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.
Characterized by systemic hypoperfusion due to cardiomyocyte necrosis and ventricular dysfunction.
Complicating acute myocardial infarction associated with high mortality rates and remains the leading cause of death in patients hospitalized with AMI.
Cardiogenic shock occurs in approximately 8 to 10% of patients with ST segment elevation myocardial infarction (STEMI) and is associated with a mortality of 40 to 50%.
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.
Affects 5 to 10% of patients presenting with acute myocardial infarction and more than half the patients with acute myocardial infarction – cardiogenic shock die during index hospitalization.
The pathophysiology of cardiac shock associated with acute MI consists of myocardial ischemia resulting in regional necrosis and decreasing cardiac contractile mass.
Among patients with STEMI and cardiogenic shock, the time from onset of symptoms to death is often less than 24 hours.
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.
Prompt reperfusion of the infected artery is the only treatment that belongs survival.
Cardiogenic shock develops when cardiac output is inadequate to meet the metabolic needs of the body.
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.
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%).
Has a 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.
The use of venoarterial extracorporeal membrane oxygenation (ECMO) is increasingly commonly used in patients with cardiogenic shock, including after cardiac arrest that is refractory to standard therapies.
The survival to hospital discharge using peripheral venoarterial ECMO in patients after cardiac arrest and with refractory cardiogenic shock is between 29% and 41%.
Extracorporal life support (ECLS) use has not shown evidence regarding its affect on mortality.
Extracorporeal life support provides both blood flow and blood oxygenation, but its routine use does not improve clinical outcomes in patients with acute myocardial infarction and cardiogenic shock, and is associated with excess bleeding complications and limb ischemia.
In patients with acute myocardial infarction, complicated by cardiogenic shock, and with planned early revascularization, the risk of death from any cause at the 30 day follow up, was not lower among patients who received ECLS therapy than among those who received medical therapy alone (ECLS-SHOCK Investigators).
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.
percutaneous, micro, axial flow pumps, drain blood from the left ventricle through a catheter and expel it into the ascending aorta.
It unloads the left ventricle but is dependent on adequate oxygenation of blood and intact right heart function to ensure adequate filling of the left ventricle.
In patients with CS there was no significant difference between milrinone or dobtamine in respected outcomes.
In patients with cardiogenic shock, especially in those with associated cardiac arrest, there may be associated ischemia reperfusion injury, a proinflammatory cytokine profile, increased nitric oxide production, which may lead to intense vasoplegia, microcirculatory dysfunction, multiple organ failure, and death.