1. health and fitness
2. disease

3 : 27
CARDIOGENIC SHOCK-MANAGEMENT
INTRODUCTION
The incidence of cardiogenic shock in community studies has not
decreased significantly over time. Despite decreasing mortality
rates associated with increasing utilisation of revascularisation,
shock remains the leading cause of death for patients hospitalised
with acute myocardial infarction (MI). Although shock often
develops early after MI onset, it is typically not diagnosed on
hospital presentation. Failure to recognise early haemodynamic
compromise and the increased early use of hypotension inducing
treatments may explain this observation.
Recently, a randomised trial has demonstrated that early
revascularisation reduces six and
12 month mortality.1,2The currentAmerican College of Cardiology/
American Heart Association (ACC/AHA) guidelines recommend
the adoption of an early revascularisation strategy for patients <
75 years of age with cardiogenic shock.3
The extent of myocardial salvage from reperfusion treatment
decreases exponentially with time to re-establishing coronary
flow. Unfortunately, there has been little progress in reducing
time to hospital presentation over the past decade,4 and this
perhaps accounts for the stagnant incidence of cardiogenic shock
in community studies (7.1%).5 Cardiogenic shock also complicates
non-ST elevation acute coronary syndromes. The incidence of
shock in the PURSUIT trial was 2.9% (1995–97),6 similar to
the 2.5% incidence reported in the non-ST elevation arm of the
GUSTO II-B trial (1994–95).7 A number of strategies that centre
on reducing the time to effective treatment may help decrease
the incidence of shock.These include public education to decrease
the time to hospital presentation, triage and early transfer of high
risk patients to selected centres, and early primary percutaneous
coronary intervention (PCI) or rescue PCI for failed thrombolysis
in high risk patients.
DEFINITION
The clinical definition of cardiogenic shock 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 (,2.2 L/min per m2) in the
presence of elevated pulmonary capillary occlusion pressure (15
mm Hg) .
M Panja, Madhumati Panja, Saroj Mandal,
Dilip Kumar, Kolkata
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 such
factors as hypovolemia, hypoxia, and acidosis.
EPIDEMIOLOGY & CAUSES
The most common cause of cardiogenic shock is extensive acute
myocardial infarction, although a smaller infarction in a patient
with previously compromised left ventricular function may also
precipitate shock. Shock that has a delayed onset may result
from infarction extension, reocclusion of a previously patent
infracted artery, or decompensation of myocardial function
in the noninfarction zone because of metabolic abnormalities.
It is important to recognize that large areas of nonfunctional
but viable myocardium can also cause or contribute to the
development of cardiogenic shock in patients after myocardial
infarction. Cardiogenic shock can also be caused by mechanical
complications—such as acute mitral regurgitation, rupture of
the interventricular septum, or rupture of the free wall—or by
large right ventricular infarctions. Other causes of cardiogenic
shock include myocarditis, end-stage cardiomyopathy, myocardial
contusion, septic shock with severe myocardial depression,
myocardial dysfunction after prolonged cardiopulmonary
bypass, valvular heart disease, and hypertrophic obstructive
cardiomyopathy (Table 1). In a recent report of the SHOCK
(SHould we emergently revascularize Occluded Coronaries for
shocK) trial registry of 1160 patients with cardiogenic shock,8, 16
74.5% of patients had predominant left ventricular failure, 8.3%
had acute mitral regurgitation, 4.6% had ventricular septal rupture,
3.4% had isolated right ventricular shock, 1.7% had tamponade
or cardiac rupture, and 8% had shock that was a result of other
causes. Patients may have cardiogenic shock at initial presentation,
but shock often evolves over several hours.17,18 In the SHOCK
trial registry.7,16
75% of patients developed cardiogenic shock within 24 hours after
presentation;the median delay was 7 hours from onset of infarction.
Medicine Update 2010  Vol. 20
Pathology and Pathophysiology
Table 1 : Causes of Cardiogenic Shock
Acute myocardial infarction
Pump failure
Large infarction
Smaller infarction with preexisting left ventricular dysfunction
Infarction extension
Reinfarction
Infarction expansion
Mechanical complications
Acute mitral regurgitation caused by papillary muscle rupture
Ventricular septal defect
Free-wall rupture
Pericardial tamponade
Right ventricular infarction
Other conditions
End-stage cardiomyopathy
Myocarditis
Myocardial contusion
Prolonged cardiopulmonary bypass
Septic shock with severe myocardial depression
Left ventricular outflow tract obstruction
Aortic stenosis
Hypertrophic obstructive cardiomyopathy
Obstruction to left ventricular filling
Mitral stenosis
Left atrial myxoma
Acute mitral regurgitation (chordal rupture)
Acute aortic insufficiency
Autopsy studies show that cardiogenic shock is generally
associated with loss of more than 40% of left ventricular
myocardium.6 Although the less common syndrome of shock
due to predominant right ventricular infarction has now been
recognized.7 Autopsy also show that more than two-third of
patients with cardiogenic shock in myocardial infarction having
stenosis more than 75% of luminal diameter of all three major
coronary arteries, usually involving the left anterior descending
coronary artery. Majority of the patients of cardiogenic shock are
found to have thrombotic occlusion of the artery supplying the
major part of recent infarction.
Other causes of shock in Acute MI include mechanical defect like
a. rupture of ventricular septum, papillary muscle, or free wall with
tamponade, right ventricular infarct (RVMI) or marked reduction
of preload due to condition like hypovolumia.
SCHEMATIC DIAGRAM SHOWING EVENTS IN
CARDIOGENIC SHOCK
MYOCARDIAL
DYSFUNCTION
SYSTOLIC
Results from the GUSTO trial15 are similar: Among patients with
shock, 11% were in shock on arrival and 89% developed shock
after admission.Among patients with myocardial infarction, shock
is more likely to develop in those who are elderly, are diabetic, and
have anterior infarction.17–21 Patients with cardiogenic shock are
also more likely to have histories of previous infarction, peripheral
vascular disease, and cerebrovascular disease.20,21 Decreased
ejection fractions and larger infarctions (as evidenced by higher
cardiac enzyme levels) are also predictors of the development
of cardiogenic shock.20,21 Cardiogenic shock is most often
associated with anterior myocardial infarction. In the SHOCK trial
registry,15,23 55% of infarctions were anterior, 46% were inferior,
21% were posterior, and 50% were in multiple locations. These
findings were consistent with those in other series.22 Angiographic
evidence most often demonstrates multivessel coronary disease
(left main occlusion in 29% of patients, three-vessel disease in
58% of patients, two-vessel disease in 20% of patients, and onevessel disease in 22% of patients).16 This is important because
compensatory hyperkinesis normally develops in myocardial
segments that are not involved in an acute myocardial infarction;
this response helps maintain cardiac output. Failure to develop
such a response because of previous infarction or high grade
coronary stenoses is an important risk factor for cardiogenic
shock and death.18,23
302
DECREASED
STROKE VOL. &
CARDIAC OUTPUT
HYPOTENSION
SYSTEMIC
DIASTOLIC
DECREASED LVEDP
(pulmonary
congestion)
CORONARY
HYPOPERFUSIO
NJ
ISCHAEMIA
VASOCONSTRICTION
&
FLUID RETENSION
Progressive
MYOCARDIAL
DAMAGE
DEATH
INCEDENCE
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.3–7
In contrast, early and aggressive monitoring can increase the
Cardiogenic Shock-Management
3. Left ventricular end diastolic pressure (LVEDP) OR Pulmonary capillary wedge pressure (PCWP) more than or equal
to 18 mm of Hg.
apparent incidence of cardiogenic shock. The Worcester Heart
Attack Study,3 a communitywide analysis, found an incidence of
cardiogenic shock of 7.5%; this incidence remained stable from
1975 to 1988. In the Global Utilization of Streptokinase and Tissue
Plasminogen Activator for Occluded Arteries (GUSTO-1) trial,8
the incidence of cardiogenic shock was 7.2%, a rate similar to that
found in other multicenter thrombolytic trials.
4. Marked reduction of cardiac index (< 1.8 L/min/m2 ).
5. Evidence of Primary cardiac abnormalities.
The onset of cardiogenic shock in a patient following ST elevation
MI heralds a dismal in-hospital prognosis. The 7.2% of patients
developing shock in the GUSTO-I trial accounted for 58% of
the overall deaths at 30 days.8 Similarly, the 30 day death rates
with non-ST elevation MI cardiogenic shock in the PURSUIT and
GUSTO-II b databases were 66% and 73%, respectively. Even with
early revascularisation, almost 50% die at 30 days.The prevention
of shock is therefore the most effective management strategy.The
opportunity for prevention is substantial, given the observation
that only a minority of patients (10–15%) present to the hospital
in cardiogenic shock.Whether due to pump failure or a mechanical
cause, shock is predominantly an early in-hospital complication
in the ST elevation MI setting. The median time post-MI for
occurrence of shock in the randomised SHOCK trial was 5.0
(interquartile range 2.2–12) hours. Similarly, median time from MI
onset to development of shock in the SHOCK registry was 6.0
(1.8–22.0) hours, and median time from hospital admission was
4 hours. Shock complicating unstable angina/non-Q MI occurs at
a later time period. In the GUSTO-IIb trial shock was recognised
at a median of 76.2 (20.6–144.5) hours for non-ST elevation MI
compared to 9.6 (1.8–67.3) hours with ST elevation MI (p < 0.001),
and median time to shock in the non-ST elevation PURSUIT trial
was 94.0 (38–206) hours.
A primary goal in preventing shock should be an effort to
reduce the large proportion of patients presenting with acute
ST elevation MI who do not receive timely reperfusion treatment.
Successful early reperfusion of the infarct related coronary artery
while maintaining integrity of the downstream microvasculature
limits ongoing necrosis, salvages myocardium, and may prevent
the development of shock in many vulnerable patients. In-hospital
development of shock often follows failed thrombolysis or
successful thrombolysis followed by evidence of recurrent MI
(ST re-elevation), infarct extension (ST elevation in new leads), and
recurrent ischaemia (new ST depression). These complications
may be significantly reduced by a primary PCI strategy.
An electrocardiogram should be obtained immediately,
since evidence of serious abnormalities should direct the
investigation toward the myocardium; conversely a normal
electrocardiogram virtually excludes the possibility of cardiogenic shock caused by myocardial infarction. A routine
chest film can provide valuable clues about the presence of
infarction, pulmonary edema or aortic dissection. Echocardiography is an excellent aid in shorting through the differential diagnosis of cardiogenic shock, it also provide information on regional and global systolic wall function valvular
integrity, and the presence or absence of pericardial effusion. Insertion of swan-ganz catheter is useful for initiating
and monitoring therapy, since the proper use of vasoactive
agents in these circumstances requires the simultaneous assessment of cardiac filling pressure and peripheral perfusion.
Management
When a patient with cardiogenic shock initially evaluated
supportive and resuscitative effort must be swift and definitive
to maximize the possibilities of survival. The initial management
protocol to combat shock is given in the table which is detailed
later.
ABG analysis
Maintain O2 saturation above 90%
May need Mech.Ventilation
Hrly. urine output record
Evidence of pulmonary Congestion:
Rales,LVS3, CXR
PRESENT
ABSENT
FLUID CHALLENGE
• ANT. MI:250ml 0.9% NS over 15 mins
• INF. MI : 400ml 0.9% NS over 15mins
NO IMPROVEMENT
PCWP less than 17 – 18 mm Hg
(Swan Ganz)
Diagnosis
DOPAMINE
INFUSION
Most patients are initially evaluated at the bedside where a
reasonably accurate clinical diagnosis of cardiogenic shock may
be made according to the following character:
1.
Evidence of organ hypo perfusion like cold clammy skin, especially on hand and feets, may be associated with peripheral cyanosis in nail beds, oliguria, and impaired mentation.
SBP less
than
90mmHg
2. Marked persistent (more than 30 min) hypotension with
systolic arterial pressure less than 80 to 90 mm of Hg.
IABP or
Add
NORADRENALI
NE infusion
303
SBP more
than 90mm
Hg
Add DOBUTAMINE and
try to decrease the dose of
DOPAMINE
Medicine Update 2010  Vol. 20
to impaired cardiac output and pulmonary pressure9 with
less effect on myocardial work.10 This agent should be reserved for those in whom therapy with catecholamine has
failed to improve cardiac performance or those in whom
arrhythmia or ischemia limits the catecholamine use.m
Long term studies show a disturbing increases in mortality among patients with heart failure who are treated with
phosphodiesterase inhibitors.11
Suggested approach to the management of cardiogenic shock complicating
acute myocardial infarction
• Asses’ volume status.
• Treat sustained arrhythmias- brady or tachyarrhythmia
• Mechanical ventilation as needed, correct acedemia, hypoxemia
• Ionotropic/vasoppresor support (dopamine)
Acute massive ST elevation
Evolving Q wave
New LBBB.
Yes
NO
B. Vasodilators :
No ST elevation
Limited ST elevation ∫ Q
Delayed cardiogenic shock
Cath Lab immediately available
Yes
Emergency
ECHO/Colour Doppler
Pump failure of right or left
ventricle or both
No
It can be beneficial for patients who are in shock, but extreme caution should be used because of the risk of precipitating further hypotension and thereby reducing coronary
blood flow. Either intravenous nitroglycerine or sodium
nitroprusside can be used; nitroglycerine is less potent as
an arteriolar vasodilator12 but it may have the advantage of
not producing coronary a. cesteala (preferential coronary
blood flow to non ischemic vascular bed).13 Vasodilators are
particularly important when mitral valvular regurgitation is
a major part of the path physiological processes. Vasodilators should generally be withheld until the blood pressure
is stabilized and hemodynamic monitoring is begun so as to
ensure that beneficial effects are produced by the drug.
On occasion, the severity of cardiac pump dysfunction will
require the use of two divergent therapeutic modalities
in order to facilitate left ventricular emptying.14 The most
commonly utilized of this combined therapies is nitroprusside and dopamine. The principal advantage offered by nitruposside in this combination is a reduction in left ventricular preload. The cardiac output not appreciably increased
by the addition of nitropusside to dopamine therapy. The
advantage offered by dopamine in this combination is an
augmentation of cardiac output and the maintenance of
systemic arterial pressure.15 A less frequently combination
dobutamine and nitropusside, has been shown to result in
higher cardiac output and lower pulmonary capillary wedge
pressures than with either drug alone.14
Aortic dissection
Tamponade
Acute severe MR
Ventricular septal
rapture
ST?------ Thrombolytic
ST?------ GP IIb/IIIa
Aspirin, heparin
Rapid IABP
Operating room ± Coronary angiography
Coronary angio ± Left ventricular angiography
Cardiac surgery,
CABG for severe 3 vessels or
Left main, LAD disease.
Correct mechanical lesion ± CABG
PTCA for 1-, 2-, or moderate 3- vessel Coronary Artery Disease
GPIIB/IIIa antagonist + Coronary Stent (s)
Fig. 1
Ionotropic Catecholamine without
predominant vasoconstrictive
properties :
Dobutamine : A I2 agonist with predominant effect ofI2 receptors
thus it increases cardiac contractility as dopamine without
causing substantial vasoconstriction and with less tachycardia
and arrythmogenesis. It also augments diastolic coronary blood
flow and collateral blood flow to ischemic area.
C. Intra Aortic Balloon Pumping (IABP):
In practice, it has little effects on peripheral vascular resistance
or lowers it and increases cardiac output.8 It does not raise
blood pressure when severe hypotension is present. It usually
administered at a starting dose 2.5 – 5 Aµg/Kg/min and increased
to 20 µg/kg/min depending on hymodynamics and heart rate.
When patients has substantial hypotension (Systolic blood
pressure <90mm of Hg) and evidence of tissue hypo perfusion
dopamine uses as intravenous ionotropic agents , but when blood
pressure is adequate but cardiac output must be augmented,
dobutamine is [preferred. When a patients is receiving a high
dose (>15 µg/Kg/min) of dopamine, norepinephrine is generally
substituted in a dose of 2-20 µg/min.
3. Phosphodiesterase Inhibitors :
Phosphodiesterase inhibitors, amrinone, milrinone can increases contractility without adrenergic stimulation, leading
304
The capacity of the intraaortic balloon pump to increases
diastolic coronary arterial perfusion and simultaneously to
decrees after load with out increasing myocardial oxygen
consumption makes it an attractive method of stabilizing
the patients with cardiogenic shock .
By inflating in the aorta during diastole and by deflating during systole the IABP reduces after load during ventricular
systole and increases coronary perfusion during diastole.
The decrees in after load and increased coronary perfusion
account for it TMs efficacy in cardiogenic shock and ischemia.
It is particularly useful as a stabilizing bridge to facilitate
diagnostic angiography, and revaswcularization and repair of
mechanical complications of acute MI.
Cardiogenic Shock-Management
velop shock within 36 hrs of MI are suitable for revascularization that can be performed within 18 hrs of MI and are
suitable if performed within 36 hrs of shock. (2008 AHA
Guieline).
Safely the pump can be inserted at the bedside; operator
experience is critical to successful placement and management. The most important contraindication of IABP insertion is
1. Aortic regirgotatopm
2. Sever peripheral vascular disease.
Although vascular and bleeding complications have been reported in 5-10 % of treated patients,2 the use of smaller vascular sheaths has reduced this risk. Vascular complications
almost are transient. Hemorrhage at the site of insertion,
particularly after removal, is relatively common. Meticulous
maintenance of the insertion site, physical examination of
the lower extremities, and attention to the timing and characteristic of balloon inflation are necessary.
Several retrospective trials have examine the effect of angiography on mortality rate in patients with cardiogenic
shock and researchers have consistently found that patients
with successful reperfusion have much better outcomes
than those without successful reperfusion.
The GUSTO-130 trial, a sub group analysis of the 2972 patients with cardiogenic shock showed that 30 day mortality
rate was significantly lower in patients who had.
Angioplasty (43% compared with 61% for patients with
shock on arrival ; 32% compared with 61% for patients who
developed shock). In this gtrial patients treated with an aggressive strategy (coronary angiography performed with in
24 hour of shock onset with revascularization PTCA or bypass surgery. Had a significantly lower mortality rate (38%,
compared with 62%.30 This benefit was present even after
adjustment for base line characteristic and persisted for up
to one year.31
Recent reports have suggested that coronary stenting may
improve outcome after either failed or suboptimal PTCA
or as a primary approach.32
A recent study of direct PTCA in patients with shock reported success rate of 94% with placement of stent in 47%
of patients ; the in hospital mortality33 rate 26%, Another
study of stenting of failed angioplasty in patients with cardiogenic shock reported a mortality rate of 27%.34
The role of ant platelet, platelet glycoprotein GP IIb/IIIa antagonists have shown to improve short term clinical outcome after angioplasty especially in patients at high risk for
complications. However published experience. With GP IIb/
IIIA receptor inhibition in patients with cardiogenic shock is
far limited to case reports,35 but extrapolation from other
settings suggest that they may play an important adjunctive
role in patients with shock who undergo angioplasty.36
Recommendation for Intra Aortic
Balloon Counterepulsation
Class I
Cardiogenic shock not quickly reversed with pharmacologic
therapy as a stabilizing measure for angiography and
revascularization. Acute mitral regurgitation or ventricular septal
defect complicating myocardial infarction as a stabilizing therapy
for angiography and repair/revascularization.
Recurrent intractitable ventricular arrhythmias with hemodynamic
instability.
Refractory post myocardial infarction angina as a bridge to
angiography and revascularization.
Randomized to tPA or rt PA in GUSTO-III.26 Although these
resultsare not definite because of broad confidence limits on the
observations, angiographic evidence supports a low reperfusion
rate in patients with shock compared with other patients with
ST. segment elevation MI.27 This is confirmed in hypotensive
experimental models.28 For this reason, thrombolytic therapy
is reserve for whom an angiographic suit and emergency
revascularization are not immediately accessible.
E. Combination of Intra – aortic Balloon Counter pulsation
and
G. Coronary Artery Bypass Surgery (CABG) :
Fibrinolytic Therapy :
Use of IABP facilitates thrombus dissolution by tPA in experimental model with and without hypotension. Non randomized data from NRMI29 and a community experience
suggest lower mortality rates with this combined therapy
. For these reasons, when primary PCI is not feasible and
fibrinolytic therapy is administered the concurrent use of
the IABP for patients in cardiogenic shock may be beneficial.
There are so many studies that show, favourable outcome
for patients with cardiogenic shock who had CABG . In
patients with cardiogenic shock left main coronary artery
disease or triple vessels diseases are common and potential
contribution of ischemia in non infarct zone to myocardial
infarction in patients with shock would support complete
revascularization.
F.
Percuteneous Transluminal Coronary Angioplasty (PTCA) :
Early revascularization is recommended for patients less
than 75 years of age with ST elevation or LBBB who de-
Published series include more than 200 patients who have
undergone surgical revascularization as a treatment of cardiogenic shock overall perioperative mortality has been low
as compared with medical therapy alone, average in 40% but
substantial selection bias is present in this non randomized
305
Medicine Update 2010  Vol. 20
Diagnosis
studies. Lone potential advantage of surbgical revascularization is that myocardium remote from the acute infarction
can also be revascularized , permitting better compensatory
function.5
Clinically the trad of elevated jugular venous pressure, systemic
hypotension and clear lung fields in presence of an inferior and
posterior infarction suggest the possibility of RVMI. Jugular venous
distention that is enhanced by inspiration (Kussmaula TM s sign) in
the setting of inferior wall MI is highly suggestive of RV involvement
byut may not be manifest with volume depletion.
THE SHOCK trial35 compared direct invasive strategies
that included urgent coronary angiography, PCI or CABG
with initial medical stabilization including IABP, thrombolytic
therapy and delayed revascularization as clinically determined. The primary end point 30 day mortality showed a
non significant 9.3% absolute and a 17% relative reduction
in favor of early revascularization. Six month and one year
mortality rate were lower (P-0.027 P- 0.025 ) in favor of
early revascularization consistent with 13 lives saved per
100 patients treated. There was an interaction between
treatment effect and age younger than 75 year versus age
more than 75 year or older. However , the SHOCK registry
demonstrated that the elderly who was clinically selected
to undergo early revascularization appear to derived benefit that is similar to younger age.
ECG shows more than one mm of ST segment elevation in lead
V3R and V4R which is the single most powerfulpredictor of RVMI
in inferior wall MI . Echocardiography also helpful in diagnosis and
can show depressed cardiac contractility. Right atrial pressure
more than 10 mm of Hg that is greater than 80% of pulmonary
capillary wedge pressure is a sensitive and specific sign of RVMI.42
Other causes of heart failure in inferior wall MI also should be
excluded (cg.Arrhythmia, ongoing ischemia, previous infarction in
another location, mechanical complications like papillary muscle
rupture and VSD.)
Management of Shock in RVMI
There are strong recommendation about urgent CAG with
IABP support and PCI or CABG, depending on the coronary anatomy for this patients younger than 75 years with
cardiogenic shock due to predominant left ventricular failure complicating acute ST segment elevation, or new left
bundle branch block MI, Elderly patients should be clinically
selecgtedaccording to their physiological age, co-morbidites
and patients a s preference. Despite the absence of data for
shock due to non ST segment elevation MI or predominant
right ventricular infarction, some author recommended
similar aggressive strategy.
Maintain Right Ventricular Preload :
Volume loading (IV normal saline)
Avoid use of nitrate and diuretics
Maintain A-V synchrony.
AV sequential pacing for sympt9omatic high degree heart
block
Prompt cardio version for hemodynamically significant SVT.
Ionotropic Support :
H. Other New Approaches :
Dobutamine (if cardiac output fails to increase after volume
loading )
New percutaneous techyniques may have important applications in patients with cardiogenic shock. In particular
percuteneous cardiopulmonary bypass38 and other methods designed to augment cardiac out put39 may be able to
sustained vital organ function while the reperfusions of the
infarct related artery and others areas of severe stenosis is
attempted. Aggressive effort to sustained life can now include use of left ventricular assisted device as a bridge to
cardiac transplantation.40
Reduce Right Ventricular After Load with Left Ventricular Dysfunction
Intra Aortic Balloon Pump (IABP)
Arterial vasodilators (nitroprusside, hydralazine)
ACE inhibitors.
Reperfusion
Thrombolytic agent
Special situation
Primary PTCA
Right ventricular myocardial infarction (RVMI) with shock :
RVMI occur up to 30% of cases with inferior and posterior MI,
and it is clinically significant upto 10% of patients.41 Mortality
rate of inferior wall MI associated with RVMI is high , 25.30% ; as
opposed to an overall mortality rate of 6% in inferior wallMI.41
RV involvement should always be considered and should be
specifically short out in inferior wall MI with clinical evidence of
low cardiac out put because of therapeutic approaches are quite
different in the presence of RV involvement from those who have
predominantly left ventricular failure.
306
CABG (in patients with multi vessel disease).
(IV; intra venous, AV : Atrioventricular , SVTY Supraventricular
Tachycardia, ACE : Angiotensine converting enzyme. PTCA
: Percutaneous Transluminal Coronary Angioplasty, CABG :
Coronary Artery Bypass Graft).
A recent study using direct angioplasty showed that restoration
of normal flow resulted in dramatic recovery of right ventricular
function and a mortality rate only 2% , where as unsuccessful
reperfusion was associated with persistent homodynamic
Cardiogenic Shock-Management
compromise and a mortality rate of 58%.
Acute Mitral Regurgitation
Ischemic mitral regurgitation is usually associated with inferior
myocardial infarction and ischemia or infarction of the posterior
papillary muscle, which has a single blood supply (usually from the
posterior descending branch of a dominant right coronary artery).
Papillary muscle rupture usually occurs 2 to 7 days after acute
myocardial infarction; it presents dramatically with pulmonary
edema, hypotension, and cardiogenic shock. When a papillary
muscle ruptures, the murmur of acute mitral regurgitation may be
limited to early systole because of rapid equalization of pressures
in the left atrium and left ventricle. More important, the murmur
may be soft or inaudible, especially when cardiac output is low.
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.
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 (a “stepup” in oxygen
saturation from right atrium to right ventricle). 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 stabilization— using intraaortic balloon pumping and pharmacologic measures—followed
by surgical repair is the only viable option for longterm 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
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
Reversible Myocardial Dysfunction
cardiopulmonary bypass, and inflammatory myocarditis. In sepsis
and, to some extent, in myocarditis, myocardial dysfunction seems
to result from the effects of inflammatory cytokines, such as
tumor necrosis factor and interleukin-1. Myocardial dysfunction
can be self-limited or fulminant, with severe congestive heart
failure and cardiogenic shock. In the latter situation, cardiovascular
support with a combination of inotropic agents (such as dopamine,
dobutamine, or milrinone) and IABP may be required for hours
or days to allow sufficient time for recovery. If these measures
fail, mechanical circula-tory support with left ventricular assist
devices can be considered.These devices can be used as a bridge
to cardiac transplantation in eligible patients or as a bridge to
myocardial recovery; functional improvement with such support
can be dramatic.
Conclusions
Mortality rates in patients with cardiogenic shock remain
frustratingly high (50% to 80%). The pathophysiology of shock
involves a downward spiral:Ischemia causes myocardial dysfunction,
which in turn worsens ischemia.Areas of nonfunctional but viable
myocardium can also cause or contribute to the development of
cardiogenic shock. 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 seem to 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. The SHOCK
multicenter randomized trial provides important data that help
clarify the appropriate role and timing of revascularization in
patients with cardiogenic shock.
References
1.
Hochman JS, Sleeper LA,Webb JG, et al. Early revascularization in acute
myocardial infarction complicated by cardiogenic shock. N Engl J Med
1999;341:625–34. Randomised controlled trial comparing an early revascularisation strategy to an initial medical stabilisation strategy in the
setting of cardiogenic shock. [PubMed]
2. Hochman JS, Sleeper LA, White HD, et al. One-year survival following
early revascularization for cardiogenic shock. JAMA 2001;285:190–2.
One year follow up of the SHOCK trial. [PubMed]
3. Ryan TJ, Anderson JL, Antman EM, et al. 1999 update: ACC/AHA guidelines for the management of patients with acute myocardial infarction.
A report of the American College of Cardiology/American Heart Association task force on practice guidelines. (Committee on management of acute myocardial infarction). Circulation 1999;100:1016–30.
[PubMed]
4. Rogers WJ, Canto JG, Lambrew CT, et al. Temporal trends in the treatment of 1.5 million patients with myocardial infarction in the US from
1990 through 1999. J Am Coll Cardiol 2000;36:2056–63. [PubMed]
5. Goldberg RJ, Samad NA, Yarzebski J, et al. Temporal trends in cardiogenic shock complicating acute myocardial infarction. N Engl J Med
1999;340:1162–68. Large community study showing a decline in
mortality but no change in incidence of shock over time. [PubMed]
In addition to hibernating and stunned myocardium, potentially
reversible causes of myocardial dysfunction include sepsisassociated myocardial depression, myocardial dysfunction after
6. Hasdai D, Harrington RA, Hochman JS, et al. Platelet glycoprotein IIb/
307
Medicine Update 2010  Vol. 20
16. Hochman J. Cardiogenic shock. Annual Scientific Sessions, American
Heart Association. Dallas, TX; 1998.
IIIa blockade and outcome of cardiogenic shock complicating acute
coronary syndromes without persistent ST- segment elevation. J Am
Coll Cardiol 2000;36:685–92. [PubMed]
17. Scheidt S, Ascheim R, Killip T 3d. Shock after acute myocardial infarction.A clinical and hemodynamic profile. Am J Cardiol.
1970;26:556-64.
7. Holmes DR Jr, Berger PB, Hochman JS, et al. Cardiogenic shock in patients with acute ischemic syndromes with and without ST-segment
elevation. Circulation 1999;100:2067–73. [PubMed]
18. Califf RM, Bengtson JR. Cardiogenic shock. N Engl J Med. 1994;330:172430.
8. Hochman JS, Boland J, Sleeper LA, Porway M, Brinker J, Col J, et al. Current spectrum of cardiogenic shock and effect of early revascularization on mortality. Results of an International Registry. SHOCK Registry
Investigators. Circulation. 1995;91:873-81.
19. Killip T 3d, Kimball JT. Treatment of myocardial infarction in a coronarycare unit. A two year experience with 250 patients. Am J Cardiol.
1967;20: 457-64.
9. Forrester JS, Diamond G, Chatterjee K, Swan HJ. Medical therapy of
acute myocardial infarction by application of hemodynamic subsets
(second of two parts). N Engl J Med. 1976;295:1404-13.
20. Hands ME, Rutherford JD, Muller JE, Davies G, Stone PH, Parker C, et al.
The in-hospital development of cardiogenic shock after myocardial infarction: incidence, predictors of occurrence, outcome and prognostic
factors. The MILIS Study Group. J Am Coll Cardiol. 1989;14:40-6.
10. Goldberg RJ, Gore JM, Alpert JS, Osganian V, deGroot J, Bade J, etal. Cardiogenic shock after acute myocardial infarction. Incidence and mortality from a community-wide perspective, 1975 to 1988. N Engl J Med.
1991;325:1117-22.
21. Leor J, Goldbourt U, Reicher-Reiss H, Kaplinsky E, Behar S. Cardiogenic shock complicating acute myocardial infarction in patients without heart failure on admission: incidence, risk factors, and outcome.
SPRINT Study Group. Am J Med. 1993;94:265-73.
11. Effectiveness of intravenous thrombolytic treatment in acute myocardial infarction. Gruppo Italiano per lo Studio della Streptochinasi
nell’Infarto Miocardico (GISSI). Lancet. 1986;1:397-402.
22. Bengtson JR, Kaplan AJ, Pieper KS, Wildermann NM, Mark DB, Pryor
DB, et al. Prognosis in cardiogenic shock after acute myocardial infarction in the interventional era. J Am Coll Cardiol. 1992;20:1482-9.
12. In-hospital mortality and clinical course of 20,891 patients with suspected acute myocardial infarction randomised between alteplase and
streptokinase with or without heparin. The International Study Group.
Lancet. 1990;336:71-5.
23. Grines CL, Topol EJ, Califf RM, Stack RS, George BS, Kereiakes D, et al.
Prognostic implications and predictors of enhanced regional wall motion of the noninfarct zone after thrombolysis and angioplasty therapy
of acute myocardial infarction. The TAMI Study Groups. Circulation.
1989;80: 245-53.
13. ISIS-3: a randomised comparison of streptokinase vs tissue plasminogen activator vs anistreplase and of aspirin plus heparin vs aspirin alone
among 41,299 cases of suspected acute myocardial infarction. ISIS-3
(Third International Study of Infarct Survival) Collaborative Group.
Lancet. 1992;339:753-70.
14. An international randomized trial comparing four thrombolytic strategies for acute myocardial infarction. The GUSTO Investigators. N Engl J
Med. 1993; 329:673-82.
24. Ryan TJ, Anderson JL, Antman EM, Braniff BA, Brooks NH, Califf RM,
et al. ACC/AHA guidelines for the management of patients with acute
myocardial infarction. A report of the American College of Cardiology/
American Heart Association Task Force on Practice Guidelines (Committee on Management of Acute Myocardial Infarction). J Am Coll Cardiol. 1996;28: 1328-428.
15. Holmes DR Jr, Bates ER, Kleiman NS, Sadowski Z, Horgan JH, MorrisDC, et al. Contemporary reperfusion therapy for cardiogenic shock:
the GUSTO-I trial experience. The GUSTO-I Investigators. Global
Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries. J Am Coll Cardiol. 1995;26:668-74.
25. Greenberg MA, Menegus MA. Ischemia-induced diastolic dysfunction:
new observations, new questions. J Am Coll Cardiol. 1989;13:10712. 26. Page DL, Caulfield JB, Kastor JA, DeSanctis RW, Sanders CA.
Myocardial changes associated with cardiogenic shock. N Engl J Med.
1971;285:
308