Summary of Case

Patient: 59-year-old male, weight 45 kg, underwent gastrectomy.

Postoperative course: On postoperative day 2 he developed supraventricular tachycardia (SVT).

Key clinical data:

• Recent transthoracic echocardiogram (23 June 2025): moderate systolic dysfunction (EF 20–40%), global left ventricular hypokinesia, grade I LV diastolic dysfunction, and mild pulmonary arterial hypertension (RVSP > 27 + RAP mmHg).
• Urine output poor (≈30 ml/hour); treated with dopamine infusion (200 mg in 50 ml at ~3 ml/hr ≈ 3.6 µg/kg/min), 20% albumin 20 ml, and furosemide 20 mg with limited response.
• At SVT onset: pulse 90 bpm with frequent PVCs (~10/min), blood pressure 110/74 mmHg.

Reference: Dunning J, Treasure T, Versteegh M, Nashef SA. Eur J Cardiothorac Surg. 2006;30(6):852–72.

Clinical Context and Echocardiographic Correlates

Cardiac compromise: The echocardiogram demonstrates reduced systolic function (EF 20–40%) and global hypokinesia, indicating limited contractile reserve. Grade I diastolic dysfunction and mild pulmonary hypertension alter ventricular filling and right-heart interaction, increasing vulnerability during stress.

Myocardial substrate: Global hypokinesia and paradoxical septal motion suggest diffuse myocardial disease rather than an isolated regional ischemic lesion. This substrate predisposes to arrhythmias under metabolic, hemodynamic, or pharmacologic stress.

Practical implication: The patient’s limited cardiac reserve, electrical instability (PVCs), and postoperative haemodynamic perturbations require careful rhythm management, invasive monitoring, and minimization of proarrhythmic interventions.

Reference: Lang RM, et al. J Am Soc Echocardiogr. 2015;28(1):1–39.e14.

Mechanisms Contributing to SVT in this Patient

Perioperative sympathetic activation

Surgery and the postoperative inflammatory state activate the hypothalamic–pituitary–adrenal axis and sympathetic nervous system, increasing circulating catecholamines. β1-adrenergic receptor stimulation raises intracellular cAMP and calcium influx through L-type channels, enhancing atrial automaticity and favoring re-entrant activity.

Catecholamine effect of dopamine infusion

At ~3.6 µg/kg/min, dopamine exerts β1 and dopaminergic receptor effects. β1 stimulation increases contractility and heart rate propensity and can facilitate early afterdepolarizations or re-entry in an irritable myocardium. In a heart with low EF and PVCs, dopamine may be proarrhythmic; alternative inotropes or vasopressors may be preferable depending on the haemodynamic goal.

Electrolyte and volume disturbances

Diuretic therapy and ongoing fluid shifts can cause hypokalemia or hypomagnesemia, which destabilize transmembrane ion gradients (Na+/K+-ATPase and potassium channels) and lower the threshold for triggered activity and re-entry. Hypovolemia or inadequate renal perfusion may also contribute indirectly.

Underlying structural/electrophysiological substrate

Myocardial fibrosis or diffuse cardiomyopathy changes ion-channel expression and conduction heterogeneity, creating fixed substrates for re-entry. Atrial stretch from elevated filling pressures or pulmonary hypertension increases ectopic activity.

Hypoxia and acid-base derangements

Hypoxia, oxidative stress, and acidosis alter ion-channel function and conduction velocity, favoring arrhythmogenesis. Maintaining adequate oxygenation and correcting acid–base disturbances reduce arrhythmic risk.

References: Maesen B, et al. Europace. 2012; Overgaard CB & Dzavík V. Circulation. 2008; Gennari FJ. N Engl J Med. 1998; Nattel S, et al. Circ Arrhythm Electrophysiol. 2008.

Pathophysiology Summary

In this postoperative patient the most likely mechanism is multifactorial: heightened sympathetic tone and β1 stimulation (endogenous catecholamines plus dopamine), electrolyte derangement and diuretic effects, and a vulnerable myocardial substrate (reduced EF, global hypokinesia, potential fibrosis) combine to produce atrial/nodal automaticity or re-entrant SVT. Frequent PVCs indicate myocardial irritability that precedes sustained supraventricular arrhythmia.

Reference: Page RL, et al. Circulation. 2016;133(14):e506–74.

Immediate Management Recommendations

1. Assess and correct reversible triggers

• Obtain urgent arterial blood gas and serum electrolytes; correct potassium (aim >4.0 mmol/L) and magnesium (aim >0.8 mmol/L) promptly.
• Ensure adequate oxygenation (SpO₂ ≥95%) and correct hypoxia or hypercarbia.
• Review acid–base status and correct marked acidosis.

1. Hemodynamic and inotropic review

• Reassess need for ongoing dopamine; if inotropic support remains necessary consider alternatives with less proarrhythmic potential (for example, dobutamine for inotropy or norepinephrine if vasoconstriction is required). Titrate to clinical endpoints (MAP, urine output, lactate).
• Optimize preload carefully—balance between improving renal perfusion and not overloading an impaired LV.

1. Acute rhythm control

• If the rhythm is SVT with haemodynamic compromise, follow ACLS/arrhythmia algorithms: synchronized cardioversion if unstable.
• For stable SVT, attempt vagal maneuvers where appropriate; administer adenosine (6 mg rapid IV push, then 12 mg if needed) for regular narrow-complex SVT while being mindful of underlying atrial fibrillation or other diagnoses.
• If atrial fibrillation or rapid atrial arrhythmia is suspected or adenosine contraindicated, consider rate control with short-acting agents: esmolol infusion or cautious diltiazem depending on blood pressure and LV function. Use calcium channel blockers with caution when systolic function is severely depressed.
• For refractory or hemodynamically significant arrhythmias, amiodarone is an option; consult cardiology.

1. Specialist input

• Urgent cardiology/electrophysiology consult for guidance on antiarrhythmic selection, need for transesophageal echocardiography (if thrombus evaluation or hemodynamic assessment is required), and advanced options.

1. Monitoring and anesthesia considerations

• Institute continuous ECG monitoring with rhythm strips; consider invasive arterial pressure monitoring if not already present.
• Avoid medications that further depress contractility or prolong QT interval. Choose sedatives and analgesics that are hemodynamically neutral when procedural sedation is needed.
• Maintain close urine-output monitoring and reassess renal perfusion strategies.

References: January CT, et al. J Am Coll Cardiol. 2014; Overgaard & Dzavík. Circulation. 2008.

Practical and Anesthetic Takeaways

• The arrhythmia is likely precipitated by a combination of exogenous catecholaminergic stimulation (dopamine), electrolyte/volume derangements, perioperative sympathetic activation, and an arrhythmogenic myocardial substrate.
• Immediate priorities are correction of reversible causes (electrolytes, oxygenation, acid–base), re-evaluation of inotropic therapy, acute rhythm management per stability, and urgent specialist involvement.
• Anesthesia and critical-care management should prioritize haemodynamic support tailored to poor LV function, minimize proarrhythmic drugs, and use short-acting agents that allow rapid titration.

Conclusion

This postoperative SVT is best viewed as a multifactorial event in a patient with limited cardiac reserve. Management must be dynamic: treat reversible precipitants, reconsider inotropic strategy, apply algorithmic arrhythmia therapy based on haemodynamic stability, and involve cardiology early. Vigilant monitoring and individualized hemodynamic support are essential to reduce recurrent arrhythmia and optimize outcome.