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Background

Cardiogenic shock is a physiologic state in which inadequate tissue perfusion results from
cardiac dysfunction, most often systolic. It is a major, and frequently fatal, complication of a
variety of acute and chronic disorders, occurring most commonly following acute myocardial
infarction (MI). (See Pathophysiology, Etiology, and Prognosis.)
Although ST-segment elevation MI (STEMI, previously termed Q-wave MI) is encountered in
most patients, cardiogenic shock may also develop in patients with non ST-segment elevation
acute coronary syndrome (NSTEMI, NSTACS, or unstable angina). (See the images below.)
Patient with an acute anterolateral myocardial infarction who
developed cardiogenic shock. Coronary angiography images showed severe stenosis of the left
anterior descending coronary artery, which was dilated by percutaneous transluminal coronary
angioplasty. Echocardiogram image from a patient with
cardiogenic shock shows enlarged cardiac chambers; the motion study showed poor left
ventricular function. Courtesy of R. Hoeschen, MD.
The clinical definition of cardiogenic shock is 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 min) and a
reduced cardiac index (< 2.2 L/min/m
2
) in the presence of elevated pulmonary capillary wedge
pressure (>15 mm Hg). (See DDx, Workup.)
Cardiogenic shock continues to be a difficult clinical problem; the management of this condition
requires a rapid and well-organized approach. (See Prognosis, Treatment, and Medication.)
The diagnosis of cardiogenic shock can sometimes be made at the bedside by observing
hypotension, absence of hypovomeia, and clinical signs of poor tissue perfusion, which include
oliguria, cyanosis, cool extremities, and altered mentation. These signs usually persist after
attempts have been made to correct hypovolemia, arrhythmia, hypoxia, and acidosis. (See
Presentation, DDx.)
Types of circulatory shock
Shock is identified in most patients based on findings of hypotension and inadequate organ
perfusion, which may be caused by either low cardiac output or low systemic vascular resistance
(SVR). Circulatory shock can be subdivided into 4 distinct classes based on the underlying
mechanism and characteristic hemodynamic findings. In all patients, before establishing a
definite diagnosis of septic shock, the following 4 classes of shock should be considered and
systematically differentiated. (See Pathophysiology, Etiology, Presentation and Workup.)
Cardiogenic shock
Cardiogenic shock characterized by primary myocardial dysfunction renders the heart to be
unable to maintain adequate cardiac output. These patients demonstrate clinical signs of low
cardiac output, with adequate intravascular volume. The patients have cool and clammy
extremities, poor capillary refill, tachycardia, narrow pulse pressure, and low urine output.
Hypovolemic shock
Hypovolemic shock results from loss of blood volume, the possible reasons for which include
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 producing direct arteriovenous shunting and is
characterized by decreased SVR or increased venous capacitance because of the vasomotor
dysfunction. These patients have high cardiac output, hypotension, high pulse pressure, low
diastolic pressure, and warm extremities with good capillary refill. Such findings upon physical
examination strongly suggest a working diagnosis of septic shock.
Patient education
Patients should receive instruction regarding the early warning signs of acute MI and how to
access the emergency medical system (eg, calling 911).
Patients must also be instructed on cardiac risk factors, particularly those that are reversible and
subject to change (eg, smoking, diet, exercise).
For patient education information, see the First Aid and Injuries Center and the Healthy Living
Center, as well as Shock and Cardiopulmonary Resuscitation (CPR).
Pathophysiology
Cardiogenic shock is recognized as a low cardiac output state secondary to extensive left
ventricular infarction, development of a mechanical defect (eg, ventricular septal defect or
papillary muscle rupture), or right ventricular infarction.
Disorders that can result in the acute deterioration of cardiac function and lead to cardiogenic
shock include myocardial infarction (MI) or myocardial ischemia, acute myocarditis, sustained
arrhythmia, severe valvular dysfunction, and decompensation of end-stage cardiomyopathy from
multiple etiologies. Autopsy studies show that cardiogenic shock is generally associated with the
loss of more than 40% of the left ventricular myocardial muscle.
Myocardial pathology
Cardiogenic shock is characterized by systolic and diastolic dysfunction. Patients who develop
cardiogenic shock from acute MI consistently have evidence of progressive myocardial necrosis
with infarct extension. Decreased coronary perfusion pressure and increased myocardial oxygen
demand play a role in the vicious cycle that leads to cardiogenic shock.
Patients suffering from cardiogenic shock often have multivessel coronary artery disease with
limited coronary blood flow reserve. Ischemia remote from the infarcted zone is an important
contributor to shock. Myocardial diastolic function is also impaired, because 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. Also, myocyte membrane transport pumps
fail, 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. These events induce fracture of the mitochondria, nuclear
envelopes, and plasma membranes.
Additionally, apoptosis (programmed cell death) may occur 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
Large areas of myocardium that are dysfunctional but still viable can contribute to the
development of cardiogenic shock in patients with MI. This potentially reversible dysfunction is
often described as myocardial stunning or as hibernating myocardium. Although hibernation is
considered a different physiologic process than myocardial stunning, the conditions are difficult
to distinguish in the clinical setting and they often coexist.
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 the hibernating (and/or stunned) myocardium generally leads to
improved myocardial function.
Consideration of 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.
Cardiovascular mechanics of cardiogenic shock
The main mechanical defect in cardiogenic shock is a shift to the right for the left ventricular
end-systolic pressure-volume curve, 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 is usually greatly increased in persons with cardiogenic
shock.
The stroke volume is decreased, and to compensate for this, the curvilinear diastolic pressure-
volume curve also shifts to the right, with a decrease in diastolic compliance. This leads to
increased diastolic filling, which is associated with an increase in end-diastolic pressure. The
attempt to enhance 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
filling pressures and 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
the intrapulmonary shunting that is often present, contributes to substantial arterial oxygen
desaturation.
Systemic effects
When a critical mass of left ventricular myocardium becomes ischemic and fails to pump
effectively, stroke volume and cardiac output are curtailed. Myocardial 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 and thereby elevating myocardial oxygen requirements. Systemic perfusion is
compromised by decreased cardiac output, with tissue hypoperfusion intensifying anaerobic
metabolism and instigating 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 the heart rate and cardiac
contractility and causes renal fluid retention, hence augmenting 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 triggered by tachycardia and
ischemia contribute to pulmonary venous congestion and hypoxemia. Sympathetically mediated
vasoconstriction to maintain systemic blood pressure amplifies myocardial afterload, which
additionally impairs cardiac performance. Finally, excessive myocardial oxygen demand with
simultaneous inadequate myocardial perfusion worsens myocardial ischemia, initiating a vicious
cycle that ultimately ends in death, if uninterrupted.
Usually, a combination of systolic and diastolic myocardial dysfunction is 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), which 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. All forms of shock are
characterized by inadequate perfusion to meet the metabolic demands of the tissues. A
maldistribution of blood flow to end organs begets cellular hypoxia and end organ damage, the
well-described multisystem organ dysfunction syndrome. The organs of vital importance are the
brain, heart, and kidneys.
A 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 propagating shock. Depressed coronary perfusion leads to worsening cardiac
dysfunction and a cycle of self-perpetuating progression of global hypoperfusion. Renal
compensation for reduced perfusion results in diminished glomerular filtration, causing oliguria
and subsequent renal failure.
Etiology
Cardiogenic shock can result from the following types of cardiac dysfunction:
Systolic dysfunction
Diastolic dysfunction
Valvular dysfunction
Cardiac arrhythmias
Coronary artery disease
Mechanical complications
The vast majority of cases of cardiogenic shock in adults are due to acute myocardial ischemia.
Indeed, cardiogenic shock is generally associated with the loss of more than 40% of the left
ventricular myocardium, although 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 persons who have had a previous inferior
myocardial infarction (MI).
Complications of acute MI, such as acute mitral regurgitation, large right ventricular infarction,
and rupture of the interventricular septum or left ventricular free wall, can result in cardiogenic
shock. Conduction abnormalities (eg, atrioventricular blocks, sinus bradycardia) are also risk
factors.
Many cases of cardiogenic shock occurring after acute coronary syndromes may be due to
medication administration. The use of beta blockers and angiotensin-converting enzyme (ACE)
inhibitors in acute coronary syndromes must be carefully timed and monitored.
[1, 2, 3]

In children, preceding viral infection may cause myocarditis. In addition, children and infants
may have unrecognized congenital structural heart defects that are well compensated until there
is a stressor. These etiologies plus toxic ingestions make up the 3 primary causes of cardiogenic
shock in children.
A systemic inflammatory response syndrometype mechanism has also been implicated in the
etiology of cardiogenic shock. Elevated levels of white blood cells, body temperature,
complement, interleukins, and C-reactive protein are often seen in large myocardial infarctions.
Similarly, inflammatory nitric oxide synthetase (iNOS) is also released in high levels during
myocardial stress. Nitric oxide production induced by iNOS may uncouple calcium metabolism
in the myocardium resulting in a stunned myocardium. Additionally, iNOS leads to the
expression of interleukins, which may themselves cause hypotension.
Left ventricular failure
Systolic dysfunction
The primary abnormality in systolic dysfunction is abated myocardial contractility. Acute MI or
ischemia is the most common cause; cardiogenic shock is more likely to be associated with
anterior MI. The causes of systolic dysfunction leading to cardiogenic shock can be summarized
as follows:
Ischemia/MI
Global hypoxemia
Valvular disease
Myocardial depressant drugs - Eg, beta blockers, calcium channel blockers, and
antiarrhythmics
Myocardial contusion
Respiratory acidosis
Metabolic derangements - Eg, acidosis, hypophosphatemia, and hypocalcemia
Severe myocarditis
End-stage cardiomyopathy - Including valvular causes
Prolonged cardiopulmonary bypass.
Cardiotoxic drugs - Eg, doxorubicin (Adriamycin)
Diastolic dysfunction
Increased left ventricular diastolic chamber stiffness contributes to cardiogenic shock during
cardiac ischemia, as well as 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 due primarily to diastolic dysfunction can be summarized as
follows:
Ischemia
Ventricular hypertrophy
Restrictive cardiomyopathy
Prolonged hypovolemic or septic shock
Ventricular interdependence
External compression by pericardial tamponade
Greatly increased afterload
Increased afterload, which can impair cardiac function, can be caused by the following:
Aortic stenosis
Hypertrophic cardiomyopathy
Dynamic aortic outflow tract obstruction
Coarctation of the aorta
Malignant hypertension
Valvular and structural abnormality
Valvular dysfunction may immediately lead to cardiogenic shock 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 a left
atrial thrombus 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.
Valvular and structural abnormalities associated with cardiogenic shock include the following:
Mitral stenosis
Endocarditis
Mitral aortic regurgitation
Obstruction due to atrial myxoma or thrombus
Papillary muscle dysfunction or rupture
Ruptured septum or free wall arrhythmias
Tamponade
Decreased contractility
Reduced myocardial contractility can result from the following:
Right ventricular infarction
Ischemia
Hypoxia
Acidosis
Right ventricular failure
Greatly increased afterload
Afterload increase associated with right ventricular failure can result from the following:
Pulmonary embolism
Pulmonary vascular disease - Eg, pulmonary arterial hypertension and veno-occlusive
disease
Hypoxic pulmonary vasoconstriction
Peak end-expiratory pressure
High alveolar pressure
Acute respiratory distress syndrome
Pulmonary fibrosis
Sleep disordered breathing
Chronic obstructive pulmonary disease
Arrhythmias
Ventricular tachyarrhythmias are often 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.
Prognosis
Cardiogenic shock is the leading cause of death in acute myocardial infarction (MI). In the
absence of aggressive, highly experienced technical care, mortality rates among patients with
cardiogenic shock are 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.
[5, 6, 7]

The overall in-hospital mortality rate for patients with cardiogenic shock is 57%. For persons
older than 75 years, the mortality rate is 64.1%; for those younger than 75 years, it is 39.5%.
Mortality rates are similar for patients with cardiogenic shock secondary to STEMI or NSTACS.
Evidence of right ventricular dilation on echocardiogram may indicate a worse outcome in
patients with cardiogenic shock, as may right ventricular infarction on a right-sided
electrocardiogram.
[8]
The prognosis for patients who survive cardiogenic shock is not well
studied but may be favorable if the underlying cause of shock is expeditiously corrected.
Morbidity and mortality
Complications of cardiogenic shock may include the following:
Cardiopulmonary arrest
Dysrhythmia
Renal failure
Multisystem organ failure
Ventricular aneurysm
Thromboembolic sequelae
Stroke
Death
The following predictors of mortality were identified from the Global Utilization of
Streptokinase and Tissue-Plasminogen Activator for Occluded Coronary Arteries (GUSTO-I)
trial
[9]
:
Increasing age
Prior MI
Altered sensorium
Cold, clammy skin
Oliguria
Echocardiographic findings such as left ventricular ejection fraction and mitral regurgitation are
independent predictors of mortality. An ejection fraction of less than 28% is associated with a
survival rate of 24% at 1 year, compared with a survival rate of 56% with a higher ejection
fraction. Moderate or severe mitral regurgitation was found to be associated with a 1-year
survival rate of 31%, compared with a survival rate of 58% in patients with no regurgitation.
Outcomes in cardiogenic shock significantly improve only when rapid revascularization can be
achieved. The SHOCK (Should We Emergently Revascularize Occluded Coronaries for
Cardiogenic Shock?) trial demonstrated that overall mortality when revascularization occurs is
38%.
[10]
When rapid revascularization is not attempted, mortality rates approach 70%. Rates vary
depending on the procedure (eg, percutaneous transluminal coronary angioplasty, stent
placement, thrombolytic therapy).
Diagnostic Considerations
Conditions to consider in the differential diagnosis of cardiogenic shock include the following:
Systemic inflammatory response syndrome
Acute coronary syndrome
Aortic regurgitation
Dilated cardiomyopathy
Restrictive cardiomyopathy
Congestive heart failure and pulmonary edema
Mitral regurgitation
Pericarditis and cardiac tamponade
Hypovolemic shock
Papillary muscle rupture
Acute valvular dysfunction
Right ventricular infarction
Right ventricular infarction occurs in up to 30% of patients with inferior myocardial infarction
(MI) and becomes hemodynamically unstable in 10% of these patients. The diagnosis is made by
identifying an ST-segment elevation in the right precordial leads (V
3
or V
4
R) and/or typical
hemodynamic findings after right heart catheterization. These are elevated right atrial and right
ventricular end-diastolic pressures with normal to low pulmonary artery wedge pressure and low
cardiac output.
Echocardiography findings can also be very helpful in the diagnosis of right ventricular
infarction. Patients with cardiogenic shock due to this condition have a better prognosis than do
patients when compared to those with cardiogenic shock due to left ventricular systolic failure.
Regarding the management of cardiogenic shock due to right ventricular infarction, supportive
therapy begins with the restoration and maintenance of right ventricular preload with fluid
administration. However, excessive fluid resuscitation may compromise left ventricular filling by
introducing an interventricular septal shift.
Inotropic therapy with dobutamine may be effective in increasing cardiac output in patients with
right ventricular infarction. Maintenance of systemic arterial pressure in order to maintain
adequate coronary artery perfusion may require vasoconstricting agents, such as norepinephrine.
In unstable patients, an intra-aortic balloon pump (IABP) may be useful for ensuring adequate
blood supply to the already compromised right ventricle.
Revascularization of the occluded coronary artery, preferably by percutaneous transluminal
coronary angioplasty (PTCA), is crucial for management and has shown to dramatically improve
outcome.
Acute mitral regurgitation
Acute mitral regurgitation is usually associated with inferior MI due to ischemia or infarction of
the papillary muscle. It occurs in approximately 1% of MIs, and posteromedial papillary muscle
is involved more frequently than anterolateral muscle. Acute mitral regurgitation usually happens
2-7 days following acute MI and manifests with an abrupt onset of pulmonary edema,
hypotension, and cardiogenic shock.
Echocardiography findings are extremely useful in making a diagnosis. The 2-dimensional (2-D)
echocardiographic image shows the malfunctioning mitral valve, and findings from a Doppler
study can be used to document the severity of mitral regurgitation. Right heart catheterization is
often 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 based on echocardiography or left ventriculography findings before definitive therapy
or surgery is initiated.
Hemodynamic stabilization by reducing afterload, either with nitroprusside or an IABP, is often
instituted. Definitive therapy requires revascularization, if ischemia is present, and/or surgical
valve repair or replacement, if a structural valvular lesion is present. The mortality rate in the
presurgical era was 50% in the first 24 hours, with a 2-month survival rate of 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, 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-
D and Doppler echocardiographic findings can be used to identify the location and severity of
the left-to-right shunt.
Rapid stabilization using an IABP and pharmacologic measures, followed by emergent surgical
repair, is lifesaving. 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 management is aggressive.
Immediate surgical repair of patients with ventricular septal rupture is reported to be associated
with survival rates of 42-75%; therefore, prompt surgical therapy is imperative 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, and inflammatory
myocarditis. In older literature, this presentation is often referred to as cold septic shock. In these
situations, myocardial dysfunction occurs from the effects of inflammatory cytokines, such as
tumor necrosis factor and interleukin 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.
Differential Diagnoses
Myocardial Infarction
Myocardial Ischemia
Myocardial Rupture
Myocarditis
Pulmonary Edema, Cardiogenic
Pulmonary Embolism
Sepsis, Bacterial
Septic Shock
Shock, Distributive
Shock, Hemorrhagic
Approach Considerations
As previously discussed, the key to achieving a good outcome in patients with cardiogenic shock
is rapid diagnosis, prompt supportive therapy, and expeditious coronary artery revascularization
in patients with myocardial ischemia and infarction.
Any patient presenting with shock must receive an early working diagnosis, urgent resuscitation,
and subsequent confirmation of the working diagnosis.
In addition to laboratory studies, workup in cardiogenic shock can include imaging studies such
as echocardiography, chest radiography, and angiography; electrocardiography; and invasive
hemodynamic monitoring.
Approach Considerations
Cardiogenic shock is an emergency requiring immediate resuscitative therapy before shock
irreversibly damages vital organs. The key to a good outcome in patients with cardiogenic shock
is an organized approach, with rapid diagnosis and prompt initiation of pharmacologic therapy to
maintain blood pressure and cardiac output.
All patients require admission to an intensive care setting, which may involve emergent transfer
to the cardiac catheterization suite, critical care transport to a tertiary care center, or internal
transfer to the intensive care unit (ICU).
Early and definitive restoration of coronary blood flow is the most important intervention for
achieving an improved survival rate. At present, it represents standard therapy for patients with
cardiogenic shock due to myocardial ischemia.
Correction of electrolyte and acid-base abnormalities, such as hypokalemia, hypomagnesemia,
and acidosis, is essential in cardiogenic shock.
Cardiogenic shock may be prevented with early revascularization in patients with myocardial
infarction (MI) and with required intervention in patients with structural heart disease.
Procedures
Placement of a central line may facilitate volume resuscitation, provide vascular access for
multiple infusions, and allow invasive monitoring of central venous pressure. Central venous
pressure may also be used to guide fluid resuscitation.
Although not necessary for the diagnosis of cardiogenic shock, invasive monitoring with a
pulmonary artery catheter may be helpful in guiding fluid resuscitation in situations in which left
ventricular preload is difficult to determine.
Pulmonary artery catheter pressure measurements may also be useful in prognosis. Retrospective
evaluation of these measurements from the SHOCK trial demonstrated that stroke volume index
(SVI) and stroke work index (SWI) vary inversely with mortality.
[10]

An arterial line may be placed to provide continuous blood pressure monitoring. This is
particularly useful if the patient requires inotropic medications.
An intra-aortic balloon pump may be placed in the emergency department as a bridge to
percutaneous coronary intervention (PCI) or coronary artery bypass graft (CABG), to decrease
myocardial workload and to improve end-organ perfusion.
PCI and coronary artery bypass
Clinicians should be alert to the fact that the SHOCK trial demonstrated that either PCI or
coronary artery bypass is the treatment of choice for cardiogenic shock and that each has been
shown to markedly decrease mortality rates at 1 year. PCI should be initiated within 90 minutes
of presentation; however, it remains helpful, as an acute intervention, within 12 hours of
presentation.
If such a facility is not immediately available, thrombolytics should be considered. However, this
treatment is second best. An increased mortality is seen in situations in which thrombolytics are
used instead of PCI. This is due to the relative ineffectiveness of the thrombolytic medications to
lyse clots in low-blood pressure situations.
[11, 1]

Consultations
Consult a cardiologist at the earliest opportunity because his or her insight and expertise may be
invaluable for facilitating echocardiographic support, placement of an intra-aortic balloon pump
(IABP), and transfer to more definitive care (eg, cardiac catheterization suite, ICU, operating
room). In severe cases, also consider discussing the case with a cardiothoracic surgeon.
Deterrence and prevention
Although cardiogenic shock is not entirely preventable, measures can be taken to minimize the
risk of occurrence, recognize it at earlier stages, and begin corrective therapy more expeditiously.
Deterrence and prevention require a high degree of suspicion and heightened awareness.
Care is required in treating patients with acute coronary syndromes who are not yet in
cardiogenic shock. Careful use of beta blockers and ACE inhibitors in these patients is essential
to avoid hypotension leading to cardiogenic shock.
[1]

Prehospital Care
Prehospital care is aimed at minimizing any further ischemia and shock. All patients require
intravenous access, high-flow oxygen administered by mask, and cardiac monitoring.
Twelve-lead electrocardiography performed in the field by appropriately trained paramedics may
be useful in decreasing door-to-PCI times and/or time to the administration of thrombolytics
because acute ST-segment elevation myocardial infarctions (STEMIs) can be identified earlier.
The emergency department (ED) can thus be alerted and may mobilize the appropriate resources.
Inotropic medications should be considered in systems with appropriately trained paramedical
personnel.
When clinically necessary, positive pressure ventilation and endotracheal intubation should be
performed. Continuous positive airway pressure (CPAP) or bilevel positive airway pressure
(BiPAP) support can be considered in appropriately equipped systems.
Resuscitation, Ventilation, and Pharmacologic Intervention
Initial management includes fluid resuscitation to correct hypovolemia and hypotension, unless
pulmonary edema is present. Central venous and arterial lines are often required. Swan-Ganz
catheterization and continuous percutaneous oximetry are routine.
Oxygenation and airway protection are critical; intubation and mechanical ventilation are
commonly required. However, although positive pressure ventilation may improve oxygenation,
it may also compromise venous return, preload, to the heart. In any event, the patient should be
treated with high-flow oxygen. Studies in patients with acute cardiogenic pulmonary edema have
shown noninvasive ventilation to improve hemodynamics and reduce the intubation rate.
Mortality is, however, unaffected.
A study by Shin et al suggested that patients who receive extracorporeal cardiopulmonary
resuscitation (CPR) versus conventional CPR for longer than 10 minutes following in-hospital
arrest have a greater chance of survival.
[12]

All patients with cardiogenic shock require close hemodynamic monitoring, volume support to
ensure adequate sufficient preload, and ventilatory support.
Pharmacologic therapy
Patients with myocardial infarction (MI) or acute coronary syndrome are given aspirin and
heparin. Both of these medications have been shown to be effective in reducing mortality in
separate studies. Before initiating therapy, however, care should be taken to ensure that the
patient does not have a myocardial wall rupture that is amenable to surgery.
There is no need to start clopidogrel until after angiography, since angiography may demonstrate
that there is a need for urgent coronary bypass.
[1]

The glycoprotein IIb/IIIa inhibitors improve the outcome of patients with nonST-segment
elevation acute coronary syndrome (NSTACS). They have been found to reduce recurrent MI
following percutaneous coronary intervention (PCI) and in cardiogenic shock.
Hemodynamic Support
Dopamine, norepinephrine, and epinephrine are vasoconstricting drugs that help to maintain
adequate blood pressure during life-threatening hypotension and help to preserve perfusion
pressure for optimizing flow in various organs. The mean blood pressure required for adequate
splanchnic and renal perfusion (mean arterial pressure [MAP] of 60 or 65 mm Hg) is based on
clinical indices of organ function.
In patients with inadequate tissue perfusion and adequate intravascular volume, initiation of
inotropic and/or vasopressor drug therapy 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;
it has the advantage of not affecting myocardial oxygen demand as much as dopamine does.
However, the resulting tachycardia may preclude the use of this inotropic agent in some patients.
Dopamine is usually initiated at a rate of 5-10 mcg/kg/min intravenously, and the infusion rate is
adjusted according to the blood pressure and other hemodynamic parameters. Often, patients
may require high doses of dopamine (as much as 20 mcg/kg/min).
If the patient remains hypotensive despite moderate doses of dopamine, a direct vasoconstrictor
(eg, norepinephrine) should be started at a dose of 0.5 mcg/kg/min and titrated to maintain an
MAP of 60 mm Hg. The potent vasoconstrictors (eg, norepinephrine) have traditionally been
avoided because of their adverse effects on cardiac output and renal perfusion.
Vasopressor supportive therapy
The following is a brief review of the mechanism of action and indications for drugs used for
hemodynamic support of cardiogenic shock.
[13, 14]

Dopamine
Dopamine is a precursor of norepinephrine and epinephrine and has varying effects according to
the doses infused. A dose of less than 5 mcg/kg/min causes vasodilation of renal, mesenteric, and
coronary beds. At a dose of 5-10 mcg/kg/min, beta1-adrenergic effects induce an increase in
cardiac contractility and heart rate.
At doses of approximately 10 mcg/kg/min, alpha-adrenergic effects lead to arterial
vasoconstriction and an elevation in blood pressure. The blood pressure increases primarily as a
result of the inotropic effect. The undesirable effects are tachycardia and increased pulmonary
shunting, as well as the potential for decreased splanchnic perfusion and increased pulmonary
arterial wedge pressure.
Norepinephrine
Norepinephrine is a potent alpha-adrenergic agonist with minimal beta-adrenergic agonist
effects. Norepinephrine can increase blood pressure successfully in patients who remain
hypotensive following dopamine. The dose of norepinephrine may vary from 0.2-1.5
mcg/kg/min, and large doses, as high as 3.3 mcg/kg/min, have been used because of the alpha-
receptor down-regulation in persons with sepsis.
Epinephrine
Epinephrine can increase the MAP by increasing the cardiac index and stroke volume, as well as
systemic vascular resistance (SVR) and heart rate. Epinephrine decreases the splanchnic blood
flow and may increase oxygen delivery and consumption.
Administration of this agent is associated with an increase in systemic and regional lactate
concentrations. The use of epinephrine is recommended only in patients who are unresponsive to
traditional agents. The undesirable effects are an increase in lactate concentration, a potential to
produce myocardial ischemia, the development of arrhythmias, and a reduction in splanchnic
flow.
Levosimendan
Levosimendan, though not approved for use in the United States, can be considered for use in
conjunction with vasopressors. It should be used with caution, however, as it can cause
hypotension. Used with vasopressors, levosimendan may improve hemodynamics and improve
coronary blood flow.
[15, 16]

Inotropic supportive therapy
Dobutamine
Dobutamine (sympathomimetic agent) is a beta1-receptor agonist, although it has some beta2-
receptor and minimal alpha-receptor activity. Intravenous dobutamine induces significant
positive inotropic effects, with mild chronotropic effects. It also induces mild peripheral
vasodilation (decrease in afterload). The combined effect of increased inotropy and decreased
afterload induces a significant increase in cardiac output.
In the setting of acute myocardial infarction (MI), dobutamine use could increase the size of the
infarct because of the increase in myocardial oxygen consumption that may ensue. In general,
avoid dobutamine in patients with moderate or severe hypotension (eg, systolic blood pressure <
80 mm Hg) because of the peripheral vasodilation.
Phosphodiesterase inhibitors
Phosphodiesterase inhibitors (PDIs), which include inamrinone (formerly amrinone) and
milrinone, are inotropic agents with vasodilating properties and long half-lives. The
hemodynamic properties of PDIs are (1) a positive inotropic effect on the myocardium and
peripheral vasodilation (decreased afterload) and (2) a reduction in pulmonary vascular
resistance (decreased preload).
PDIs are beneficial in persons with cardiac pump failure, but they may require concomitant
vasopressor administration. Unlike catecholamine inotropes, these drugs are not dependent on
adrenoreceptor activity; therefore, patients are less likely to develop tolerance to these
medications.
PDIs are less likely than catecholamines to cause adverse effects known to be associated with
adrenoreceptor activity (eg, increased myocardial oxygen demand, myocardial ischemia). They
are also associated with less tachycardia and myocardial oxygen consumption. However, the
incidence of tachyarrhythmias is greater with PDIs than with dobutamine.
Thrombolytic Therapy
Although thrombolytic therapy (TT) reduces mortality rates in patients with acute myocardial
infarction (MI), its benefits for patients with cardiogenic shock secondary to MI are
disappointing. When used early in the course of MI, TT 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 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 employing a tissue plasminogen activator did not show reductions in
mortality rates from cardiogenic shock. Lower rates of reperfusion of the infarct-related artery in
patients with cardiogenic shock may help to explain the disappointing results from TT. Other
reasons for the decreased efficacy of TT are the existence of hemodynamic, mechanical, and
metabolic causes of cardiogenic shock that are unaffected by TT.
Thrombolytic therapy plus IABP
A prospective cohort study demonstrated the potential survival benefit of combining TT with
IABP counterpulsation in patients with MI complicated by cardiogenic shock.
[17]

Out of 1190 patients enrolled, the treatments were (1) no TT and no IABP counterpulsation
(33%, n = 285), (2) IABP counterpulsation only (33%, n = 279), (3) TT only (15%, n = 132), and
(4) TT and IABP counterpulsation (19%, n = 160).
Patients in cardiogenic shock who were treated with TT had lower in-hospital mortality rates
than did those who did not receive TT (54% vs 64%), and patients selected for IABP
counterpulsation had lower in-hospital mortality rates than did those who did not receive IABP
counterpulsation (50% vs 72%).
Furthermore, a significant difference was noted in inhospital mortality rates among the 4
treatment groups; ie, TT plus IABP counterpulsation (47%), IABP counterpulsation only (52%),
TT only (63%), no TT and no IABP counterpulsation (77%).
Revascularization influenced in-hospital mortality rates significantly (39% with revascularization
vs 78% without revascularization).
Patients who are unsuitable for invasive therapy should be treated with a thrombolytic agent in
the absence of contraindications. This is a class I recommendation by American College of
Cardiology (ACC)/American Heart Association (AHA) guidelines.
Intra-Aortic Balloon Pump
The use of the IABP reduces systolic left ventricular afterload and augments diastolic coronary
perfusion pressure, thereby increasing cardiac output and improving coronary artery blood flow.
The IABP is effective for the initial stabilization of patients with cardiogenic shock. However, an
IABP is not definitive therapy; the IABP stabilizes patients so that definitive diagnostic and
therapeutic interventions can be performed.
[18, 19]

The IABP 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 rates in patients with
myocardial infarction (MI) and cardiogenic shock treated with an IABP and subsequent
revascularization, as previously mentioned.
Complications may be documented in up to 30% of patients who undergo IABP therapy; these
relate primarily to local vascular problems, embolism, infection, and hemolysis.
The impact of treatment with an IABP on long-term survival is controversial and depends on the
patients hemodynamic status and the etiology of the cardiogenic shock. Patient selection is the
key issue; inserting the IABP early, rather than waiting until full-blown cardiogenic shock has
developed, may result in clinical benefit.
Ramanathan et al found that rapid and complete reversal of systemic hypoperfusion with IABP
counterpulsation in the SHOCK trial and SHOCK registry was independently associated with
improved inhospital, 30-day, and 1-year survival, regardless of early revascularization. This
suggests that complete reversal of systemic hypoperfusion with IABP counterpulsation is an
important early prognostic feature.
[20]

In the IABP-SHOCK II study, 600 patients with cardiogenic shock complicating acute
myocardial infarction were randomized to intraaortic balloon counterpulsation or no intraaortic
balloon counterpulsation. All patients were expected to undergo early revascularization. Use of
intraaortic balloon counterpulsation did not significantly reduce 30-day mortality in these
patients.
[21]

Ventricular Assist Devices
In recent years, left ventricular assist devices (LVADs) capable of providing complete short-term
hemodynamic support have been developed. The application of LVAD during reperfusion, after
acute coronary occlusion, causes reduction of the left ventricular preload, increases regional
myocardial blood flow and lactate extraction, and improves general cardiac function. The LVAD
makes it possible to maintain the collateral blood flow as a result of maintaining the cardiac
output and aortic pressure, keeping wall tension low and reducing the extent of microvascular
reperfusion injury.
[18, 19, 22]

A pooled analysis from 17 studies showed that the mean age of this group of patients with
LVADs was 59.5 4.5 years and that mean support duration was 146.2 60.2 hours. In 78.5%
of patients (range, 53.8-100%), adjunctive reperfusion therapy, mainly percutaneous
transluminal coronary angioplasty (PTCA), was used. Mean weaning and survival rates were
58.5% (range, 46-75%) and 40% (range, 29-58%), respectively.
[18]

In any case, comparing studies is difficult because important data are usually missing, mean age
of patients were different, and time to treatment is not standardized. Hemodynamic presentation
seems to be worse compared with data reported in the SHOCK trial, with lower cardiac index,
lower systolic aortic pressure, and higher serum lactates. Taking these considerations into
account, LVAD support seems to give no survival improvement in patients with cardiogenic
shock complicating acute myocardial infarction (MI), compared with early reperfusion alone or
in combination with IABP.
In a randomized, controlled trial in which 129 patients with end-stage heart failure who were
ineligible for cardiac transplantation were assigned either to receive an LVAD (68 patients) or to
undergo optimal medical management, survival rates were higher in the LVAD group. The rates
of survival at 1 year were 52% in the device group and 25% in the medical therapy group, while
the rates at 2 years were 23% and 8%, respectively. In addition, the quality of life was
significantly improved at 1 year in the device group.
[23]

Implantable LVADs are being used as a bridge to heart transplantation for patients with acute MI
and cardiogenic shock.
[24]
According to the HeartMate Data Registry
[25]
, from 1986-1998, 41
patients (5% of the total number of HeartMate IP patients) were supported with this implantable
pneumatic device for acute MI, and 25 (61%) were successfully bridged to heart transplantation.
However, LVADs as a bridging option for patients with cardiogenic shock must be considered
cautiously and must be avoided in patients who are unlikely to survive or are not likely to be
transplant candidates. Further investigations are required to better define indications, support
modalities, and outcomes.
The indications for insertion of a ventricular assist device are controversial. Such an aggressive
approach to support the circulatory system in cardiogenic shock is appropriate (1) after the
failure of medical treatment and an IABP, (2) when the cause of cardiogenic shock is potentially
reversible, or (3) if the device can be used as a bridging option.
Percutaneous Transluminal Coronary Angioplasty
The retrospective and prospective data favor aggressive mechanical revascularization in patients
with cardiogenic shock secondary to myocardial infarction (MI).
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 (TT).
Several retrospective clinical trials have shown that patients with cardiogenic shock due to
myocardial ischemia benefitted (reduction in 30d mortality rates) when treated with angioplasty.
A study of direct (primary) PTCA in patients with cardiogenic shock reported lower mortality
rates in patients treated with angioplasty combined with the use of stents than in patients treat
with medical therapy.
A study by Antoniucci et al found that mortality rates increase in relation to the length of time to
treatment in patients with acute MI who are not considered to be at low risk. To study the
relationship of time to treatment and mortality in patients with acute MI, a series of 1336 patients
who underwent successful primary PTCA were stratified into low-risk and not low risk patient
groups. The 6-month mortality rate was 9.3% for notlow risk patients and 1.3% for the low-risk
patients. An increase in the mortality rate from 4.8% to 12.9% with increasing time to
reperfusion was observed in the not lowrisk group. A delay from symptom onset to treatment
resulted in higher mortality rates for the not lowrisk patients.
[26]

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 the deterioration of already compromised myocardial function.
Coronary artery bypass grafting (CABG) in the setting of cardiogenic shock is generally
associated with high surgical morbidity and mortality rates. Because the results of percutaneous
interventions can be favorable, routine bypass surgery is often discouraged for these patients.
A 2004 task force of the ACC and the AHA gave a class I recommendation to the performance
of primary PCI or emergent CABG in patients younger than 75 years who have STEMI who
develop shock within 36 hours of myocardial infarction (MI) and can be treated within 18 hours
of shock onset. Performance of primary PCI or emergent CABG was considered reasonable in
patients older than 75 years (class IIa recommendation).
Revascularization in the SHOCK Trial
Results from the SHOCK trial supported the superiority of a strategy that combines early
revascularization with medical management in patients with cardiogenic shock. In the study,
patients were assigned to receive either optimal medical management, including an IABP and
TT, or cardiac catheterization followed by revascularization using PTCA or CABG.
[27, 11, 28]

The mortality rates at 30 days were 46.7% in the early intervention group and 56% in patients
treated with optimal medical management. Although these 30-day results did not reach statistical
significance, the mortality rate at 6 months was significantly lower in the early intervention
group (50.3% vs 63.1%).
[27]

The 1-year survival rates were also reported from the SHOCK trial.
[11]
The survival rate at 1-year
was 46.7% for patients in the early revascularization group and 33.6% in the conservative
management group. The treatment benefit was apparent only for patients younger than 75 years
(51.6% survival rate in early revascularization group vs 33.3% in patients treated with optimal
medical management).
Based on the outcome of this study, the recommendation is that patients with acute myocardial
infarction (MI) complicated by cardiogenic shock, particularly those younger than 75 years,
should be rapidly transferred to a center with personnel capable of performing early angiography
and revascularization procedures.
Patient Transfer
Immediately transfer a patient who develops cardiogenic shock to an institution at which
invasive monitoring, coronary revascularization, and skilled personnel are available to provide
expert care.
Patients with cardiogenic shock who are admitted to a hospital without facilities for
revascularization should be immediately transferred to a tertiary care center with such facilities.
If time to PCI is more than 1 hour and onset of symptoms has been within 3 hours, rapid
administration of TT is recommended.
It should be kept in mind, however, that attempts to transfer a patient with cardiogenic shock
must be made only when everything possible has been done to stabilize his or her condition and
when the level of care during the transfer will not significantly decrease.
Medication Summary
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
for persons with cardiogenic shock. Dopamine and dobutamine are the drugs of choice to
improve cardiac contractility, with dopamine the preferred agent in patients with hypotension.
Vasodilators relax vascular smooth muscle and reduce the SVR, allowing for improved forward
flow, which improves cardiac output.
Diuretics are used to decrease plasma volume and peripheral edema. The reduction in
extracellular fluid and plasma volume associated with diuresis may initially decrease cardiac
output and, consequently, blood pressure, with a compensatory increase in peripheral vascular
resistance. With continuing diuretic therapy, the plasma volume and peripheral vascular
resistance usually return to pretreatment values.
Inotropic Agents
Class Summary
These agents augment coronary and cerebral blood flow during the low-flow state associated
with cardiogenic shock. They also improve cardiac output in refractory hypotension and shock.
View full drug information
Dopamine

Dopamine stimulates adrenergic and dopaminergic receptors. Its hemodynamic effect depends
on the dose. Lower doses primarily stimulate dopaminergic receptors that produce renal and
mesenteric vasodilation. Higher doses produce cardiac stimulation and vasoconstriction.
View full drug information
Dobutamine

Dobutamine is a sympathomimetic amine with stronger beta effects than alpha effects. It
produces systemic vasodilation and increases the inotropic state. Higher doses may cause an
increase in heart rate, exacerbating myocardial ischemia.
View full drug information
Norepinephrine (Levophed)

Norepinephrine is a naturally occurring catecholamine with potent alpha-receptor and mild beta-
receptor activity. It stimulates beta1- and alpha-adrenergic receptors, resulting in increased
cardiac muscle contractility, heart rate, and vasoconstriction. Norepinephrine increases blood
pressure and afterload. Increased afterload may result in decreased cardiac output, increased
myocardial oxygen demand, and cardiac ischemia.
Norepinephrine is generally reserved for use in patients with severe hypotension (eg, systolic
blood pressure < 70 mm Hg) or hypotension unresponsive to other medication.
View full drug information
Milrinone

Milrinone is a selective phosphodiesterase inhibitor in cardiac and vascular tissue with positive
inotropic and vasodilator effects; it has little chronotropic activity. This agent's mode of action
differs from that of either digitalis glycosides or catecholamines.
View full drug information
Inamrinone

Formerly known as amrinone, inamrinone is a phosphodiesterase inhibitor with positive
inotropic and vasodilator activity. It produces vasodilation and increases the inotropic state.
Inamrinone is more likely to cause tachycardia than is dobutamine, and it may exacerbate
myocardial ischemia.
Vasodilators
Class Summary
Vasodilators decrease preload and/or afterload.
View full drug information
Nitroglycerin IV

This agent causes relaxation of vascular smooth muscle by stimulating intracellular cyclic
guanosine monophosphate production. The result is a decrease in preload and blood pressure (ie,
afterload).
Antiplatelet Agents, Cardiovascular
Class Summary
Agents that irreversibly inhibit platelet aggregation may improve morbidity.
View full drug information
Aspirin (Anacin, Ascriptin Regular Strength, Bayer Aspirin Regimen Regular,
Bufferin, Ecotrin)

Aspirin is an odorless, white, powdery substance available in 81 mg, 325 mg, and 500 mg, for
oral use. When exposed to moisture, aspirin hydrolyzes into salicylic acid and acetic acids. It is a
stronger inhibitor of prostaglandin synthesis and platelet aggregation than are other salicylic acid
derivatives. The acetyl group is responsible for inactivation of cyclo-oxygenase via acetylation.
Aspirin is hydrolyzed rapidly in plasma, and elimination follows zero order pharmacokinetics.
Aspirin irreversibly inhibits platelet aggregation by inhibiting platelet cyclo-oxygenase. This, in
turn, inhibits the conversion of arachidonic acid to prostaglandin 12 (a potent vasodilator and
inhibitor of platelet activation) and thromboxane A2 (a potent vasoconstrictor and platelet
aggregate). Platelet-inhibition lasts for the life of the cell (approximately 10 d).
Aspirin may be used at a low dose to inhibit platelet aggregation and improve complications of
venous stases and thrombosis. It reduces the likelihood of myocardial infarction (MI) and is also
very effective in reducing the risk of stroke. Early administration of aspirin in patients with acute
MI may reduce cardiac mortality in the first month.
Opioid Analgesics
Class Summary
Analgesics reduce pain, which decreases sympathetic stress and provides some preload
reduction.
View full drug information
Morphine sulfate (Duramorph, Astramorph, MS Contin, Kadian, Oramorph
SR)

Morphine sulfate is the drug of choice for narcotic analgesia due to its reliable and predictable
effects, safety profile, and ease of reversibility with naloxone. Various intravenous doses are
used; the drug is commonly titrated until the desired effect is achieved.
Diuretics, Loop
Class Summary
These drugs cause diuresis to decrease plasma volume and edema and thereby decrease cardiac
output and, consequently, blood pressure. The initial decrease in cardiac output causes a
compensatory increase in peripheral vascular resistance. With continuing diuretic therapy,
extracellular fluid and plasma volumes return almost to pretreatment levels. Peripheral vascular
resistance decreases below that of the pretreatment baseline.
View full drug information
Furosemide (Lasix)

Furosemide increases the excretion of water by interfering with the chloride-binding cotransport
system, which, in turn, inhibits sodium and chloride reabsorption in the ascending loop of Henle
and the distal renal tubule.
Individualize the dose to the patient. Depending on the response, administer furosemide at
increments of 20-40mg no sooner than 6-8 hours after the previous dose, until the desired
diuresis occurs. When treating infants, titrate the drug in increments of 1mg/kg/dose until a
satisfactory effect is achieved.
Cardiovascular, Other
Class Summary
These drugs cause arterial and venous dilation by binding to the cyclic guanosine
monophosphate (GMP) receptors on vascular smooth muscle, causing smooth muscle relaxation.
Natriuretic peptides produce dose-dependent decreases in pulmonary capillary wedge pressure
and systemic arterial pressure.
View full drug information
Nesiritide (Natrecor)

Nesiritide is a recombinant deoxyribonucleic acid (DNA) form of human B-type natriuretic
peptide (hBNP), which dilates veins and arteries.
Human BNP binds to the particulate guanylate cyclase receptor of vascular smooth muscle and
endothelial cells. Binding to the receptor causes an increase in cyclic GMP, which serves as a
second messenger to dilate veins and arteries. Pulmonary capillary wedge pressure is reduced
and dyspnea is improved in patients with acutely decompensated congestive heart failure.
Nesiritide may be considered in the treatment of patients with cardiogenic shock. Although
nesiritide has been shown to increase mortality and renal dysfunction, it continues to be studied
as a treatment for acute congestive heart failure and currently retains US Food and Drug
Administration (FDA) approval. However, it should be used with caution in the setting of
cardiogenic shock because it has been shown to cause hypotension.
http://emedicine.medscape.com/article/152191-overview

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