Cardiogenic shock is characterized by low cardiac output and tissue hypoxia due to inadequate pumping function of the heart. It is a leading cause of death for acute myocardial infarction patients without aggressive medical care. Clinically, cardiogenic shock patients appear pale with cool skin and demonstrate signs of hypoperfusion. Treatment involves fluid resuscitation, inotropes to support blood pressure, mechanical circulatory support like IABP, and most importantly reversal of the underlying cause through procedures like PCI or CABG. While supportive care buys time, definitive treatment of the precipitating cardiac problem is needed for long term recovery from cardiogenic shock.

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2. The clinical definition of cardiogenic shock is
decreased cardiac output and evidence of tissue
hypoxia in the presence of adequate
intravascular volume.
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3. Cardiogenic shock is the leading
cause of death in acute MI, with
mortality rates of up to 70-90%
in the absence of aggressive,
highly experienced technical
care.
Hemodynamic criteria for cardiogenic
shock are sustained hypotension (systolic
blood pressure below 90 mm Hg for at
least 30 min) and a reduced cardiac index
(<2.2 L/min/m2) in the presence of normal
or elevated pulmonary capillary wedge
pressure (>15 mm Hg) or right ventricular
end-diastolic pressure (RVEDP) (>10 mm
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4. 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.
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Cardiogenic shock is recognized as a low cardiac output
state secondary to extensive left ventricular (LV)
infarction, development of a mechanical defect (eg,
ventricular septal defect or papillary muscle rupture), or
right ventricular (RV) infarction.
Patients who develop cardiogenic shock from
acute MI consistently have evidence of
progressive myocardial necrosis with infarct
extension. Decreased coronary perfusion
pressure and cardiac output as well as increased
myocardial oxygen demand play a role in the
vicious cycle that leads to cardiogenic shock
and potentially death.
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.
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.

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Myocardial
Hibernation
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.
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.

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Systemic Effects !
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 salt and fluid retention,
hence augmenting the LV preload.
The elevated heart rate and
contractility increases myocardial
oxygen demand, further
worsening myocardial ischemia.
Fluid retention and impaired LV diastolic filling triggered by tachycardia
and ischemia worsen pulmonary venous congestion and hypoxemia.
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.
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.

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Etiology !
• Systolic dysfunction
• Diastolic dysfunction
• Valvular dysfunction
• Cardiac arrhythmias
• Coronary artery disease
• Mechanical complications

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Characteristics of a patient with Cardiogenic shock !
• 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 also may be present.
• Heart sounds are usually distant, and third and
fourth heart sounds may be present
• The pulse pressure may be low, and patients are
usually tachycardic
• Patients show signs of hypoperfusion, such as
altered mental status and decreased urine
output

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Approach to such case !
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.

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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 and respiratory
support, as well as reversal of the underlying cause.
Approach to such case !
Placement of a central line may facilitate volume
resuscitation, provide vascular access for multiple
infusions, and allow invasive monitoring of central
venous pressure.
An arterial line may be placed to provide continuous
blood pressure monitoring. This is particularly useful
if the patient requires inotropic medications.
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.
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.

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Initial management includes fluid resuscitation to
correct hypovolemia and hypotension, unless
pulmonary edema is present. Central venous and
arterial lines are often required.
Oxygenation and airway protection are critical;
intubation and mechanical ventilation are commonly
required.Patients with myocardial infarction (MI) or
acute coronary syndrome are given aspirin and
heparin.
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.
Dopamine increases myocardial contractility and supports the blood pressure; however, it may increase myocardial
oxygen demand.
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 use of the intra-aortic balloon pump (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.
New trials suggests the usage of LVAD in the clinical setting of cardiogenic shock. And the results have been
promising.

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How ever the definitive treatment of
cardiogenic shock should be reversal of the
etiologic factor.
Eg – PCI, CABG etc.

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