Phase i vs phase ii block

6 min read Last updated April 9, 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 &lt,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 &#039,more Phase I&#039,—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.
  • Prolonged apnoea after suxamethonium: differentiate pseudocholinesterase deficiency (prolonged duration) from Phase II block (usually after prolonged administration).
  • Monitoring: Phase I may look like &#039,deep block&#039, 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.

Test yourself…

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 &#039,fade&#039, 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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