Lecture 13 Flashcards
Causes of tachycardia
Ectopic beats - ischaemic muscle spontaneously depolarises
-AVN more dominant
After depolarisations - abnormal depolarisation after AP
Atrial fibrillation
Re - entry loop - Conduction delay and accessory pathway
Causes of Bradycardia
Sick sinus syndrome - intrinsic SAN dysfunction
- extrinsic factors e.g. drugs
Conduction block - AVN, Bundle of His defects
Delayed after depolarisations
Intracellular calcium conc increased
Reverses NCX
Ventricular tachycardia
Early after depolarisations
Long AP causing longer QT interval - longer repolarisation
Oscillations
Ventricular tachycardia
Multiple re-entrant circuits
Chaotic signals passed down AV node
Rapid atrial and ventricular impulses
Atrial fibrillation
Irregularly irregular rhythm
Ventricular pre-excitation
Accessory pathway between atria and ventricles - re entrant loop
Wolff - Parkinson white syndrome
Atrium depolarise early
Class I anti arrhythmic drugs
Sodium channel blocker
Lidocaine
Blocks open or inactivated sodium channels
More activity in damaged muscle less in normal - does not affect normal tissue
Blocks channel after depolarisation and then dissociates in time for next AP - preventing inappropriate AP firing
Class II anti arrhythmic drugs
Beta adrenoreceptor antagonists - beta blockers
Propanolol, atenolol
Block sympathetic activity
Beta 1 - decreases HR - decreases pacemaker slope
- slower AVN conduction
Used in:
post MI patients
Atrial fibrillation
Prevents supraventricular tachycardia
Class III- anti arrhythmic drugs
Block potassium channels
QT interval longer - repolarisation longer
Reality: early after depolarisations
Ventricular tachycardia
Na+ recover from inactivation
Amiodarone
Class III
Not very selective - acts on other channels
Treats:
Tachycardia associated Wolff - Parkinson white syndrome
Ventricular arrhythmia post MI
Class IV anti arrhythmic drugs
Block calcium channels
Decrease AP upstroke
Decreased AVN conductance
Decreased force of contraction - Negative inotropy
Adenosine
Acts on A1 receptors on AV node
Increases K+ conductance - delays successive APs
Very short half life
Prevents supraventricular tachycardia
Digoxin
Cardiac glycoside
Blocks Na+ pump
Build up of Na+ intracellularly
NCX reverses - build up of calcium intracellularly stored in SR
Increased force of contraction
Treatment of angina
Reduce work load of heart:
Nitrates - venodilation
B blockers - decrease HR
Class IV anti arrhythmic - calcium channel antagonists
Improve blood supply to heart:
Reperfusion
High risk conditions of thrombosis
Atrial fibrillation
Acute MI
Prosthetic valves
Left atrial appendages - common site
