Pharmacology - Heart Flashcards
Explain the conduction pathway in the heart
SA Node excitation
AV Node excitation
HIS Bundle and Branches
Purkinje Fibres
What does each part of an ECG mean?
P Wave –> Depolarisation of the atria
QRS Complex –> Depolarisation of the ventricles
T Wave –> Repolarisation of the ventricles
Why can the pacemaker of the heart undergo spontaneous depolarisation?
Because its 4th phase has no true baseline (creaps upwards)
This is due to sodium influx via hyperpolarisation-activated, cAMP-gated, non-selective channels (funny channel)
What occurs at the 4 (5) phases of the Cardiac Action Potential?
Phase 0 –> Rapid depolarisation
Due to rapid sodium influx via voltage-activated Na+ channels
Phase 1 –> Rapid repolarisation
Phase 2 –> Plateau
Due to slow Ca2+ influx via L-type channels, and efflux via K+ channels (both voltage-gated)
Phase 3 –> Repolarisation
Due to increased K+ efflux via voltage-gated K+ channels
Phase 4 –> Stable baseline
What’s the difference between an Absolute and an Relative refractory period?
Absolute/Effective –> When a second AP isn’t possible regardless of the strength of the stimuli (as phase 0 can’t be reached)
Relative –> If a very strong stimulus is created, then a second AP can be caused
How is the if ‘funny’ channel modulated?
And what drug inhibits it?
Stimulates –> Sympathetic NS via B1/2 receptors
Inhibits –> Parasympathetic (vagus nerve) NS via M2 receptors
Ivabradine
What are Channelopathies?
Cardiac ion channel genetic diseases
What are the classifications and types of Cardiac Arrhythmias?
Site of Origin in the Heart
Supraventricular (SAN/AVN/Atria)
Ventricular (HIS Bundles/Purkinje Fibres/Ventricles)
Effect on the Heart Rate
Bradycardia (below 60bpm)
Tachycardia/arrhythmia (above 100bpm)
Effect on the Heart Rhythm
Regular
Irregular
The type of QRS complex
Narrow
Broad (>120ms in duration of the ECG)
What can cause Cardiac Arrhythmias?
Existing heart diseases/myocardial iscaemia
Drugs –> eg, digoxin
Electrolyte disturbances (K+/Ca2+)
Hyper/hypothyroidism
Phenocrymocytoma (increased circulating catecholamines)
Genetic disorders –> eg, channelopathies
What different parts of the heart do Rate controlling and Rhythm controlling drugs act on?
Rate Controlling –> The Pacemaker AP
Rhythm Controlling –> The Cardiac AP
What is the Vaughan Williams Classification of antiarrhythimic drugs?
Class 1 –> Sodium channel blockers (preventing depolarisation….phase 0)
Class 2 –> Beta-Blockers (inhibits phase 2 and 4)
Class 3 –> Drugs that prolong the AP duration (inhibits repolarisation…..phase 3)
Class 4 –> Calcium Channel Blockers (inhibit the plateau….phase 2)
Explain Class I antiarrhythmic drugs
Sodium channel blockers –> so slow down depolarisation (phase 0)….and so the cardiac AP and AP conduction
There are 3 different types
1a (Disopyramide) –> Intermediate dissociation rate
Also block K+ channels, so prolong the QT interval (phase 3)
1b (Lidocaine) –> Fast dissociation rate
1c (Flecanide)–> Slow dissociation rate
How do Beta-Blockers (Class II) work?
Block B1-adrenoceptors
Slow conduction of at the AV node
How do class III drugs, like amiodarone, work?
Block voltage-activated K+ channels, preventing repolarisation in phase 3
So they prolong the duration of the cardiac AP and the QT interval –> Increasing the refractory period….so slowing the HR
Also blocks Na+, Ca2+ channels
Decreases expression of B1-adrenoceptors
A modest A-adrenergic receptor antagonist
What Beta-Blocker is also a Class III drug?
Sotalol