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![References
• Graudins A, Lee HM, Druda D. Calcium Channel Antagonists And Beta-Blocker Overdose: Antidotes and
Adjunct Therapies. British Journal of Clinical Pharmacology, 2015;81(3):453-461. doi: 10.111/bcp.12763
• Barrueto F. Calcium channel blocker poisoning. In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA.
Accessed 01 May 2016.
• Hoffman RS, Howland MA, Lewin NA, et al. (2015) Goldfrank’s Toxocologic Emergencies, 10th Edition.
McGraw-Hill.
• Harris NS. Case 24-2006: A 40-Year-Old Woman with Hypotension after an Overdose of Amlodipine. N Engl J
Med 2006;355:602-611
• Nasa P, Singh A, Juneja D, et al. Continuous venovenous hemodiafiltration along with charcoal
hemoperfusion for the management of life-threatening lercanidipine and amlodipine overdose. Saudi Journal
of Kidney Diseases and Transplantation. 2014; 25(6):1255-1258.
• Kamp TJ, Hell JW. Regulation of Cardiac L-Type Calcium Channels by Protein Kinase A and Protein Kinase
C. Circulation Research. 2000;87:1095-1102.
• Clinical Pharmacology [database online]. Tampa, FL: Gold Standard, Inc.; 2016. URL:
http://www.clinicalpharmacology.com.](https://image.slidesharecdn.com/f48aad89-f45b-4144-9805-8335601655fa-160802033355/85/Amlodipine-Overdose-41-320.jpg)
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Amlodipine Overdose
- 1. Amlodipine Overdose Kimberly M.Treier Internal Medicine APPE May 3, 2016
- 2. Patient Case 4/15/16 • A64 y/o male was transported from Massena, NY to UVM MC ED after ingesting fifty 5mg amlodipine tablets • Per family, patient has been depressed and suicidal for several days
- 3. AMLODIPINE THE BASICS Class DHP-typecalcium channel blocker MOA Directly inhibits vascular and myocardial L-type calcium channels Side effects Common: edema, dizziness, flushing, palpitations Other: fatigue, nausea, abdominal pain, somnolence Therapeutic range 2.5 to 10 mg daily Max dose 10 mg daily
- 4. Why Is ThisImportant? • Calcium… • Initiates excitation-contraction coupling (muscles) • SA node depolarization (heart) • Maintains smooth muscle tone (vascular and GI system) • Reduces insulin secretion (pancreas)
- 6. Harris NS. NEngl J Med 2006;355:602-611
- 7. Methods of Toxicity •Calcium Channel Blockers… • Initiates excitation-contraction coupling (muscles) • inotropy • SA node depolarization (heart) • chronotropy • Maintains smooth muscle tone (vascular and GI system) • vasodilation • Reduces insulin secretion (pancreas) • blood glucose • glucose utilization by the heart
- 8. Methods of Toxicity •Calcium Channel Blockers… • Initiates excitation-contraction coupling (muscles) • inotropy **non-DHP • SA node depolarization (heart) • chronotropy **non-DHP • Maintains smooth muscle tone (vascular and GI system) • vasodilation **DHP • Reduces insulin secretion (pancreas) • blood glucose • glucose utilization by the heart
- 9. Harris NS. NEngl J Med 2006;355:602-611
- 10. Early Symptoms • Fatigue,dizziness and lightheadedness • Severe poisoning: syncope, altered mental status, coma, sudden death • DHP CCBs: • Primarily peripheral vasodilation reflex tachycardia • Loss of selectivity during severe poisoning bradycardia
- 11. AMLODIPINE TOXICITY Mild to ModerateSevere - Reflex tachycardia and hypotension - Drowsiness - Nausea - Vomiting - Peripheral vasodilation - Profound hypotension refractory to inotropic therapy - Conduction disturbances - Shock - Metabolic acidosis - Acute renal failure - Respiratory failure/hypoxemia
- 12. Interventions • General • Goal:supportive • Cardiogenic shock • Goal: improve contractility and bradycardia • Vasodilatory shock • Goal: improve vascular tone
- 13. Initial • GI decontamination •Immediate release: activated charcoal • Within 4 hours of ingestion • Extended release: whole bowel irrigation • Only if asymptomatic • Airway and respiratory support • IV isotonic crystalloid • 1-2 L max
- 14. First-Line • Isotonic fluids •Atropine • Glucagon • Calcium
- 15. Atropine Indication MOA EffectsDose Adverse Effects Symptomatic bradycardia ACH- mediated bradycardia HR (may not be significant or persistent) 0.5-1 mg IV q2-3 minutes (max 3 mg) Anti-ACH effects Treatment failure should be anticipated with severe poisoning
- 16. Glucagon Indication MOA EffectsDose Adverse Effects Cardiogenic shock Ca2+ channel activation (via adenylate cyclase and cAMP) HR 5 mg IV bolus (can repeat x 2 every 10 min) N/V Hyperglycemia
- 17. Harris NS. NEngl J Med 2006;355:602-611
- 18. Calcium Indication MOA EffectsDose Adverse Effects Hypotension and bradycardia Ca2+ concentration gradient across cellular membrane BP, CO and vascular tone Loading dose: 13-25 mEq Ca2+ Infusion: 0.5 mEq Ca2+/kg/hr Hypercalcemia Hypophosphat emia ECG changes Tissue injury with extravasation Effects may not last and may not be significant in severe poisoning
- 19. Harris NS. NEngl J Med 2006;355:602-611
- 20. Second-Line • High-Dose InsulinEuglycemic Therapy • Catecholamines • Vasopressors • Intravenous fat emulsion (refractory shock or cardiac arrest) • Methylene blue (refractory shock)
- 21. Indication MOA EffectsDose Adverse Effects Cardiogenic shock Myocardial energy Inotropy Arterial vasodilation (endothelial nitric oxide) CO and BP Loading dose: 1 unit/kg Infusion: 1-10 units/kg/hr + D50W Hypoglycemia Hypokalemia Vasodilation High-Dose Insulin Euglycemic Therapy
- 22. • Primary myocardialenergy source • Healthy: free fatty acids • Shock: glucose • CCBs inhibit insulin secretion from pancreatic β cells • Diffusion vs. insulin-mediated uptake • Myocardium becomes insulin resistant due to IP3 dysregulation ( glucose transporters and contraction) • insulin secretion + glucose utilization = hyperglycemia High-Dose Insulin Euglycemic Therapy (HIET)
- 23. Indication MOA EffectsAgents Adverse Effects Cardiogenic shock Adrenergic stimulation (inotropy and chronotropy) BP, CO and tissue profusion Epinephrine Dopamine Dobutamine Epinephrine: blood glucose lactic acid Limb ischemia Catecholamines
- 24. Harris NS. NEngl J Med 2006;355:602-611
- 25. Indication MOA EffectsAgents Adverse Effects Vasodilatory shock α1-mediated vasoconstrictio n vascular tone (and BP) systemic vascular resistance Norepinephrin e Phenylephrine blood glucose lactic acid Alpha-Adrenergic Agonists
- 26. Indication MOA EffectsDose Adverse Effects Vasodilatory shock Vasoconstrictio n via: Vascular V1 receptor activation ATP-activated K+ channels nitric oxide Adrenergic potentiation BP systemic vascular resistance Titrate to effect Max 0.04 units/min CO Limb ischemia Vasopressin
- 27. Third-Line • Intravenous fatemulsion (refractory shock or cardiac arrest) • Methylene blue (refractory shock) • Phosphodiesterase inhibitors
- 28. Indication MOA EffectsDose Adverse Effects Refractory cardiogenic or vasodilatory shock Muscle contraction Energy Active drug BP, HR and perfusion Loading dose: 1-1.5 mL/kg of 20% ILE Infusion: 0.25-0.5 ml/kg/min of 20% ILE Blood viscosity Pancreatitis Noncardiogeni c pulmonary edema Intravenous Lipid Emulsion
- 29. Three proposed mechanisms: •Ca2+ channel activation • intracellular metabolism • “Lipid Sink” • Inactivation via sequestration • Dependent on lipophilicity • Amlodipine LogP = 3.72 • Verapamil LogP = 4.91 Intravenous Lipid Emulsion Images courtesy of Google Images
- 30. Indication MOA EffectsAdverse Effects Refractory vasodilatory shock Nitric oxide: (nitric oxide-cGMP pathway, scavenges and inhibits synthesis) BP vasopressor dosing Blue discoloration (skin, secretions) Hemolysis Methemoglobinemia Serotonin syndrome (inhibits MAO-A) Methylene Blue
- 31. Indication MOA EffectsAgents Adverse Effects Cardiogenic shock Ca2+ channel activation (via adenylate cyclase and cAMP) Vasodilation HR and CO Milrinone Inamrinone Enoximone HoTN Phosphodiesterase Inhibitors Not readily available and may exacerbate HoTN
- 32. Harris NS. NEngl J Med 2006;355:602-611
- 33. Other • Cardiac transvenous/cutaneouspacing • Indication: bradycardia, heart block • Effect: HR • Extracorporeal cardiac assist devices • Indication: cardiogenic shock • Effect: CO • Not effective in vasodilatory shock
- 34. What Happened tothe Patient? • Respiratory failure • Refractory cardiogenic and vasodilatory shock • Atrial fibrillation and other conduction abnormalities • Metabolic acidosis • AKI • Peripheral and pulmonary edema • Pneumonia/septic shock • Limb ischemia (nonviable right leg) • Ileus
- 35. DAY 2 Scheduled ContinuousPRN Acid/Base/Electrolytes/Gl ucose: KCl 20 mEq IV x1 MgSO4 2 g in D5W IV x1 (repeated x1) Insulin R 70 units IV x1 Cardiovascular: Fat emulsion 275 mg/kg x1 GI: Famotidine 20 mg IV BID Pain/Neuromuscular Blockade: Ketamine 20 mg IV x1 Vecuronium 10 mg IV x1 VTE prophylaxis: Heparin 5,000 units SQ q8h Glucose: D10W IV at 100 ml/hr Dextrose 20% IV at 25-150 ml/hr Insulin R 548 units/hr IV Insulin R 70 units/hr IV Cardiovascular: Dopamine 12.32-138.78 mg/hr IV Epinephrine 0.0608-0.6 mg/hr IV Norepinephrine 0.1216-1.8 mg/hr IV Cardiovascular: Atropine 0.5-1 mg IV DAY 1
- 36. DAY 2 Scheduled ContinuousPRN Acid/Base/Electrolytes/Glucos e: CaCl 1,000 mg IV x1 (repeated x 3) KCl 20 mEq IV every hour NaHCO3 100 mEq IV x1 D50W 12.5 g IV x1 (repeated x2) Cardiovascular: Methylene blue 2 mg/kg IV x1 (repeated x 1) GI: Docusate 100 mg PO BID Senna 1-2 tabs PO qHS Miralax 17 g PO daily Famotidine 20 mg IV BID Respiratory: Hydrocortisone 50 mg IV q6h Antibiotics: Vancomycin 15 mg/kg IV q12h Zosyn 4.5g IV q8h VTE prophylaxis: Heparin 5,000 units SQ q8h Acid/Base/Electrolytes/Glucos e: NaHCO3 30 mEq/hr IV Dextrose 20% IV at 25-150 ml/hr Insulin 548 units/hr IV Cardiovascular: Dopamine 12.32-138.78 mg/hr IV Epinephrine 0.0608-0.6 mg/hr IV Norepinephrine 0.1216-1.8 mg/hr IV Methylene blue 69 mg/hr IV Acid/Base/Electrolytes/Glucos e: D50W 12.5 g IV KCl 20 mEq IV every hour Pain/Sedation: Hydromorphone 0.5-1 mg IV q2h DAY 2
- 37. DAY 3 Scheduled ContinuousPRN Acid/Base/Electrolytes/Glucose: CaCl 1,000 mg IV x1 (repeated x3) MgSO4 2g IV x1 NaHCO3 50 mEq IV x1 (repeated x1) Cardiovascular: Furosemide 20 mg IV x1 Hydrocortisone 50 mg IV q6h Antibiotics: Vancomycin 15 mg/kg IV q12h Zosyn 4.5g IV q8h GI: Docusate 100 mg PO BID Famotidine 20 mg IV BID Miralax 17 g PO daily Senna 1-2 tabs PO qHS Respiratory: Duoneb q4h via neb Sedation/Neuromuscular blockade: Midazolam 1mg IV x1 Vecuronium 10 mg IV x1 Anticoagulation: Heparin 5,000 units SQ q8h Acid/Base/Electrolytes/Glucose: NaHCO3 30 mEq/hr IV Dextrose 20% IV at 25-150 ml/hr Insulin 548 units/hr IV Cardiovascular: Dopamine 12.32-138.78 mg/hr IV Epinephrine 0.0608-0.6 mg/hr IV Norepinephrine 0.1216-1.8 mg/hr IV Vasopressin 1.8 units/hr IV Pain: Hydromorphone 0.4-1 mg/hr IV Anticoagulation: Heparin 750 units/hr IV Acid/Base/Electrolytes/Glucose: D50W 12.5 g IV KCl 20 mEq IV every hour Pain/Fever: APAP 650 mg PR q6h Hydromorphone 0.5-1 mg IV q2h DAY 3
- 38. DAY 3 Scheduled ContinuousPRN Acid/Base/Electrolytes/Glu cose: NaHCO3 50 mEq IV x1 (repeated x1) Cardiovascular: Hydrocortisone 50 mg IV q6h Antibiotics: Zosyn 4.5g IV q8h Respiratory: Duoneb q4h via neb Acid/Base/Electrolytes/Glu cose: NaHCO3 30 mEq/hr IV Dextrose 20% IV at 25-150 ml/hr Insulin 548 units/hr IV Cardiovascular: Dopamine 12.32-138.78 mg/hr IV Epinephrine 0.0608-0.6 mg/hr IV Norepinephrine 0.1216-1.8 mg/hr IV Vasopressin 20 units/100 ml IV at 9 ml/hr Pain: Hydromorphone 1 mg/ml IV at 0.4-1 ml/hr Anticoagulation: Heparin 750 units/hr IV Acid/Base/Electrolytes/Glu cose: D50W 12.5 g IV KCl 20 mEq IV every hour Pain/Sedation/Anxiety: Hydromorphone 0.5-1 mg IV q2h Lorazepam 1-4 mg IV q30 min DAY 4
- 39. What Happened tothe Patient? Pronounced deceased on 4/18/16
- 40. Case Report • 40y/o female ingested 1,000 mg amlodipine • Presentation: • AMS, HoTN (42/32 mmHg), normal HR, no edema, no cyanosis • Treatment: • IV fluid, charcoal, whole-bowel irrigation, glucagon, high- dose insulin, dextrose, dopamine, norepinephrine, phenylephrine, calcium chloride, calcium gluconate • Disposition: • Survived • Discharged to in-patient psychiatric unit on day 27
- 41. References • Graudins A,Lee HM, Druda D. Calcium Channel Antagonists And Beta-Blocker Overdose: Antidotes and Adjunct Therapies. British Journal of Clinical Pharmacology, 2015;81(3):453-461. doi: 10.111/bcp.12763 • Barrueto F. Calcium channel blocker poisoning. In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA. Accessed 01 May 2016. • Hoffman RS, Howland MA, Lewin NA, et al. (2015) Goldfrank’s Toxocologic Emergencies, 10th Edition. McGraw-Hill. • Harris NS. Case 24-2006: A 40-Year-Old Woman with Hypotension after an Overdose of Amlodipine. N Engl J Med 2006;355:602-611 • Nasa P, Singh A, Juneja D, et al. Continuous venovenous hemodiafiltration along with charcoal hemoperfusion for the management of life-threatening lercanidipine and amlodipine overdose. Saudi Journal of Kidney Diseases and Transplantation. 2014; 25(6):1255-1258. • Kamp TJ, Hell JW. Regulation of Cardiac L-Type Calcium Channels by Protein Kinase A and Protein Kinase C. Circulation Research. 2000;87:1095-1102. • Clinical Pharmacology [database online]. Tampa, FL: Gold Standard, Inc.; 2016. URL: http://www.clinicalpharmacology.com.
- 43. VITALS/LABS DATE: 4/15/16 4/16/16 TIME:12-16 16-20 20-00 00-04 04-08 08-12 12-16 16-20 20-00 Temp 91.9 95.5 95.2 95.9 95.9 96.8 97 HR 61 71 73 87 74 80 79 98 95 ABP 75/42 84/37 83/31 101/38 94/34 96/46 107/49 102/48 101/53 RR 22 22 28 23 29 25 28 28 Na+ 129 129 127 128 125 124 125 124 K+ 4.2 5.6 3.0 3.6 4.0 3.9 4.3 4.0 CO2 19 11 12 13 15 16 20 24 Cl- 97 98 99 96 98 98 98 93 SCr 0.82 1.09 cCa2+ 11.9 PO42- 7.6 7.2 4.9 3.6 2.9 3.8 3.8 3.0 Mg+ 1.9 1.8 1.6 2.9 2.3 2.1 1.9 1.8 Glucos e 346 324 354 312 221 103 72 87 139 pH (art) 7.10 7.11 7.15 7.16 7.15 7.21 7.23 O2 sat. 100 87 98 98 84 82 94 LA 4.5 WBC
- 44. VITALS/LABS DATE: 4/17/16 4/18/16 TIME:00-04 04-08 08-12 12-16 16-20 20-00 00-04 04-08 08-12 Temp 98.2 97.5 99.9 101.1 101.1 101.8 101.1 HR 95 105 117 119 123 131 131 0 ABP 98/52 96/54 93/58 94/51 109/52 91/49 99/48 17/10 RR 28 32 32 30 29 30 0 Na+ 123 123 122 122 120 121 124 124 K+ 3.7 3.9 3.9 4.2 4.4 4.3 4.3 5.6 CO2 24 23 21 20 18 23 19 16 CL- 93 94 97 96 96 93 95 95 SCr 1.06 2.26 cCa2+ 10.8 10.3 10.1 PO42- 3.1 2.6 2.2 2.4 2.9 2.8 3.7 5.5 Mg+ 1.6 2.1 1.8 1.7 1.7 1.8 1.8 1.9 Glucos e 109 96 86 144 120 137 159 201 pH (art) 7.24 7.19 7.12 7.18 O2 sat. 80 73 81 94 LA 3.0 6.5 11.3 WBC
- 45. Case Report • 69y/o male ingested 300 mg lercandipine + 50 mg amlodipine • Presentation: • HoTN, right BBB, metabolic acidosis, respiratory and cardiac arrest • Treatment: • IV fluid, calcium gluconate, charcoal gastric lavage, WBI, dopamine, norepinephrine, epinephrine, terlipressin, pacemaker, glucagon, sodium bicarbonate, intra-aoritc balloon pump, charcoal hemoperfusion • Disposition: • Survived, discharged day 7
Editor's Notes
- #2 0003299955
- #7 Harris NS. N Engl J Med 2006;355:602-611 Figure 2. Role of L-Type Calcium Channels and Amlodipine Activity in Myocytes. The extracellular concentration of calcium is 10,000 times the intracellular concentration. The gradient is maintained by the impermeability of the cell membrane to calcium and through pumps that excrete intracellular calcium ions into the extracellular space (Ca2+/H+-ATPase and Na+/Ca2+ exchanger), as well as by the active uptake and release of calcium by intracellular organelles (endoplasmic reticulum and mitochondria). Calcium flows into the cell through a voltage-gated calcium channel in response to a variety of stimuli, including β-adrenergic receptors. The influx of calcium into the cell and from the endoplasmic reticulum ultimately increases the activity of the actin–myosin–troponin complex. Amlodipine binds the α1c subunit of voltage-gated L-type calcium channels on the myocyte membrane, blocking the flow of calcium and reducing the activity of the actin–myosin–troponin complex.
- #8 Hallmark of CCB poisoning = depressed myocardial contraction and peripheral vasodilation
- #9 Hallmark of CCB poisoning = depressed myocardial contraction and peripheral vasodilation Hypotension most common and life-threatening finding d/t decreased inotropy bradycardia, and peripheral vasodilation
- #10 Harris NS. N Engl J Med 2006;355:602-611 Figure 2. Role of L-Type Calcium Channels and Amlodipine Activity in Myocytes. The extracellular concentration of calcium is 10,000 times the intracellular concentration. The gradient is maintained by the impermeability of the cell membrane to calcium and through pumps that excrete intracellular calcium ions into the extracellular space (Ca2+/H+-ATPase and Na+/Ca2+ exchanger), as well as by the active uptake and release of calcium by intracellular organelles (endoplasmic reticulum and mitochondria). Calcium flows into the cell through a voltage-gated calcium channel in response to a variety of stimuli, including β-adrenergic receptors. The influx of calcium into the cell and from the endoplasmic reticulum ultimately increases the activity of the actin–myosin–troponin complex. Amlodipine binds the α1c subunit of voltage-gated L-type calcium channels on the myocyte membrane, blocking the flow of calcium and reducing the activity of the actin–myosin–troponin complex.
- #14 d/c WBI at onset of bradycardia and HoTN b/c reduced GI function and ileus
- #18 Harris NS. N Engl J Med 2006;355:602-611 Figure 2. Role of L-Type Calcium Channels and Amlodipine Activity in Myocytes. The extracellular concentration of calcium is 10,000 times the intracellular concentration. The gradient is maintained by the impermeability of the cell membrane to calcium and through pumps that excrete intracellular calcium ions into the extracellular space (Ca2+/H+-ATPase and Na+/Ca2+ exchanger), as well as by the active uptake and release of calcium by intracellular organelles (endoplasmic reticulum and mitochondria). Calcium flows into the cell through a voltage-gated calcium channel in response to a variety of stimuli, including β-adrenergic receptors. The influx of calcium into the cell and from the endoplasmic reticulum ultimately increases the activity of the actin–myosin–troponin complex. Amlodipine binds the α1c subunit of voltage-gated L-type calcium channels on the myocyte membrane, blocking the flow of calcium and reducing the activity of the actin–myosin–troponin complex.
- #20 Harris NS. N Engl J Med 2006;355:602-611 Figure 2. Role of L-Type Calcium Channels and Amlodipine Activity in Myocytes. The extracellular concentration of calcium is 10,000 times the intracellular concentration. The gradient is maintained by the impermeability of the cell membrane to calcium and through pumps that excrete intracellular calcium ions into the extracellular space (Ca2+/H+-ATPase and Na+/Ca2+ exchanger), as well as by the active uptake and release of calcium by intracellular organelles (endoplasmic reticulum and mitochondria). Calcium flows into the cell through a voltage-gated calcium channel in response to a variety of stimuli, including β-adrenergic receptors. The influx of calcium into the cell and from the endoplasmic reticulum ultimately increases the activity of the actin–myosin–troponin complex. Amlodipine binds the α1c subunit of voltage-gated L-type calcium channels on the myocyte membrane, blocking the flow of calcium and reducing the activity of the actin–myosin–troponin complex.
- #23 Inhibited insulin secretion and impaired glucose utilization
- #25 Harris NS. N Engl J Med 2006;355:602-611 Figure 2. Role of L-Type Calcium Channels and Amlodipine Activity in Myocytes. The extracellular concentration of calcium is 10,000 times the intracellular concentration. The gradient is maintained by the impermeability of the cell membrane to calcium and through pumps that excrete intracellular calcium ions into the extracellular space (Ca2+/H+-ATPase and Na+/Ca2+ exchanger), as well as by the active uptake and release of calcium by intracellular organelles (endoplasmic reticulum and mitochondria). Calcium flows into the cell through a voltage-gated calcium channel in response to a variety of stimuli, including β-adrenergic receptors. The influx of calcium into the cell and from the endoplasmic reticulum ultimately increases the activity of the actin–myosin–troponin complex. Amlodipine binds the α1c subunit of voltage-gated L-type calcium channels on the myocyte membrane, blocking the flow of calcium and reducing the activity of the actin–myosin–troponin complex.
- #30 Most often used for anesthesia (e.g. bupivocaine)
- #33 Harris NS. N Engl J Med 2006;355:602-611 Figure 2. Role of L-Type Calcium Channels and Amlodipine Activity in Myocytes. The extracellular concentration of calcium is 10,000 times the intracellular concentration. The gradient is maintained by the impermeability of the cell membrane to calcium and through pumps that excrete intracellular calcium ions into the extracellular space (Ca2+/H+-ATPase and Na+/Ca2+ exchanger), as well as by the active uptake and release of calcium by intracellular organelles (endoplasmic reticulum and mitochondria). Calcium flows into the cell through a voltage-gated calcium channel in response to a variety of stimuli, including β-adrenergic receptors. The influx of calcium into the cell and from the endoplasmic reticulum ultimately increases the activity of the actin–myosin–troponin complex. Amlodipine binds the α1c subunit of voltage-gated L-type calcium channels on the myocyte membrane, blocking the flow of calcium and reducing the activity of the actin–myosin–troponin complex.
- #41 Harris NS. Case 24-2006: A 40-Year-Old Woman with Hypotension after an Overdose of Amlodipine. N Engl J Med 2006;355:602-611 No third-line interventions
- #46 Nasa P, Singh A, Juneja D, et al. Continuous venovenous hemodiafiltration along with charcoal hemoperfusion for the management of life-threatening lercanidipine and amlodipine overdose. Saudi Journal of Kidney Diseases and Transplantation. 2014; 25(6):1255-1258.