The Cardiac Electrical system and the ECG Flashcards
Specialized excitatory and conductive system of the Heart
Sinus Node/Sinoatrial Node/SA Node
Internodal Pathways
Atrioventricular Node/AV Node
AV Bundle
Left and Right Bundle of branches of Purkinje Fibres
Sinus(Sinoatrial) Node
Small,flattened,ellipsoid strip oof specialized cardiac tissue.
Located: Superior posterolateral wall of the right atrium immediatly below and slightly lateral to the opening of the SVC
Fibrres of this node have no contractile muscle filaments
SA nodal fibres connect directly to the atrial muscle fibres so that any AP that begins in the sinus node spreads immediatly into the atrial muscle wall
Automatic Electrical Rhythmicity of the Sinus Fibres
Some cardiac fibres have the capability of self excitation, a process that can cause autonomic rhythmical discharge and contraction
Mechanism of Sinus Nodal Rhythmicity
The RMP of the sinus nodal fibre between discharges has a negativity of about -55 - -60mV in comparison with the -85 - -90 mV for the ventricular muscle fibre.
What is the cause for the negative RMP for the sinus fibre
The reason is that the cell membrane of the sinus fibre are naturally leaky to sodium and calcium ions and positive charges of the entering calcium and sodium ions neutralize some of the intracellurlar negativity.
Types of membrane ion channels which play important roles in causing the voltage changes of the AP in cardiac muscle.
Fast Sodium channels
L-type calcium channels/Slow sodium-calcium channels
Potassium Channels
Discuss the action potential which is observed in ventricular muscle
- Opening of the fast sodium channels is responsible for the upstroke spike in AP because of rapid influx of positive ions to the interior of the fibre
- The plateau of the Ventricular AP is caused by the slower opening of the the sodium-calcium channels/L-type calcium channels
- Opening of the potassium channels allows diffusion of large amounts of positive k+ ions in the outward direction through through fiber membrane and returns the Membrane potrntial to its resting level.
Self-excitation of the Sinus Nodal Fibre
Because of the high sodium ion concentration in the ECF outside the nodal fibre as well as a moderate number of the already open sodium channels,positive sodium ions from outside the fibre normally tend to leak to the inside.
Therefore between heartbeats,influx of +ve charged sodium ions cause a slow rise in the RMP in the +ve direction.
The RMP gradually rises and becomes less +ve between each two heartbeats.
When the potential reaches a threshold voltage of about -40 mV, the L-type calcium channels become activated causing an AP.
Therefore,basically the inherent leakiness of the sinus nodal fibres to the sodium and calcium ions cause their self-excitation
Why does the leakiness to the sodium and calcium ions not cause the sinus nodal fibre to remain depolarised all the time.
First, the l-type calcium channels become inactivated after opening
Second, At about the same time,greatly increased numbers of the potassium channels open.
Therefore the influx of positive calcium and sodium ions through the l-type calcium channels ceases while at the same time large quantities of positive ions diffues out the fibre.
Both of the effects reduce the intracellular potential back to its negative resting level and therefore terminating the AP.
The potassium channels remain open for a few seconds temporarily continuing the movement of positve charges out the cell with resultant excess negativity inside the fibre-Hyperpolarization
Hyperpolarization
It initially carriers the RMP down to about -55 - -60 mV at the termination of the action potential
Why is the new state of hyperpolarization not maintained forever?
During the next feew seconds after the AP is over,progressively more and more potassium channels close.
The inward-leaking sodium and calcium ions once again over balance the outward flux of potassium ions which cause the resting potential to drfit upward reaching the threshold for discharge
fibres
fibre
The AV node delays impulse conduction from the atria to the ventricles
The atrial conductive system is organized so that the cardiac impulses does not travel from the atria to the ventricles to rapidly
The av node and its adjacent conductive fibres that delay this transmission.
What is the location ot the AV-Node
It is located in the posterior wall of the right atrium immediatly behind the tricuspid valve.
The duration in the AV Nodal delay
The Total delay in the AV bundle and the AV bundle system is about 0.13 second-0,09 0,04
This delay as well as the intial conduction delay of 0.03 seconds from the sinus node to the av node
What the causes of the slow conductance
The slow conduction in nthe transitional,nodal and penetrating AV bundle fibre is caused mainly by diminished number of gap junctions between succesive cells inthe conducting pathways. son theree is grat resistance to conduction of excitatiry ions from one conducting fibre.
Rapid Transmission in the Ventricualr Purkinje System
The special purkinje fibres lead from the AV node though the the AV bundle into the the ventricles but there are not present in the intitial fewlenghths of these fibres where they pentrate the AV fibrous barrier,They have quite opposite functional characteristics to those of the AV nodal fibres
They are large fibres and they traansmit AP at a high velocity of about 1.5-4.0 m/sec, a velcity 6 times that in the usual ventricular muscle and 150 times in some of the AV nodal fibres
The velocity allows almsot intantnoues transmission of the cardiac impulse throughout the entire remainded of the ventricular muscle
What is the rapid transmission of AP by Purkinje fibres caused by
It is believed to be caused by a very high levels of permeability of the gap junctions at the intercalated discs between the successive cells that make up the the purkinje fibres,therfore ions are transmitted easily from one cell to the next thus enhancing the velocity of transmission
They also have very few myofibrils which means that they contract little or not at all during the course of impulse transmission
How does the one way conduction through the AV bundle occur
A special characteristic of the Av bundle is the inability except in abnormal states, of the AP to travel backward from the ventricles to the atria.
This characteristics prevents re-entry of cardiac impulses by this route from the ventricles to the atria,allowning only forwad conduction from the atria to the ventricles
What is the function of the Fibrous Barrier
The barrier normally acts as an insulator to prevent passage of the cardiac impulse between atrial and ventricular muscle through any other route besides forward conduction though the Av bundle
In rare instances, an abnormal muscle bridge does penetrate the fibrous barrier elsewhere at the av bundle.Under such circumstances, the cardiac impulse can re-enter the atria from the ventricles causing serous cardiac arrhythmias.
Distributuion of the purkinje fibres
page 126
Transmission of the cardiac impulse in the ventricular muscle
page 126
The sinus node is the normal pacemaker of the heart
ff
Role of the purkinjee system in casuing synchromus contraction of ventriclualr muscles
jkkf
Sympathetic and parasympthatheis nerves
gg
para
hdh
Summary of the main ion channle events during t=each oth the five main paheses of the AP of a typical fast myocardial fibre
It occurs in 5 phases
Phase 0:
Depolarization,fast sodium channels open,the mebrane potential becomes more positive,Voltgae gated sodium channels open and permit sodium to rapidly flow into the cell and depolarizes
Phase 1:
Intial Repolarization.
Fast sodium channels close,The sodium channels closes the cells begins to repolarize and potassium ions leave the cell through open potassium channels
Phase 2:
Plataeu:
Calcium channels open and fast potassium channels close. A brief initial repolarization occurs and the AP then platueas as a result of increased calcium ion permeability annd decreased potassium ion permeabilty
The voltage-gated calcium ion channels open slowly during phase 0 and 1, and calcium ion enter the cell. Potassium channels then close and the combination of decreased potassium efflux and increased calcium ion reflux causes the action potential to plaetuea
Phase 3:
Rapid repolarization
Calcium channels close and slow pottasium channels open.The closure of calcium ion channels and increased potassium ion permeabilty,permitting potasssium ions to rapidly exit the cells,ends the platuesa and returns the cell membrane potential back its resting level.
Phase 4:
Resting Membrane Potential
Which averages about -90 mV
What may Hypoxia Do
It may convert fast fibres into slow fibres
What are the conditions which may increase the automaticity in latent pacemakers which may overide SA nodal pacemaking
Ishaemia
Hypokalaemia
Fibre Stretch
Local Catecholamine Release
How may Atrial and ventricular ectopic pacemakers develop
When the membrane potential is sufficiently depolarized
The impartance of the delay at AV node
Ensures atrial contraction completes ventricular filling before ventricular contraction
Ensures simulatanoues depolarization of all His Bundle fibres/AV bundle
Protects ventricles from a rapidly discharging SA node
What is the clinical value of performing a 12 lead elcetrocardiography
- Abnormal cardiac excitation
- Arrhythmias
- Conduction defects
- Myocardial damage (e.g. due to myocardial i
schaemia or necrosis) - Cardiac enlargement
- Electrolyte disorders
Main complaints of PTs
CLINICAL PRESENTATIONS:
1. Acute chest pain at rest Acute coronary syndrome: Up- or downward ST segment displacement T wave inversion Normal ECG
- Cardiac palpitations
Ectopic beats (supra-ventricular/ventricular)
Tachycardia
Atrial fibrillation - Extreme tiredness or syncope
Conduction block: first, second or third degree; bundle branch block - Cardiovascular collapse
Asystole (cardiac arrest)
Ventricular fibrillation
Electrocardiogram:
Standardized two dimensional representation of cardiac vectors (which differs from lead to lead, depending on the orientation/perspective of a particular lead.)
Electrocardiograph
volt- / galvanometer (electrical apparatus) that registers electrocardiograms.
