The Conducting System of the Heart & ECG Flashcards
(43 cards)
how is cardiac muscle different from skeletal muscle? (2)
- cardiac muscle cells in atria and ventricles are joined by intercalated disks (hold cells together)
- gap junctions within the the intercalated disks link adjacent cardiac muscle cells electrically, so that an action potential in any one cell in any one cell spreads into adjacent cells: synchronous contractation of the whole tissue
what is atria or ventricular tissue known as because of its electrical and mechanical connectivty?
syncytium
what is the pace-maker of the heart?
location?
how does it work?
pace-maker of heart: sino-atrial node (SAN).
- modified cardiac muscle cells. (NOT NERVE CELLS)
- connected by gap junctions
function: impulse generating tissue
location: near entrance to the SVC
mechanism of action:
- electrical activity starts in the SA node, depolarises the atrial muscle, atrial muscle starts to contract, spread across to atrioventrincular node
- here it STOPS (not transmitted to ventricles)
-
where is the AVN located?
what is importnat role of this ?
inter-atrial septum, close to tricuspid valve
slightly delays the contraction of the ventricles, so that atria can fully contract / empty before ventricles contract
what can happen if the SAN is damaged?
other sites in the right atria can take over as pacemaker
explain how action potentials occur in pacemaker cells
what determines the race of firing of pacemaker cells?
- *regular, spontaneous action potentials:**
- special K channels open during AP, but slowly, spontaneously close (aka funny current)
- causes a progressive depolarisation
- normal K channels are not present
- eventually this pacemaker / prepotential potenential reaches threshold for the Na AP channels to open: new AP generated
- the rate of firing of pacemaker cells is determined by rate of closure of K channels
explain what the innervation is like in the SAN from the para and sympathetic nerves
what action do they cause and how?
SAN innervation from:
- parasympathetic nerve: from vagus nerve. inhibit the closure of K channels via muscarinic receptors (pacemaker cells slow down)
- sympathetic nerves: from thoracic spinal cord in symp trunk. increase the closure of K channels by beta adrenoreceptor actions. (pacemaker cells increase) -
what is sinus arrythmia?
parasympathetic outflow in the vagus nerve increases during expiration and decreases during inspiration
causes a decrease in HR during expiration
(is perfectly normal)
Sinus arrhythmia refers to a changing sinus node rate with the respiratory cycle, on inspiration and expiration. This is quite common in young, healthy individuals and has no clinical significance. The heart rate increases with inspiration, due to the Bainbridge reflex, and decreases with expiration.
what can make sinus arrthymia disappear?
admisitration of atropine (blocks para effects)
how does the action potential work down from right atria to right ventricle?
how long after AP from SAN does AV node contract?
-action potentials in the atria reach the AV node before the atria have finished contracting.
SO
- delay of 60ms at the start of the AV node allows time for the atria to physically contract and so to push tho blood into the ventricles before the ventricles start to contract
- AV node does not start to transmit action potentials down into the Bundle of His in the ventricles until 120ms after the start of the SA node action potential
The delay of 60ms at the start of the AV node allows time for the atria to physically contract and so to push their blood into the ventricles before the ventricles start to contract
what does delay mechanism mean
makes vulnerable to ischaemia - can get partial or full blockage of AP at this site
what are Purkinje fibres? what is their role?
where are the first purkinje fibres activated?
- function: conduct the AP down the AV node, into interventricular septum to activate the ventricles. they are large diameter muscle fibres, joined by gap junctions.
- first muscles activated: muscles at the apex and muscles which contract capillary muscles that close the AV vavales
- get the left bundle (conducts the impulse to the Purkinje fibres of the right ventricle) and right bundle (conducts the impulse to the Purkinje fibres of the left ventricle)
. at the top: bundle of His
what happens if get right bundle / left bundle block of purkinje fibres?
Conduction through these bundles can be damaged by ischaemia. If the conduction fails at the right or left bundle we get ‘bundle branch block’ where the ventricles is activated late or not activated
what are the first part of the ventricles to contract?
papillary muscles - they close the AV valves before main ventricular contraction
what are the papillary muscles attached to the AV valves by?
what is their function?^
chordae tedinea - pull the AV valves together and close them
describe what the ventricular AP is like during the depolarisation stage AND during the refractory period (and why)
what substance can change in depolarisation and whats the name for that change?
- *-** starts wth normal nerve AP with Na influx, yet a prolonged depolarisation occurs: the plateau
- the plateau is from prolonged entry of calcium into the cell, which comes from **extracellular space
- causes the heart muscle tocontract for much longer than skeletal muscle**
THEN
- get a long refractory period before a new AP
- this prevents the muscle contracting prematurely and keeps cells synchronous
depolarisation can be altered by:
- adrenaline: increases Ca2+ entry - causes increased force of contraction of the heart: inotropic effect
which drugs can block calcium channels in the heart & what does this do to ventricular contraction?
- amlodopine & verapamil block the Ca2+ channels
what do each of Class 1-4 antiarrhythmic drug classes block?
whats an example of a beta and calcium channel blocker?
Class 1: Na+ channel blocker
Class II: B blocker - e.g. Propranolol
Class III - Potassium-channel blockers
Class IV - Calcium-channel blockers. e.g Verapamil
what is fibrillation? what does a defibrillator do?
fibrillation: when different parts of ventricles are contracting at different times - not enough pressure from ventricle to open valves
defibrillator shocks all the muscles and makes it contract synchronously -> all cells go into refractory period together
are the shapes recorded on an ECG the same as AP inside cell?
No ! (upwards projection on ECG doesnt neccessarily mean depolarisation, BUT time between ECG recordings is the same as time between AP)
what is an ECG lead?
where do lead I, II & III record voltages betweenn?
which plane do all three ^ give electrical activity of together?
where are the aVR, aVL, and aVF leads go?
ECG lead: the voltage recorded between two points on the body
Lead I: records the signal voltage between the left and right axillae
Lead II: records the voltage betwen the right axila and leg
Lead III: records the voltage between the left axilla and leg
togther: give a picture of the electrical activity of the heart in a frontal plane
- *aVR:** points up to right axilla
- *aVL:** points up to left axilla
- *aVF:** points down to groin
= 6 limb leads
why do augmented leads detect?
help id the locus of an abnormality in heart
which is the standard ECG (i.e. from which lead?)
what are the deflections (PQRST) visible in healthy subjects? which one might not be present
- lead II (gives largest signal of all 3 leads)
- *- P wave**: start of depol of atria
- *- QRS wave:** start of depol of ventricles
- T wave: repolaristion of ventricles
how long should the QRS complex last?
how long should the PR interval last?
QRS: 60-100 ms
PR: 120-200 ms
