Cardiac electrophysiology and arrhythmia Flashcards Preview

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Flashcards in Cardiac electrophysiology and arrhythmia Deck (37):

Sinus rhythm maintained by?

Entrainment and suppression of lower pacemakers
Coordination and excitation via specialised conduction system
Existence of a prolonged refractory period in the myocardium


Draw the cardiac myocyte action potential diagram

check book



Absolute / effective refractory period, cannot stimulate heart again during this time



Relative RP, can generate slow propagating AP but need larger than normal stimulus



supra normal period, can generate slow propagating AP with smaller than normal stimulus


The 2 categories of causes of arrhythmia

1. Disorders of impulse formation
- Early discharge of a pacemaker (abnormal automaticity) or activity triggered by an unstable RMP in working myocardial cells (DAD, EAD) causing extrasytoles
2. Disorders of impulse conduction
- Conduction abnormalities such as partial or complete AV block = slow HR or bradycardia, left or right bundle branch block and reentry = altered time course of ventricular activation sequence


Conduction abnormalities may arise because of?

spatial or temporal dispersion or repolerisation


the vulnerable window?

Stimulation during the T wave period on an ECG
because much of the ventricular myocardium is in relative refractory period and escalation elicits slowly propagating action potentials, which is a risk factor for generating re entrant arrhythmia.


movement of the depolarisation wavefront through the heart?

endocardium to epicardium
apex to base


overdrive suppression

SAN normally drives the lowest pacemakers because it has the fastest spontaneous rate, this surpasses the inherent automaticity of the lower pacemakers
AVN and purkingie


what is the definition of an arrhythmia

and deviation in sinus rhythm


Definition of a reentrant arrhythmia

repeated circulation of a wave of activation within a region of the ventricular wall
Gives rise to a ventricular tachycardia --> VF


Definition of ventricular fibrillation

chaotic reentrant activity at multiple sites throughout ventricles, heart loses capacity to pump


Atrial flutter

caused by single atrial reentrant circuit
fast regular atrial rate (250-350bpm)


at high atrial rates what is likely to occur?

partial AV block


Atrial fibrillation

is characterised by rapid disorganised atrial activation (300-600bpm) can lead to rapid disorganised ventricular rhythm


atrial flutter and fibrillation can occur as a result of? common demographic

heart valve lesions and congestive heart failure
Relatively common in the elderly, rhythm disturbances can be distressing and impair clot formation theyre not directly life threatening. Yet there is increased risk of clot formation, and subsequent PE and stroke.


Ventricular fib and tachycardia can occur in?

acute myocardial ischaemia
result of structural remodelling associated with healed myocardial infarct
heart failure
hereditary ion channel mutations


VT associated with

rapid ventricular activation (110-250bpm) and impaired mechanical function


What does atrial fib look like on an ECG?
what is it defined as when taking a pulse?

no organised activity on baseline, AVN cant protect the ventricles forever
Irregularly irregular pulse


The actual ionic currents that cross the cardiac cell membrane during the AP are determined by?

the status of membrane channels that carry specific ions and also influenced by the membrane potential.


Importance of the fast acting sodium channel

Activation gates shut at resting potential but open rapidly with depolarisation, whereas inactivation gates that reopen at rest shut as the cell membrane is depolarised, therefore brief delay between activation and inactivation, when channel is open.
The membrane potential dependance of sodium channel inactivation is responsible for prolonged refractory period of cardiac AP. The myocutes cannot be reactivated during the ERP because membrane potential is > - 50mV and inactivation gates are closed.


How can a myocardial block cause a reentrant arrhythmia?

If the block is unidirectional: say the activation is arriving at the top and unable to propagate around the left had side but can on the right, yet can pass retrogradely back up the left side back up to the top where it reactivates tissue to generate sustained action potential around the reentrant circuit, which can occur if the time taken to propagate is the same as the ERP.


Why will you not get a reentrant model circuit working in a normal heart?

ERP = 250-300msec
activation spreads through the myocardium at 1m/sec
therefore the wave length needed to support reentrant arrhythmia is around 250-300mm, a path distance that is quite long when compared to the dimensions of the human heart

wavelength = ERP x CV
venerability increases with
- decreased CV
- Decreased refractory period


A sustained reentrant activation can be set up around a region of anatomic or functional block provided there is??

a trigger
unidirectional block
slow conduction occur and / or short ERP (said conditions most probable when depolarisation is not spatially homogenous)
and a curcit


WPW syndrome

Bundle of kent provides accessory pathway from A --> V
Normally early activation occurs via said pathway and collides with activation that has propagated via AVN (ECG = wide QRS complex and slurred blurring (delta wave), and associated short PR interval)
Normally little effect on function but possibility for macro reentry to occur: so if ectopic atrial activation blocked in the accessory pathway but propagates to the ventricles via the AVN, the conduction delays through the AVN are sufficiently long to enable this activation of reexcite the atria and set up a stable reentrant curcuit with a repetition rate that is faster than than the SAN, in this case ventricular activation via the fast conduction system and thus tachycardia is a narrow complex. If reentrant curcuit in the opposite direction, going though the AVN in the retrograde direction then a wide complex tachycardia generated


Rate of propagation of electrical activation determined by?

Electrical properties of myocytes
- increased electrical coupling between myocytes increases propagation rate,
- propagation rate greatest in large diameter cells
Inward current during excitation
- Density and status of sodium channels important - greater current = faster prorogation


Why does ectopic activation in the vulnerable period have a high probability of inducing re entrant arrhythmia?

During the vulnerable period the V. myocardium's membrane potential is around -50mV and as a result relatively few of the inactivation gates which close shortly after depolarisation will have reset, so the numbers of sodium channels that can be opened are small and hence prorogation of electrical activity is slow.
Also repolarisation not uniform throughout ventricles which increases probability that local conduction block will occur


Myocardial ischaemia results in

Slow conduction
reduced AP duration
Non-Uniform depolarisation
Ectopic activation DAD's


Mechanism behind slow conduction in myocardial ischemia

Sodium / potassium ATPase reduced
Transmembrane Na+ / K+ gradients reduced
Partial membrane depolarisation
Inactivation of sodium channels
Reduced gap junction coupling (low pH due to regional metabolic acidosis)


How does the AP change in myocardial ischemia

Sodium/ potassium ATPase reduced = increased intracellular Na+ and increased extracellular K+
Transmembrane potassium gradient reduced
Ina reduced
Hyperkalemia shortens AP duration, external inc in K+ = increased conduction of IKR channel


DAD's in myocardial ischemia

Hard to pump calcium out of the cell due to ischemia
Increase Ca2+ in the SR
When the SR reaches levels above some threshold they automatically release calcium now you suddenly have a lot of calcium inside the cytoplasm that generates inward going current because its electrogenic
If this depolarisation reaches threshold you have ectopic beat which could be a trigger for generating arrhythmia


Factors that help VT develop to VF with acute MI

if VT develops
- +ve feedback
- Rapid rate, poor contraction
- Increased O2 demand, reduced O2 supply
- Ischemia more severe
--> VF


Cardiac rhythm with healed MI

Infarct borderline complex
- structural heterogeneity
- Substrate for abnormal electrical activity and reentry
- Often monomorphic VT - stabilised by structure


Why do people with heart failure also die of arrhythmias?

the atria and ventricles become fibrosed over time, scar tissue forming in small patches everywhere through the heart,
A and V become dilated = greater possibility for larger path lengths for re entry
Increased atrial pressure because pump isn't working so well, sets of stretch activated channels

* a;tered expression and function of NCX - can cause DADs which trigger re entrant arrhythmia
AF begets AF


Long QT syndrome and EADs
- increased Ap duration may be caused by?

EAD's caused by prolonged action potentials which enable Lca(L) to reactivate
- Drugs (amiodarone)
- Reduced extracellular K+ conc (hypokalemia - decreased [K+]o --> decreases Ikr
- Potassium channel mutation that lead to reduced effectiveness of delayed rectifier Ikr: LQT1 [Ikr] + LQT2 [Ikr]
- Sodium ion channel mutations that affect inactivation of Ina (LQT3)


EAD's can result in?

continuously varying polymorphic VT
Torsade de pointes - "twisting of the points" may resolve spontaneously or progress to VF