Case 1: Cardiogenic ShockIntroduction Cardiogenic shock could be described as a medical emergency that requires a complete clinical assessment of the cause and a therapy targeted at the cause. Its occurrence is as frequent as, a 8.6% of patients with ST segment elevation and 29% with MI are prone to shock which in turn has a leading mortality rate of 57%. Most cardiogenic shock is found to have an MI. The causes range from MI to others as Beta blockers overdose, respiratory acidosis, valvular or structural and preexisting condition as heart disease, diabetes, dysarrythmia etc.
Cardiagenic shock might be defined as the sustained hypo tension arising due to tissues hypo perfusion despite adequate left ventricular filling pressures. Thus in cardiogenic shock, insufficient perfusion of tissues (heart) is seen which renders it to be in adequate to meet the demand of oxygen and nutrients. This is theoretically followed by the cell death arising due to oxygen starvation – hypoxia, that inter leads to cardiac arrest in other terms, circulatory arrest that ultimately culminates the cardiac pump function. Thus it could be understood that the cardiogenic cause might be caused by the failure of heart to pump effectively.
This is usually a condition that occurs secondary to the damage of heart muscle most of an MI, Arrhythmia, Cardiacmyopathy, Cardiac valve problems, Ventricular outflow obstruction as Aortic valve stenosis, Aortic valve. (Holmes etal. ,2003)Case Details and Patient Presentation: The patient discussed here is a 51 year old male with a history of Acute Myocardial Infarction AMI that was followed by an acute cardiogenic shock. On admission the patient’s blood pressure was measured to be 78/48 mmHg, pulse was 100 beats per minute that was highly irregular and thready with an altered mental status, hypotension and pulmonary edema.
The anxiety and restless and altered mental state might be due to decrease cerebral perfusion followed by subsequent hypoxia. Hypo tension might be due to decreased cardiac output. The patient’s skin was cool, clammy and mottled, might be due to vasoconstriction that is due to the subsequent hypo perfusion of skin. Also a distended jugular vein was seen that might be due to the increased jugular venous pressure.
The patient was observed to have hyper ventilation – with a rapid and deep respiration mainly due to the sympathetic nervous system stimulation and acidosis. The patient appeared fatigue. The patient had refused to eat for past few days and had chest pain from last night. Patient was reported to be Oligouric. The heart sounds were distant with both third and fourth heart sound heard with low pulse, tachycardia. Also an hour before the patient reported an abrupt onset of squeezing pain, atypical near the chest. Immediately patient was ventilated with a BVM device at the rate of 50 breaths per minute and patient had oxygen saturation of 94% and was ventilated with 100% oxygen.
The patient’s pal our on admission was ashen. On enquiry to the patient’s son, who admitted the patient explained that the patient was a case of hyper tension, diabetic. Pathophysiology: cardiac output increased ventricular filling pressures, cardiac chamber and ultimately univentricular or biventricular that result in systemic hypotension and/or pulmonary edema. ystemic inflammatory response syndrometype mechanism the pathophysiology of cardiogenic shock. levated levels of white blood cells, body temperature, complement, interleukins, and C-reactive protein are seen inflammatory nitric oxide synthetase (iNOS) induces nitric oxide production, which uncouple calcium metabolism in the myocardium resulting in a stunned myocardium.
Additionally, iNOS expression of interleukins, which cause hypotension.