- Rate >100
- Causes
- Anaemia
- Anxiety
- Exercise
- Pain
- Sepsis
- Hypovolaemia
- Heart failure
- Pulmonary embolism
- Pregnancy
- Thyrotoxicosis
- Beri beri
- CO2 retention
- Autonomic neuropathy
- Sympathomimetics e.g. caffeine, adrenaline, and nicotine
Sinus bradycardia
- Rate <60
- Causes
- Physical fitness
- Vasovagal attacks
- Sick sinus syndrome
- Acute MI (inferior most likely)
- Hypothyroidism
- Hypothermia
- Increased intracranial pressure
- Cholestasis
- Drugs e.g. Beta blockers, digoxin, amiodarone, verapamil
AF
- Causes
- IHD
- Thyrotoxicosis
- Hypertension
1st and 2nd degree (Mobitz I/II) heart block
- Causes
- Normal variant
- Athletes
- Sick sinus syndrome
- IHD
- Acute carditis
- Drugs (digoxin, Beta-blockers)
3rd degree complete heart block
- Causes
- Idiopathic (fibrosis)
- Congenital
- IHD
- Aortic valve calcification
- Cardiac surgery/trauma
- Digoxin toxicity
- Infiltration (abscesses, granulomas, tumours, parasites)
Q waves
- Pathological Q waves are usually >0.04s wide and >2mm deep
- Causes
- Infarction
- Acute MI
ST elevation
- Causes
- Normal variant (high take-off)
- Acute MI
- Prinzmetal's angina
- Acute pericarditis (saddle-shaped)
- Left ventricular aneurysm
ST depression
- Causes
- Normal variant (upward sloping)
- Digoxin (downward sloping)
- Ischaemic (horizontal)
- Angina
- Acute posterior MI
T inversion
- V1-V3
- Normal (Blacks and children)
- Right bundle branch block (RBBB)
- Pulmonary embolism
- V2-V5
- Subendocardial MI
- HCM
- Subarachnoid haemorrhage
- Lithium
- V4-V6 and aVL
- Ischaemia
- LVH
- Left bundle branch block (LBBB)
- Within hours, the T wave may become peaked and ST segments may begin to rise
- Within 24 hours, the T wave inverts, as ST segment elevation begins to resolve
- ST elevation rarely persists, unless a left ventricular aneurysm develops
- T wave inversion may or may not persist
- Within a few days, pathological Q waves begin to form
- Q waves usually persist, but may resolve in 10%
- The leads affected reflect the site of the infarct
- Inferior (II, III, aVF)
- Anteroseptal (V1-V4)
- Anterolateral (V4-V6, I, aVL)
- Posterior (V1-V2, tall R)
- Subendocardial (No Q waves, ST and T changes present)
Pulmonary embolism
- Sinus tachycardia is commonest
- There may be RAD, RBBB, right ventricular strain pattern (R-axis deviation, dominant R wave and T wave inversion/ST depression in V1 and V2, leads II, III and aVF may show similar changes)
- Rarely, the 'SIQIIITIII' pattern occurs: deep S waves in I, pathological Q waves in III, inverted T waves in III
Metabolic abnormalities
- 'Digoxin effect': ST depression and inverted T wave in V5-6 (reversed tick)
- In digoxin toxicity, ANY arrhythmia can occur (ventricular ectopics and nodal bradycardia are common)
- Hyperkalaemia: Tall, tented T wave, widened QRS, absent P waves, 'sine wave' appearance
- Hypokalaemia: Small T waves, prominent U waves
- Hypercalcaemia: Short QT interval
- Hypocalcaemia: Long QT interval, small T waves
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