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The heart is the pump responsible for maintaining adequate circulation of oxygenated blood around the vascular network of the body. It is a four-chamber pump, with the right side receiving deoxygenated blood from the body at low presure and pumping it to the lungs (the pulmonary circulation) and the left side receiving oxygenated blood from the lungs and pumping it at high pressure around the body (the systemic circulation).
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Cardiac muscle has three types of membrane ion channels that play important roles in causing the voltage changes of the action potential. They are (1) fast sodium channels, (2) slow sodium-calcium channels, and (3) potassium channels Depolarization: First, the action potential of cardiac muscle is caused almost entirely by sudden opening of large numbers of so-called fast sodium channels that allow tremendous numbers of sodium ions to enter the cardiac muscle fiber from the extracellular fluid. These channels are called “fast” channels because they remain open for only a few thousandths of a second and then abruptly close. After depolarization, there's a brief repolarization that takes place with the efflux of potassium through fast acting potassium channels. Plateau: Secondly, another entirely different population of slow calcium channels, which are also called calcium-sodium channels. This second population of channels differs from the fast sodium channels in that they are slower to open and, even more important, remain open for several tenths of a second. During this time, a large quantity of both calcium and sodium ions flows through these channels to the interior of the cardiac muscle fiber, and this maintains a prolonged period of depolarization, causing the plateau in the action potential. Repolarization: When the slow calcium-sodium channels do close at the end of 0.2 to 0.3 second and the influx of calcium and sodium ions ceases, the membrane permeability for potassium ions also increases rapidly; this rapid loss of potassium from the fiber immediately returns the membrane potential to its resting level, thus ending the action potential.
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These are simplified slides discussing the regulation of cardiac output and venous return. Learning objectives: 1. Comprehend the determinants of cardiac output and factors affecting cardiac output 2. Comprehend the factors affecting stroke volume and heart rate and total peripheral resistance 3. Identify the factors regulating venous return 4. Discuss the causes of high and low output cardiac failure 5. Enlist the functions of veins and recognise the significance of venous reservoirs Study Resources: 1. Chapter 20, Guyton and Hall Textbook of Medical Physiology, 14th edition 2. Chapter 30 and 32, Ganong’s Review of Medical Physiology, 26th edition 3. Chapter 10, Human Physiology by Lauralee Sherwood, 9th edition 4. Physiology, Cardiac Output - StatPearls https://www.ncbi.nlm.nih.gov/books/NBK470455/
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Dr. Faiza delivers an insightful lecture on the distinguishing characteristics of skeletal, smooth, and cardiac muscles, offering a comprehensive understanding of their histology, physiological anatomy, electrophysiological properties, and contractile mechanisms. Through meticulous tabulation and comparison, she aims to equip learners with a detailed comprehension of the unique features and functionalities of each muscle type. Beginning with a detailed exploration of histological differences, Dr. Faiza outlines key distinctions such as multinucleation in skeletal muscle, mononucleation in smooth and cardiac muscles, and the presence of striations in skeletal and cardiac muscles. She meticulously elucidates the structural arrangement of each muscle type, highlighting their cellular morphology and organization within tissues. Transitioning to physiological anatomy, Dr. Faiza navigates through various aspects including innervation, level of control, initiation of contraction, and modification by hormones. By delineating the role of the somatic nervous system in skeletal muscle control, and contrasting it with the autonomic nervous system's influence on smooth and cardiac muscles, she offers a nuanced understanding of neural regulation in muscle physiology. Furthermore, Dr. Faiza delves into electrophysiological properties, elucidating the mechanisms underlying action potential generation, duration, and ionic basis in each muscle type. Through insightful analysis, she reveals how differences in action potential characteristics contribute to variations in muscle contraction speed, duration, and resistance to fatigue. Finally, Dr. Faiza meticulously examines the contractile mechanisms of skeletal, smooth, and cardiac muscles, shedding light on the sliding filament theory, mechanisms of calcium action, and speed of contraction. By comprehensively comparing these mechanisms, she provides learners with a deep understanding of the intricate processes governing muscle contraction and function. Through engaging presentation and meticulous analysis, Dr. Faiza's lecture serves as a valuable resource for students seeking a thorough understanding of the fundamental differences between skeletal, smooth, and cardiac muscles.
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