PHIS 206 1st Edition Lecture 15 Outline of Last Lecture I Osmotic Pressure II Regulating Pressure III Pulmonary Circulation IV Renal Function Curve Outline of Current Lecture I Circulation in the Heart II Heart Failure congestive III Shock IV Why Heart is Not Working Current Lecture I 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 damaged protective mechanism aerobic exercise promotes collateral circulation development o 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 dioxide II 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 oxygen III Shock cardiac output low so tissue damage is inevitable inadequate arterial pressure for tissues to perfuse and prevent damage These 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 Shock 1 hypovolemic reduced plasma volume Venus return goes down Hemorrhage shock severe bruises internal external damage in body cavities 2 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 shock 3 cardiogenic heart is not working well so go into shock most common way people die IV 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 stretch o some blood will stretch wall of the heart which increases the end systolic volume o 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 anymore
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