Cardiogenic Shock Treatment & Management

  • Author: Andrew Lenneman, MD; Chief Editor: Henry H Ooi, MBBCh   more...
 
Updated: Aug 25, 2011
 

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 alpha-receptor 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 beta2-receptor 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, 53.8-100%), 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, 0.34-0.78; 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 1986-1998, 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.

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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 low–risk patient groups. The 6-month mortality rate was 9.3% for not low–risk 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 low–risk group. A delay from symptom onset to treatment resulted in higher mortality rates for the not low–risk 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 1-year 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, 2.2-24.1%; 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.

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Consultations

Consultation with a cardiologist and/or an intensivist should be sought early in the patient's clinical course. The patient is usually admitted to a coronary care unit or intensive care unit. All patients with cardiogenic shock should be cared for in a facility at which right heart catheterization, coronary arteriography, and revascularization facilities are readily available.

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Contributor Information and Disclosures
Author

Andrew Lenneman, MD 

Disclosure: Nothing to disclose.

Coauthor(s)

Henry H Ooi, MBBCh  Director, Advanced Heart Failure and Cardiac Transplant Program, Nashville Veterans Affairs Medical Center; Assistant Professor of Medicine, Vanderbilt University School of Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Russell F Kelly  MD, Assistant Professor, Department of Internal Medicine, Rush Medical College; Chairman of Adult Cardiology and Director of the Fellowship Program, Cook County Hospital

Russell F Kelly is a member of the following medical societies: American College of Cardiology

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Ronald J Oudiz, MD, FACP, FACC, FCCP  Professor of Medicine, University of California, Los Angeles, David Geffen School of Medicine; Director, Liu Center for Pulmonary Hypertension, Division of Cardiology, LA Biomedical Research Institute at Harbor-UCLA Medical Center

Ronald J Oudiz, MD, FACP, FACC, FCCP is a member of the following medical societies: American College of Cardiology, American College of Chest Physicians, American College of Physicians, American Heart Association, and American Thoracic Society

Disclosure: Actelion Grant/research funds Clinical Trials + honoraria; Encysive Grant/research funds Clinical Trials + honoraria; Gilead Grant/research funds Clinical Trials + honoraria; Pfizer Grant/research funds Clinical Trials + honoraria; United Therapeutics Grant/research funds Clinical Trials + honoraria; Lilly Grant/research funds Clinical Trials + honoraria; LungRx Clinical Trials + honoraria; Bayer Grant/research funds Consulting

Amer Suleman, MD  Private Practice

Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

Chief Editor

Henry H Ooi, MBBCh  Director, Advanced Heart Failure and Cardiac Transplant Program, Nashville Veterans Affairs Medical Center; Assistant Professor of Medicine, Vanderbilt University School of Medicine

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of eMedicine gratefully acknowledge the contributions of previous authors Sat Sharma, MD, FRCPC, and Michael E Zevitz, MD, to the original writing and development of this article.

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  53. Wong SC, Sanborn T, Sleeper LA, et al. Angiographic findings and clinical correlates in patients with cardiogenic shock complicating acute myocardial infarction: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK?. J Am Coll Cardiol. Sep 2000;36(3 Suppl A):1077-83. [Medline].

 
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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.
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.
A coronary angiogram image of a patient with cardiogenic shock demonstrates severe 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.
Echocardiogram image from a patient with cardiogenic shock shows enlarged cardiac chambers; the motion study showed poor left ventricular function. Courtesy of R. Hoeschen, MD.
 
 
 
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