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Physiology

Renal

Question 6 of 180

A patient is sent into ED by his GP with an abnormal blood test result. His ECG performed at triage is shown below. What is the likely abnormality seen on his blood test:

Answer:

The ECG shows peaked T waves most likely secondary to hyperkalaemia. Effects of hyperkalaemia on the ECG:
  • Peaked T waves (usually the earliest sign of hyperkalaemia)
  • P wave widens and flattens
  • PR segment lengthens
  • P waves eventually disappear
  • Prolonged QRS interval with bizarre QRS morphology
  • High-grade AV block with slow junctional and ventricular escape rhythms
  • Any kind of conduction block (bundle branch blocks, fascicular blocks)
  • Sinus bradycardia or slow AF
  • Development of a sine wave appearance (a pre-terminal rhythm)
  • Cardiac arrest due to:
    • Asystole
    • Ventricular fibrillation
    • PEA with bizarre, wide complex rhythm

Hyperkalaemia

RCEM defines normal values for total serum potassium as 3.0 - 4.5 mmol/L.

Causes

The causes of hyperkalaemia may be divided into:

  • Renal retention
    • Renal failure
    • Hypoaldosteronism (e.g. Addison's disease)
    • K+ sparing diuretics
    • ACE inhibitors/ARBs
    • NSAIDs
    • Trimethoprim and pentamidine therapy
  • Increased intake
    • Excess dietary K+
  • Transcellular shift of K+ out of cells
    • Metabolic acidosis
    • Insulin deficiency
    • Beta-blockers
    • Cellular injury/rhabdomyolysis
      • Tumour lysis syndrome, trauma, burns, crush syndrome, chemotherapy
  • Pseudohyperkalaemia
    • Prolonged tourniquet time
    • Difficulty collecting the sample
    • Test tube haemolysis
    • Length of storage of the specimen
    • Sample from limb receiving IV fluids containing potassium

Clinical Features

Clinical features of hyperkalaemia may include:

  • Asymptomatic
  • Paraesthesia
  • Muscle weakness or paralysis
  • Cardiac conduction abnormalities and dysrhythmias

ECG Changes

Hyperkalaemia causes a rapid reduction in resting membrane potential leading to increased cardiac depolarisation and muscle excitability. This in turn results in ECG changes which can rapidly progress to ventricular fibrillation or asystole.

Classic ECG changes:

  • Tall peaked T waves
  • Shortening of the QT interval
  • Lengthening of the PR interval
  • Widening of the QRS complex
  • Loss of the S-T segment
  • Loss of p waves
  • Sine wave appearance

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  • Biochemistry
  • Blood Gases
  • Haematology
Biochemistry Normal Value
Sodium 135 – 145 mmol/l
Potassium 3.0 – 4.5 mmol/l
Urea 2.5 – 7.5 mmol/l
Glucose 3.5 – 5.0 mmol/l
Creatinine 35 – 135 μmol/l
Alanine Aminotransferase (ALT) 5 – 35 U/l
Gamma-glutamyl Transferase (GGT) < 65 U/l
Alkaline Phosphatase (ALP) 30 – 135 U/l
Aspartate Aminotransferase (AST) < 40 U/l
Total Protein 60 – 80 g/l
Albumin 35 – 50 g/l
Globulin 2.4 – 3.5 g/dl
Amylase < 70 U/l
Total Bilirubin 3 – 17 μmol/l
Calcium 2.1 – 2.5 mmol/l
Chloride 95 – 105 mmol/l
Phosphate 0.8 – 1.4 mmol/l
Haematology Normal Value
Haemoglobin 11.5 – 16.6 g/dl
White Blood Cells 4.0 – 11.0 x 109/l
Platelets 150 – 450 x 109/l
MCV 80 – 96 fl
MCHC 32 – 36 g/dl
Neutrophils 2.0 – 7.5 x 109/l
Lymphocytes 1.5 – 4.0 x 109/l
Monocytes 0.3 – 1.0 x 109/l
Eosinophils 0.1 – 0.5 x 109/l
Basophils < 0.2 x 109/l
Reticulocytes < 2%
Haematocrit 0.35 – 0.49
Red Cell Distribution Width 11 – 15%
Blood Gases Normal Value
pH 7.35 – 7.45
pO2 11 – 14 kPa
pCO2 4.5 – 6.0 kPa
Base Excess -2 – +2 mmol/l
Bicarbonate 24 – 30 mmol/l
Lactate < 2 mmol/l
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