Arrhythmias Flashcards
describe cardiac arrhtymias
disturbances of heart rate, rhythm
describe in terms of rate; bradycardia tachycardia describe in terms of origin; supra-ventricular (atria and AV node) ventricular
describe causes of cardiac arrhythmia
changes in;
impulse formation - changes in automaticity, triggered activity
impulse conduction - re-entry, conduction block, accessory tracts
describe changes in automaticity
SA is pacemaker (highest, 70-80 BPM, dominant over latent pacemakers) but all components of cardiac conduction system demonstrate a slower spontaneous phase 4 depolarisation and thus possess automaticity (AV node, 50-60 BPM, Purkinje fibres 30-40 BPM) => overdrive suppression
In order for the SA node to exert its normal control of rate and rhythm it must discharge action potentials at a regular frequency greater than any other structure in the heart
if not, the function of the SA node as normal pacemaker is taken over by another latent pacemaker as the result of loss of overdrive suppression
describe loss of overdrive suppression
May occur if the SA node firing frequency is pathologically low, or if conduction of the impulse from the SA node is impaired;
latent pacemaker may initiate an impulse that generates an escape beat
a run of such impulses may give rise to an escape rhythm, a series of escape beats
May occur if a latent pacemaker fires at an intrinsic rate faster than the SA node rate (even if the SA node is functioning normally);
latent pacemaker initiates an ecoptic beat, or a series of such beats generating an ectopic rhythm (i.e. one not generated by the SA node – ectopic meaning in an abnormal place, or position)
ectopic rhythms can result from ischaemia, hypokalaemia, increased sympathetic activity, fibre stretch and other causes
Can occur in response to tissue damage (e.g. post myocardial infarction);
even non-pacemaker cells (i.e. myocytes), when partially depolarized, may assume spontaneous activity
describe triggered acitivty
A normal action potential may trigger abnormal oscillations in membrane potential termed afterdepolarizations (ADs) that occur during, or after, repolarization
ADs of amplitude sufficient to reach threshold cause premature action potentials and beats
Afterdepolarizations may be either (PP);
early afterdepolarizations (EADs)
delayed afterdepolarizations (DADs)
Repeated afterdepolarizations of either type may cause a sustained arrhythmia
describe early afterdepolarizations
occur during the inciting action potential within; phase 2 (terminal plateau) – AD mediated by Ca2+ channels (when Na+ channels are still inactivated) phase 3 (repolarization) – AD mediated by Na+ channels (when partial recovery of Na+ channels from inactivation has occurred)
are most likely to occur when heart rate is slow
often occur in Purkinje fibres
are associated with prolongation of the action potential and drugs (e.g. sotalol) prolonging the QT interval
when sustained can lead to the life threatening arrhythmia ‘torsades de pointes’
describe delayed afterdepolarizations
occur after complete repolarization
are caused by large increases in [Ca2+]i
excessive [Ca2+]i results in;
oscillatory release of Ca2+ from the sarcoplasmic reticulum (SR)
a transient inward current (Iti, involving Na+-influx) that occurs in phase 4
are most likely to occur when heart rate is fast
are increased and decreased in incidence by prolongation and shortening of the duration of the action potential by drugs, respectively (predictably from alterations in Ca2+ influx during phase 2)
may be triggered by drugs that increase Ca2+ influx (e.g. catecholamines), or release, from the SR (e.g. digoxin)
describe defects in impulse conduction
re-entry
conduction block
accessory tracts
describe re-entry defect in impulse conduction
Self sustaining electrical circuit (anatomically may be two parallel conduction pathways), stimulates an area of myocardium repeatedly/rapidly The re-entrant circuit requires; unidirectional block anterograde conduction prohibited retrograde conduction allowed slowed retrograde conduction velocity
describe conduction block defect in impulse conduction - partial
partial - slowed conduction - tissue conducts all impulses but more slowly than usual
e.g. first degree AV block
intermittent block - tissue conducts some impulses, but not others
e.g. second degree AV block occurring as 2 types;
Mobitz type I – PR interval gradually increases from cycle to cycle until AV node fails completely and a ventricular beat is missed
Mobitz type II –PR interval is constant but every nth. ventricular depolarization is missing
describe conduction block defect in impulse conduction - complete
no impulses are conducted through affected area
e.g. third degree AV block ;
atria and ventricles beat independently, governed by their own pacemakers
ventricular pacemaker is now the Purkinje fibres – fire relatively slowly and unreliably – manifest as bradycardia and low cardiac output
describe accessory tract pathways
Some individuals possess electrical pathways in parallel to the AV node
a common pathway is the bundle of Kent
impulse through bundle of Kent is conducted more quickly than that through the AV node
ventricles receive impulses from both the normal and accessory pathways – can set up the condition for a re-entrant loop predisposing to tachyarrhythmias
describe action of anti-arrhythmic drugs
inhibit specific ion channels (or activate/block specific receptors) with the intention of suppressing abnormal electrical activity classified pharmacologically based upon their effects upon the cardiac action potential (the Vaughn Williams classification The scheme defines four classes I, II, III and IV, with class I subdivided into subclasses Ia, Ib and Ic many antiarrhythmic agents are not entirely selective blockers of Na+, K+, or Ca2+ channels, and may block more than one channel type (e.g. amiodarone) Some drugs do not fit in to the Vaughn Williams classification (e.g. adenosine, digoxin)
describe class I anti-arrhthmic drugs - IA
phase 0
rhythm control
acts on atria, ventricles, AV accessory pathways
targets voltage activated Na+ channel (PP);
Voltage-activated Na+ channels cycle between resting, open and inactivated (refractory) states. Relative proportions of time spent in each depend upon firing frequency
During high frequency firing (e.g. tachyarrhythmias) relatively more time is spent in the open and inactivated states. Class I agents bind preferential to these targeting areas of the myocardium in which firing frequency is highest in a use-dependent manner without preventing the heart from beating at normal frequencies
Associate with and dissociate from Na+ channels at a moderate rate. Slow rate of rise of AP and prolong refractory period
e.g. Disopyramide
describe class I anti-arrhthmic drugs - IB
phase 0
rhythm control
acts on ventricles
targets voltage activated Na+ channel
Associate with and dissociate from Na+ channels at a rapid rate. Prevent premature beats
e.g. Lignocaine
