CASE STUDY: POST MI TORSADE ARREST

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CASE STUDY:

POST MI TORSADE ARREST

ALMERO OOSTHUIZEN

UCT/US EMERGENCY MEDICINE

1 APRIL 2009

PATIENT BACKGROUND

• Mrs. AS, 70y female

• PMH:

– Hypertension, 40py smoker (COPD)

– No previous ischemic events

• Medication:

– Ridaq 12,5mg od

– Currently using amoxil and paracodol for ‘flu’

• No allergies

PRESENTING COMPLAINT

• Presented to VHW ED at 16h10

• 15h00 - Generalised weakness; legs felt numb; vomited twice; appeared confused; could not understand speech or speak clearly

• 15h30 – Chest discomfort; sweating; tremulous. Lasted 30min, then came and went

• Also c/o leg discomfort ; 2 weeks of productive cough

PHYSICAL EXAM 1

• General:

– Frail, poor concentration, slightly slurred speech

– HR 75 ; BP 140/82 ; Temp 36,7 ; RR 24 ; Hb 11

• CVS:

– Regular pulse ; limb pulses not documented ; no failure ; no murmurs ; JVP not documented

• Chest:

– No abnormalities documented

PHYSICAL EXAM 2

• Abd:

– No abnormalities documented

• CNS

– GCS 14 (slightly confused); power both legs 4/5

– Nil more documented

INITIAL ECG’S 1

INITIAL ECG’S 2

INITIAL ASSESMENT

• Casualty Officer (2’nd year intern) notes

– ?MI ; ?TIA ; ?LRTI

• Central question: In light of possible IC event, is it safe to strep patient?

INITIAL MANAGEMENT

• O

2

; Aspirin 300mg ; Morphine 4mg ; Isordil sl

• Trop T (neg)

• Casualty officer referred the patient to medical registrar (actually a cosmo)

– Recommended they phone GSH cardiology

– Said he’d be down as soon as possible

• GSH Cardiology

– “we don’t give advice re thrombolysis over the phone” AAARGHH! Intern! AAARGHH!

THEN…

• Patient now comfortable and pain free

• Spoke to medics again

– Recommended ED hold off on strep until they have reviewed patient

19h00

• Patient became unresponsive (noticed immediately by attending nurse) and pulseless

• CPR commenced at once with chest compressions, and patient rushed to resuscitation area (cpr en route, transit time about 20 sec)

RESUSCITATION 1

• BVM vent 2:30 high quality chest compressions ongoing

• Monitor attached within 40 seconds of initial arrest

• Arrest rhythm: Torsade du Pointes

• Immediate async. biphasic cardio version at

200J

• CPR commenced, adrenalin 1mg IV ordered, but not given yet

TORSADE ECG’S

RESUSCITATION 2

• During first cycle of chest compressions post shock, patient displayed signs of ROSC

– Moaning, moving

• Good pulse felt; rhythm = AF with incomplete

RBBB at 75bpm

• Patient woke up and was conversant within about two minutes, complaining of ‘sore ribs’

• By this time the medic arrived at last

SUBSEQUENT CARE

• Post resuscitation care consisted of O

2 mask and ongoing cardiac monitoring via face

• 2g MgSO

4 infused IV over 5 minutes

• After discussion with the medical consultant, thrombolysis with streptokinase was started once the patient had been transferred to ICU.

NEXT MORNING

• Stable post strep course in ICU

• Bilateral, severe PVD noted

• Critical ischemia of right leg

• Transferred to GSH ICU

• Right leg embolectomy and fasciotomy, with eventual right sided BKA (septic, non healing wound)

• Transferred back to VHW on 25-2-2009, and is doing well!

FINAL ASSESSMENT

• Inferior STEMI with RV extension

– Possible intermittent complete AV block with bradycardia

– Complicated by Torsade arrest

– Post version/strep AF

• Acute limb ischemia (right leg)

– Initial embolectomy

– Eventual right BKA

• Probably never had a ‘TIA’

PEARLS

• ACS patients are not stable patients

– They should be intensively monitored

• Difficult management decisions on sick or complicated patients like this should be made by the most senior person available

• Torsade with arrest is still arrest: initial treatment remains good CPR and early cardio version. Other treatments may then be considered

Pause Dependent (Acquired)

• Drug induced: 1A and 1C antidysrhythmics, phenothiazines, cyclic antidepressants, organophosphates, antihistamines.

• Electrolyte abnormalities: hypokalemia, hypomagnesemia, hypocalcemia (rarely)

• Diet related: starvation, low protein

• Severe bradycardia or atrioventricular block

• Hypothyroidism

• Contrast injection

• Cerebrovascular accident (especially intraparenchymal)

• Myocardial ischemia

OVERDRIVE WHY?

• Acquired Torsade is due to prolongation of the

QT interval and is usually precipitated by bradycardia

• The so-called short-long-short phenomenon

• Brady – early ectopic beat (‘escape’) – comp pause – recovery beat with long QT - R on T -

Torsade

OVERDRIVE WHY?

• Speeding up the rate will shorten ventricular repolarisation

• This decreases the effective QT (and therefore vulnerable time) interval and decreases the chances of an early ectopic beat

• Voila!

OVERDRIVE WHAT?

• NB: Overdrive to prevent recurrent TdP vs.

Overdrive to convert resistant TdP

• Electrical overdrive to a ventricular rate of about 100 – 120

– Discussion of technique during lecture

• Chemical overdrive with Isoproterenol

– 2 to 10 mcg/kg/min

– Titrate to increase HR till VT suppressed

Adrenergic Dependent

Congenital

Jervell and lange-Nielsen syndrome (deafness, autosomal recessive)

Romano-Ward syndrome (normal hearing, autosomal dominant)

Sporadic (normal hearing, no familial tendency)

Mitral valve prolapse.

Acquired

Cerebrovascular disease (especially subarachnoid hemorrhage)

Autonomic surgery: radical neck dissection, carotid endarterectomy, truncal vagotomy

TORSADE: MANAGEMENT

• Unstable: Unsynchronized cardio version

– Sync not effective due to variable R wave amplitude, morphology and axis

• Other options

– Correct precipitant

– MgSO

4

1-2g IV in 10 ml D5W as a push for everyone

(may also consider K supplementation)

– Consider lidocaine or amiodarone (effectiveness not demonstrated)

• Class 1A and 1C contraindicated

REFERENCES

• ACLS resource text (ACLS EP)

• 5 Minute emergency medicine consult, Rosen and Barkin

• Textbook of Emergency Medicine, Rosen and

Barkin

• Emedicine.com

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