Broad complex following gastro illness
A 55 year old man presents to triage with a 2 day history of lethargy following a gastro illness. He has a past medical history of ischaemic heart disease, asthma and chronic renal impairment.
An ECG is performed and is shown below:
An ECG is performed and is shown below:
1. Interpret the ECG
Wide complex tachycardia
Rate 100 bpm
Absent p waves
Left axis deviation
Atypical LBBB morphology
Sine wave appearance
2. What is your differential diagnosis?
Consistent with severe hyperkalaemia
Differential is limited given the atypical morphology of the QRS complexes, but should consider toxic ingestion of tricyclics, flecainide or other Na channel blocking agents.
In general ECG changes correspond to different plasma levels of potassium:
K+ in mmol/L ECG characteristics
6 - 7 Tall peaked T waves (>5mm)
7 - 8 QRS widening, small-amplitude P waves
8 - 9 Fusion of QRS complex with T wave production sine wave
>9 AV dissociation, ventricular tachycardia, ventricular fibrillation
Making this patient's K+ at least 8 mmol/L
3. What is your emergent management?
a. Treat the hyperkalaemia
c. Ongoing monitoring and disposition
Reference: "Textbook of Adult Emergency Medicine" 3rd Edition, Cameron et al pg 502-503
For an excellent run down of the ECG in hyperkalaemia see lifeinthefastlane.com
Wide complex tachycardia
Rate 100 bpm
Absent p waves
Left axis deviation
Atypical LBBB morphology
Sine wave appearance
2. What is your differential diagnosis?
Consistent with severe hyperkalaemia
Differential is limited given the atypical morphology of the QRS complexes, but should consider toxic ingestion of tricyclics, flecainide or other Na channel blocking agents.
In general ECG changes correspond to different plasma levels of potassium:
K+ in mmol/L ECG characteristics
6 - 7 Tall peaked T waves (>5mm)
7 - 8 QRS widening, small-amplitude P waves
8 - 9 Fusion of QRS complex with T wave production sine wave
>9 AV dissociation, ventricular tachycardia, ventricular fibrillation
Making this patient's K+ at least 8 mmol/L
3. What is your emergent management?
a. Treat the hyperkalaemia
- Antagonise potassium cardiac toxicity: IV Ca chloride 10% 5-10ml or IV Ca gluconate 10% 5-10ml (nb. this stabilises the cardiac membrane but does NOT decrease K levels)
- Shift potassium into the cells:
- IV insulin 10-20U with dextrose 50g or
- nebulised salbutamol 10-20mg or IV 0.5mg dilutes in 100ml over 10-15min) or
- IV sodium bicarbonate 50-200mmol
- Enhance potassium excretion:
- oral and/or rectal resonium 50g
- frusemide diuresis
- haemodialysis
- Most likely dehydration and acute on chronic renal failure in this patient
- Consider other causes based on history and examination such as: rhabdomyolysis, digoxin toxicity exacerbating hyperkalaemia, tumour lysis syndrome
c. Ongoing monitoring and disposition
- Remember that K+ levels can easily rebound after mechanisms to shift K+ into cells and that Ca++ only lasts 30-60 mins
- You need to monitor and repeat treatments until the potassium is excreted by the body and the underlying cause is addressed
- Monitor vitals, UO, K+, ECG (cardiac monitoring)
- Disposition will be to a renal dialysis unit or intensive care/HDU cardiac monitored environment
Reference: "Textbook of Adult Emergency Medicine" 3rd Edition, Cameron et al pg 502-503
For an excellent run down of the ECG in hyperkalaemia see lifeinthefastlane.com