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CARDIOGENIC SHOCK-MANAGEMENT
INTRODUCTION
M Panja, Madhumati Panja, Saroj Mandal,
The incidence of cardiogenic shock in community studies has not Dilip Kumar, Kolkata
decreased significantly over time. Despite decreasing mortality
rates associated with increasing utilisation of revascularisation,
Circulatory shock is diagnosed at the bedside by observing
shock remains the leading cause of death for patients hospitalised
hypotension and clinical signs indicating poor tissue perfusion,
with acute myocardial infarction (MI). Although shock often
including oliguria; clouded sensorium; and cool, mottled
develops early after MI onset, it is typically not diagnosed on
extremities. Cardiogenic shock is diagnosed after documentation
hospital presentation. Failure to recognise early haemodynamic
of myocardial dysfunction and exclusion or correction of such
compromise and the increased early use of hypotension inducing
factors as hypovolemia, hypoxia, and acidosis.
treatments may explain this observation.
Recently, a randomised trial has demonstrated that early EPIDEMIOLOGY & CAUSES
revascularisation reduces six and
The most common cause of cardiogenic shock is extensive acute
12 month mortality.1,2The currentAmerican College of Cardiology/ myocardial infarction, although a smaller infarction in a patient
American Heart Association (ACC/AHA) guidelines recommend with previously compromised left ventricular function may also
the adoption of an early revascularisation strategy for patients < precipitate shock. Shock that has a delayed onset may result
75 years of age with cardiogenic shock.3 from infarction extension, reocclusion of a previously patent
The extent of myocardial salvage from reperfusion treatment infracted artery, or decompensation of myocardial function
decreases exponentially with time to re-establishing coronary in the noninfarction zone because of metabolic abnormalities.
flow. Unfortunately, there has been little progress in reducing It is important to recognize that large areas of nonfunctional
time to hospital presentation over the past decade,4 and this but viable myocardium can also cause or contribute to the
perhaps accounts for the stagnant incidence of cardiogenic shock development of cardiogenic shock in patients after myocardial
in community studies (7.1%).5 Cardiogenic shock also complicates infarction. Cardiogenic shock can also be caused by mechanical
non-ST elevation acute coronary syndromes. The incidence of complications—such as acute mitral regurgitation, rupture of
shock in the PURSUIT trial was 2.9% (1995–97),6 similar to the interventricular septum, or rupture of the free wall—or by
the 2.5% incidence reported in the non-ST elevation arm of the large right ventricular infarctions. Other causes of cardiogenic
GUSTO II-B trial (1994–95).7 A number of strategies that centre shock include myocarditis, end-stage cardiomyopathy, myocardial
on reducing the time to effective treatment may help decrease contusion, septic shock with severe myocardial depression,
the incidence of shock.These include public education to decrease myocardial dysfunction after prolonged cardiopulmonary
the time to hospital presentation, triage and early transfer of high bypass, valvular heart disease, and hypertrophic obstructive
risk patients to selected centres, and early primary percutaneous cardiomyopathy (Table 1). In a recent report of the SHOCK
coronary intervention (PCI) or rescue PCI for failed thrombolysis (SHould we emergently revascularize Occluded Coronaries for
in high risk patients. shocK) trial registry of 1160 patients with cardiogenic shock,8, 16
74.5% of patients had predominant left ventricular failure, 8.3%
DEFINITION had acute mitral regurgitation, 4.6% had ventricular septal rupture,
3.4% had isolated right ventricular shock, 1.7% had tamponade
The clinical definition of cardiogenic shock is decreased cardiac or cardiac rupture, and 8% had shock that was a result of other
output and evidence of tissue hypoxia in the presence of adequate causes. Patients may have cardiogenic shock at initial presentation,
intravascular volume. Hemodynamic criteria are sustained but shock often evolves over several hours.17,18 In the SHOCK
hypotension (systolic blood pressure, 90 mm Hg for at least 30 trial registry.7,16
minutes) and a reduced cardiac index (,2.2 L/min per m2) in the
presence of elevated pulmonary capillary occlusion pressure (15 75% of patients developed cardiogenic shock within 24 hours after
mm Hg) . presentation;the median delay was 7 hours from onset of infarction.
Medicine Update 2010 Vol. 20
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Cardiogenic Shock-Management
apparent incidence of cardiogenic shock. The Worcester Heart 3. Left ventricular end diastolic pressure (LVEDP) OR Pulmo-
Attack Study,3 a communitywide analysis, found an incidence of nary capillary wedge pressure (PCWP) more than or equal
cardiogenic shock of 7.5%; this incidence remained stable from to 18 mm of Hg.
1975 to 1988. In the Global Utilization of Streptokinase and Tissue
4. Marked reduction of cardiac index (< 1.8 L/min/m2 ).
Plasminogen Activator for Occluded Arteries (GUSTO-1) trial,8
the incidence of cardiogenic shock was 7.2%, a rate similar to that 5. Evidence of Primary cardiac abnormalities.
found in other multicenter thrombolytic trials.
An electrocardiogram should be obtained immediately,
The onset of cardiogenic shock in a patient following ST elevation since evidence of serious abnormalities should direct the
MI heralds a dismal in-hospital prognosis. The 7.2% of patients investigation toward the myocardium; conversely a normal
developing shock in the GUSTO-I trial accounted for 58% of electrocardiogram virtually excludes the possibility of car-
the overall deaths at 30 days.8 Similarly, the 30 day death rates diogenic shock caused by myocardial infarction. A routine
with non-ST elevation MI cardiogenic shock in the PURSUIT and chest film can provide valuable clues about the presence of
GUSTO-II b databases were 66% and 73%, respectively. Even with infarction, pulmonary edema or aortic dissection. Echocar-
early revascularisation, almost 50% die at 30 days.The prevention diography is an excellent aid in shorting through the differ-
of shock is therefore the most effective management strategy.The ential diagnosis of cardiogenic shock, it also provide infor-
opportunity for prevention is substantial, given the observation mation on regional and global systolic wall function valvular
that only a minority of patients (10–15%) present to the hospital integrity, and the presence or absence of pericardial effu-
in cardiogenic shock.Whether due to pump failure or a mechanical sion. Insertion of swan-ganz catheter is useful for initiating
cause, shock is predominantly an early in-hospital complication and monitoring therapy, since the proper use of vasoactive
in the ST elevation MI setting. The median time post-MI for agents in these circumstances requires the simultaneous as-
occurrence of shock in the randomised SHOCK trial was 5.0 sessment of cardiac filling pressure and peripheral perfu-
(interquartile range 2.2–12) hours. Similarly, median time from MI sion.
onset to development of shock in the SHOCK registry was 6.0
(1.8–22.0) hours, and median time from hospital admission was Management
4 hours. Shock complicating unstable angina/non-Q MI occurs at
When a patient with cardiogenic shock initially evaluated
a later time period. In the GUSTO-IIb trial shock was recognised
supportive and resuscitative effort must be swift and definitive
at a median of 76.2 (20.6–144.5) hours for non-ST elevation MI
to maximize the possibilities of survival. The initial management
compared to 9.6 (1.8–67.3) hours with ST elevation MI (p < 0.001),
protocol to combat shock is given in the table which is detailed
and median time to shock in the non-ST elevation PURSUIT trial
later.
was 94.0 (38–206) hours.
ABG analysis
A primary goal in preventing shock should be an effort to Maintain O2 saturation above 90%
May need Mech.Ventilation
reduce the large proportion of patients presenting with acute Hrly. urine output record
Diagnosis
DOPAMINE
Most patients are initially evaluated at the bedside where a INFUSION
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Cardiogenic Shock-Management
Safely the pump can be inserted at the bedside; operator velop shock within 36 hrs of MI are suitable for revascular-
experience is critical to successful placement and manage- ization that can be performed within 18 hrs of MI and are
ment. The most important contraindication of IABP inser- suitable if performed within 36 hrs of shock. (2008 AHA
tion is Guieline).
1. Aortic regirgotatopm Several retrospective trials have examine the effect of an-
2. Sever peripheral vascular disease. giography on mortality rate in patients with cardiogenic
shock and researchers have consistently found that patients
Although vascular and bleeding complications have been re-
with successful reperfusion have much better outcomes
ported in 5-10 % of treated patients,2 the use of smaller vas-
than those without successful reperfusion.
cular sheaths has reduced this risk. Vascular complications
almost are transient. Hemorrhage at the site of insertion, The GUSTO-130 trial, a sub group analysis of the 2972 pa-
particularly after removal, is relatively common. Meticulous tients with cardiogenic shock showed that 30 day mortality
maintenance of the insertion site, physical examination of rate was significantly lower in patients who had.
the lower extremities, and attention to the timing and char- Angioplasty (43% compared with 61% for patients with
acteristic of balloon inflation are necessary. shock on arrival ; 32% compared with 61% for patients who
developed shock). In this gtrial patients treated with an ag-
Recommendation for Intra Aortic gressive strategy (coronary angiography performed with in
Balloon Counterepulsation 24 hour of shock onset with revascularization PTCA or by-
Class I pass surgery. Had a significantly lower mortality rate (38%,
compared with 62%.30 This benefit was present even after
Cardiogenic shock not quickly reversed with pharmacologic adjustment for base line characteristic and persisted for up
therapy as a stabilizing measure for angiography and to one year.31
revascularization. Acute mitral regurgitation or ventricular septal
defect complicating myocardial infarction as a stabilizing therapy Recent reports have suggested that coronary stenting may
for angiography and repair/revascularization. improve outcome after either failed or suboptimal PTCA
or as a primary approach.32
Recurrent intractitable ventricular arrhythmias with hemodynamic
instability. A recent study of direct PTCA in patients with shock re-
ported success rate of 94% with placement of stent in 47%
Refractory post myocardial infarction angina as a bridge to of patients ; the in hospital mortality33 rate 26%, Another
angiography and revascularization. study of stenting of failed angioplasty in patients with car-
Randomized to tPA or rt PA in GUSTO-III.26 Although these diogenic shock reported a mortality rate of 27%.34
resultsare not definite because of broad confidence limits on the The role of ant platelet, platelet glycoprotein GP IIb/IIIa an-
observations, angiographic evidence supports a low reperfusion tagonists have shown to improve short term clinical out-
rate in patients with shock compared with other patients with come after angioplasty especially in patients at high risk for
ST. segment elevation MI.27 This is confirmed in hypotensive complications. However published experience. With GP IIb/
experimental models.28 For this reason, thrombolytic therapy IIIA receptor inhibition in patients with cardiogenic shock is
is reserve for whom an angiographic suit and emergency far limited to case reports,35 but extrapolation from other
revascularization are not immediately accessible. settings suggest that they may play an important adjunctive
E. Combination of Intra – aortic Balloon Counter pulsation role in patients with shock who undergo angioplasty.36
and G. Coronary Artery Bypass Surgery (CABG) :
Fibrinolytic Therapy : There are so many studies that show, favourable outcome
Use of IABP facilitates thrombus dissolution by tPA in ex- for patients with cardiogenic shock who had CABG . In
perimental model with and without hypotension. Non ran- patients with cardiogenic shock left main coronary artery
domized data from NRMI29 and a community experience disease or triple vessels diseases are common and potential
suggest lower mortality rates with this combined therapy contribution of ischemia in non infarct zone to myocardial
. For these reasons, when primary PCI is not feasible and infarction in patients with shock would support complete
fibrinolytic therapy is administered the concurrent use of revascularization.
the IABP for patients in cardiogenic shock may be beneficial. Published series include more than 200 patients who have
F. Percuteneous Transluminal Coronary Angioplasty (PTCA) : undergone surgical revascularization as a treatment of car-
diogenic shock overall perioperative mortality has been low
Early revascularization is recommended for patients less as compared with medical therapy alone, average in 40% but
than 75 years of age with ST elevation or LBBB who de- substantial selection bias is present in this non randomized
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compromise and a mortality rate of 58%. cardiopulmonary bypass, and inflammatory myocarditis. In sepsis
and, to some extent, in myocarditis, myocardial dysfunction seems
Acute Mitral Regurgitation to result from the effects of inflammatory cytokines, such as
tumor necrosis factor and interleukin-1. Myocardial dysfunction
Ischemic mitral regurgitation is usually associated with inferior
can be self-limited or fulminant, with severe congestive heart
myocardial infarction and ischemia or infarction of the posterior
failure and cardiogenic shock. In the latter situation, cardiovascular
papillary muscle, which has a single blood supply (usually from the
support with a combination of inotropic agents (such as dopamine,
posterior descending branch of a dominant right coronary artery).
dobutamine, or milrinone) and IABP may be required for hours
Papillary muscle rupture usually occurs 2 to 7 days after acute
or days to allow sufficient time for recovery. If these measures
myocardial infarction; it presents dramatically with pulmonary
fail, mechanical circula-tory support with left ventricular assist
edema, hypotension, and cardiogenic shock. When a papillary
devices can be considered.These devices can be used as a bridge
muscle ruptures, the murmur of acute mitral regurgitation may be
to cardiac transplantation in eligible patients or as a bridge to
limited to early systole because of rapid equalization of pressures
myocardial recovery; functional improvement with such support
in the left atrium and left ventricle. More important, the murmur
can be dramatic.
may be soft or inaudible, especially when cardiac output is low.
Echocardiography is extremely useful in the differential diagnosis,
Conclusions
which includes free-wall rupture, ventricular septal rupture, and
infarction extension pump failure. Hemodynamic monitoring Mortality rates in patients with cardiogenic shock remain
with pulmonary artery catheterization may also be helpful. frustratingly high (50% to 80%). The pathophysiology of shock
Management includes afterload reduction with nitroprusside and involves a downward spiral:Ischemia causes myocardial dysfunction,
intra-aortic balloon pumping as temporizing measures. Inotropic which in turn worsens ischemia.Areas of nonfunctional but viable
or vasopressor therapy may also be needed to support cardiac myocardium can also cause or contribute to the development of
output and blood pressure. Definitive therapy, however, is surgical cardiogenic shock. The key to a good outcome is an organized
valve repair or replacement, which should be undertaken as approach with rapid diagnosis and prompt initiation of therapy to
soon as possible because clinical deterioration can be sudden. maintain blood pressure and cardiac output. Expeditious coronary
Ventricular Septal Rupture Patients who have ventricular revascularization is crucial. When available, emergency cardiac
septal rupture have severe heart failure or cardiogenic shock, catheterization and revascularization with angioplasty or coronary
with a pansystolic murmur and a parasternal thrill. The classic surgery seem to improve survival and represent standard therapy
finding is a left-to-right intracardiac shunt (a “stepup” in oxygen at this time. In hospitals without direct angioplasty capability,
saturation from right atrium to right ventricle). On pulmonary stabilization with IABP and Thrombolysis followed by transfer
artery occlusion pressure tracing, ventricular septal rupture can to a tertiary care facility may be the best option. The SHOCK
be difficult to distinguish from mitral regurgitation because both multicenter randomized trial provides important data that help
can produce dramatic “V” waves. The diagnosis is most easily clarify the appropriate role and timing of revascularization in
made with echocardiography. Rapid stabilization— using intra- patients with cardiogenic shock.
aortic balloon pumping and pharmacologic measures—followed
by surgical repair is the only viable option for longterm survival. References
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