6.Discuss the etiology, pathophysiology, and clinical manifestations of pulmonary arterial hypertension.
7.Discuss the etiology, pathophysiology and clinical manifestations of Cor Pulmonale. 2ndary to PAH, RV eventually fails pushing against high pressure; CM- Rsided HF 8. Examine the etiology, clinical manifestations and pathophysiology of shock states. a. Differentiate between the etiology, clinical manifestations, and pathophysiology of hypovolemic, cardiogenic, septic, neurogenic and anaphylactic shock in adults. Patho-decrease CO, decrease in circulating volume, widespread vasodilation Minimum BP to perfuse body is SBP 90mmHg Patho-lack of cell o2 d/t lack of perf to cell or increased consumption, shock states cause cells to extract more o2 from hgb, decrease available o2, leads to production of lactic acid d/t cells using anaerobic metabolism (lactic acid good marker of perfusion), svo2 levels reflect o2 extraction from cells, low levels mean more o2 extracted; normal with elevated lactic is ominous sign, anaerobic metabolism uses ATP faster so lack of ATP---failure in NaK pump, Na accumulates inside cell, potassium exits cell, action potentials of neurons/myocardial cells immediately affected—myocardial depressant factor is released and this suppresses myocardial contraction, increased Na draws H20 into cells—cell edema, leaves interstitial space dry & draw water from vascular space and swells, decreases intravascular volume, albumin consumed for energy, so decreases oncotic pressure, further decreasing intravascular volume Impaired glucose delivery/use d/t impaired perfusion—body releases cortisol, growth hormone, catecholamine which leads to hyperglycemia, insulin resistance tachycardia, increased SVT, increase cardiac contractility; cells shift to glycogenolysis, gluconeogenesis and lipolysis to generate fuel for survival Impaired protein metabolism/deletion of protein stores results in organ failure; gluconeogenesis cause proteins metabolized for fuel, not available to help maintain cell structure, fxn, repair, replication; metabolism of proteins leads to production ammonia/urea, ammonia toxic to cells, albumin first protein to be consumed Disease Etiology Clinical Manifestations Pathophysiology Hypovolemic Hemorrhage, burns, Tachycardia, low Loss of volume leads to
V/D, dehydration BP, fluid shifting into cells then out of vasculature into interstitial—low volume, vasoconstriction and tachycardia d/t release of catecholamine, low vol lead to decrease hydrostatic pressure which allow fluids from interstitium to enter intravascular space; liver/spleen release stored RBCs, kidney
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