What are the expected Electrocardiogram (ECG) changes in Gastric Outlet Obstruction (GOO) with hypokalemic metabolic alkalosis?

ECG Changes in Gastric Outlet Obstruction with Hypokalemic Metabolic Alkalosis

The most characteristic ECG change in hypokalemic metabolic alkalosis associated with gastric outlet obstruction (GOO) is the presence of prominent U waves.

Pathophysiology and ECG Manifestations

Gastric outlet obstruction leads to persistent vomiting, which causes significant loss of gastric contents. This results in:

1. Metabolic alkalosis: Due to loss of hydrogen ions from gastric acid
2. Hypokalemia: Due to:
   • Direct potassium loss in vomitus
   • Secondary renal potassium wasting (as hydrogen ions are retained in exchange for potassium)
   • Increased aldosterone secretion from volume depletion

ECG Changes in Hypokalemia

According to the American Heart Association guidelines, hypokalemia produces characteristic ECG changes that progress with severity 1:

• Mild hypokalemia (3.0-3.5 mEq/L):

  • Flattening of T waves
  • ST-segment depression

• Moderate to severe hypokalemia (<3.0 mEq/L):

  • Prominent U waves (most characteristic finding)
  • Broadening of T waves
  • ST-segment depression
  • Prolonged QT interval (technically QU interval as U wave merges with T wave)

The U wave is particularly evident in leads V2 and V3, where it appears as a low-amplitude, low-frequency deflection after the T wave 1. In severe hypokalemia, the U wave may become more prominent and even exceed the T-wave amplitude in the same lead 1.

Clinical Significance and Complications

The ECG changes in hypokalemic metabolic alkalosis associated with GOO are clinically significant because:

1. They can lead to life-threatening arrhythmias including:

   • First or second-degree atrioventricular block
   • Atrial fibrillation
   • Ventricular arrhythmias (PVCs, VT, Torsades de Pointes)
   • Ventricular fibrillation and cardiac arrest 1

2. The ECG changes may be the first indicator of severe electrolyte disturbance before clinical symptoms appear

Case Evidence

Case reports confirm these ECG findings in patients with GOO:

• A 61-year-old man with gastric pyloric stenosis due to adenocarcinoma presented with severe metabolic alkalosis (pH 7.66) and hypokalemia (K 2.9 mEq/L) that was associated with prolonged QTc interval (0.52 seconds) on the ECG 2

• Another case report described a patient with severe hypokalemia (1.31 mmol/L) who showed typical ECG characteristics including dynamic changes in T-wave morphology, ST-segment depression, and prominent U waves, best seen in the mid-precordial leads (V2-V4) 3

Management Implications

Recognition of these ECG changes is crucial because:

1. They may be the first indication of severe electrolyte disturbance
2. They guide urgent treatment decisions
3. They help monitor response to therapy

Treatment should focus on:

• Correcting volume depletion with IV fluids
• Potassium repletion
• Addressing the underlying cause (GOO)
• Continuous ECG monitoring during correction 1

Conclusion

In the context of GOO with hypokalemic metabolic alkalosis, the most characteristic ECG change is the presence of prominent U waves (option B), which is a direct manifestation of hypokalemia. While QT prolongation (option A) may occur, it's often due to fusion of the U wave with the T wave rather than true QT prolongation. QRS widening (option C) is more characteristic of hyperkalemia, not hypokalemia.