L2. Cardiac Rhythm and Rhythm Disturbance Flashcards
Describe the initiation and spread of electrical activation in the healthy heart = Sinus rhythm
- Spontaneous depolarisation of cells in SA node –> Atrial chambers –> AV node–> bundle of His –> bundle branches either side of interventricular septum then –> Purkinje fibres.
Explain how sinus rhythm is maintained
- Entrainment and suppression of lower pacemakers by the SA node which has fastest spontaneous rate.
- Programmed excitiation via specialised conduction system
- Existence of prolonged refractory period in the myocardium
Describe how ventricular myocyte excitability varies during a cardiac action potential with reference to the FRT, ARP/ERP, RRP and SNP.
ARP/ERP = absolute/effective refractory period where AP can’t propogate regardless of signal strength
RRP= relative refractive period following ARP where slower AP can be generated if stimuli is greater than normal
SNP= period following RRP where slower AP can be generated with smaller stimuli than normal.
FRT = full refractory time which is ARP + RRP + SNP.
State the roles of disorders of impulse formation and conduction in initiating and maintaining an arrhythmia.
Faults in
- Impulse formation=
- Abnormal automaticity eg. early discharge of pacemaker
- Activity triggered by unstable resting membrane potential in working myocardial cells - Impulse conduction=
- Partial/complete AV block causing bradycardia
Alteration of the time course of ventricular activation sequence possible because of spatial/temporal dispersion of repolarisation.
- Left or right bundle branch block
- Re-entry
Describe the ECG features of common re-entrant arrythmia: VT, VF, AFL and AF
- VT: Ectopic stimulus during the T wave (RRP of most myocytes) causes short run of re-entry in one section of the wall - fast repeating high peaks
- This progresses to VF: reentrant activity at multiple sites causes irregular v short squiggles
- Atrial flutter is caused by single reentrant circuit: irregular repetition of saw toothed P waves
- Atrial fibrillation: rapid disorganised atrial activation which make lead to disordered ventricular rhythm: no discernable p waves, with irregular QRS
Provide an overview of the ionic basis of the cardiac action potential.
- Initially depolarisation is caused by rapid influx of Na into cell.
- L type Ca2+ channel opens giving inward slower ca2+ which gives the plateau period. This is important for ca-mediated ca release
- Na/Ca2+ exchanger
- K channel open to make an ouward K+ current. This causes repolarisation
Describe the re-entrant circuit model that describes propagation of electrical activity around an area of block/refractoriness
Re-entrant model proposes that
1. activation begins at the top of the block and propagates with equal velocity around both sides
- Normally it will collide at the bottom, then stop.
- In re-entrant arrythmia, there is a block on one path on the side so that there is only 1 unidirectional propagation
- If the time taken to travel around the area back up to the start is same as the ERP, then it is possible to reactivate tissue and create sustained re-entrant circuit.
Explain the Wolff-Parkinson-White syndrome + ECG features using the re-entrant circuit model
In WPW The bundle of Kent provides an accessory pathway for electrical activity to pass from atria to ventricle (other than AV node).
This causes early activation of the ventricle which collides with the slowly propogated activation via AV node.
This results in ECG with wide QRS and slurred beginning and short PR interval .
Explain how the rate of propagation of electrical activation is determined
Increased Propagation rate proportional to
- Electrical properties of myocytes:
- increased electrical coupling
- diameter of cell - Inward current during excitation
- Density and
- Status of activation/ inactivation gates of sodium channels:
Explain how reduced activation propagation velocity can increase the probability of re-entry.
Re-entrant arrhthymia requires a wavelength = time of the Effective Refractory Period * CV
Slower conduction increases the likelihood that the unidirectional propagation will be able to cycle back to activate cells that have finished their refractory period
Explain how slow conduction, reduced action potential duration, DADs and non-uniform repolarization increase the potential for arrhythmia in myocardial ischemia and how they came about from MI
- Slow conduction / Reduced AP duration comes from reduced Na2+ current due to low ATP affecting transmembrane Na+ and K+ gradients, increased K+ outside,
= reduces wavelength
- Ectopic activation (delayed after depolarisation) comes from impaired Ca2+ homeostasis leading to increased intracellular Ca2+ concentration during diastole.
=trigger for re-entry arrythmia
- Non-uniform repolarisation comes from heterogeneity in perfusion to certain areas.
=increased probability of local conduction block
Explain why heart failure increases the potential for arrhythmia. (6 causes). It also has increased risk of VT and VF
- In HF, atria becomes dilated increasing pathlength for potential re-entrant currents- promote AF
- Increased atrial stretch stimulates stretch activated ion channels
- HF->Atrial Fibrosis creates a marked regional slowing of conduction
- In congestive HF expression and function of Na/Ca2+ exchanger can cause Delayed after depolarisation which trigger arrhythmia
- Heterogenous remodelling of ANS inputs can influence electrical properties and slow conduction
- AF causes changes in cellular electrical properties that sustain it.
Describe how Long QT Syndrome can cause ventricular arrhythmia.
- there is increased risk due to increased non-uniformity of repolarisation in LQTs.
- LQTS has prolonged ventricular AP induced by drugs or hereditary membrane ion channel mutations
- This allows enough time for L-type calcium channels to re-activate
- Generation of after-depolarisations late in plateau phase or early in repolarisation causes re-entrant arrythmia
- This results in continuously varying polymorphic VT - twisting of points which may spontaneously resolve or progress to VF
