***understanding arrhythmias and actions of drugs on the CVS Flashcards
causes of tachycardia
ectopic pacemaker activity - where damaged area of myocardium becomes depolarised and spontaneously activate or activated due to ischaemia = dominates over SA node
afterdolparisations - abnormal depolarisation following the AP
atrial flutter/fibrillation
re-entry loop - conduction delay or accessory pathway
causes of Brady cardia
sinus bradycardia- where SAN dysfunction or due to extrinsic factors such as drugs
conduction block- problems with AVN or bundle of His or slow conduction at AVN from extrinsic factors e.g drugs
what is a delayed after-depolarisation
due to high intracellular calcium levels causes another extra depolarisation after the AP before full refractory period. due to high calcium levels. can cause atrial tachycardia if continuously happens. look at pic
what is an early after depolarisation
more likely to happen if have a prolonged AP. happen before AP is over. oscillations can lead to ventricular tachycardia
what causes prolonged AP
hypokalaemia (not enough K+ to repolarise quick enough)
bradycardia
lots of drugs cause this
overactive sodium/calcium (more K+ needed to repolarise)
problems with potassium channels
describe how re-entrent arrhythmias occur
there is a partial block which can’t conduct impulses forward BUT because its only partial for some unknown reason the impulse can be conducted back up past the partial block. on the other side of the block the cells have recovered from their refractory period and these cells depolarise and this cycle continues. **complex look at notes
what is a multiple re-enterent circuit in the atria (atrial fibrillation)
multiple re-entry cicuits= chaotic signals to ventrciles= irregular, no P waves, narrow QRS and wavy baseline
what is a AVN re-entry circuit
goes back around redepolarises atria and ventricles straight away = VERY high heart rate, up to 200bpm = trachycardia
what is a ventricular pre-excitation (wolf-parkinson white syndrome)
accessory pathway -can cause an extra beat through atria and ventricles causing tachycardia
drugs blocking voltage sensitive sodium channels
e.g lidocaine - blocks open sodium channels = the ones that must be injured because dissociates before next AP due to short half life. = little effect on normal tissue.
used after MI if patient showing ventricular tachycardia due to damaged areas of myocardium firing automatically - lidocaine prevents this and savours working tissue
beta adrenoreceptor antagonists
e.g propanol. blocks sympathetic action of heart. decreases upstroke and slows conduction of AVN.
what are beta blockers
prevent supraventricular tachycardia by slowing conduction of AVN. used after MI BUT usually causes increased sympathetic activity = increased chance chance of arrhythmia. slower heart reduces o2 demand beneficial after MI
drugs that block potassium channels
prolongs AP - prevents another AP in theory but actually if too long increases chance of arrhythmia
what is amiodarone
a drug that blocks potassium channels. not very selective = makes it better and blocks lots of other channels. treats tachycardia by prolonging AP and preventing arrhythmia after MI. don’t know why this is better than selective ones
function of calcium channel blockers
eg verapamil and ditazem. decreases force of contraction= less chance of arrhythmia BUT actually may increase risk. (they are non-dihydropyridine meaning they are calcium blockers acting in the heart)
