Antiarrhythmic drugs and anaesthesia Flashcards
Cardiac conduction system
SA node: impulse generator, 60-100bpm, travels through the LA & RA ->
AV Node: Provides a delay to conduction of approx 0.15secs allowing the atria to fill the ventricles with blood ->
His-Purkinje fibres: Rapid depolarisation throughout both ventricles causing ejection from the ventricles
SA and AV Node Action Potentials
4- If channels allow Na and K into the cell at a constant rate slowly increasing the resting membrane potential.
0- At -50mV T-type Ca channels open and Ca influx raises the membrane potential to the threshold potential opening L-type Ca channels and causing a rapid rise in membrane potential
3- Ca channels close and K channels open allowing K efflux and restoration of resting membrane potential
Myocyte Action Potential
4 - Resting membrane potential maintained at -85mV by the Na/K ATPase pump
0 - At the threshold potential voltage-gated Na channels open and there is a rapid influx of Na leading to a membrane depolarised at +30mV. At this mV the Na channels close and enter an inactivated state.
1 - Outward K channels open and K effluxes from the cell forming a notch in the action potential
2 - The membrane potential plateaus when L-type Ca channels open allowing calcium influx and therefore Ca moves into the cell as K moves out
3 - Ca channels decline and close and K moves out restoring the resting membrane potential.
In phase 2 a strong enough repeat action potential can force sodium channels to open again prematurely creating a new action potential
Bradyarrhythmia pathogenesis
Failure of impulse generation of the SA node or failure of propagation at the AV node or His-Purkinje fibres.
Tachyarrhythmia pathogenesis
Enhanced automaticity
- normal automaticity is sympathetic stimulation, mechanical stretch or hypokalaemia stimulation of the SA node to increase the slope of depolarisation at phase 4
- enhanced automaticity occurs when myocardial cells are injured and the resting membrane potential sits at -60 to -40mV increasing the likelihood of ectopic action potential generation.
Triggered automaticity
- occurs when a premature action potential occurs before the previous action potential is complete
- Seen as delayed: MI, hypercalcaemia, digoxin toxicity, adrenergic stimulation
- Or early: Long QT syndromes and MI
Re-entry
- Occurs when areas of normal conduction become diseased or there is an accessory pathway overriding the AV node delay
- The diseased area does not respond to the action potential as Na channels are still inactivated, they then get propagated downstream later causing a loop effect as the action potential now propogates in the wrong direction
Patient-related risk factors for developing arrhythmias in the perioperative period
- Increased sympathetic activity: sepsis, laryngoscopy, hypoxia, pain
- Severe bradycardia: can lead to triggered automaticity arrhythmias developing
- Myocardial ischaemia
- Electrolyte disturbances: K <3.5 or >6, Ca <1.17 or >1.4 (ionised) and Mg <0.74 or >4
- Metabolic and respiratory abnormalities
Pharmacological-related risk factors for developing arrhythmias in the perioperative period
- IV induction agents: reduce sympathetic tone leading to bradycardia and risk of ectopic arrhythmia generation
- Ketamine: increase in sympathetic tone and prolongation of QT
- Opioids: especially remifentanil will cause a bradycardia
- Anticholinesterases: Stimulate muscarinic ACh receptors causing a bradycardia and AV nodal delay
- Vasoconstrictors: stimulate the baroreceptor and cause a bradycardia
Indications for starting an anti-arrhythmic drug
- Alleviation of symptoms
- Improve cardiac function as a result of tachycardia
- Prevent progression to life-threatening arrhythmias
- Reduce the need for electrical cardioversion
Modified Vaughn Williams Classification of Antiarrhythmic Drugs
Class 0
- If channel modulators
- Ivabradine
- Used for rate control in tachycardia
Class 1
- Voltage-gated Na channel blockers can be split into a, b and c (intermediate, fast and slow dissociation kinetics)
- a: quinidine : SVT, AF, VT/VF
- b: lidocaine, phenytoin: VT after MI
- c: Flecainide: AF and atrial flutter
Class 2
- Autonomic modulators, either…
- B-adrenergic blockers: propranolol (Non-selective), metoprolol (selective)
- Muscarinic blockers: atropine and glycopyrrolate
- Muscarinic activators: digoxin
- A1 receptor activators: adenosine
Class 3
- K channel blockers
- Soltalol, amiodarone
Class 4
- L-type calcium channel blockers
- Verapamil and diltiazem
Class 5 & Class 6- no drugs available clinically, effect gap junctions and mechanosensitive channel blockers
Class 7
- Upstream target modulators
- Ace inhibitors and ATII receptor blockers
Treatment options for haemodynamically unstable bradyarrhythmia in the perioperative period
- Atropine 600mcg bolus up to 3mg
- Glycopyrrolate 200-600mcg bolus
- Dopamine infusion
- Adrenaline infusionn
- Transcutaneous pacing
Treatment options for haemodynamically unstable tachyarrhythmia in the perioperative period
- Synchronised DCCV up to 3x shocks
- Amiodarone 300mg over 10 mins and 900mg over 23 hrs
Treatment options for haemodynamically stable bradyarrhythmia in the perioperative period
- Monitor
- Consider need to pace
Treatment options for haemodynamically stable broad complex tachyarrhythmia in the perioperative period
Irregular Rhythm (Torsarde)
- Magnesium
Regular Rhythm (Pulsed VT)
- Amiodarone 300mg over 10 mins and 900mg over 23 hrs
- Lidocaine 2mg/kg bolus followed by 1-4mg/min
- DCCV x3
Treatment options for haemodynamically stable narrow complex tachyarrhythmia in the perioperative period
Regular Rhythm (SVT)
- Adenosine 6mg, 12mg
- B-blocker or amiodarone
Irregular Rhythm (AF or flutter)
- Amiodarone
- B-blocker metoprolol 1-5mg
- Digoxin 0.25-0.5mg
