PHIS 206 1st EditionLecture 15Outline of Last Lecture I. Osmotic PressureII. Regulating PressureIII. Pulmonary CirculationIV. Renal Function CurveOutline of Current LectureI. Circulation in the HeartII. Heart Failure (congestive)III. ShockIV. Why Heart is Not Working?Current LectureI. Circulation in the Heart-collateral circulation: unlike anywhere else, arterioles in the heart have shunts if one arteriole is blocked by a blood clot, the capillaries perfuse reduces damage of having one arteriole damagedprotective mechanism aerobic exercise promotes collateral circulation developmento growth of collateral circulation: if O2 is reduced, heart grows more arterioles and increases collateral circulation, which in turn helps the heart muscle anaerobic exercise: lactic acid produced from carbon dioxideII. Heart Failure (congestive)-cardiac output falls away from 5 L and output is not matching Venus Return -fluid accumulates on Venus Return-increased fluid levels in lungs and open spaces reserved for air-cardiac output low and trouble releasing carbon dioxide and capturing oxygenIII. Shock-cardiac output low so tissue damage is inevitable -inadequate arterial pressure for tissues to perfuse and prevent damageThese notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.-Causes/Types of Shock1. hypovolemic: reduced (plasma) volume Venus return goes down Hemorrhage shock severe bruises, internal/external damage in body cavities2. neurogenic: basal motor center in brain stem is damaged or changes from sympathetic to parasympathetic. so decreased pressure in neurogenic volume pain, anxiety, fear facilitate neurogenic shock3. cardiogenic: heart is not working well, so go into shock most common way people dieIV. Why Heart is Not Working?-Most common: thrombosis (clot lodged somewhere)-Heart can recover, and dead piece can become scarred tissue less muscle, less contractile cells When the heart contracts, scarred tissue will stretcho some blood will stretch wall of the heart, which increases the end systolic volumeo increased end-systolic (systolic stretch)-Heart can develop a leak when damaged fills passively blood squirted in pericardial when heart contracts space where heart expands is less since pericardial sac is NOT empty reduction in end-diastole: cardiac tamponade -Fibrillation: heart muscle damaged so will become hyperexcitable (generate action potentials at a high frequency action potentials travel around heart, so any given heart piece is alternating between relaxation and contraction the heart is not in unison, so cardiac output decreases fibrillator: gives shock to heart simultaneously to stimulate all heart cells (refractory)o 1st cell out of refractory will have the greatest frequency of action potentials (S-A node) works if hyperexcitable cell is not hyperexcitable
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