Background:
Cardiogenic shock is a major, and frequently fatal, complication of a
variety of acute and chronic disorders that impair the ability of the heart to
maintain adequate tissue perfusion. Cardiac failure with cardiogenic shock
continues to be a frustrating clinical problem; the management of this condition
requires a rapid and well-organized approach.
Cardiogenic shock is a physiologic state in which inadequate tissue perfusion
results from cardiac dysfunction, most commonly following acute myocardial
infarction (MI). The clinical definition of cardiogenic shock is a decreased
cardiac output and evidence of tissue hypoxia in the presence of adequate
intravascular volume. Hemodynamic criteria for cardiogenic shock are sustained
hypotension (systolic blood pressure <90 mm Hg for at least 30 minutes) and a
reduced cardiac index (<2.2 L/min/m2) in the presence of an
elevated pulmonary capillary occlusion pressure (>15 mm Hg).
The diagnosis of cardiogenic shock sometimes can be made at the bedside by
observing hypotension and clinical signs of poor tissue perfusion, including
oliguria, cyanosis, cool extremities, and altered mentation. These signs usually
persist after attempts at correcting hypovolemia, arrhythmia, hypoxia, and
acidosis have been made.
Historical Aspects
Myocardial infarction is the most common cause of cardiogenic shock in modern
times. Morgagni first recognized myocardial infarction in 1761, subsequently
described by Caleb Parry in 1788 and by Heberden in 1802. John Hunter, a surgeon
at St. George’s Hospital, London, described his personal experience with
myocardial infarction in 1773. Adam Hammer, a physician in Mannheim, identified
the role of coronary thrombosis in causation of myocardial infarction in 1878.
The clinical features of acute myocardial infarction and survival of patients
after such an event were reported in 1912 in the Journal of the American
Medical Association by James Herrick, a Chicago physician. In the late
20th century, clinicians recognized cardiogenic shock as a low
cardiac output state, secondary to extensive left ventricular infarction,
development of a mechanical defect (eg, ventricular septal or papillary muscle
rupture), and right ventricular infarction.
Pathophysiology: Disorders that can result in the acute
deterioration of cardiac function leading to cardiogenic shock include MI or
ischemia, acute myocarditis, sustained arrhythmia, acute valvular catastrophe,
and decompensation of end-stage cardiomyopathy from multiple etiologies. Autopsy
studies show that cardiogenic shock generally is associated with the loss of
more than 40% of the left ventricular myocardial muscle. The pathophysiology of
cardiogenic shock, which is well understood in the setting of coronary artery
disease, is described below.
Myocardial pathology
Cardiogenic shock is characterized by both systolic and diastolic
dysfunction. In patients who develop cardiogenic shock from acute MI,
progressive myocardial necrosis with infarct extension is consistently observed
and is accompanied by decreased coronary perfusion pressure and increased
myocardial oxygen demand. These patients often have multi-vessel coronary artery
disease with limited coronary flow reserve. Ischemia remote from the infarcted
zone is an important contributor to shock. Myocardial diastolic function also is
impaired as ischemia causes decreased myocardial compliance, thereby increasing
left ventricular filling pressure, which may lead to pulmonary edema and
hypoxemia.
Cellular pathology
Tissue hypoperfusion, with consequent cellular hypoxia, causes anaerobic
glycolysis, the accumulation of lactic acid, and intracellular acidosis. Failure
of myocyte membrane transport pumps also occurs, which decreases transmembrane
potential and causes intracellular accumulation of sodium and calcium, resulting
in myocyte swelling. If ischemia is severe and prolonged, myocardial cellular
injury becomes irreversible and leads to myonecrosis, which includes
mitochondrial swelling, the accumulation of denatured proteins and chromatin,
and lysosomal breakdown, resulting in fracture of the mitochondria, nuclear
envelopes, and plasma membranes. Additionally, apoptosis (programmed cell death)
may be found in peri-infarcted areas and may contribute to myocyte loss.
Activation of inflammatory cascades, oxidative stress, and stretching of the
myocytes produces mediators that overpower inhibitors of apoptosis, thus
activating the apoptosis.
Reversible myocardial dysfunction
It is extremely important to understand that large areas of dysfunctional but
viable myocardium can contribute to the development of cardiogenic shock in
patients with myocardial infarction. This potentially reversible dysfunction is
often described as myocardial stunning and/or hibernating myocardium.
Myocardial stunning represents post-ischemic dysfunction that persists
despite restoration of normal blood flow. By definition, myocardial dysfunction
from stunning eventually resolves completely. The mechanism of myocardial
stunning involves a combination of oxidative stress, abnormalities of calcium
homeostasis and circulating myocardial depressant substances.
Hibernating myocardium is a state of persistently impaired myocardial
function at rest, which occurs because of the severely reduced coronary blood
flow. Hibernation appears to be an adaptive response to hypoperfusion that may
minimize the potential for further ischemia or necrosis. Revascularization of
hibernating (and/or stunned) myocardium generally leads to improved myocardial
function.
It is extremely important to understand that large areas of dysfunctional but
viable myocardium can contribute to the development of cardiogenic shock in
patients with myocardial infarction. This potentially reversible dysfunction
often is described as myocardial stunning or hibernating myocardium. Myocardial
stunning represents postischemic dysfunction that persists despite restoration
of normal blood flow. By definition, myocardial dysfunction from stunning
eventually resolves completely. The mechanism of myocardial stunning involves a
combination of oxidative stress, abnormalities of calcium homeostasis, and
circulating myocardial-depressant substances.
Hibernating myocardium is a state of persistently impaired myocardial
function at rest, which occurs because of the severely reduced coronary blood
flow. Hibernation appears to be an adaptive response to hypoperfusion that may
minimize the potential for further ischemia or necrosis. Revascularization of
hibernating or stunned myocardium generally leads to improved myocardial
function. Consideration for the presence of myocardial stunning and hibernation
is vital in patients with cardiogenic shock because of the therapeutic
implications of these conditions. Hibernating myocardium improves with
revascularization, whereas the stunned myocardium retains inotropic reserve and
can respond to inotropic stimulation. Although hibernation is considered a
different physiologic process than that of myocardial stunning, the conditions
are difficult to distinguish in the clinical setting and often coexist.
Cardiovascular mechanics of cardiogenic shock
The main mechanical defect in cardiogenic shock is that the left ventricular
end-systolic pressure-volume curve is shifted to the right because of a marked
reduction in contractility. As a result, at a similar or even lower systolic
pressure, the ventricle is able to eject less blood volume per beat. Therefore,
the end-systolic volume usually is greatly increased in cardiogenic shock, and
the stroke volume is decreased. To compensate for the decrease in stroke volume,
the curvilinear diastolic pressure-volume curve shifts to the right, with a
decrease in diastolic compliance. This leads to increased diastolic filling that
is associated with an increase in end-diastolic pressure. The increase in
cardiac output by this mechanism comes at the cost of having a higher left
ventricular diastolic filling pressure, which ultimately increases myocardial
oxygen demand and causes pulmonary edema.
As a result of decreased contractility, the patient develops elevated left
and right ventricular (RV) filling pressures and a low cardiac output. Mixed
venous oxygen saturation falls because of the increased tissue oxygen
extraction, which is due to the low cardiac output. This, combined with
intrapulmonary shunting that often is present, contributes to substantial
arterial desaturation.
Systemic effects
When a critical mass of left ventricular myocardium becomes ischemic and
fails to pump effectively, stroke volume and cardiac output decrease. Ischemia
is further exacerbated by compromised myocardial perfusion due to hypotension
and tachycardia. The pump failure increases ventricular diastolic pressures
concomitantly, causing additional wall stress, hence elevating myocardial oxygen
requirements. Systemic perfusion is compromised by decreased cardiac output,
with tissue hypoperfusion causing increased anaerobic metabolism, leading to the
formation of lactic acid, which further deteriorates the systolic performance of
the myocardium.
Depressed myocardial function also leads to the activation of several
physiologic compensatory mechanisms. These include sympathetic stimulation,
which increases heart rate and contractility and renal fluid retention, which
increases the left ventricular preload. The raised heart rate and contractility
increases myocardial oxygen demand, further worsening myocardial ischemia. Fluid
retention and impaired left ventricular diastolic filling caused by tachycardia
and ischemia contribute to pulmonary venous congestion and hypoxemia.
Sympathetic-mediated vasoconstriction to maintain systemic blood pressure
increases myocardial afterload, which impairs cardiac performance. Increased
myocardial oxygen demand with simultaneous inadequate myocardial perfusion
worsens myocardial ischemia, initiating a vicious cycle that ultimately ends in
death if uninterrupted.
Usually, both systolic and diastolic myocardial dysfunction are present in
patients with cardiogenic shock. Metabolic derangements that impair myocardial
contractility further compromise systolic ventricular function. Myocardial
ischemia decreases myocardial compliance, thereby elevating left ventricular
filling pressure at a given end-diastolic volume (diastolic dysfunction). This
further leads to pulmonary congestion and congestive heart failure.
Shock state
Shock state, irrespective of the etiology, is described as a syndrome
initiated by acute systemic hypoperfusion that leads to tissue hypoxia and vital
organ dysfunction. A maldistribution of blood flow to end organs leads to
cellular hypoxia and end-organ damage, the well-described multisystem organ
dysfunction syndrome. All forms of shock are characterized by inadequate
perfusion to meet the metabolic demands of the tissues. Three organs are of
vital importance, the brain, heart, and kidneys.
Decline in higher cortical function may indicate diminished perfusion of the
brain, which leads to an altered mental status ranging from confusion and
agitation to flaccid coma. The heart plays a central role in perpetuating shock.
Depressed coronary perfusion leads to worsening cardiac dysfunction and a cycle
of self-perpetuating progression of global hyperperfusion. Renal compensation
for reduced perfusion results in diminished glomerular filtration, causing
oliguria and subsequent renal failure.
Frequency:
In the US: The incidence of cardiogenic shock ranges from
5-10% in patients with acute myocardial infarction. In the Worcester Heart
Attack Study, a community-wide analysis, an incidence of 7.5% was reported.
The literature contains few data on cardiogenic shock in nonischemic
patients.
Internationally: Several multicenter thrombolytic trials
in Europe reported a prevalence of cardiogenic shock following MI of
approximately 7%.
Mortality/Morbidity: The historic mortality rate from
cardiogenic shock is 80-90%; recent studies have reported somewhat less
in-hospital mortality, in the range of 56-67%. With the advent of thrombolytics,
improved interventional coronary procedures, and better medical therapies for
heart failure, the overall incidence of cardiogenic shock is likely to decline
from historic highs.
Sex: The overall incidence of cardiogenic shock is higher in
men because of the increased incidence of coronary artery disease in males.
However, the percentage of female patients with MI who develop cardiogenic shock
is higher than that of their male counterparts.
CLINICAL
History:
Cardiogenic shock is a medical emergency. Performance of a complete
clinical assessment is critical to understanding the cause of the shock and for
targeting therapy towards correcting the cause.
Cardiogenic shock following acute myocardial infarction generally develops
after admission to the hospital, although a small number of patients are in
shock at presentation. Patients demonstrate clinical evidence of low cardiac
output, which is manifested by sinus tachycardia, low urine output, and cool
extremities. Systemic hypotension, defined as systolic blood pressure below 90
mm Hg or a decrease in mean blood pressure by 30 mm Hg, ultimately develops
and further propagates tissue hypoperfusion.
Most patients who develop acute myocardial infarction present with abrupt
onset of squeezing or heavy substernal chest pain; the pain may radiate to
left arm or to the neck. The chest pain may be atypical, the location being
epigastric or the neck or the arm only. The pain quality may be burning,
sharp, or stabbing. The pain may be absent in persons with diabetes or elderly
individuals.
Associated autonomic symptoms including nausea, vomiting, and sweating
also may occur.
A history of previous cardiac disease, use of cocaine, previous myocardial
infarction or previous cardiac surgery should be obtained. A patient thought
to have myocardial ischemia should have assessment of cardiac risk factors.
The evaluation should include history of hyperlipidemia, left ventricular
hypertrophy, family history of premature coronary artery disease, history of
hypertension, and cigarette smoking. Presence of two or more risk factors
increases the likelihood of acute myocardial infarction.
Other associated symptoms are diaphoresis, exertional dyspnea, or dyspnea
at rest. The feeling of presyncope or syncope, palpitations, generalized
anxiety, or depression are other features indicative of poor cardiac
function.
Physical: Cardiogenic shock is diagnosed after documentation
of myocardial dysfunction and exclusion of alternative causes of hypotension,
such as hypovolemia, hemorrhage, sepsis, pulmonary embolism, pericardial
tamponade, aortic dissection, and preexisting valvular disease. Shock is present
if evidence of multisystem organ hypoperfusion is detected on physical
examination.
Patients in shock usually appear ashen or cyanotic and have cool skin and
mottled extremities.
Peripheral pulses are rapid and faint and may be irregular if arrhythmias
are present.
Jugular venous distention and crackles in the lungs are usually (but not
always) present. Peripheral edema may be present, as well.
Heart sounds usually are distant, and both third and fourth heart sounds
(S3 and S4) may be present.
The pulse pressure may be low, and patients usually are
tachycardic.
Patients show signs of hypoperfusion, such as altered mental status and
decreased urine output.
A systolic murmur may be heard in patients with acute mitral regurgitation
or ventricular septal rupture. The associated parasternal thrill indicates
ventricular septal defect, whereas murmur of mitral regurgitation may be
limited to early systole. The systolic murmur, which becomes louder on
Valsalva and prompt standing, suggests hypertrophic obstructive cardiomyopathy
(idiopathic hypertropic subaortic stenosis).
Causes: Acute or acute on chronic left ventricular failure
is a classic scenario in cardiogenic shock.
The causes of cardiogenic shock can be divided into the following sections,
based on etiology:
Systolic dysfunction: The primary abnormality in systolic dysfunction is
decreased myocardial contractility. Acute MI or ischemia is the most common
cause; cardiogenic shock is more likely to be associated with anterior MI. The
other causes of systolic dysfunction leading to cardiogenic shock are severe
myocarditis, end-stage cardiomyopathy (including valvular causes), myocardial
contusion, and prolonged cardiopulmonary bypass.
Diastolic dysfunction: Increased left ventricular diastolic chamber
stiffness contributes to cardiogenic shock commonly during myocardial
ischemia, but also in the late stages of hypovolemic shock and septic shock.
Increased diastolic dysfunction is particularly detrimental when systolic
contractility is also depressed. The causes of cardiogenic shock primarily due
to the diastolic dysfunction are listed at the end of this section.
Valvular dysfunction: Valvular dysfunction may lead to cardiogenic shock
acutely or may aggravate other etiologies of shock. Acute mitral regurgitation
secondary to papillary muscle rupture or dysfunction is caused by ischemic
injury. Rarely, acute obstruction of the mitral valve by left atrial thrombus
also may result in cardiogenic shock by means of severely decreased cardiac
output. Aortic and mitral regurgitation reduce forward flow, raise
end-diastolic pressure and aggravate shock associated with other etiologies.
Cardiac arrhythmia: Ventricular tachyarrhythmias often are associated with
cardiogenic shock. Furthermore, bradyarrhythmias may cause or aggravate shock
due to another etiology. Sinus tachycardia and atrial tachyarrhythmias
contribute to hypoperfusion and aggravate shock.
Coronary artery disease: Cardiogenic shock generally is associated with
the loss of more than 40% of the left ventricular myocardium, although
predominantly RV infarction or the mechanical complications of MI (eg, acute
mitral regurgitation, ventricular septal rupture, free wall rupture) also may
lead to cardiogenic shock. In patients with previously compromised left
ventricular function, even a small infarction may precipitate shock.
Cardiogenic shock is more likely to develop in people who are elderly or
diabetic or in those who have had a previous inferior infarction.
Other causes: Mechanical complications such as acute mitral regurgitation,
large RV infarction, and rupture of the interventricular septum or left
ventricular free wall are other causes of cardiogenic shock.
Causes of cardiogenic shock include the following:
Approach to the initial clinical evaluation of a patient in
shock
Any patient presenting with shock must have an early working
diagnosis, an approach to urgent resuscitation, and confirmation of the working
diagnosis. Shock is identified in most patients by hypotension and inadequate
organ perfusion, which may be caused either by low cardiac output or by low
systemic vascular resistance. Circulatory shock can be subdivided into 4
distinct classes on the bases of underlying mechanism and characteristic
hemodynamics. These classes of shock should be considered and systemically
differentiated before establishing a definite diagnosis of septic
shock.
Hypovolemic shock
Hypovolemic shock results from
loss of blood volume caused by conditions such as gastrointestinal bleeding,
extravasation of plasma, major surgery, trauma, and severe
burns.
Obstructive shock
Obstructive shock results from
impedance of circulation by an intrinsic or extrinsic obstruction. Pulmonary
embolism, dissecting aneurysm, and pericardial tamponade all result in
obstructive shock.
Distributive shock
Distributive shock is
caused by conditions such as direct arteriovenous shunting and is characterized
by decreased resistance or increased venous capacity from the vasomotor
dysfunction. These patients have high cardiac output hypotension, large pulse
pressure, low diastolic pressure, and warm extremities with good capillary
refill. Such findings on physical examination strongly suggest a working
diagnosis of septic shock.
Cardiogenic shock
Cardiogenic
shock is characterized by primary myocardial dysfunction resulting in the
inability of the heart to maintain adequate cardiac output. These patients
demonstrate clinical signs of low cardiac output, with evidence of adequate
intravascular volume. The patients have cool and clammy extremities, poor
capillary refill, tachycardia, narrow pulse pressure, and low urine output.
WORKUP
Lab Studies:
Biochemical profile: Measurement of routine biochemistry, such as
electrolytes, renal function (urea and creatinine), and liver function tests
(eg, bilirubin, aspartate aminotransferase [AST], alanine aminotransferase
[ALT], and lactic acid dehydrogenase [LDH]) all are useful in appraisal of
proper functioning of vital organs.
Complete blood count: Measurement of CBC generally is helpful to exclude
anemia; a high white cell count may indicate an underlying infection, and
platelet count may be lowered secondary to coagulopathy of sepsis.
Cardiac enzymes
Diagnosis of acute myocardial infarction is aided by a variety of serum
markers, which include creatine kinase (CK) and its subclasses, troponin,
myoglobin, and lactate dehydrogenase. The CK-MB is most specific but may be
falsely elevated in myopathy, hypothyroidism, renal failure, and skeletal
muscle injury.
Cardiac troponins T and I are widely used for diagnosis of myocardial
injury. The rapid release and metabolism of myoglobin occurs in myocardial
infarction. A 4-fold rise of myoglobin over 2 hours appears to be a
sensitive test for myocardial infarction. Serum lactate dehydrogenase (LDH)
increases approximately 10 hours after onset of myocardial infarction, peaks
at 24-48 hours, and gradually returns to normal in 6-8 days. LD-1 isoenzyme
is primarily released by the heart but also may come from kidney, stomach,
pancreas, and red blood cells.
Arterial blood gases: Arterial blood gases indicate overall acid-base
homeostasis and level of arterial blood oxygenation. Base deficit elevation
(normal is +3 to –3 mmol/L) correlates with the occurrence and severity of
shock. Base deficit also is an important marker to follow during resuscitation
of a patient from shock.
Lactate: Serial lactate measurements are useful markers of hypoperfusion
and also are used as indicators of prognosis. Elevated lactate in a patient
with signs of hypoperfusion indicates a poor prognosis; rising lactate during
resuscitation portends a very high mortality rate.
Imaging Studies:
Echocardiography should be performed early to establish the cause of
cardiogenic shock.
Echocardiography provides information on global and regional systolic
function, as well as diastolic dysfunction.
Echocardiography also can lead to a rapid diagnosis of mechanical causes
of shock, such as papillary muscle rupture causing acute myocardial
regurgitation, acute ventricular septal defect, free myocardial wall
rupture, and pericardial tamponade.
Chest x-ray: Chest x-ray is useful in excluding other causes of shock or
chest pain. A widened mediastinum may indicate aortic dissection; tension
pneumothorax or pneumomediastinum may present as low-output shock. Most
patients with established cardiogenic shock exhibit findings of left
ventricular failure. These radiological features include pulmonary vascular
redistribution, interstitial pulmonary edema, enlarged hilar shadows, presence
of Kerley-B lines, cardiomegaly, bilateral pleural effusions, and, finally,
the alveolar edema manifests as bilateral perihilar opacities in a so-called
butterfly distribution.
Other Tests:
Electrocardiogram: Acute myocardial ischemia is diagnosed by the presence
of ST segment elevation, ST segment depression, or the presence of Q waves. T
wave inversion, although less sensitive, is seen in myocardial ischemia.
Therefore, perform electrocardiography immediately to diagnose MI and/or
ischemia.
Procedures:
Invasive hemodynamic monitoring
Invasive hemodynamic monitoring (right heart catheterization) is very
useful for excluding other causes of shock, eg, volume depletion, or
obstructive and septic shock.
The hemodynamic measurements of cardiogenic shock are a pulmonary
capillary wedge pressure (PCWP) greater than 15 mm Hg and a cardiac index of
less than 2.2 L/min/m2.
The presence of large V waves on the pulmonary capillary wedge pressure
tracing suggests severe mitral regurgitation.
A step-up in oxygen saturation between the right atrium and the RV is
diagnostic of ventricular septal rupture.
High right-sided filling pressures in the absence of an elevated
pulmonary capillary wedge pressure, when accompanied with
electrocardiographic criteria, indicates RV infarction.
Coronary artery angiography
Coronary angiography is urgently indicated in patients with myocardial
ischemia or MI who also develop cardiogenic shock. Angiography is required
to assess the anatomy of the coronary arteries and the need for urgent
revascularization.
Coronary angiography often demonstrates multivessel coronary artery
disease in cardiogenic shock. In these patients, a compensatory hyperkinesis
cannot occur in the noninfarct territory because of the severe coronary
artery atherosclerosis. The most common cause of cardiogenic shock is
extensive MI, although a smaller infarction in a previously compromised left
ventricle also may precipitate shock. Following MI, large areas of
nonfunctional but viable myocardium (hibernating myocardium) also can cause
or contribute to cardiogenic shock.
TREATMENT
Medical Care:
Initial management includes fluid resuscitation to correct hypovolemia
and hypotension, unless pulmonary edema is present. Central venous and arterial
lines often are required; right heart catheterization and oximetry are routine.
Oxygenation and airway protection are critical; intubation and mechanical
ventilation commonly are required. Correction of electrolyte and acid-base
abnormalities, such as hypokalemia, hypomagnesemia, and acidosis, are essential.
In patients with inadequate tissue perfusion and adequate intravascular
volume, initiation of an inotropic and/or vasopressor drug may be necessary.
Dopamine increases myocardial contractility and supports the blood pressure;
however, it may increase myocardial oxygen demand. Dobutamine may be preferable
if the systolic blood pressure is higher than 80 mm Hg and has the advantage of
not affecting myocardial oxygen demand. However, the resulting tachycardia may
preclude the use of this inotrope in some patients.
Thrombolytic therapy
Although thrombolytic therapy reduces mortality rates in patients with
acute MI, its benefits for patients with cardiogenic shock secondary to MI
are less certain. When used early in the course of MI, thrombolytic therapy
reduces the likelihood of subsequent development of cardiogenic shock after
the initial event.
In the Gruppo Italiano Per lo Studio Della Streptokinase Nell’Infarto
Miocardio (GISSI) trial, 30-day mortality rates were 69.9% in patients with
cardiogenic shock who received streptokinase, compared to 70.1% in patients
who received a placebo. Similarly, other studies with a tissue plasminogen
activator did not show any benefit in mortality rates from cardiogenic
shock. Lower rates of reperfusion of the infarct-related artery in patients
with cardiogenic shock might explain the disappointing results from
thrombolytic therapy. The other reasons for decreased efficacy of
thrombolytic therapy in cardiogenic shock are a result of hemodynamic,
mechanical, and metabolic factors that are unaffected by such
therapy.
Intra-aortic balloon pump
The use of the intra-aortic balloon pump (IABP) reduces systolic left
ventricular afterload and augments the diastolic coronary perfusion
pressure, thereby increasing cardiac output and improving coronary artery
blood flow. Intra-aortic balloon pumping is effective for the initial
stabilization of patients with cardiogenic shock. However, intra-aortic
balloon pumping is not a definitive therapy; the IABP stabilizes the
patients so that definitive diagnostic and therapeutic maneuvers can be
performed.
Intra-aortic balloon pumping also may be a useful adjunct to
thrombolysis for initial stabilization and transfer of patients to a
tertiary care facility. Some studies have shown lower mortality in patients
with MI treated with intra-aortic balloon pumping and subsequent
revascularization.
Complications may be documented in up to 30% of patients who undergo
intra-aortic balloon pumping and mainly relate to local vascular problems,
emboli, infection, and hemolysis. The impact of intra-aortic balloon pumping
on long-term survival is controversial and depends on the hemodynamic status
and etiology of cardiogenic shock. Patient selection is the key issue; the
early insertion of the IABP may result in clinical benefit rather than
waiting until full-blown cardiogenic shock has developed.
Ventricular assist devices
These devices function as prosthetic ventricles but most require a
sternotomy for insertion. Assist devices may be used to support left
ventricular performance, RV performance, or a combination, depending on the
underlying condition. The Pierce-Donachy left ventricular assist device has
been used as a bridge to cardiac transplantation. Insertion of this device
allowed survival to transplant in 75% of 29 patients.
The Nimbus Hemopump circumvents the problem associated with median
sternotomy and allows a percutaneous placement of cannula across the aortic
valve, which is coupled to an extracorporeal power source. The major
complications of this device are ventricular arrhythmias and embolic
phenomenon.
The indications for insertion of a ventricular assist device are
controversial. Thus, aggressive approach to support the circulatory system
may be used after failure of medical treatment and intra-aortic balloon
pumping; and in the presence of the potentially reversible cause of
cardiogenic shock.
Surgical Care: The retrospective and prospective data favor
aggressive mechanical revascularization in patients with cardiogenic shock
secondary to MI.
Percutaneous transluminal coronary angioplasty
Reestablishing blood flow in the infarct-related artery may improve left
ventricular function and survival following MI. In acute MI, studies show
that percutaneous transluminal coronary angioplasty (PTCA) can achieve
adequate flow in 80-90% of patients, compared with 50-60% of patients after
thrombolytic therapy.
Several retrospective clinical trials have shown that patients with
cardiogenic shock due to myocardial ischemia benefitted from a reduction in
30-day mortality rates when treated with angioplasty. A recent study of
direct (primary) PTCA in patients with cardiogenic shock reports lower
mortality rates in patients treated with angioplasty combined with the use
of stents, compared to medical therapy.
Coronary artery bypass grafting
Critical left main artery disease and 3-vessel coronary artery disease
are common findings in patients who develop cardiogenic shock. The potential
contribution of ischemia in the noninfarcted zone contributes to
deterioration of already compromised myocardial function.
Coronary artery bypass grafting (CABG) in the setting of cardiogenic
shock generally is associated with high surgical morbidity and mortality.
Because the results of percutaneous interventions can be favorable, routine
bypass surgery for these patients often is discouraged.
Shock trial
A recent study known as the Shock Trial addressed the question of
revascularization in patients with cardiogenic shock. Patients were assigned
to receive either optimal medical management, including an IABP and
thrombolytic therapy, or cardiac catheterization followed by
revascularization using PTCA or CABG.
The mortality rates at 30 days were 46.7% in the early intervention
group, compared with 56% in patients treated with optimal medical
management. Although this did not reach a statistical significance at 1
month, the mortality at 6 months was significantly lower in the early
intervention group. This study supports the superiority of a strategy that
combines early revascularization with medical management in patients with
cardiogenic shock.
Consultations: Consultation with a cardiologist and/or an
intensivist should be done early in the patient's clinical course. The patient
usually is admitted to a coronary care unit or intensive care unit.
MEDICATION
Vasopressors augment
the coronary and cerebral blood flow during the low-flow state associated with
shock. Sympathomimetic amines with both alpha- and beta-adrenergic effects are
indicated in cardiogenic shock. Dopamine and dobutamine are the drugs of choice
to improve cardiac contractility, with dopamine the preferred agent in
hypotensive patients.
Vasodilators relax vascular smooth muscle and reduce the systemic vascular
resistance (SVR), allowing for improved forward flow, which improves cardiac
output. Adequate pain control is essential for quality patient care and patient
comfort. Diuretics are used to decrease plasma volume and peripheral edema. The
reduction in plasma volume and stroke volume associated with diuresis may
decrease cardiac output and, consequently, blood pressure, with a compensatory
increase in peripheral vascular resistance. With continuing diuretic therapy,
the volumes of the extracellular fluid and of the plasma return to near
pretreatment levels, and the peripheral vascular resistance usually falls below
its pretreatment baseline.
Drug Category: Vasopressors/inotropes -- These
drugs augment both the coronary and the cerebral blood flow during the low-flow
state associated with cardiogenic shock.
Drug Name
Dopamine (Intropin) -- Stimulates both
adrenergic and dopaminergic receptors. Hemodynamic effect depends on the
dose. Lower doses stimulate mainly dopaminergic receptors that produce
renal and mesenteric vasodilation. Cardiac stimulation and
vasoconstriction is produced by higher doses.
Adult Dose
5-20 mcg/kg/min IV continuous infusion;
dose may be increased by 1-4 mcg/kg/min q10-30min until the optimal
response is achieved; >50% of patients are maintained satisfactorily on
doses <20 mcg/kg/min
Phenytoin, alpha- and beta-adrenergic
blockers, general anesthesia, and MAOIs increase and prolong effects of
dopamine
Pregnancy
C - Safety for use during pregnancy has
not been established.
Precautions
Must be administered via central
vein Closely monitor urine flow, cardiac output, pulmonary wedge
pressure, and blood pressure during infusion; prior to infusion, correct
hypovolemia with either whole blood or plasma, as indicated; monitoring
central venous pressure or left ventricular filling pressure may be
helpful in detecting and treating hypovolemia
Drug Name
Dobutamine (Dobutrex) -- Sympathomimetic
amine with stronger beta than alpha effects. Produces systemic
vasodilation and increases the inotropic state. Higher dosages may cause
an increase in heart rate, exacerbating myocardial ischemia.
Adult Dose
5-20 mcg/kg/min IV continuous infusion,
titrate to desired response; not to exceed 40 mcg/kg/min
Pediatric Dose
Administer as in adults
Contraindications
Documented hypersensitivity to the agent,
hypertrophic cardiomyopathy, atrial fibrillation or flutter, severe
tachycardia
Interactions
Beta-adrenergic blockers antagonize the
effects of dobutamine; general anesthetics may increase its toxicity.
Pregnancy
B - Usually safe but benefits must
outweigh the risks.
Precautions
Following a myocardial infarction, use
dobutamine with extreme caution; correct hypovolemic state before
using May exacerbate hypotension Cautious use indicated when
ventricular or life-threatening tachyarrhythmias are
present
Drug Category: Phosphodiesterase
enzyme inhibitors -- Induce peripheral vasodilation and provide
inotropic support.
Drug Name
Milrinone (Primacor) -- Positive inotrope
and vasodilator with little chronotropic activity. Different in mode of
action from either cardiac glycosides (digoxin) or catecholamines.
Adult Dose
50 mcg/kg IV loading dose over 10 min,
followed by 0.375-0.75 mcg/kg/min continuous IV infusion
Pediatric Dose
Administer as in adults; although DOC in
many pediatric ICUs, safety and efficacy are not well established
Contraindications
Documented hypersensitivity
Interactions
May precipitate if infused in the same IV
line as furosemide
Pregnancy
C - Safety for use during pregnancy has
not been established.
Precautions
Monitor fluid, electrolyte changes, and
renal function during therapy; excessive diuresis may cause an increase in
potassium loss and predispose digitalized patients to arrhythmias (correct
hypokalemia by potassium supplementation prior to treatment); slow or stop
the infusion in patients showing excessive decreases in blood pressure; if
vigorous diuretic therapy has caused significant decreases in cardiac
filling pressure, cautiously administer the drug and monitor blood
pressure, heart rate, and clinical symptomatology
Drug Name
Inamrinone - formerly amrinone (Inocor)
-- Phosphodiesterase inhibitor with positive inotropic and vasodilator
activity. Produces vasodilation and increases inotropic state. More likely
to cause tachycardia than dobutamine and may exacerbate myocardial
ischemia.
Adult Dose
Initial dose: 0.75 mg/kg IV bolus slowly
over 2-3 min Maintenance infusion: 5-10 mcg/kg/min; not to exceed 10
mg/kg; adjust dose according to patient response
Pediatric Dose
Administer as in adults; safety and
efficacy not well established
Contraindications
Documented hypersensitivity
Interactions
Diuretics may cause significant
hypovolemia and a decrease in filling pressure; inamrinone has additive
effects with cardiac glycosides
Pregnancy
C - Safety for use during pregnancy has
not been established.
Precautions
Causes thrombocytopenia in 2-3% of
patients; hypotension may occur following a loading dose; requires
adequate preload; ventricular dysrhythmias may occur but may be related to
the underlying condition; do not use in patients with cardiac outlet
obstruction (eg, aortic stenosis, pulmonic stenosis, hypertrophic
cardiomyopathy); discontinue therapy if clinical symptoms of liver
toxicity occur; correct hypokalemic states before using
inamrinone
Drug Category: Vasodilators
-- Decrease preload and/or afterload
Drug Name
Nitroglycerin (Nitro-Bid) -- Causes
relaxation of vascular smooth muscle by stimulating intracellular cyclic
guanosine monophosphate production. The result is a decrease in preload
and blood pressure (afterload).
Adult Dose
10-200 mcg/min IV continuous infusion
Pediatric Dose
0.1-1 mcg/kg/min IV infusion
Contraindications
Documented hypersensitivity; severe
anemia, shock, postural hypotension, head trauma, closed-angle glaucoma,
cerebral hemorrhage
Interactions
Aspirin may increase nitrate serum
concentrations; marked symptomatic orthostatic hypotension may occur with
coadministration of calcium channel blockers (dose adjustment of either
agent may be necessary)
Pregnancy
C - Safety for use during pregnancy has
not been established.
Precautions
Caution in 3-vessel, left main coronary
artery disease, aortic stenosis, or low systolic blood
pressure
Drug Category: Analgesics
Drug Name
Morphine sulfate (Duramorph, Astramorph,
MS Contin) -- DOC for narcotic analgesia due to its reliable and
predictable effects, safety profile, and ease of reversibility with
naloxone. Various IV doses are used, commonly titrated until the desired
effect is obtained.
Adult Dose
Starting dose: 0.1 mg/kg
IV/IM/SC Maintenance dose: 5-20 mg/70 kg IV/IM/SC
q4h Relatively hypovolemic patients: start with 2 mg IV/IM/SC,
reassess hemodynamic effects of the dose
Pediatric Dose
0.1-0.2 mg/kg/dose IV/IM/SC q2-4h prn;
not to exceed 15 mg/dose; may initiate at 0.05 mg/kg/dose
Contraindications
Documented hypersensitivity; hypotension,
potentially compromised airway where establishing rapid airway control
would be difficult
Interactions
Phenothiazines may antagonize analgesic
effects of opiate agonists; tricyclic antidepressants, MAOIs, and other
CNS depressants may potentiate the adverse effects of morphine.
Pregnancy
C - Safety for use during pregnancy has
not been established.
Precautions
Avoid in hypotension, respiratory
depression, nausea, emesis, constipation, and urinary retention; caution
in atrial flutter and other supraventricular tachycardias; has vagolytic
action and may increase ventricular response rate
Drug Category: Diuretics -- Decrease plasma volume and
peripheral edema. Excessive reduction in plasma volume and stroke volume
associated with diuresis may decrease cardiac output and, consequently, blood
pressure.
Drug Name
Furosemide (Lasix) -- Increases excretion
of water by interfering with chloride-binding cotransport system, which in
turn inhibits sodium and chloride reabsorption in ascending loop of Henle
and distal renal tubule. Individualize dose to patient. Depending
on response, administer at increments of 20-40 mg no sooner than 6-8 h
after the previous dose, until desired diuresis occurs. When treating
infants, titrate with 1 mg/kg/dose increments until a satisfactory effect
is achieved.
Adult Dose
20-80 mg/d PO/IV/IM; titrate up to 600
mg/d for severe edematous states; may be administered as a continuous
infusion as well
Pediatric Dose
1 mg/kg IV/IM slowly under close
supervision; not to exceed 6 mg/kg
Contraindications
Documented hypersensitivity, hepatic
coma, anuria, and a state of severe electrolyte depletion
Interactions
Metformin decreases furosemide
concentrations; furosemide interferes with the hypoglycemic effect of
antidiabetic agents and antagonizes the muscle-relaxing effect of
tubocurarine; auditory toxicity appears to be increased with the
coadministration of aminoglycosides and furosemide; hearing loss of
varying degrees may occur; the anticoagulant activity of warfarin may be
enhanced when taken concurrently with this medication; increased plasma
lithium levels and toxicity are possible when taken concurrently with this
medication
Pregnancy
C - Safety for use during pregnancy has
not been established.
Precautions
Observe for blood dyscrasias, liver or
kidney damage, or idiosyncratic reactions; perform frequent serum
electrolyte, carbon dioxide, glucose, uric acid, calcium, creatinine, and
BUN determinations during the first few months of therapy and periodically
thereafter; loop diuretics may increase urinary excretion of magnesium and
calcium
FOLLOW-UP
Further Inpatient Care:
Cardiogenic shock is an emergency requiring immediate resuscitative
therapy, before shock irreversibly damages vital organs. Simultaneously,
elucidating the cause of shock is important so that therapy can be directed to
correcting the cause.
Transfer:
Immediately transfer a patient who develops cardiogenic shock to an
institution where invasive monitoring, coronary revascularization, and skilled
personnel are available to provide expert care to the patient.
Prognosis:
In the absence of aggressive, highly experienced technical care, mortality
among patients with cardiogenic shock is exceedingly high (up to 70-90%). The
key to achieving a good outcome is rapid diagnosis, prompt supportive therapy,
and expeditious coronary artery revascularization in patients with myocardial
ischemia and infarction. The mortality rate in patients treated aggressively
can be lowered to 40-60%. The prognosis of patients who survive cardiogenic
shock is not well studied but may be reasonable, if the underlying cause of
shock is corrected.
MISCELLANEOUS
Medical/Legal Pitfalls:
Cardiogenic shock has a very high mortality rate (60-80%), although
mortality rates have decreased over the last 2 decades.
Areas of nonfunctioning but viable (hibernating) myocardium can cause or
contribute to the development of cardiogenic shock.
The key to a good outcome in cardiogenic shock is an organized approach,
with rapid diagnosis and prompt initiation of therapy to maintain blood
pressure and cardiac output. Early and definitive restoration of coronary
blood flow is the most important intervention for producing improvement in
survival, and it represents standard therapy at present for patients with
cardiogenic shock due to myocardial ischemia.
The development of cardiogenic shock may be prevented with early
revascularization in patients with myocardial infarction when accompanied with
appropriate pharmacological management; and with required intervention in
patients with structural heart disease.
Special Concerns:
Right ventricular infarction
RV infarction occurs in up to 30% of patients with inferior MI and
becomes hemodynamically unstable in 10% of those patients. Diagnosis is made
by identifying ST segment elevation in the right precordial leads
(V3 or V4R) and/or typical hemodynamic findings on
right heart catheterization (elevated right atrial and RV end-diastolic
pressures with normal to low pulmonary artery wedge pressure and low cardiac
output). Echocardiography also can be very helpful in the diagnosis of RV
infarction. Patients with cardiogenic shock from RV infarction have a better
prognosis when compared to those with cardiogenic shock due to left
ventricular systolic failure.
Management of cardiogenic shock from right ventricular infarction:
Supportive therapy for patients with RV infarction begins with the
restoration and maintenance of RV preload with fluid administration.
However, excessive fluid resuscitation may compromise left ventricular
filling by introducing interventricular septal shift. Inotropic therapy with
dobutamine may be effective in increasing cardiac output in patients with RV
infarction. Maintenance of systemic arterial pressure in order to maintain
adequate coronary artery perfusion may require vasoconstricting agents, such
as norepinephrine. In unstable patients, IABP may be useful for ensuring
adequate blood supply to the already compromised right ventricle.
Revascularization of the occluded coronary artery, preferably by PTCA is
crucial for management and has shown to dramatically improved
outcome.
Acute mitral regurgitation
Acute mitral regurgitation usually is associated with inferior
myocardial infarction due to ischemia or infarction of the papillary muscle.
The incidence is approximately 1% of MIs, posteromedial papillary muscle is
involved more frequently than the anterolateral muscle. Acute mitral
regurgitation usually occurs 2-7 days following acute MI and presents with
abrupt onset of pulmonary edema, hypotension, and cardiogenic shock.
Echocardiography is extremely useful in making a diagnosis. The
2-dimensional echocardiogram will show the malfunctioning mitral valve, and
the Doppler study can be used to document the severity of mitral
regurgitation. Right heart catheterization often is required for stabilizing
the patient. Tall V waves identified on pulmonary arterial and wedge
pressure waveforms indicate acute mitral regurgitation. However, the
diagnosis must be confirmed by echocardiography or left ventriculography
before definite therapy or surgery.
Hemodynamic stabilization by reducing afterload either with
nitroprusside or IABP often is instituted. Definitive therapy requires
revascularization, if ischemia is present, and/or surgical valve repair or
replacement, if structural valvular lesion is present. The mortality in the
presurgical era was reported at 50% in the first 24 hours, with 2-months
survival reported at 6%.
Cardiac rupture
Rupture of the free wall of the left ventricle occurs within 2 weeks of
the MI and may occur within the first 24 hours. The rupture may involve the
anterior or posterior or lateral wall of the ventricle.
Cardiac rupture often presents as sudden cardiac death. Premortem
symptoms include chest pain, agitation, tachycardia, and hypotension. This
diagnosis should be considered in patients with electromechanical
dissociation who have a history of anginal pain. Patients rarely, if ever,
survive cardiac rupture.
Ventricular septal rupture
Approximately 1-3% of acute MIs are associated with ventricular septal
rupture. Most septal ruptures occur within the week following MI. Patients
with acute ventricular septal rupture develop acute heart failure and/or
cardiogenic shock, with physical findings of a harsh holosystolic murmur and
left parasternal thrill. A left-to-right intracardiac shunt as demonstrated
by a step-up (>5% increase in oxygen saturation) between the right atrium
and right ventricle confirms the diagnosis. Alternatively, 2-dimensional and
Doppler echocardiography can be used to identify the location and severity
of the left-to-right shunt.
Rapid stabilization using IABP and pharmacologic measures, followed by
emergent surgical repair, is life saving. The timing of surgical
intervention is controversial, but most experts suggest operative repair
within 48 hours of the rupture. Ventricular septal rupture portends a poor
prognosis unless an aggressive approach to management is utilized. Immediate
surgical repair of patients with ventricular septal rupture is reported to
be associated with survival rates of 42-75%; therefore, it is imperative
that prompt surgical therapy be undertaken as soon as possible after the
diagnosis of ventricular septal rupture is confirmed.
Reversible myocardial dysfunction
Other causes of severe reversible myocardial dysfunction are
sepsis-associated myocardial depression, myocardial depression following
cardiopulmonary bypass, or inflammatory myocarditis. This presentation is
often referred to as cold septic shock in older literature. In these
situations, myocardial dysfunction occurs from the effects of inflammatory
cytokines, such as tumor necrosis factor (TNF) and interleukin (IL)-1.
Myocardial dysfunction may vary from mild to severe and may lead to
cardiogenic shock. For patients in cardiogenic shock, cardiovascular support
with inotropic agents may be required until recovery, which generally occurs
after the underlying disease process resolves.
Constructed
by Dr N.A. Nematallah Consultant in perioperative medicine and intensive
therapy, Al Razi Orthopedic Hospital ,
State of Kuwait, email : razianesth@freeservers.com
