Arrhythmias and CVS drugs Flashcards
define supraventricular tachycardia.
Tachycardia originating at or above the atrioventricular (AV) node ( AVN, SAN, atrium). Includes conditions like atrial fibrillation. *narrow irregularly irregular QRS.
what could cause tachycardia?
- ectopic pacemakers due to damaged myocardium depolarisation, latent pacemaker activated due to ischaemia and dominated over SAN.
- afterdepolarisations : abnormal depolarisations.
- atrial flutter/ fibrillations.
- conduction delays.
what could cause bradycardia?
- sinus bradycardia : intrinsic SAN dysfunction.
- extrinsic factors like drugs ( beta blockers )
- conduction block at AVN or bundle of HIS.
- conduction problems due to extrinsic factors like drugs ( beta blockers ).
differentiate between the impact of early after-depolarisations and delayed after-depolarisations.
- early can lead to oscillations, more likely to happen if AP prolonged, longer AP = longer QT. more time for inactive calcium channels to recover.
- another fired before repolarised.
- delayed can trigger activity, self-perpetuating causing oscillations. more likely if calcium high involving Na/Ca exchanger.
- faster depolarization.
how does the re-entrant mechanism generate arrhythmias?
- due to blocks in conduction the excitation takes long route to spread the wrong way through damaged myocardium, setting up a circus of excitation.
- eg : multiple re-entry loops in atrium leads to A-fib.
: fast and slow pathways in AVN create re-entry loop at supra-ventricular tachycardia.
: accessory pathway between atria and ventricles such as in Wolff-parkinson-white syndrome
what type of drugs are used to treat arrhythmias?
ON PAPER NOTES
- voltage sensitive sodium channel blockers.
- Beta adrenoreceptor antagonists.
- potassium channel blockers.
- calcium channel blockers.
describe the use and effect of IV lidocaine.
- used following an MI incase of ventricular tachycardia.
- effect : mild Na+ channel block, slows upstroke of depolarisation, shorten AP and slows conduction velocity.
- not used as much anymore
why would beta adrenoreceptor blockers be useful to treat supra-ventricular tachycardia post MI?
- MI usually increases sympathetic activity of heart causing arrhythmias so beta blockers help reduce that and prevent ventricular arrhythmia’s.
- reduces O2 demand as sympathetic effects like HR, contractility reduced so risk of ischaemia less.
K+ channel blockers prolong AP and can have pro-arrhythmic effects. one exception is Amiodarone. explain why.
- has other effects. slope phase of upstroke slowed down similar to Na+ blockers, beta blocking effect, weak calcium channel blocking effect and vasodilation.
- effective for suppressing ventricular arrhythmias post MI.
give examples for each drug type.
- Na+ blockers : Lidocaine.
- B-adreno blockers : propranolol, atenolol (more selective).
- K+ blockers : Amiodarone.
- Ca2+ blockers : Verapramil.
how does adenosine work?
- IV administration acts on A1 receptors at AVN and enhances K+ conductance and hyperpolarises cells on conducting tissue.
- Anti-arrhythmatic.
why are ACEi important in treatment of heart failure?
- reduces work load of heart by reducing preload, afterload.
- side effect may include dry cough as ACE breaks down bradykinin and it is inhibited.
- important in hypertension too.
what drug would be given for patients who cannot tolerate ACEi?
- Losartan which is an angiotensin II receptor blocker.
- used to treat hypertension and heart failure.
how might diuretics be useful in heart failure medication?
- especially loop diuretics prevent NA+ retention so more water is lost.
- reduces pulmonary and peripheral oedema.
calcium channel blockers act to reduce workload for heart by acting on heart itself or vasculature. how does this work?
- acting on vasculature to reduce peripheral resistance, lower arterial pressure, and workload by reducing afterload.
- verapamil acts on heart to reduce contraction by blocking calcium channels.
