Arrhythmias

This page is included because the curriculum asks specifically for knowledge of the 'electrophysiological basis of arrhythmias'.

Relevant pages from elsewhere include those on bradycardia & tachycardia.

There are separate pages concerning arrhythmia in pregnancy and arrhythmia following cardiac surgery.

One may wish to brush up on some Primary FRCA cardiac action potential physiology...

Resources

Perioperative arrhythmias are common, albeit usually transient and often require no (significant) intervention

Patient factors	Anaesthetic factors	Physiological factors	Surgical factors
↑ Age	Cardiac depression → reflex sympathetic activation	Hypoxia \| hypercarbia	Pain
Existing coronary or cardiac disease HTN, IHD, CM, congenital cardiac dx	CVC/PA catheter	Hypovolaemia	Trauma
Respiratory disease e.g. OSA, COPD, pulmonary HTN	Excessive stimulation e.g. laryngoscopy	Electrolyte disturbance esp. K⁺, Ca²⁺ & Mg²⁺	Mediastinal manipulation
Endocrine: ↑T₄, ↓T₄, phaeo	Light planes of anaesthesia/inadequate analgesia	Hypo-/hyper-thermia	Infection
Malignancy	Drugs: volatile agents, ketamine, inotropes, suxamethonium, β-blockers	Hypo-/hyper-glycaemia	'SIRS'
Drugs: alcohol, caffeine, recreational	LA toxicity	Perioperative MI	Anaemia
Intracranial pathology e.g. SAH, raised ICP		Post-operative pulmonary complications

Arrhythmias are, in general, caused by disturbance of cardiac action potential generation and/or conduction
Bradyarrhythmias typically arise due to:

Enhanced automaticity

This refers to a steeper (shorter) slope of phase 4 of the pacemaker cell action potential, lowering the threshold potential
The net effect is an increase in the pacemaker rate, and thus the heart rate

'Normal' enhanced automaticity refers to sinus tachycardia i.e. arising at the SA node, e.g. due to sympathetic stimulation, vagolytic stimuli, or hypokalaemia

Typically in areas of myocyte injury, which leaves the cells with a partially depolarised membrane (-60 to -40mV)
These cells have an increased tendency to spontaneously depolarise, causing atrial ectopic beats

Triggered automaticity

Describes generation of a premature action potential prior to completion of the previous one
These 'after-depolarisations' can be categorised as delayed (DAD) or early (EAD)

DADs occur during the early stage of phase 4 of the normal action potential due to intracellular calcium overload

Example pathologies include myocardial ischaemia, adrenergic stimulation or digoxin toxicity
Excess intracellular calcium triggers the 3Na⁺/Ca²⁺ exchanger, with electrogenic inflow of sodium leading to pacemaker-like activity

EADs occur during phase 3 of the normal action potential, thereby prolonging the action potential

Example pathologies include myocardial injury or K⁺ channel inhibitors e.g. amiodarone
They cause prolongation of the QT interval and may lead to torsade de pointes

Re-entrant movements

Arises in regions of functional (e.g. post-MI) or structural (e.g. WPW) conduction delays
This leads to a unidirectional block i.e. an action potential cannot propagate through the affected region due to ongoing inactivation of Na⁺ channels in the area
The action potential therefore enters the diseases area from downstream, leading to retrograde conduction
These areas of non-uniform rates of conduction/refractory periods within a ring of excitable tissue lead to a self-sustaining circus movement
If there are multiple re-entry circuits, one is at risk of either AF or VF