Monday 27 August 2012

ECG abnormalities

Sinus tachycardia

  • 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)
Myocardial infarction
  • 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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