Cardiac Rhythm Flashcards
Electrical activation in sinus rhythm (3)
- SAN suppresses lower pacemakers as it is the fastest- overdrive suppression
- coordinated excitation via specialised conduction system
- Prolonged refractory period in myocardium
Different refractory periods and what they are (where they are on graph, look at graph)
ARP: absolute refractory period- unable to stimulate myocyte
RRP: relative, can restimulate, but a greater than normal stimulus required. Poor and slow propagation as not all channels restored
SRP: supernormal, smaller stimulus than normal. Response if stimulated poorer than normal
Arrythmia is a deviaton from sinus rhythm due to an abnormal stimulus. What are the two common ways this occurs?
- Disorder of impulse formation: early discharge of a pacemaker, or activity triggered by an unstable RMP in working myocardial cells (DAD, EAD)
- Disorder of impulse conduction: partial or complete AV blck, LBBB, RBBB an reentry. Partial block gives rise to bradycardia, others alter time course of ventricular activation sequence.
Re-entrant arrythmias and how they cause VT and VF
There is a vulnearble period, in the RRP or the T wave area (repolarisation).
Ectopic stimulation during the T wave, stimulating slow AP’s
Can initiate a re-entrant arrhythmia, repeated wave of activation within ventricles, leads to VT
Can lead to VF
Other types of re-entrant arrythmias
Atrial flutter: sawtooth appearance on ECG, a single re-entrant atrial circuit with a fast atrial rate. A slower ventricular response, can cause heart block
Atrial fibrillation: rapid disorganised atrial rhythm, not all conducted to ventricles. (irregulalrly irregular rhythm). Risk of clot formation, treatment with warfarin/dabigatran
V tach: Rapid ventricular activation, MONOMORPHIC VT, abent/unrelated p wave. Impaired mechanical function, risk of VF. Wide QRS
V fib: loss of ventricular coordination
Ionic currents during the cardiac AP: I(Na) I(CaL) I(Na/Ca) I(to) I(K1) I(Kr/Ks)
I(Na): rapid activation and inactivation, fast inward depolarisation, causing decreased I(K1) permeability and opens I(CaL)
I(CaL): Rapid activation, slowly switches off over plateau, drives slow AP in SAN/AVN
I(Na/Ca): Exchanger (3Na,1Ca), During plateau, calcium in, sodium out. reverse during plateau
I(to): early repolarisation due to transient outward K+ and Cl-
I(K1): determines RMP, Causes potassium influx, but is balanced out by concentration gradient which causes efflux
I(Kr/Ks): delayed rectifier currents, activate during plateau and start repolarization, increases the I(K1), K+ influx
Activation and inactivation of the sodium channel
At rest
Depolarisation
When inactivation gate is closed what must happen?
Rest: Inactivation open, activation closed
Depolarisation: Inactivation gate will close, and activation gate will open. Causes a small window of current, the sodium inflow, switches on then off very rapidly
gates must reset for another Ap to occur. RRP is thus when some channels are reset and some have not. Occurs during repolarisation. Is inactivated during plateau
Re-entrant circuit model
Normal heart
Abnormal heart
equation that links and re-entrant requirements
examples that can cause these re-entrants
Normal heart: In a region of block, no conduction. Activation in this area propogates around block and collide and dissipate
Abnormal: Able to propogate around one way (unidirectional block), and pass up side with block on top, restimulating. Re-entrant circuit.
However can only occur if region it comes back up to is not refractory.
Wavelength= ERP x conduction velocity, thus a slower ERP and slower CV mean more likely to start a re-entrant (more vulnerable). Thus need a circuit, slow conduction + low ERP, unidirectional block and a trigger
Anatomical: scar
Functional: non-responsive tissue
Wolf-Parkinson White syndrome
if trigger two ECG findings
consequence if AF
Additional muscle between A and V that conducts AP.
may seem normal but will exhibit on ECG a short PR, wide QRS and delta wave
However a trigger can cause macro re-entry if activation occurs during RRP. Unidirectional block formed
Can lead to rapid tachycardia, faintness and death
1) Re-entrant down through the AVN, leading to a narrow complex VT (SVT?)
2) Re-entrant up through the AVN a wide complex VT
In afib, signal can be transduced due to AVn not slowing it down.
What is the rate of propogation of electrical activation determined by?
Electrical properties of myocytes: increased electrical coupling between myocytes increases rate; increased diameter of cells increases rate (purkinje>AVN)
Inward current during excitation: Density and status of sodium channel, greater current, faster propogation.
This is because I(Na) propogates AP’’s by bringing adjacent myocytes to cross threshold via nexin junctions. thus amount of Na influx affects time taken for tissue to reach threshold
Propogation of electrical activity in an ectopic beat
Ectopic activation during the vulnerable period increases likelihood of re-entrant arrythmia
- Sodium channels not fully reset, so reduced Na current, slower propogation (less CV)
- Repolarisation non-uniform, greater probability of local conduction block
Why does myocardial ischaemia result in possibility for arrhythmia
- Slow conduction
- reduced AP duration (decreased ERP, decreased wavelength)
- Non-uniform repolarisation (increased prob of loacl conduction block)
- Ectopic activations (DADs)
Why is there slow conduction in myocardial ischaemia
low wavelength
low ATP
Reduced Na+/K+ ATPase function reduced (3Na+ out, 2 K+ in)
Results in increased intracellular Na more extracellular K+
This reduces gradient for the I(Na), so less I(Na).
Means inactivation gate is already partially closed due to altered MP
Less gap junction coupling also due to lower pH (regional metabolic acidosis)
Why is the AP duration shorter in myocardial ischaemia
low wavelength
Altered ion gradients (more Na(i) and K(o))
Transmembrane K+ gradient reduced also
Hyperkalaemia increases the I(Kr), quicker repolarisation
Activation of I(K,ATP) channels increases repolarisation too (open when ATP is low)
regional differences
DADs, a type of trigger (delayed after depolarisations)
Due to less ATP, impaired Ca2+ release, causing increased intracellular calcium
Increases ER calcium, likelihood of CICR from SR
Increases calcium out of cell by exchanger, sodium influx may cause depolarisation and activation
