Theme: Cardiogenic shock

Plan

Introduction
Etiology
Pathophysiology
Conclusion
Used materials

Introduction
Cardiogenic shock - systemic
hypoperfusion secondary to severe
depression of cardiac output and
sustained systolic arterial hypotension
despite elevated filling pressures.

Etiology

Systolic dysfunction
Diastolic dysfunction
Valvular dysfunction
Cardiac arrhythmias
Coronary artery disease
Mechanical complications

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)

Left ventricular failure

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

Left ventricular failure

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
Decreased contractility
Reduced myocardial contractility can result from the following:
Right ventricular infarction
Ischemia
Hypoxia
Acidosis

Left ventricular failure

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

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.

Pathophysiology

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.

Reversible myocardial dysfunction

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.

Systemic effects
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.

Conclusion
The clinical definition of cardiogenic shock is
decreased cardiac output and evidence of
tissue hypoxia in the presence of adequate
intravascular volume. 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.

Used materials
Reynolds HR, Hochman JS. Cardiogenic shock: current concepts and
improving outcomes. Circulation. Feb 5 2008; [Medline].
Chen ZM, Pan HC, Chen YP, Peto R, Collins R, Jiang LX, et al. Early
intravenous then oral metoprolol in 45,852 patients with acute myocardial
infarction: Nov 5 2005;[Medline].
Goldberg RJ, Samad NA, Yarzebski J, Gurwitz J, Bigelow C, Gore JM.
Temporal trends in cardiogenic shock complicating acute myocardial
infarction. Apr 15 [Medline].
Babaev A, Frederick PD, Pasta DJ, Every N, Sichrovsky T, Hochman JS.
Trends in management and outcomes of patients with acute myocardial
infarction complicated by cardiogenic shock. Jul 27 2005;
Garatti A, Russo C, Lanfranconi M, Colombo T, Bruschi G, Trunfio S,
Mechanical circulatory support for cardiogenic shock complicating acute
myocardial infarction: an experimental and clinical review. May-Jun 2007.

Thanks for attention!!!