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Cardiac Dysrhythmias And Heart Block Notes

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Cardiac Dysrhythmias and heart block

Dysrhythmias
-classified by site (atrial, nodal, ventricular) and by type (ectopics, tachycardia, flutter, fibrillation)
-ventricular dysrhythmia has the greatest effect on cardiac output. Ventricular fibrillation is fatal is untreated
-Atrial fibrillation is the commonest dystrhymia and is associated with increased risk of stroke, due to thrombus in the fibrillating left atrium
-Dysrhythmia occurs in normal, healthy hearts but the difference is that dysrhythmia is self terminating
-Heart rate is less than 60 (bradycardia) or more than 100
-if origin of action potentials is not from the sinus-ectopic pacemaker activity
-abnormal conduction pathways
-abnormal conduction velocity Normal dysrythmias Sinus Tachycardia: Heart rate faster than normal driven by the sinus node - frightened/ startled individuals or during excercise. It can be pathological for acute hyperthyroidism Sinus arrhythmia... Change in heart rate that occurs with each respiratory cycle- inspiration accelearates the heart whilst the expiration slows it- cyclic variations in sympathetic and parasympathetic tone Variation in the sinus rhythm where the P-P interval varies by more than 10%
-Normally: due to respiration the P-P interval lengthens with inspiration and shortens with expiration a) Conduction abnormalities: Heart block
-AV node/bundle of His, or bundle branch may fail to transmit electrical excitation properly due to fibrosis or ischaemic heart disease Ischaemia- fall in intracellular ATP, this activates ATP sensitive K channels- so less is inhibited- cells become less excitable- slowing or blocking of conduction during ischaemia
-1st degree heart block: The tissue conducts all impulses but more slowly than usual, damage to the gap junctions, increase in electrical resistance, fibrosis Lengthening of the PR interval (more than 0.2 seconds)- slowing of conduction between the AV node and ventricle
-2nd degree heart block: intermittent block, tissue conducts some atrial impulses but not all, Mobitz type 1/ Wenckeback block - PR internal gradually lengthens from

one cycle to the next until AV node fails completely, skipping a ventricular depolarisation (every 3/4th beat fails to conduct) Mobitz type 2 PR interval is constant but every nth ventricular depolarisation is missing
-3rd degree heart block/ Complete heart block: transmission fails completely so the atria and ventricles beat independently at different rates. The atria (P waves) are beating at 72/minute driven by the SA node. Ventricles beat at 30/minute driven by latent pacemaker in bundle of His or purkinje system
-can lead to Stroke-Adams attack- sudden temporary loss of consciousness-treated with artificial pacemaker implantation b) Conduction abnormalities-velocity 2: Abnormal propogation Re-entry mechanisms sustain pathological fibrillation Unidirectional block-Ischaemia or chronic heart failure causes long refractory period and slow conduction velocities in the certain regions of the heart. When normal excitations reach these regions- unidirectional bock, the ischaemic myocytes are refractory from previous impulse so it propagates no further. So the actionpotentials bypass this area and by the time the propagating wave has spread down it is retrogradely propagated to the ischaemic regions as the myocytes are no longer refractory - so the impulse is conducted back to the origin
-Due to the slow wave of conduction, by the time the impulse reaches the origin, the myocytes have had enough time to repolarise, regain their excitability after their refractory period so are depoalrised again self perpetuating loop
-Re entry sustains fibrillation after a triggering delayed after depolarisation - reentry pathways can be seen using a voltage sensitive dye
-Frequency of re-entry generally outpaces the SA nodal pacemaker- leads to tachyarryhtmias, atrial and ventricular fibrillation
-acessory conduction pathway: wolff-parkinson-white syndrome- abnormal anatomy, accessory conduction pathway made of muscle cells -bundle of kentconducts action potentials from the atria to the ventricular septum depolarising some of the septal muscle earlier than if the depolarisation reached by slower AV nodal pathway

-Ventricular depolarisation is more spread out, broader QRS complex,small delta wave, interval between the P and QRS complex is shortened
-The aberrant conduction pathway also results in a loop- re-entry, supraventricular tachycardia, more than 200 beats per minute due to re-entry pathway in the accessory bundle of Kent. Ventricular depolarisation wave passes up the bundle of kent to re-excite the atria and producing a self perpetuating circus pathway and tachycardia
-sensation of palpitations, truncated diastolic filling interval reduces the cardiac output- collapse
-treatment: destruction of the bundle of kent

TREATMENT: Increase the conduction velocity, so depolarisation arrives before the cells have repolarised
-increasing the refractory period (so cells are still refractory when the next circuit of depolarisation arrives) Atrial Fibrillation
-Firbillation is uncoordinated, repetitive excitation of myocytes- writhing movement of chamber wall-no effective ejection of blood-fibrillation is sustained by multiple local re-entry circuits- common in elderly and people with sedentary lifestyles
-Re-entry loop within the atria generates a rapid succession of action potentialsbecomes the fastest pacemaker in the heart and outpaces the SA node- bombards the AV node- AV node can't repolarise fast enough to pass all of the impulses, only some of it make it to the ventricles
-atria acts mostly as a booster pump so many patients are unware they have it
-excitation is transmitted sporadically through the AV to the ventricles resulting in characteristic radial pulse of irregular rhythm Ventricular fibrillation
-More lifethreathening- heart can't generate cardiac output a) Abnormal initiation - altered automacity Depolarisation dependent triggered activity Calcium overload: Digitalis intoxication leads to increase in intracellular calcium concentration- leads to SR sequestering too much calcium- so SR begins to

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