PSIO 202, Lecture 7

PSIO 202, Lecture 7 - PSIO 202 Human Anatomy and Physiology...

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Unformatted text preview: PSIO 202 Human Anatomy and Physiology Lecture 7 The Heart; Mechanics and Cardiac Output Objectives and Reading Assignment Reading: Tortora, pages 738-742 Objectives Discuss the relationship between pressure and volume in the heart chambers, as well as the position of the various heart valves, in both systole and diastole Define cardiac output and know how to calculate it, given values for heart rate and stroke volume Define and describe the major determinants of stroke volume, and the underlying mechanisms of each Define the Frank-Starling mechanism Definition of Systole and Diastole Ventricular systole starts when the AV valves close and the pressure within the ventricles begins to rise as the cardiac muscle fibers are depolarized and then contract Ventricular diastole starts with ventricular muscle repolarization, leading to a drop in ventricular pressure, and filling of the ventricle Atrial systole is very brief; thus, ventricular filling is largely passive Figure 17.18b Cardiac Output (CO, or Q) CO is the volume of blood pumped by the ventricles in a given unit of time CO (L/min) = SV (L/beat) x HR (beats/min) At rest, HR = 75 beats/min and stroke volume = 0.07 L/beat CO = 5.25 L/min Determinants of Stroke Volume aortic (or pulmonary artery) blood pressure (also called the "afterload") end-diastolic volume (or "preload") contractility Afterload the ventricles cannot eject blood into the aorta or pulmonary artery until the pressure in the ventricle exceeds the pressure in the vessel Thus, an increase in pressure will have a major impact on the work of the heart, and on the stroke volume. Preload The cardiac chambers are mechanical pumps, and therefore can pump only what is delivered to them The "preload" is slang for "end-diastolic volume", and has a major impact on the stroke volume The stroke volume cannot increase unless the rate of cardiac filling also increases Preload and Afterload Figure 17.20 Contractility Contractility refers to the strength of cardiac muscle contraction Contractility has both active and passive components Active contractility - stimulation of the sympathetic nerves to the heart Passive contractility - the result of changing the length of the cardiac muscle fibers ("Frank-Starling mechanism") Control of Active Contractility Due to the actions of norepinephrine (or epinephrine) Increased rate of pacemaker activity Increased force of cardiac muscle contraction Control of Active Contractility, Con't. The action potential invades the ttubules, and calcium is released from the sarcoplasmic reticulum The norepinephrine also increases the permeability of the cardiac muscle fibers to calcium As a result, the number of actin/myosin crossbridge interactions is increased Contractility and Norepinephrine Sympathetic stimulation releases norepinephrine and initiates a cyclic AMP secondmessenger system Figure 17.21 The "Frank-starling" Mechanism refers to the relationship between the rise in stroke volume and the rise in preload if the preload is increased--even in a heart with no nerve supply--the stroke volume will increase systematically The Frank-starling Mechanism In vitro, no nerve supply Stroke volume Preload ...
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This note was uploaded on 09/23/2008 for the course PSIO 202 taught by Professor Staff during the Fall '08 term at Arizona.

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