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Official reprint from UpToDate®

www.uptodate.com ©2013 UpToDate®

AuthorJudith S Hochman, MD

Section EditorsBernard J Gersh, MB, ChB, DPhil,FRCP, MACCJames Hoekstra, MD

Deputy EditorGordon M Saperia, MD, FACC

Prognosis and treatment of cardiogenic shock complicating acute myocardial infarction

Disclosures

All topics are updated as new evidence becomes available and our peer review process is complete.Literature review current through: Oct 2013. | This topic last updated: Sep 9, 2013.

INTRODUCTION — Cardiogenic shock (CS) is a clinical condition of inadequate tissue (end-organ) perfusion

due to cardiac dysfunction. The definition includes the following hemodynamic parameters: persistent

hypotension (systolic blood pressure <80 to 90 mmHg or mean arterial pressure 30 mmHg lower than baseline)

with severe reduction in the cardiac index (<1.8 L/ min per m2 without support or <2.0 to 2.2 L/min per m2 with

support) and adequate or elevated filling pressures [1]. Short-term prognosis is directly related to the severity of

the hemodynamic disorder.

The most common etiology of CS is an acute myocardial infarction (usually ST elevation myocardial infarction)

with left ventricular failure, but it can also be caused by mechanical complications, such as acute mitral

regurgitation or rupture of either the ventricular septal or free walls. However, any cause of acute, severe left or

right ventricular dysfunction may lead to CS.

The prognosis and therapy of CS complicating acute myocardial infarction (MI) will be reviewed here. The larger

discussion of the causes of CS, other presentations that mimic CS secondary to MI, as well as the clinical

manifestations and diagnosis of this disorder are discussed separately. (See "Clinical manifestations and

diagnosis of cardiogenic shock in acute myocardial infarction".)

PROGNOSIS

Temporal trends — The incidence of cardiogenic shock (CS) appears to be falling since the mid 1970s. In a

report from one United States metropolitan area (Worcester, Massachusetts), the incidence of CS was around 7

percent between 1975 and 1990 and has decreased to between 5.5 to 6.0 percent since then [2].

The historic mortality rate for CS complicating an acute myocardial infarction (MI) was 80 to 90 percent [3].

However, lower values for in-hospital mortality have been noted in more studies, ranging from 48 to 74 percent

[4-9]. Studies have suggested short-term mortality rates between 42 and 48 percent [2,9,10].

Two reports from the National Registry of Myocardial Infarction showed evidence of continued improvement in

mortality from CS between 1994 and 2004 [5]. Similar findings were noted in an analysis of over 23,000 acute

coronary syndrome patients in a Swiss registry (1997 to 2006) [11].

These improvements in the incidence of shock and the associated mortality in part reflect increased use of

coronary reperfusion strategies, particularly primary percutaneous coronary intervention, which, by restoring

patency to the infarct-related artery, can limit infarct size [5-7,12]. The time trend toward better outcomes may

also be attributable to improvements in the medical care of these patients. (See "Primary percutaneous

coronary intervention in acute ST elevation myocardial infarction: Determinants of outcome".)

Predictors of mortality — A number of studies have attempted to identify risk factors for mortality in CS. An

analysis from the GUSTO-I database identified the following predictors of 30-day survival for patients with CS

complicating an ST elevation myocardial infarction (STEMI) who receive initial fibrinolysis [13]:

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Increasing age (odds ratio 1.49 for each 10 year increase)

Prior MI

Physical findings at the time of diagnosis (the presence of altered sensorium and cold, clammy skin)

Oliguria

Hemodynamic parameters (including basic vital signs and measurements obtained from pulmonary artery

catheterization) also correlate with mortality in patients with CS. These parameters include mean arterial

pressure (MAP), systolic and diastolic blood pressure, cardiac output (CO), and cardiac index, with cardiac

power index (MAP x CO/451 x body surface area in m2) being the strongest hemodynamic predictor on

multivariate analysis [14].

STEMI versus NSTEMI — The mortality rate in patients in CS in GUSTO-IIb was similar in those with

STEMI or non-ST elevation acute coronary syndrome (ACS) [8]. Although CS was significantly less common

with non-ST elevation infarcts (2.5 versus 4.2 percent, odds ratio 0.58), patients with non-ST elevation acute

coronary syndromes were older and more likely to have three vessel disease and diabetes mellitus.

Coronary anatomy — Most patients with CS complicating an acute MI have severe and extensive coronary

disease. In the SHOCK trial registry, for example, 16 percent of those who underwent angiography had

significant left main disease and 53 percent had three vessel disease [15]. Mortality varied significantly with the

location of the culprit lesion and was noted to be higher in patients with a left main or saphenous vein graft

lesion than in those with circumflex, left anterior descending, or right coronary artery lesions (79 and 70 percent

versus 37 to 42 percent). Right coronary culprit lesions were associated with the best prognosis [16].

Echocardiographic predictors — In a substudy from the SHOCK trial, 169 patients had echocardiograms

[17]. The only independent echocardiographic predictors of outcome were left ventricular ejection fraction (LVEF)

and severity of mitral regurgitation (MR). For those with an LVEF <28 percent, survival at one year was 24

percent (versus 56 percent for those with a higher LVEF). For those with moderate or severe MR, survival at one

year was 31 percent (versus 58 percent for those with mild or no MR). However, there was benefit of early

revascularization at all levels of LVEF and MR grade. (See 'SHOCK trial' below.)

Symptom onset to reperfusion time — The time from symptom onset to reperfusion is an important

determinant of mortality in patients with STEMI who undergo primary PCI. An analysis of 80 such patients who

were in CS showed that in-hospital mortality was only 6.2 percent in patients reperfused within two hours of

symptom onset; this was more likely to occur in patients diagnosed with MI in the prehospital arena [18]. (See

"Primary percutaneous coronary intervention in acute ST elevation myocardial infarction: Determinants of

outcome".)

After successful reperfusion therapy — Early successful reperfusion therapy, particularly with percutaneous

coronary intervention, improves outcomes compared with conservative (medical) therapy. The magnitude of this

benefit is discussed below. (See 'Reperfusion' below.)

GENERAL MEASURES — Severe systemic hypoperfusion leads to hypoxemia and lactic acidosis, which can

cause further myocardial depression both directly and by decreasing the responsiveness to vasopressors such

as dopamine and norepinephrine. Thus, if possible, correction of these metabolic disturbances is important

(table 1). In addition, shock in the setting of myocardial infarction (MI) may be caused by factors not directly

related to the MI. These include hypovolemia, use of blood pressure lowering drugs, rate slowing drugs, and

other types of cardiovascular disease; they are discussed in greater detail elsewhere. (See "Clinical

manifestations and diagnosis of cardiogenic shock in acute myocardial infarction", section on 'Contributing

factors'.)

The following discussion is generally in accord with recommendations made in the 2004 American College of

Cardiology/American Heart Association (ACC/AHA) guidelines on the management of patients with ST elevation

myocardial infarction (STEMI), which were not changed in the 2007 Focused Update [19,20]. Similar principles

apply to patients with non-ST elevation myocardial infarction (NSTEMI) (table 2).

Medications — Aspirin, heparin, and vasopressors are frequently given in cardiogenic shock (CS), while certain

other medications should be avoided or used in reduced dose. Medications that have hepatic or renal clearance

should be used in reduced doses because of hypoperfusion of these organs. One important example is use of a

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lower dose of lidocaine, which is rarely given to treat ventricular arrhythmias.

Oral antiplatelet therapy — Both Aspirin and clopidogrel reduce mortality from acute MI [19]. (See

"Antiplatelet agents in acute ST elevation myocardial infarction" and "Antiplatelet agents in acute non-ST

elevation acute coronary syndromes".)

We recommend that all patients with CS complicating an acute MI receive aspirin even though its efficacy has

not been specifically studied in this setting. Alternative routes of administration for patients who are intubated

without a nasogastric tube include crushing a tablet for absorption through the buccal mucosa or administration

of a rectal suppository.

Clopidogrel should be deferred until after angiography, as many with MI and CS will require urgent coronary

artery bypass surgery. When clopidogrel is deferred, we suggest the use of glycoprotein (GP) IIb/IIIa inhibitors

as soon as possible after the decision has been made to proceed to angiography. (See 'GP IIb/IIIa inhibitors'

below.)

Heparin — Intravenous heparin infusion, especially in conjunction with reperfusion therapy, reduces

mortality in acute MI [19]. Even though heparin has not been evaluated in CS, there are compelling reasons that

full-dose intravenous heparin therapy should be given. Patients in shock are in a low flow state with high

fibrinogen concentrations. As a result, they are at risk for left ventricular and deep vein thrombosis. Heparin may

also maintain coronary artery patency. (See "Anticoagulant therapy in acute ST elevation myocardial infarction"

and "Anticoagulant therapy in non-ST elevation acute coronary syndromes".)

GP IIb/IIIa inhibitors — GP IIb/IIIa inhibitors improve the outcome of patients with non-ST elevation acute

coronary syndrome (ACS). (See "Antiplatelet agents in acute non-ST elevation acute coronary syndromes".)

The impact of eptifibatide on patients with CS was evaluated in a post-hoc subgroup analysis from the PURSUIT

trial [21]. Randomization to eptifibatide did not affect the incidence of shock. However, in patients who were

treated with eptifibatide and developed shock, compared to those receiving placebo, a significantly reduced

incidence of death at 30 days was noted (48 versus 58 percent in patients without an MI and 69 versus 85

percent in patients with an MI). A possible mechanism of benefit is relief of microvascular obstruction.

Another possible mechanism for benefit is the possible therapeutic effect of GP IIb/IIIa inhibitors in patients with

an STEMI and CS who undergo primary percutaneous coronary intervention (PCI). (See "Primary percutaneous

coronary intervention in acute ST elevation myocardial infarction: Determinants of outcome".)

Bivalirudin — Patients with CS have been excluded from pivotal trials that have examined the role of

bivalirudin. In a small single center experience, outcomes were similar in patients who received bivalirudin and

provisional GP IIb/IIIa inhibitor (n = 37) compared to patients (n = 49) treated with heparin and GP IIb/IIIa

inhibitors [22].

Beta blockers and other negative inotropes — Drugs that have negative inotropic activity should be

avoided in patients with CS or "pre-shock" in which the cardiac output is severely diminished but hypotension

has not yet developed. Included in this group are beta blockers and calcium channel blockers [19]. Evidence for

this recommendation comes from the COMMIT trial in which randomization to early beta blockade was

associated with a 30 percent higher occurrence of cardiogenic shock in patients over the age of 70, those with

systolic blood pressure (BP) <120 mm Hg or presenting heart rate greater than 110 beats per minute, and those

with Killip Class >1. In addition, antiarrhythmic drugs with negative inotropic or vasodilating properties, such as

lidocaine, procainamide, bretylium, and quinidine, should be used with caution. Amiodarone, although it has

beta blocking properties, is the preferred antiarrhythmic agent when one is required for sustained ventricular or

atrial tachyarrhythmias.

Vasopressors and inotropes — Prompt treatment of hypotension and hypoperfusion is essential to the

management of CS. Both pharmacologic and nonpharmacologic methods of circulatory support are employed to

reverse hypotension, maintain vital organ perfusion, and maintain coronary perfusion pressures as high as

possible. (See 'Mechanical support' below.)

Sympathomimetic inotropic and vasopressor agents remain the mainstay of first-line therapy [19] (see "Use of

vasopressors and inotropes"):

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Norepinephrine is a potent vasopressor with positive inotropic properties that may be used for rapid initial

circulatory support for CS. The minimum required dose should be used.

Dopamine in alpha-agonist doses (greater than 15 µg/kg per min). It also has positive inotropic effects,

which may be beneficial but produces an undesirable elevation in pulmonary capillary wedge pressure

(PCWP). The minimum required dose should be used.

While dopamine has often been chosen/recommended before norepinephrine, and the latter used when the

response to dopamine is inadequate, some evidence suggests that outcomes may be better with

norepinephrine. In a trial of 1679 patients with circulatory shock due to varying etiologies (septic, hypovolemic,

and CS) who were randomly assigned to initial therapy with either dopamine or norepinephrine, there was a

trend toward higher rate of death at 28 days with dopamine and there were significantly more arrhythmias,

predominantly atrial fibrillation. There was no difference in the treatment effect based on shock type, including in

the subset of 280 patients with cardiogenic shock [23].

There is insufficient evidence upon which a firm recommendation for the choice of the first vasopressor in

patients with cardiogenic shock can be made. Our experts suggest starting with norepinephrine, but emphasize

that efforts should be made to minimize both the number of agents and their dose. In some patients,

measurement of hemodynamic parameters such as cardiac output and arterial pressure (as well as the

calculation of systemic vascular resistance) may guide the choice of vasopressors and inotropes. However,

there is no evidence that titrating medications based on hemodynamics improves outcomes.

Unfortunately, increasing systemic vascular resistance (SVR) with vasopressors in patients who already have an

elevated SVR induced by endogenous norepinephrine and angiotensin II limits the improvement in cardiac

output, increases cardiac work, and raises the PCWP. As a result, mechanical support devices are preferred as

soon as they can be instituted.

A possible alternative is the administration of dobutamine or a phosphodiesterase inhibitor, such as milrinone,

which are inotropic agents that also produce vasodilation. However, these drugs do not reverse the hypotension

in post-MI shock, which, as noted above, is sometimes accompanied by vasodilation rather than

vasoconstriction.

Dobutamine should not be used as first-line single therapy when hypotension is present, but can be given to

less sick patients with a low cardiac index and high PCWP but no hypotension. An additive effect can be

achieved by combining moderate dose dobutamine with dopamine. Milder cases (ie, nonhypotensive patients in

low output state) can also be treated with dobutamine in combination with vasodilators (such as intravenous

nitroglycerin), which will further reduce both afterload and preload.

Phosphodiesterase inhibitors have not been studied in patients with an acute MI and CS and are not

recommended. The possible role of intravenous L-NMMA (tilarginine acetate), an inhibitor of nitric oxide

synthase that produces vasoconstriction, was evaluated in the TRIUMPH trial [10]. Enrollment was stopped

prematurely based upon a prespecified futility analysis. There was no statistically significant difference in all-

cause mortality at 30 days between treatment and placebo (48 and 42 percent, respectively) [10].

We generally begin therapy with a vasopressor (norepinephrine or dopamine) in hypotensive patients with

systemic hypoperfusion. The administration of dobutamine is limited to less sick patients with a low cardiac

index, high PCWP, and borderline blood pressure without frank hypotension. An additive effect can be achieved

by combining moderate dose dobutamine and norepinephrine or dopamine. Non-hypotensive patients in a low

output state can also be treated with dobutamine plus a vasodilator (intravenous nitroglycerin or nitroprusside).

This combination will further reduce both afterload and preload.

Differences compared to patients without shock — Based upon the discussion above, the following

summarizes potential differences in care compared to patients without CS:

In most cases, clopidogrel should be held until after angiography.

If used, lidocaine should be used in lower doses.

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Drugs with negative inotropic properties such as beta blockers and calcium channel blockers should be

avoided during the period of shock.

Hemodynamic monitoring — The insertion of a balloon-tipped pulmonary artery (Swan-Ganz) catheter and an

intraarterial blood pressure monitoring catheter are in general useful as part of the diagnostic evaluation of the

patient with CS. (See "Clinical manifestations and diagnosis of cardiogenic shock in acute myocardial

infarction", section on 'Hemodynamic monitoring'.)

Reperfusion therapy should not be delayed for the placement of a pulmonary artery catheter. Hemodynamic

monitoring is useful in patients with refractory shock despite revascularization.

Repeated determination of hemodynamics is in general useful to guide therapeutic intervention [19,24,25]:

Assessment of cardiac filling pressures so that hypovolemia and volume overload can be identified and

corrected. (See 'Volume management' below.)

Evaluation of the response of cardiac output to therapeutic interventions, including volume management,

sympathomimetics, and mechanical support.

Detection and quantification of intracardiac shunting in ventricular septal defect complicating acute MI.

(See "Mechanical complications of acute myocardial infarction", section on 'Rupture of the interventricular

septum'.)

Calculation of systemic vascular resistance and discrimination of vasoconstrictive from vasodilatory

shock. (See "Clinical manifestations and diagnosis of cardiogenic shock in acute myocardial infarction".)

Volume management — Hypovolemia may be present, particularly in the setting of diuretic use or vomiting.

Intravenous fluid replacement should be guided by measurement of the PCWP, arterial oxygen saturation

(SaO2), systemic arterial pressure, and cardiac output. (See 'Hemodynamic monitoring' above.) Each patient's

optimal PCWP is the lowest value that results in the highest cardiac output as long as the SaO2 is above 90

percent. The usual value in CS is between 18 and 25 mmHg [26].

An empiric intravenous volume challenge of 250 mL of isotonic saline can be given prior to right heart

catheterization in patients with suspected CS when there is no evidence of pulmonary congestion on physical

examination or chest x-ray and the patient is not in respiratory distress [19]. Overly vigorous fluid challenges in

patients with extensive left ventricular infarction, particularly older adults, will result in pulmonary edema and

should be avoided.

On the other hand, there are two settings in which more volume support is indicated: right ventricular shock due

to a right ventricular MI, in which high filling pressures are required to maximize flow to the left ventricle; and the

venodilation and hypotension that are common with inferior MI, but do not constitute a shock state. The

diagnosis of right ventricular MI is suspected in patients with inferior MI, clear lung fields, and shock. It can also

be confirmed by the use of right sided electrocardiogram (ECG) leads. In patients with presumed right ventricular

shock, vigorous intravenous (IV) fluid replacement is indicated if jugular (central) venous pressure is not

elevated. An early echocardiogram can be performed in this setting to guide clinical management. (See "Right

ventricular myocardial infarction".)

Patients with volume overload and cardiogenic pulmonary edema without hypotension may require therapy with

diuretics, morphine, supplemental oxygen, and vasodilators. The management of this complication is discussed

separately. (See "Treatment of acute decompensated heart failure: General considerations".)

Ventilatory support — Ventilatory support may be required for several reasons in patients with CS (see

"Overview of mechanical ventilation"):

To protect the airway and maintain oxygen supply in patients with a deterioration in consciousness or

cardiac arrest.

To treat acute respiratory failure, most often due to cardiogenic pulmonary edema. (See "Treatment of

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acute decompensated heart failure: General considerations".)

To raise the arterial pH in metabolic acidosis. (See "Bicarbonate therapy in lactic acidosis".)

The use of mechanical ventilation may increase the likelihood of successful weaning from intraaortic balloon

pump (IABP) support. This was suggested by a report of 28 patients with strictly defined CS receiving inotropic

medication and IABP counterpulsation; 10 patients were also supported with mechanical ventilation [27]. A

significantly larger proportion of ventilated patients were weaned from IABP (90 versus 44 percent) and

discharged from the hospital (80 versus 28 percent).

In selected patients who require mechanical ventilation, endotracheal intubation may not be necessary and a

trial of noninvasive positive pressure ventilation is warranted (table 3). This issue is discussed separately. (See

"Noninvasive positive pressure ventilation in acute respiratory failure in adults".)

Glucose control — The optimal blood glucose target in patients with MI, including those who are critically ill, is

unknown. The data addressing the issue of glucose targets during the acute phase of myocardial infarction,

including very ill patients, are presented separately. (See "Glycemic control for acute myocardial infarction in

patients with and without diabetes mellitus" and "Glycemic control and intensive insulin therapy in critical

illness".)

MECHANICAL SUPPORT

Intraaortic balloon pump — The available evidence does not support the routine use of an intraaortic balloon

pump (IABP)in most patients with acute myocardial infarction (MI) complicated by cardiogenic shock (CS) in

whom primary percutaneous coronary intervention (PCI) is attempted or performed or in whom fibrinolytic

therapy is administered. However, benefit may exist in patients with mechanical defects (such as mitral

regurgitation or a ventricular septal defect) and selected other patients who are rapidly deteriorating. (See

"Intraaortic balloon pump counterpulsation" and "Mechanical complications of acute myocardial infarction",

section on 'Rupture of the interventricular septum' and "Mechanical complications of acute myocardial

infarction", section on 'Acute mitral regurgitation'.)

The best evidence against the routine use of IABP for patient with MI comes from the IABP-SHOCK II trial in

which 600 patients with CS complicating acute MI (ST elevation myocardial infarction [STEMI] and non-ST

elevation myocardial infarction [NSTEMI]) were randomly assigned to the device or no device [28]. All patients

were expected to undergo early revascularization (predominantly with PCI) and to receive best available medical

care. At 30 days, there was no difference in the rate of all-cause mortality (39.7 versus 41.3 percent,

respectively; relative risk 0.96, 95% CI 0.79-1.17). There were no significant differences in secondary end points

such as length of stay in the intensive care unit, renal function, or the rates of major bleeding, peripheral

ischemic complications, sepsis, or stroke. These outcomes were similar at 12-month follow-up; for example,

there was no difference in the rate of all-cause death (52 versus 51 percent, respectively) [29].

One weakness of the study was a high rate of crossover of patients in the control group to IABP for reasons

other than the development of a mechanical complication (26 of 30 insertions were thought to be protocol

violations). However, a per protocol adjusted analysis that excluded patients who crossed over came to the

same conclusions. It is possible that rapidly deteriorating patients may not have been enrolled and if enrolled,

crossed over; the study cohort may represent those who stabilized on vasopressor/inotropic support. Thus, the

trial results may not apply to severe shock with rapid deterioration. Further data and longer follow-up is needed

to better understand subsets that may benefit from IABP.

Two earlier observational studies support the findings in IABP-SHOCK II.

The National Registry of Myocardial Infarction (NRMI) 2 found no reduction in in-hospital mortality

associated with the use of an IABP in patients undergoing primary percutaneous coronary intervention

(PCI) for CS (47 versus 42 percent without IABP) [30], although some benefit was found in hospitals with

a higher rate of IABP use [31]. (See "Intraaortic balloon pump counterpulsation".)

A 2009 meta-analysis of nine observational studies including over 10,000 patients with CS found no

significant benefit with IABP in the entire cohort, but a significant decrease in 30-day mortality in patients

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treated with fibrinolysis [32]. However, this meta-analysis is limited due to selection bias and the lack of

randomization of IABP in this setting. (See 'Use with fibrinolysis' below.)

For those patients with CS undergoing PCI in whom an IABP is chosen, the optimal timing of placement is

unknown as the observational evidence is conflicting. In IABP SHOCK II, there was no difference in outcomes

between those who received an IABP before or after PCI. In a study of 48 patients with MI and CS, a

significantly lower in-hospital mortality at 30 days (19 versus 69 percent) was found in those who received the

IABP before as opposed to after PCI [33]. However, an earlier analysis from the SHOCK trial registry suggested

that the mortality was similar whether IABP was placed before or after PCI [34].

Use with fibrinolysis — The role of IABP in MI patients treated with fibrinolytic therapy who will be

transferred for possible revascularization is not well established, as there is little evidence that can be used to

guide the formation of recommendations. (See "Management of failed fibrinolysis (thrombolysis) or threatened

reocclusion in acute ST elevation myocardial infarction", section on 'Primary failure'.)

Animal studies have suggested that the rate of clot dissolution with fibrinolysis in CS can be restored to normal

levels if the blood pressure is raised by aggressive use of vasopressors [35] or insertion of an IABP (figure 1)

[36]. There are no randomized clinical data demonstrating the efficacy and safety of combined IABP and

fibrinolysis in CS complicating MI. However, there is some evidence suggesting efficacy.

The National Registry of Myocardial Infarction 2 evaluated 23,180 patients who had CS during hospitalization; an

IABP, which was used in 31 percent of patients, was associated with a significantly lower in-hospital mortality in

those who received fibrinolytic therapy (49 versus 67 percent without IABP) [30]. A similar benefit from IABP

combined with fibrinolytic therapy was noted in the SHOCK trial registry [34] and the GUSTO-1 trial [37]. The

potential for bias in these studies is great.

Few MI patients with CS will present to hospitals where fibrinolysis will be administered instead of

revascularization but where an IABP is available. For these uncommon patients whose hemodynamic

parameters and clinical status are rapidly deteriorating while on vasopressor and inotropic support and who will

be transferred for cardiac catheterization, our authors and reviewers have differing approaches, with some

recommending placement of an IABP and others not. The decision to place an IABP or not should be made in

consultation with physicians at the receiving cardiac catheterization laboratory. The decision should be included

by the expertise of the team placing the IABP, potential delays in transfer, and patient-related factors such as

risk of bleeding and quality of vascular access.

Other mechanical devices — Other circulatory support devices are sometimes used or are being investigated

in patients with CS. (See "Circulatory assist devices: Cardiopulmonary assist device and short-term left

ventricular assist devices", section on 'Short-term VAD'.)

These include:

Left ventricular and biventricular assist devices. In the setting of CS, these surgically placed devices are

usually placed as a bridge to transplantation in eligible patients in whom ventricular function is not

expected to recover.

Percutaneous left atrial-to-femoral arterial ventricular assist device. This device (Tandem Heart) is placed

via the femoral vein and across the interatrial septum to provide temporary circulatory support while

performing high-risk PCI or awaiting ventricular recovery.

Percutaneous cardiopulmonary bypass support with use of an extracorporeal membrane oxygenator is

utilized when oxygenation is severely impaired.

Percutaneous transvalvular left ventricular assist device (LVAD). This device (Impella LP 2.5) is placed via

the femoral artery, retrograde across the aortic valve into the left ventricle. It has a microaxial pump that

decompresses the left ventricle and delivers a maximum flow of 2.5 L/min into the ascending aorta. In a

multicenter observational registry of 120 patients with CS after acute myocardial infarction who received

the Impella-2.5 device following initial IABP support, 30-day mortality was 64.2 percent [38]. Without a

compactor group, we do not know how this would compare to no device or to other devices.

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Two small, randomized trials have compared a percutaneous LVAD to an IABP in patients with CS after an

acute MI:

The first study compared the LVAD (Tandem Heart) in 41 patients [39]. Although hemodynamic and

metabolic parameters were more effectively reversed with the LVAD, complications such as severe

bleeding and limb ischemia were more common. The mortality rates were similar, but this study was not

powered to assess mortality.

In the second study, 25 patients were randomly assigned to LVAD (Impella) or an IABP [40]. The LVAD

was placed safely in all assigned patients and significantly improved hemodynamic parameters, such as

cardiac index at 30 minutes to a greater extent than IABP (0.5 versus 0.1 L/min/m2). Important outcomes

such as death could not be meaningfully assessed due to the small sample size, but as noted above for

the Tandem Heart study, mortality rates were similar for the two groups.

The efficacy of these devices is discussed in detail elsewhere. (See "Circulatory assist devices:

Cardiopulmonary assist device and short-term left ventricular assist devices".)

Recommendations of others — We agree with the 2004 American College of Cardiology/American Heart

Association (ACC/AHA) guidelines on STEMI, which recommended an IABP as a stabilizing measure in an

acute MI in patients with CS that is not quickly reversed with pharmacologic therapy (table 2 and table 4) [41].

No changes to this approach were made in the 2007 focused update [42]. The 2008 European Society of

Cardiology task force on the management of ST-segment elevation acute myocardial infarction made similar

recommendations [43]. The use of an IABP, in addition to assisting hemodynamic management, is an important

measure to stabilize the patient to permit angiography and revascularization.

Primary PCI in patients in CS should be performed with IABP support, and many feel strongly that this support

should be instituted prior to the first coronary angiographic dye injection (table 4). This regimen might allow the

patient to tolerate the procedure better and has documented efficacy for reducing acute closure after PCI. Other

experts recommend opening the culprit artery as soon as possible, and then placing an IABP.

REPERFUSION — As mentioned above, there is evidence that the high mortality associated with CS has

improved over time [5,7,9,44]. This benefit is thought to be predominantly due to increased use of coronary

reperfusion strategies, which, by restoring patency to the infarct-related artery, can limit infarct size, as well as

interrupt the vicious spiral that characterizes cardiogenic shock (CS) [5-7,12]. (See "Clinical manifestations and

diagnosis of cardiogenic shock in acute myocardial infarction", section on 'Pathophysiology'.)

Most of the evidence of benefit for early reperfusion therapy has come from observations of patients with ST

elevation myocardial infarction (STEMI). However, in patients without shock, reperfusion with fibrinolytic therapy

has not been shown to be of benefit in patients with non-ST elevation myocardial infarction (NSTEMI). Therefore,

most of the discussion below is directed at patients with STEMI; for those patients in whom a diagnosis of

NSTEMI with CS is made, we believe that early reperfusion with revascularization (percutaneous coronary

intervention [PCI] or coronary artery bypass graft surgery [CABG]) is useful.

Observational data suggest that an open infarct-related artery in patients with CS complicating an acute MI

correlates strongly with in-hospital survival. In a report of 200 patients from Duke, for example, the in-hospital

mortality was much lower in patients with a patent compared to a closed infarct-related artery (33 versus 75

percent); this relationship was independent of how patency was achieved (eg, spontaneous or pharmacologic

fibrinolysis or mechanical intervention) [45]. Similar findings were noted in the SHOCK trial registry [15]. In-

hospital mortality was lower in patients with TIMI grade 3 (normal) flow (26 versus 47 percent with TIMI grade 0/1

[no or faint flow]).

Coronary reperfusion can be achieved with fibrinolysis (in patients with STEMI), PCI, or emergency CABG.

Outcomes are better when successful reperfusion can be delivered early in the course of MI.

We support the approach to reperfusion recommended in the 2004 American College of Cardiology/American

Heart Association (ACC/AHA) guidelines for the management of patients with ST-elevation myocardial infarction

(which was not changed in the 2007 update) [46]. This approach was refined in a 2008 publication and is

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presented in algorithmic form [1].

Fibrinolysis — There are limited randomized data assessing the efficacy of fibrinolysis compared to either

placebo or PCI in patients who have CS at presentation. The available studies have demonstrated some benefit

of fibrinolysis compared to placebo, but superiority of PCI or CABG compared to fibrinolysis. Fibrinolysis is

recommended if PCI is not possible or if it is delayed. (See "Fibrinolytic therapy in acute ST elevation

myocardial infarction: Initiation of therapy".)

The 1994 meta-analysis from the Fibrinolytic Therapy Trialists' (FTT) Collaborative Group found that, among

patients with a systolic blood pressure <100 mmHg and a heart rate >100 beats per minute, fibrinolysis was

associated with a 7 percent absolute reduction in mortality at one month compared to control (54 versus 61

percent) [47]. The apparently limited efficacy of fibrinolysis may have reflected failure to augment coronary

perfusion pressure during administration of the fibrinolytic agent. In animal studies, the rate of dissolution of a

coronary artery thrombus by fibrinolytic therapy is markedly depressed when hypotension is present [35,36].

In a post-hoc analysis of the SHOCK trial, the use of fibrinolytic therapy was associated with a significant

reduction in mortality at 12 months (60 versus 78 percent without fibrinolysis) in the group assigned to medical

therapy [48].

Based upon the apparent benefit in those who did not receive immediate revascularization and the absence of

adverse effects in those who underwent invasive procedures, fibrinolytic therapy should be given to patients who

present to a facility without primary PCI or timely transfer for primary PCI capability, particularly those who

present within three hours of symptoms. (See "Selecting a reperfusion strategy for acute ST elevation

myocardial infarction" and 'Use with fibrinolysis' above.)

Choice of agent — There are limited data, derived only from subset analyses of major fibrinolytic therapy

trials, evaluating the comparative efficacy of different fibrinolytic agents. There is no evidence to suggest greater

benefit of one agent compared with another [6,49]. Thus, the choice of agent should probably not be different

from patients without CS (table 5). (See "Characteristics of fibrinolytic (thrombolytic) agents and clinical trials in

acute ST elevation myocardial infarction".).

Late shock — The preceding observations on fibrinolysis were primarily made in patients who had CS at or

soon after presentation. However, the majority of patients develop shock after initial emergency department

presentation [6,8,21,41,50]. Such patients have a somewhat lower in-hospital mortality than those in CS on

admission [41,50]. (See "Clinical manifestations and diagnosis of cardiogenic shock in acute myocardial

infarction", section on 'Time of onset'.)

The only role for fibrinolysis administered more than 12 to 24 hours after onset of an MI is if the development of

late shock is thought to be due to recurrent coronary artery occlusion and if urgent angiography and

revascularization cannot be performed; prompt transfer to a tertiary center with revascularization facilities should

be arranged for patients in whom late shock is thought to be due to recurrent coronary artery occlusion, unless

impossible.

Primary PCI — Primary percutaneous coronary intervention (PCI) is preferred to fibrinolysis for CS complicating

acute MI [42,51-55]. PCI is usually performed only on the infarct-related artery; however, some patients have

undergone multivessel intervention [56]. The decision should be guided by the clinical profile of the patient,

anatomic characteristics, operator experience, lack of response to PCI of the infarct-related artery, and

documentation of hypokinesis in the remote zones.

Initial experience with coronary intervention in CS was obtained in studies of the benefits of early angiography

following fibrinolysis. Nonrandomized [53] and randomized trials [54] have shown benefit.

SHOCK trial — The benefits of early revascularization in patients with CS were confirmed in the SHOCK

trial, a randomized comparison of emergency revascularization versus a strategy of initial medical stabilization

including fibrinolysis and intraaortic balloon pump (IABP) in patients with an ST elevation MI (or new left bundle

branch block) and CS.

The SHOCK trial included 302 patients with confirmed CS developing within 36 hours of an acute MI [54]. The

patients were randomly assigned within 12 hours of the diagnosis of shock to emergency revascularization

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(CABG in 40 percent and PCI in 60 percent) within six hours of randomization or to initial medical stabilization.

Almost half of the patients assigned to emergency revascularization had had prior fibrinolysis, and therefore

underwent rescue PCI or CABG; 63 percent of patients in the medical arm also received fibrinolytic therapy.

Late revascularization was performed in 25 percent of patients in the medical stabilization arm at a minimum of

54 hours after randomization at the discretion of the local physician. Intraaortic balloon counterpulsation was

utilized in 86 percent of patients in both groups.

At 30 days, there was an insignificant 9 percent absolute difference in total mortality (primary end point)

between the two treatment groups (47 versus 56 percent with initial medical therapy with fibrinolysis); the lack of

significance could represent beta error since the trial was underpowered to detect such a difference. The benefit

increased over time and became significant at six months. (See 'Long-term outcome' below.)

Patients in CS on admission have a higher in-hospital mortality than the majority of patients who develop shock

after hospitalization [41,50]. However, in the SHOCK trial and registry, patients in shock on admission derived

the same in-hospital mortality benefit from emergency revascularization (60 versus 82 percent) as those who

developed shock later (46 versus 62 percent) [41]. (See 'Late shock' above.)

Determinants of outcome — The clinical response to primary PCI is highly variable. While some patients

improve rapidly after PCI, others show no immediate hemodynamic improvement, and a few transiently

deteriorate after reperfusion is established, particularly if there is late reperfusion. This is also true for late

reperfusion with fibrinolysis. Concurrent use of an IABP protects against sudden hemodynamic deterioration.

(See 'Intraaortic balloon pump' above.)

Data from the nonrandomized SHOCK trial registry suggest that the in-hospital mortality after PCI is related to

the degree of reperfusion achieved in the infarct related artery [57]. Among 276 patients undergoing PCI, the

mortality for TIMI grade 3 (normal), grade 2, or grade 0/1 flow was 33, 50, and 86 percent, respectively. A similar

relationship to TIMI flow grade was noted in a report from the ALKK primary PCI registry in Germany (37, 66,

and 78 percent in-hospital mortality, respectively) [44]. (See "Fibrinolytic (thrombolytic) agents in acute ST

elevation myocardial infarction: Markers of efficacy", section on 'TIMI flow grade'.)

The time from symptom onset to PCI may be another determinant of outcome. In the ALKK report, the in-

hospital mortality was 44 percent in patients receiving primary and rescue PCI as well as urgent CABG within

three hours from symptom onset, 45 percent from three to six hours, 54 percent from 6 to 12 hours, and 58

percent from 12 to 24 hours [44]. However, the benefits of primary PCI were seen in both early and late

presenters in the SHOCK trial [54]. As a result, late presenters should not be denied emergency

revascularization based upon timing alone. (See 'SHOCK trial' above.)

In a prespecified subset analysis of the SHOCK trial, the benefit of revascularization on survival was limited to

patients <75 years old, but there were too few elderly patients in this subgroup to be confident of the observation

[55]. Subsequent studies, including the SHOCK registry, have found the same magnitude of benefit in patients

≥75 years old [58,59]. At present, no firm conclusion regarding the magnitude of benefit (or harm) can be made

in older patients.

Use in left main stenosis — In the SHOCK trial registry, 16 percent of patients with CS had significant left

main disease (although not necessarily left main occlusion) [15]. Although emergent CABG is a

revascularization option, it appears to be seldom utilized in contemporary clinical practice [9].

Potential efficacy of PCI in patients with CS and left main disease was suggested in an observational registry of

unprotected left main stenosis; 40 patients with an acute MI (37 of whom had CS) underwent emergency PCI

(17 with stenting) [60]. The rate of in-hospital death (35 versus 70 percent) was lower in those who received a

stent compared to primary balloon angioplasty alone. Stenting was also associated with a higher survival rate at

12 months (53 versus 35 percent). A much higher in-hospital mortality rate of 81 percent was noted after primary

PCI among 80 patients with a left main stem infarct-related artery in the ALKK primary PCI registry in Germany

[44]. (See "Management of left main coronary artery disease".)

Coronary artery bypass surgery — The majority of patients with CS after MI have significant left main or three

vessel disease (16 and 53 percent, respectively, in the SHOCK trial registry) [15]. In such patients, the ability to

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achieve complete revascularization makes CABG a potentially critical therapeutic strategy. A surgical approach

also permits the correction of concomitant severe mitral regurgitation, which is often present. Pooled data on

370 patients in 22 studies revealed an in-hospital mortality rate of 36 percent when CABG was performed during

the hospitalization for acute MI with CS [51]. (See "Coronary artery bypass graft surgery after acute ST elevation

myocardial infarction", section on 'Cardiogenic shock'.)

The relatively low mortality rate in these nonrandomized series may reflect a true benefit or selection bias, in

which patients at lowest risk are selected for CABG. However, similar findings (41 percent overall mortality) were

noted in the patients who underwent emergency CABG in the SHOCK trial within six hours of randomization

[54]. Despite this benefit, CABG is underutilized in the community setting. In a review from the National Registry

of Myocardial Infarction of 25,311 patients with CS seen from 1995 to 2004 in the United States, the overall rate

of immediate CABG was stable at about 3 percent [9].

PCI versus CABG — The relative efficacy of PCI and CABG was evaluated in the 128 patients with

predominant left ventricular failure who underwent emergency revascularization in the SHOCK trial [61]. Not

surprisingly, the 47 patients (37 percent) who underwent CABG were significantly more likely to have diabetes

and three-vessel or left main disease; 85 percent of these patients received two or more grafts and 52 percent

received three or more grafts. Despite the more extensive disease in the CABG group, overall survival was

similar to PCI at 30 days (57 versus 56 percent with PCI) and one year (47 versus 52 percent). The similar

outcomes, despite the worse disease in patients undergoing CABG, may reflect in part the higher rate of

complete revascularization (87 versus 23 percent with PCI).

In clinical practice, a combination of these two revascularization strategies is often indicated. This may involve

emergent percutaneous recanalization of the infarct related artery in the catheterization laboratory followed by

emergent/urgent revascularization with CABG.

Population-based studies — Observations from population-based studies suggest that the results of the

SHOCK trial itself can be applied to clinical practice. As an example, similar 30-day survival benefits with early

revascularization were noted in the larger nonrandomized SHOCK trial registry [59,62]. The outcome with

revascularization was the same in men and women [63]. (See "Management of coronary heart disease in

women".)

Observations were comparable in the review cited above from the National Registry of Myocardial Infarction

(NRMI) of 25,311 patients with CS seen between 1995 and 2004 [9].

Long-term outcome — In addition to the short-term benefits, follow-up reports from the SHOCK trial

demonstrated that the benefit of revascularization persists for many years. At one year, early revascularization

was associated with a lower mortality rate (eg, 53 versus 66 percent) [55]. In addition, the patients who were

assigned to emergency revascularization were significantly more likely to remain stable after discharge (71

versus 44 percent at one year) and less likely to worsen or die after 30 days (15 versus 34 percent) [64].

The mortality benefit persisted at six years (67 versus 80 percent with medical stabilization) (figure 2) [65]. The

previously observed significant interaction between age and treatment effect was no longer evident on long-term

follow-up.

Evidence of long-term benefit was also suggested in a subset analysis from the GUSTO-I trial of over 39,000

patients who were alive at 30 days after an acute MI, 1306 of whom had been in CS [66]. Revascularization

within 30 days was performed in 44 percent of the patients with CS; the one-year mortality in these patients was

significantly lower than in those who were not revascularized (8 versus 15 percent, odds ratio 0.6 after adjusting

for differences in baseline characteristics). Not surprisingly, the survivors of CS had higher one-year mortality

than those without shock (12 versus 3 percent).

Major society guidelines — The ACC/AHA guidelines for the management of patients with STEMI recommend

primary PCI or emergent CABG in patients less than 75 years of age with an STEMI or MI with new or

presumably new left bundle branch block who develop shock within 36 hours of MI, can be treated within 18

hours of the onset of shock, and are suitable for revascularization [19,20,67]. It is considered reasonable to

perform primary PCI or emergent CABG in selected patients ≥75 years of age who meet the same criteria and

are suitable for revascularization.

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Fibrinolytic therapy (in the absence of contraindications) is given a strong recommendation in the ACC/AHA

guidelines for patients who are unsuitable for invasive therapy (because of age, comorbidities, or personal

preference) [19]. (See 'Fibrinolysis' above.)

Summary — The optimal strategy for the management of CS is characterized by an early revascularization

strategy with adjunctive IABP support. Our approach is as follows:

Revascularization with either PCI or CABG is preferred to fibrinolytic therapy, if it can be performed in a

timely manner (within 90 minutes from initial hospital presentation for PCI). This is consistent with the

management of patients without CS. (See "Selecting a reperfusion strategy for acute ST elevation

myocardial infarction", section on 'Summary and recommendations'.)

Primary PCI is preferred to CABG for patients with one- or two-vessel coronary disease and technically

suitable lesions [68]. Immediate CABG may be considered for left main or severe three-vessel disease. If

CABG cannot be performed, single-vessel or multivessel PCI may be attempted. CABG is the treatment

of choice if there are associated mechanical complications.

We suggest the prompt administration of fibrinolytic therapy if the PCI related delay is anticipated to

exceed 60 minutes and/or the door-to-balloon time is anticipated to exceed 90 minutes. In addition, we

suggest fibrinolytic therapy for patients who are unsuitable for invasive therapy (because of age,

comorbidities, or personal preference). This approach was given a class I recommendation in the

ACC/AHA guidelines [19]. (See 'Fibrinolysis' above.)

For patients who appear to have successfully reperfused with fibrinolytic therapy and who no longer

manifest CS, we suggest not taking the patient to the catheterization laboratory urgently, based on the

evidence of harm with PCI soon after fibrinolysis. (See "Percutaneous coronary intervention after

fibrinolysis for acute ST elevation myocardial infarction", section on 'Facilitated PCI'.)

When fibrinolytic agents are given, they should be combined with vigorous vasopressor use and IABP

(inserted cautiously to reduce the risk of bleeding) in an attempt to normalize coronary perfusion

pressure. As mentioned above, fibrinolysis is relatively ineffective when administered to hypotensive

patients (figure 1).

Patients admitted to hospitals without facilities for revascularization should be immediately transferred to

a tertiary care center with such facilities [19]. Such patients can be treated with insertion of an IABP (if

available) if there is a delay in transfer or the tertiary care center is far away. If there is an anticipated very

long delay in transport for cardiac catheterization AND the risks of fibrinolysis are low AND the duration

of MI symptoms is <3 hours, we recommend rapid initiation of fibrinolytic therapy (<30 minutes) prior to

transfer.

Patients who survive initial therapy that does not include emergency PCI or CABG should be referred for

coronary angiography and potential revascularization [19]. This recommendation is based upon the high

prevalence of a low left ventricular ejection fraction and three vessel or left main disease [15], settings in

which revascularization is associated with a long-term reduction in mortality.

SUMMARY AND RECOMMENDATIONS — Mortality in patients with cardiogenic shock (CS) complicating

myocardial infarction (MI) approaches 50 percent, despite advances in therapeutic interventions such as the

early use of percutaneous coronary intervention and improvements in medical care, particularly aggressive

antithrombotic therapy. (See 'Prognosis' above.)

This high mortality can be lowered with further improvements in the speed with which reperfusion is delivered,

and vigilant observation of those hospitalized patients with MI at risk. (See "Clinical manifestations and

diagnosis of cardiogenic shock in acute myocardial infarction", section on 'Risk factors'.)

The following is a summary of our approach to the treatment of patients with CS.

Diagnostic testing — An emergency echocardiogram should be performed to determine the etiology of shock

in the absence of a large MI [19]. Echocardiography can be useful to estimate left atrial pressure as well as to

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identify the etiology of shock. (See "Clinical manifestations and diagnosis of cardiogenic shock in acute

myocardial infarction", section on 'Echocardiography'.)

Hemodynamic monitoring, including pulmonary artery catheterization, may be useful to guide optimal medical

management, particularly when the diagnosis is in doubt. Monitoring is also useful in distinguishing

vasoconstrictive from vasodilatory shock. However, placement of a pulmonary artery catheter should not delay

transferring the patient to the catheterization laboratory. (See 'Hemodynamic monitoring' above and "Clinical

manifestations and diagnosis of cardiogenic shock in acute myocardial infarction".)

Medical management — Initial therapy of CS consists of early identification, optimally before frank

hypotension is present, and rapid stabilization with correction of metabolic abnormalities.

Antiplatelet agents — The recommendations for the use of antiplatelet agents in patients with MI are given

separately. (See "Antiplatelet agents in acute ST elevation myocardial infarction", section on 'Summary and

recommendations' and "Antiplatelet agents in acute non-ST elevation acute coronary syndromes", section on

'Summary and recommendations'.)

In patients with CS in whom revascularization is planned, we recommend not giving a thienopyridine until after

diagnostic coronary angiography (and percutaneous coronary intervention [PCI] is to be performed) and adding a

glycoprotein (GP) IIb/IIIa inhibitor to heparin as early as possible after diagnosis (Grade 1B). This

recommendation is based upon the fact that a higher percentage of patients with CS complicating MI will require

coronary artery bypass graft surgery (CABG) compared to those without and the potential benefits for GP IIb/IIIa

agents with PCI in the highest risk subsets. (See 'Oral antiplatelet therapy' above.)

Beta blockers — We recommend withholding beta blockers and calcium channel blockers in patients with

CS (Grade 1B). (See 'Beta blockers and other negative inotropes' above.)

Vasopressors — We recommend vasopressors for patients with cardiogenic shock (Grade 1B). Although

there is no definitive evidence of the superiority of one vasopressor over another, we suggest beginning with

norepinephrine (Grade 2B). (See 'Vasopressors and inotropes' above.)

IABP — Our recommendations for the use of an intraaortic balloon pump (IABP) in patients with acute MI and

cardiogenic shock are as follows (see 'Intraaortic balloon pump' above):

For patients in whom mechanical complications (eg, acute mitral regurgitation or rupture of the ventricular

septum) are not present and for whom revascularization is planned, we suggest not placing an IABP as a

routine strategy (Grade 2B).

However, for such patients whose hemodynamic parameters and clinical status are rapidly deteriorating

while on vasopressor and inotropic support, we suggest placement of an IABP (Grade 2C). Deterioration

is considered present when the systolic blood pressure is persistently below 80 mmHg, there is a fall

urine output or a worsening of mentation, the arterial oxygen saturation is falling, or cardiac arrhythmias

(including heart block or ventricular tachycardia or fibrillation) develop or worsen.

The role of IABP is not well studied in the uncommon patient treated with fibrinolytic therapy whose

hemodynamic parameters and clinical status are rapidly deteriorating while on vasopressor and inotropic

support and for whom transfer to a facility capable of performing urgent revascularization is planned. Our

authors and reviewers have differing approaches, with some recommending placement of an IABP before

transfer and other not. (See 'Use with fibrinolysis' above.)

Reperfusion — All patients with CS complicating MI should undergo an attempt at reperfusion. (See

'Reperfusion' above.)

Our recommendations for the use of reperfusion therapy in patients with MI complicated by CS are similar to

those for most patients with MI and differ principally in the level of evidence (see "Selecting a reperfusion

strategy for acute ST elevation myocardial infarction", section on 'Summary and recommendations'):

For patients with ST elevation MI, we recommend revascularization as opposed to fibrinolytic therapy

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(Grade 1A). This recommendation requires that diagnostic coronary angiography be performed within 90

minutes of initial hospital presentation. For those patients who cannot undergo timely coronary

angiography, we recommend fibrinolytic therapy rather than no immediate reperfusion (Grade 1B).

For patients with one or two vessel disease who do not have mechanical complications, we recommend

percutaneous coronary intervention (PCI) of the infarct related artery as opposed to CABG (Grade 1B).

For patients with three vessel disease or left main disease who do not have mechanical complications

(such as acute mitral regurgitation or rupture of either the ventricular septal or free walls), we suggest

immediate PCI as opposed to CABG (Grade 2C). In many cases it may be appropriate to prefer CABG

based on factors such as the likelihood of successful revascularization with PCI, the extent of disease,

the skill level/experience of the PCI team, or the availability of immediate CABG.

For patients with mechanical complications, we recommended immediate CABG and attempt at repair of

the mechanical defect as opposed to PCI (Grade 1B).

For patients with non-ST elevation MI, we recommend that revascularization be performed as soon as

possible as opposed to either fibrinolytic therapy or no reperfusion (Grade 1B).

ACKNOWLEDGMENT — The UpToDate editorial staff would like to thank Dr. Venu Menon for his contributions

as an author to previous versions of this topic review.

Use of UpToDate is subject to the Subscription and License Agreement.

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30:459.

33. Abdel-Wahab M, Saad M, Kynast J, et al. Comparison of hospital mortality with intra-aortic ballooncounterpulsation insertion before versus after primary percutaneous coronary intervention for cardiogenicshock complicating acute myocardial infarction. Am J Cardiol 2010; 105:967.

34. Sanborn TA, Sleeper LA, Bates ER, et al. Impact of thrombolysis, intra-aortic balloon pumpcounterpulsation, and their combination in cardiogenic shock complicating acute myocardial infarction: areport from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries forcardiogenic shocK? J Am Coll Cardiol 2000; 36:1123.

35. Prewitt RM, Gu S, Garber PJ, Ducas J. Marked systemic hypotension depresses coronary thrombolysisinduced by intracoronary administration of recombinant tissue-type plasminogen activator. J Am CollCardiol 1992; 20:1626.

36. Prewitt RM, Gu S, Schick U, Ducas J. Intraaortic balloon counterpulsation enhances coronarythrombolysis induced by intravenous administration of a thrombolytic agent. J Am Coll Cardiol 1994;23:794.

37. Anderson RD, Ohman EM, Holmes DR Jr, et al. Use of intraaortic balloon counterpulsation in patientspresenting with cardiogenic shock: observations from the GUSTO-I Study. Global Utilization ofStreptokinase and TPA for Occluded Coronary Arteries. J Am Coll Cardiol 1997; 30:708.

38. Lauten A, Engström AE, Jung C, et al. Percutaneous left-ventricular support with the Impella-2.5-assistdevice in acute cardiogenic shock: results of the Impella-EUROSHOCK-registry. Circ Heart Fail 2013;6:23.

39. Thiele H, Sick P, Boudriot E, et al. Randomized comparison of intra-aortic balloon support with apercutaneous left ventricular assist device in patients with revascularized acute myocardial infarctioncomplicated by cardiogenic shock. Eur Heart J 2005; 26:1276.

40. Seyfarth M, Sibbing D, Bauer I, et al. A randomized clinical trial to evaluate the safety and efficacy of apercutaneous left ventricular assist device versus intra-aortic balloon pumping for treatment of cardiogenicshock caused by myocardial infarction. J Am Coll Cardiol 2008; 52:1584.

41. Jeger RV, Harkness SM, Ramanathan K, et al. Emergency revascularization in patients with cardiogenicshock on admission: a report from the SHOCK trial and registry. Eur Heart J 2006; 27:664.

42. O'Neill WW. Angioplasty therapy of cardiogenic shock: are randomized trials necessary? J Am CollCardiol 1992; 19:915.

43. Van de Werf F, Bax J, Betriu A, et al. Management of acute myocardial infarction in patients presentingwith persistent ST-segment elevation: the Task Force on the Management of ST-Segment Elevation AcuteMyocardial Infarction of the European Society of Cardiology. Eur Heart J 2008; 29:2909.

44. Zeymer U, Vogt A, Zahn R, et al. Predictors of in-hospital mortality in 1333 patients with acute myocardialinfarction complicated by cardiogenic shock treated with primary percutaneous coronary intervention(PCI); Results of the primary PCI registry of the Arbeitsgemeinschaft Leitende KardiologischeKrankenhausärzte (ALKK). Eur Heart J 2004; 25:322.

45. Bengtson JR, Kaplan AJ, Pieper KS, et al. Prognosis in cardiogenic shock after acute myocardialinfarction in the interventional era. J Am Coll Cardiol 1992; 20:1482.

46. Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA guidelines for the management of patients withST-elevation myocardial infarction--executive summary: a report of the American College ofCardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revisethe 1999 Guidelines for the Management of Patients With Acute Myocardial Infarction). Circulation 2004;110:588.

47. Indications for fibrinolytic therapy in suspected acute myocardial infarction: collaborative overview of earlymortality and major morbidity results from all randomised trials of more than 1000 patients. FibrinolyticTherapy Trialists' (FTT) Collaborative Group. Lancet 1994; 343:311.

48. French JK, Feldman HA, Assmann SF, et al. Influence of thrombolytic therapy, with or without intra-aorticballoon counterpulsation, on 12-month survival in the SHOCK trial. Am Heart J 2003; 146:804.

49. Hasdai D, Holmes DR Jr, Topol EJ, et al. Frequency and clinical outcome of cardiogenic shock duringacute myocardial infarction among patients receiving reteplase or alteplase. Results from GUSTO-III.Global Use of Strategies to Open Occluded Coronary Arteries. Eur Heart J 1999; 20:128.

50. Webb JG, Sleeper LA, Buller CE, et al. Implications of the timing of onset of cardiogenic shock afteracute myocardial infarction: a report from the SHOCK Trial Registry. SHould we emergently revascularize

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Occluded Coronaries for cardiogenic shocK? J Am Coll Cardiol 2000; 36:1084.

51. Bates ER, Topol EJ. Limitations of thrombolytic therapy for acute myocardial infarction complicated bycongestive heart failure and cardiogenic shock. J Am Coll Cardiol 1991; 18:1077.

52. Antoniucci D, Valenti R, Santoro GM, et al. Systematic direct angioplasty and stent-supported directangioplasty therapy for cardiogenic shock complicating acute myocardial infarction: in-hospital and long-term survival. J Am Coll Cardiol 1998; 31:294.

53. Berger PB, Holmes DR Jr, Stebbins AL, et al. Impact of an aggressive invasive catheterization andrevascularization strategy on mortality in patients with cardiogenic shock in the Global Utilization ofStreptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO-I) trial. Anobservational study. Circulation 1997; 96:122.

54. Hochman JS, Sleeper LA, Webb JG, et al. Early revascularization in acute myocardial infarctioncomplicated by cardiogenic shock. SHOCK Investigators. Should We Emergently RevascularizeOccluded Coronaries for Cardiogenic Shock. N Engl J Med 1999; 341:625.

55. Hochman JS, Sleeper LA, White HD, et al. One-year survival following early revascularization forcardiogenic shock. JAMA 2001; 285:190.

56. Mylotte D, Morice MC, Eltchaninoff H, et al. Primary percutaneous coronary intervention in patients withacute myocardial infarction, resuscitated cardiac arrest, and cardiogenic shock: the role of primarymultivessel revascularization. JACC Cardiovasc Interv 2013; 6:115.

57. Webb JG, Sanborn TA, Sleeper LA, et al. Percutaneous coronary intervention for cardiogenic shock in theSHOCK Trial Registry. Am Heart J 2001; 141:964.

58. Lim HS, Farouque O, Andrianopoulos N, et al. Survival of elderly patients undergoing percutaneouscoronary intervention for acute myocardial infarction complicated by cardiogenic shock. JACC CardiovascInterv 2009; 2:146.

59. Dzavik V, Sleeper LA, Cocke TP, et al. Early revascularization is associated with improved survival inelderly patients with acute myocardial infarction complicated by cardiogenic shock: a report from theSHOCK Trial Registry. Eur Heart J 2003; 24:828.

60. Marso SP, Steg G, Plokker T, et al. Catheter-based reperfusion of unprotected left main stenosis duringan acute myocardial infarction (the ULTIMA experience). Unprotected Left Main Trunk Intervention Multi-center Assessment. Am J Cardiol 1999; 83:1513.

61. White HD, Assmann SF, Sanborn TA, et al. Comparison of percutaneous coronary intervention andcoronary artery bypass grafting after acute myocardial infarction complicated by cardiogenic shock:results from the Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock(SHOCK) trial. Circulation 2005; 112:1992.

62. Hochman JS, Buller CE, Sleeper LA, et al. Cardiogenic shock complicating acute myocardial infarction--etiologies, management and outcome: a report from the SHOCK Trial Registry. SHould we emergentlyrevascularize Occluded Coronaries for cardiogenic shocK? J Am Coll Cardiol 2000; 36:1063.

63. Wong SC, Sleeper LA, Monrad ES, et al. Absence of gender differences in clinical outcomes in patientswith cardiogenic shock complicating acute myocardial infarction. A report from the SHOCK Trial Registry.J Am Coll Cardiol 2001; 38:1395.

64. Sleeper LA, Ramanathan K, Picard MH, et al. Functional status and quality of life after emergencyrevascularization for cardiogenic shock complicating acute myocardial infarction. J Am Coll Cardiol 2005;46:266.

65. Hochman JS, Sleeper LA, Webb JG, et al. Early revascularization and long-term survival in cardiogenicshock complicating acute myocardial infarction. JAMA 2006; 295:2511.

66. Berger PB, Tuttle RH, Holmes DR Jr, et al. One-year survival among patients with acute myocardialinfarction complicated by cardiogenic shock, and its relation to early revascularization: results from theGUSTO-I trial. Circulation 1999; 99:873.

67. Kushner FG, Hand M, Smith SC Jr, et al. 2009 Focused Updates: ACC/AHA Guidelines for theManagement of Patients With ST-Elevation Myocardial Infarction (updating the 2004 Guideline and 2007Focused Update) and ACC/AHA/SCAI Guidelines on Percutaneous Coronary Intervention (updating the2005 Guideline and 2007 Focused Update): a report of the American College of CardiologyFoundation/American Heart Association Task Force on Practice Guidelines. Circulation 2009; 120:2271.

68. Hochman JS. Cardiogenic shock complicating acute myocardial infarction: expanding the paradigm.Circulation 2003; 107:2998.

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Topic 83 Version 18.0

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GRAPHICS

Treatment options for cardiogenic shock due to left ventricular

dysfunction

General measures

Ventilation support to correct hypoxemia and, in part, acidosis

Optimize intravascular volume

Sodium bicarbonate only for severe metabolic acidosis (arterial pH less than 7.10 to 7.15)

Aspirin

Intravenous heparin

Possible glycoprotein IIb/IIIa inhibitor with NSTEMI

Insertion of pulmonary artery catheter

Specific measures

Pharmacologic support

Sympathomimetic inotropes (eg, dopamine)

Norepinephrine (for refractory hypotension)

Mechanical support

IABP, usually combined with percutaneous coronary intervention or coronary artery bypass graft

surgery or possible thrombolytic therapy

Newer devices

Left ventricular or biventricular assist devices

Percutaneous cardiopulmonary bypass

Reperfusion/revascularization

Primary percutaneous coronary intervention

Coronary artery bypass graft

Thrombolytic therapy for patients not receiving PCI in a timely manner

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ACC/AHA/ESC guideline summary: Treatment of cardiogenic shock

in patients with acute myocarial infarction (MI)*

Class I - There is evidence and/or general agreement that the following

approaches are indicated in the treatment of cardiogenic shock in

patients with an acute MI:

• Intraaortic balloon counterpulsation when cardiogenic shock is not quickly reversed with

pharmacologic therapy. The IABP is a stabilizing measure for angiography and prompt

revascularization.

• Intraarterial monitoring.

• Early revascularization with either PCI or CABG for patients less than 75 years of age

who develop shock within 36 hours of MI and who are suitable for revascularization that

can be performed within 18 hours of shock. This recommendation does not apply when

further support is futile because of the patient's wishes or contraindications to or

unsuitability for further invasive care.

• Among patients with ST elevation MI, fibrinolytic therapy in those who are not suitable

for revascularization and have no contraindications to fibrinolysis.

• Unless assessed by invasive testing, echocardiography to evaluate for possible

mechanical complications.

Class IIa - The weight of evidence or opinion is in favor of the usefulness

of the following approaches in the treatment of cardiogenic shock in

patients with an acute MI:

• Pulmonary artery catheterization

• Early revascularization with either PCI or CABG for selected patients 75 years of age or

older (eg, patients with good functional status who agree to invasive care) who develop

shock within 36 hours of MI and who are suitable for revascularization that can be

performed within 18 hours of shock.

* These guidelines were for patients with ST elevation MI or MI associated with left bundlebranch block. Similar principles apply to cardiogenic shock developing in patients with a non-STelevation MI.Data from Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA guidelines for the management ofpatients with ST-elevation myocardial infarction--executive summary: a report of the AmericanCollege of Cardiology/American Heart Association Task Force on Practice Guidelines (WritingCommittee to Revise the 1999 Guidelines for the Management of Patients With Acute MyocardialInfarction). Circulation 2004; 110:588.

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Potential indicators of success in noninvasive positive pressure

ventilation

Younger age

Lower acuity of illness (APACHE score)

Able to cooperate, better neurologic score

Less air leaking, intact dentition

Moderate hypercarbia (PaCO >45 mmHG, <92 mmHG)

Moderate acidemia (pH <7.35, >7.10)

Improvements in gas exchange and heart respiratory rates within first two hours

Reproduced with permission from: International Concensus Conferences in Intensive Care Medicine:Noninvasive positive pressure ventilation in acute respiratory failure. Am J Respir Crit Care Med2001; 163:288. Copyright © 2001 American Thoracic Society.

2

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Importance of blood pressure on clot dissolution

Dogs with a left anterior descending coronary artery occlusion bythrombus were made hypotensive by phlebotomy. Rates ofthrombolysis (percent per 30 min) were depressed by low BP andrestored with norepinephrine (NE) titrated to a systolic BP of 130mmHg or with intraaortic balloon counterpulsation (IABC).Data from: Prewitt RM, Gu S, Garger PJ, Ducas J. J Am Coll Cardiol 1992;20:1626, and Prewitt RM, Gu S, Schick U, Ducas J. J Am Coll Cardiol 1994;23:794.

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ACC/AHA guideline summary: Intraaortic balloon pump (IABP) in

acute myocardial infarction (MI)

Class I - There is evidence and/or general agreement that an IABP

should be used in patients with acute MI in the following settings

• Hypotension (systolic pressure less than 90 mm Hg or ≥30 mmHg below the baseline

mean arterial pressure) that does not respond to other interventions unless further

support is limited by patient's wishes or contraindications or unsuitability for further

invasive care.

• Low-output state

• Cardiogenic shock not quickly reversed with pharmacologic therapy as a stabilizing

measure for angiography and prompt revascularization.

• Recurrent ischemic-type chest discomfort and hemodynamic instability, poor left

ventricular function, or a large area of myocardium at risk. Such patients should be

referred for urgent cardiac catheterization and, if appropriate, revascularization.

Class IIa - The weight of evidence or opinion is in favor of benefit from

an IABP in patients with acute MI in the following setting

• Refractory polymorphic ventricular tachycardia in an attempt to diminish myocardial

ischemia.

Class IIb - The evidence or opinion is less well established for an IABP in

patients with acute MI in the following setting

• Refractory pulmonary congestion.

Data from Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA guidelines for the management ofpatients with ST-elevation myocardial infarction--executive summary: a report of the AmericanCollege of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation2004; 110:588.

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Preferred thrombolytic regimens for acute ST elevation myocardial

infarction

DrugRecommended

IV regimen*Advantages and limitations

Alteplase

(accelerated

regimen)

15 mg bolus Better outcomes than streptokinase in GUSTO-1 (30-

day mortality 6.3 versus 7.3 percent); costlier than

streptokinase; more difficult to administer because of

short half-life

then 0.75 mg/kg

(maximum 50 mg)

over 30 minutes

then 0.5 mg/kg

(maximum 35 mg)

over the next 60

minutes

Tenecteplase Single bolus over

five to ten

seconds based

upon body

weight:

As effective as alteplase in ASSENT-2 with less

noncerebral bleeding and need for transfusion;

easier to administer (single bolus due to longer half-

life) both in and out of hospital; these advantages

make tenecteplase the drug of choice in many US

hospitals<60 kg: 30 mg

60 to 69 kg: 35

mg

70 to 79 kg: 40

mg

80 to 89 kg: 45

mg

≥90 kg: 50 mg

Reteplase 10 units over two

minutes then

repeat 10 unit

bolus at 30

minutes

Similar outcomes as alteplase but easier to

administer

Streptokinase 1.5 million units

over 30 to 60

minutes

Generally a much less costly option than other

fibrinolytics but outcomes are inferior. Neutralizing

antibodies develop, which can diminish efficacy of

subsequent use. Elevated risk of hypersensitivity

reaction with repeated doses. Used extensively

outside North America due to lower cost. (Not

available in US or CAN).

* All patients are also given non enteric-coated aspirin 162 to 325 mg and, with alteplase,reteplase, and tenecteplase, unfractionated heparin as a 60 units/kg bolus (maximum 4000units) followed by an intravenous infusion of 12 units/kg per hour (maximum 1000 units perhour) adjusted to target aPTT of 50 to 70 seconds. Heparin has not been definitively shown toimprove outcomes with non-fibrin-specific agents such as streptokinase. However, heparin isrecommended with streptokinase in patients who are at high risk for systemicthromboembolism (large or anterior myocardial infarction, atrial fibrillation, previous embolus, orknown left ventricular thrombus).

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Kaplan-Meier long-term survival of all patients and those

discharged alive following hospitalization

Among all patients, the survival rates in the early revascularization (ERV)and initial medical stabilization (IMS) groups, respectively, were 41.4 versus28.3 percent at three years and 32.8 versus 19.6 percent at six years. Withexclusion of eight patients with aortic dissection, tamponade, or severemitral regurgitation identified shortly after randomization, the survivalcurves remained significantly different (P = .02), with a 14.0 percentabsolute difference at six years. Among hospital survivors, the survivalrates in the ERV and IMS groups, respectively, were 78.8 versus 64.3percent at three years and 62.4 versus 44.4 percent at six years.Reproduced with permission from: Hochman JS, Sleeper LA, Webb JG, et al. Earlyrevascularization and long-term survival in cardiogenic shock complicating acutemyocardial infarction. JAMA 2006; 295:2511. Copyright ©2006 American MedicalAssociation. All Rights Reserved.