4. Heartbeat and ECG Flashcards
Describe the SAN and it’s role
SAN is a group of specialised cells positioned on the wall of the right atrium, near the entrance of the superior vena cava
It is the impulse generating tissue i.e. the pacemaker
SAN receives blood from the right coronary artery - occlusion of this artery will cause iscaemia in the SAN
Describe the cells of the SAN
These are nodal cells - modified cardiac muscle cells - NOT nerve cells
All myocardial cells have the potential to be pacemaker cells
The cells with the fastest pace are the pacemaker cells
These cells are connected to adjacent atrial cells by gap junctions
Give the location of the AVN and how it relates to the SAN
Cardiac electrical activity starts in the SAN and spreads across to the AVN where it stops
The AVN is located on the inter-atrial septum close to the tricuspid valve
Give the mechanism of the cardiac pacemaker cell
There is a constant (leak) sodium influx into the cell at rest
This would normally depolarise the cell but a simultaneous outward potassium current prevents this
The outward potassium current decays with time SO the membrane potential slowly depolarises - outward potassium current is reduced
When this reaches a critically low level, the cell is sufficiently depolarised to trigger a sodium influx and an action potential
During the action potential, the potassium current is ‘reset’ to a high level and then starts to decay again
SO the rate of spontaneous contraction of cardiac pacemaker cells is dependent on the rate of decay of the outward potassium current
Describe the innervation of the SAN
The SAN is innervated by the parasympathetic (vagal) nerve and sympathetic nerve fibres
Parasympathetic nerves from vagus nerve inhibit the closure of the potassium channels via muscarinic receptors - this makes the pacemaker cells slow down
Sympathetic nerves at the SAN increase the closure of the channels via B-adrenoreceptors - this makes the pacemaker speed up
NB. both systems also have weaker inputs to the AVN
Describe and explain the transmission of action potentials from the SAN to AVN and the delay that occurs
Action potential from the SAN spreads over both atria 60ms after the SAN is activated
The AVN does not start to transmit action potentials down the bundle of His until 120ms
This means that there is a delay at the AVN for 60ms
This allows time for the atria to physically contract and push their blood into the ventricles before the ventricles start to contract
This delay means that this part is the ‘weak link’ in the cardiac cycle
Describe the transmission of the action potentials down to the ventricles
The Purkinje fibres cause the activation of the ventricles
Ventricles have uniquely shaped action potentials - starts like a normal action potential with Na+ influx and there is then a plateau - this is a prolonged depolarisation phase caused by a late and prolonged entry of Ca2+ into the cell
This helps the muscles contract for much longer than skeletal muscle because the more Ca2+ that enters, the stronger the contraction
What is the strength of the contraction of the ventricles determined by?
Determined by the calcium influx
How do Ca2+ ions enter the cardiac cells?
How can this be used clinically?
Enter through slow (L type) calcium channels in the membrane of cardiac cells
Drugs can be used to block these channels to reduce the force of ventricular contraction and the work/oxygen demand of the heart
Describe the refractory period of cardiac cells in the ventricle
The cells have a long refractory period before the action potential - this prevents the muscle from contracting prematurely and keeps all the cells synchronous
What happens when cardiac cells go out of synchronisation?
How does a defibrillator fix this?
This is ‘fibrillation’
Different parts of the ventricle are contracting at different times - ventricular pressure cannot rise enough to generate any cardiac output and this leads to death
A defibrillator shocks all the muscle and makes it contract synchronously - it causes all of the cells to go into the refractory period together and hence restores the rhythm
What is an ECG - how does it occur?
The action potentials in the cardaic muscle generate electrical voltages outside the heart which can be detected on the surface of the body - this is an ECG
NB. the changes are smaller than the action potentials and the shapes are different BUT the timings are important
Describe how ECGs work
Consist of 12 recordings called ‘leads’ - these generate 12 images
An ECG lead is the voltage recorded between two points on the body
The leads give you a picture of the heart in a frontal plane
Describe the typical leads of an ECG
These are known as the ‘basic limb leads’
Lead 1 - records the signal between the left and right axillae
Lead 2 - records signal between right axillae and leg
Lead 3 - records signal between left axillae and leg
Standard ECG is recorded from lead 2 - this normally gives the largest signal of the three leads
Describe and explain the different parts of an ECG wave
P wave
-Due to atrial depolarisation
-Should be smooth and rounded
-Normally positieve in leads 1, 2 and sometimes 3
Notched or peaked P waves are seen in COPD or CHF
Q wave
- Negative
- SO no Q wave is present if QRS signal starts upwards
- Size depends on what lead you’re looking at
- Normally small or absent on lead 2
R and S waves
- R wave usually positive
- R wave present on leads 1, 2 and 3
- S wave is negative
- Forms QRS complex - polarity depends on which lead is viewed; can be positive, negative or bipolar
ST segment
- This is when all the ventricular muscles are contracting
- Normally starts flat and curves upwards into T wave
- ST segment changes are important for diagnosis of Acute Myocardial Infarction (AMI)
T wave
- Due to the difference in time of the repolarisation of the ventricles
- Normally orientated in the same direction as the QRS complex
