G26i: Relate the surface ECG to the events of the cardiac cycle

ECG

P wave (~0.1 sec): wave of depol. spreading from SA Node throughout atria

PR segment (0.12 – 0.2sec): isoelectric interval between end of P wave and start of QRS

PR interval (<0.12 sec): time from atrial depol → ventricular depol <0.12 sec

QRS complex (<0.12 sec): ventricular depolarisation

ST segment (<0.15 sec): isoelectric period end of S wave → start of T wave. Entire ventricle has been depolarised. Plateau phase of AP

T wave: ventricular repolarisation

QT interval: beginning of Q wave → end of T wave. Entire ventricular depol & repolarisation. 200 – 400 millisecs depending on HR, ↑HR, shorter PA, ↓QT

PR interval (<0.12 secs)

  • Beginning of P wave → beginning of R wave
  • Atrial contraction & conduction through AV node
  • Conduction in SA & AV node depend on Ca2+ entry during Ph0
  • Cardiac activity also controlled by ANS

DIGOXIN

  • Blocks Na/K/ATPase
  • Directly ↑vagal activity which augments AV node slowing
  • → ↑PR interval

β-Blockers

  • Competitively inhibits β receptors
  • ↓AV node conduction
  • ↑PR interval

Adenosine

  • Stimulates adenosine sensitive K channels
  • ↑K conductance
  • ∴hyperpolarises supraventricular myocytes
  • Inhibition of AV conduction
  • ↑PR interval

Amiodarone

  • Anti-adrenergic
  • Non-competitive block of α & β receptors
  • ↓HR & ↓AV conduction
  • ↑PR interval

QRS Complex (<0.12 secs)

  • Ventricular depolarisation (from Bundle of His)
  • Atrial & ventricular myocardial contraction and conduction through His-Purkinje system depends on Na+ entry via Fast Na channel in Ph0

Amiodarone

  • Na+ channel blockade
  • ↓slope Ph0
  • ↓amplitude AP
  • ↓conduction velocity ∴AP slower transmitted

especially through His-Purkinje & ventricles

  • ↑QRS

Class Ic Na+ channel blockers i.e. flecainide

  • Inhibit Fast Na+ channels
  • ↓rate of rise of AP esp. in His-Purkinje

Class Ia Na+ channel blockers i.e. procainamide = ↑QRS

QT Interval

  • Period from first depol → ventricular repolarisation

Outward K channel blockers

  • Blocking outward K+ channels prolongs AP
  • Delay of repolarisation causes myocyte to have less charge difference across its membrane
  • ∴resulting in activation of inward depol current (early after depol)
  • Danger of this is possible triggered activity which can progress to re-entry & polymorphic VT

NB: main ECG ∆ with K+ OUTWARD CHANNEL BLOCKADE = Prolonged QT

Antiarrythmics

  • Class Ia → flecainide
  • Class Ic → procainamide
  • Class III → amiodarone

Ψ Drugs

  • TCAs → amitryptline
  • SSRI → venlafaxine
  • Antipsychotics
    • Haloperidol
    • Quetiapine
    • Droperidol
    • Risperidone

Antimicrobials

  • Ciprofloxacin
  • Clarithromycin
  • Erythromycin

Toxins

  • Organophosphates