IJCS | Volume 33, Nº1, January / February 2019

99 Rodrigues et al. Cardiac arrest after metoclopramide infusion Int J Cardiovasc Sci. 2020;33(1):98-101 Case Report renal function. She remained under sedation and mechanical ventilation until the beginning of the ninth day, being weaned without any major incidents. The prokinetic agent prescription was maintained even after gastroparesis improvement. However, by the tenth day, the administration of bolus metoclopramide was immediately followed by bradyarrhythmia and CRA (Cardiorespiratory Arrest) with Pulseless Electrical Activity (PEA). The management was performed according to the ACLS (Advanced Cardiovascular Life Support) protocol, with CPR (Cardiopulmonary Resuscitation), orotracheal intubation and administration of epinephrine (1 mg intravenously). The condition was reversed after one cycle, with no evidence of sequelae and followed by extubation one hour after the CRA. The electrocardiogram performed later showed sinus rhythm, with an electrical axis around +60º, with no changes in the Pwave or PR interval, heart rate of 83 bpm, QRS interval with normal morphology and amplitudes, no changes in the ST-segment and T wave and QTc interval of 376 msec. The p r e v i ou s l y pe r f o rmed t r an s t ho r a c i c echocardiogram, carried out on the 4 th day of ICU stay, had shown only discrete mitral regurgitation, without segmental alterations, with normal-sized cardiac chambers, with an ejection fraction of 69% (Teichholz). Before the event, the patient was breathing ambient air, with stable vital signs (HR: 98 bpm; blood pressure levels: 121x71 mmHg; RR: 20 breaths per minute; SO 2 : 99%; temperature: 36.3º C), conscious and oriented, with no alterations at the physical examination. The laboratory exams showed normal glycemia (112 mg/dL; and 127 mg/dL after the event) and potassium (4.6 mEq/L) levels and arterial blood gas analysis with mild respiratory alkalosis (pH: 7.469; PO 2 : 114.4 mmHg; PCO 2 : 31.8 mmHg; HCO 3 : 23.3 mmol/L; BE: 0.5 mmol/L). Immediately after the adverse reaction, the prescription of metoclopramide was modified to “if necessary” and withdrawn from the prescription for the next day. The patient was discharged from the ICU on the following day without further complications. Eight days later, after diabetes treatment adjustments, she was discharged from the hospital and is currently being followed in an outpatient endocrinology unit. Discussion Blockade of the dopaminergic pathways (D1 and D2 receptors) associated with gastrointestinal motility inhibition is characterized as the pharmacodynamic basis of metoclopramide, and in particular, blockade of central D2 receptors by the drug can cause dystonic extrapyramidal reactions and increase prolactin levels, considered the most common mechanisms of metoclopramide toxicity. 4 Moreover, this drug is a derivative of procainamide 3 and its cardiotoxic effect seems to involve the blocking of sodium channels, affecting the cardiac electrophysiology. 5 Despite the arrhythmogenic potential, there have been few reports of CRA associated with its use. These involved patients of both genders between 28 and 66 years of age, with a variety of clinical conditions and CRA after infusion of themedication (Table 1). There have been reports of five episodes following metoclopramide infusions in one patient with subarachnoid hemorrhage, two episodes of asystole inone patient at the postoperative period of partial mastectomy, one case in a patient admitted for abdominal pain and emesis, one report of bradycardia followed by cardiac arrest in a patient at the preoperative period for gastrectomy and one case of a patient with scleroderma who had CRA five minutes after the medication infusion. 4,6-9 All these cases have in common the intravenous administration of the same bolus dose ofmetoclopramide. It seems that the infusion time can have an impact on the occurrenceof the event, suchas extrapyramidal reactions. 10 It is noteworthy that there were no complications when the medication was administered by slow infusion in saline solution during the first days of treatment. Other medications prescribed on the day of the event were also evaluated. In addition to metoclopramide, unfractionated heparin, glargine and regular insulin, meropenem, methylcellulose eye drops, pantoprazole, nystatin, and topical triamcinolone were prescribed. At the time of the event, the patient remained under hydrationwith lactated Ringer’s solution in a continuous intravenous infusion at 21 mL/hour. Meropenem and methylcellulose were scheduled at the same time as metoclopramide but had not yet been administered. We emphasize the patient`s clinical stability on this day, including a scheduled ICU discharge. According to the Naranjo algorithm, CRA as a consequence of metoclopramide administration may be characterized as a probable adverse reaction (7 points). The risk can be higher in critically-ill patients with predisposing conditions, use of multiple medications, or it may be associated with prolonged use without