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Transcript
Cardiovascular dynamics-abbreviated • For bio 260 • Source:mixed Topics to be covered • Chapter 18-The Heart • Chapter 19-Blood vessels • Physio Ex-Cardiovascular Dynamics-Print data w/explanations. • Physio Ex-Frog Cardiovascular Physiology-read only. Topics to be covered • Chapter 18-The Heart • Chapter 19-Blood vessels • Physio Ex-Cardiovascular Dynamics-Print data w/explanations. • Physio Ex-Frog Cardiovascular Physiology-read only. Cardiac Output 14-3 Cardiac Output (CO) • Is volume of blood pumped/min by each ventricle • Stroke volume (SV) = blood pumped/beat by each ventricle • CO = SV x HR • Total blood volume is about 5.5L 14-4 Regulation of Cardiac Rate • Without neuronal influences, SA node will drive heart at rate of its spontaneous activity • Normally Symp & Parasymp activity influence HR (chronotropic effect) • Autonomic innervation of SA node is main controller of HR – Symp & Parasymp nerve fibers modify rate of spontaneous depolarization 14-5 Regulation of Cardiac Rate continued • Cardiac control center of medulla coordinates activity of autonomic innervation • Sympathetic endings in atria & ventricles can stimulate increased strength of contraction 14-7 14-8 Stroke Volume • Is determined by 3 variables: – End diastolic volume (EDV) = volume of blood in ventricles at end of diastole – Total peripheral resistance (TPR) = impedance to blood flow in arteries – Contractility = strength of ventricular contraction 14-9 Regulation of Stroke Volume • EDV is workload (preload) on heart prior to contraction – SV is directly proportional to preload & contractility • Strength of contraction varies directly with EDV • Total peripheral resistance = afterload which impedes ejection from ventricle • Ejection fraction is SV/ EDV – Normally is 60%; useful clinical diagnostic tool 14-10 Frank-Starling Law of the Heart • States that strength of ventricular contraction varies directly with EDV Fig 14.2 – Is an intrinsic property of myocardium – As EDV increases, myocardium is stretched more, causing greater contraction & SV 14-11 Frank-Starling Law of the Heart continued • (a) is state of myocardial sarcomeres just before filling – Actins overlap, actin-myosin interactions are reduced & contraction would be weak • In (b, c & d) there is increasing interaction of actin & myosin allowing more force to be developed Fig 14.3 14-12 Extrinsic Control of Contractility • At any given EDV, contraction depends upon level of sympathoadrenal activity – NE & Epi produce an increase in HR & contraction (positive inotropic effect) • Due to increased Ca2+ in sarcomeres Fig 14.4 14-13 Fig 14.5 14-14 Venous Return • Is return of blood to heart via veins • Controls EDV & thus SV & CO • Dependent on: – Blood volume & venous pressure – Vasoconstriction caused by Symp – Skeletal muscle pumps – Pressure drop during inhalation Fig 14.7 14-15