Vomiting, NG Suction, and 'Therapeutic' Digoxin: Reading the Electrolytes
Mr. A., 63, has been admitted for four days of persistent vomiting followed by nasogastric suction for a small-bowel obstruction. He takes digoxin 0.125 mg daily for atrial fibrillation and furosemide 40 mg daily for heart failure. Overnight his urine output has fallen and he is drowsy and anorexic. Morning results:
pH 7.50 | PaCO2 47 mmHg | HCO3 36 mEq/L | Na 134 | K 2.9 | Cl 92 | Creatinine 1.5 mg/dL (baseline 0.9) | Digoxin 1.9 ng/mL | Mg 1.6 mg/dL
Telemetry shows a heart rate of 52 with a PR interval that has lengthened from 0.18 to 0.24 seconds since admission. The covering clinician says the digoxin level is 'within range, so it is not the digoxin.'
1. Interpret the acid–base picture, including whether the PaCO2 represents appropriate compensation or a second primary disorder.
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Primary disorder: metabolic alkalosis with appropriate respiratory compensation.
- pH 7.50 = alkalaemia, so the dominant process is alkalosis.
- HCO3 36 mEq/L is far above 24, confirming a metabolic alkalosis.
- Is the CO2 rise appropriate? Expected PaCO2 rises about 0.7 mmHg for every 1 mEq/L rise in HCO3. ΔHCO3 = 36 − 24 = 12, so expected PaCO2 ≈ 40 + (12 × 0.7) ≈ 48 mmHg. The measured 47 mmHg fits - this is compensation (hypoventilation), not a primary respiratory acidosis. If the CO2 were much higher than predicted, you would look for a coexisting respiratory acidosis.
- Anion gap = 134 − (92 + 36) = 6 - normal. This is a chloride-responsive, hypochloraemic alkalosis, consistent with loss of gastric H+ and Cl− from vomiting and NG suction, worsened by loop diuretic use.
- A urine chloride under 20 mEq/L would support the chloride-responsive state and predict response to saline.
The rising creatinine (0.9 → 1.5) signals volume depletion and reduced renal clearance - which matters directly for the digoxin question.
2. Explain why this patient can show digoxin toxicity at a level of 1.9 ng/mL, and what findings you would monitor for.
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A 'therapeutic' level is not reassuring when potassium and renal function are abnormal.
Mechanisms:
- Digoxin binds the Na+/K+-ATPase at a site that competes with potassium. When serum K falls, more digoxin binds and the same level produces a greater effect. A level of 1.9 ng/mL with K 2.9 mEq/L is functionally much higher than the number suggests.
- Alkalosis increases myocardial sensitivity to digoxin.
- Volume depletion and a creatinine rise from 0.9 to 1.5 mean reduced digoxin clearance: the level will continue to climb if nothing changes.
- Furosemide contributes to both hypokalaemia and chloride loss, perpetuating the alkalosis.
Monitor for:
- Cardiac: bradycardia (already 52), lengthening PR interval (0.18 → 0.24 s), AV block, junctional rhythm, PVCs, bigeminy, VT.
- GI: anorexia (already present), nausea, vomiting - easily misattributed to the bowel obstruction.
- Neurologic: confusion, drowsiness, weakness.
- Visual: blurred vision, yellow-green halos.
The clinician's reasoning is the trap here: the level is interpreted without the potassium, the pH, or the trend in creatinine.
3. List your priority interventions and monitoring over the next few hours, with the physiological rationale for each.
Read the worked answer
Priorities: stop the offending drugs, correct the chloride and potassium deficits, and watch the rhythm.
- Hold digoxin and furosemide and notify the prescriber with the full picture (K 2.9, HCO3 36, creatinine 1.5, HR 52, prolonged PR) - not just 'the level is 1.9.'
- Telemetry on, and print rhythm strips. Bradycardia with PR prolongation is the earliest objective sign of toxicity here.
- Replace potassium, mindful of urine output - never infuse potassium rapidly into an oliguric patient. Follow facility limits for peripheral versus central rates.
- Replace magnesium (1.6 mg/dL): hypomagnesaemia makes hypokalaemia refractory to correction.
- Restore chloride and volume with 0.9% sodium chloride. Chloride is what corrects a chloride-responsive alkalosis - potassium chloride and saline both supply it; adding KCl to D5W alone will not fix the alkalosis.
- Treat the ongoing losses: optimize NG decompression, record output, consider H2 blockade to reduce gastric acid loss.
- Reassess labs (BMP, magnesium, repeat digoxin level) at an interval the prescriber specifies, and trend creatinine and urine output hourly.
- Anticipate escalation: if there is high-grade AV block, haemodynamic compromise, or ventricular dysrhythmia, the antidote is digoxin-specific antibody fragments - ask early rather than late.
- Do not overcorrect: rapid full correction of chronic alkalosis can cause seizures and dysrhythmias. Aim for steady, monitored correction.