Overdose
Approach, Assessment and Management
Dr. Kirsty Dunn
FACEM
Emergency Department
Ballarat Health Services
Key Issues
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Heterogenous clinical presentation
Myriad toxins – ingestion, exposure
Risk assessment knows pt weight (?) and comorbidities (?)
Dynamic medical illness (some anticipated
clinical decline)
Tailored Mx plan for individual patient
Conventional resuscitation methods may not
apply
GCS 12 vs 8 for ETT
Approach
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“RESUS RSI DEAD”
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Typically management simultaneous with
assessment. Coal face – no past medical
history, limited drug history, reliant on
bystanders/ ambulance officers / old notes.
Assessment
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Criticality
Aetiology
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Most likely
Most fatal
Impact on underlying
comorbidities
Rule out non-accidental
injury.
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History
Examination
Investigations
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Bedside
Labs
Imaging
Specialist
Management
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Resuscitate
Specific
Supportive
Referral
Disposition
Education
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RESUS RSI DEAD
Resuscitate + Antidote
Risk assess
Supportive care +
monitoring
Investigations
Decontaminate
Enhance elimination
Disposition
RESUS RSI DEAD
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ABC…. DEFG
Seek and treat
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Emergency antidote
Screening ECG
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Bloods
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hypoglycaemia
Seizures
Hypo/erthermia
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Levels
ABG
glucose
alcohols, antiepileptics, paracetamol,
salicylates, digoxin, lithium, methotrexate,
iron
ABC’s in toxicology
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A – corrosive injury
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Alkalis, acids, paraquat
B – hyperV (acidosis)
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hypoV
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Opiates, benzodiazepines
Increased secretions
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Salicylates, toxic alcohols
imminent compromise so early ETT
or surgical airway
avoid normoV iff ETT need to resp
compensate with inc tidal vol. Soda bic 1-2
mmol/kg
naloxone 200mcg im, slow 200mcg iv titrate
NB do not give flumazenil (unless iatrogenic w
nil PMH)
Organophosphates, nerve agents, carbamates
Hypoxia w acidosis and MOFailure

Paraquat
1 mouthful fatal - herbicide
Oxygen therapy injurious - aim SpO2 90 (PaO2 60)
Huge dose atropine - 1.2mg iv doubling every 3/60
titrate to drying secretions
ABC’s in toxicology
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C – VF
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Do ABG seeking hypocalcaemia
Systemic flurosis in hydrofluric acid vapourisation
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VT
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(glass etching, chrome cleaning – mechanics)
high dose iv calcium GLUCONATE (not chloride) not the
usual "10ml 10% 10 mins" but 90ml 10% stat repeating
every TWO mins with attempts at defibrillation
ammiodarone contraindicated (further prolongs blocks as cardiac domestos)
don't a/w VBG prior to sodabic 50mmol, intubate, hyperV, sodabic 50mmol.
Seek TCA o/d
Seek the Ia,c and III drugs (cocaine, lignocaine,
flecainide, PROPRANOLOL, quinine
V ectopics
immigrants
Bblock
ABC’s in Toxicology continued
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C – refractory hypotension
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Amphetamines, cocaine, serotonin syndrome
Asystole
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Bblocker, CaCh blocker, local anaesthetics
Refractory hypertension / tachycardia
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HIET, intralipid
Digoxin
benzo's+++,
cyproheptadine. do
not give BBlockers
(unopposed alpha
with ICH)
digibind . 5 vials and repeat
Calcium Chloride contraindicated despite
looking like hyperkalaemia
D – refractory seizure

Seek TCA w long QRS. Risk stratify for isoniazid
benzo's, phenobarbitone, pyridoxine
(immigrant, Tb)
residue 1Giv.
ABC’s in toxicology
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E – febrile
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Serotonin syndrome, neuroleptic malignant syndrome,
benzo's +++, cyproheptadine 4mg NG
(malignant hyperthermia)
G – hypoglycaemia
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Gliclazide, insulin, Bblockers
Hyperglycaemia
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Salicylates (CNS gluc zero)
or PO 4/24, cease offending agents,
active cooling, seek rhabdo.
octreotide
Risk assessment
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Agent (s)
Dose
Time ingested
Time lapsed
Clinical features and course
Patient factors (Wt, liver and renal F,
anorexia, cardiac)
Toxic Drug Levels
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Paracetamol >200mg/kg
Iron 60mg/kg elemental iron
Colchicine >500mg/kg
Digoxin > 4mg (16 x 250 mic tabs)
Warfarin or rat sac >1 sachet
Aspirin >300mg / kg
Paeds 1 pill (CCB, BB, amphetamines, TCA,
propranolol, gliclazide, opioids)
Decontamination
PROS
Improved morb / mortality
More benign clinical
course
Reduce need for
hazardous intervention
Reduce hosp LOS

CONS
Aspiration
GIT obstruction / perf
Distraction from
supportive Mx
Resource intense
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Decontamination
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Charcoal (“activated”)
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50G adults, 1G/kg kids
(mixed w ice cream)
Benefit must outweigh
risk (aspirn)
Ci Altered or anticipated
drop in GCS / Seizure
risk
Safe in pregnancy
steamed wood pulp
to increase surface area for binding
Charcoal
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Indications….(*dubious)
Almost everything else
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But never really used
Paracetamol (*)
Benzo’s (*)
Barbiturates (*)
TCA’s (*)
Phenothiazines
Anticonvulsants (*)
Aspirin
Theophylline
Digoxin
Amphetamines (*)
Quinine
Blockers
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Contraindications
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PHAILS
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Pesticides
Hydrocarbons
Acids / alkalis / alcohols
/arsenic
Iron / lead
Lithium or ionic elements
Solvents
Patient:
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unstable,
non-toxic ingestion,
antidote available,
ACS,
will require gastroscopy,
bowel obstruction
Whole bowel irrigation
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PEG
Takes 1 nurse 6 hours as sole job
Needs commode and antiemetics (and lots of toilet
paper)
When charcoal ineffective and poor prognosis with
no antidote and not amenable to purely supportive
care
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Eg enteric coated or slow release preps.
 IRON, slow K, SR CaCh Block, arsenic, lead, body
packers.
Elimination
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Never carried out to the detriment of
resuscitation or antidote.
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Multi-dose activated charcoal
Urinary alkalinisation
Haemodialysis / CVVHDF
Charcoal haemoperfusion
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Pearls for Elimination
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MDAC causes aspiration, bowel obstruction,
corneal abrasions
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listen for bowel sounds every 2/24 50g bottle.
Takes up to 6 hours.
Urinary alkalinisation
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Aim urine pH >7.5
1-2 mmol soda bic / Kg then 100mmol over 4/24.
give KCl and monitor K. Stop when tox resolving.
Scenarios
FACEM 2011.1 Q7

A 46 year old man is brought to your emergency
department by ambulance following an overdose of
unknown medications. He has had a brief
generalized seizure en route.

On arrival his observations are:
Broad complex tachy
LAD
RSR in V1, slurred upstroke V6
I-V conduction delay (QRS) ®
Terminal R wave aVR >3mm
Prolonged QTc >550ms
Critical TCA overdose. QRS seizure.
QT torsades / VT
Management
Mx in resus area, treatment with NaHCo3 50-100mmol aiming to
reduce R wave and shorten QRS. pH 7.55,
 Fluid Mx for hypotension and Benzodiazepines for seizures.
 Use of RSI to assist is accepted but was felt that in this Stem
was secondary to above
Features of unsuccessful answers
 Lack of detail & precision or systematic approach to part A
 Inadequate management – focus was NaHCo3 is the antidote
and 1st line treatment.
 No titration or endpoints – to pH 7.55 & QRS , and no detail in
doses or utalising cardioversion in Mx

Scenario 2
FACEM 2013/1. Q1
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A 20 year old man is brought to your ED by ambulance after
being found collapsed at home following a large polypharmacy
drug overdose that included Venlafaxine. He has been intubated
and received 500mls of normal saline prior to arrival. The time of
ingestion is not known.

Observations:
capture
broad complex
tachycardia, rate 180
bpm
peaked T waves
no mans land axis ventricular origin
FACEM VAQ Exam 2013.1 - Question 6
•The overall pass rate for this question was 68/134 (50.7%)
•Pass Criteria ECG
•Broad complex tachycardia with differential of VT and possible Na channel
blockade. May pass if Na blockade not mentioned but management
includes appropriate use of NaHCO3
•Pass Criteria Treatment
•Hyperventilation (patient intubated, key initial therapy) or ventilation
strategy to achieve this
•Use of NaHCO3 with initial bolus of minimum 50 - 100 mmol aiming pH
7.55, narrowing of QRS
•DO NOT use amiodarone. Safe to try DC cardioversion however.
•Fluid loading with minimum 1 litre stat (in view of initial 500 ml bolus,
further min 500ml required though more ideal)
•Features of Higher level answers
Description of ECG features supporting VT.
Recognition of potential Na Channel blockade/ coingestion (eg TCA).
Recognition that atypical for Venlafaxine.
Consideration of hyperkalaemia
Aggressive management of possible Na channel blockade with alkalinisation
Hyperventilation of intubated patient. pH 7.50-7.55
NaHCO3 (100mmol or 2 mmol/kg repeated to end points of ECG, cardiovascular
stability, pH)
Description of measures to improve BP (fluids + 2nd line of pressors) + endpoints
DCCV likely ineffective. Appropriate to delay until after NaHO3, hyperventilation,
fluids.
Recognition of hyperthermia, concern for serotonin syndrome. Sedation with
benzodiazepines, probable paralysis, simple cooling measures, core temp.
Consideration possible differential for this re other causes (other toxidromes,
sepsis, aspiration etc)
Recognition of significant seizure risk due to Venlafaxine with mention of
management with benzodiazepines 1st line, and consideration of monitoring
implications.
Consideration of co-ingestants, hyperkalaemia, rhabdomyolysis, renal failure
etc.
Fail criteria
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Inappropriate use of anti-arrhythmics. Class I agent
use is contraindicated and dangerous (=Fail).
Use of amiodarone is also inappropriate as 1st line
= fail if used prior to hyperventilation, NaHCO3,
DCCV
Displaying no significant knowledge of the
management of an unstable broad complex
tachyarrhythmia in a toxicological setting (managing
along standard ALS lines with no use of NaHCO3 or
hyperventilation).
Scenario 3
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FACEM2007.2 Q3
A 77 year old man presents to your emergency
department feeling generally unwell for several
days. He is noted to have a pulse rate of 36 beats /
minute and is normotensive.
Arterial blood gases and serum biochemical tests
are performed
Describe and Interpret
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Life threatening metabolic acidaemia with a HAGMA
likely related to Acute on CRF causing life
threatening digoxin toxicity requiring urgent antidote
and correction of acid base balance and renal
winters formula
supportive therapy.
Expected pCO2 = 1.5x HCo3 +8 = 29
Anion Gap = (Na +K) –(HCO3 +Cl) = 27
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carbon monoxide, AKA,
toluene, methanol, metformin,
uraemia, DKA, paraldehyde
[R], iron, isoniazid [seizure],
lactate, ethylene glycol,
salicylates
Ddx – LTKR or CATMUDPILES
Expected K = 3.5 +[0.1(7.35-7.19) x 0.5] = 4.3
can also do Aa gradient, Delta gap, Ur:Cr ratio
Outline Management
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Move to resus, full physiological monitoring with a team
approach.
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Resus: A/B fine. Allow to hyperV
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C – gain IVC and commence aggressive rehydration 1
Lstat aiming for UO >1ml/kg/hr
D – do not sedate (avoid resp acidosis)
Specific:
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Delegate staff for digibind 2 vials and repeat 15/60 aiming
for HR >60
Hyperkalaemia
 Ins dext / salbutamol / resonium / Soda bic. FAIL IF USE
CALCIUM CHLORIDE
 Monitor VBG 30/60, serial ECG’s seeking automaticity and
peaked T waves.
Outline management
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Supportive
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Renal failure – ivf. Cvvhdf. Monitor fluid balance, K and
urea. Cease nephrotoxics.
Glucose – avoid hypoglycaemia (K Rx)
Antiemetics for nausea
Seek cause of ARF--- digoxin tox --N/V
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?stroke / myocardial event / infection / change meds
Outline management
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Referral
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Disposition
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ICU, renal med, poisons information, and cause initial
illness – cardiol / neurol / etc
ICU for monitoring, correction of fluid / elec’s/ treating
cause
Education
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NOK, GP, altering prescription
Scenario 4
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A 27-year old female presents to ED one hour after
swallowing 70 x 40mg propranolol tablets (= 2.8
grams) with suicidal intent.
At the time of assessment she is drowsy (GCS 13)
with a heart rate of 46 bpm.
Fifteen minutes earlier she had been awake and
able to give a history to paramedics… You need to
act fast to save this patient. Are you up to the
challenge?
LITFL
terminal R wave in aVR >3mm.
Sodium channel blockade
RSR in V1 and slurred upstroke V6.
broad complex RBBB pattern
1st degree heart block.
general rate not as anticholinergic as
expected in a TCA O/D.
rate = 13 x 6 = 78
prolonged QTc
Basetts formula QTc = QT/square root of
the R-R (medcalc.com)
Propranolol overdose
Question for Pharmacy
Primary
Describe the toxicokinetics of propranolol.

Absorption: Rapidly absorbed orally. Peak blood levels occur at 1-3
hours following oral administration.
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Distribution: Highly lipophilic agent with a wide volume of distribution.
Rapidly distributed to all tissues, including CNS.
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Protein Binding: Approximately 93% protein bound.
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Metabolism: Undergoes extensive hepatic metabolism, with
hydroxylation of the aromatic nucleus and degradation of the
isoprenaline side-chain. Over 20 metabolites identified. The 4-hydroxy
metabolite has active beta-blocking properties.

Elimination: 95-100% of an ingested dose is excreted in the urine as
metabolites and their conjugates.

Half-life: Plasma half-life is around 3-6 hours. The pharmacological
effects last much longer than this. Elimination half-life is 12 hours and
may be prolonged following overdose.
Question for Pharmacy
Primary
Describe the toxicokinetics of propranolol.

Absorption: Rapidly absorbed orally. Peak blood levels occur at 1-3
hours following oral administration.

Distribution: Highly lipophilic agent with a wide volume of distribution.
Rapidly distributed to all tissues, including CNS.

Protein Binding: Approximately 93% protein bound.

Metabolism: Undergoes extensive hepatic metabolism, with
hydroxylation of the aromatic nucleus and degradation of the
isoprenaline side-chain. Over 20 metabolites identified. The 4-hydroxy
metabolite has active beta-blocking properties.

Elimination: 95-100% of an ingested dose is excreted in the urine as
metabolites and their conjugates.

Half-life: Plasma half-life is around 3-6 hours. The pharmacological
effects last much longer than this. Elimination half-life is 12 hours and
may be prolonged following overdose.
Propranolol O/D
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Behave like TCA but slower ventricular rate
Treated as per TCA
Excess beta-blockade causes:
 Hypotension and bradycardia
 Bradyarrhythmias, including sinus bradycardia, 1st-3rd degree
heart block, junctional or ventricular bradycardia
 Bronchospasm
 Hyperkalaemia and hypo/hyperglycaemia
Sodium-channel blockade causes:
 Cardiotoxicity – QRS widening, ventricular arrhythmias and
cardiac arrest
 Neurotoxicity – coma, seizures and delirium
Massive propranolol overdose typically presents with coma,
seizures, bradycardia and progressive cardiogenic shock.
In TCA O/D anticholinergic effects create tachycardia relative protection against prolonged QTc and
torsades. BUT in propranolol O/D Bblockade means
R-on-T a high risk.
Beta Blocker O/D

Propranolol and sotalol are really the ones to worry
about

Risk Assessment (what,where,when,how)
 Prop / sotalol
 Underlying cardiac or lung disease
 Co-ingested CCB or digoxin
 Elderly or children (1 pill can kill)
 Even 1G propranolol is severe tox
 Anticipate early DECLINE (unless SR sotalol)
Toxic Mechanism
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Inhibit B1 and B2 receptors
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Inhibit response to catecholamines
Negative chronotropy, negative inotropy,
hypoglycaemia
Sodium channel blockade
Lipid soluble so crosses BBB -seizure, coma,
DEATH
Propranolol toxicity is associated with QRS
widening and a positive R’ wave in aVR
(signs of sodium channel blockade), which
portend the onset of coma, seizures,
hypotension and ventricular arrhythmias.
Sotalol blocks myocardial potassium
channels, causing QT prolongation and
Torsades de Pointes in overdose.
Management BB O/D
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In resus with INVASIVE monitoring
Resus ABC’s
Antidote?
Management BB O/D
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In resus with INVASIVE monitoring
Resus ABC’s
Antidote?
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SODIUM BICARBONATE
Management BB O/D
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In resus with INVASIVE monitoring
Resus ABC’s
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Intubate, hyperventilate
Antidote?
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SODIUM BICARBONATE
Dose?
Management BB O/D
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In resus with INVASIVE monitoring
Resus ABC’s
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Intubate, hyperventilate
Antidote?
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SODIUM BICARBONATE
Dose?

100mmol IV and repeat 15/60
Management BB O/D
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In resus with INVASIVE monitoring
Resus ABC’s
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Intubate, hyperventilate
Antidote?
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SODIUM BICARBONATE
Dose?

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100mmol IV and repeat 15/60
Aims?
Management BB O/D
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In resus with INVASIVE monitoring and…
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Resus ABC’s
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PACING PADS in situ
Intubate, hyperventilate
Antidote?
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SODIUM BICARBONATE
Dose?
 100mmol IV and repeat 15/60
Aims?
 Narrowing QRS, shortening R wave in aVR, pH 7.55
Management BB O/D

C – what are the options?
Management BB O/D
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C – what are the options?
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Atropine 600mcg iv 2 minutely up to 3mg
Isoprenaline 0.5-5 mcg / min
Adrenaline start at 10mcg/min and titrate aiming for
BP and secretions
AVOID bradyarrythmia – torsades. ESP sotalol.



Isoprenaline
(magnesium)
Overdrive pacing
New Management BB O/D
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HIET
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High Insulin Euglycaemic Therapy
What is it used for??
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

Propranolol, sotalol and any symptomatic BB O/D with
anticipated decline (underlying cardiac or pulm)
CaCh Blocker O/D
INTRALIPID

(100ml iv)
HIET

Allows glucose into myocytes eliminating FFacid metabolism

How to give HIET… 3 IV lines


50ml 50% dextrose push
After DXT give massive dose actrapid



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
1 unit/kg bolus
Infusion of 0.5 un/kg.
If ongoing HD instability can inc infusion to 1 un/kg
50ml 50% dextrose ivi titrated to BSL (hrly)
Monitor K+
p waves
nil correlation with atrium and
ventricular impulses
rate is 5 x 6 =30bpm
Calcium Channel O/D


Verapamil and diltiazem the ones to worry
about
Risk Ax




Just TWICE the usual dose of v or d can cause
tox in susceptible pt (liver F)
ALL taken seriously
10 tabs life threatening adult
1 pill can kill kids
Calcium Ch O/D

If altered consc state then due to profound
hypoT or a co-ingestant



CCB do not Cross BBB
Cause hyperglycaemia as suppress insulin
release
Must keep SR preps 16hrs for observation.
Not the usual 4 hour rule.
Ix in CCB
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Screening ECG, paracetamol
Cardiac monitor
U+E
CCa
ABG – lactate (shock),
Glucose (H)
CXR (APO)
Mx in CCB

Resus –

Anticipate rapid decline. Calamity of hypotension
and brady arrythmia. Need concurrent resus,
antidote and decontamination
 A – early ETT if risk Assess high risk. Intubate
anyone not responding to 20ml/kg IVF
 C – Calcium. 20ml 10% 10mins CaChloride (x3
potency Ca gluconate). Aim CCa 2-3 mEq/L
atropine
calcium
PEG
ECMO
intralipid
Balloon
pump
pacing
HIET
Reading list
Murray Toxicology Handbook
 Life in the fast lane
 EM RAP
 Cameron
Resources:
Life in the Fast Lane
(http://lifeinthefastlane.com)
