Lecture 5.5: Drugs affecting arrhythmias Flashcards
What is the effect of atropine? What kind of a drug is it?
Atropine is a muscarinic receptor antagonist of the parasympathetic nervous system. Blocking it results in a faster heart rate.
True or false? PNS provides a basal level of activity to keep heart rate low.
True.
What is the effect of propranolol? What kind of a drug is it?
Propranolol is a beta adrenoceptor antagonist of the sympathetic nervous system. Blocking it results in a slower heart rate.
SA/AV node pacemaker has how many phases? What are they?
3 phases. Phase 0 - Depolarisation (Ca2+ in) Phase 3 - Repolarisation (K+ out) Phase 4 - Spontaneous depolarisation (ifunny) - calcium.
What is the mechanism of effect of acetylcholine on SA/AV nodes?
Via muscarinic (M2) GPCR, decrease cAMP, open K+ channels. Results in hyperpolarisation. Decreases HR.
What is the mechanism of effect of NA on SA nodes?
NA via B1-adrenoceptors (GPCR) increase cAMP, opens Ca2+ channels. Ca2+ entry increased slope of phase 4 depolarisation. Thereby increasing rate of firing (SA node) and more rapid conduction (AV node). This can however, trigger dysrhythmias.
What are the phases of Ventricular action?
Phase 0 - Depolarisation with Na going in. Phase 1 - Rapid repolarisation K+ efflux. Phase 2 - Plateau Ca2+ influx. Phase 3 - Repolarisation K+ efflux Phase 4 - Stable membrane potential.
What are the clinical signs of dysrhythmias?
SOB, fluttering, palpitations, fainting, fatigue, chest pain.
Briefly describe the mechanism of dysrhythmias.
Altered impulse formation leads to the pacemaker cells’ automaticity. Altered impulse conduction results in conduction block so ventricles beat at their own rate around 30-40bpm. (AV node speed).
Triggered activity such as early/late after depolarisations, due to excess sympathetic activity.
What are the 4 major classes of antiarrhythmics?
- Sodium channel blockers.
- B-adrenoceptor antagonism.
- K+ channel blockade.
- Ca2+ channel blockade.
Briefly go through type 1 drugs.
Sodium channel blockers reduce phase 0 slope and peak of ventricular AP. An example is lignocaine, which also happens to be an anaesthetic with a small therapeutic window.
Briefly go through type 2 drugs.
Decreases rate and conduction (SA node). Inhibits sympathetic influence on heart, stabilising membrane in purkinje fibres, hard to excite.
Adverse effects include bradycardia, fatigue, hypotension. Also bronchoconstriction, so is contraindicated in asthmatics. Also can’t be used for diabetics, as hypoglycaemia is a problem.
Briefly go through type 3 drugs.
K+ channel blockade delays phase 3 of ventricular action potential. It essentially prolongs the cardiac action potential, and slows down phase 3 repolarisations.
It is particularly useful for ventricular arrhythmias where there is muscle damage and possibly also backward conduction as it decreases re-entry.
Amioradone is an example, but it does more than just class 3 stuff, also can blocks NA and B adrenoceptors, thereby acting as class 1,2.
Adverse side effects unique to amiodarone include reversible photosensitisation, skin discolouration, hypothyroidism and pulmonary fibrosis (long term).
Briefly go through type 4 drugs.
Ca2+ channel blockade. Most effective at SA and AV nodes, reduces rate and conduction.
Cardio selective Ca2+ blockers. Verapamil is an example.
Acts preferentially on SA and AV nodal tissue, prevents atrial tachycardias.
Slows down conduction velocity, increases refractory period.
Adverse effects include flush, peripheral oedema, dizziness, bradycardia, headache, nausea.
