CVS 4 - Arrhythmia Flashcards
SA and AV nodal cells
Phase 0- voltage gated Ca2+ channel opens due to depolarization
Phase 4- Slow depolization
spontaneous (automatic) pacemaker mostly due to Na+ influx until membrane potential reaches threshold to open calcium channels
Ventricular myocytes
Phase 2- K+ and Ca2+ channels open Ca2+ channels inactive with time
Phase 1- Na+ channels automatically inactivate
Phase 0- voltage gated Na+ channel opens
Phase 3
Ca2+ channel close K+ channels open cell repolarizes
Refractory period
refractory period between 0-2 where the channels are already open so another action potential cannot cause another contraction tot take place. However in phase 3 if another action potential arises and is sufficiently strong it can start further depolarisation
Why does arrhythmia occur? Several potential causes:
– M.I., – heart failure, – hyperthyroidism, – electrolyte abnormalities: hypokalaemia (speeds up SA phase 4), hypomagnesemia, alkalosis, acidosis – autonomic dysfunction, – drugs: eg β antagonists slow SA phase 4 – inherited mutation in ion channels, – fever
Cardiac tissue goes through a cycle
At rest -> Response -> Refractory period -> At rest….
• Different regions respond at different times (so the pump works)
• One region may be refractory while other can respond
• abnormality in:
– automaticity: site of origin of impulse, rate and regularity of pacemaker
– conduction of impulse
• leads to non-coordinated contraction
• Goal is to restore this by fixing electrical abnormalities
Arrhythmia: electrical defects
Defects in impulse from SA /AV node
• AV sets frequency if SA node slows -extra impulse when SA node does fire
• Alternatively AV node may fire too frequently- also creates extra impulse
Bypass
• Additional pathway bypassing AV node
Conduction block
Re-entry
• Common cause of tachyarrhythmia
Afterdepolarizations
• Normal action potential triggers additional oscillations
Classes of Arrhythmia
• Supraventricular
– origin is SA, AV nodes or atria
– sinus tachycardia/ bradycardia
» faster (>100 bpm)/slower (<60 bpm) than normal but regular beat
» altered SA firing
– atrial tachycardia (supraventicular tachycardia)
» atrial pacemaker other than SA node
– atrial flutter
» atrial rate 280-300 bpm but ventricle cant respond (AV node refractory period)
– atrial fibrillation
» re-entry impulses in atrium
• Ventricular
– origin is in ventricles
– Ventricular tachycardia
» normal atrial function
» Monomorphic – ventricular pacemaker causes additional systole
» Polymorphic – eg Torsades des pointes, caused by sustained early after depolarizations
– ventricular fibrillation
» re-entry impulses in ventricle.
» Fatal if untreated. Defibrillation essential
• Heart block
– pacemaker impulse delayed or fails to reach ventricles
Arrhythmia: pharmacological treatment goals
•Treatment goals – Restore normal cardiac rhythm – Prevent recurrence of arrhythmia – Prevent more severe arrhythmia – Deal with haemodynamic consequences
Vaughan Williams classification of anti-arrhythmic drugs
– Class I Na+ channel blockers
» reduce SA rate:
– Shift threshold to higher potential – Decrease slope phase 4
» decrease re-entry in contractile tissue – slow down phase 0 so refractory for longer
– Sub-classified:
» Ia bind open Na+ channel and also block K+ channels
» Ib bind open as well as refractory Na+ channel more effective at high rates » Ic not rate dependant
– Class II β adrenergic receptor antagonists
– Class III K+ channel blockers
– Class IV Ca2+ channel blockers
Pharmacologically induced arrhythmia
– All antiarrhythmic drugs can precipitate arrhythmia
– Many drugs which prolong QT → ↑ risk torsades des pointes (twisting the points)
– Several non-cardiac drugs can induce arrhythmia
Class Ia
Mechanism
Drug Example
- prolong action potential
• Mechanism
– Block Na+ channel- slow phase 0 →↓conduction velocity
– Block K+ -prolongs repolarization →↑refractory period
– prolongs QRS duration (ECG)
– Also cholinergic antagonist so blocks parasympathetic inhibition of AV node- faster AV conduction can cause increased ventricular rate in patients with atrial flutter
• Drugs
– disopyramide
Effects of cholinergic blockade
Blurred Vision, mydriasis - (pupillary constrictor muscle) Tachycardia – relief of P-ANS inhibition of SA and AV nodes Dry mouth – P-ANS promotes salivation
Constipation –P-ANS promotes GI motility
Dry skin, less sweating – P-ANS promotes these secretions
Disopyramide contraindication in heart failure
“additive” ↓cardiac output
Class Ib
Mechanism
Drug example
- shorten action potential
• Mechanism
– Na+ channel block, although relatively weak (fast dissociation)
– Advantage – most effective on frequently depolarizing tissue
– Bind both open and refractory channel
• Drugs
– Lidocaine