Cardiogenic Shock

Olivier Collange
Cardiogenic shock (CS) is the most common cause of death in patients hospitalized with
acute myocardial infarction (MI) and is associated with a poor prognosis. CS needs to be
recognized and diagnosed rapidly. Treatment strategies using intra-aortic balloon
counterpulsation and emergency revascularization by percutaneous coronary interventions or
coronary bypass surgery improve outcomes.
A. Definition
The clinical definition of CS is decreased cardiac output and evidence of tissue hypoxia in
the presence of adequate intravascular volume. Hemodynamic criteria are sustained
hypotension (systolic blood pressure < 90 mm Hg for at least 30 minutes) and a reduced
cardiac index (CI<2.2 L/min/m2) in the presence of elevated pulmonary artery occlusion
pressure (PAOP>15 mm Hg) [1, 2].* Circulatory shock is diagnosed at the bedside by
observing hypotension and clinical signs indicating poor tissue perfusion, including oliguria;
clouded sensorium; and cool, mottled extremities. Cardiogenic shock is diagnosed after
documentation of myocardial dysfunction and exclusion or correction of hypovolemia and
hypoxemia.
*NB: Most of the studies define CS as a state secondary to cardiac dysfunction with systolic
blood pressure < 90mmHg for at least 1 hour that is not responsive to fluid administration
alone, associated with sign of hypoperfusion or a CI< 2.2L/min/m2 and PAOP>18 mmHg.
Other investigators regarded measurement of CI<1.8L/min /m2 as indicative for cardiogenic
shock [3].
B. Epidemiology, prognosis and etiologies
Recent estimates of the incidence of cardiogenic shock have ranged from 5% to 10% of
patients with myocardial infarction. The precise incidence is difficult to measure because
patients who die before reaching the hospital are not given the diagnosis. In contrast, early and
aggressive monitoring can increase the apparent incidence of cardiogenic shock. However,
several trials show that CS complicate approximately 5% to 8% of ST-elevation myocardial
infarction (STEMI) [4] and 2.5% of non-ST-elevation myocardial infarction (non-STEMI)
cases [5]. This translates to 40 000 to 50 000 cases per year in the United States [6].
Prognosis
In-hospital mortality in the SHOCK Trial Registry was 60% [7]. In the NRMI data, the
overall in-hospital mortality decreased from 60.3% in 1995 to 47.9% in 2004 [8]. 29% of
patients with CS were in shock as they presented to hospital, and 71% developed CS after
admission. CS patients were more likely to have a history of hypertension, dyslipidemia, and
prior coronary angioplasty and to be older than 75 years. In the SHOCK Trial Registry, the
median time from onset of myocardial infarction to shock was 7 hrs.
Etiologies
The distribution of causes of cardiogenic shock complicating acute myocardial inarction on
the prospective SHOCK trial registry is shown in the table 1. LV failure accounts for 79% of
cases, mechanical causes comprising 12% and isolated RV infraction comprising 3%. Causes
as coexistent severe valvular heart disease, excess dosing of betablocker or calcium channel

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blocker therapy, severe dilated cardiomyopathy, recent hemorrage or cardiac catheterization

laboratory complicccations accounted for the remaining 7%. Of course, concurrent conditions,
such as hemorrhage or infection, may contribute to shock. Concerning MI, infarction location
is anterior in 55% of cases and in multiple locations in 50%.
Some treatment may contribute to CS development
Several different classes of medications used to treat MI have been associated with shock,
including -blockers, angiotensin-converting enzyme inhibitors, and morphine. Although early
use of each of these medications is associated with only a small excess risk of CS, the large
number of patients treated with these therapies translates into a substantial potential number of
events.
C. Pathophysiology
The predominant cause of cardiogenic shock is left ventricular (LV) failure in the setting of
acute myocardial infarction. Cardiogenic shock usually results from an extensive acute
infarction, although a smaller infarction in a patient with previously compromised LV function
may also precipitate shock.
1.
Systemic effects
1.1. Classic paradagim [1]
Myocardial dysfunction resulting from ischemia worsens that ischemia, creating a downward spiral (figure 1). When a critical mass of LV myocardium becomes ischemic or nectrotic
and fails to pump, stroke volume and cardiac output decrease. Myocardial perfusion, which
depends on the pressure gradient between the coronary arterial system and the left ventricle,
and on the duration of diastole, is compromised by hypotension and tachycardia. The increased
ventricular diastolic pressure caused by pump failure further reduces coronary perfusion
pressure. Finally, the additional wall stress elevates myocardial oxygen requirements, further
worsening ischemia.
LV dysfunction increases left atrial (LA) pressure and ischemia increases diastolic stiffness,
increasing LA pressure. This in turn may result in pulmonary congestion and consequent
hypoxia, which can exacerbate myocardial ischemia as well as impair RV performance. Fluid
retention and impaired diastolic filling caused by tachycardia and ischemia may result in
pulmonary congestion and hypoxia.
When myocardial function is depressed, several compensatory mechanisms designed to
increase cardiac output are activated, including sympathetic stimulation to increase heart rate
and contractility and activation of the rennin/angiotensin/aldosterone system, which leads to
renal fluid retention and increase preload. These compensatory mechanisms may become
maladaptive and can actually worsen the situation when carcinogenic shock develops.
Increased heart rate and contractility increase myocardial oxygen demand and exacerbate
ischemia.
The vascular response to impaired cardiac output is vasoconstriction to maintain systemic
blood pressure and coronary perfusion. However, this increases myocardial afterload and may
further impair cardiac performance and increase myocardial oxygen demand. The increased
oxygen demand facing inadequate perfusion worsens ischemia and begins a vicious cycle that
may end in death if not interrupted.
1.2. Effect of inflammation on hemodynamics [2, 9]
Recent data suggest that not all the patients fit into this classic paradigm. In the SHOCK
trial, the average systemic vascular resistance (SVR was not elevated and the range of value
was wide, suggesting that compasotory vasoconstriction is not universal. Supporting this
notion is the fact that the mean ejection fraction in the SHOCK trial was only moderately
decreased (30%), indicating that mechanisms other than pump failure were at work. The
systemic inflammatory response syndrome also plays a role. The heart releases cytokines after

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MI, which can activate inductible nitric oxide synthase (iNOS), leading to vasodilatation and
worsening hypotension. NO can also combine with superoxide to form peroxynitrite, a toxic
radical that can impair myocardial contractility
1.3. Preshock
Some patients will demonstrate signs of tissue hypoperfusion with systolic blood pressure
>90 mm Hg. This has been termed nonhypotensive cardiogenic shock or preshock. In the
SHOCK Trial Registry, these patients demonstrated the hemodynamic profile of elevated
pulmonary artery occlusion pressure with low cardiac index and high systemic vascular
resistance. The hospital mortality rate in this group of patients was 43%, very high but lower
than in patients diagnosed with full-blown cardiogenic shock. The mortality in patients with
preshock compares with a mortality rate of 26% in patients with hypotension without signs of
hypoperfusion.
2.
Myocardial pathology
2.1. Infarct extension and infarct expansion: the gray area
Acute myocardial infarction is a dynamic process that evolves over hours. There is a central
zone of infarction, surrounded by a border zone of jeopardized ischemic myocardium that
mays be salvageable by reperfusion. Loss of myocardium is not confined to the initial
infarction period. Progressive myocardial necrosis is frequently observed in clinical and
pathologic studies. This is consistent with epidemiologic observations that indicate that the
majority of hospital patients develop shock over a period of hours to days after initial
presentation. Patients who develop shock after admission often have evidence of infarct
extension, which represents additional myocardial necrosis after the initial insult. Infarct
extension can result from reocclusion of a transiently patent infarct artery, propagation of
intracoronary thrombus or a combination of decreased coronary perfusion pressure and
increased myocardial oxygen demand. Myocites at the border zone of an infarction are more
susceptible to additional ischemic episodes; therefore, theses adjacent segments are at
particular risk. This marginal extension has been termed piecemeal necrosis.
Infarct expansion is conceptually distinct and refers to expansion and thinning of the infarct
area in the first hours to days of acute MI as myocite slip past each other. Infarct expansion is
an early form of pathologic remodelling that can distort both regional and global ventricular
geometry and lead to increased wall stress. Infarct expansion causes enlargement of left
ventricle, which initially serves as a compensatory mechanism stroke volume. However, this
increases wall stress, which in turn imposes additional mechanical strain on myocytes,
potentially causing further slippage. Infarct expansion is seen most dramatically after extensive
anterior myocardial infarction and is often an important contributor to late development of
cardiogenic shock.
Despite the conceptual distinction between infarct expansion and infarct extension, there is a
gray area in which infarcts may enlarge by a combination of both mechanisms.
2.2. Diastolic function
Myocardial diastolic function is also impaired in patients with CS. MI decreases compliance,
increasing LV filling pressure at a given end-diastolic volume. Greater LV diastolic pressures
increase myocardial oxygen demand and decrease coronary perfusion pressure, further
exacerbating ischemia and ventricular dysfunction. Elevation of LV pressure leads to
pulmonary edema and hypoxemia.
3.
Mechanical Complications of Acute Myocardial Infarction
3.1. Right Ventricular Infarction
Right ventricular infarction occurs in up to 30% of patients with inferior infarction and is
clinically significant in 10% [10]. Patients usually present with hypotension, elevated neck
veins, and clear lung fields. Diagnosis is made by identifying ST-segment elevation in right

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precordial leads or characteristic hemodynamic findings on right-heart catheterization

(elevated right atrial and right ventricular end-diastolic pressures with normal to low
pulmonary artery occlusion pressure and low cardiac output). Echocardiography can show
depressed right ventricular contractility. Patients with cardiogenic shock on the basis of right
ventricular infarction have a better prognosis than those with left-sided pump failure [10]. This
may be due in part to the fact that right ventricular function tends to return to normal over time
with supportive therapy [11], although such therapy may need to be prolonged.
Supportive therapy for patients with right ventricular infarction begins with maintainance of
right ventricular preload with fluid administration. In some cases, however, fluid resuscitation
may increase pulmonary capillary occlusion pressure but may not increase cardiac output, and
overdilation of the right ventricle can compromise left ventricular filling and cardiac output
[11]. Inotropic therapy with dobutamine may be more effective in increasing cardiac output in
some patients, and monitoring with serial echocardiography may also be useful to detect right
ventricular overdistention [11]. Maintenance of atrioventricular synchrony is also important in
these patients to optimize right ventricular filling. For patients with continued hemodynamic
instability, intra-aortic balloon pumping may be useful, particularly because elevated right
ventricular pressures and volumes increase wall stress and oxygen consumption and decrease
right coronary perfusion pressure, exacerbating right ventricular ischemia. Reperfusion of the
occluded coronary artery is also crucial, restoration of normal flow resulted in dramatic
recovery of right ventricular function and a mortality rate of only 2%, whereas unsuccessful
reperfusion was associated with persistent hemodynamic compromise and a mortality rate of
58%.
3.2. Acute Mitral Regurgitation
Ischemic mitral regurgitation is usually associated with inferior myocardial infarction and
ischemia or infarction of the posterior papillary muscle. Papillary muscle rupture usually
occurs 2 to 7 days after acute myocardial infarction; it presents dramatically with pulmonary
edema, hypotension, and cardiogenic shock.
Echocardiography is extremely useful in the differential diagnosis, which includes free-wall
rupture, ventricular septal rupture, and infarction extension pump failure. Hemodynamic
monitoring with pulmonary artery catheterization may also be helpful. Management includes
afterload reduction with nitroprusside and intra-aortic balloon pumping as temporizing
measures. Inotropic or vasopressor therapy may also be needed to support cardiac output and
blood pressure. Definitive therapy, however, is surgical valve repair or replacement, which
should be undertaken as soon as possible because clinical deterioration can be sudden [1].
3.3. Ventricular Septal Rupture
Patients who have ventricular septal rupture have severe heart failure or cardiogenic shock,
with a pansystolic murmur and a parasternal thrill. The classic finding is a left-to-right
intracardiac shunt. On pulmonary artery occlusion pressure tracing, ventricular septal rupture
can be difficult to distinguish from mitral regurgitation because both can produce dramatic V
waves. The diagnosis is most easily made with echocardiography.
Rapid stabilizationusing intra-aortic balloon pumping and pharmacologic measures
followed by surgical repair is the only viable option for long-term survival. The timing of
surgery is controversial, but most experts now suggest that operative repair should be done
early, within 48 hours of the rupture.
3.4. Free-Wall Rupture
Ventricular free-wall rupture usually occurs during the first week after myocardial infarction;
the classic patient is elderly, female, and hypertensive. The early use of thrombolytic therapy
reduces the incidence of cardiac rupture, but late use may increase the risk. Free-wall rupture
presents as a catastrophic event with a pulseless rhythm. Salvage is possible with prompt
recognition, pericardiocentesis to relieve acute tamponade, and thoracotomy with repair.

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D. Treatment
1.
Initial management
1.1. Early CS recognition: as simple as clinical examination
The most important aspects of the initial care of the patient with cardiogenic shock are
recognizing the condition early in its course and understanding its cause. Rapid assessment of
the history, physical examination, and chest radiograph is mandatory, recognizing the signs of
heart failure, pulmonary edema (sometimes with clear lung fields on examination), and tissue
hypoperfusion, manifesting as low blood pressure, rapid heart rate, agitation, confusion,
oliguria, cyanosis, and cool and clammy skin. Appreciating the electrocardiographic signs of
acute myocardial ischemia, myocardial infarction, new left bundle branch block, and
arrhythmias is critical. Rapid echocardiographic assessment is key. The echo-Doppler study
will assess regional and global left ventricular function, right ventricular size and function, the
presence of mitral regurgitation and other valve abnormalities, pericardial effusion, and
possible septal rupture.
1.2. Echocardiography is crucial
Echocardiographic assessment of left ventricular ejection fraction was found to be similar to
ejection fraction as assessed by left ventriculography and can be used as the sole initial
evaluation of systolic left ventricular function in patients with CS. Differential diagnoses to
consider in patients with CS include hemorrhage, sepsis, aortic dissection, and massive
pulmonary embolism.
1.3. Immediate measures
Patients must be assessed regarding the need for sedation, intubation, and mechanical
ventilation in order to correct hypoxemia and reduce the work of breathing [12, 13]. Initial
medical therapy includes intravenous fluid challenge for patients with significant hypotension,
if there is no evidence for pulmonary edema or significant elevation of jugular venous
pressure. If CS is due to acute myocardial infarction or ischemia, emergency cardiac
catheterization and revascularization need to take place in patients believed suitable for this
approach.
1.4. Pulmonary artery catheter
Pulmonary artery catheterization can assist in the precise measurement of volume status, left
and right ventricular filling pressures, and cardiac output. It is also valuable in diagnosing right
ventricular infarction and the mechanical complications of acute myocardial infarction.
Hemodynamic measurements can help guide fluid management and the use of inotropic agents
and vasopressors. The American College of Cardiology/American Heart Association
(ACC/AHA) guidelines list pulmonary artery catheterization as a class I recommendation in
patients with hypotension not responding to fluid administration or when mechanical
complications of myocardial infarction are suspected and echocardiography is not available.
Pulmonary artery catheterization is a class IIa recommendation for patients in CS who have
persistent signs of hypoperfusion and in patients receiving inotropic and vasopressor drugs
[14].
2.
Medical treatment
2.1. Choose the inotropic/vasopressive drug
The goal of the initial medical therapy of CS is to maintain arterial pressure adequate for
tissue perfusion. Initially, dopamine is the drug of choice because it acts as an inotrope as well
as a vasopressor. Intravenous norepinephrine is a more potent vasoconstrictor, with somewhat
less effect on heart rate, and should be used in patients with more severe hypotension. These
drugs increase heart rate and systemic vascular resistance and thus increase myocardial oxygen
demand, and they may aggravate ischemia and lead to cardiac arrhythmias. Doses should be
adjusted to the lowest levels that improve tissue perfusion [3, 13, 14].

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Dobutamine, an inotrope with arterial dilator properties, can be used in patients with less
severe hypotension or can be combined with vasopressors to improve cardiac output [13].
The figure 2 shows symptomatic treatments for supporting CS hemodynamic.
2.2. Diuretics
Intravenous diuretics are used in patients with pulmonary edema and elevated pulmonary
artery occlusion pressure.
2.3. Aspirin
Aspirin should be given to patients with acute myocardial infarction.
2.4. Amiodarone
Intravenous amiodarone can be given for patients with severe arrhythmia.
2.5. Other? No.
The use of [beta]-blockers should be avoided in the acute phase of CS. Nitrates are not
recommended when the patient is hypotensive.
3.
Emergency Early Revascularisation
3.1. Emergency Revascularization: PCI and CABG
The most successful strategy to successfully treat acute myocardial infarction is rapid
restoration of flow in the infarct-related artery [15], and primary coronary angioplasty results
in better outcomes than fibrinolytic therapy [16]. Early mechanical revascularization with
either PCI or coronary artery bypass graft surgery (CABG) is associated with survival benefit.
The SHOCK trial prospectively randomized 302 patients with CS due to acute myocardial
infarction and left ventricular failure to emergency early revascularization (ERV) with PCI or
CABG vs. initial medical stabilization (IMS) with drug therapy and IABP. PCI accounted for
64% of revascularization and CABG was performed in 36%. The 30-day mortality rate, the
primary outcome measured, was lower in the early revascularization group (47% vs. 56%),
which was not statistically significant. However, late mortality rates were significantly
improved in patients who received ERV [17]. At 6 months, 1 yr, and 6 yrs, a statistically
significant absolute survival difference of 13% was seen in patients who received ERV [18].
At 6 yrs, overall survival was 32.8% in the ERV group and 19.6% in the IMS group. In
patients who survived hospitalization, the 6-yr survival rate in patients with ERV was 62.4%
vs. 44.4% in IMS patients. There was no significant difference in long-term survival between
patients treated with PCI or CABG. Quality of life measures were also better in patients who
had received ERV.
3.2. Fibrinolytic Therapy: second intention
Urgent transfer to the cardiac catheterization laboratory for coronary angiography and
emergency coronary intervention has largely supplanted thrombolytic therapy as first-line
treatment for patients with acute myocardial infarction and CS. Fibrinolytics are not as
effective as accomplishing reperfusion in STEMI with CS as in patients with STEMI without
cardiogenic shock [13]. This is hypothesized to be due to decreased penetration of the coronary
thrombus by fibrinolytics in hypotensive patients, a greater incidence of coronary artery
reocclusion after thrombolysis, and longer times required to achieve coronary patency [12].
However, in the SHOCK Trial Registry, the addition of IABP to thrombolytic therapy
decreased mortality significantly from 63% with thrombolysis alone to 47% with thrombolysis
and IABP. Thrombolytic therapy was associated with a lower mortality than in patients who
did not receive any reperfusion therapy [19].
Current guidelines have relegated thrombolytic therapy for CS as a class I recommendation
only in patients with STEMI who are unsuitable for invasive therapy with PCI or bypass
surgery [14].

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4.
Mechanical assistance
4.1. Intra-Aortic Balloon Counterpulsation (IABP)
IABP is very useful to support patients with CS. This device will increase coronary blood
flow, decrease left ventricular afterload, and decrease left ventricular end-diastolic pressure
without increasing oxygen demand [1]. Cardiac output is increased only modestly, and this
device does not provide total circulatory support.
The efficacy of IABP in acute myocardial infarction complicated by CS has not been
evaluated in a randomized controlled trial. However, current ACC/AHA guidelines list IABP
as a class I recommendation for patients with low cardiac output states, hypotension, and CS
not responding quickly to other measures [14].
Complications of IABP include bleeding, thrombocytopenia, hemolysis, leg ischemia, aortic
dissection, femoral artery injury, thromboembolism, and sepsis. The complication rate has
been reduced with percutaneous insertion and with smaller pumps. Complication rates have
been reported at 10% to 30%, with major complication rates of 2.5% to 3.0% [20]. Patients
usually must be anticoagulated during IABP use. Contraindications to the use of IABP include
severe aortic insufficiency, severe peripheral vascular disease, and aortic aneurysm.
The use of IABP in CS improves the short-term hemodynamic profile and may allow for
improvement in function of ischemic myocardium. It likely does not improve outcomes unless
it is combined with definitive coronary revascularization [20].
4.2. Ventricular Assist Devices (VADs): a bridge to heart transplantation
VADs have been used in small series of highly selected patients with CS refractory to IABP
and reperfusion strategies. The use of VADs should be considered in patients with very low
cardiac output, <1.2 L/min/m2 [12].
The TandemHeart percutaneous VAD a bridge to...the bridge?
The TandemHeart percutaneous VAD, inserted in the catheterization laboratory, uses a
catheter directed into the left atrium via a transseptal puncture, unloading the left atrium and
left ventricle. Blood is then pumped into a 15- to 17-Fr catheter inserted in the femoral artery,
producing flows of 3.54.0 L/min. This technique could be effective as a bridge to implanted
VADs or cardiac transplant therapy, with a low incidence of adverse effects. This device
cannot be used in patients with right ventricular failure or severe peripheral vascular disease
[21].
Conclusion
Mortality rates in patients with cardiogenic shock are high (50%) but should be limited
following recent guidelines. The key to a good outcome is an organized approach with rapid
diagnosis and prompt initiation of therapy to maintain blood pressure and cardiac output.
Expeditious coronary revascularization is crucial. When available, emergency cardiac
catheterization and revascularization with angioplasty or coronary surgery improve survival
and represent standard therapy at this time. In hospitals without direct angioplasty capability,
stabilization with IABP and thrombolysis followed by transfer to a tertiary care facility may be
the best option.

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Table 1 : Etiologies of CS, from [2]

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Figure 1: Current concept of CS physiopathology, from [9]

Figure 2: Emergency management of complicated ST-segment elevation myocardial

infarction, from ACA/AHA Practice guidelines [14].

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REFERENCES
1. Hollenberg, S.M., C.J. Kavinsky, and J.E. Parrillo, Cardiogenic shock. Ann Intern Med,
1999. 131(1): p. 47-59.
2. Topalian, S., F. Ginsberg, and J.E. Parrillo, Cardiogenic shock. Crit Care Med, 2008. 36(1
Suppl): p. S66-74.
3. Hochman, J.S. and E.M. Ohlman, Cardiogenic Shock. AHA clinical series, ed. E.M.
Antman. 2009, Singapore: Wiley-Blackwell.
4. Fox, K.A., et al., Intervention in acute coronary syndromes: do patients undergo
intervention on the basis of their risk characteristics? The Global Registry of Acute
Coronary Events (GRACE). Heart, 2007. 93(2): p. 177-82.
5. Hasdai, D., et al., Platelet glycoprotein IIb/IIIa blockade and outcome of cardiogenic
shock complicating acute coronary syndromes without persistent ST-segment elevation. J
Am Coll Cardiol, 2000. 36(3): p. 685-92.
6. Thom, T., et al., Heart disease and stroke statistics--2006 update: a report from the
American Heart Association Statistics Committee and Stroke Statistics Subcommittee.
Circulation, 2006. 113(6): p. e85-151.
7. Hochman, J.S., et al., Cardiogenic shock complicating acute myocardial infarction-etiologies, management and outcome: a report from the SHOCK Trial Registry. SHould
we emergently revascularize Occluded Coronaries for cardiogenic shocK? J Am Coll
Cardiol, 2000. 36(3 Suppl A): p. 1063-70.
8. Babaev, A., et al., Trends in management and outcomes of patients with acute myocardial
infarction complicated by cardiogenic shock. JAMA, 2005. 294(4): p. 448-54.
9. Reynolds, H.R. and J.S. Hochman, Cardiogenic shock: current concepts and improving
outcomes. Circulation, 2008. 117(5): p. 686-97.
10. Zehender, M., et al., Right ventricular infarction as an independent predictor of
prognosis after acute inferior myocardial infarction. N Engl J Med, 1993. 328(14): p. 9818.
11. Dell'Italia, L.J., et al., Comparative effects of volume loading, dobutamine, and
nitroprusside in patients with predominant right ventricular infarction. Circulation, 1985.
72(6): p. 1327-35.
12. Duvernoy, C.S. and E.R. Bates, Management of cardiogenic shock attributable to
acute myocardial infarction in the reperfusion era. J Intensive Care Med, 2005. 20(4): p.
188-98.
13. Ellis, T.C., et al., Therapeutic strategies for cardiogenic shock, 2006. Curr Treat
Options Cardiovasc Med, 2006. 8(1): p. 79-94.
14. Antman, E.M., et al., 2007 focused update of the ACC/AHA 2004 guidelines for the
management of patients with ST-elevation myocardial infarction: a report of the American
College of Cardiology/American Heart Association Task Force on Practice Guidelines. J
Am Coll Cardiol, 2008. 51(2): p. 210-47.
15. The effects of tissue plasminogen activator, streptokinase, or both on coronary-artery
patency, ventricular function, and survival after acute myocardial infarction. The GUSTO
Angiographic Investigators. N Engl J Med, 1993. 329(22): p. 1615-22.
16. Keeley, E.C., J.A. Boura, and C.L. Grines, Primary angioplasty versus intravenous
thrombolytic therapy for acute myocardial infarction: a quantitative review of 23
randomised trials. Lancet, 2003. 361(9351): p. 13-20.
17. Hochman, J.S., et al., Early revascularization in acute myocardial infarction
complicated by cardiogenic shock. SHOCK Investigators. Should We Emergently
Revascularize Occluded Coronaries for Cardiogenic Shock. N Engl J Med, 1999. 341(9):
p. 625-34.
18. Hochman, J.S., et al., Early revascularization and long-term survival in cardiogenic
shock complicating acute myocardial infarction. JAMA, 2006. 295(21): p. 2511-5.

192

Cardiogenic shock

19. Sanborn, T.A., et al., Impact of thrombolysis, intra-aortic balloon pump

counterpulsation, and their combination in cardiogenic shock complicating acute
myocardial infarction: a report from the SHOCK Trial Registry. SHould we emergently
revascularize Occluded Coronaries for cardiogenic shocK? J Am Coll Cardiol, 2000. 36(3
Suppl A): p. 1123-9.
20. Trost, J.C. and L.D. Hillis, Intra-aortic balloon counterpulsation. Am J Cardiol, 2006.
97(9): p. 1391-8.
21. Lee, M.S. and R.R. Makkar, Percutaneous left ventricular support devices. Cardiol
Clin, 2006. 24(2): p. 265-75, vii.

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