To find out more clearly the relationship anemia with heart disease need to be behind the reciprocal relationship between these two things. Red blood cells function carry O2 from the lungs to the entire body of network involving the heart. Be clear to the network oxygen's, cardiac output (heart load), ventilation tuberculosis, red blood cells and capillary play an important role. How the relationship of Hb with the compensation can be seen in the heart curve below. (Lefrandt R.L, 2004).
When mild anemia, compensation is usually only a shift in curve desosiasi oxygen to the left. But when the Hb falls below 7-8 g%, increase in rainfall will be a heart, as shown in the activity. Contents load average will increase, happen circulation hiperkinetiky who marked with tachycardia, pulsasi on capillary and arterial, and pulse pressure increase arising sitolik usually noisy at all Costa. Left circulation period, left ventricular stroke work increased, the flow of circulation increases with the increase in coronary heart rainfall. (Lefrandt R.L, 2004).
Haemodinamik changes in the patients anemia was not caused by a decrease in blood Hb level, but also seen in other things that have not been known as a whole. Suspected of vasodilatasi perifer and decreasing blood viscosity's in patients with anemia clearly play an important role. Hemodinamik changes could not occur even if Hb is low, especially if blood viscosity is quite high, for example, in anemia infuse get the fluid in the dextran or multiple myeloma. Increased rainfall in the heart anemia occurs because the decrease in blood viskositas and a decrease in after load because the left ventricular decreasing tonus arteriole perifer. Decrease in tonus mechanism arteriole perifer is not clear, but allegedly related to the network hypoxia, asidemia lactate and accumulation bradikinin and vasodilator metabolic adenosin. (Lefrandt R.L, 2004).
Also note that the order autonomous nerve holds an important role in the adaptation mechanism in the circulation anemia. Pressure diastolic end ventricle left / left ventricular end diastolic pressure (LVED) usually remain normal despite anemia in weight, until symptoms arise dekompensasi. Ventricle left function (left ventricular function) usually does not interfere even if anemia is severe and longstanding (hematokrit 20-25%) but the anemia hematokrit with a weight of less than 15% function left ventricle decreased, although not accompanied by organic heart disease before. (Lefrandt R.L, 2004).
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