Cardiogenic Shock

Cardiogenic Shock
 Introduction
 Cardiogenic shock is a major, and frequently fatal, complication of a
variety of acute and chronic disorders that impair the ability of the heart to
maintain adequate tissue perfusion.
Cardiogenic Shock
 Causes
1) Ventricular fibrillation
2) Very slow heart rhythm (bradycardia) or heart conduction block
3) MI
4) Aortic stenosis,Aortic dissection
5) Mitral stenosis
6) Cardiomyopathy
7) Tear or rupture of the wall (septum) between the left and right ventricle
8) Tear or rupture of the muscles or tendons that support the heart valves,
especially the mitral valve
9) Rupture of the heart muscle due to damage from the heart attack
Cardiogenic Shock
 Pathophysiology
 Disorders that can result in the acute deterioration of cardiac function and
can lead to cardiogenic shock include MI or myocardial ischemia,
sustained arrhythmia, acute valvular catastrophe, and decompensation of
end-stage cardiomyopathy from multiple etiologies.
Cardiogenic Shock
 Myocardial pathology
 Cardiogenic shock is characterized by both 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.
 These patients 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
Cardiogenic Shock
 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 pathophysiologic 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.
Cardiogenic Shock
 Clinical Presentation
o Rapid breathing
o Rapid and Weak (thready) pulse
o Restlessness, agitation, confusion
o Skin that feels cool to the touch
o Pale skin color
o Decreased mental status
o Loss of ability to concentrate
o Increase JVP
o Oliguria
o Coma
Cardiogenic Shock
 Investigation
 Arterial blood gas
 Blood chemistry (electrolytes, cardiac enzymes)
 CBC
 Coronary angiography
 Echocardiogram
 Electrocardiogram
 Nuclear scans
Cardiogenic Shock
Management
A)General management-
 Complete bed rest
 O2 inhalation
 Relief of pain by opiates

B)Specific measures-
• 1.i.v fliud administration
• 2.glyceral trinitrate
• 3.dopamine 4-10 μg/kg/min
• 4.dobutamine 2.5-10 μg/kg/min
• 5.adrenaline
Cardiogenic Shock
 Management(Other’s)
 Mechanical assist device-
 Intra-aortic balloon counter pulsation
 Ventricular assist device
Cardiogenic Shock
 Monitoring
 ECG
 BP
 Pulse
 Skin temp
 U.O
 CVP(Central Venous pressure)
 PCWP(Pulmonary Capillary Wedge Pressure)
 Oxygen saturation