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Mansoura University

Mahmoud El Tohamy

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cardiac physiology heart function medical physiology human anatomy

Summary

This document is a lecture on cardiac properties, focusing on the mechanism of rhythmicity of the sinoatrial node (SAN). The document explores the different phases of the SAN action potential, including pacemaker potential, depolarization, and repolarization. It also discusses factors affecting the rhythmicity such as nervous, physical, and chemical factors and clinical notes. The document is aimed at undergraduate medical students.

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M D Hello Everyone Hope You Are Having A Wonderful Physiological Day ☺☺☺ ARE YOU READY ? LET'S GET STARTED! Cardiac Prosperities 1 Sem 3 Mahmoud El Tohamy M.D, Ph.D. Lecturer of Medical Physiology Faculty of Medicine, MNU Dr.m.el...

M D Hello Everyone Hope You Are Having A Wonderful Physiological Day ☺☺☺ ARE YOU READY ? LET'S GET STARTED! Cardiac Prosperities 1 Sem 3 Mahmoud El Tohamy M.D, Ph.D. Lecturer of Medical Physiology Faculty of Medicine, MNU [email protected] Phases of Action Potential +++++++++++++++++++++++ ------------------------------------- RMP or Polarization state Na+ ------------------------------------- +++++++++++++++++++++++ Depolarization Action Potential +++++++++++++++++++++++ ------------------------------------- K+ Repolarization Properties Of Cardiac Muscle The cardiac muscle has four basic properties which are essential for its functioning as the central pump of the circulatory system. Rhythmicity Excitability Conductivity Contractility Rhythmicity ❖Definition: It is the ability of heart to beat regularly. ❖Origin: Myogenic (not neurogenic). The nerves control the rate but do not initiate the beat. ❖Evidence that rhythmicity is myogenic: Heart of human fetus start to beat before development of nerves. Transplanted heart (no nerve supply) continues to beat. Rhythmicity ❖Nature of spontaneous rhythmicity: Most cardiac fibers have the ability Tissue Ryhthmicity of self excitation especially nodal SAN 110 beats / min and conducting fibers. AVN 90 beats / min Bundle tissues 45 beats / min SAN has the greatest rhythm, so it Purkinje fibers 35 beats / min is called Ventricles 25 beats / min Pacemaker of the heart Rhythmicity ❖Self excitation of SAN fibers: RMP of SAN = - 55mv to - 60mv. Natural leakiness of membrane to Na+ which leads to a) Unstable & Low RMP (-55 to -60mv). b) Self excitation of SAN. Mechanism of rhythmicity of the SAN (SAN action potential) The action potential is composed of the 3 phases (403): 1. Pacemaker potential or prepotential (phase 4) The membrane potential rises gradually from the resting level of -55\-60 mv to the firing level of -40 mv. It occurs during diastole, so it is also called the Diastolic Depolarization (DD). Mechanism of rhythmicity of the SAN (SAN action potential) 1. Pacemaker potential or prepotential (phase 4) It is due to: A. Na influx through funny (slow) Na channels B. Ca influx through T (transient) type Ca channel C. ↓ K+ efflux. Importance: It is the cause of rhythmicity. Rate of slope of prepotential determine the heart rate (the more rapid slope → the more the heart rate). Mechanism of rhythmicity of the SAN (SAN action potential) 2. Depolarization (upstroke) phase (phase 0): From membrane potential (–40 mv) to (+10 mv). Generated by inward Ca current through L (long lasting) Ca channels (Na current is negligible in SA node cells). Mechanism of rhythmicity of the SAN (SAN action potential) 3. Repolarization (phase 3): Occurs due to : Stoppage of Ca++ influx increase K+ efflux which brings back the membrane potential to the unstable RMP (-55 to -60 mv) Then, this process is repeated continuously through life. Factors affecting the Rhythmicity 1. Nervous factors Sympathetic Stimulation Vagal Stimulation Effect ↑ rhythmicity ↓ rhythmicity. Mechanism Symp stimulation ➔ NA release Vagal stimulation ➔ A.ch release ➔ ➔ ↑ permeability to Na+ & ↑ permeability to K+ ➔ ↑ K+ efflux Ca2+ ➔ ↑ slope of prepotential ➔ hyperpolarization ➔ ↓ slope of ➔ threshold is reached rapidly prepotential ➔ threshold is reached ➔ ↑ rhythmicity. slowly ➔ ↓ rhythmicity. NB: Chronotropism = influence on rhythmicity (heart rate). * + ve chronotropic factor is one that  heart rate. * - ve chronotropic factor is one that  heart rate. Clinical note Vagal tone → ↓ sinus rhythm from 110 to 75/min (normal HR) Mild vagal stimulation → ↓ sinus rhythm. Strong vagal stimulation → stop sinus rhythm but not the ventricles which beat by idioventricular rhythm ????? (Vagus not supply the ventricles) Factors affecting the Rhythmicity 2. Physical factors Warming Cooling Moderate ➔  rhythmicity by: Moderate ➔  rhythmicity. (1)  membrane permeability to K+ (i.e. rapid slope of prepotential). (2)  speed of ionic fluxes. This explains tachycardia in fever. (each 1℃ → ↑ HR 8-10 beat/minute) - Excessive ➔ denaturation of - Excessive ➔  intracellular metabolism ➔ intracellular proteins ➔ cardiac stops rhythmicity. damage. Factors affecting the Rhythmicity 3. Chemical factors A. Drugs and hormones Increase rhythmicity Decrease rhythmicity - Catecholamines. - Cholinergic drugs (methacholine). - Thyroxine (stimulate SAN - Digitalis (depress nodal tissue) ➔ metabolism)  K+ efflux ➔ hyperpolarization Factors affecting the Rhythmicity 3. Chemical factors B. Blood gases O2 decrease CO2 increase Changes in H+ conc Mild ➔  rhythmicity  rhythmicity (by Acidosis ➔  affinity (direct effect on SAN) producing acidemia) between catecholamines & Sever ➔  rhythmicity cardiac receptors ➔  ➔ cardiac arrest rhythmicity. Alkalosis ➔  rhythmicity. Factors affecting the Rhythmicity 3. Chemical factors D. Ions Potassium ions: - Mild hyperkalemia decrease rhythmicity by decreasing K+ efflux thus prolong repolarization phase and delay prepotential Calcium ions: - Mild hypercalcemia decreases rhythmicity by activating K+ channels ➔ hyperpolarization ➔ so longer time is needed to reach threshold potential N.B. A balanced concentration of Na+, K+ and Ca++ ions in the extracellular fluid is essential for normal heart function. Factors affecting the Rhythmicity 3. Chemical factors D. Toxins e.g. typhoid ➔  rhythmicity due to direct inhibitory effect on nodal tissue. Clinical note the Faget sign sometimes called sphygmothermic dissociation: Relative bradycardia in association with fever (Temperature-pulse dissociation) Faget sign is often seen in: Yellow fever Typhoid fever ??? Brain abscess Conductivity ❖Definition: Ability of cardiac muscle to conduct excitation wave from one part to another. Normally AP starts from SAN (pacemaker) and is propagated to the rest of the cardiac tissue in the following steps 1. Transmission of cardiac impulse through atria 2. Transmission of cardiac impulse through AVN (AVN delay) 3. Transmission in Purkinje system 4. Transmission of cardiac impulse in ventricular muscle (1)Transmission of cardiac impulse through atria ❖The action potential is initiated in SAN then travel as follows: Right and left atrial mass. Anterior interatrial band to left atrium. Anterior, middle, and posterior internodal bundles, directly to AVN. Velocity in atria = 1m/sec. (2) Transmission of cardiac impulse through AVN (AVN delay): ❖Velocity : 0.02 – 0.05 m/s. ❖Sites of AVN delay Site of delay sec. Initial conduction delay between 0.03 SAN and AVN AVN 0.09 Penetrating portion of AVB 0.04 Total delay in the heart 0.16 (2) Transmission of cardiac impulse through AVN (AVN delay): ❖Causes of AVN delay: 1. Smaller size of nodal fibers than atrial fibers. 2. Few gap junctions. ❖Significance of AVN delay: 1. Allow sufficient time for atria to empty their blood into ventricle before ventricular contraction begins. 2. Protect the ventricle from pathological high atrial rhythm as AF and atrial flutter. (3) Transmission in purkinje system: ❖Purkinje system transmit impulses from AVN through AV bundle & right and left bundle branches into ventricles. ❖Velocity: 4 m/sec → immediate transmission of cardiac impulse through the entire ventricles. ❖Cause of rapid conduction in the Purkinje system: 1. Large fibers. 2. High permeability of gap junctions. Time for transmission of impulse from Bundle branches to end of Purkinje fibers: 0.03 sec. AVB conduct impulse in one direction only from AVN to the ventricles. This prevents re-entry of cardiac impulses from ventricles to atria. (4) Transmission of cardiac impulse in ventricular muscle ❖Impulses are transmitted from the end of Purkinje fibers toward the surface of heart through the ventricular muscles. ❖Speed: 0.3 – 0.5 m/sec. Factors affecting the Conductivity The Same as Rhythmicity ☺☺☺☺ Dromotropism ➔ influence on conductivity. * + ve dromotropic factor is one that  conductivity. * - ve dromotropic factor is one that  conductivity. Any Questions ?? Thank You

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