Lecture 7 (Cardiovascular II) PDF

Summary

This lecture note covers Cardiovascular II, focusing on cardiac function and control. It details the electrical activity of the heart, cardiac action potentials, the conduction system, and the role of the autonomic nervous system. The lecture also discusses cardiac muscle composition and contraction mechanisms.

Full Transcript

Cardiovascular II: Cardiac Function and Control ANSC 3080 G. Bedecarrats Learning Objectives  Describe the electrical activity of the heart  Explain cardiac action potentials  Describe the cardiac conduction system and its functional significance  Explain the role pla...

Cardiovascular II: Cardiac Function and Control ANSC 3080 G. Bedecarrats Learning Objectives  Describe the electrical activity of the heart  Explain cardiac action potentials  Describe the cardiac conduction system and its functional significance  Explain the role played by the autonomic nervous system in controlling the heart  Describe the determinant of cardiac performance Cardiac Muscle Composition Myocardium composed of 2 types of muscle cells Contractile cells: 99 % of the cells Action potential required for contraction Autorhythmic cells: Modified non-contractile cells Concentrated is specific regions of the heart SPONTANEOUSLY generate ACTION POTENTIAL Autorhythmicity = pacemaker Gap junctions In the heart, adjacent cells are connected by water- filled pores forming open connections = GAP JUNCTIONS Allow ion to move freely from 1 cell to another = electrical activity can pass from cell to cell Water filled channels Electrical Conduction System  Generated by the pacemaker cells = Autorhythmic  Sino-Atrial (SA) node: Command center (determine heart contraction) Rhythmical self excitation  Atrio-Ventricular (AV) node Also have autorhythmic ability BUT: pace slower so UNDER SA CONTROL Gateway for electrical conduction between atria and ventricles  Bundle of His and Purkinje fibers Help to quickly propagate electrical activity from the AV node to the rest of the ventricles Significance of the Electrical Activity  Role of the electrical “system”  Maintain appropriate heart rate  Coordinate contraction of atria and ventricles  Coordinate contraction of each chamber  Clinical relevance  Use electrocardiogram (ECG) to determine heart rhythm  Problems with conduction – abnormal rhythm (arrhythmia) Sequence of Excitation 1. SA node self excitation (generation of APs) 2. APs propagate through atria = atrial contraction 3. AV node activated by AP wave, transmit electrical activity to the bundle of His and Purkinje fibers with a little delay (allows packing of blood in ventricles and closure of the AV valves) 4. Electrical activity propagate through ventricles = ventricular contraction 1 2 3 4 Generation of AP in the SA Node Under normal condition (a):  Cells from SA node gradually depolarize. This drift in potential is caused by the leakage of Na+ inside the cell and reduced diffusion of K+ outside the cell  When threshold in met, an AP is generated  Cycle is repeated = pacemaker potential Controlled by the Autonomic Nervous System (b):  Sympathetic fibers: reduce the time required to reach the threshold = faster pace  Parasympathetic fibers: prolong the time required to reach the threshold = slower pace Cardiac Muscle Contraction  Action potentials from the autorhythmic cells propagate to the contractile cells  Action potentials in contractile cells is responsible for muscle contraction  Due to the gap junction Heart can be considered a “functional syncytium” Contraction will follow the “all or none rule” Action Potential of Contractile Cells  Differs from AP in autorhythmic cells Stable resting membrane potential (no drift)  Differs from skeletal muscle AP Duration Skeletal muscle: very short, milliseconds Cardiac muscle: long, 100’s of milliseconds Length of refractory period Skeletal muscle shorter than cardiac muscle  What is the functional impact of these differences? 3 Ca+ in Cardiac output:4 Blood pumped by each half of the heart per minute Na+ in 5 K out + 2 1 Voltage Gated Channels Phase 1 Phase 2 Phase 3 Phase 4 Phase 5 Na+ Closed Open Closed Closed Closed K+ Closed Closed Open (Open) Open Ca+ Closed Closed Closed Open Closed  Phase 1: resting membrane potential  Phase 2: rapid depolarization, mainly due to influx of Na+ into cell  Phase 3: short phase of repolarization; loss of K+ from cell  Phase 4: plateau phase – influx of Ca2+ into cell  Phase 5: repolarization phase – outward movement of K+ from cell  Panel a: skeletal muscle  Short AP, short refractory period  Ability to be re-stimulated quickly and reach “tetanic contraction”  Different fibers stimulated separately (summation)  Panel b: heart muscle  With gap junction all the cells contract at once  AP longer, refractory period longer  Prevent rapid repeated contraction (no tetanic state) Comparison Between Contractile and Autorhythmic Excitation – Contraction Coupling Calcium-stimulated-calcium-release (next slide): 1. Depolarization 2. Voltage-gated Ca++ channels open 3. Ca++ entry induces an avalanche of Ca++ release from sarcoplasmic reticulum (10-fold increase in Ca++) 4. Large increase in intracellular Ca++ triggers contraction 5. Ca++ pumped back in its pre-stimulation compartment Control of the Heart Contraction Effect of the Sympathetic Nervous System:  Stimulates the heart rate  Stimulates the firing of the SA node  Stimulates the velocity of the AV node conduction (shorter delay)  Increases the contraction force  Increases the release of Ca2+ from sarcoplasmic store  Reduces the contraction time  Increases the speed of Ca2+ transport (reduces the plateau length)  Actions mediated by epinephrine/norepinephrine on - adrenergic receptors present in ALL cardiac cells Effect of the Parasympathetic Nervous System (Vagus nerve):  Decreases the heart rate  Reduces the firing of the SA node  Decreases the velocity of the AV node conduction (longer delay)  Actions mediated by binding of acetylcholine on muscarinic receptors in autorhythmic cells  Increase K+ permeability  Hyperpolarization increase time required to reach the AP threshold Electrocardiogram (ECG)  In the heart, lots of cells are firing an AP simultaneously Generate a strong current Current conducted through body fluid to the skin  ECG = measure heart membrane potential throughout the cardiac cycle  Electrode placed at different location on the skin will read the progression of the electric current wave  Standard ECG has 3 waves  P wave = depolarization of the atria  QRS wave = depolarization of the ventricles (why appears larger?)  T wave = repolarization of the ventricles  Base-apex lead configuration One lead on the left chest, second lead over the neck (jugular groove) Normal rate and rhythm Use of the ECG  Assessment of the heart rate and rhythm  Heart rate: measure the intervals between cycles  Contraction force: measure amplitude of waves  Rhythm: measure the intervals between each waves  Detection of abnormalities  Heart rate (under resting condition)  Bradycardia = slower rate  Tachycardia = faster rate  Rhythm  Abnormally long P-Q interval = AV conduction problem  “Ectopic” beats (extrasystole) = action potential generated independently of the SA node, results in extracontraction Normal horse ECG What is that?

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