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CD
DR. CHINTAN
DAVE
CLINICAL EP 25
BEDSIDE PHYSIOLOGY
CASE CHALLENGE - 61F, THREE DAYS OF DYSPNEA
Would you
intubate her?
Lungs clear. Chest Xray clean. She is saturating
97% and she cannot hold her head off the pillow.
SpO2 97%
pCO2 58
FVC 1.1 L
NIF -24
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DR. CHINTAN
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WHAT THE BEDSIDE GAVE YOU
Six findings, none of them
pulmonary
VOICE
Soft, fading through the
afternoon
EYES
Heavy lids, diplopia by
evening
COUNT TEST
Reaches 12 in a single
breath
SWALLOW
Coughs on water, repeated
choking
NECK
Head off the pillow < 3
SECONDS
TIMING
"She always looks worse at
night"
Chest exam is clear. CXR shows only low lung
volumes. VBG: pH 7.31, pCO2 58.
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ANSWER - D
Myasthenic crisis
Impending neuromuscular respiratory failure
- a clinical diagnosis, not a test result.
01 Fatigable ptosis and diplopia, worse at night
02 Bulbar failure: choking, weak voice, secretions
03 pCO2 58 behind a normal pulse oximeter
04 Ciprofloxacin and magnesium, both triggers
05 Neurology referral pending for droopy eyelids
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DR. CHINTAN
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THE PHYSIOLOGY
Ventilation fails first
Oxygenation is a membrane problem. Her membrane
is fine.
Ventilation is a muscle problem. Her muscles are
failing.
So CO2 rises for hours while the sat reads 97%.
Hypoxemia is the last thing to go wrong!
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DR. CHINTAN
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KEY PRINCIPLE
The 20/30/40 rule
Three bedside thresholds that say the respiratory
pump is failing, long before the saturation moves.
20
FVC below 20 mL/kg
Vital capacity - the volume she can still move
30
NIF weaker than -30 cmH₂O
Inspiratory strength - the muscle that fills the lung
40
PEMax below 40 cmH₂O
Expiratory strength - the cough that clears
secretions
She breaches the first two, and PEMax was never
checked. A single effort-dependent value proves
nothing - trend them frequently (q1h or q2h).
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WHY THE SAT MISLEADS
The oximeter measures
the lung, not the pump
Supplemental oxygen holds the saturation up while
tidal volume quietly falls.
CO2 retention is the first measurable failure and it
needs a blood gas to see.
By the time she desaturates, the reserve is already
gone.
TELLS YOU LITTLE
SpO2, oxygen
requirement, chest film
TELLS YOU EVERYTHING
pCO2, single-breath count,
neck flexion, secretions
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DR. CHINTAN
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BULBAR WEAKNESS
A swallowing problem is an airway problem
SECRETIONS
She can no longer clear what she
makes.
COUGH
Expiratory muscle weakness makes it
useless.
VOICE
A weakening voice is a weakening
airway.
CONSEQUENCE
Aspiration arrives before fatigue does.
Bulbar failure alone justifies intubation,
whatever the respiratory numbers say.
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SHE WAS GIVEN BOTH
Drugs that unmask
myasthenia
FLUOROQUINOLONES
Ciprofloxacin - started 5 days ago for
UTI
MAGNESIUM
IV in the ER for presumed bronchospasm
MACROLIDES
Azithromycin, erythromycin
AMINOGLYCOSIDES
Gentamicin, tobramycin
BETA-BLOCKERS
Including topical ophthalmic drops
NM BLOCKERS
Profound, prolonged sensitivity
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THE DECISION
BiPAP or intubate?
BiPAP MAY BUY TIME
Early hypercapnia, intact
bulbar function, protected
airway, a reversible trigger
already being treated, and
a nurse at the bedside.
INTUBATE HER
Bulbar failure with
aspiration, secretions she
can't clear, a voice still
fading, neck flexor
weakness, and
deterioration over hours.
She has every feature in the right-hand column. A
controlled ICU intubation beats a crash airway on
the ward, every time.
Avoid depolarising and non-depolarising agents where you can; if
you paralyse, expect an exaggerated and prolonged response.
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ONCE THE AIRWAY IS SECURED
Treating the crisis
01 Find the trigger. Infection is the commonest; drugs are
the most missed.
02 IVIG 2 g/kg over 2-5 days, or plasma exchange.
Comparable efficacy - choose on severity, access
and comorbidity.
03 Hold pyridostigmine in most intubated patients - it
floods the airway with secretions. Restart as
mechanics recover.
04 Start corticosteroids once support is in place,
expecting transient early worsening.
05 Extubate on mechanics and secretion control, not on
gas exchange alone.
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THE ICU MISTAKE
Watching her overnight
Serial numbers get checked once a shift instead of every
few hours.
A poor-effort NIF gets recorded as reassurance.
Sedatives and opioids are given to a patient with no
reserve.
The team waits for a saturation that only falls at the very
end.
Every one of these turns a planned intubation into a
peri-arrest airway at 3am.
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TAKE THIS TO THE BEDSIDE
In neuromuscular disease,
never ask how well the lungs
are oxygenating. Ask how much longer
the muscles can keep
working.
Myasthenia, Guillain-Barré, ALS, brainstem
disease - the question is the same, and it is
answered at the bedside.
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EVIDENCE
Where this comes from
01 Narayanswami P, Sanders DB, et al. International
consensus guidance for management of myasthenia
gravis: 2020 update. Neurology. 2021.
02 Wendell LC, Levine JM. Myasthenic crisis. The
Neurohospitalist. 2011.
03 Damian MS, Widjicks EFM. The clinical management
of neuromuscular disorders in intensive care.
Neuromuscular Disorders. 2019.
04 Rabinstein AA, Widjicks EFM. Warning signs of imminent
respiratory failure in neurological patients. Seminars
in Neurology. 2003.
05 Gajdos P, Chevret S, Toyka KV. Plasma exchange for
generalised Myasthenia gravis. Cochrane Database of
Systematic Reviews. 2002.
06 Sheikh S, Alvi U, Soliven B, Rezania K. Drugs that
induce or cause deterioration of myasthenia gravis.
Journal of Clinical Medicine. 2021.
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TAKE-HOME
Ask how long the muscles can
keep working
That question is the difference between a
planned intubation and an arrest.
SAVE THIS
SHARE WITH
YOUR TEAM
FOLLOW
@DRCHINTANDAVE
BEDSIDE PHYSIOLOGY EP 25 EDUCATIONAL ONLY, NOT MEDICAL ADVICE
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