ECG Changes in Drug and Electrolyte Abnormalities

Hypokalemia
• Slowed conduction,

• Delayed ventricular repolarization,

• Shortened refractory period

• Increased automaticity
• Flattening and inversion of T waves in mild hypokalemia,
• Followed by Q-T interval prolongation,
• Visible U wave
• Mild ST depression

• Severe hypokalemia
• Torsades de points
• Ventricular tachycardia
Hyperkalemia
• Hyperkalaemia is defined as a potassium level > 5.5 mEq/L

• Moderate hyperkalaemia is a serum potassium > 6.0 mEq/L

• Severe hyperkalaemia is a serum potassium > 7.0 mE/L

Effects of hyperkalaemia on the ECG
• Mid Hyperkalemia
• Serum potassium > 5.5 mEq/L is associated with repolarization
abnormalities:
• Peaked T waves (usually the earliest sign of hyperkalaemia)

• Serum potassium > 6.5 mEq/L is associated with progressive

paralysis of the atria:
• P wave widens and flattens
• PR segment lengthens
• P waves eventually disappear
• Serum potassium > 7.0 mEq/L is associated with conduction
abnormalities and bradycardia:
• 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)
• Serum potassium level of > 9.0 mEq/L causes cardiac arrest due to:
• Asystole
• Ventricular fibrillation
• PEA with bizarre, wide complex rhythm
Hypocalcemia
• Normal serum corrected calcium = 2.2 – 2.6 mmol/L.

• Mild-moderate hypocalcaemia = 1.9 – 2.2 mmol/L.

• Severe hypocalcaemia = < 1.9 mmol/L.

• Causes of Hypocalcaemia
• Hypoparathyroidism
• Vitamin D deficiency
• Acute pancreatitis
• Hyperphosphataemia
• Hypomagnesaemia
• Diuretics (frusemide)
• Pseudohypoparathyroidism
• Congenital disorders (e.g. DiGeorge syndrome)
• Critical illness (e.g. sepsis)
• Factitious (e.g. EDTA blood tube contamination)
• ECG changes in Hypocalcaemia
• Hypocalcaemia causes QTc prolongation primarily by prolonging the
ST segment.
• The T wave is typically left unchanged.
• Dysrhythmias are uncommon, although atrial fibrillation has been
reported.
• Torsades de pointes may occur, but is much less common than with 
hypokalaemia or hypomagnesaemia.
Hypercalcemia
• Causes of Hypercalcaemia
• Hyperparathyroidism (primary and tertiary)
• Myeloma
• Bony metastases
• Paraneoplastic syndromes
• Milk-alkali syndrome
• Sarcoidosis
• Excess vitamin D (e.g. iatrogenic)
• ECG Changes in Hypercalcaemia
• The main ECG abnormality seen with hypercalcaemia is 
shortening of the QT interval
• In severe hypercalcaemia, Osborn waves (J waves) may be seen
• Ventricular irritability and VF arrest has been reported with
extreme hypercalcaemia
Quinine toxicity
Toxicity Mechanism:
• Class 1A antiarhythmic with both sodium and potassium blocking
properties thereby prolonging the QRS and QT intervals
B Blockers and Calcium Channel Blockers
• Effects on the ECG
• Sinus bradycardia.
• 1st degree, 2nd degree and 3rd degree AV block.
• Junctional bradycardia.
• Ventricular bradycardia.
• “A prolonged PR interval is an early sign of beta-blocker or calcium-
channel blocker toxicity — even in the absence of significant
bradycardia.”
Tricyclic Antidepressant Overdose
• ECG Features of Sodium-Channel Blockade
• Features consistent with sodium-channel blockade:
• Interventricular conduction delay — QRS > 100 ms in lead II
• Right axis deviation of the terminal QRS:
– Terminal R wave > 3 mm in aVR
– R/S ratio > 0.7 in aVR
• Patients with tricyclic overdose will also usually demonstrate sinus
tachycardia secondary to muscarinic (M1) receptor blockade.
• Typical ECG of TCA toxicity demonstrating:
• Sinus tachycardia with first-degree AV block (P waves hidden in the
T waves, best seen in V1-2).
• Broad QRS complexes.
• Positive R’ wave in aVR.