1) In a retrospective review of reported citalopram overdoses in 26 patients, QTc interval prolongation occurred in 8 patients and bundle-branch block (BBB) occurred in 3 patients (2 patients with left BBB and 1 patient with right BBB). Atrioventricular block was reported in 1 patient and extrasystoles, in 2 patients. Among the 26 patients, the estimated amounts ingested ranged from 200 to 4960 mg (median 1190 mg) (Jimmink et al, 2008).
2) In a series of 225 cases of overdose with newer antidepressants, patients suffering citalopram overdose (n=88) had significantly longer QT intervals on ECG than those taking venlafaxine, mirtazapine, or nefazodone (Kelly et al, 2004).
3) In a review of 108 cases of citalopram overdose, approximately 25% of the patients had ECG changes such as nonspecific changes of the ST-T region and moderate widening of the ECG complexes. However, no clinically significant arrhythmias were reported (Personne et al, 1997).

1) A 54-year-old woman with psychotic depression treated with citalopram 20 mg/day and zopiclone 7.5 mg/day developed delayed dysrhythmias after intentionally ingesting an unknown amount of citalopram with alcohol. She presented to the emergency department (time of ingestion unknown) with altered mental status, hypotension, and low O2 saturation. A positive bilateral Babinski (without sensory motor deficit) and jugular vein distension were noted upon examination. Laboratory analysis showed a blood ethanol level of 0.2 g/L, lactic acidosis, hypokalemia, metabolic acidosis, and a serum citalopram level of 5.88 mg/L (therapeutic range 0.01 to 0.2 mg/L). Urine screening was negative for opiates, cocaine, benzodiazepines, and tricyclic antidepressants. She was treated with 50 g activated charcoal and admitted to ICU. Upon admission to ICU, she seized and developed ventricular fibrillation (VF) which was treated successfully with midazolam and defibrillation. A prolonged QT interval of 0.44 seconds (QTc 0.62 seconds) with left bundle branch block was noted on ECG; however, cardiac enzymes were negative for myocardial infarction. Sustained ventricular tachycardia with VF episodes occurred 10 hours after ICU admission and continued for 48 hour, requiring repeated defibrillation. She recovered fully and was discharged 16 days after admission (Liotier & Coudore, 2011).
2) A 31-year-old man developed sinus tachycardia (130 beats/min) with a widened QRS complex (124 msec) with a left bundle-branch block, and prolonged QTc (506 msec) after ingesting 400 mg citalopram. The QRS complex narrowed (96 msec) with resolution of the left bundle-branch block pattern, and the QTc interval shortened (495 msec) after administration of sodium bicarbonate (Engebretsen et al, 2003).
3) An 82-year-old woman developed a generalized tonic-clonic seizure approximately 12 hours after ingesting citalopram 1.6 g in a suicide attempt. Although her cardiovascular and pulmonary examinations were unremarkable, an initial ECG showed sinus bradycardia with a ventricular rate of 58 beats/min, left axis deviation, and left bundle-branch block, which were consistent with her previous ECGs. In addition, the QRS duration, QT interval, and QTCs interval were 146 msec, 544 msec, and 534 msec, respectively. Three hours after she was transferred to telemetry service, marked bradycardia was observed. A 12-lead ECG showed a junctional escape rhythm with a ventricular rate of 40 beats/min, retrograde ventriculoatrial activation, and an underlying left bundle-branch block. The QRS duration, QT interval, and QTc interval were 152 msec, 646 msec, and 527 msec, respectively. The administration of sodium bicarbonate solution 50 mEq (50 mL of 8.4% solution) by direct intravenous injection on 2 different occasions caused a dramatic but temporary impact on the ECG findings. These effects quickly reverted to the previous junctional bradycardia. Approximately 3 hours after starting a continuous infusion of sodium bicarbonate 150 mEq in 1 liter of 5% dextrose in water (a rate of 75 mL/hour or 11.25 mEq/hour), normal sinus rhythm with a rate of 63 beats/min, a QT interval of 510 msec, and a QTc interval 504 msec were noted. After 36 hours, the infusion was stopped and no new ECG abnormalities were observed (Brucculeri et al, 2005).
4) Persistent bidirectional wide-complex tachycardia, QRS prolongation, QTc widening, left bundle-branch block, and seizures were reported in a 22-year-old woman who ingested citalopram 1200 mg in a suicide attempt. She reverted to normal sinus rhythm within 5 hours of presentation (Sztajnkryeer et al, 2003).
5) A 36-year-old woman developed palpitation, weakness, nausea, and numbness 36 hours after taking citalopram 1000 mg with alcohol. On day 3, her vital signs were blood pressure, 84/44 mmHg; temperature, 99.3 degrees F; pulse, 102 to 160 beats/min; and respiratory rate, 17 breaths/min. ECG revealed intermittent runs of wide-complex tachycardia with a QTc of 600 msec. Despite saline and magnesium sulfate infusions, she developed intermittent bigeminy, and despite IV lidocaine, intermittent torsade de pointes occurred. After receiving potassium chloride, transvenous pacemaker insertion, and isoproterenol infusion, she converted to normal sinus rhythm, and QTCs interval narrowed to 442 msec after 2 days. Her plasma citalopram level was 477 ng/mL (therapeutic range 40 to 110 ng/mL), with a corresponding desmethylcitalopram level of 123.2 ng/mL (therapeutic range 14 to 40 ng/mL) (Tarabar et al, 2003).
6) A 21-year-old ingested 20 citalopram 20 mg tablets after drinking a "couple of beers" (blood alcohol 121 mg/dL) and taking one alprazolam 0.25 mg tablet. The patient received gastrointestinal decontamination. One hour after ingestion, the patient was in normal sinus rhythm with a QTc interval of 380 msec, and within 2 hours she had a QTc interval of 438 msec. At 7 hours the QTc was 450 msec, and at 13 hours it was 457 msec. Subsequent monitoring showed a QTc of 393 msec approximately 20 hours after ingestion. The delay in peaked effect was likely due to the cardiotoxicity of the metabolite DDCT. The authors noted that this overdose was relatively small (less than 7 times the recommended maximum daily dose of 60 mg), but QT prolongation still occurred (Catalano et al, 2001).
7) Right bundle-branch block and QRS prolongation (136 msec) were reported in a 21-year-old man following an overdose of citalopram 1800 mg, fluoxetine 1000 mg, and acetaminophen 2500 mg. The patient's citalopram serum level was 840 ng/mL (ten times the reported therapeutic concentration of 80 ng/mL). ECG abnormalities resolved spontaneously (QRS 100 msec; normal axis) within 36 hours of ingestion (Grover & Caravati, 2001).
8) Five cases of QTc prolongation and sinus tachycardia have been reported following severe nonfatal citalopram overdoses (range 400 to 5200 mg) (Grundemar et al, 1997).
9) Wide-complex right bundle-branch block with multiple episodes of monomorphic ventricular tachycardia, and a widened QRS were reported in a 19-year-old man who intentionally ingested an unknown amount of citalopram. The serum citalopram concentration, obtained at time of presentation, was 1500 ng/mL (therapeutic, 9 to 200 ng/mL). The patient's ECG abnormalities resolved following supportive therapy (Maddry et al, 2013).
10) ESCITALOPRAM: A 32-year-old woman developed nausea, vertigo, confusion, palpitation, drowsiness, slight leukocytosis, mild fever, tachycardia (pulse 120 beats/min), and mild hypotension (blood pressure 100/70 mmHg) after ingesting escitalopram 190 mg. ECG revealed an increased QT interval and sinus tachycardia. Following supportive care, she recovered and was discharged 24 hours after hospitalization (Yuksel et al, 2005). Another patient, a 14-year-old girl, experienced a prolonged QTc interval after ingesting escitalopram 200 mg. She presented to the emergency department approximately 24 hours postingestion, and an ECG showed normal sinus rhythm with a QTc interval of 450 msec. The following day (2 days postingestion), a repeat ECG showed a QTc interval of 469 msec. That same day, her QTc interval normalized to 420 msec spontaneously, and she was transferred to a psychiatric facility (Scharko & Schumacher, 2008).
11) Approximately 16 hours after a 46-year-old woman intentionally ingested 1400 mg of citalopram, an ECG was performed revealing a prolonged QTc interval of 541.6 ms. At approximately 29 hours post-ingestion, the initial citalopram serum concentration was 1231 ng/mL. Over the course of several days, the patient's serum citalopram concentration and QTc interval were determined within 24 hours of each other in 6 different instances, and determined on the same date in 5 cases, showing a similar rate of decline, indicating a direct correlation between the serum concentration of citalopram and QTc interval prolongation that was statistically significant (r=0.943; p<0.005) (Unterecker et al, 2012).
12) ESCITALOPRAM: A 16-year-old girl, with a history of depression, presented to the emergency department with vomiting and slight lethargy approximately 2.5 hours after ingesting 500 mg of escitalopram, 25 tablets of tramadol/acetaminophen, and an unknown amount of hydrocodone/acetaminophen. An ECG revealed an incomplete right bundle branch block with a widened QRS complex (110 ms) and a QTc interval of 482 ms. Ten minutes following administration of an IV bolus of sodium bicarbonate (100 mEq), a repeat ECG revealed narrowing of the QRS complex (102 ms) and QTc interval prolongation (509 ms). A sodium bicarbonate infusion and IV magnesium sulfate were subsequently initiated, resulting in normalization of her QRS complex and QTc interval. The patient's serum escitalopram concentration, obtained approximately 8 hours post-ingestion, was 45 mcg/L (Schreffler et al, 2013).

1) In a similar case, a 21-year-old man developed a seizure 14 hours after an intentional ingestion of citalopram 1800 mg (serum level 10 times the normal therapeutic range of 840 ng/mL), fluoxetine 1000 mg (normal serum level), and acetaminophen 2500 mg. The patient recovered without sequelae (Grover & Caravati, 2001).

1) A 54-year-old woman with psychotic depression treated with citalopram 20 mg/day and zopiclone 7.5 mg/day intentionally ingested an unknown amount of citalopram with alcohol. She presented to the emergency department (time of ingestion unknown) with a Glasgow coma scale score of 8, severe hypotension, and low O2 saturation. A positive bilateral Babinski (without sensory motor deficit) and jugular vein distension were noted upon examination. She was treated with 50 g activated charcoal and admitted to ICU. Upon admission to ICU, she seized twice and developed ventricular fibrillation (VF) which was treated successfully with midazolam and defibrillation. Sustained ventricular tachycardia with VF episodes occurred 10 hours after ICU admission and continued for 48 hours, requiring repeated defibrillation. She recovered fully and was discharged 16 days after admission (Liotier & Coudore, 2011).
2) Generalized tonic-clonic seizures occurred in 2 patients who developed severe hypoglycemia following overdose ingestions of citalopram (2760 mg in one patient and an unknown amount in the other patient). Both patients recovered with supportive care (Duncan et al, 2008).
3) A 10-month-old child ingested an unknown amount of her grandmother's citalopram and developed refractory seizures shortly thereafter. Seizures recurred despite treatment with midazolam and fosphenytoin, and she required intubation and paralysis with succinylcholine as well as the addition of a third anticonvulsant, phenobarbital. Initial citalopram plasma level 1 hour after ingestion was 1400 ng/mL. She was discharged 48 hours postingestion without evident sequelae (Masullo et al, 2006).
4) An 82-year-old woman developed a generalized tonic-clonic seizure approximately 12 hours after ingesting citalopram 1.6 g in a suicide attempt (Brucculeri et al, 2005).
5) A 23-year-old man ingested citalopram 920 mg and developed a generalized tonic-clonic seizure which lasted approximately 2 minutes and was treated with ativan 1 mg. No further seizures occurred (Cuenca et al, 2004).
6) A 31-year-old man had a witnessed generalized clonic seizure approximately 13 hours after an intentional ingestion of citalopram 400 mg and alcohol. No recurrence was reported (Engebretsen et al, 2003).
7) A 45-year-old man developed tonic-clonic seizures approximately 2 hours after ingesting citalopram 3000 mg (citalopram 2400 mg as a racemic mixture). The seizures resolved following administration of IV diazepam (Kelly et al, 2003).
8) Persistent bidirectional wide-complex tachycardia, QRS prolongation, QTc widening, left bundle-branch block (LBBB), and seizures were reported in a 22-year-old woman who ingested citalopram 1200 mg in a suicide attempt. She reverted to normal sinus rhythm within 5 hours of presentation (Sztajnkryeer et al, 2003).
9) A 21-year-old man presented to the emergency department (ED) unresponsive and with seizures after an overdose ingestion of citalopram and olanzapine, with potential maximum ingestions of 11.6 g and 600 mg, respectively. An ECG indicated wide complex tachycardia. Peak serum citalopram concentration, measured within 30 minutes post-presentation, was 522 ng/mL. Approximately 2.5 hours after arrival to the ED, following a second seizure, the patient developed hypotension that worsened over the next several hours, requiring an epinephrine infusion to maintain a mean arterial pressure of 60 mmHg. Bradycardia (less than 40 beats/min) developed approximately 6.5 hours post-presentation, and was unresponsive to atropine and isoproterenol, necessitating placement of a transvenous pacemaker. Approximately 10 hours post-presentation, a third seizure occurred. Because of progressive cardiac and neurotoxicity, IV lipid emulsion therapy was administered, with a total dose of 10% lipid emulsion at 21 mL/hour (0.005 mL/kg/min for a total of 17 hours). This is a 50-fold lower dose than what is recommended. Following the infusion, the patient's condition stabilized with no further clinical worsening. The pacemaker was discontinued 24 hours post-presentation and the epinephrine infusion was titrated down and discontinued 5 hours later (Lung et al, 2013).

1) Citalopram serum concentration was at a therapeutic level in one patient and 2 and 5 times therapeutic levels in the other cases.
2) Moclobemide serum concentrations were 5 times therapeutic levels in one patient and 20 to 50 times higher in the other two cases.

1) In patients who are at risk for the abrupt onset of seizures or mental status depression, activated charcoal should not be administered in the prehospital setting, due to the risk of aspiration in the event of spontaneous emesis.
2) The addition of flavoring agents (cola drinks, chocolate milk, cherry syrup) to activated charcoal improves the palatability for children and may facilitate successful administration (Guenther Skokan et al, 2001; Dagnone et al, 2002).

1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).

1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).

1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).

1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).

1) VALPROATE SODIUM: ADULT DOSE: An initial dose of 20 to 40 mg/kg IV, at a rate of 3 to 6 mg/kg/minute; may give an additional dose of 20 mg/kg 10 minutes after loading infusion. PEDIATRIC DOSE: 1.5 to 3 mg/kg/minute (Brophy et al, 2012).
2) LEVETIRACETAM: ADULT DOSE: 1000 to 3000 mg IV, at a rate of 2 to 5 mg/kg/min IV. PEDIATRIC DOSE: 20 to 60 mg/kg IV (Brophy et al, 2012; Loddenkemper & Goodkin, 2011).
3) LACOSAMIDE: ADULT DOSE: 200 to 400 mg IV; 200 mg IV over 15 minutes (Brophy et al, 2012). PEDIATRIC DOSE: In one study, median starting doses of 1.3 mg/kg/day and maintenance doses of 4.7 mg/kg/day were used in children 8 years and older (Loddenkemper & Goodkin, 2011).
4) TOPIRAMATE: ADULT DOSE: 200 to 400 mg nasogastric/orally OR 300 to 1600 mg/day orally divided in 2 to 4 times daily (Brophy et al, 2012).

1) Contraindicated in patients with preexisting dysrhythmias; tachycardia or heart block due to digitalis toxicity; ventricular dysrhythmias that require inotropic therapy; and angina. Use with caution in patients with coronary insufficiency (Prod Info Isuprel(TM) intravenous injection, intramuscular injection, subcutaneous injection, intracardiac injection, 2013).

1) PREPARATION: Add 4 mL of 0.1% solution to 1000 mL of dextrose 5% in water to produce 4 mcg/mL.
2) INITIAL DOSE
3) MAINTENANCE DOSE

1) MAXIMUM RATE: Administer diazepam IV over 2 to 3 minutes (maximum rate: 5 mg/min).
2) ADULT DIAZEPAM DOSE: 5 to 10 mg initially, repeat every 5 to 10 minutes as needed. Monitor for hypotension, respiratory depression and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after diazepam 30 milligrams.
3) PEDIATRIC DIAZEPAM DOSE: 0.2 to 0.5 mg/kg, repeat every 5 minutes as needed. Monitor for hypotension, respiratory depression and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after diazepam 10 milligrams in children over 5 years or 5 milligrams in children under 5 years of age.
4) RECTAL USE: If an intravenous line cannot be established, diazepam may be given per rectum (not FDA approved), or lorazepam may be given intramuscularly.

1) MAXIMUM RATE: The rate of IV administration of lorazepam should not exceed 2 mg/min (Prod Info Ativan(R), 1991).
2) ADULT LORAZEPAM DOSE: 2 to 4 mg IV. Initial doses may be repeated in 10 to 15 minutes, if seizures persist (Prod Info ATIVAN(R) injection, 2003).
3) PEDIATRIC LORAZEPAM DOSE: 0.1 mg/kg IV push (range: 0.05 to 0.1 mg/kg; maximum dose 4 mg); may repeat dose in 5 to 10 minutes if seizures continue. It has also been given rectally at the same dose in children with no IV access (Sreenath et al, 2009; Chin et al, 2008; Wheless, 2004; Qureshi et al, 2002; De Negri & Baglietto, 2001; Mitchell, 1996; Appleton, 1995; Giang & McBride, 1988).

1) If seizures cannot be controlled with diazepam or recur, give phenobarbital or propofol.

1) SERUM LEVEL MONITORING: Monitor serum levels over next 12 to 24 hours for maintenance of therapeutic levels (15 to 25 mcg/mL).
2) ADULT PHENOBARBITAL LOADING DOSE: 600 to 1200 mg of phenobarbital IV initially (10 to 20 mg/kg) diluted in 60 mL of 0.9% saline given at 25 to 50 mg/minute.
3) ADULT PHENOBARBITAL MAINTENANCE DOSE: Additional doses of 120 to 240 mg may be given every 20 minutes.
4) MAXIMUM SAFE ADULT PHENOBARBITAL DOSE: No maximum safe dose has been established. Patients in status epilepticus have received as much as 100 mg/min until seizure control was achieved or a total dose of 10 mg/kg.
5) PEDIATRIC PHENOBARBITAL LOADING DOSE: 15 to 20 mg/kg of phenobarbital intravenously at a rate of 25 to 50 mg/min.
6) PEDIATRIC PHENOBARBITAL MAINTENANCE DOSE: Repeat doses of 5 to 10 mg/kg may be given every 20 minutes.
7) MAXIMUM SAFE PEDIATRIC PHENOBARBITAL DOSE: No maximum safe dose has been established. Children in status epilepticus have received doses of 30 to 120 mg/kg within 24 hours. Vasopressors and mechanical ventilation were needed in some patients receiving these doses.
8) NEONATAL PHENOBARBITAL LOADING DOSE: 20 to 30 mg/kg IV at a rate of no more than 1 mg/kg/min in patients with no preexisting phenobarbital serum levels.
9) NEONATAL PHENOBARBITAL MAINTENANCE DOSE: Repeat doses of 2.5 mg/kg every 12 hours may be given; adjust dosage to maintain serum levels of 20 to 40 mcg/mL.
10) MAXIMUM SAFE NEONATAL PHENOBARBITAL DOSE: Doses of up to 20 mg/kg/min up to a total of 30 mg/kg have been tolerated in neonates.
11) CAUTION: Adequacy of ventilation must be continuously monitored in children and adults. Intubation may be necessary with increased doses.

1) In a series of 30 citalopram deaths, mean postmortem blood concentration in suicide cases (n=20) was 1.83 mcg/mL (range 0.04 to 13.9 mcg/mL), and in accidental deaths (n=8) the average blood level was 1.12 mcg/mL (range 0.09 to 5.72 mcg/mL). In this study, citalopram overdose was not considered the cause of death in subjects with postmortem blood levels of less than 0.35 mcg/mL, when citalopram was taken alone. In addition, citalopram levels between 0.37 and 0.83 mcg/mL did not always produce toxicity in all cases (Segura & Bravo, 2004).
2) In a retrospective review involving 26 patients, nausea and vomiting, tachycardia, QTc interval prolongation, seizures, drowsiness, and coma were reported following citalopram overdose ingestions in amounts ranging from 200 to 4960 mg (median 1190 mg). Serum citalopram concentrations, obtained from 20 minutes to 8 hours (median 3 hours) postingestion, ranged from 0.21 to 7.5 mg/L (median 1.13 mg/L) (Jimmink et al, 2008).

1) A serum citalopram level of 5.88 mg/L (therapeutic range 0.01 to 0.2 mg/L) was detected in a 54-year-old woman after she intentionally ingested an unknown amount of citalopram with alcohol. She presented to the emergency department (time of ingestion unknown) with altered mental status, hypotension, and low O2 saturation. Laboratory analysis showed a blood ethanol level of 0.2 g/L and urine screening was negative for opiates, cocaine, benzodiazepines, and tricyclic antidepressants. She was treated with 50 g activated charcoal and admitted to ICU. Sustained ventricular tachycardia with VF episodes occurred 10 hours after ICU admission and continued for 48 hours. External electric shocks and sternum strikes were administered. She recovered fully and was discharged 16 days after admission (Liotier & Coudore, 2011).
2) An overdose of 840 mg in an adult resulted in death. At necropsy, citalopram concentration was 6.1 mcg/g femoral vein blood (Ostrom et al, 1996).
3) A combined overdose of trimipramine and citalopram in an adult woman resulted in postmortem femoral blood levels of 2.33 mg/kg and 4.81 mg/kg, respectively (Musshoff et al, 1999).
4) At autopsy a serum citalopram level of 3,402 ng/mL was thought to be the cause of death in a 38-year-old man who had a history of depression and was found pulseless (Carlton & Hughes, 2001).
5) A seizure and transient ECG abnormalities occurred in an adult man following an overdose of citalopram (total 1800 mg, with a serum level of 840 ng/mL) and fluoxetine (serum level within normal limits) (Grover & Caravati, 2001).
6) A maximum serum citalopram concentration of 1.92 mg/L occurred 2 hours following an intentional ingestion of citalopram hydrobromide 3000 mg (citalopram 2400 mg free base). The maximum serum norcitalopram concentration of 0.27 mg/L occurred approximately 24 hours postingestion (Kelly et al, 2003).
7) A 36-year-old woman developed palpitation, weakness, nausea, and numbness 36 hours after taking citalopram 1000 mg with alcohol. On day 3, her vital signs were blood pressure, 84/44 mmHg; temperature, 99.3 degrees F; pulse, 102 to 160 beats/min; and respiratory rate, 17 breaths/min. ECG revealed intermittent runs of wide-complex tachycardia with a QTc of 600 msec. Despite saline and magnesium sulfate infusions, she developed intermittent bigeminy, and despite IV lidocaine, intermittent torsade de pointes occurred. After receiving potassium chloride, transvenous pacemaker insertion, and isoproterenol infusion, she converted to normal sinus rhythm, and QTCs interval narrowed to 442 msec after 2 days. Her plasma citalopram level was 477 ng/mL (therapeutic range 40 to 110 ng/mL), with a corresponding desmethylcitalopram level of 123.2 ng/mL (therapeutic range 14 to 40 ng/mL) (Tarabar et al, 2003).
8) A 22-year-old woman died following intentional ingestion of citalopram 2880 mg. Citalopram concentrations in her body fluids and organ tissues were as follows (Luchini et al, 2005):