Phase i vs phase ii block

6 min read Last updated April 8, 2026

How to recognise Phase I vs Phase II at the bedside (nerve stimulator)

  • Use a peripheral nerve stimulator early if suxamethonium effect seems prolonged or atypical.
  • Phase I (depolarising) pattern: reduced twitch height with preserved TOF ratio (no fade).
    • TOF: all four twitches reduced similarly; TOF ratio ~1 (despite low absolute twitch).
    • Tetanic stimulation: no significant fade; may see post-tetanic potentiation is absent/minimal.
  • Phase II (desensitisation) pattern: fade appears (resembles non-depolarising block).
    • TOF: T4/T1 reduced (TOF ratio <0.9), often with marked fade.
    • Tetanic stimulation: fade present; post-tetanic facilitation may be seen.
  • Clinical clue: prolonged suxamethonium exposure (large dose/infusion) increases likelihood of Phase II features.

Immediate management implications

  • If paralysis persists: ensure adequate sedation/anaesthesia, ventilate, and reassess with nerve stimulator.
  • Do not assume Phase II is reliably reversible; consider cautious anticholinesterase only if clear Phase II pattern and recovery has begun.
    • Anticholinesterase can worsen Phase I block (by increasing ACh at endplate and inhibiting plasma cholinesterase → prolonging sux metabolism).
  • If prolonged block after a single intubating dose: consider pseudocholinesterase deficiency (quantitative/qualitative) rather than Phase II.

Definitions

  • Phase I block: depolarising neuromuscular block produced by suxamethonium causing persistent endplate depolarisation and inactivation of voltage-gated Na+ channels → failure of propagation of action potentials.
  • Phase II block: block that develops after prolonged exposure to suxamethonium; endplate repolarises but transmission fails due to receptor/ion channel changes (desensitisation) and behaves like a non-depolarising block on monitoring (fade).

Mechanistic comparison (what to say in a viva)

  • Phase I: sux acts as an acetylcholine receptor agonist → opens nicotinic ACh receptor channel → depolarisation; sustained depolarisation prevents recovery of voltage-gated Na+ channels → flaccid paralysis after initial fasciculations.
  • Phase II: with continued exposure, the endplate becomes less responsive to ACh (desensitised) and/or channel function changes; membrane repolarises but neuromuscular transmission shows fade due to impaired safety margin and presynaptic effects.
  • Key concept: Phase II is not simply 'more Phase I'—it is a qualitatively different pattern with fade and partial reversibility characteristics.

Triggers and risk factors for Phase II features

  • Most commonly associated with: large cumulative doses or infusion of suxamethonium (e.g., historically for ECT or long procedures).
  • Other contributors: prolonged exposure in the presence of reduced clearance (e.g., pseudocholinesterase deficiency) may complicate the picture; however, deficiency classically causes prolonged Phase I-type block after a single dose.

Neuromuscular monitoring patterns (high-yield table in words)

  • Train-of-four (TOF): Phase I = no fade (T4/T1 ~1); Phase II = fade (T4/T1 reduced).
  • Tetanic stimulation: Phase I = sustained response; Phase II = tetanic fade.
  • Post-tetanic count/facilitation: Phase I = minimal/absent; Phase II = may show facilitation (like non-depolarising).

Effect of anticholinesterases (neostigmine/edrophonium)

  • Phase I: anticholinesterases tend to prolong/intensify block.
    • Mechanisms: increased ACh at the endplate augments depolarisation; inhibition of plasma cholinesterase reduces sux metabolism.
  • Phase II: may show partial reversal with anticholinesterase, but response is variable and should be guided by monitoring and clinical recovery.
    • Practical: only consider if clear fade consistent with Phase II and there is evidence of spontaneous recovery; otherwise continue ventilation and sedation.

Clinical relevance and common exam link-ins

  • Prolonged apnoea after suxamethonium: differentiate pseudocholinesterase deficiency (prolonged duration) from Phase II block (usually after prolonged administration).
  • Monitoring: Phase I may look like 'deep block' if you only consider twitch height; TOF ratio is key to identifying fade.
  • Management: supportive ventilation and sedation are definitive; pharmacological reversal is secondary and pattern-dependent.
You give suxamethonium for RSI. The patient remains apnoeic at 15–20 minutes. How do you approach this problem and what are your differentials?

Structure your answer into immediate management, assessment/monitoring, and likely causes.

  • Immediate: maintain oxygenation/ventilation, ensure adequate anaesthesia/sedation, protect airway, and check haemodynamics/temperature.
  • Assess: peripheral nerve stimulator (TOF/tetanus), review drugs given (opioids, hypnotics, magnesium, antibiotics), check acid–base/electrolytes (K+, Ca2+, Mg2+), temperature.
  • Differentials: pseudocholinesterase deficiency (most likely after single dose), drug interactions potentiating weakness, hypothermia, severe metabolic disturbance; Phase II block is less likely after a single intubating dose.
  • If pseudocholinesterase deficiency suspected: continue ventilation/sedation; send blood for cholinesterase activity and dibucaine number (later confirmation).
Describe the differences between Phase I and Phase II block produced by suxamethonium, including nerve stimulator findings.
  • Phase I: depolarising block; fasciculations then flaccid paralysis; TOF shows no fade (T4/T1 ~1) though twitch height reduced; tetanus sustained.
  • Phase II: desensitisation-type block after prolonged exposure; behaves like non-depolarising block; TOF fade (T4/T1 reduced), tetanic fade, possible post-tetanic facilitation.
  • Anticholinesterase response: Phase I worsens/prolongs; Phase II may partially reverse (unreliable).
Why do anticholinesterases prolong Phase I block?
  • They increase acetylcholine at the neuromuscular junction, which augments depolarisation at nicotinic receptors when sux is present.
  • They inhibit plasma cholinesterase, reducing suxamethonium hydrolysis and prolonging its effect.
A patient has received a suxamethonium infusion and now shows TOF fade. What does this suggest and what are your options?
  • TOF fade after prolonged sux exposure suggests Phase II characteristics (non-depolarising-like).
  • Stop suxamethonium; maintain ventilation and sedation; monitor recovery with quantitative NM monitoring if available.
  • Consider cautious neostigmine only if there is clear evidence of Phase II pattern and spontaneous recovery; be prepared for incomplete reversal and continued ventilation.
How would you explain 'fade' physiologically in Phase II block?
  • Fade reflects reduced ability to sustain neuromuscular transmission during repetitive stimulation due to reduced safety margin and impaired mobilization/release of ACh (presynaptic contribution) plus postsynaptic receptor/channel changes.
  • This is why Phase II resembles non-depolarising block on TOF and tetanus.
What is the relationship between pseudocholinesterase deficiency and Phase I/Phase II block?
  • Pseudocholinesterase deficiency reduces suxamethonium metabolism, prolonging its action; classically this presents as prolonged Phase I-type depolarising block after a single dose.
  • Phase II features are more associated with prolonged exposure/cumulative dosing; deficiency may increase exposure time but the key clinical exam point is: single-dose prolonged apnoea → think cholinesterase problem first.
How can you distinguish deep Phase I block from Phase II block if both show small twitch responses?
  • Look at TOF ratio and fade rather than absolute twitch height: Phase I has no fade (ratio preserved), Phase II has fade (ratio reduced).
  • Use tetanus/post-tetanic responses: Phase II tends to show tetanic fade and post-tetanic facilitation.
Give a concise comparison of Phase I vs Phase II block suitable for a 60-second viva answer.
  • Phase I: depolarising; fasciculations; reduced twitch height but no TOF/tetanic fade; anticholinesterases prolong.
  • Phase II: after prolonged exposure; desensitisation-type; TOF and tetanic fade with possible post-tetanic facilitation; may be partially reversible with anticholinesterase but unpredictable.
What practical errors can occur if you misinterpret Phase I block as non-depolarising block?
  • Giving neostigmine during Phase I may prolong paralysis and delay recovery.
  • Assuming fade is present without measuring TOF ratio can lead to incorrect diagnosis and management; always use objective monitoring where possible.

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