Which electrolyte imbalances can cause Non-ST-Elevation Myocardial Infarction (NSTEMI) in susceptible individuals, particularly those with a history of cardiovascular disease, hypertension, diabetes, or hyperlipidemia?

Electrolyte Imbalances That Can Cause NSTEMI

While electrolyte imbalances do not directly "cause" NSTEMI in the traditional sense of plaque rupture and thrombosis, severe disturbances—particularly hypokalemia, hyperkalemia, hypomagnesemia, and hypocalcemia—can precipitate myocardial ischemia and infarction by creating supply-demand mismatch, triggering lethal arrhythmias, or causing coronary vasospasm.

Understanding the Pathophysiology

The key distinction is that NSTEMI fundamentally results from an imbalance between myocardial oxygen supply and demand 1. While the most common mechanism involves coronary artery narrowing from thrombus on disrupted plaque, the guidelines explicitly recognize that supply-demand mismatch from other causes can produce NSTEMI 1.

Electrolyte imbalances contribute through several mechanisms:

• Increased myocardial oxygen demand in the presence of fixed coronary stenosis (tachyarrhythmias from electrolyte disturbances) 1
• Dynamic coronary obstruction via vasospasm triggered by electrolyte abnormalities 1
• Severe arrhythmias causing hemodynamic compromise and reduced coronary perfusion 2

Specific Electrolyte Imbalances and Their Cardiac Impact

Hypokalemia (Most Clinically Significant)

Hypokalemia is the most important electrolyte disturbance in acute coronary syndromes, occurring in 17-34% of patients with acute myocardial infarction 3, 4, 5.

Critical thresholds and risks:

• Potassium <4.0 mEq/L significantly increases ventricular arrhythmia risk (59% vs 42% in normokalemic patients) 4
• Patients with potassium <4.0 mmol/L have 26% incidence of life-threatening ventricular arrhythmias versus 11.9% with normal levels 5
• Hypokalemia is an independent risk factor for lethal ventricular arrhythmias in acute MI 2

Mechanisms of cardiac injury:

• Prolongs QT interval, creating substrate for torsades de pointes and ventricular fibrillation 6
• Causes T-wave flattening, ST-segment depression, and prominent U waves 6, 7
• Can progress to ventricular tachycardia, ventricular fibrillation, or asystole 7
• Increases digitalis toxicity in patients on cardiac glycosides 7, 8

Common causes in cardiac patients:

• Loop and thiazide diuretics (most common) 7, 8
• Gastrointestinal losses with secondary hyperaldosteronism 7
• Primary aldosteronism (8-20% of hypertensive patients) 7

Hyperkalemia

Severe hyperkalemia can cause cardiac arrest and myocardial injury through direct effects on cardiac conduction 6.

Progressive ECG changes by severity:

• 5.5-6.5 mmol/L: Peaked T waves (often first sign) 6
• 6.5-7.5 mmol/L: Flattened P waves, prolonged PR interval, widened QRS complex 6

• 7.0-8.0 mmol/L: Sine-wave pattern, idioventricular rhythms, progression to asystole 6

Clinical significance:

• Hyperkalemia directly caused sudden cardiac arrest in hospitalized patients 6
• Can precipitate supply-demand mismatch through severe bradycardia and hemodynamic compromise 6

Hypomagnesemia

Magnesium deficiency amplifies the arrhythmogenic effects of other electrolyte disturbances and occurs in 4-22% of acute MI patients 4, 5.

Key clinical points:

• Hypomagnesemia frequently coexists with hypokalemia and makes potassium repletion difficult 7
• Contributes to QT prolongation and increases risk of torsades de pointes 6
• Associated with ventricular arrhythmias, particularly when combined with hypokalemia (10 of 13 patients with both had ventricular arrhythmias) 4
• Magnesium deficiency has been implicated in sudden death in heart failure patients 8

Treatment consideration:

• Magnesium bolus or infusion is recommended for torsades de pointes regardless of baseline magnesium level 6

Hypocalcemia

Hypocalcemia occurs in 9% of acute MI patients and predicts mortality 3.

Clinical significance:

• Hypocalcemia was a significant independent predictor of 1-month mortality (OR = 0.221, P = 0.014) in patients with myocardial infarction 3
• Contributes to QT prolongation and arrhythmia risk 6
• Changes in intracellular calcium contribute to arrhythmias with acute ischemia and reperfusion 2

Hyponatremia

Hyponatremia is highly prevalent (36% of acute MI patients) and predicts mortality 3.

Clinical significance:

• Significant independent predictor of 1-month mortality (OR = 0.789, P = 0.010) 3
• More common in STEMI than NSTEMI patients (significant difference, P < 0.001) 3
• Results from enhanced vasopressin and angiotensin release in heart failure, exacerbated by diuretics 8

Clinical Algorithm for Assessment

When evaluating patients with suspected NSTEMI:

1. Obtain immediate electrolyte panel including sodium, potassium, magnesium, and calcium on all patients with chest pain 3, 5

2. Identify high-risk electrolyte patterns:

   • Potassium <4.0 mEq/L (not just <3.5 mEq/L) 4, 5
   • Any degree of hypomagnesemia, especially with concurrent hypokalemia 4, 8
   • Hypocalcemia or hyponatremia in acute MI setting 3

3. Recognize ECG manifestations:

   • Hypokalemia: T-wave flattening, ST depression, prominent U waves, QT prolongation 6, 7
   • Hyperkalemia: Peaked T waves progressing to widened QRS and sine waves 6
   • Combined deficiencies: Marked QT prolongation suggesting torsades risk 6

4. Correct aggressively in acute MI:

   • Target potassium ≥4.0 mEq/L (not just >3.5 mEq/L) in all cardiac patients 7, 4
   • Correct magnesium concurrently with potassium (magnesium deficiency prevents effective potassium repletion) 7, 8
   • Use slow IV infusion for potassium; bolus administration is dangerous 7

Critical Pitfalls to Avoid

Do not dismiss borderline-low electrolytes (potassium 3.5-4.0 mEq/L) in acute coronary syndromes—this range still carries significantly increased arrhythmia risk 4, 5.

Do not correct hypokalemia without checking and correcting magnesium—magnesium is essential for maintaining intracellular potassium, and isolated potassium repletion will fail 7, 8.

Do not rely solely on serum magnesium levels—serum measurements poorly reflect intracellular magnesium status, and tissue depletion can exist with normal serum levels 8.

Do not overlook diuretic-induced electrolyte depletion as a contributor to acute coronary events—loop and thiazide diuretics cause substantial losses of both potassium and magnesium 7, 8.

Do not forget that patients on digoxin require more aggressive electrolyte management—hypokalemia and hypomagnesemia dramatically increase digitalis toxicity 7, 8.