Cardiogenic Shock Research Paper
Cardiogenic shock is characterized by the heart’s acute inability to deliver the amount of oxygen that the peripheral tissues and organs demand. [DCCN 2008]
Patho psychology of Cardiogenic Shock
When a critical mass of ventricular myocardium becomes ischemic or necrotic, the ventricular pump fails, and there is a decrease in stroke volume and cardiac output. Decreased stroke volume causes increased filling pressures and wall tension for the left ventricle, with a corresponding increase in myocardial oxygen demand. The increased filling pressures are reflected back into the left atrium and the pulmonary vasculature, leading to vascular congestion and pulmonary oedema with impaired gas exchange.
The acute decrease in cardiac output can
result in multi organ failure and systemic inflammation. As hypotension occurs because of the decrease in cardiac output, the aortic diastolic pressure is also decreased, compromising the coronary artery perfusion and decreasing oxygen delivery to the myocardium.
With a decrease in cardiac output, the heart rate increases, further decreasing diastolic time. In response to the decrease in cardiac output, there are several compensatory mechanisms that activated. The sympathetic nervous system causes an increase in heart rate and systemic vascular resistance (SVR) in an attempt to increase blood pressure and maintain cardiac output, whereas the rennin-angiotensin-aldosterone system causes the retention of sodium and water to increase blood volume and preload. Tachycardia further compromises coronary perfusion as well as the perfusion to the left ventricle. The pre-existing ischemia is worsened, and the downward spiral that characterizes cardiogenic shock begins.
Patho psychology of Cardiogenic Shock
When a critical mass of ventricular myocardium becomes ischemic or necrotic, the ventricular pump fails, and there is a decrease in stroke volume and cardiac output. Decreased stroke volume causes increased filling pressures and wall tension for the left ventricle, with a corresponding increase in myocardial oxygen demand. The increased filling pressures are reflected back into the left atrium and the pulmonary vasculature, leading to vascular congestion and pulmonary oedema with impaired gas exchange.
The acute decrease in cardiac output can
result in multi organ failure and systemic inflammation. As hypotension occurs because of the decrease in cardiac output, the aortic diastolic pressure is also decreased, compromising the coronary artery perfusion and decreasing oxygen delivery to the myocardium.
With a decrease in cardiac output, the heart rate increases, further decreasing diastolic time. In response to the decrease in cardiac output, there are several compensatory mechanisms that activated. The sympathetic nervous system causes an increase in heart rate and systemic vascular resistance (SVR) in an attempt to increase blood pressure and maintain cardiac output, whereas the rennin-angiotensin-aldosterone system causes the retention of sodium and water to increase blood volume and preload. Tachycardia further compromises coronary perfusion as well as the perfusion to the left ventricle. The pre-existing ischemia is worsened, and the downward spiral that characterizes cardiogenic shock begins.