Thoughts from the lists' collective brains welcome for a situation I have
not previously come across
73 year old man, under treatment for panic attacks arrives in sinusoidal VT,
clammy, central pulses, no BP, talking. On amytriptiline. Rapidly given
midazolam and DC shock x 1 200J - into SR. Immediate 12 lead is completely
normal, no iscahemia, and we were interested to note he had not a single
ectopic on the monitor. BP then recorded as 140/80. Unconscious from the
midazolam but things seemed to be going OK.
Gases taken immediately post shock show gross metabolic acidosis, pH 7.0.
Receiving IV saline though lungs wet and JVP in his exernal auditory meatus.
His myocardium then became increasingly irritable 15 minutes or so post
shock - increasing VE's and n/s bursts of VT. I had just put up a nitrate
infusion and stopped it as his BP progressively fell to 90 systolic. Given
lignocaine bolus and infusion and magnesium 2g, to no effect. Remained
hypotensive, flumazenil given to reverse his sedation. Over the next 30
minutes he remained hypotensive, systolics around 90-100 but increasingly
well perfused peripherally. Central access obtained and amiodarone given,
lignocaine tailed off.
My questions
why the delayed myocardial irritability? Is it related to peripheral
reperfusion?
why didn't it respond to lignocaine?
Would anyone have done an RSI rather than just midazolam? My reason was time
- he looked close to losing output but obviously I left his airway at risk.
Steve Meek
RUH Bath
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