Abstract
Mammalian heart, constituted with each two atriums and ventricles, supplies atmospheric oxygen to the body tissues. Right ventricle drives un-oxygenated blood to lung circuit via pulmonary artery by contracting the ventricular muscle, of which process is so-called pulmonary circulation. While, the blood oxygenated by lung circuit flows to the peripheral tissues and organs through the aorta (systemic circulation).
The cardiac ventricular weights are depending on the pumping abilities of the heart, i.e., the left ventricular weight is proportional to arterial blood pressure and cardiac output, whereas the right one is correlated with pulmonary arterial pressure and cardiac output. Therefore, the mechanisms of adaptation to high altitude are resulted in (1) the increased hypoxic pulmonary vasoconstriction (HPV), (2) the raised Ht due to polycythemia. Both increases in HPV and Ht contributes to marked pulmonary arterial hypertension, resulted in right ventricular hypertrophy. In short, the pathological cardiac changes at high altitude are characterized by the right ventricular hypertrophy associated with pulmonary arterial hypertension. On the contrary, “sports heart” observed in athletes is characterized by the bilateral ventricular hypertrophy, caused by the increased cardiac output and systemic hypertension.
Changes of the cardiac weight are depending the severity of the load to the heart, accordingly the hypertrophied cardiac muscle is reversible by removing the load. The reversible phenomenon is similar to the case of skeletal muscles. We can see several established examples indicated the reversibility of the right hypertrophied ventricles: (1) seasonal changes (the right ventricular hypertrophy observed during winter is superior to that during summer), (2) latitude of habitat (animals living in the north area develop right ventricular hypertrophy compared with the southern area), (3) global warming (warm climate reduces the rate of right ventricular weight to left one).
