origin and conduction of cardiac impulse Flashcards
where in the heart does excitation originate?
- in the pacemaker cells in the SA node (a cluster of specialised pacemaker cells)
where is the SA node located?
upper right atrium (close to where the SVC enters the right atrium)
what does sinus rhythm mean?
when the heart is controlled by the SA node
how does cardiac excitation originate?
- the cells in the SA node have no stable resting membrane potential and generate spontaneous pacemaker potentials
- the spontaneous pacemaker potential takes the membrane potential to a threshold and an action potential is generated, resulting in the generation of regular spontaneous action potentials in the SA nodal cells
what is the pacemaker potential due to?
- a decrease in K+ efflux
- Na+ and K+ influx
- transient Ca++ influx
(pacemaker potential is the upward stroke at the bottom)
what happens once the threshold is reaches?
- the rising phase of action potential (depolarisation) is caused by activation of L-type Ca++ channels which results in Ca++ influx
what causes the falling phase of action potential? (repolarisation)
- inactivation of L-type Ca++ channels and activation of K+ channels which result in K+ efflux
what is the AV node, where is it located and what does it do?
- bundle of specialised cardiac cells
- located at the base of the right atrium, above junction of arita and ventricles
- AV node is the only point of electrical contact between atria and ventricles
- AV node cells are small in diameter and have slow conduction velocity
how does cardiac excitation spread?
- across the atria (cells to cell conduction via gap junctions)
- from SA node to AV node (cells to cell via gap junctions but also some internodal pathways)
- the conduction is delayed in the AV node (this allows artial systole to precede ventricular systole = contraction)
- the bundle of his and its branches and the network of purkinje fibres allows rapid spread of action potential to the ventricles
- ventricular muscle (cells to cell)
what happens in phase 0 of action potential in contractile cardiac muscle cells?
- the resting membrane = -90mV
- rising phase of action potential (depolarisation) is caused by fast Na+ influx
- membrane potenetial is then +20mV
what are the phases of ventricular muscle action potential?
0 = fast Na+ influx
1 = closure of Na+ channels and transient K+ efflux
2 = mainly Ca++ influx
3 (falling phase)= closure of Ca++ channels and K+ efflulx
4 = resting membrane potential
what is the plateau phase?
- the membrane potential is . maintained near the peak of action potential for a few hundred milliseconds
- it is a unique characteristic of contractile cardiac muscle cells
- the plateau phase is mainly due to influx of Ca++ through L-type Ca++ channels
what is the falling phase of ventricular muscles action potential?
- (repolarisation)
- caused by inactivation of Ca++ channels and activation of K+ channels
- resulting in K+ efflux
what changes the heart rate?
- HR is mainly influenced by the autonomic nervous system
- sympathetic stimulation increases the heart rate
- parasympathetic stimulation decreases the heart rate
- changes in HR involve a reciprocal action of sympathetics and parasympathetics
how does the autonomic nervous system influence the normal HR?
- the vagus nerve (para) exerts a continuous influence on the SA node under resting conditions
- vagal tone dominates under normal resting conditions
- vagal tone slows the intrinsic HR from 100bpm to 70bmp
what is normal resting HR?
between 60 and 100 bpm
what is bradycardia?
resting HR under 60bpm
what is tachycardia?
resting HR over 100bpm
how does parasympathetic influence the heart?
- vagus nerve supplies SA node and AV node
- vagal stimulation slows heart rate and increase aV nodal delay
how does sympathetic influence the heart?
- cardiac sympa nerve supply the SA node and AV node and myocardium
- sympa stimulation increases HR and decreases AV nodal delay
- also increases the force of contraction
what is the neurotransmitter for parasympathetic?
- neurotransmitter is acetyle choline acting through M2
- atropine is a competitive inhibitor of acetylcholine - used in extreme bradycardia to speed up the heart rate
what is the neurotransmitter for sympathetic?
neurotransmitter is noradrenaline acting through B1 adenoceptors.
what are the standard leads?
1 = RA - LA 2 = RA - LL 3 = LA - LL
what are the ECG records?
P = atrial depolarisation (first small bump) ORS = ventricular depolarisaiton (spike) T = ventricular repolarisation (seond large bump) PR = largery AV node delay (line after spike) ST = segment ventricular systole (line after spike) TP = diastole (long line)