History

Cardiogenic shock is a medical emergency. A complete clinical assessment is critical to understanding the cause of the shock and to targeting therapy for correcting the cause. Cardiogenic shock following acute MI generally develops after admission to the hospital, although a small number of patients are in shock at presentation. Patients demonstrate clinical evidence of hypoperfusion (low cardiac output), which is manifested by sinus tachycardia, low urine output, and cool extremities. Systemic hypotension, defined as systolic blood pressure below 90 mm Hg or a decrease in mean blood pressure by 30 mm Hg, ultimately develops and further propagates tissue hypoperfusion. Most patients who develop acute MI present with an abrupt onset of squeezing or heavy substernal chest pain; the pain may radiate to the left arm or the neck. The chest pain may be atypical, the location being epigastric or only in the neck or arm. The pain quality may be burning, sharp, or stabbing. The pain may be absent in persons with diabetes or in elderly individuals. Patients also may report associated autonomic symptoms, including nausea, vomiting, and sweating.A history of previous cardiac disease, use of cocaine, previous MI, or previous cardiac surgery should be obtained. A patient thought to have myocardial ischemia should have an assessment for cardiac risk factors. The evaluation should reveal a history of hyperlipidemia, left ventricular hypertrophy, hypertension, or cigarette smoking or should reveal a family history of premature coronary artery disease. The presence of 2 or more risk factors increases the likelihood of acute MI. Other associated symptoms are diaphoresis, exertional dyspnea, or dyspnea at rest. Presyncope or syncope, palpitations, generalized anxiety, and depression are other features indicative of poor cardiac function.

Physical
Cardiogenic shock is diagnosed after documentation of myocardial dysfunction and exclusion of alternative causes of hypotension, such as hypovolemia, hemorrhage, sepsis, pulmonary embolism, pericardial tamponade, aortic dissection, or preexisting valvular disease. Shock is present if evidence of multisystem organ hypoperfusion is detected upon physical examination. Patients in shock usually appear ashen or cyanotic and have cool skin and mottled extremities.Peripheral pulses are rapid and faint and may be irregular if arrhythmias are present.Jugular venous distention and crackles in the lungs are usually (but not always) present. Peripheral edema also may be present.Heart sounds are usually distant, and both third and fourth heart sounds may be present.The pulse pressure may be low, and patients are usually tachycardic.Patients show signs of hypoperfusion, such as altered mental status and decreased urine output.A systolic murmur is generally heard in patients with acute mitral regurgitation or ventricular septal rupture.The associated parasternal thrill indicates the presence of a ventricular septal defect, whereas the murmur of mitral regurgitation may be limited to early systole. The systolic murmur, which becomes louder upon Valsalva and prompt standing, suggests hypertrophic obstructive cardiomyopathy (idiopathic hypertropic subaortic stenosis).

Causes
Based on the etiology and pathophysiology, cardiogenic shock can be divided into systolic dysfunction, diastolic dysfunction, valvular dysfunction, cardiac arrhythmias, coronary artery disease, and mechanical complications

Systolic dysfunction

The primary abnormality in systolic dysfunction is abated myocardial contractility. Acute MI or ischemia is the most common cause; cardiogenic shock is more likely to be associated with anterior MI. The other causes of systolic dysfunction leading to cardiogenic shock are severe myocarditis, end-stage cardiomyopathy (including valvular causes), myocardial contusion, and prolonged cardiopulmonary bypass.
Diastolic dysfunction

Increased left ventricular diastolic chamber stiffness contributes to cardiogenic shock during cardiac ischemia, but also in the late stages of hypovolemic shock and septic shock. Increased diastolic dysfunction is particularly detrimental when systolic contractility is also depressed. The causes of cardiogenic shock due primarily to diastolic dysfunction are listed in Diastolic dysfunction.
Valvular dysfunction

Valvular dysfunction may immediately lead to cardiogenic shock or may aggravate other etiologies of shock. Acute mitral regurgitation secondary to papillary muscle rupture or dysfunction is caused by ischemic injury. Rarely, acute obstruction of the mitral valve by left atrial thrombus may result in cardiogenic shock by means of severely decreased cardiac output. Aortic and mitral regurgitation reduce forward flow, raise end-diastolic pressure, and aggravate shock associated with other etiologies.
Cardiac arrhythmias

Ventricular tachyarrhythmias are often associated with cardiogenic shock. Furthermore, bradyarrhythmias may cause or aggravate shock due to another etiology. Sinus tachycardia and atrial tachyarrhythmias contribute to hypoperfusion and aggravate shock.
Coronary artery disease

Cardiogenic shock is generally associated with the loss of more than 40% of the left ventricular myocardium, although in patients with previously compromised left ventricular function, even a small infarction may precipitate shock. Cardiogenic shock is more likely to develop in people who are elderly or diabetic or in those who have had a previous inferior infarction.

Mechanical complications

Complication of acute MI, such as acute mitral regurgitation, large RV infarction, and rupture of the interventricular septum or left ventricular free wall, are other causes of cardiogenic shock. Specific causes of cardiogenic shock include the following:
Left ventricular failure

Systolic dysfunction (decreased contractility) o Ischemia/MI o Global hypoxemia o Valvular disease (see Valvular or structural abnormality) o Myocardial depressant drugs (eg, beta-blockers, calcium channel antiarrhythmics) o Myocardial contusion o Respiratory acidosis o Metabolic derangements (eg, acidosis, hypophosphatemia, hypocalcemia) Diastolic dysfunction/increased myocardial diastolic stiffness o Ischemia o Ventricular hypertrophy o Restrictive cardiomyopathy o Consequence of prolonged hypovolemic or septic shock o Ventricular interdependence o External compression by pericardial tamponade Greatly increased afterload o Aortic stenosis o Hypertrophic cardiomyopathy o Dynamic aortic outflow tract obstruction o Coarctation of the aorta o Malignant hypertension Valvular or structural abnormality o Mitral stenosis o Endocarditis o Mitral aortic regurgitation o Obstruction due to atrial myxoma or thrombus o Papillary muscle dysfunction or rupture o Ruptured septum or free wall arrhythmias Decreased contractility o RV infarction o Ischemia o Hypoxia o Acidosis

blockers,

Right ventricular failure

Greatly increased afterload

Pulmonary embolism Pulmonary vascular disease (eg, pulmonary arterial hypertension, veno-occlusive disease) o Hypoxic pulmonary vasoconstriction o Peak end-expiratory pressure o High alveolar pressure o Acute respiratory distress syndrome o Pulmonary fibrosis o Sleep disordered breathing o Chronic obstructive pulmonary disease Arrhythmias o Atrial and ventricular arrhythmias (tachycardia-mediated cardiomyopathy) o Conduction abnormalities (eg, atrioventricular blocks, sinus bradycardia)

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Differentials

Myocardial Infarction Myocardial Ischemia Myocardial Rupture Myocarditis Pulmonary Edema, Cardiogenic Pulmonary Embolism Sepsis, Bacterial Septic Shock Shock, Distributive Shock, Hemorrhagic Systemic Inflammatory Response Syndrome

Laboratory Studies
Biochemical profile

Measurement of routine biochemistry parameters, such as electrolytes, renal function (eg, urea and creatinine), and liver function tests (eg, bilirubin, aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase [LDH]), are all useful for assessing proper functioning of vital organs.
CBC count

A CBC count is generally helpful to exclude anemia; a high WBC count may indicate an underlying infection, and the platelet count may be low because of coagulopathy related to sepsis.

Cardiac enzymes

The diagnosis of acute MI is aided by a variety of serum markers, which include creatine kinase and its subclasses, troponin, myoglobin, and LDH. The value for the isoenzyme of creatine kinase with muscle and blood subunits is most specific but may be falsely elevated in persons with myopathy, hypothyroidism, renal failure, or skeletal muscle injury. The rapid release and metabolism of myoglobin occurs in persons with MI. A 4-fold rise of myoglobin over 2 hours appears to be a test result sensitive for MI. The serum LDH value increases approximately 10 hours after the onset of MI, peaks at 24-48 hours, and gradually returns to normal in 6-8 days. The LDH fraction 1 isoenzyme is primarily released by the heart but also may come from the kidneys, stomach, pancreas, and red blood cells. Cardiac troponins T and I are widely used for the diagnosis of myocardial injury. Troponin elevation in the absence of clinical evidence of ischemia should prompt a search for other causes of cardiac damage, such as myocarditis. Troponin I and T can be detected in serum within the first few hours after onset of acute myocardial infarction. Troponin levels peak at 14 hours after acute myocardial infarction, peak again several days later (biphasic peak), and remain abnormal for 10 days. This characteristic could make troponin T (in combination with CK-MB) useful for retrospective diagnosis of acute myocardial infarction in patients who seek care very late. Troponin T is an independent prognosticator of adverse outcomes and can be used as a patient risk-stratifying tool in patients with unstable angina or non Q-wave myocardial infarction.

Arterial blood gases

Arterial blood gas values indicate overall acid-base homeostasis and the level of arterial blood oxygenation. A base deficit elevation (reference range is +3 to -3 mmol/L) correlates with the occurrence and severity of shock. A base deficit is also an important marker to follow during resuscitation of a patient from shock.
Lactate

Serial lactate measurements are useful markers of hypoperfusion and are also used as indicators of prognosis. Elevated lactate values in a patient with signs of hypoperfusion indicate a poor prognosis; rising lactate values during resuscitation portend a very high mortality rate.

Imaging Studies
Echocardiography should be performed early to establish the cause of cardiogenic shock. Echocardiography provides information on global and regional systolic function and on diastolic dysfunction. Echocardiography findings can also lead to a rapid diagnosis of mechanical causes of shock, such as papillary muscle rupture causing acute myocardial regurgitation, acute ventricular septal defect, free myocardial wall rupture, and pericardial tamponade. Chest radiography findings are useful for excluding other causes of shock or chest pain. A widened mediastinum may indicate aortic dissection. Tension pneumothorax or pneumomediastinum readily detected on x-ray films may manifest as low-output shock.

Most patients with established cardiogenic shock exhibit findings of left ventricular failure. The radiological features of left ventricular failure include pulmonary vascular redistribution, interstitial pulmonary edema, enlarged hilar shadows, the presence of Kerley B lines, cardiomegaly, and bilateral pleural effusions; alveolar edema manifests as bilateral perihilar opacities in a so-called butterfly distribution.

Other Tests
Electrocardiogram

Acute myocardial ischemia is diagnosed based on the presence of ST-segment elevation, STsegment depression, or Q waves. T-wave inversion, although a less sensitive finding, may be seen in persons with myocardial ischemia. Therefore, perform electrocardiography immediately to help diagnose MI, myocardial ischemia, or both. See the images below

This ECG shows evidence of an extensive anterolateral myocardial infarction; this patient subsequently developed cardiogenic shock.

ECG tracing shows further evolutionary changes in a patient with cardiogenic shock.

ECG tracing in a patient who developed cardiogenic shock secondary to pericarditis and pericardial tamponade. A 63-year-old man admitted to the emergency department with clinical features of cardiogenic shock. The ECG revealed findings indicative of wide-complex tachycardia, likely ventricular tachycardia. Following cardioversion, his shock state improved. The cause of ventricular tachycardia was myocardial ischemia.

Procedures
Invasive hemodynamic monitoring

Invasive hemodynamic monitoring (Swan-Ganz catheterization) is very useful for helping exclude other causes of shock, eg, volume depletion, or obstructive and septic shock. The hemodynamic measurements of cardiogenic shock are a pulmonary capillary wedge pressure (PCWP) greater than 15 mm Hg and a cardiac index of less than 2.2 L/min/m2. The presence of large V waves on the PCWP tracing suggests severe mitral regurgitation. A step-up in oxygen saturation between the right atrium and the right ventricle is diagnostic of ventricular septal rupture. High right-sided filling pressures in the absence of an elevated PCWP, when accompanied with electrocardiographic criteria, indicate RV infarction.

Coronary artery angiography

Coronary angiography is urgently indicated in patients with myocardial ischemia or MI who also develop cardiogenic shock (see the image below). Angiography is required to help assess the anatomy of the coronary arteries and the need for urgent revascularization.

Patient with an acute anterolateral myocardial infarction who developed cardiogenic shock. Coronary angiography images showed severe stenosis of the left anterior descending coronary artery, which was dilated by percutaneous transluminal coronary angioplasty.

Coronary angiography findings often demonstrate multivessel coronary artery disease in persons with cardiogenic shock. In these patients, a compensatory hyperkinesis cannot occur in the noninfarct territory because of the severe coronary artery atherosclerosis. The most common cause of cardiogenic shock is extensive MI, although a smaller infarction in a previously compromised left ventricle also may precipitate shock. Following MI, large areas of nonfunctional but viable myocardium (hibernating myocardium) can also cause or contribute to cardiogenic shock. See the images below.

demonstrates

severe

A coronary angiogram image of a patient with cardiogenic shock stenosis of the left anterior descending coronary artery.

A coronary angiogram image of a patient with cardiogenic shock demonstrates severe stenosis of the left anterior descending coronary artery. Following angioplasty of the critical stenosis, coronary flow is reestablished. The patient recovered from cardiogenic shock.

Medical Care
Initial management includes fluid resuscitation to correct hypovolemia and hypotension, unless pulmonary edema is present. Central venous and arterial lines are often required. Swan-Ganz catheterization and continuous percutaneous oximetry are routine. Oxygenation and airway protection are critical; intubation and mechanical ventilation are commonly required. Correction of electrolyte and acid-base abnormalities, such as hypokalemia, hypomagnesemia, and acidosis, are essential. A study by Shin et al suggests that patients who receive extracorporeal cardiopulmonary resuscitation (CPR) versus conventional CPR for longer than 10 minutes following in-hospital arrest have a greater chance of survival.[3] Patients with MI or acute coronary syndrome are given aspirin and heparin. Both of these medications have been shown to be effective in reducing mortality in separate studies. The glycoprotein IIb/IIIa inhibitors improve the outcome of patients with NSTACS. Their benefit has been proven in reducing recurrent MI following percutaneous coronary intervention (PCI) and in cardiogenic shock. All patients with cardiogenic shock require close hemodynamic monitoring, volume support to ensure adequate sufficient preload, and ventilatory support as discussed in Respiratory Failure.
Hemodynamic support

Dopamine, norepinephrine, and epinephrine are vasoconstricting drugs that help maintain adequate blood pressure during life-threatening hypotension and help preserve perfusion pressure for optimizing flow in various organs. The mean blood pressure required for adequate splanchnic and renal perfusion (mean arterial pressure [MAP] of 60 or 65 mm Hg) is based on clinical indices of organ function.

In patients with inadequate tissue perfusion and adequate intravascular volume, initiation of inotropic and/or vasopressor drug therapy may be necessary. Dopamine increases myocardial contractility and supports the blood pressure; however, it may increase myocardial oxygen demand. Dobutamine may be preferable if the systolic blood pressure is higher than 80 mm Hg and has the advantage of not affecting myocardial oxygen demand as much as dopamine. However, the resulting tachycardia may preclude the use of this inotropic agent in some patients. Dopamine is usually initiated at a rate of 5-10 mcg/kg/min intravenously, and the infusion rate is adjusted according to the blood pressure and other hemodynamic parameters. Often, patients may require high doses of dopamine (as much as 20 mcg/kg/min). If the patient remains hypotensive despite moderate doses of dopamine, a direct vasoconstrictor (eg, norepinephrine) should be started at a dose of 0.5 mcg/kg/min and titrated to maintain an MAP of 60 mm Hg. The potent vasoconstrictors (eg, norepinephrine) have traditionally been avoided because of their adverse effects on cardiac output and renal perfusion.
Vasopressor supportive therapy

The following is a brief review of the mechanism of action and indications for drugs used for hemodynamic support of cardiogenic shock. Dopamine is a precursor of norepinephrine and epinephrine and has varying effects according to the doses infused. A dose of less than 5 mcg/kg/min causes vasodilation of renal, mesenteric, and coronary beds. At a dose of 5-10 mcg/kg/min, beta1-adrenergic effects induce an increase in cardiac contractility and heart rate. At doses of approximately 10 mcg/kg/min, alpha-adrenergic effects lead to arterial vasoconstriction and an elevation in blood pressure. The blood pressure increases primarily as a result of inotropic effect, and the undesirable effects are (1) tachycardia and increased pulmonary shunting and (2) the potential to decrease splanchnic perfusion and increase pulmonary arterial wedge pressure. Norepinephrine is a potent alpha-adrenergic agonist with minimal beta-adrenergic agonist effects. Norepinephrine can increase blood pressure successfully in patients who remain hypotensive following dopamine. The dose of norepinephrine may vary from 0.2-1.5 mcg/kg/min, and large doses, as high as 3.3 mcg/kg/min, have been used because of the alphareceptor down-regulation in persons with sepsis. Epinephrine can increase the MAP by increasing the cardiac index and stroke volume, along with an increase in SVR and heart rate. Epinephrine may increase oxygen delivery and consumption and decreases the splanchnic blood flow. Administration of this agent is associated with an increase in systemic and regional lactate concentrations. The use of epinephrine is recommended only in patients who are unresponsive to traditional agents. The undesirable effects are an increase in lactate concentration, a potential to produce myocardial ischemia, the development of arrhythmias, and a reduction in splanchnic flow.

Inotropic supportive therapy

Dobutamine (sympathomimetic agent) is a beta1-receptor agonist, although it has some beta2receptor and minimal alpha-receptor activity. Intravenous dobutamine induces significant positive inotropic effects with mild chronotropic effects. It also induces mild peripheral vasodilation (decrease in afterload). The combined effect of increased inotropy and decreased afterload induces a significant increase in cardiac output. In the setting of acute MI, dobutamine use could increase the size of the infarct because of the increase in myocardial oxygen consumption that may ensue. In general, avoid dobutamine in patients with moderate or severe hypotension (eg, systolic blood pressure < 80 mm Hg) because of the peripheral vasodilation. Phosphodiesterase inhibitors (PDIs), currently inamrinone (formerly amrinone) and milrinone, are the PDI inotropes that have proved valuable. These are inotropic agents with vasodilating properties, and each has a long half-life. The hemodynamic properties of PDIs are (1) a positive inotropic effect on the myocardium and peripheral vasodilation (decreased afterload) and (2) a reduction in pulmonary vascular resistance (decreased preload). PDIs are beneficial in persons with cardiac pump failure, but they may require concomitant vasopressor administration. Unlike catecholamine inotropes, these drugs are not dependent on adrenoreceptor activity; therefore, patients are less likely to develop tolerance to these medications. PDIs are less likely than catecholamines to cause adverse effects known to be associated with adrenoreceptor activity (eg, increased myocardial oxygen demand, myocardial ischemia). They are also associated with less tachycardia and myocardial oxygen consumption. However, the incidence of tachyarrhythmias is greater with PDIs compared to dobutamine.
Thrombolytic therapy

Although thrombolytic therapy (TT) reduces mortality rates in patients with acute MI, its benefits for patients with cardiogenic shock secondary to MI are disappointing. When used early in the course of MI, TT reduces the likelihood of subsequent development of cardiogenic shock after the initial event. In the Gruppo Italiano Per lo Studio Della Streptokinase Nell'Infarto Miocardio trial, 30-day mortality rates were 69.9% in patients with cardiogenic shock who received streptokinase, compared to 70.1% in patients who received a placebo. Similarly, other studies with a tissue plasminogen activator did not show any benefit in mortality rates from cardiogenic shock. Lower rates of reperfusion of the infarct-related artery in patients with cardiogenic shock might help explain the disappointing results from TT. The other reasons for the decreased efficacy of TT are the presence of hemodynamic, mechanical, and metabolic factors causative of cardiogenic shock; these factors are unaffected by TT.

A recent prospective study investigated the potential benefit of TT and intra-aortic balloon pump (IABP) counterpulsation on in-hospital mortality rates of patients with MI complicated by cardiogenic shock. Out of 1190 patients enrolled, the treatments were (1) no TT and no IABP counterpulsation (33%, n = 285), (2) IABP counterpulsation only (33%, n = 279), (3) TT only (15%, n = 132), and (4) TT and IABP counterpulsation (19%, n = 160). Patients in cardiogenic shock treated with TT had lower in-hospital mortality rates compared to those who did not receive TT (54% vs 64%, P = .005), and those selected for IABP counterpulsation had lower in-hospital mortality rates compared to those who did not receive IABP counterpulsation (50% vs 72%, P < .0001). Furthermore, a significant difference was noted in in-hospital mortality rates among the 4 treatment groups, ie, TT plus IABP counterpulsation (47%), IABP counterpulsation only (52%), TT only (63%), no TT and no IABP counterpulsation (77%) (P < .0001). Revascularization influenced in-hospital mortality rates significantly (39% with revascularization vs 78% without revascularization, P < .0001). Patients who are unsuitable for invasive therapy should be treated with a thrombolytic agent in the absence of contraindications. This is a class I recommendation by American College of Cardiology (ACC)/American Heart Association (AHA) guidelines.
Intra-aortic balloon pump

The use of the IABP reduces systolic left ventricular afterload and augments diastolic coronary perfusion pressure, thereby increasing cardiac output and improving coronary artery blood flow. The IABP is effective for the initial stabilization of patients with cardiogenic shock. However, an IABP is not definitive therapy; the IABP stabilizes the patients so that definitive diagnostic and therapeutic interventions can be performed. The IABP also may be a useful adjunct to thrombolysis for initial stabilization and transfer of patients to a tertiary care facility. Some studies have shown lower mortality rates in patients with MI and cardiogenic shock treated with an IABP and subsequent revascularization, as previously mentioned. Complications may be documented in up to 30% of patients who undergo IABP therapy and mainly relate to local vascular problems, embolism, infection, and hemolysis. The impact of an IABP on long-term survival is controversial and depends on the hemodynamic status and etiology of the cardiogenic shock. Patient selection is the key issue; early insertion of the IABP may result in clinical benefit, rather than waiting until full-blown cardiogenic shock has developed. Ramanathan et al found that rapid and complete reversal of systemic hypoperfusion with IABP counterpulsation in the SHOCK Trial and SHOCK Registry was independently associated with

improved in-hospital, 30-day, and 1-year survival, regardless of early revascularization, suggesting complete reversal of systemic hypoperfusion with IABP counterpulsation is an important early prognostic feature.[4]
Ventricular assist devices

In recent years, left ventricular assist devices (LVADs) capable of providing complete short-term hemodynamic support have been developed. The application of LVAD during reperfusion, after acute coronary occlusion, causes reduction of the left ventricular preload, increases regional myocardial blood flow and lactate extraction, and improves general cardiac function. The LVAD makes it possible to maintain the collateral blood flow as a result of maintaining the cardiac output and aortic pressure, keeping wall tension low, and reducing the extent of microvascular reperfusion injury. The pooled analysis from 17 studies showed that the mean age of this group of patients was 59.5 4.5 years, mean support duration was 146.2 60.2 hours. In 78.5% of patients (range, 53.8100%), adjunctive reperfusion therapy, mainly PTCA, was used. Mean weaning and survival rates were 58.5% (range, 46-75%) and 40% (range, 29-58%), respectively. In any case, comparing studies is difficult because important data are usually missing, patients were younger, and time to treatment is not standardized. Hemodynamic presentation seems to be worse compared with data reported in the SHOCK trial, with lower cardiac index, lower systolic aortic pressure, and higher serum lactates. Taking these considerations into account, LVAD support seems to give no survival improvement in patients with CS complicating acute MI, compared with early reperfusion alone or in combination with IABP. One randomized controlled trial assigned 129 patients with end-stage heart failure who were ineligible for cardiac transplantation to receive a left ventricular assist device (68 patients) or optimal medical management. Survival analysis that received left ventricular assist devices as compared with the medical therapy group (relative risk, 0.52; 95% confidence interval, 0.340.78; P=0.001). The rates of survival at 1 year were 52% in the device group and 25% in the medical therapy group (P=0.002), and the rates at 2 years were 23% and 8% (P=0.09), respectively. The quality of life was significantly improved at 1 year in the device group.[5] Implantable LVAD is being used as a bridge-to-heart transplantation for patients with acute MI and CS. Farrar and colleagues reported the best outcome in a multicenter trial that included 17 patients in CS from acute MI.[6] Thirteen patients (76%) underwent HTx and all were discharged after support with the Thoratec LVAD. According to the HeartMate Data Registry[7] , from 19861998, 41 patients (5% of the total number of HeartMate IP patients) were supported with this implantable pneumatic device for acute MI and 25 (61%) were successfully bridged to heart transplantation. However, LVADs as a bridging option for patients with CS must be considered cautiously and must be avoided in patients unlikely to survive or unlikely to be transplant candidates. Further investigations are required to better define indications, support modalities, and outcomes. The indications for insertion of a ventricular assist device are controversial. Such an aggressive approach to support the circulatory system in cardiogenic shock is appropriate (1) after the

failure of medical treatment and the IABP and (2) when the cause of cardiogenic shock is potentially reversible or as a bridging option.

Surgical Care
The retrospective and prospective data favor aggressive mechanical revascularization in patients with cardiogenic shock secondary to MI.
Percutaneous transluminal coronary angioplasty

Reestablishing blood flow in the infarct-related artery may improve left ventricular function and survival following MI. In acute MI, studies show that percutaneous transluminal coronary angioplasty (PTCA) can achieve adequate flow in 80-90% of patients, compared with 50-60% of patients after TT. Several retrospective clinical trials have shown that patients with cardiogenic shock due to myocardial ischemia benefitted (reduction in 30-d mortality rates) when treated with angioplasty. A recent study of direct (primary) PTCA in patients with cardiogenic shock reports lower mortality rates in patients treated with angioplasty combined with the use of stents, compared to medical therapy. To study the relationship of time to treatment and mortality in patients with acute MI, a series of 1336 patients who underwent successful primary PTCA were stratified into low-risk and not lowrisk patient groups. The 6-month mortality rate was 9.3% for not lowrisk patients and 1.3% for the low-risk patients (P < .001). An increase in the mortality rate from 4.8% to 12.9% with increasing time to reperfusion was observed in the not lowrisk group. A delay from symptom onset to treatment resulted in higher mortality rates for the not lowrisk patients.[8]
Coronary artery bypass grafting

Critical left main artery disease and 3-vessel coronary artery disease are common findings in patients who develop cardiogenic shock. The potential contribution of ischemia in the noninfarcted zone contributes to the deterioration of already compromised myocardial function. Coronary artery bypass grafting (CABG) in the setting of cardiogenic shock is generally associated with high surgical morbidity and mortality rates. Because the results of percutaneous interventions can be favorable, routine bypass surgery is often discouraged for these patients. A 2004 task force of the ACC and the AHA gave a class I recommendation to the performance of primary PCI or emergent CABG in patients younger than 75 years who have STEMI and who develop shock within 36 hours of MI and can be treated within 18 hours of onset of shock. Performance of primary PCI or emergent CABG was considered reasonable in patients older than 75 years (class IIa recommendation).

SHOCK trial

A recent study known as the SHOCK (ie, SHould we emergently revascularize Occluded Coronaries in cardiogenic shocK) trial addressed the question of revascularization in patients with cardiogenic shock. Patients were assigned to receive either optimal medical management, including an IABP and TT, or cardiac catheterization followed by revascularization using PTCA or CABG.[9] The 1-month and 6-month survival rates were reported from the SHOCK Trial.[10] The mortality rates at 30 days were 46.7% in the early intervention group and 56% in patients treated with optimal medical management. Although this did not reach a statistical significance at 1 month, the mortality rate at 6 months was significantly lower in the early intervention group (50.3% vs 63.1%, P = .027). The results of this study support the superiority of a strategy that combines early revascularization with medical management in patients with cardiogenic shock. The 1-year survival rates were also reported from the SHOCK Trial.[11] The survival rate at 1year was 46.7% for patients in the early revascularization group and was 33.6% in the conservative management (absolute difference in survival, 13.2%; 95% confidence interval, 2.224.1%; P < .03; relative risk for death, 0.72; 95% confidence interval, 0.54-0.95) group. The treatment benefit was apparent only for patients younger than 75 years (51.6% survival rate in early revascularization group vs 33.3% in patients treated with optimal medical management). Based on the outcome of this study, the recommendation is that patients with acute MI complicated by cardiogenic shock, particularly those younger than 75 years, should be rapidly transferred to a center with personnel capable of performing early angiography and revascularization procedures

Medication Summary
Vasopressors augment the coronary and cerebral blood flow during the low-flow state associated with shock. Sympathomimetic amines with both alpha- and beta-adrenergic effects are indicated for persons with cardiogenic shock. Dopamine and dobutamine are the drugs of choice to improve cardiac contractility, with dopamine the preferred agent in patients with hypotension. Vasodilators relax vascular smooth muscle and reduce the SVR, allowing for improved forward flow, which improves cardiac output. Adequate pain control is essential for quality patient care and patient comfort. Diuretics are used to decrease plasma volume and peripheral edema. The reduction in extracellular fluid and plasma volume associated with diuresis may initially decrease cardiac output and, consequently, blood pressure, with a compensatory increase in peripheral vascular resistance. With continuing diuretic therapy, the plasma volume and peripheral vascular resistance usually return to pretreatment values.

Vasopressors/inotropic agents

Class Summary

Augment coronary and cerebral blood flow during low-flow state associated with cardiogenic shock.
View full drug information Dopamine (Intropin)

Stimulates adrenergic and dopaminergic receptors. Hemodynamic effect depends on dose. Lower doses stimulate mainly dopaminergic receptors that produce renal and mesenteric vasodilation. Higher doses produce cardiac stimulation and vasoconstriction.
View full drug information Dobutamine (Dobutrex)

Sympathomimetic amine with stronger beta than alpha effects. Produces systemic vasodilation and increases the inotropic state. Higher doses may cause increase in heart rate, exacerbating myocardial ischemia.

Phosphodiesterase enzyme inhibitors

Class Summary

Induce peripheral vasodilation and provide inotropic support.

View full drug information Milrinone (Primacor)

Positive inotrope and vasodilator with little chronotropic activity. Different in mode of action from either cardiac glycosides (digoxin) or catecholamines.
View full drug information Inamrinone (Inocor)

Formerly known as amrinone. Phosphodiesterase inhibitor with positive inotropic and vasodilator activity. Produces vasodilation and increases inotropic state. More likely to cause tachycardia than dobutamine and may exacerbate myocardial ischemia.

Vasodilators
Class Summary

Decrease preload and/or afterload.

View full drug information Nitroglycerin IV (Nitro-Bid)

Causes relaxation of vascular smooth muscle by stimulating intracellular cyclic guanosine monophosphate production. Result is a decrease in preload and blood pressure (ie, afterload).

Analgesics
Class Summary

Reduce pain, which decreases sympathetic stress, in addition to providing some preload reduction.
View full drug information Morphine sulfate (Duramorph, Astramorph, MS Contin)

DOC for narcotic analgesia due to its reliable and predictable effects, safety profile, and ease of reversibility with naloxone. Various IV doses are used, commonly titrated until desired effect is achieved.

Diuretics
Class Summary

Decrease plasma volume and peripheral edema. Excessive reduction in plasma volume and stroke volume associated with diuresis may decrease cardiac output and, consequently, blood pressure.
View full drug information Furosemide (Lasix)

Increases excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in ascending loop of Henle and distal renal tubule. Individualize dose to patient. Depending on response, administer at increments of 20-40 mg no sooner than 6-8 h after previous dose, until desired diuresis occurs. When treating infants, titrate in increments of 1 mg/kg/dose until satisfactory effect is achieved.