Additive effect of propofol and fentanyl precipitating cardiogenic shock.

The intravenous administration of propofol and fentanyl has become a common practice in a variety of clinical settings including outpatient dermatologic, cosmetic and oral surgery. The combination provides both systematic sedation and analgesia with low incidence of unwanted side effects. The cardiogenic shock is very uncommon in healthy individuals. The cardiovascular depressive effect of propofol and fentanyl has been well established, but the development of cardiogenic shock is very rare when these drugs are used together. Hence the awareness of this effect is advantageous to the patients undergoing such surgeries.

INTRODUCTION

The sedatives and analgesics used during anesthetic procedures are known to produce undesirable effects on cardiac hemodynamics. This hemodynamic deterioration sometimes leads to multiple organ failure in post operative period.[1] But there is no other diagnostic test to evaluate this emergency situation except a meticulous clinical observation of sustained hypotension with tissue hypoperfusion despite adequate left ventricular filling pressure and oliguria. The development of advanced technology in the line of treatment such as extracorporeal life support (ELS), a variation of cardiopulmonary bypass, can improve the outcomes of cardiogenic shock.[2] Although propofol and fentanyl are known to depress the myocardial function with reduced left ventricular ejection fraction (LVEF),[34] cardiogenic shock is not yet reported when the patients are treated with these drugs. This case has been reported to create awareness among the prescribers to evaluate and manage the outcome of critical clinical situation during administration of these drugs.

CASE REPORT

A 34-year-old woman presented with complaints of umbilical hernia and had no secondary infection on clinical examination. The surgery was performed under conscious sedation and analgesia procedure which is routinely preferred by the anesthetists for minor surgeries. The patient experienced sudden, severe hemodynamic deterioration after undergoing this minor surgical procedure. Spontaneous breathing was maintained by continuous infusion of propofol at a rate of 100 μg/kg/min to achieve conscious sedation after administering fentanyl 100 μg intravenously. During surgery, the patient remained hemodynamically stable. Patient had nausea and vomiting in the early postoperative period, which were treated with 4 mg of intravenous ondansetron. A few minutes later, the patient experienced hemodynamic instability with sinus tachycardia and hypotension. Her heart rate was 122 regular beats/minute, and the blood pressure was 50/30 mmHg. The oxygen saturation had decreased to 80% as recorded by pulse oximetry, despite oxygen supply through face mask. She was immediately treated with intravenous dopamine and dobutamine as well as with ventilator support due to acute respiratory failure. The arterial gasometry showed oxygen pressure 40 mmHg and carbon dioxide pressure 49 mmHg; the electrocardiogram monitor showed sinus tachycardia. The signs of heart failure (HF) were found in the bedside digital X-ray of chest and emergency transthoracic echocardiography (TTE) revealed severe biventricular dysfunction with global hypokinesia. The LVEF was 42%. Coronary angiography showed no coronary lesions. An intra-aortic balloon pump was introduced for counterpulsation. The repeat TTE revealed LVEF 32% and a left ventricular extracorporeal membrane oxygenation (ECMO) device was inserted to assist the impaired clinical course of the patient. The LVEF gradually improved and on the 5th postoperative day the ventilatory support and circulatory perfusion assistance were removed. Troponin T and C reactive protein levels remained within normal limits. The other routine investigations like chemistry panel, complete blood cell count, and coagulation profile were within normal limits. The serology battery for myocarditis, blood cultures, urine cultures, and cytotoxic antibodies were found insignificant. An endomyocardial biopsy was not performed because of its low diagnostic yield. Three weeks later, a new TTE showed a non-dilated left ventricle, absence of segmental contractility alterations, and an LVEF in the normal range. She was reviewed for 6 months in out-patient department and was found asymptomatic and required no further treatment.

DISCUSSION

In this patient, the etiology of cardiogenic shock can be discussed to rule out many other possibilities which can cause cardiogenic shock. Postpartum cardiomyopathy usually develops in late pregnancy or during first few months after delivery.[5] It is very unlikely since this patient had delivery 6 years ago and underwent sterilization surgery. A viral infection can cause myocarditis, but her sudden clinical deterioration, with no history of infection, and negative serological tests make this diagnosis unlikely. Propofol infusion syndrome includes arrhythmias, hemodynamic deterioration, metabolic acidosis, rhabdomyolysis, and impaired renal and hepatic function.[6] This clinical entity has been described mainly in pediatric critical care patients and has been associated with prolonged use (>48 h) and high doses (>4 mg/kg/h).[7] Ondansetron is considered to be a safe class of medications for postoperative nausea and vomiting.[8] Takotsubo cardiomyopathy (TTC) is an acute cardiac syndrome mimicking elevated ST-segment myocardial infarction, characterized by transient regional wall motion abnormalities involving the apical and middle portions of the left ventricle in the absence of significant obstructive coronary disease.[9] In this patient, the absence of electrocardiographic and echocardiographic alterations suggestive of TTC leads us to reject this diagnostic possibility. The association of propofol and fentanyl as a cause of severe, acute HF has been described.[10] Both propofol and fentanyl may cause depression of ventricular function and decreased blood pressure. Propofol dilates the arteries by inducing nitric oxide synthesis, blocks calcium channels, and activates protein kinase C, all of which, taken together, lead to a decrease in pre-load and a decline in cardiac output. Apart from this possibility, dose-dependent intrinsic negative inotropic effect attributable to propofol itself has also been reported.[1112] It occurs most often when used in combination with fentanyl and in patients with or without previous heart disease.[13] Both mechanisms might trigger a state of cardiogenic shock in patients with individual susceptibility.

CONCLUSION

Various causes can be attributed to cardiogenic shock during the anesthetic procedures. In this case, the abrupt hemodynamic deterioration in the absence of clear causative factor could be related to the use of propofol and fentanyl.