Description of Event or Problem · 0
AS A RESPONSIBLE MANDATED REPORTER, I SUBMIT THIS ON BEHALF OF THE AUTHORS IN AN EFFORT TO CLOSE THE GAP BETWEEN RESEARCH AND FDA ACKNOWLEDGED OUTCOMES: "THE FIRST MECT WAS COMPLETED UNEVENTFULLY WITHOUT SIGNIFICANT INCREASES IN BPAND HEART RATE (HR). ON HIS SECOND SCHEDULED MECT 2 DAYS LATER, BP AND HR WITH NORMAL SINUS RHYTHM WERE 100/60 MMHG AND 69 BPM, RESPECTIVELY, ON ARRIVAL IN THE OPERATING ROOM. THE FIRST STIMULUS, WHICH INDUCED CONSIDERABLE HYPERTENSION (BP 182/134 MMHG), SINUS TACHYCARDIA (HR 130 BPM), AND A SLIGHT PROLONGATION (0.46 S) OF QTC INTERVALS (FIG. 1A), COULD NOT ACHIEVE THE EXPECTED EFFICACY OF SEIZURE. THEREFORE, ABOUT 1 MIN AFTER THE FIRST STIMULUS, A SECOND ONE WAS APPLIED CONSECUTIVELY WITHOUT ADDITIONAL ADMINISTRATION OF THIOPENTAL, AND EFFECTIVE CONVULSIONS WERE OBTAINED. HOWEVER, THIS SECOND STIMULUS TRIGGERED MONOFOCAL ISOLATED AND COUPLETS OF PRE- MATURE VENTRICULAR CONTRACTIONS LASTING FOR APPROXIMATELY 20 S (FIG. 1B) ON ECG, FOLLOWED BY ABOUT 10 S OF VT CAUSING A LOSS OF PULSE AND THE DISAPPEARANCE OF THE FINGER PLETHYSMOGRAM ON A PULSE OXIMETER (FIG. 1C). IMMEDIATELY, CHEST COMPRESSION WAS PERFORMED SEVERAL TIMES, RESULTING IN THE SUCCESSFUL RESTORATION OF SPONTANEOUS AND NORMAL SINUS RHYTHM USING NO ANTIARRHYTHMIC AGENT. INTRAVENOUS 0.5 MG OF NICARDIPINE FOR PERSISTENT HYPERTENSION AFTER THE RESTORATION OF SINUS RHYTHM RESTORED A NORMOTENSIVE STATE. SPO2 WAS MAINTAINED AT BETWEEN 97 AND 100% THROUGHOUT THE COURSE OF EVENTS. HE RECOVERED SMOOTHLY FROM ANESTHESIA WITHOUT ANY ADVERSE CONSEQUENCES OR POSTOPERATIVE COMPLICATIONS. BECAUSE OF THIS INCIDENTAL VT, ALL SUBSEQUENT ATTEMPTS TO PERFORM MECT WERE CANCELED. POSTOPERATIVELY, CLOSE EXAMINATION--INCLUDING AN ECG AT REST, HOLTER ECG, ECHOCARDIOGRAM, CHEST ROENTGENOGRAM, AND BIOCHEMICAL LABORATORY DATA--FAILED TO CLARIFY ANY POSSIBLE CAUSE OF VT, SUCH AS LONG QT SYNDROME, BRUGADA SYNDROME, EARLY REPOLARIZATION SYNDROME, TORSADES DE PO- INTES, ISCHEMIC HEART DISEASES, DISORDERED ELECTROLYTES OF CALCIUM, MAGNESIUM, POTASSIUM OR OTHER CONDITIONS. IN RECENT YEARS, MECT UNDER GENERAL ANESTHESIA HAS BEEN WIDELY EMPLOYED TO TREAT VARIOUS KINDS OF DRUG-RESISTANT DEPRESSIVE STATES. IT IS WELL KNOWN THAT MECT INDUCES STIMULATION OF THE AUTONOMIC NERVOUS SYSTEM WITH INITIAL PARASYMPATHETIC OUTFLOW IMMEDIATELY FOLLOWED BY SYMPATHOTONIC RESPONSES. MOST OF THESE RESPONSES, CONSISTING OF INITIAL BRADYCARDIA, ARRHYTHMIAS, AND SUBSEQUENT HYPER-TENSION AND TACHYCARDIA, ARE IN GENERAL TRANSIENT AND RECOVER SPONTANEOUSLY. HOWEVER, THERE HAVE BEEN SEVERAL REPORTS OF LIFE-THREATENING ARRHYTHMIAS IN RELATION TO MECT, INDICATING THAT PREDISPOSING FACTORS TO THESE ARRHYTHMIAS MIGHT INVOLVE PRE-EXISTING ISCHEMIC HEART DISEASE, SUXAMETHONIUMINDUCED HYPERKALEMIA, AND TACHYCARDIA DUE TO THE USE OF ATROPINE AS PREMEDICATION. CONCERNING ATROPINE, THE AUTHORS ADMINISTERED IT 30 MIN BEFORE TRANSFERRING THE PATIENT TO THE OPERATING ROOM AS ROUTINE PREMEDICATION FOR MECT IN ORDER TO DECREASE THE SALIVARY SECRETION, WHICH IS OCCASIONALLY FACILITATED BY ANTIPSYCHOTICS. HOWEVER, THE PATIENT DID NOT DEMONSTRATE TACHYCARDIA, POSSIBLY INDUCED BY ATROPINE, ON ARRIVAL IN THE OPERATING ROOM. IN OUR PATIENT, THEREFORE, THESE FACTORS COULD BE RULED OUT. WITH RESPECT TO THE QTC INTERVAL, IT HAS BEEN POINTED OUT THAT MECT CAN PROVOKE PROLONGATION OF QTC INTERVALS. IN OUR PATIENT, THE QTC INTERVAL SPREAD TO 0.46 S FOLLOWING THE CONVULSIONS. HOWEVER, THE DEGREE OF PROLONGATION WAS SO SMALL THAT IT APPEARS TO SUGGEST LITTLE CLINICAL SIGNIFICANCE. DRUG-INDUCED QTC PROLONGATION HAS BEEN INDICATED FOR ANTIPSYCHOTICS SUCH AS CHLORPROMAZINE AND HALOPERIDOL, TRICYCLIC ANTIDEPRESSANTS SUCH AS IMIPRAMINE, AMITRIPTYLINE AND DOXEPIN, AND SELECTIVE SEROTONIN RECEPTOR INHIBITORS LIKE FLUOXETINE, WHILE NONE OF THE DRUGS POTENT ENOUGH TO INDUCE PROLONGATION OF THE QTC INTERVAL WERE PRESCRIBED FOR OUR PATIENT. MACRO-AND MICROSHOCK CAN BE RESPONSIBLE FOR CARDIAC ARRHYTHMIAS THROUGH ELECTRICAL IMPLEMENTS. THE LEAKAGE CURRENTS DERIVED FROM THE PULSE WAVE GENERATOR USED FOR HIM, MEASURED USING A TESTER (3155 LEAK CURRENT HITESTER, HIOKI E.E., UEDA, NAGANO, JAPAN), WERE 11¿17 LA: WELL BELOW THE VALUES PERMITTED BY JAPANESE INDUSTRIAL STANDARDS FOR MEDICAL EQUIPMENT. ACCORDINGLY, MACRO- SHOCK WAS RULED OUT AS THE REASON FOR HIS ARRHYTHMIAS. THUS, IN OUR CASE, THE REASON THAT THE FIRST ELECTRIC STIMULUS FAILED TO PRODUCE AN EFFECTIVE CONVULSION AND VT IS STILL UNCLEAR. HOWEVER, IT IS CLEAR THAT, UNDER THE CONDITION OF UNCONTROLLED HEMODYNAMICS, CONSIDERABLE SYMPATHOTONIC INCREASES IN BP AND HR FOLLOWING THE ELECTRIC STIMULI AUGMENTED THE CARDIAC OXYGEN DEMAND, MYOCARDIAL CONTRACTILITY, AND SERUM CATECHOLAMINE LEVEL, RESULTING IN RELATIVE MYOCARDIAL ISCHEMIA. THEREFORE, THE USE OF CALCIUM CHANNEL AND/OR BETA BLOCKERS BEFORE APPLYING ELECTRIC STIMULI SHOULD BE CONSIDERED IN ORDER TO ATTENUATE HEMODYNAMIC HYPERACTIVITY [8, 15, 17]. WE USED NICARDIPINE, A CALCIUM CHANNEL BLOCKER, AGAINST PERSISTING HYPERTENSION EVEN AFTER THE RESTORATION OF NORMAL SINUS RHYTHM. HAD THE NICARDIPINE BEEN ADMINISTERED PROPHYLACTICALLY, THESE ADVERSE EVENTS COULD HAVE BEEN PREVENTED (ALTHOUGH, TO OUR REGRET, THE BP AND HR WERE NOT MEASURED JUST BEFORE AND AFTER THE SECOND ELECTRIC STIMULUS). THE AUTHORS DID NOT ADMINISTER THIOPENTAL ADDITIONALLY BEFORE THE SECOND STIMULUS. HOWEVER, IT MIGHT BE NECESSARY TO CHECK THE LEVEL OF AWARENESS WITH THE EEG IN ORDER TO PREVENT AWARENESS AND, IF NECESSARY, ADDITIONAL THIOPENTAL SHOULD BE GIVEN IF THE FIRST STIMULUS FAILS. THE PRECISE INCIDENCE OF MECT-INDUCED ARRHYTHMIAS IS UNKNOWN, BUT CAUTION IS ADVISED, ESPECIALLY IN PATIENTS AT HIGH RISK FOR CARDIAC ARRHYTHMIAS. IT IS HIGHLY IMPORTANT TO BE AWARE THAT MECT HAS THE POTENTIAL TO INDUCE UNPREDICTABLE AND LIFE-THREATENING ARRHYTHMIAS LIKE VT. HTTP://LINK.SPRINGER.COM/10.1007/S00540-011-1166-8. FDA SAFETY REPORT ID# (B)(4).