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Cardiovascular system lectures 19-21 w2012 _DF_

Cardiovascular system lectures 19-21 w2012 _DF_ -...

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Cardiovascular system: I. The Blood Vessels and Control of Blood Flow Lectures 19-21 Recommended (not required) reading in Sherwood 7th edition: Main topics: Chapter 10: 343-376 Plus, a brief mention of cardiac blood supply in Chapter 9: 332-333 And, recall smooth muscle properties Chapter 8: pp 289-294 Dr. David Furlow 274 Briggs e-mail: [email protected] office hours: T,R 4:10-5 at 2064 Sciences Lab Bldg
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Topics to be covered in these lectures: Control of Cardiac Output (“basically” continue with Dr. Ishida’s notes for this) Autonomic control of the heart Effect of venous return volume on heart contraction strength Frank-Starling law of the heart Sympathetic control of heart contraction strength & venous return General structure of the cardiovascular system Blood flow to organs at rest and during exercise A special note about the coronary circulation How blood flow is regulated (general concepts) Structure and function of different components of the vascular tree =>Definition of mean arterial pressure Arteries Arterioles: major resistance vessels Vasodilation versus vasoconstriction Extrinsic versus intrinsic control Important side note: General properties of smooth muscle Nitric oxide as a vasodilating signal Capillaries Determinants of bulk flow Veins and venous return
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1) Autonomic control of heart rate @ SA node 2) Autonomic control of conduc<on velocity @ AV node 3) Effect of venous return volume on heart contrac<on strength 4) Sympathe<c control of heart contrac<on strength & venous return What determines & adjusts cardiac output? para symp Symp can & Parasymp can heart rate these schema)cally show where different controls are exerted in a 4-­૒chambered heart Larger venous return can ventricular contrac<on volume 3 Symp can ventricular contrac<on (& also increase venous return) symp volume 4 1 para Parasymp can conduc<on @ AV node 2
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If stimulate Sympathetic Parasympathetic Then heart rate Increases Decreases Spike interval Shorter than control Longer than control Mechanism Norepinephrine increases pacemaker current ACh decreases pacemaker current & hyperpolarize SA node by increasing P(K) Vagus Symp can & Parasymp can heart rate… 1
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autonomic control is usually a combination of sympathetic & parasympathetic inputs increase in sympathetic input and decrease in parasympathetic input combine to increase heart rate; opposite for decrease in heart rate this implies parasympathetic input at rest: in fact, this input is relatively strong if stop all autonomic input to heart, heart rate rises from 70 beats/min to approx 100 beats/min also, see tonic (continuous) sympathetic control of blood pressure creates vasomotor tone without this, blood pressure can fall to 40-60 mm Hg. this can occur when spinal anesthesia induces spinal shock by blocking efferent sympathetic fibers also, see mutual pre-synaptic inhibition (not shown in this figure) vagus nerve (ACh) can inhibit norE release; sympathetic fiber can inhibit ACh release are these entirely separate controls ?
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