Analytic Review

Journal of Intensive Care Medicine

28(3) 151-165
Post Myocardial Infarction Cardiogenic ª The Author(s) 2013
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Shock: A Review of Current Therapies DOI: 10.1177/0885066611411407
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Ramford Ng, MD1 and Yerem Yeghiazarians, MD1

Abstract
Cardiogenic shock is often a devastating consequence of acute myocardial infarction (MI) and portends to significant mortality and
morbidity. Despite improvements in expediting the time to treatment and enhancements in available medical therapy and
reperfusion techniques, cardiogenic shock remains the most common cause of mortality following MI. Post-MI cardiogenic shock most
commonly occurs as a consequence of severe left ventricular dysfunction. Right ventricular (RV) MI must also be considered. Mechan-
ical complications including acute mitral regurgitation, ventricular septal rupture, and ventricular free-wall rupture can also lead to
cardiogenic shock. Rapid diagnosis of cardiogenic shock and its underlying cause is pivotal to delivering definitive therapy. Intravenous
vasoactive agents and mechanical support devices may temporize the patient’s hemodynamic status until definitive therapy by percu-
taneous or surgical intervention can be performed. Despite prompt management, post-MI cardiogenic shock mortality remains high.

Keywords
cardiogenic shock, myocardial infarction, mechanical complications

Received October 15, 2010, and in revised form March 15, 2011. Accepted for publication March 17, 2011.

Background complications of MI that may lead to cardiogenic shock. These

include acute severe mitral regurgitation (MR), ventricular sep-
Cardiogenic shock is often a devastating consequence of acute
tal rupture (VSR), and left ventricular free-wall rupture leading
myocardial infarction (MI) and portends to significantly
to cardiac tamponade. In the era of prompt percutaneous coron-
increased mortality and morbidity.1,2 Despite improvements in
ary intervention (PCI), acute stent thrombosis must also be con-
the delivery of prompt medical care and significant advances
sidered when cardiogenic shock presents in the post-PCI setting
in effective reperfusion strategies, the incidence of cardiogenic
(Table 2).7 Other causes of shock to carefully consider include
shock complicating acute MI is improving but remains unaccep- blood loss, sepsis, pulmonary embolism, aortic dissection, stress
tably high. Based on the Should We Emergently Revascularize
cardiomyopathy (Takotsubo), medication overdose, or adrenal
Occluded Coronaries for Cardiogenic Shock (SHOCK)3 registry
crisis.
published in 1995, the incidence of cardiogenic shock compli-
This review will focus on the pathophysiology, presentation,
cating MI was estimated at 7%. More recently, the Global Reg-
diagnostic workup, and medical/supportive therapy for each of
istry of Acute Coronary Events (GRACE) registry demonstrated
the most common causes of cardiogenic shock following MI.
a 24% decline in shock complicating MI in the GRACE cohort
The presently available mechanical circulatory support devices
from 1999 to 2006. This group comprises the vast majority of
will also be briefly reviewed.
deaths associated with acute MI. Even with expedient treatment,
the prognosis remains poor with mortality of cardiogenic shock
as high as 60%.4
Cardiogenic shock more often occurs following ST segment Major Causes of Shock Post-MI
elevation MI ([STEMI] 5%-9%)1,2,5 than in the setting of non- In the following section, we will outline the major causes of
ST segment elevation MI ([NSTEMI] 2.1%).6 It occurs when cardiogenic shock post-MI and discuss the etiology, risk
cardiac pump failure leads to inadequate end-organ tissue perfu-
sion, with systolic blood pressure (SBP) of less than 90 mm Hg, a
reduction in cardiac index ([CI] <1.8 L/min per m2), in the set-
ting of elevated left ventricular diastolic pressure (Table 1).7
1
University of California, San Francisco, CA, USA
The overwhelming preponderance9 of post-MI cardiogenic
Corresponding Author:
shock cases are due to left ventricular failure (74.5%). Like- Yerem Yeghiazarians, University of California San Francisco, Division of
wise, isolated right ventricular (RV) infarction needs to be con- Cardiology, 505 Parnassus Avenue, Box 0103, San Francisco, CA 94143, USA.
sidered. It is also important to recognize the mechanical Email: yeghiaza@medicine.ucsf.edu

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152
Table 1. Cardiogenic Shock: Diagnostic Criteria.7,8
Clinical
Hypotension with evidence of inadequate end-organ tissue
perfusion due to cardiac pump failure
Hemodynamic
Persistent hypotension (systolic blood pressure <90 mm Hg)
Reduced cardiac index (<1.8 L/min/m2)
Elevated left ventricular diastolic pressure (>18 mm Hg)7
factors, clinical presentation/diagnosis, therapy, and prognosis
of each condition.
Severe Left Ventricular Dysfunction
Etiology
The most common cause of cardiogenic shock complicating
an MI is resultant severe LV dysfunction. Myocardial
infarction is caused most commonly by atherothrombosis,
but may also be precipitated by stent thrombosis, coronary
artery dissection, or rarely coronary embolism. Cardiogenic
shock due to severe LV dysfunction accounted for nearly
75% of all acute MI cardiogenic shock presentations based
on the SHOCK trial registry.3In all, 27% presented to the
hospital already in shock, while 47% and 72% developed
shock within the first 6 hours and 24 hours of MI onset,
respectively.3 With older patients who present with STEMI
and shock, critical aortic stenosis should also be recognized
quickly as that can further deteriorate the clinical syndrome.
The increased use of primary PCI over thrombolysis as a
reperfusion strategy for acute MI has lowered the rate of
congestive heart failure (CHF).11,12 The 30-day mortality
for acute MI complicated by cardiogenic shock was as high
as 80% in the prereperfusion era and up to 58% in GUSTO I
patients treated with thrombolysis.13 Data on PCI reperfu-
sion in the setting of cardiogenic shock have shown
improvements in mortality.14 This is further supported with
data from the GRACE registry, which demonstrated a 24%
decline in shock, complicating MI in the GRACE cohort
from 1999 to 2006.
Patients with cardiogenic shock due to LV dysfunction com-
monly have multivessel disease including the left anterior des-
cending (LAD) artery or left main coronary artery.9,13,15 Based
on the autopsy studies, at least 40% of the LV mass is involved
when cardiogenic shock develops.13 This may be due to a large
territory infarct or a smaller infarct in a patient with an under-
lying impairment of LV function prior to the current presenta-
tion. Patients with cardiogenic shock following acute MI have
an LV ejection fraction on average of 30%.7,13 In the acute MI
setting with impaired segmental wall motion, LV chamber size
dilates to accommodate an increased end-diastolic volume and
maintain overall stroke volume and cardiac output. While
hemodynamically stabilizing in the immediate setting, the
LV adaptation serves to further increase myocardial wall stress,
LV dilation, and heart failure.7
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Journal of Intensive Care Medicine 28(3)
Table 2. Causes of Cardiogenic Shock.8,10
Severe left ventricular dysfunction
Right ventricular infarction
Acute mitral regurgitation
Ventricular septal rupture
Free-wall rupture
Table 3. Risk Factors for Developing Cardiogenic Shock.7,13,17
Older age
Prior myocardial infarction (MI)
Female gender
Diabetes mellitus
Anterior wall MI
Risk Factors
Based on the GUSTO-I trial, age, Killip Class >2, anterior MI,
and heart rate (HR) >100 bpm are seen in a majority of the
cases16 Other noted risk factors have included prior MI, female
gender, and diabetes mellitus (Table 3).13,18
Clinical Presentation/Diagnosis
Physical examination may reveal a S3 auscultated on cardiac
examination, auscultation of new murmurs, signs of pulmonary
congestion, and evidence of inadequate end-organ perfu-
sion.7,13 These include impaired mentation, cool or clammy
extremities, and oliguria. With patients who develop cardio-
genic shock after PCI has recently been performed, particularly
by femoral artery approach, close examination of the vascular
access site should be performed to rule out significant bleed
from an access site complication.
Electrocardiogram (ECG) may reveal the patient’s initial MI
but may be nonspecific in 15% to 30% of patients.7 If the
patient has recently had a coronary stent placed, ECG may
be useful in diagnosing a reinfarction caused by stent thrombo-
sis. The absence of profound ECG changes should heighten the
consideration of other causes of cardiogenic shock.
Echocardiography is useful to visualize the extent of LV
dysfunction. Additionally, RV function and mechanical causes
of cardiogenic shock can be evaluated in search of other conco-
mitant explanations of the patient’s clinical status.
Therapy
The paramount goal of any therapy should be attempts to
achieve prompt revascularization. The patient should be
brought expediently to the cardiac catheterization laboratory
for coronary angiography. Revascularization should be per-
formed without delay by PCI or emergency coronary artery
bypass graft (CABG) surgery if the anatomy is suitable. If there
is no cardiac catheterization laboratory at the presenting
facility and transfer to a cardiac catheterization capable facility
with emergent PCI revascularization cannot be achieved within
Ng and Yeghiazarians 153

Table 4. Receptor Activity of Commonly Used Inotropic and A recently published study comparing the use of norepi-
Vasopressor Agents. nephrine and dopamine in patients with shock challenges the
preferential use of dopamine over norepinephrine.21 De Backer
Receptor Activity20 et al examined the randomized blinded first-line use of
Vasoactive
Agent Infusion Range a1 b1 b2 Dopamine dopamine or norepinephrine in 1679 patients presenting with
various types of shocks. Although the primary endpoint of
Epinephrine 0.01-0.1 mg/kg/min """"" """" """ — 28-day mortality was not statistically different between groups,
or (2-10 mg/min) the dopamine as first-line agent group experienced nearly twice
Norepinephrine 0.01-3 mg/kg/min """"" """ "" —
the number of serious arrhythmic (ventricular tachycardia, ven-
Phenylephrine 0.4-9.1 mg/kg/min """"" — — —
Dopamine 2.0-20 mg/kg/min """ """" "" """"" tricular fibrillation, or atrial fibrillation) events (24.1% in the
Dobutamine 2.0-20 mg/kg/min " """"" """ — dopamine-treated group and 12.4% in the norepinephrine
group). Further, when looking at the prespecified subgroup
Increasing number of arrows indicates greater effect. analysis of cardiogenic shock (280 patients, with 58% having
MI as the underlying etiology), the rate of death at 28 days was
90 minutes, immediate thrombolytic therapy should be higher for those in cardiogenic shock managed with dopamine
considered. Successful reperfusion following STEMI is sug- as compared to norepinephrine (P ¼ .03). The mechanistic
gested by relief of symptoms, maintenance/restoration of explanation of this finding is unclear but may be related to the
hemodynamic and electrical stability, and a reduction by at increased HR and more frequent arrhythmias seen in the dopa-
least 50% in the ST-segment pattern of injury on ECG per- mine group.
formed 60 to 90 minutes following initiation of therapy.19 Vasodilators, while useful in reducing wall stress by after-
Following reperfusion, the goal of therapy is to support the load reduction, should not be used in the hypotensive patient.
patient clinically and hemodynamically to allow for recovery Acute coronary event inhibitors mitigate infarct expansion and
of stunned or hibernating myocardium. reduce preload and afterload but should not be started in the
Arrhythmias should be treated and hypoxemia should be cor- setting of cardiogenic shock. Likewise, b-blockers, useful for
rected. Careful volume assessment and continuous monitoring is secondary prevention, should not be routinely started early in
required. In the setting of acute MI and cardiogenic shock, fluid the course of an acute STEMI. The Clopidogrel and Metoprolol
can redistribute into the lungs, even in the setting of intravascular in Myocardial Infarction Trial (COMMIT) demonstrated that
hypovolemia.13 When signs of pulmonary edema are present, a starting IV b-blockade early in the presentation of an acute
trial of intravenous (IV) diuretic may be warranted. Placement MI followed by an oral b-blocker reduced in-hospital reinfarc-
of a pulmonary artery (PA) catheter can help assess the patient’s tion and ventricular fibrillation rates, but increased the risk of
fluid status. cardiogenic shock. This was most notable within the first 12
Patients with cardiogenic shock due to severe LV dysfunc- hours of admission and translated to no overall mortality
tion commonly require the addition of IV vasopressor support. benefit.22
The American College of Cardiology / American Heart Asso- Because unexpectedly low systemic vascular resistance is
ciation (AHA/ACC) STEMI guidelines list as a Class I recom- often seen in the setting of cardiogenic shock, inflammatory
mendation for the use of vasopressor support in patients with and neurohormonal mediators have been speculated to play a
hypotension if volume loading does not correct the hypoten- role in the development and propagation of this clinical dete-
sion.19 There are several vasoactive agents used in the manage- rioration.23-25 Inflammatory cytokines increase the expression
ment of shock (Table 4). Norepinephrine is a direct-acting of inducible nitric oxide synthase (NOS). This increases the
agent that acts on both a- and b-adrenergic receptors of the levels of NO, thereby decreasing systemic vascular resistance
postganglionic sympathetic nerve to provide vasoconstriction and myocardial contractility. Initial small nonrandomized
and to a lesser degree, augmentation of cardiac output.20 Dopa- single-center studies of a nonselective NOS inhibitor showed
mine acts as a direct agent stimulating the a- and b-adrenergic improved hemodynamic parameters and 30-day mortality.23,24
receptors and indirectly by both stimulating increased norepi- Subsequently, a larger international, multicenter, randomized-
nephrine release and conversion into norepinephrine.20 The controlled, double-blind, placebo-controlled trial (TRIUMPH)
ACC/AHA guidelines specifically favor the use of dopamine evaluated the use of the NOS inhibitor L-n-monomethyl-
as the agent of first choice, beginning at 2.5 mg/kg per min and arginine (L-NMMA), in post-MI cardiogenic shock patients
titrating up to 15 mg/kg per min.19 If the patient’s SBP is mark- who had undergone PCI.25 This demonstrated a blood pressure
edly reduced (<80 mm Hg), the guidelines support the use of IV improvement, but the study was discontinued early for failure
norepinephrine, as a more potent vasoconstrictor with less poten- to demonstrate a 30-day morality benefit. The use of nonselec-
tial to precipitate arrhythmia. Norepinephrine can be started at tive NOS inhibitors has not been widely demonstrated to
0.1 mg/kg per min and titrated up in increments of 0.02 mg/kg/ improve the overall clinical patient outcome.
min. Norepinephrine should be promptly transitioned to dopa- There should be a low threshold to initiate mechanical circu-
mine when SBP improves to >80 mmHg. Additionally, the latory support. An intra-aortic balloon pump (IABP) can be
guidelines suggest adding IV dobutamine once the SBP reaches quickly and percutaneously inserted. The IABP augments car-
>90 mmHg to limit the dopamine dose.19 diac output by afterload reduction. If available, an Impella left

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154
ventricular assist device (LVAD) may be considered. Inserted
percutaneously, the Impella device functions by preload reduc-
tion with a greater degree of cardiac output support. Other
mechanical circulatory support devices to consider include the
LVAD and extracorporeal membrane oxygenation (ECMO)
support. These devices will be discussed in more detail later
in this review.
Prognosis
Ultimately, the patient’s prognosis and ability to wean off tem-
porizing measures will depend on the amount of myocardium
recovered following expedient revascularization. Multiple
studies have shown improved survival with early PCI or surgi-
cal revascularization.26-28 Despite aggressive therapeutic mea-
sures, mortality remains high. Overall in-hospital mortality of
the 1116 post-MI patients with cardiogenic shock due to LV
dysfunction was 59.2% in the SHOCK trial and registry.9 The
mortality of post-MI LV dysfunction patients undergoing
percutaneous transluminal coronary angioplasty (PTCA) at any
time during hospitalization for cardiogenic shock is 45% based
on 936 patients (including SHOCK trial and registry patients).9,26-28
Right Ventricular Infarction
Etiology
Right ventricular infarction occurs most commonly with MI of
the inferior or inferior-posterior wall. Patients typically present
with a right coronary artery occlusion proximal to the RV mar-
ginal or with a left circumflex occlusion in a left dominant
system.29
The incidence of RV infarction ranges widely from 14% to
84%, depending on the study and criteria used.30,31 Cardio-
genic shock caused by ‘‘isolated’’ RV infarct accounted for
2.8% of cardiogenic shock patients from the SHOCK registry.9
Risk Factors
Patients with cardiogenic shock due to RV MI compared with
LV MI are likely to be younger, present with their first MI,
present with single-vessel coronary disease, and less likely to
have anterior wall MI.32
Clinical Presentation/Diagnosis
In the absence of underlying or concomitant LV dysfunction,
physical examination reveals signs of right heart failure with
a clear pulmonary examination. The triad of hypotension, jugu-
lar venous distention, and clear lungs in a patient with an infer-
ior infarct is well recognized but sensitivity of the triad is poor
(25%).33,34 Other findings may include tricuspid regurgitation,
RV gallop, pulsus paradoxus, and potentially high-grade atrio-
ventricular block.31 Elevated jugular venous pressure (JVP)
alone is sensitive (88%) but poorly specific (69%) for RV
MI.34 Kussmaul’s sign, defined by increase in jugular venous
pressure with inspiration and often associated with constrictive
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Journal of Intensive Care Medicine 28(3)
pericarditis, is a useful finding.31 The presence of elevated JVP
and Kussmaul’s sign is both sensitive (88%) and highly spe-
cific (100%) for the presence of hemodynamically significant
RV MI.34
The ECG, particularly with right-hand side leads, is a quick
but vital diagnostic tool to rapidly identify RV MI and typically
shows an inferior territory MI. There are several ECG criteria
that exist.35,36 The ECG criterion most frequently used is >1 mm
ST-segment elevations seen in lead V4R of a right-hand side
ECG; it has a positive predictive value of 87% (sensitivity
80% and specificity 88%).37-39 It is also a strong independent
predictor of major complications and in-hospital mortal-
ity.38,39 Other electrocardiographic findings may include
sinus bradycardia,36 atrial fibrillation,40 complete heart block,
and new right bundle branch block.39
An echocardiogram is the study of choice for a quick defi-
nitive assessment of RV function. Echocardiographic findings
include RV hypokinesis or akinesis, RV dilation, and right
atrial (RA) enlargement.41 Additionally, flattening or reversed
bowing of the intraventricular septum may be seen and is
caused by RV pressure and/or volume overload.42 Echocardio-
graphy can also be used to assess the degree of LV impairment
and to exclude the mechanical causes of cardiogenic shock.
Because of the utility of echocardiography, PA catheter
measurements are often not needed to diagnose RV infarction.
Accepted hemodynamic criteria for RV infarct include an RA
pressure greater than 10 mm Hg, ratio of RA:pulmonary capil-
lary wedge pressure (PCWP) of 0.8 or greater, or an RA pres-
sure no less than 5 mm Hg less than the PCWP.13,42 The PCWP
is often normal or low unless there is concomitant or underly-
ing LV dysfunction. Because of delayed upstroke and impaired
relaxation, the RV pressure waveform is often described as
bifid.30
Therapy
Following prompt reperfusion, medical therapy for RV infarc-
tion includes supporting preload while reducing afterload until
RV function returns. In the absence of other mechanical com-
plications, IV fluid administration may be needed to maintain
preload and cardiac output. Close volume and hemodynamic
assessment should be monitored in all patients, especially those
with LV dysfunction to avoid precipitating pulmonary edema.
A PA catheter may be useful in managing the fluid status. Pre-
load reducing agents such as nitrates and diuretics should be
avoided. If fluid administration fails to improve cardiac output,
inotropic support with dobutamine can be tried to improve RV
performance. Dobutamine is thought to improve RV output by
increasing the interventricular septal contractility, in addition
to decreasing pulmonary vascular resistance.43,44 Small studies
suggest a possible benefit of the IABP in the setting of cardio-
genic shock from RV MI.45-47 The speculated mechanism of
benefit is by increased coronary perfusion and decreased pul-
monary arterial resistance. If intravenous fluids (IVF) and
vasopressor support are unable to maintain the patient’s
Ng and Yeghiazarians
hemodynamic status, a right ventricular assist device (RVAD)
may be an option to provide temporizing mechanical RV
support.
Atrioventricular (AV) synchrony should be maintained.
Advanced heart block may occur in up to 48% of patients pre-
senting with RV infarct.48 In patients with complete heart
block, AV sequential pacing aides in cardiac output and rever-
sing cardiogenic shock while ventricular pacing alone provides
no benefit.49
Prognosis
Prognosis is based on the ability to reperfuse the affected RV
wall territory. The RV has lower oxygen requirements, is thin-
ner walled, is perfused during systole and diastole, and often
has collateral blood flow from the LAD and Thesbian
veins.13,30 Most patients will respond to reperfusion and
adjunctive therapy in 48 to 72 hours. Overall in-hospital mor-
tality32 of cardiogenic shock due to RV MI patient in the
SHOCK registry was 55%. A retrospective look by Brodie and
colleagues demonstrated the benefit of early PCI. Of the 30
patients, with cardiogenic shock attributable to RV MI, those
treated with PCI had an in-hospital mortality of 23%, with
96% (22 of 23) hospital survivors remaining alive at a median
follow-up of 3.5 years.50
Acute MR
Etiology
Acute MR accounts for 8.3% of cardiogenic shock presenta-
tions based on the SHOCK registry.51 Although traditionally
thought to occur 2 to 7 days post-MI, the SHOCK registry
showed a median time for papillary muscle rupture of 13 hours
post-MI.51
Most ischemic MR is associated with inferior or posterior
MIs, self-resolving, and of little clinical significance. However,
acute ischemic MR causing cardiogenic shock can be cata-
strophic and needs to be recognized and treated promptly.52
The mechanism of acute ischemic MR can be classified as
functional or structural in etiology. Functional MR results from
MI causing an adaptive LV dilatation and resultant mitral valve
annular dilation. Papillary muscle dysfunction with segmental
wall motional abnormality at the muscle insertion can also lead
to poor valve leaflet coaptation. Structural causes include chor-
dae or papillary muscle rupture resulting in a flail mitral leaflet.
Risk Factors
Patients with cardiogenic shock from acute MR tend to be more
commonly female, older age, diabetes mellitus, and have
underlying cerebrovascular disease and preexisting sympto-
matic coronary artery disease.52
Patients presenting with RCA infarcts with a right dominant
coronary circulation are at greatest risk of papillary muscle rup-
ture. The mitral valve posteromedial papillary muscle, which is
perfused by the posterior descending artery (PDA), is 6 to 12
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155
times more likely to rupture than the anterolateral papillary
muscle, which receives dual blood supply from both the LAD
artery and the left circumflex coronary artery.53,54
Clinical Presentation/Diagnosis
Cardiac auscultation reveals a soft pansystolic murmur best
heard at the apex with radiation to the left axilla. In patients
with impaired LV systolic function or elevated left atrial pres-
sure, this murmur may be absent.7,55 There is no thrill. Physical
examination may reveal signs of pulmonary edema.
Electrocardiogram may show tachycardia and a recent infer-
ior or posterior MI, but otherwise adds little to the diagnostic
workup.
An echocardiogram with color flow Doppler is often the
diagnostic test of choice and can help differentiate acute MR
from intraventricular rupture, which may have similar clinical
findings. The presence of severe MR with normal LV cavity
size is suggestive of acute MR.55 The size and direction of the
regurgitant jet and any evidence of a flail leaflet can be visua-
lized. A transesophageal echocardiogram may be needed for
more definitive assessment if a papillary muscle rupture is sus-
pected but not seen by transthoracic echocardiogram.
PA catheterization may reveal a large V wave in the PCWP
tracing.53 A large V wave may also be seen in the setting of a
ventricular septal defect (VSD) or a poorly compliant LV.
There should not be any right heart step-up of oxygen satura-
tion, but oxygen saturation drawn from a distal pulmonary
artery branch may likewise be contaminated with the large
mitral regurgitant jet flow.54
A left ventriculogram performed during cardiac catheteriza-
tion can also provide a qualitative assessment of the MR
severity.
Therapy
Immediate medical management is based on the aggressive use
of vasodilator therapy, such as nitroprusside, to provide after-
load reduction and maintain forward cardiac output. This, how-
ever, cannot be used in the patients with acute hypotension.
Mechanical circulatory support with an IABP should be
considered in the patients with hypotension unable to tolerate
vasodilator therapy, in order to improve forward cardiac flow
while reducing shunt regurgitant fraction.
The decision for prompt surgical repair as well as prognosis
is based on the degree of MR and whether the MR is due to
papillary muscle rupture or functional MR as a consequence
of annular dilation in the setting of severe LV dilation.
In the setting of functional MR, an initial strategy of agg-
ressive medical management with temporizing mechanical
device circulatory support to stabilize the hemodynamic sta-
tus is warranted. With recovery of stunned myocardium fol-
lowing PCI reperfusion and with the mitral valve (MV)
apparatus intact, the degree of MR may improve and obviate
any need for surgical intervention.
156
In patients with a ruptured papillary muscle causing flail
leaflet, patients should be promptly stabilized with medical and
mechanical device therapy followed by urgent surgical correc-
tion. Surgery should not be delayed when a correctable lesion is
present. Hemodynamic collapse in these patients can be sudden
and life threatening.13 Surgical survival is predicted by early
operation, short duration of shock, and mild degree of LV and
RV involvement.7,56 Surgical correct may be achieved by
mitral valve repair or valve replacement.
Prognosis
Uncorrected, post-MI acute MR due to complete papillary mus-
cle rupture is associated with a 75% mortality at 24 hours and
95% mortality at 2 weeks.57 Operative mortality58 approaches
50%. Overall in-hospital mortality in the SHOCK registry of
post-MI cardiogenic shock due to acute MR was 55%.9
Ventricular Septal Rupture
Etiology
As with most mechanical complications of MI, VSR was his-
torically thought to occur several days post-MI, with an aver-
age onset of 2 to 4 days post-MI.59,60 This correlates with
pathologic findings demonstrating necrotic tissue most abun-
dant at this time and subsequent development of collateral cor-
onary flow and connective tissue to this territory beginning at
day 4.61,62 More recent registries have shown a median time
to the development of VSR to be 16 to 24 hours.51,63 Ventricu-
lar septal rupture accounted for 4.6% of the cases of cardio-
genic shock in the SHOCK registry.9
Risk Factors
Ventricular septal rupture is seen more often in men compared
to women (3-2),64 with a mean age of presentation of 62.5
years.65 Ventricular septal rupture most commonly occurs after
a patient’s initial MI.60,66 Systemic hypertension prior to MI
was present in over half of those patients developing VSR, but
this is comparable to those experiencing MI without VSR.67
Traditionally, VSR occurs in the setting of a transmural MI
and is more commonly associated with anterior or anterolateral
MIs with the LAD coronary artery as the culprit (up to 60% of
the time).68,69 In 20% to 40% of cases, an inferior VSR is the
cause, attributable to an occluded dominant right coronary
artery, or less frequently, a dominant left circumflex coronary
artery.70 Pathologically, they can be classified as simple, a
direct through-and-through any defect, or complex, having a
serpigenous dissection tract away from the primary VSR site.62
Simple defects are typically anterior VSR defects, while com-
plex forms are more commonly found in inferior VSRs.
Clinical Presentation/Diagnosis
The left-to-right shunting resulting from VSR typically leads to
CHF and hemodynamic decompensation. Patients are often
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Journal of Intensive Care Medicine 28(3)
stable before developing sudden onset of recurrent angina (up
to 50% of cases), cardiogenic shock, and pulmonary edema
with right-hand side heart failure.7 The physical examination
may reveal a new harsh holosystolic murmur most prominent
at the lower left sternal border in 90% of presentations, with
a thrill noted in half of the cases.53,62 The new onset systolic
murmur and sudden hemodynamic compromise in the post-
MI patient can be mistaken for acute MR, which can occur con-
comitantly with VSR. Absence of a murmur does not rule out a
VSR.
An echocardiogram with spectral and color flow Doppler is
a powerful tool in diagnosing the presence of VSR and demon-
strates the shunt size and location.71 PA catheterization can be
used to confirm the diagnosis and calculate shunt fraction when
echocardiographic images are nondiagnostic. Oxygen satura-
tion step up of 8% to 9% or greater will be seen between RA
and PA.72
A left ventriculogram performed during cardiac catheteriza-
tion can also be used in identifying the presence, location, and
size of the VSR.
Therapy
Once the diagnosis is made, medical stabilization with inotro-
pic support such as dopamine or dobutamine should be started.
Vasodilators therapy may reduce the degree of shunting but
should be avoided in the patients with hypotension. The goals
of immediate temporizing management include (a) reducing
systemic vascular resistance to reduce left-to-right shunt, (b)
maintaining cardiac output and arterial blood flow to ensure
adequate end-organ perfusion, and (c) maintaining coronary
artery blood flow.62 Mechanical circulatory support is fre-
quently necessary as a temporizing measure prior to surgical
repair. Placing an IABP assists in each of the above mea-
sures.73-75 The transient benefit of the IABP peaks at 24 hours,
with no further benefit derived from prolonged use.73,75 The
Impella circulatory support device is contraindicated in intra-
ventricular rupture. Because of the high mortality associated
with untreated VSR and high surgical mortality in the setting
of concomitant cardiogenic shock, early surgical repair is the
treatment of choice, even in the hemodynamically stable
patient.63 Age, CI, and shunt volume are related to surgical out-
come.76 Despite the high in-hospital mortality, hospital survi-
vors treated surgically do well on a long-term basis.63 Of the
20 patients taken for urgent surgical repair of postinfarct VSR
performed by Scanlon and colleagues, 12 survived to hospital
discharge.73 At a mean follow-up of 47.9 months, there was
1 late noncardiac death. Of the 12 patients, 11 survived, all
in NYHA CHF class I or II.73
Transcatheter closure of post-MI VSR has been demon-
strated in case reports and limited single-center series with
varying results.77-79 Despite the less invasive approach, mortal-
ity remains high.80 Transcatheter VSR closure has been used
with some success in postsurgical repair patients with residual
or recurrent defects.80,81 The optimal use of transcatheter
devices in the overall treatment strategy currently remains
Ng and Yeghiazarians
unclear although may be a consideration in the very high-risk
patients.62
Prognosis
Without surgical intervention, postinfarction VSR mortality is
high and notably highest in the acute setting. It is associated
with 25% mortality at 24 hours, 50% at 1 week, and 80% at
4 weeks; only 7% live beyond 1 year.64,82 Even with prompt
surgical attention, mortality is quite poor. In the SHOCK
registry examination of 55 patients manifesting a VSR in the
setting of cardiogenic shock, in-hospital mortality of postin-
farction VSR was 96% in the medically managed group (1 of
24 survived to hospital discharge) compared to 81% mortality
of the surgically treated group (6 of 31 patients surviving to
hospital discharge).83 The overall mortality the post-MI VSR
group was 87.3%, significantly higher than mortality by other
causes of post-MI cardiogenic shock.83
Free-Wall Rupture/Tamponade
Etiology
Ventricular free-wall rupture typically occurs within the first
week after a transmural MI. In all, 50% present within the first
5 days after MI, with 90% presenting by the first 2 weeks.84,85
It accounted for 1.7% of cardiogenic shock patients in the
SHOCK registry and had a 30-day mortality of 55% based on
the SHOCK registry data.85 Cardiac rupture (free-wall rupture
and VSR) constitutes the second most common cause of in-
hospital death in patients with acute MI.86-88
As with VSR, free-wall ruptures can be classified as simple
or complex and can occur over the anterior or lateral and pos-
terior LV wall.84,85 Lateral and posterior wall MIs are specu-
lated to be more prone to free-wall rupture but seen less
frequently due to the overall higher proportion of anterior wall
MIs.89 Free-wall rupture can present with an acute, subacute, or
chronic course with those associated with cardiogenic shock
typically having an acute or subacute course. With acute rup-
ture, the patient develops sudden onset of chest pain followed
by cardiac tamponade, rapid hemodynamic collapse, and sud-
den death.90 Because of the rapid clinical deterioration with
hemorrhagic rupture into the pericardium, acute free-wall rup-
ture is not amenable to current therapies.62 Subacute presenta-
tions result in a smaller contained rupture that may be
temporarily stabilized by clot or fibrinous pericardial adhesions
and may account for up to one third of free-wall ruptures.62,89
Risk Factors
Risk factors for free-wall rupture resulting from MI include
female gender, age91,92 greater than 55, hypertension, large
infarct size, and delayed or incomplete revascularization.67,93-
95
Patients presenting with their first MI (90%) and those with
single-vessel disease are also more likely to rupture,67,92 sug-
gesting a limited collateral coronary blood supply.96,97
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157
Clinical Presentation/Diagnosis
Physical examination findings may be consistent with cardiac
tamponade and include jugular venous distension, pulsus para-
doxus, and diminished heart sounds in addition to hypoten-
sion.7,86 The ECG may reveal low voltages throughout. The
cardiac rhythm commonly seen at the time of rupture includes
sinus bradycardia, junctional rhythm, complete heart block, or
idioventricular rhythm.98 An echocardiogram reveals pericar-
dial effusion and may show signs of cardiac tamponade includ-
ing RV diastolic collapse and >25% respiratory variation in
mitral inflow. The ventricular wall defect may also be appre-
ciated on echocardiography. PA catheterization will reveal
equalization of right-hand side diastolic pressures if cardiac
tamponade has developed.
Therapy
Medical therapy with fluids and inotropes can be initiated as
the operating room is readied but should not delay surgical
intervention. Prompt recognition and urgent surgical repair are
key to the outcome.
Immediate pericardiocentesis may be performed as the oper-
ating room is being readied. Emergent surgical repair remains
the patient’s best chance for survival.99 Surgical repair of free-
wall rupture includes resection of the infracted area and closure
of the rupture territory either by Teflon or Dacron patches or
with the use of biological glues.62
Prognosis
Without prompt surgical attention, post-MI free-wall rupture is
exceedingly high. Figueras et al examined 425 consecutive
free-wall ruptures over a 30-year period from single-center
experience and found that the mortality rate associated with
free-wall rupture had decreased from 94% to 75%.86 This was
likely due to increased use of reperfusion therapy and improved
post-MI care. Because of the rapid hemodynamic deterioration,
acute free-wall ruptures are almost always fatal before surgical
intervention can be initiated. Subacute free-wall ruptures, how-
ever, do provide a window of opportunity for prompt interven-
tion. Lopez-Sendon et al prospectively examined 1247
consecutive patients with acute MI including 33 patients with
subacute free-wall rupture diagnosed at operation. In all, 76%
(25 of 33) of the patients with subacute free-wall rupture sur-
vived the surgical correction, with 48.5% (16) being long-
term survivors.99
Mechanical Circulatory Support Devices
In the setting of post-MI cardiogenic shock, pharmacologic
therapy offers inotropic support at the expense of increased
myocardial tissue oxygen demand. Despite its benefits, phar-
macologic therapy alone may not be adequate to maintain sys-
temic perfusion. For this reason, mechanical circulatory
support devices should be considered for additional adjunctive
therapy. The mechanical circulatory assist devices require
158 Journal of Intensive Care Medicine 28(3)

intensive care unit monitoring, systemic anticoagulation, and

significant limitation in patient mobility. Mechanical assist
devices should not be inserted into patients when there is no
anticipation of recovery.

Intra-Aortic Balloon Pump

Intra-aortic balloon pump counterpulsation is the most com-
monly used circulatory support device used in the presence
of cardiogenic shock7 and can provide temporizing circulatory
augmentation in an acutely decompensating patient. This is due
in part to its wide availability at most community and tertiary
hospitals. It can be quickly placed in an emergent setting.
Device sizing is based on patient height and most commonly
8F (2.7 mm) in caliber, although 7F (2.3 mm) IABPs are less
commonly available. The device is percutaneously inserted
through a common femoral artery sheath or sheathless and
positioned in the descending thoracic aorta. It is ideally seated
below the takeoff of the left subclavian artery and above the
level of the renal arteries. The counterpulsation is timed with
the cardiac cycle by surface ECG or arterial pressure tracings.
The theoretical benefits of IABP are 2-fold: inflation of the
balloon during diastole to augment coronary artery perfusion
and rapid presystolic deflation of the balloon to provide reduc-
tion in systemic afterload. There is no increase in myocardial
tissue oxygen demand.7 This circulatory support is intended
to aid as a temporizing bridge to myocardial recovery or defi-
nitive surgical therapy. It is approved for use up to 72 hours but
can remain in place longer (up to 14 days) if closely monitored
and no complications have arisen.15
Estimations of hemodynamic benefit provided by this
device range from ‘‘modest’’ to 20% increase in cardiac output,
while decreasing the mean pulmonary capillary wedge pressure
by the same degree.15,46
Intra-aortic balloon pump therapy is considered a class I
indication (ACC/AHA guidelines) for the management of
cardiogenic shock not rapidly reversed by pharmacological
therapy.11 Observational data from the GUSTO-1 and SHOCK
registry suggest improved survival with early IABP use in this Figure 1. Illustration of TandemHeart device (CardiacAssist, Inc,
setting. The most common vascular complications of IABP Pittsburgh, Pennsylvania). http://www.cardiacassist.com/TandemHeart/.
use is limb ischemia, which can occur in up to 14% to 45%
of patients.100 Other IABP complications include cerebral
embolism during device insertion, renal embolism, infection, circulation independent of the native cardiac rhythm. Limited
dissection of the aorta or iliac artery, or aortic perforation. studies have examined their use in post-MI patients with refrac-
The IABP is contraindicated in patients with no anticipation tory cardiogenic shock.101,102 Based on the type of device, flow
of recovery, aortic dissection, severe peripheral vascular dis- can be pulsatile or continuous. They can be implantable or
ease, or aortic regurgitation. extracorpeal. Percutaneously inserted LVADs include the Tan-
demHeart (CardiacAssist Inc, Pittsburgh, Pennsylvania), and
the Impella device (Abiomed Inc., Danvers, Massachusetts;
Ventricular-Assist Devices
Figures 1-3 and Table 5). Use of LVAD and referral for cardiac
A host of ventricular-assist devices (VADs) are available to transplantation may be considered in appropriate cases.
maintain circulatory support. In contrast to the IABP, which are
synchronized to the cardiac cycle and reduced afterload, VADs
provide hemodynamic stability by maintaining systemic flow
Tandem Heart
while reducing preload.7,15 Originally designed for intraopera- The TandemHeart is a left atrial to femoral artery bypass
tive circulatory support, these devices can maintain systemic device, which can be inserted for up to 14 days and provides

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Ng and Yeghiazarians
Figure 2. Illustration of Impella device (ABIOMED, Inc., Danvers,
Massachusetts) seated in its functional positional across the aortic
valve. http:// www.abiomed.com/products/Impella.cfm
up to 4 L/min per m2 of flow.15,103 It requires a 21F (7 mm)
transatrial septal puncture and the insertion of a single 15F to
17F (5-5.7 mm) cannula into the common femoral artery.
Alternatively, a 12-F (4 mm) cannula can be inserted into both
common femoral arteries. Blood is continuously removed from
the left atrium and delivered through the pump and an arterial
perfusion catheter into the 15F to 17F (5-5.7 mm) common
femoral artery perfusion catheter.15 This results in delivering
left atrial oxygenated blood into the systemic circulation. The
preload and afterload is decreased while cardiac output in
augmented.103
Impella
The Impella device is a percutaneously placed left ventricular
mechanical support device. It is an impeller-driven axial flow
device based on the Archimedes screw principle with a rotor
that can operate at up to 50 000 rpm.103,104
The catheter-based device can be rapidly placed through the
femoral or brachial artery with the electrical motor drive screw
seated across the aortic valve. The inflow cannula is located at
the pigtail end of the device, which rests in the left ventricle
with the outflow port situated above the motor in the ascending
aorta.
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159
Figure 3. Percutaneous Impella 2.5L device seated in the left ventricle of
a patient with cardiogenic shock due to left ventricular (LV) dysfunction.
There are 2 sizes presently available. The 2.5 L/min device
requires a 13F (4.3 mm) sheath and can be placed percuta-
neously in a cardiac catheterization laboratory, while the 5 L/
min device requires a surgical cut down of the femoral or axi-
ally artery to place a 21F (7 mm) sheath. The Impella 2.5-L
device can remain in place for up to 5 days.103
The ISAR-SHOCK trial evaluated 26 patients presenting
with cardiogenic shock due to acute MI and randomized them
to post-PCI IABP or Impella placement.105 The Impella group
met its primary end point of a greater change in CI from base-
line to 30 minutes (P ¼ .02). The Impella arm demonstrated an
improvement in CI of 0.49 L/min per m2 (from 1.71 L/min per
m2 at baseline to 2.2 L/min per m2), while the IABP arm
improvement in CI was 0.11 L/min per m2 (1.73-1.84 L/min
per m2). However, the CI between groups at all measured time
points up to 30 hours was similar. At 30 hours, the Impella arm
CI was 2.51 L/min per m2 compared to the IABP arm CI of 2.40
L/min per m2. There was no difference in the 30-day mortality,
but this trial was underpowered for clinical outcomes. Larger
trials of this device are needed before its widespread use can
be advocated in this context.
The Impella device is contraindicated in the presence of aor-
tic valve disease, ventricular septal defect, hypertrophic
obstructive cardiomyopathy, or LV thrombus.
Conclusion
Despite improvements in time to deliver MI treatment and
enhancements in available medical therapy and revasculariza-
tion techniques, cardiogenic shock remains an all too prevalent
 160
Table 5. Comparison of Available Mechanical Support Devices.15

Complications Effect Time Advantage Limitation Contraindication

IABP Limb ischemia; aortic 0.5-1 L/min Up to Prolonged support; Requires stable rhythm; Moderate-to severe AI;
dissection 14 days unloads LV; lowest level of support aortic disease;
ease of use uncontrolled sepsis;
coagulopathy PAD

CPS bleeding; hemolysis;
stroke; embolus
pVAD (Tandem Heart) Pericardial tamponade;
aortic puncture; limb
ischemia
Transvalvular LVAD Aortic valve damage
(Impella)
Provides complete
circulatory support
3.5 L/min
2.5 L/min, 5 L/min
Up to6 hours Independent of rhythm; Limited duration of Moderate-to severe AI;
allows controlled trans- support; PAD; coagulopathy
fer to; or full support requires perfusionist;
does not unload LV
Up to 14 days Prolonged support; Large cannula; requires VSD; PAD; LA thrombus
full support trans-septal puncture
Up to 5 days Unloads LV Aortic stenosis; LV thrombus; VSD;
RV failure aortic valve disease;
hypertrophic
obstructive CM

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Abbreviations: IABP, intra-aortic balloon pump; CPS, cardiopulmonary support; pVAD, percutaneous ventricular-assist device; LVAD, left ventricular-assist device; VSD, ventricular septal defect; PAD, peripheral arterial
disease; LA, left atrial; CM, cardiomyopathy.
Ng and Yeghiazarians
sequelae following acute MI. Expedient cardiac catheterization
and coronary artery revascularization are the key to restoring
cardiac function and preventing subsequent development of
cardiogenic shock. This can be achieved by PCI and/or surgical
revascularization if anatomy is suitable and provide improved
mortality benefit compared to medical therapy alone. With car-
diogenic shock complicating MI, patient mortality precipi-
tously increases. Most commonly, post-MI cardiogenic shock
occurs as a consequence of LV dysfunction. Similarly, RV
MI must be considered. In patients with cardiogenic shock
despite recent cardiac revascularization, mechanical causes of
cardiogenic shock should also be considered. Mechanical
causes include acute severe MR, VSR, and ventricular free-
wall rupture leading to tamponade. In the immediate post-
PCI setting, acute stent thrombosis should also be considered.
Prompt recognition of cardiogenic shock and diagnosis of its
cause remains key to providing the appropriate initial manage-
ment and delivering definitive therapy.106-126 In addition to
understanding the patient’s clinical course and performing a
focused physical examination, an ECG and a bedside echocar-
diogram often provide a quick noninvasive determination of
the cause of cardiogenic shock.
Following prompt revasularization, initiating IV inotropic
and vasopressor agents may support the patient’s clinical sta-
tus. The patient’s hemodynamic support needs, however, may
be exceeded by those provided from pharmacologic therapy
alone. In these instances, a mechanical circulatory support
device may provide temporizing hemodynamic stabilization
until LV recovery occurs or definitive nonpharmacologic
therapy is performed. Mechanical complications including
acute MR resulting from papillary muscle rupture, VSR, and
free-wall rupture require surgical intervention. Despite expedi-
ent management, post-MI cardiogenic shock mortality remains
high.
Declaration of Conflicting Interests
The author(s) declared no potential conflicts of interest with respect to
the research, authorship, and/or publication of this article.
Funding
The author(s) received no financial support for the research, author-
ship, and/or publication of this article.
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