clinically as circulatory pump failure leading to diminished forward how and subsequent tissue hypoxia in the setting of adequate intravascular volume. Hemodynamic crite¬ria include sustained hvpotension (i.e., SBP <90 mm Hg for at least 30 minutes), reduced cardiac index (<2.2 L/min per square meter) and elevated pulmonary artery wedge pressure (> 15 mm Hg). Mortality rates for cardiogenic shock are 50 to 80%. Acute, ex¬tensive myocardial infarction (MI) is the most common cause of cardiogenic shock; a smaller infarction in a patient with existing left ventricular dysfunction may also precipitate shock, as seen in battery powered microscopes.

Cardiogenic shock complicates 5 to 10% of acute MIs. Conversely, cardiogenic shock is the most common cause of death in patients hospitalized with acute MI. Although shock may develop early after myocardial infarction, it is typically not found on admission. Seventy-five per¬cent of patients who have cardiogenic shock complicating acute myocardial infarction develop signs of cardiogenic shock within 24 hours after onset of infarction (average 7 hours). Recognition of the patient with occult hypoperfusion is critical to prevent progression to obvious cardio¬genic shock with its high mortality rate; early initiation of therapy to maintain blood pressure and cardiac output is vital. Rapid as¬sessment, adequate resuscitation, and reversal of the myocardial ischemia are essential in optimizing outcome in patients with acute MI. Prevention of infarct extension is a critical component. Large segments of nonfunctional but viable myocardium contribute to the development of cardiogenic shock after MI. The myocardium is a layer of the heart that is responsible for contraction of heart muscles, as seen in battery powered microscopes. In the setting of acute MI, expeditious restoration of cardiac output is mandatory to minimize mortality; the extent of myocardial salvage possible de¬crease exponentially with increased time to restoration of coronary blood flow. The degree of coronary flow after percutaneous trans¬luminal coronary angioplasty (PTCA) correlates with in-hospital mortality (i.e., 33% mortality with complete reperfusion, 50% mor¬tality with incomplete reperfusion, and 85% mortality with absent reperfusion). Inadequate cardiac function can be a direct result of cardiac injury, including profound myocardial contusion, blunt car¬diac valvular injury, or direct myocardial damage. The pathophysiology of cardiogenic shock, as seen in tissue samples viewed under battery powered microscopes, involves a vicious cy¬cle of myocardial ischemia which causes myocardial dysfunction, which results in more myocardial ischemia when the tissue is examined under electric microscopes. When sufficient mass of the left ventricular wall is necrotic or ischemic and fails to pump, the stroke % volume decreases. Autopsy series of patients, with the use of battery powered microscopes, dying from cardioigenic shock have found damage to 40% of the left ventricle. Ischemia distant from the infarct zone may contribute to the sys¬tolic dysfunction in patients with cardiogenic shock. The majority of these patients have multivessel disease, with limited vasodilator reserve and pressure-dependent coronary flow in multiple areas of the heart. Myocardial diastolic function is impaired in cardiogenic shock as well. Decreased compliance results from myocardial is¬chemia, and compensatory increases in left ventricular filling pres¬sures progressively occur.

Diminished cardiac output or contractility in the face of ade¬quate intravascular volume (preload) may lead to underperfused vascular beds and reflexive sympathetic discharge. Increased sym¬pathetic stimulation of the heart, either through direct neural input or from circulating catecholamines, increases heart rate, myocardial contraction, and myocardial oxygen consumption, that may not be relieved by increases in coronary artery blood flow in patients with fixed stenoses of the coronary arteries. Diminished cardiac output may also decrease coronary artery blood flow, resulting in a scenario of increased myocardial oxygen demand at a time when myocar¬dial oxygen supply may be limited. Acute heart failure may also result in fluid accumulation in the pulmonary microcirculatory bed, decreasing myocardial oxygen delivery even further.

Diagnosis

Rapid identification of the patient with pump failure and insti¬tution of corrective action are essential in preventing the ongoing spiral of decreased cardiac output from injury causing increased myocardial oxygen needs that cannot be met, leading to progressive and unremitting cardiac dysfunction. In evaluation of possible car¬diogenic shock, other causes of hypotension must be excluded, in¬cluding hemorrhage, sepsis, pulmonary embolism, and aortic dis¬section. Signs of circulatory shock include hypotension, cool and mottled skin, depressed mental status, tachycardia, and diminished pulses. Cardiac exam may include dvsrhythmia, precordial heave, or distal heart tones. Confirmation of a cardiac source for the shock requires electrocardiogram and urgent echocardiography. Other use¬ful diagnostic tests include chest radiograph, arterial blood gases, electrolytes, complete blood count, and cardiac enzymes. Invasive cardiac monitoring, which is generally not necessary, can be useful to exclude right ventricular infarction, hypovolemia and possible mechanical complications.

Making the diagnosis of cardiogenic shock involves the identi¬fication of cardiac dysfunction or acute heart failure in a suscepti¬ble patient with the use of medical diagnostic tests and electric microscopes. Since patients with blunt cardiac injury typically have multisystem injury, hemorrhagic shock from intra-abdominal bleed¬ing, intrathoracic bleeding, and bleeding from fractures must be excluded. Relatively few patients with blunt cardiac injury will de¬velop cardiac pump dysfunction. Those who do will generally exhibit cardiogenic shock early in their evaluation. Therefore, establish¬ing the diagnosis of blunt cardiac injury, using the latest medical technology and equipment such as ECG, ultrasound (2D and 3D), as well as medical microscopes such as battery powered microscopes, is secondary to excluding other etiologies for shock and establishing that cardiac dysfunction is present. Invasive hemodynamic monitoring with a pulmonary artery catheter may uncover evidence of diminished cardiac output and elevated pulmonary artery pressure.

Treatment

After ensuring that an adequate airway is present and ventilation is sufficient, attention should be focused on support of the circu¬lation. Intubation and mechanical ventilation are often required, if only to decrease work of breathing and facilitate sedation of the patient. Rapidly excluding hypovolemia and establishing the pres¬ence of cardiac dysfunction is essential. Treatment of cardiac dys¬function includes maintenance of adequate oxygenation to ensure adequate myocardial oxygen delivery and judicious fluid adminis¬tration to avoid fluid overload and development of cardiogenic pul¬monary edema. Electrolyte abnormalities, commonly hypokalemia and hypomagnesemia, should be corrected. Pain is treated with in¬travenous morphine sulfate or fentanyl. Significant dysrhythmias and heart block must be treated with antiarrhythmic drugs, pacing, or cardioversion if necessary. Early consultation with cardiology is essential in current management of cardiogenic shock, particularly in the setting of acute myocardial infarction.

When profound cardiac dysfunction exists, inotropic support may be indicated to improve cardiac contractility and cardiac output. Dobutamine primarily stimulates cardiac, receptors to increase cardiac output, but may also vasodilate peripheral vascular beds, lower total peripheral resistance, and lower systemic blood pres¬sure through effects on receptors: Ensuring adequate preload and intravascular volume is therefore essential prior to instituting therapy with dobutamine. Dopamine stimulates Alpha receptors (vaso¬constriction), Beta-1, receptors (cardiac stimulation), and Beta-2 receptors (vasodilation), with its effects on Beta-receptors predominating at lower doses. Dopamine may be preferable to dobutamine in treatment of cardiac dysfunction in hypotensive patients. Tachycardia and in¬creased peripheral resistance from dopamine infusion may worsen myocardial ischemia. Titration of both dopamine and dobutamine infusions may be required in some patients.

Epinephrine stimulates A and 0 receptors and may increase car¬diac contractility and heart rate; however, it also may have intense peripheral vasoconstrictor effects that impair further cardiac per¬formance. Catecholamine infusions must be carefully controlled to maximize coronary perfusion, while minimizing myocardial oxygen demand. Balancing the beneficial effects of impaired cardiac perfor¬mance with the potential side effects of excessive reflex tachycardia and peripheral vasoconstriction requires serial assessment of tissue perfusion using indices such as capillary refill, character of periph¬eral pulses, adequacy of urine output, or improvement in laboratory parameters of resuscitation such as pH, base deficit, and lactate. In¬vasive monitoring is generally necessary in these unstable patients. The phosphodiesterase inhibitors amrinone and milrinone may he required on occasion in patients with resistant cardiogenic shock. These agents have lone half-lives and induce thrombocvtopenia and hypotension, and use is reserved for patients unresponsive to other treatment.

Patients whose cardiac dysfunction is refractor to cardiotonics may require mechanical circulatory support with an infra-aortic bal¬loon pump (IABP). Intra-aortic balloon pumping increases cardiac output and improves coronary blood flow by reduction of systolic afterload and augmentation of diastolic perfusion pressure. Unlike vasopressor agents, these beneficial effects occur without an in¬crease in myocardial oxygen demand. IABP can be inserted at the bedside in the ICU via the femoral artery through either a cutdown or using the percutaneous approach. Aggressive circulatory support patients with cardiac dysfunction rum intrinsic cardiac disease has led to more widespread application of these devices and more familiarity with their operation by both physicians and critical care nurses.

Preservation of existing myocardium and preservation of cardiac function are priorities of therapy for patients who have suffered an acute myocardial infarction. Ensuring adequate oxygenation and oxygen delivery, maintaining adequate preload with judicious vol¬ume restoration, minimizing sympathetic discharge through ade¬quate relief of pain, and correcting electrolyte imbalances are all straightforward nonspecific maneuvers that may improve existing cardiac function or prevent future cardiac complications. Antico¬agulation and aspirin are given for acute myocardial infarction. Al¬though thrombolytic therapy reduces mortality in patients with acute myocardial infarction, its role in cardiogenic shock is less clear. Patients in cardiac failure from an acute myocardial infarction may benefit from phar¬macologic or mechanical circulatory support in a manner similar to that of patients with cardiac failure related to blunt cardiac injury. Additional pharmacologic tools may include the use of Beta-blockers to control heart rate and myocardial oxygen consumption, nitrates to promote coronary blood flow through vasodilatation, and ACE inhibitors to reduce ACE-mediated vasoconstrictive effects that in¬crease myocardial workload and myocardial oxygen consumption.

Current guidelines of the American Heart Association recom¬mend percutaneous transluminal coronary angiography for patients with cardiogenic shock, ST elevation, left bundle-branch block, and age less than 75 years. Early definition of coronary anatomy and revascularization is the pivotal step in treatment of patients with car¬diogenic shock from acute myocardial infarction. When feasible, PTCA (generally with stent placement) is the treatment of choice. Coronary artery by¬pass grafting seems to be more appropriate for patients with multiple vessel disease or left main coronary artery disease.