Lecture 7 (Cardiovascular II) PDF

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 sign...

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 1  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 2  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 3  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? 4  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) 5  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 6  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 7  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 8  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? 9