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Cardiogenic shock

Cardiogenic shock is described as a clinical condition of inadequate tissue end-organ perfusion due to inability of the heart to pump adequate amounts of blood.

Complicating acute myocardial infarction associated with high mortality rates and remains the leading cause of death in patients hospitalized with AMI.

It is a clinical condition of inadequate organ perfusion related to the inability of the heart to pump an adequate amount of blood.

The reduced tissue perfusion result in decreased oxygen and nutrients delivery to the tissues and, if prolonged can add end organ damage and multi system failure.

The pathophysiology of cardiac shock associated with acute MI consists of myocardial ischemia  resulting in regional necrosis and decreasing cardiac contractile mass.

The decreased ventricular function and decreasing cardiac output and systemic hypotension is perceived by carotid baroreceptors juxtaglomerular cells in the kidney leading to reflexive sympathetic/neurohormone activation increased circulating catecholamines.

In this setting vascular endothelial cells typically constrict to maintain systemic perfusion and the renin-angiotensin-aldosterone cascade is activated to increase salt and water retention.

Together in the reflex responses lead to increased myocardial overload and circulating plasma volume which can reduce pressure cardiac performance and lead to pulmonary edema.

If the ventricular function cannot be restored, or the congestion does not occur, a cycle of decreasing cardiac output and progressive volume overload ensues  ultimately  leading to a reduction in coronary artery perfusion pressure, myocardial ischemia, worsening cardiac functioning, and cardiac and circulatory collapse.

Its most common etiology is acute myocardial  ischemia due to occlusion of an epicardial coronary artery, resulting in regional cardiac myocyte necrosis and loss of ventricular function.

CS is defined as a state of low cardiac output resulting in clinical and bio chemical manifestations of end organ hypoperfusion.
CS is the most common presentation with severe left ventricular dysfunction in the setting of an AMI, and most frequently after an anterior MI.
In a study of 686 patients with CS in the setting of AMI: 42% had a left anterior descending MI and 7.7% had a left main main coronary artery MI.
Occurs in 5 to 10% of people with acute myocardial infarction.
CS is the leading cause of hospital death in patients with AMI.
Between 40 and 50,000 patients in the US have CS associated with AMI each year, corresponding to an incidence of approximately 5-10% of all patients with AMI.

A 30 day mortality in patients with CS is nearly 40% and approaches approximately 50% it one year.About 7% of patients with AMI develop cardiogenic shock.(4-12%).

Cardiogenic shock is more frequent in older adults.
Acute myocardial infarction-cardiogenic shock is associated with in-house mortality in excess of 50% even in the contemporary treatment area.
30 day mortality is nearly 40% and approaches 50% at one year.
Emergency revascularization reduces the risk of death in patients with myocardial infarction complicated by cardiogenic shock.

Female sex is an independent predictor of worse in-hospital outcomes in older adults with acute myocardial infarction-cardiogenic shock in the US.

As with 50-70% mortality within 30 days.

Death from cardiogenic shock results from one or more of three factors: hemodynamic deterioration, multi-organ dysfunction, and the development of a systemic inflammatory response syndrome.

Mortality as high as 80% in the prethrombolytic era.

Complicating myocardial infarction treated with early mechanical revascularization can reduce 6 and 12 month mortality compared to initial medical stabilization including use of intra-aortic balloon pump, and fibrinolytic therapy followed by late or no revascularization.

Early revascularization after myocardial infarction does not benefit patients older than 75 years of age.

Associated with loss of 40% or more of the left ventricular mass based on autopsy studies.

Association between 40% necrosis or more and the development of cardiogenic shock accepted principle.

The pathophysiology of CS associated with AMI consists of a myocardial ischemia insult resulting in regional necrosis and decreasing cardiac contracttile mass.

Subsequently a decrease in ventricular function with an associated decreasing cardiac output and systemic systemic hypotension is perceived by carotid baroreceptors and juxta glomerular cells in the kidney.

Decreased perfusion leads to sympathetic/neurohormonal activation and increased circulating catecholamines.

With cardiogenic shock vascular and endothelium cells constrict to maintain systemic perfusion and the renin-angiotensin-Aldosterone cascade is activated to increase salt and water retention.

These reflexes increase myocardial afterload and circulating plasma volume which can reduce cardiac performance and lead to pulmonary edema.

If ventricular function cannot be restored, a cycle of decreasing cardiac output and progressive volume overload occurs.

Ultimately this cycle leads to decreased coronary artery perfusion pressure, myocardial ischemia, worsening cardiac function, and circulatory collapse.

Coronary angiography and revascularization of the infarct related artery reduces 30 day mortality from 51.6 243.3 percent (CULPRIT-Shock trial).

In patient with CS associated with AMI due to left ventricular infarction, the inability to inject blood efficiently leads to increased LV end diastolic pressure, which is associated with elevated pulmonary capillary wedge pressure.

Patient with increased left ventricular end diastolic pressure,typically present with an S3 gallup, tachypnea, and hypoxemia due to pulmonary edema.

The use of intravascular microaxial left ventricular assist device compared with intra aortic balloon pumps may be associated with worse in hospital clinical outcomes among patients with AMI in cardiogenic shock undergoing percutaneous coronary intervention.
Vasopressors and inotropes remain in the cornerstone of therapy for most patients with CS.
 Norepinephrine is the preferred vasopressor over epinephrine and dopamine.

In patients  with CS there was no significant difference between milrinone or dobtamine in respected outcomes.

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