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BMS 508

by: Jess Graff
Jess Graff

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About this Document

These notes cover the lecture from February 19th
Human Anatomy and Physiology II
Mary Katherine Lockwood, PhD
Class Notes
Anatomy & Physiology
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This 5 page Class Notes was uploaded by Jess Graff on Saturday February 20, 2016. The Class Notes belongs to BMS 508 at University of New Hampshire taught by Mary Katherine Lockwood, PhD in Spring 2016. Since its upload, it has received 18 views. For similar materials see Human Anatomy and Physiology II in Biological Sciences at University of New Hampshire.

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Date Created: 02/20/16
BMS 508.03 2/19/2016 Chapter 20 (cont) The Cardiovascular System (cont) Cardiodynamics (cont) • Effects on the SA Node • Sympathetic and parasympathetic stimulation • Greatest at SA node (heart rate) • ACh (parasympathetic stimulation) • Slows the heart • NE (sympathetic stimulation) • Speeds the heart • Atrial Reflex • Also called Bainbridge reflex • Adjusts heart rate in response to venous return • Stretch receptors in right atrium • Trigger increase in heart rate • Through increased sympathetic activity • Hormonal Effects on Heart Rate • Increase heart rate (by sympathetic stimulation of SA node) • Epinephrine (E) • Norepinephrine (NE) • Thyroid hormone • Factors Affecting the Stroke Volume • The EDV – amount of blood a ventricle contains at the end of diastole • Filling time • Duration of ventricular diastole • Venous return • Rate of blood flow during ventricular diastole • Preload • The degree of ventricular stretching during ventricular diastole • Directly proportional to EDV • Affects ability of muscle cells to produce tension • The EDV and Stroke Volume • At rest • EDV is low • Myocardium stretches less • Stroke volume is low • With exercise • EDV increases • Myocardium stretches more • Stroke volume increases • The Frank–Starling Principle • As EDV increases, stroke volume increases • Physical Limits • Ventricular expansion is limited by: • Myocardial connective tissue • The cardiac (fibrous) skeleton • The pericardial sac • End-Systolic Volume (ESV) • The amount of blood that remains in the ventricle at the end of ventricular systole • Three Factors That Affect ESV  Preload • Ventricular stretching during diastole  Contractility • Force produced during contraction, at a given preload  Afterload • Tension the ventricle produces to open the semilunar valve and eject blood • Contractility  Is affected by: • Autonomic activity • Hormones • Effects of Autonomic Activity on Contractility  Sympathetic stimulation • NE released by postganglionic fibers of cardiac nerves • Epinephrine and NE released by adrenal medullae • Causes ventricles to contract with more force • Increases ejection fraction and decreases ESV  Parasympathetic activity • Acetylcholine released by vagus nerves • Reduces force of cardiac contractions • Hormones  Many hormones affect heart contraction  Pharmaceutical drugs mimic hormone actions • Stimulate or block beta receptors • Affect calcium ions (e.g., calcium channel blockers) • Afterload  Is increased by any factor that restricts arterial blood flow  As afterload increases, stroke volume decreases • Summary: The Control of Cardiac Output  Heart rate control factors • Autonomic nervous system • Sympathetic and parasympathetic • Circulating hormones • Venous return and stretch receptors  Stroke volume control factors • EDV • Filling time and rate of venous return • ESV • Preload, contractility, afterload • Cardiac Reserve  The difference between resting and maximal cardiac outputs • The Heart and Cardiovascular System  Cardiovascular regulation • Ensures adequate circulation to body tissues  Cardiovascular centers • Control heart and peripheral blood vessels  Cardiovascular system responds to: • Changing activity patterns • Circulatory emergencies


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