- Arrhythmias arise from disturbances of impulse generation, conduction, or both
Structurally normal heart
- Haemodynamic: ↑ blood volume, HR and stroke volume, with physiological LVH, stretch the myocytes
- Causes early afterdepolarisations, a shortened refractory period and slowed conduction
- Hormonal: oestrogen and progesterone are proarrhythmic
- Oestrogen ↑ L-type calcium channel expression in the SA node, accelerating pacemaker depolarisation and HR
- ↑ automaticity and adrenergic responsiveness
- Autonomic: ↑ sympathetic activity, particularly during labour and delivery
- Pharmacokinetic: ↑ volume of distribution, altered protein binding and ↑ renal clearance may cause subtherapeutic antiarrhythmic levels
Other causes
- Structural heart disease: congenital (particularly scar-related after Fontan, Mustard/Senning or ToF repair), valvular, ischaemic, cardiomyopathy including PPCM
- Inherited channelopathies: long QT, Brugada, CPVT
- Accessory pathways e.g. WPW
- Triggers: electrolyte disturbance (K+, Mg2+), sepsis, thromboembolism, thyroid disease, OSA, obesity, drugs (alcohol, cocaine, amphetamines)
ECG changes in normal pregnancy
- Sinus tachycardia
- Shortened PR, QRS and QT intervals
- Left axis deviation (15-20°) from diaphragmatic elevation
- Small Q waves and T wave inversion in the inferior leads and V1-3
- Atrial and ventricular ectopics
- There is no upper limit of normal HR in pregnancy, but a resting HR of 100-115/min or more may warrant investigation