Prognosis and treatment of cardiogenic shock complicating acute myocardial infarction

11/5/13 Prognosis and treatment of cardiogenic shockcomplicating acute myocardial infarction
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Author
Judith S Hochman, MD
Section Editors
Bernard J Gersh, MB, ChB, DPhil,
FRCP, MACC
James Hoekstra, MD
Deputy Editor
Gordon 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]:

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

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"):

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.

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

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

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.

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

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

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.

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

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

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

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elderly patients with acute myocardial infarction complicated by cardiogenic shock: a report from the
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etiologies, management and outcome: a report from the SHOCK Trial Registry. SHould we emergently
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revascularization for cardiogenic shock complicating acute myocardial infarction. J Am Coll Cardiol 2005;
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Circulation 2003; 107:2998.

Topic 83 Version 18.0

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

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 bundle
branch block. Similar principles apply to cardiogenic shock developing in patients with a non-ST
elevation MI.
Data from Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA guidelines for the management of
patients with ST-elevation myocardial infarction--executive summary: a report of the American
College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing
Committee to Revise the 1999 Guidelines for the Management of Patients With Acute Myocardial
Infarction). Circulation 2004; 110:588.

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 Med
2001; 163:288. Copyright © 2001 American Thoracic Society.
2

Importance of blood pressure on clot dissolution
Dogs with a left anterior descending coronary artery occlusion by
thrombus were made hypotensive by phlebotomy. Rates of
thrombolysis (percent per 30 min) were depressed by low BP and
restored with norepinephrine (NE) titrated to a systolic BP of 130
mmHg 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.

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 of
patients with ST-elevation myocardial infarction--executive summary: a report of the American
College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation
2004; 110:588.

Preferred thrombolytic regimens for acute ST elevation myocardial
infarction
Drug
Recommended
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 4000
units) followed by an intravenous infusion of 12 units/kg per hour (maximum 1000 units per
hour) adjusted to target aPTT of 50 to 70 seconds. Heparin has not been definitively shown to
improve outcomes with non-fibrin-specific agents such as streptokinase. However, heparin is
recommended with streptokinase in patients who are at high risk for systemic
thromboembolism (large or anterior myocardial infarction, atrial fibrillation, previous embolus, or
known left ventricular thrombus).

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 versus
28.3 percent at three years and 32.8 versus 19.6 percent at six years. With
exclusion of eight patients with aortic dissection, tamponade, or severe
mitral regurgitation identified shortly after randomization, the survival
curves remained significantly different (P = .02), with a 14.0 percent
absolute difference at six years. Among hospital survivors, the survival
rates in the ERV and IMS groups, respectively, were 78.8 versus 64.3
percent 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. Early
revascularization and long-term survival in cardiogenic shock complicating acute
myocardial infarction. JAMA 2006; 295:2511. Copyright ©2006 American Medical
Association. All Rights Reserved.

Prognosis and treatment of cardiogenic shock complicating acute myocardial infarction

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