This document describes a 52-year-old male patient who presented with fatigue and was found to have hypokalemia. The patient has a history of type 2 diabetes, hypertension, congestive heart failure, smoking, and asthma. An ECG showed changes consistent with hypokalemia including increased P-wave amplitude, prolonged PR interval, widespread ST depression and T-wave flattening. The patient was taking furosemide and a salbutamol-containing inhaler, and it was unclear how long his potassium had been low. The treatment plan included IV potassium supplementation, medication reconciliation to address the cause of hypokalemia, and follow-up labs and potential cardiac testing.

1. Dr. Robert Ferris

2. (it’s upside down)

4.  M, 52 y/0, presents with fatigue++
 T2DM
 HTN + CCF
 Smoker + reported hx. of asthma
 No history of MI
 Good adherence to medication, but unsure
what these are:
 “Blood pressure tablet(s)”
 “Inhaler”

6. U&E → K+ 2.3
↓
HYPOKALAEMIA

7.  Increased amplitude of P-waves
 PR interval prolongation
 Widespread ST depression andT wave
flattening/inversion
 U-waves
 Long QU interval: QT interval appears
prolonged, due to flattenedT-wave and
presence of U-Wave

12.  Pt. found to be taking regular furosemide
alongside salbutamol-containing inhaled
medication
 Unclear when furosemide was commenced, and
whether meant to be a regular medication, as
patient also on ramipril
 Unclear how long potassium had been low
 No other complaints, no chest discomfort, no
syncopes/collapse

13.  Telemetry
 IV K+, slow
 Repeat U&E
 ?repeat echo, if one due
 Take the opportunity for a proper medication
reconciliation
 Inform the patient’s GP once this has been done!!

14.  HypoK+ often associated with hypoMg2+
 A combination of low K+ and Mg2+ ahave
potentiating destabilising effects on
myocardial cells
 This combination is associated with increased
risk of malignant ventricular arrhythmias

15. References:
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