SalioSAM/toxsample11 huggingface dataset:
Poisoning cause: Severe isoniazid toxicity
Toxic dose : <50 kg:	>10 mg/kg OR >300 mg
≥50 kg:	>15 mg/kg OR >900 mg
Toxic serum or urine levels: >15 mg/kg OR >900 mg
Management: Intractable seizures are the hallmark of severe isoniazid ingestions. Following adequate airway, respiratory, and circulatory support, primary treatment is aimed at terminating seizure activity. The patient should receive intravenous pyridoxine on a gram for gram basis of isoniazid ingested or 5 grams empirically for unknown doses. Standard anticonvulsant therapy is likely to be of marginal benefit as sole treatment, but benzodiazepines or barbiturates may act synergistically with pyridoxine and should be administered as well. Sodium bicarbonate can be administered for severe metabolic acidosis. Coma should be treated with standard supportive care. Administration of pyridoxine may reverse isoniazid-induced coma. Treat severe hypotension with IV 0.9% NaCl at 10 to 20 mL/kg. Add vasopressors (eg, norepinephrine) if unresponsive to fluids. ANTIDOTE 1) Pyridoxine can be used to reverse the isoniazid-induced pyridoxine deficiency, which can terminate seizures and may be helpful in reversing isoniazid-induced coma. DOSES: ADULTS: The recommended dose is 4 g IV followed by 1 g IM every 30 minutes, to reach an amount equal to the number of grams of isoniazid ingested. Another source recommended an initial first dose of up to 5 g IV administered at a rate of 1 g every 2 to 3 minutes, to reach an amount equal to the number of grams of isoniazid ingested. If the amount of isoniazid is unknown, an initial pyridoxine dose of no more than 5 g should be considered. CHILDREN: 70 mg/kg (not to exceed 5 g), administered at a rate of 1 g every 2 to 3 minutes. However, the exact dosing regimen has not been established and some sources have found such doses to be insufficient. Oral pyridoxine can be administered via nasogastric tube if intravenous supplies are exhausted, but there is no data demonstrating the utility of oral pyridoxine for severe isoniazid toxicity. Benzodiazepines and/or barbiturate should also be administered to patients with seizures secondary to isoniazid Overdose
Clinical effect 1: Seizure
Clinical effect 2: Lactic acidosis
Clinical effect 3: Coma
Clinical effect 4: Hyperthermia
Clinical effect 5: Rhabdomyolysis
Clinical effect 6: Renal failure
Clinical effect 7: Hypotension
Clinical effect 8: Hepatic enzyme elevations
Clinical effect 9: Fulminant hepatic failure
Clinical effect 10: Persisting dementia
Poisoning cause: Mild to moderate metronidazole toxicity
Toxic dose : <50 kg	>26 mg/kg
≥50 kg	>12 g
Management: Treatment is symptomatic and supportive. Patients may only need observation
Clinical effect 1: Asymptomatic
Clinical effect 2: Nausea
Clinical effect 3: Vomiting
Clinical effect 4: Ataxia
Clinical effect 5: Dark (green/black) urine
Clinical effect 6: Increased liver enzymes
Clinical effect 7: Disulfiram like reactions
Poisoning cause: Severe acute metronidazole toxicity
Toxic dose : <50 kg	>26 mg/kg
≥50 kg	>12 g
Management: Treatment is symptomatic and supportive. Orotracheal intubation for airway protection should be performed early in cases of CNS depression or repeated seizure activity. Treat seizures with IV benzodiazepines; barbiturates or propofol may be needed if seizures persist or recur. QT prolongation has been reported with metronidazole, particularly when administered with drugs with the potential for prolonging the QT interval. Concomitant use of metronidazole and other drugs that prolong the QT interval may increase the risk of torsades de pointes. Treat torsades de pointes with IV magnesium sulfate, and correct electrolyte abnormalities, Overdrive pacing may be necessary. 2) DISULFIRAM-LIKE REACTION: If patient is hypotensive, it is either from a disulfiram-like reaction or a co-ingestant. Manage hypotension with IV fluids. If hypotension persists, use direct-acting vasopressors such as norepinephrine. Benzodiazepines may be used for associated agitation or anxiety. Fomepizole inhibits alcohol dehydrogenase, preventing the formation of acetaldehyde, and could theoretically be useful in treating severe disulfiram-like reactions, although there is limited experience with this therapy.
Clinical effect 1: CNS depression
Clinical effect 2: Peripheral neuropathy
Clinical effect 3: Seizure
Poisoning cause: Severe chronic metronidazole toxicity
Management: 1)Treatment is symptomatic and supportive. Orotracheal intubation for airway protection should be performed early in cases of CNS depression or repeated seizure activity. Treat seizures with IV benzodiazepines; barbiturates or propofol may be needed if seizures persist or recur. QT prolongation has been reported with metronidazole, particularly when administered with drugs with the potential for prolonging the QT interval. Concomitant use of metronidazole and other drugs that prolong the QT interval may increase the risk of torsades de pointes. Treat torsades de pointes with IV magnesium sulfate, and correct electrolyte abnormalities, Overdrive pacing may be necessary. 
2) DISULFIRAM-LIKE REACTION: If patient is hypotensive, it is either from a disulfiram-like reaction or a co-ingestant. Manage hypotension with IV fluids. If hypotension persists, use direct-acting vasopressors such as norepinephrine. Benzodiazepines may be used for associated agitation or anxiety. Fomepizole inhibits alcohol dehydrogenase, preventing the formation of acetaldehyde, and could theoretically be useful in treating severe disulfiram-like reactions, although there is limited experience with this therapy. 
Clinical effect 1: Sensory neuropathy
Clinical effect 2: Dizziness
Clinical effect 3: Diplopia
Clinical effect 4: Disorientation
Clinical effect 5: Ataxia
Poisoning cause: Mild to moderate rifampin toxicity
Toxic dose : 6 months - 79 years	>100 mg/kg OR >7 g
Management: Treatment is symptomatic and supportive. Gastrointestinal symptoms (eg, nausea, vomiting, abdominal pain, diarrhea) should be anticipated. Administer IV fluids in patients with significant vomiting and/or diarrhea. Antiemetics may be necessary to control severe nausea and vomiting. Monitor vital signs and assess liver enzymes and bilirubin levels. Monitor neuro function; lethargy is an early finding. Reversible brownish-red or orange discoloration of the skin and bodily fluids is likely to occur and is dose-dependent
Clinical effect 1: Nausea
Clinical effect 2: Vomiting
Clinical effect 3: Abdominal pain
Clinical effect 4: Pruritus
Clinical effect 5: Headache
Clinical effect 6: Increasing lethargy
Clinical effect 7: Orange to red vomitus
Clinical effect 8: Brownish-red or orange skin
Clinical effect 9: Bodily fluid discoloration
Clinical effect 10: Transient alterations in liver enzymes
Clinical effect 11: Increased bilirubin levels
Clinical effect 12: Facial edema
Clinical effect 13: Periorbital edema
Clinical effect 14: Red urine
Clinical effect 15: Tears
Poisoning cause: Severe rifampin toxicity
Toxic dose : 6 months - 79 years	>100 mg/kg OR >7 g
Management: Treatment is symptomatic and supportive. Alterations in mental status may develop; symptoms may be significant in patients with underlying hepatic disease. Monitor liver enzymes and bilirubin levels until evidence of patient recOvery. There have been rare reports of conduction abnormalities, hypotension, seizures and pulmonary edema following severe toxicity. Monitor vital signs, neuro status, obtain a baseline ECG and institute cardiac monitoring. Treat seizures with benzodiazepines, barbiturates as necessary. Perform a chest radiograph in a symptomatic patient
Clinical effect 1: Hepatotoxicity
Clinical effect 2: Jaundice
Clinical effect 3: Seizure
Clinical effect 4: Dysrhythmias
Clinical effect 5: Pulmonary edema
Clinical effect 6: Cardiac arrest
Clinical effect 7: Death
Poisoning cause: Mild to moderate tetracycline toxicity
Toxic dose : 6 months - 79 years	>200 mg/kg OR >5000 mg
Management: Treatment is symptomatic and supportive. Patients may only need observation. 
Clinical effect 1: Nausea
Clinical effect 2: Vomiting
Poisoning cause: Severe tetracycline toxicity
Toxic dose : 6 months - 79 years	>200 mg/kg OR >5000 mg
Management: Abdominal pain, nausea, vomiting, pancreatitis Cardiac toxicity, wide-complex bradycardia, prolonged QTc interval, third-degree atrioventricular block
Clinical effect 1: Abdominal pain
Clinical effect 2: Nausea
Clinical effect 3: Vomiting
Clinical effect 4: Pancreatitis
Clinical effect 5: Wide-complex bradycardia
Clinical effect 6: QTc prolongation
Clinical effect 7: Conduction disturbances/AV block
Poisoning cause: Rivaroxaban (xarelto)  
Toxic dose : 6 months - 17 years	>0.6 mg/kg OR >50 mg
18 years - 64 years	>0.6 mg/kg OR >150 mg
65 years - 79 years	>30 mg
Management: Treatment is symptomatic and supportive. An antidote (ie, coagulation factor Xa) has been developed and may be indicated in patients that require reversal of anticoagulation following a clinically significant rivaroxaban or apixaban exposure (See Antidote). Alternatively, four-factor prothrombin complex concentrates can be used for urgent reversal. Transfusion of packed red cells and fresh frozen plasma may be indicated in patients with severe bleeding.
Clinical effect 1: Hemorrhage
Clinical effect 2: Asymptomatic
Poisoning cause: apixaban Overdose
Toxic dose : <50 kg:	≥1 mg/kg OR >20 mg
≥50 kg	: ≥1 mg/kg OR >50 mg
Management: Treatment is symptomatic and supportive. An antidote (ie, coagulation factor Xa) has been developed and may be indicated in patients that require reversal of anticoagulation following a clinically significant rivaroxaban or apixaban exposure (See Antidote). Alternatively, four-factor prothrombin complex concentrates can be used for urgent reversal. Transfusion of packed red cells and fresh frozen plasma may be indicated in patients with severe bleeding.
Clinical effect 1: Hemorrhage
Clinical effect 2: Asymptomatic
Poisoning cause: Mild to moderate levetiracetam(keppra) toxicity
Toxic dose : 6 months - 23 months	:>40 mg/kg,
2 years - 16 years:	>70 mg/kg,
17 years - 79 years:	>7000 mg
Management: Treatment is symptomatic and supportive. Correct any significant fluid and/or electrolyte abnormalities in patients with severe diarrhea and/or vomiting. Manage mild hypotension with IV fluids
Clinical effect 1: Vomiting
Clinical effect 2: Drowsiness/lethargy
Clinical effect 3: Apathy
Clinical effect 4: Profound hypotonia
Clinical effect 5: Ataxia
Clinical effect 6: Agitation/Irritability/Restlessness
Clinical effect 7: Aggression
Poisoning cause: Severe levetiracetam( keppra) toxicity
Toxic dose : 6 months - 23 months:	>40 mg/kg,
2 years - 16 years:	>70 mg/kg,
17 years - 79 years:	>7000 mg
Management: Treatment is symptomatic and supportive. Closely monitor neurologic function. Treat seizures with IV benzodiazepines; barbiturates or propofol may be needed if seizures persist or recur. In patients with acute allergic reaction, oxygen therapy, bronchodilators, diphenhydramine, corticosteroids, vasopressors and epinephrine may be required. Treat severe hypotension with IV 0.9% NaCl at 10 to 20 mL/kg. Add vasopressors (eg, norepinephrine) if unresponsive to fluids. Treat bradycardia with atropine; if unresponsive, use beta adrenergic agonists (eg, isoproterenol). Consider temporary pacemaker insertion.
Clinical effect 1: Coma
Clinical effect 2: Bradycardia
Clinical effect 3: Hypotension
Clinical effect 4: Respiratory depression
Poisoning cause: Mild to moderate Oxcarbazepine (trileptal) toxicity
Toxic dose : acute ingestion of as little as 15-40 mg/kg can produce toxicity.
Management: Treatment is symptomatic and supportive. Manage mild hypotension with IV fluids. Treat mild hyponatremia with water restriction and/or 0.9% sodium chloride
Clinical effect 1: Vomiting
Clinical effect 2: Abdominal pain
Clinical effect 3: Ataxia
Clinical effect 4: Hyponatremia
Clinical effect 5: Ophthalmoplegia
Clinical effect 6: Movement disorders
Clinical effect 7: Electrolyte disturbances
Clinical effect 8: Tachycardia
Clinical effect 9: Vertigo
Clinical effect 10: Diplopia
Clinical effect 11: Blurred vision
Clinical effect 12: Nystagmus
Clinical effect 13: Somnolence
Clinical effect 14: Respiratory depression
Clinical effect 15: Lethargy
Clinical effect 16: Dystonia
Clinical effect 17: Dyskinesia
Poisoning cause: Severe Oxcarbazepine (trileptal) toxicity
Toxic dose :  Severe toxicity is common after ingestion of 80-150 mg/kg. With chronic use, 10-20% of patients will develop hepatic toxicity when the dose is 10 mg/kg/day, but less than 2% will develop this toxicity if the dose is 3-5 mg/kg/day. Older persons are more susceptible to chronic toxicity​​.
Management:  Treatment is symptomatic and supportive. Treat severe hypotension with IV 0.9% NaCl at 10 to 20 mL/kg. Add vasopressors (eg, norepinephrine) if unresponsive to fluids. Treat seizures with IV benzodiazepines; barbiturates or propofol may be needed if seizures persist or recur. In patients with acute allergic reaction, oxygen therapy, bronchodilators, diphenhydramine, corticosteroids, vasopressors and epinephrine may be required. Manage severe hyponatremia with 0.9% sodium chloride; 3% sodium chloride may be necessary only with severe, symptomatic hyponatremia.
Clinical effect 1: Vomiting
Clinical effect 2: Abdominal Pain
Clinical effect 3: Bradycardia
Clinical effect 4: Tachycardia
Clinical effect 5: Hypertension
Clinical effect 6: Hypotension
Clinical effect 7: Electrolyte disturbances
Clinical effect 8: Tinnitus
Clinical effect 9: Vertigo
Clinical effect 10: Diplopia
Clinical effect 11: Blurred vision
Clinical effect 12: Nystagmus
Clinical effect 13: Somnolence
Clinical effect 14: Respiratory depression
Clinical effect 15: Lethargy
Clinical effect 16: Hyponatremia
Clinical effect 17: Seizure
Clinical effect 18: Coma
Poisoning cause: Mild to moderate pregabalin (lyrica) toxicity
Toxic dose : 6 months - 3 years:	>75 mg,
4 years - 15 years:	>150 mg,
16 years - 64 years:	>300 mg,
65 years - 79 years:	>150 mg
Management:  Treatment is symptomatic and supportive.
Clinical effect 1: CNS depression
Clinical effect 2: Anxiety
Clinical effect 3: Agitation/Irritability/Restlessness
Clinical effect 4: Restlessness
Poisoning cause: Severe pregabalin (lyrica) toxicity
Toxic dose : 6 months - 3 years:	>75 mg,
4 years - 15 years:	>150 mg,
16 years - 64 years:	>300 mg,
65 years - 79 years:	>150 mg
Management:  Treatment of pregabalin exposure is largely supportive in nature with careful attention to airway protection in severe cases. Hypotension is usually mild responding to intravenous fluid boluses. If hypotension persists, add vasopressors (eg, norepinephrine) if unresponsive to fluids. Admit all severely symptomatic patients. Treat seizures with IV benzodiazepines or barbiturates.
Clinical effect 1: CNS depression
Clinical effect 2: Coma
Clinical effect 3: Delirium/encephalopathy
Clinical effect 4: Seizure
Clinical effect 5: Heart block
Clinical effect 6: Death
Poisoning cause: Mild to moderate topiramate toxicity
Toxic dose : For individuals aged 6 months to 79 years, triage to the ER is recommended if the ingested amount of topiramate exceeds 3 mg/kg.
Management: Treatment is symptomatic and supportive. Monitor vital signs, mental status and serum electrolytes
Clinical effect 1: Drowsiness/lethargy
Clinical effect 2: Lethargy
Clinical effect 3: Seizure
Clinical effect 4: Dizziness
Clinical effect 5: Agitation/Irritability/Restlessness
Clinical effect 6: Confusion
Clinical effect 7: Nausea
Clinical effect 8: Vomiting
Clinical effect 9: Ataxia
Clinical effect 10: Tremor
Clinical effect 11: Hypotension
Clinical effect 12: Depression
Clinical effect 13: Speech disturbances
Clinical effect 14: CNS depression
Clinical effect 15: Abnormal coordination
Clinical effect 16: Blurred vision
Clinical effect 17: Diplopia.
Poisoning cause: Severe topiramate toxicity
Toxic dose : For individuals aged 6 months to 79 years, triage to the ER is recommended if the ingested amount of topiramate exceeds 3 mg/kg.
Management: Treatment is symptomatic and supportive. Non-anion gap metabolic acidosis has been reported in some cases of Overdose and therapeutic use. Alterations in mental status including drowsiness, confusion, psychomotor slowness and, in rare cases, coma have been observed. Monitor serum electrolytes, ABGs and CNS function as indicated. Administer fluids, sodium bicarbonate to correct acidosis. Monitor respiratory effort; intubation and mechanical ventilation may be necessary
Clinical effect 1: Acidosis
Clinical effect 2: Coma
Poisoning cause: Mild to moderate benzodiazepines  toxicity
Management: Supportive care.
Clinical effect 1: CNS depression
Clinical effect 2: Drowsiness/lethargy
Clinical effect 3: Confusion
Clinical effect 4: Dysarthria
Clinical effect 5: Lethargy
Clinical effect 6: Hypnotic state
Clinical effect 7: Diminished reflexes
Clinical effect 8: Ataxia
Clinical effect 9: Hypotonia
Clinical effect 10: Paradoxical reactions
Clinical effect 11: Agitation/Irritability/Restlessness
Clinical effect 12: Irritability
Clinical effect 13: Impulsivity
Clinical effect 14: Aggressive behavior
Clinical effect 15: Restlessness
Clinical effect 16: Excitement
Clinical effect 17: Talkativeness
Clinical effect 18: Respiratory depression
Poisoning cause: Severe benzodiazepines toxicity(rapid iv injection)
Management: Coma and respiratory depression require intubation. Hypotension responds to fluids and rarely vasopressors. Anion gap metabolic acidosis from prolonged, high-dose lorazepam or diazepam can be treated with medication cessation.
Clinical effect 1: Respiratory depression
Clinical effect 2: Respiratory arrest
Clinical effect 3: Coma
Clinical effect 4: Hypotension
Clinical effect 5: Hypothermia
Clinical effect 6: Rhabdomyolysis
Poisoning cause: Severe methotrexate toxicity
Toxic dose : 6 months - 12 months:	>5 mg,
13 months - 5 years:	>20 mg,
6 years - 50 years:	>30 mg,
51 years - 79 years:	>20 mg
Management: If methotrexate serum levels are between 0.1–1 mcmol/L, administer 10–15 mg/m2 of leucovorin every 6 hours for 12 doses.
If levels are between 1–5 mcmol/L, increase the leucovorin dose to 50 mg/m2 every 6 hours until the serum level is less than 0.1 mcmol/L.
For levels between 5–10 mcmol/L, administer 100 mg/m2 of leucovorin every 6 hours until the serum level drops below 0.1 mcmol/L.Additionally, if serum creatinine increases by 50% in the first 24 hours after methotrexate exposure, the dose frequency of leucovorin should be increased to every 3 hours until the methotrexate level is less than 5 mcmol/L​​.Administer intravenous leucovorin as soon as possible. Administer intravenous fluids. Begin alkaline diuresis with a bicarbonate infusion to prevent renal precipitation of methotrexate. Administer colony stimulating factors (filgrastim or sargramostim) as these patients are at risk for severe neutropenia. Transfusion of platelets and/or packed red cells may be needed in patients with severe thrombocytopenia, anemia, or hemorrhage. Severe nausea and vomiting may respond to a combination of agents from different drug classes. Glucarpidase (formerly known as carboxypeptidase CPDG2) rapid Methotrexate therapy necessitates close monitoring: A) Hematologic: •
Clinical effect 1: Renal failure
Clinical effect 2: Pancytopenia
Clinical effect 3: Nausea
Clinical effect 4: Vomiting
Clinical effect 5: Diarrhea
Clinical effect 6: Stomatitis
Clinical effect 7: Acute lung injury
Clinical effect 8: Respiratory depression
Poisoning cause: Mild to moderate naphthalene toxicity
Management: Care is symptomatic and supportive. Treat nausea and vomiting with antiemetics
Clinical effect 1: Nausea
Clinical effect 2: Vomiting
Clinical effect 3: Diarrhea
Clinical effect 4: Headache
Clinical effect 5: Restlessness
Poisoning cause: Severe naphthalene toxicity
Toxic dose : As little as one mothball containing naphthalene (250–500 mg) may produce hemolysis in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency.
The amount necessary to produce lethargy or seizures is not precisely known but may be as little as 1–2 grams (equivalent to about 4–8 mothballs).
Management: Care is symptomatic and supportive. Treat symptomatic methemoglobinemia with methylene blue. Severe hemolysis may require transfusion
Clinical effect 1: Lethargy
Clinical effect 2: Hemolysis
Clinical effect 3: Hemolytic anemia
Clinical effect 4: Methemoglobinemia
Clinical effect 5: Hyperkalemia
Clinical effect 6: Hepatomegaly
Clinical effect 7: Splenomegaly
Clinical effect 8: Dysuria
Clinical effect 9: Hematuria
Clinical effect 10: Hemoglobinuria
Clinical effect 11: Seizure
Clinical effect 12: Coma
Clinical effect 13: Acidosis
Clinical effect 14: Renal failure
Clinical effect 15: Acute lung injury
Poisoning cause: Mild to moderate codeine poisoning
Management: Patients may only need observation. 
Clinical effect 1: Euphoria
Clinical effect 2: Drowsiness/lethargy
Clinical effect 3: Constipation
Clinical effect 4: Nausea
Clinical effect 5: Vomiting
Clinical effect 6: Miosis
Clinical effect 7: Bradycardia
Clinical effect 8: Hypotension
Poisoning cause: Severe codeine poisoning
Management:  Administer oxygen and assist ventilation for respiratory depression. Naloxone is the antidote indicated for severe toxicity (respiratory or CNS depression). Orotracheal intubation for airway protection should be performed early in cases of obtundation and/or respiratory depression that do not respond to naloxone. 
Clinical effect 1: Respiratory depression
Clinical effect 2: Respiratory arrest
Clinical effect 3: Hypoxia
Clinical effect 4: Coma
Clinical effect 5: Bradycardia
Clinical effect 6: Acute lung injury
Clinical effect 7: Seizure
Clinical effect 8: Death
Poisoning cause: Mild to moderate meperidine toxicity
Toxic dose : The toxic dose of meperidine is greater than 0.25 mg/kg or greater than 10 mg. 
Management: Patients may need only observation for CNS excitation or depression and respiratory depression
Clinical effect 1: Lightheadedness
Clinical effect 2: Dizziness
Clinical effect 3: Nausea
Clinical effect 4: Vomiting
Clinical effect 5: Urinary retention
Clinical effect 6: CNS depression
Clinical effect 7: Disorientation
Poisoning cause: Severe meperidine toxicity
Toxic dose : Severe toxicity is indicated when the dosage exceeds 2 mg/kg or 50 mg. 
Management: Administer oxygen and assist ventilation for respiratory depression. Naloxone is the antidote indicated for respiratory or CNS depression. Orotracheal intubation for airway protection should be performed early in cases of obtundation and/or respiratory depression that do not respond to naloxone, or in patients who develop severe acute lung injury. Treat seizures with benzodiazepines. 
Clinical effect 1: Agitation/Irritability/Restlessness
Clinical effect 2: Tremors
Clinical effect 3: Myoclonus
Clinical effect 4: Motor weakness
Clinical effect 5: Seizure
Clinical effect 6: Respiratory depression
Clinical effect 7: CNS depression
Clinical effect 8: Serotonin syndrome
Clinical effect 9: Muscle rigidity
Clinical effect 10: Tremor
Clinical effect 11: Confusion
Clinical effect 12: Behavioral changes/Bizarre behavior / altered mentation
Clinical effect 13: Autonomic instability
Clinical effect 14: Orofacial dyskinesias
Clinical effect 15: Arm flexion
Clinical effect 16: Stiffening of the legs
Poisoning cause: Mild to moderate morphine toxicity
Management:  Patients may need only observation for CNS excitation or depression and respiratory depression. 
Clinical effect 1: Euphoria
Clinical effect 2: Drowsiness/lethargy
Clinical effect 3: Constipation
Clinical effect 4: Nausea
Clinical effect 5: Vomiting
Clinical effect 6: Miosis
Clinical effect 7: Bradycardia
Clinical effect 8: Hypotension