Summary

These notes cover cardiovascular physiology, focusing on topics like cardiac output, blood pressure, and myocardial oxygen utilization during exercise and at rest. They include details on the heart's response to different exercise intensities and discuss the importance of blood supply to the heart.

Full Transcript

Concentric (shortening) contractions compress peripheral vasculature causing an increase in resistance Magnitude of increase is related to the intensity of effort and the amount of muscle mass used Submax Upper Body Exercise ○ UBE ex...

Concentric (shortening) contractions compress peripheral vasculature causing an increase in resistance Magnitude of increase is related to the intensity of effort and the amount of muscle mass used Submax Upper Body Exercise ○ UBE exercise requires greater O2 consumption than leg exercise at any submaximal power output Lower mechanical efficiency Recruitment of stabilizing muscles Greater physiological strain than LBE Higher HR, Ve, BP, and RPE Upper Body Exercise ○ Maximal exercise VO2 values are typically 20-30% below those of lower body exercise Lower max HR and pulmonary ventilation Smaller musculature activated Cardiac Output and TPR Example ○ SBP=210 ○ DBP= 90 ○ CO= 20 L/min ○ TPR = DBP + [⅓ (SBP-DBP)]/ CO ○ TPR= 6.5 Hypotensive Recovery Response ○ After a bout of sustained light to moderate exercise, SBP temporarily decreases below pre-exercising levels for up to 12 hours in normal and hypertensive subjects ○ Mechanism Blood pools in skeletal muscle vascular beds during recovery What is the clinical significance of an exaggerated BP response? ○ Future development of hypertension ○ Increased risk for cardiovascular mortality and cardiovascular events ○ Presence of cardiac hypertrophy Increased muscle Heart's Blood Supply ○ No nutrients are taken from the blood in the heart chambers ○ Coronary circulation supplies the heart muscle 5% (250ml) of total output ○ Right and left coronary arteries start at the aorta behind the aortic valve ○ Arteries divide into a dense capillary networks that feeds the myocardium ○ Coronary sinus and anterior cardiac veins collect blood and empty directly into the right atrium Myocardial Oxygen Utilization ○ At rest the myocardium extracts 70-80% of the oxygen from the blood flowing in the coronary vessels Most other tissues only use 25% ○ In vigorous exercise coronary blood flow increases 4-6 times above resting level Impaired coronary blood supply ○ Coronary muscle is purely aerobic ○ If blood flow is interrupted chest pain results (angina pectoris) ○ Exercise increases energy requirements Stress test us used as a diagnostic tool for myocardial blood flow (ischemia) ○ A blood clot within these vessels results in myocardial infarction Damage ranges from mild to severe ○ Ischemia: restriction in blood supply to tissues ○ Hypoxia: a region of the body is deprived of adequate O2 supply ○ Infarction: tissue death caused by a local lack of oxygen Rate Pressure Product ○ Provides a non-invasive estimation of myocardial workload (myocardial oxygen uptake) ○ RPP= SBP x HR ○ RPP= linear relationship with exercise intensity ○ Chronic exposure to higher myocardial workload can lead to cardiac hypertrophy Cardiovascular Regulation and Integration ○ Cardiac muscle has an ability to maintain its own rhythm (i.e heart rate) ○ Without extrinsic stimuli the intrinsic heart rate 100 BPM ○ Extrinsic control of the heart (i.e neurohumoral factors) can adjust heart rate from 40 bpm at rest to 220 bpm at peak exercise Autorhythmic/Automaticity ○ The heart can beat on its own without the need for exogenous commands ○ Don’t rely on a nerve to contract the heart Intrinsic Regulation of Heart Rate ○ Membrane potential from negative to positive and will start depolarization ○ Starts at the SA node but will propagate outwards ○ Sinoatrial node to the Atrioventricular node to the purkinje fibers and then to the bundle of HIS ○ As it gets to the bottom of the ventricle the signal will travel up the walls of the heart ○ AV node delays the electrical signal ○ 0.10 second delay allows atria to contract before ventricular filling

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