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Ventricular tachycardia medical therapy

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Sara Zand, M.D.[2] Cafer Zorkun, M.D., Ph.D. [3], Avirup Guha, M.B.B.S.[4]

Overview

Overview

The mainstay of medical therapy in hemodynamic stable VT is suppression of tachyarrhythmia with antiarrhythmic medications such as amiodarone, sotalol, lidocaine, betablocker alongside with correction of hypokalemia, hypomagnesemia and hypocalcemia. In addition, treating the underlying causes of VT including ischemic heart disease or decompensated heart failure are warranted.

Medical Therapy

Medical Therapy

Common medications for treatment of VT include:[1]

Antiarrhythmic medications

Antiarrhythmic medications

[2]

Sodium channel blocker

Ranolazine

  • NO efficacy in reduction the fist VT, VF in high risk patients, but significant reduction of recurrent VT, VF requiring ICD implantation.[7]

Beta blocker

Amiodarone, sotalol

Calcium channel blocker



Arrhythmiac medication, class, dose Indication Receptor target Electrophysiologic effect Pharmacological characteristics Common advers effects
Acebutolol

PO 200–1200 mg daily, up to 600 mg bid

VT, PVC B1, mild internistic sympathetic activity Slowing sinus rate, increasing AV nodal refractoriness Prolonged haft life in renal impairment, metabolism: hepatic Bradycardia, hypotension, HF, AV block, Dizziness, fatigue, anxiety, impotence, hyperesthesia,hypoesthesia
Amiodarone (III)

IV:VF/pulseless VT arrest: 300 mg bolus, stable VT: 150-mg bolus then 1 mg/min x 6 h, then 0.5 mg/min x 18 h PO: 400 mg q 8 to 12 h for 1–2 wk, then 300–400 mg daily; reduce dose to 200 mg daily if possible

VT, VF, PVC INa, ICa, IKr, IK1, IKs, Ito, Beta receptor, Alpha receptor, nuclear T3

recepto

Slowed sinus rate, QRS prolongation, QTc prolongation, increased AV nodal refractoriness ,increased defibrilation threshold Metabolism: hepatic, half life: 26-107 days Hypotension, bradycardia, AV block, TdP, slowing VT below programmed ICD detection rate, increased defibrillation threshold, corneal microdeposits, thyroid abnormalities, ataxia, nausea, emesis, constipation, photosensitivity, skin discoloration, ataxia, dizziness, peripheral neuropathy, tremor, hepatitis, cirrhosis, pulmonary fibrosis, pneumonitis
Atenolol (II)

PO: 25–100 mg qd or bid

VT, PVC, ARVC, LQTS Beta 1 Slowed sinus rate , 
increased AV nodal refractoriness
Metabolism: hepatic Bradycardia, hypotension, heart failure, AV block, dizziness, fatigue, depression, impotence
Bisoprolol (II)

PO: 2.5–10 mg once daily

VT, PVC Beta 1 receptor Slowed sinus rate, increased AV nodal refractoriness Metabolism: hepatic Chest pain, bradycardia, AV block, Fatigue, insomnia, diarrhea
Carvedilol (II)

PO: 3.125–25 mg q 12 h

VT, PVC Beta 1, Beta 2, Alpha Slowed sinus rate, increased AV nodal refractoriness Metabolism: hepatic Bradycardia, hypotension, AV block, edema, syncope, Hyperglycemia, dizziness, fatigue, diarrhea
Carvedilol (II)

PO: 3.125–25 mg q 12 h

VT, PVC Beta 1, Beta 2, Alpha Slowed sinus rate, increased AV nodal refractoriness Metabolism: hepatic Bradycardia, hypotension, AV block, edema, syncope, Hyperglycemia, dizziness, fatigue, diarrhea
Diltiazem (IV)

IV: 5–10 mg,qd: 15–30 min, Extended release: PO: 120–360 mg/da, PO: 3.125–25 mg q 12 h

RVOT VT, ideopathic left VT ICa-L Slowed sinus rate, slowed AV node conduction, PR prolongation Metabolism: hepatic Bradycardia, hypotension, AV block, edema, exacerbation of HF reduced EF, Headache, rash, constipation
Esmolol (II)

IV: 0.5 mg/kg bolus, 0.05 mg/kg/min

VT B1 Slowed sinus rate, increased AV node refractoriness Metabolism: RBC Bradycardia, hypotension, AV block, HF, dizziness, neusea
Flecainide (IC) PO: 50–200 mg q 12 h VT, PVC (in the absence of structural heart disease), CPVT INa, IKr, IKur Prolonged PR interval, prolonged QRS duration, increased defibrillation threshold Metabolism: RBC Sinus node dysfunction, AV block, drug-induced Brugada syndrome, monomorphic VT in patients with a myocardial scar, exacerbation of HFrEF
Lidocaine (IB)

IV: 1 mg/kg bolus, 1–3 mg/min, 1–1.5 mg/kg. Repeat 0.5–0.75 mg/kg bolus every 5–10 min (max cumulative dose 3 mg/kg), maintenance infusion: 1–4 mg/min or starting 0.5 mg/min

VT, VF INa Slightly shortening of QTc interval Metabolism: hepatic, prolonged half life in HF, liver disease, shock, severe renal disease Bradycardia, hemodynamic collapse, AV block, sinus arrest, delirium, psychosis, seizure, nausea, tinnitus, dyspnea, bronchospasm
Metoprolol (II) IV: 5 mg q 5 min up to 3 doses, PO: 25–100 mg Extended release qd or q 12 h VT, PVC B1 Slowed sinus rate, increased AV nodal refractoriness Metabolism: None, Excretion: urine Bradycardia, hypotension, AV block, dizziness, fatigue, diarrhea, depression, dyspnea
Metoprolol (II) IV: 5 mg q 5 min up to 3 doses, PO: 25–100 mg Extended release qd or q 12 h VT, PVC B1 Slowed sinus rate, increased AV nodal refractoriness Metabolism: None, Excretion: urine Bradycardia, hypotension, AV block, dizziness, fatigue, diarrhea, depression, dyspnea
Mexiletine (IB), PO: 150–300 mg q 8 h or q 12 h VT, PVC, VF, Long QT3 INa Slightly shortening of QTc interval Metabolism: hepatic HF, AV block, lightheaded, tremor, ataxia, paresthesias, nausea, blood dyscrasias
Nadolol (II)

PO: 40–320 mg daily

VT, PVC, LQTS, CPVT B1, B2 Slowed sinus rate, increased AV nodal refractoriness Metabolism: none, excretion: urine Bradycardia, hypotension, HF, AV block, edema, dizziness, cold extremities, bronchospasm
Procainamide (IA), IV: loading dose 10–17 mg/kg at 20–50 mg/min, maintenance dose: 1–4 mg/min, PO (SR preparation): 500–1250 mg q 6 h VT, PVC, LQTS, CPVT B1, B2 Slowed sinus rate, increased AV nodal refractoriness Metabolism: none, excretion: urine Bradycardia, hypotension, HF, AV block, edema, dizziness, cold extremities, bronchospasm
Propafenone (IC), PO: Immediate release 150–300 mg q 8 h, Extended release 225–425 mg q 12 h VT, PVC (in the absence of structural heart disease) INa, IKr, IKur, Beta receptor, Alpha recept Prolonged PR interval, prolonged QRS duration, increased defibrillation threshold Metabolism: hepatic HF, AV block, drug-induced Brugada syndrome, dizziness, fatigue, nausea, diarrhea, xerostomia, tremor, blurred vision
Propranolol (II), IV: 1–3 mg q 5 min to a total of 5 mg, PO: Immediate release 10–40 mg q 6 h; Extended release 60–160 mg q 12 h VT, PVC, Long QT syndrome Beta 1 , B2 , INa Slowed sinus rate, increased AV nodal refractoriness Metabolism: hepatic Bradycardia, hypotension, HF, AV block, sleep disorder, dizziness, nightmares, hyperglycemia, diarrhea, bronchospasm
Quinidine (IA), PO: sulfate salt 200–600 mg q 6 h to q 12 h, gluconate salt 324–648 mg q 8 h to q 12 h, IV: loading dose: 800 mg in 50 mL infused at 50 mg/min VT, VF, short QT syndrome, brugada INa, Ito, IKr, M, Alpha receptor QRS prolongation, QTc prolongation, increased defibrillation threshold Metabolism: hepatic Syncope, torsades de pointes, AV block, dizziness, diarrhea, nausea, esophagitis, emesis, tinnitus, blurred vision, rash, weakness, tremor, blood dyscrasias
Ranolazine (not classified), PO: 500–1000 mg q 12 h VT INa, IKr Slowed sinus rate, QTc prolongation Metabolism: hepatic Bradycardia, hypotension, headache, dizziness, syncope, nausea, dyspnea
Sotalol (III), IV: 75 mg q 12 h, PO: 80–120 mg q 12 h, may increase dose every 3 d; max 320 mg/d VT, VF, PVC B1, B2 IKr Slowed sinus rate, QTc prolongation, increased AV nodal refractoriness, decreased defibrillation threshold Metabolism: none Bradycardia, hypotension, HF, syncope, TdP, fatigue, dizziness, weakness, dyspnea, bronchitis, depression, nausea, diarrhea
Verapamil, IV: 2.5–5 mg q 15–30 min, sustained release PO: 240–480 mg/d RVOT VT, verapamil-sensitive idiopathic Left VT ICa-L Slowed sinus rate,PR prolongation, slowed AV nodal conduction Metabolism: hepatic Hypotension, edema, HF, AV block, bradycardia, exacerbation of HF reduced EF, headache, rash, gingival hyperplasia, constipation, dyspepsia
Electrolytes

Electrolytes


Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]Mohamadmostafa Jahansouz M.D.[3]

Synonyms and keywords: abnormal electrolytes, abnormal lytes, lytes

Overview

Electrolytes are electrically charged solutes necessary to maintain body homeostasis. The main electrolytes include Sodium (Na), Potassium (K), Chloride (Cl), Calcium (Ca), Phosphorus (P), and Magnesium (Mg). These electrolytes are involved in multiple physiologic and neurohormonal reactions necessary to maintain neuromuscular, neuronal, myocardial, and acid-base balance. Their balance are mainly regulated by renal and endocrine systems, any changes in their balance may be life threatening. Electrolytes are in balance to achieve neutral electrical charges. Electrolytes could be classified based on their electrical charge to anions and cations. Anions include bicarbonate, chloride, and phosphorus. Cations are calcium, magnesium, potassium, and sodium. Sodium and chloride are the major extracellular ions that has the greatest impact on serum osmolality (solute concentration in 1 liter of water). Calcium and bicarbonate are the other major extracellular electrolytes. Main intracellular electrolytes are potassium, phosphorus, and magnesium.

Causes

The following table summarize the common causes for electrolytes imbalance.

Electrolyte Ionic formula Normal limits (meq/l) Disturbance Lab value Common causes
Sodium Na+ 135-145 Hyponatremia <135 meq/L Hypovolemic[1]
Euvolemic[2][3][4] SIADH, glucocorticoid deficiency, psychogenic polydipsia
Hypervolemic[5][6][7] CHF, cirrhosis, nephrotic syndrome, renal failure
Hypernatremia >145 meq/L Extrarenal loss[8][9] Vomiting, diarrhea, insensible loss
Renal loss[10] Diuretics, diabetes insipidus (central and nephrogenic)
Potassium K+ 3.5-5 Hypokalemia <3.5 meq/L Transcellular shifts[11][12] Insulin therapy, alkalosis
GI loss[13][14] Diarrhea, laxative abuse, vomiting
Renal loss[15][16][17][18]
Hyperkalemia[19][20][21] >5 meq/L ACE inhibitors, acidosis, addisonian crisis, beta blockers, blood transfusion, cirrhosis, diabetic nephropathy, high potassium diet, malnutrition, renal tubular acidosis type IV, renal failure
Calcium Ca2+ 8.5-10.2 Hypocalcemia[22][23][24] <8.5 meq/L Hypoparathyroidism, pseudohypoparathyroidism, hypomagnesemia, hypovitaminosis D,

chronic kidney disease, hypoalbuminemia

Hypercalcemia[25][26][27][28] >10.2 meq/L Hyperparathyroidism, familial hypocalciuric hypercalcemia, malignancy, Milk-alkali syndrome,

vitamin D toxicity, sarcoidosis, diuretics, lithium

Phosphate PO43- 2.5-4.5 Hypophosphatemia[29][30][31] <2.5 meq/L Refeeding syndrome, respiratory alkalosis, alcohol abuse, malabsorption
Hyperphosphatemia[32][33] >4.5 meq/L Transcellular shift, tumor lysis syndrome , rhabdomyolysis, hypoparathyroidism, pseudohypoparathyroidism, acute kidney injury, chronic kidney disease
Magnesium Mg2+ 1.5-2.5 Hypomagnesemia[34][35][36] <1.5 meq/L Alcohol use, uncontrolled diabetes mellitus, hypercalcemia, Gitelman syndrome, loop and thiazide diuretics
Hypermagnesemia[37][38] >2.5 meq/L Renal failure, massive oral ingestion

Diagnosis

Diagnosis of electrolyte disturbances is suspected by clinical presentation and will be confirmed by laboratory values. Clinical manifestations depend on the severity of disturbances and their chronicity however, the presentation may vary according to underlying condition. The following table summarizes common symptoms and signs of electrolytes disturbances and important ECG findings.


Disturbance Chronicity/ Level (meq/L) Common clinical manifestations ECG findings
Symptoms Signs
Hyponatremia Early/125-130 Nausea, malaise Muscle cramps N/A
Late/115-120 Headache, lethargy Respiratory distress, coma, seizure Non specific ST-T changes
Hypernatremia >145 Malaise Lethargy, confusion, coma Non specific ST-T changes
Hypokalemia[39] <2.5-3 Nausea, anorexia, vomiting, muscle weakness, muscle cramps Rhabdomyolysis, respiratory failure
Hyperkalemia[40][41] >7.5 Muscle weakness, polyuria, polydipsia Paralysis
Hypocalcemia[42][43] <7-7.5 Paresthesias, muscle spasm Trousseau’s sign, Chvostek’s sign, seizures
Hypercalcemia[44] >12 Fatigue, depression, insomnia, nausea, vomiting, constipation, polyuria Hyperreflexia, confusion, coma
Hypophosphatemia[45][46][47] <1 Irritability, paresthesias, dysphagia Delirium, seizure, coma Ventricular arrhythmias
Hyperphosphatemia[48] >4.5 Muscle cramps, paresthesias Tetanus QT interval prolongation (mainly due to associated hypocalcemia)
Hypomagnesemia[49] <1 Tremor, tetanus, weakness Apathy, delirium, coma
Hypermagnesemia[50] >4 Nausea, flushing, headache Somnolence, hypotension, absent DTR

References

  1. ↑ Alam NH, Majumder RN, Fuchs GJ (July 1999). “Efficacy and safety of oral rehydration solution with reduced osmolarity in adults with cholera: a randomised double-blind clinical trial. CHOICE study group”. Lancet. 354 (9175): 296–9. PMID 10440307.
  2. ↑ Pham PC, Pham PM, Pham PT (May 2006). “Vasopressin excess and hyponatremia”. Am. J. Kidney Dis. 47 (5): 727–37. doi:10.1053/j.ajkd.2006.01.020. PMID 16632011.
  3. ↑ Ellison DH, Berl T (May 2007). “Clinical practice. The syndrome of inappropriate antidiuresis”. N. Engl. J. Med. 356 (20): 2064–72. doi:10.1056/NEJMcp066837. PMID 17507705.
  4. ↑ Oelkers W (August 1989). “Hyponatremia and inappropriate secretion of vasopressin (antidiuretic hormone) in patients with hypopituitarism”. N. Engl. J. Med. 321 (8): 492–6. doi:10.1056/NEJM198908243210802. PMID 2548097.
  5. ↑ Leier CV, Dei Cas L, Metra M (September 1994). “Clinical relevance and management of the major electrolyte abnormalities in congestive heart failure: hyponatremia, hypokalemia, and hypomagnesemia”. Am. Heart J. 128 (3): 564–74. PMID 8074021.
  6. ↑ Rodríguez-Iturbe B, Colic D, Parra G, Gutkowska J (September 1990). “Atrial natriuretic factor in the acute nephritic and nephrotic syndromes”. Kidney Int. 38 (3): 512–7. PMID 2146429.
  7. ↑ Ginès P, Guevara M (September 2008). “Hyponatremia in cirrhosis: pathogenesis, clinical significance, and management”. Hepatology. 48 (3): 1002–10. doi:10.1002/hep.22418. PMID 18671303.
  8. ↑ Rose BD (December 1986). “New approach to disturbances in the plasma sodium concentration”. Am. J. Med. 81 (6): 1033–40. PMID 3799631.
  9. ↑ Shamsuddin AK, Yanagimoto S, Kuwahara T, Zhang Y, Nomura C, Kondo N (June 2005). “Changes in the index of sweat ion concentration with increasing sweat during passive heat stress in humans”. Eur. J. Appl. Physiol. 94 (3): 292–7. doi:10.1007/s00421-005-1314-7. PMID 15765239.
  10. ↑ Thompson CJ, Baylis PH (October 1987). “Thirst in diabetes insipidus: clinical relevance of quantitative assessment”. Q. J. Med. 65 (246): 853–62. PMID 3449889.
  11. ↑ Adrogué HJ, Lederer ED, Suki WN, Eknoyan G (May 1986). “Determinants of plasma potassium levels in diabetic ketoacidosis”. Medicine (Baltimore). 65 (3): 163–72. PMID 3084904.
  12. ↑ Adrogué HJ, Madias NE (September 1981). “Changes in plasma potassium concentration during acute acid-base disturbances”. Am. J. Med. 71 (3): 456–67. PMID 7025622.
  13. ↑ Ho JM, Juurlink DN, Cavalcanti RB (March 2010). “Hypokalemia following polyethylene glycol-based bowel preparation for colonoscopy in older hospitalized patients with significant comorbidities”. Ann Pharmacother. 44 (3): 466–70. doi:10.1345/aph.1M341. PMID 20124467.
  14. ↑ Beloosesky Y, Grinblat J, Weiss A, Grosman B, Gafter U, Chagnac A (April 2003). “Electrolyte disorders following oral sodium phosphate administration for bowel cleansing in elderly patients”. Arch. Intern. Med. 163 (7): 803–8. doi:10.1001/archinte.163.7.803. PMID 12695271.
  15. ↑ Wang WH, Giebisch G (May 2009). “Regulation of potassium (K) handling in the renal collecting duct”. Pflugers Arch. 458 (1): 157–68. doi:10.1007/s00424-008-0593-3. PMC 2730119. PMID 18839206.
  16. ↑ Vallon V, Schroth J, Lang F, Kuhl D, Uchida S (September 2009). “Expression and phosphorylation of the Na+-Cl- cotransporter NCC in vivo is regulated by dietary salt, potassium, and SGK1”. Am. J. Physiol. Renal Physiol. 297 (3): F704–12. doi:10.1152/ajprenal.00030.2009. PMC 2739704. PMID 19570885.
  17. ↑ Kurtz I (October 1998). “Molecular pathogenesis of Bartter’s and Gitelman’s syndromes”. Kidney Int. 54 (4): 1396–410. doi:10.1046/j.1523-1755.1998.00124.x. PMID 9767561.
  18. ↑ Monnens L, Bindels R, Grünfeld JP (July 1998). “Gitelman syndrome comes of age”. Nephrol. Dial. Transplant. 13 (7): 1617–9. PMID 9681697.
  19. ↑ Smellie WS (March 2007). “Spurious hyperkalaemia”. BMJ. 334 (7595): 693–5. doi:10.1136/bmj.39119.607986.47. PMC 1839224. PMID 17395950.
  20. ↑ Gonick HC, Kleeman CR, Rubini ME, Maxwell MH (May 1971). “Functional impairment in chronic renal disease. 3. Studies of potassium excretion”. Am. J. Med. Sci. 261 (5): 281–90. PMID 5092154.
  21. ↑ Arthur S, Greenberg A (June 1990). “Hyperkalemia associated with intravenous labetalol therapy for acute hypertension in renal transplant recipients”. Clin. Nephrol. 33 (6): 269–71. PMID 2376088.
  22. ↑ Riccardi D, Brown EM (March 2010). “Physiology and pathophysiology of the calcium-sensing receptor in the kidney”. Am. J. Physiol. Renal Physiol. 298 (3): F485–99. doi:10.1152/ajprenal.00608.2009. PMC 2838589. PMID 19923405.
  23. ↑ Neufeld M, Maclaren NK, Blizzard RM (September 1981). “Two types of autoimmune Addison’s disease associated with different polyglandular autoimmune (PGA) syndromes”. Medicine (Baltimore). 60 (5): 355–62. PMID 7024719.
  24. ↑ Cholst IN, Steinberg SF, Tropper PJ, Fox HE, Segre GV, Bilezikian JP (May 1984). “The influence of hypermagnesemia on serum calcium and parathyroid hormone levels in human subjects”. N. Engl. J. Med. 310 (19): 1221–5. doi:10.1056/NEJM198405103101904. PMID 6709029.
  25. ↑ Meric F, Yap P, Bia MJ (November 1990). “Etiology of hypercalcemia in hemodialysis patients on calcium carbonate therapy”. Am. J. Kidney Dis. 16 (5): 459–64. PMID 2239937.
  26. ↑ Glendenning P, Gutteridge DH, Retallack RW, Stuckey BG, Kermode DG, Kent GN (April 1998). “High prevalence of normal total calcium and intact PTH in 60 patients with proven primary hyperparathyroidism: a challenge to current diagnostic criteria”. Aust N Z J Med. 28 (2): 173–8. PMID 9612524.
  27. ↑ Alikhan Z, Singh A (October 1996). “Hyperthyroidism manifested as hypercalcemia”. South. Med. J. 89 (10): 997–8. PMID 8865795.
  28. ↑ Distler W (1989). “[The climacteric–physiology or pathology?]”. Arch. Gynecol. Obstet. (in German). 245 (1–4): 947–52. PMID 2679445.
  29. ↑ Marinella MA (2005). “Refeeding syndrome and hypophosphatemia”. J Intensive Care Med. 20 (3): 155–9. doi:10.1177/0885066605275326. PMID 15888903.
  30. ↑ MOSTELLAR ME, TUTTLE EP (January 1964). “EFFECTS OF ALKALOSIS ON PLASMA CONCENTRATION AND URINARY EXCRETION OF INORGANIC PHOSPHATE IN MAN”. J. Clin. Invest. 43: 138–49. doi:10.1172/JCI104888. PMC 289504. PMID 14105225.
  31. ↑ Murer H, Lötscher M, Kaissling B, Levi M, Kempson SA, Biber J (June 1996). “Renal brush border membrane Na/Pi-cotransport: molecular aspects in PTH-dependent and dietary regulation”. Kidney Int. 49 (6): 1769–73. PMID 8743494.
  32. ↑ Tsokos GC, Balow JE, Spiegel RJ, Magrath IT (May 1981). “Renal and metabolic complications of undifferentiated and lymphoblastic lymphomas”. Medicine (Baltimore). 60 (3): 218–29. PMID 6894477.
  33. ↑ Grossman RA, Hamilton RW, Morse BM, Penn AS, Goldberg M (October 1974). “Nontraumatic rhabdomyolysis and acute renal failure”. N. Engl. J. Med. 291 (16): 807–11. doi:10.1056/NEJM197410172911601. PMID 4423658.
  34. ↑ Shah GM, Kirschenbaum MA (1991). “Renal magnesium wasting associated with therapeutic agents”. Miner Electrolyte Metab. 17 (1): 58–64. PMID 1722865.
  35. ↑ Elisaf M, Merkouropoulos M, Tsianos EV, Siamopoulos KC (December 1995). “Pathogenetic mechanisms of hypomagnesemia in alcoholic patients”. J Trace Elem Med Biol. 9 (4): 210–4. doi:10.1016/S0946-672X(11)80026-X. PMID 8808192.
  36. ↑ Tosiello L (June 1996). “Hypomagnesemia and diabetes mellitus. A review of clinical implications”. Arch. Intern. Med. 156 (11): 1143–8. PMID 8639008.
  37. ↑ RANDALL RE, COHEN MD, SPRAY CC, ROSSMEISL EC (July 1964). “HYPERMAGNESEMIA IN RENAL FAILURE. ETIOLOGY AND TOXIC MANIFESTATIONS”. Ann. Intern. Med. 61: 73–88. PMID 14178364.
  38. ↑ Clark BA, Brown RS (1992). “Unsuspected morbid hypermagnesemia in elderly patients”. Am. J. Nephrol. 12 (5): 336–43. doi:10.1159/000168469. PMID 1489003.
  39. ↑ Knochel JP, Schlein EM (July 1972). “On the mechanism of rhabdomyolysis in potassium depletion”. J. Clin. Invest. 51 (7): 1750–8. doi:10.1172/JCI106976. PMC 292322. PMID 5032523.
  40. ↑ Mattu A, Brady WJ, Robinson DA (October 2000). “Electrocardiographic manifestations of hyperkalemia”. Am J Emerg Med. 18 (6): 721–9. doi:10.1053/ajem.2000.7344. PMID 11043630.
  41. ↑ Bashour T, Hsu I, Gorfinkel HJ, Wickramesekaran R, Rios JC (February 1975). “Atrioventricular and intraventricular conduction in hyperkalemia”. Am. J. Cardiol. 35 (2): 199–203. PMID 1119378.
  42. ↑ Benoit SR, Mendelsohn AB, Nourjah P, Staffa JA, Graham DJ (August 2005). “Risk factors for prolonged QTc among US adults: Third National Health and Nutrition Examination Survey”. Eur J Cardiovasc Prev Rehabil. 12 (4): 363–8. PMID 16079644.
  43. ↑ Meyer T, Ruppert V, Karatolios K, Maisch B (2007). “Hereditary long QT syndrome due to autoimmune hypoparathyroidism in autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy syndrome”. J Electrocardiol. 40 (6): 504–9. doi:10.1016/j.jelectrocard.2006.12.013. PMID 17289071.
  44. ↑ Rosenqvist M, Nordenström J, Andersson M, Edhag OK (July 1992). “Cardiac conduction in patients with hypercalcaemia due to primary hyperparathyroidism”. Clin. Endocrinol. (Oxf). 37 (1): 29–33. PMID 1424189.
  45. ↑ Silvis SE, DiBartolomeo AG, Aaker HM (March 1980). “Hypophosphatemia and neurological changes secondary to oral caloric intake: a variant of hyperalimentation syndrome”. Am. J. Gastroenterol. 73 (3): 215–22. PMID 6773412.
  46. ↑ Weisinger JR, Bellorín-Font E (August 1998). “Magnesium and phosphorus”. Lancet. 352 (9125): 391–6. doi:10.1016/S0140-6736(97)10535-9. PMID 9717944.
  47. ↑ Ognibene A, Ciniglio R, Greifenstein A, Jarjoura D, Cugino A, Blend D, Whittier F (January 1994). “Ventricular tachycardia in acute myocardial infarction: the role of hypophosphatemia”. South. Med. J. 87 (1): 65–9. PMID 7506845.
  48. ↑ Ketteler M, Block GA, Evenepoel P, Fukagawa M, Herzog CA, McCann L, Moe SM, Shroff R, Tonelli MA, Toussaint ND, Vervloet MG, Leonard MB (July 2017). “Executive summary of the 2017 KDIGO Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD) Guideline Update: what’s changed and why it matters”. Kidney Int. 92 (1): 26–36. doi:10.1016/j.kint.2017.04.006. PMID 28646995.
  49. ↑ VALLEE BL, WACKER WE, ULMER DD (January 1960). “The magnesium-deficiency tetany syndrome in man”. N. Engl. J. Med. 262: 155–61. doi:10.1056/NEJM196001282620401. PMID 13840893.
  50. ↑ Krendel DA (March 1990). “Hypermagnesemia and neuromuscular transmission”. Semin Neurol. 10 (1): 42–5. doi:10.1055/s-2008-1041252. PMID 2161126.

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Fatty acids, Lipids

Fatty acids, Lipids


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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

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In chemistry, especially biochemistry, a fatty acid is a carboxylic acid often with a long unbranched aliphatic tail (chain), which is either saturated or unsaturated. Carboxylic acids as short as butyric acid (4 carbon atoms) are considered to be fatty acids, whereas fatty acids derived from natural fats and oils may be assumed to have at least 8 carbon atoms, e.g., caprylic acid (octanoic acid). Most of the natural fatty acids have an even number of carbon atoms, because their biosynthesis involves acetyl-CoA, a coenzyme carrying a two-carbon-atom group (see fatty acid synthesis).

In industry, fatty acids are produced by the hydrolysis of the ester linkages in a fat or biological oil (both of which are triglycerides), with the removal of glycerol. See oleochemicals.

Types of fatty acids

Three dimensional representations of several fatty acids

Saturated fatty acids

Main article: Saturated fat

Saturated fatty acids do not contain any double bonds or other functional groups along the chain. The term “saturated” refers to hydrogen, in that all carbons (apart from the carboxylic acid [-COOH] group) contain as many hydrogens as possible. In other words, the omega (ω) end contains 3 hydrogens (CH3-), and each carbon within the chain contains 2 hydrogen

Saturated fatty acids form straight chains and, as a result, can be packed together very tightly, allowing living organisms to store chemical energy very densely. The fatty tissues of animals contain large amounts of long-chain saturated fatty acids. In IUPAC nomenclature, fatty acids have an [-oic acid] suffix. In common nomenclature, the suffix is usually –ic.

The shortest descriptions of fatty acids include only the number of carbon atoms and double bonds in them (e.g., C18:0 or 18:0). C18:0 means that the carbon chain of the fatty acid consists of 18 carbon atoms, and there are no (zero) double bonds in it, whereas C18:1 describes an 18-carbon chain with one double bond in it. Each double bond can be in either a cis- or trans- conformation and in a different position with respect to the ends of the fatty acid; therefore, not all C18:1s, for example, are identical. If there is one or more double bonds in the fatty acid, it is no longer considered saturated, rather mono- or polyunsaturated.

Most commonly-occurring saturated fatty acids are:

Common name IUPAC name Chemical structure Abbr.
Butyric Butanoic acid CH3(CH2)2COOH C4:0
Caproic Hexanoic acid CH3(CH2)4COOH C6:0
Caprylic Octanoic acid CH3(CH2)6COOH C8:0
Capric Decanoic acid CH3(CH2)8COOH C10:0
Lauric Dodecanoic acid CH3(CH2)10COOH C12:0
Myristic Tetradecanoic acid CH3(CH2)12COOH C14:0
Palmitic Hexadecanoic acid CH3(CH2)14COOH C16:0
Stearic Octadecanoic acid CH3(CH2)16COOH C18:0
Arachidic Eicosanoic acid CH3(CH2)18COOH C20:0
Behenic Docosanoic acid CH3(CH2)20COOH C22:0

Unsaturated fatty acids

Main article: Unsaturated fat

File:Isomers of oleic acid.png Unsaturated fatty acids are of similar form, except that one or more alkenyl functional groups exist along the chain, with each alkene substituting a single-bonded ” -CH2-CH2-” part of the chain with a double-bonded “-CH=CH-” portion (that is, a carbon double-bonded to another carbon).

The two next carbon atoms in the chain that are bound to either side of the double bond can occur in a cis or trans configuration.

cis
A cis configuration means that adjacent carbon atoms are on the same side of the double bond. The rigidity of the double bond freezes its conformation and, in the case of the cis isomer, causes the chain to bend and restricts the conformational freedom of the fatty acid. The more double bonds the chain has in the cis configuration, the less flexibility it has. When a chain has many cis bonds, it becomes quite curved in its most accessible conformations. For example, oleic acid, with one double bond, has a “kink” in it, whereas linoleic acid, with two double bonds, has a more pronounced bend. Alpha-linolenic acid, with three double bonds, favors a hooked shape. The effect of this is that, in restricted environments, such as when fatty acids are part of a phospholipid in a lipid bilayer, or triglycerides in lipid droplets, cis bonds limit the ability of fatty acids to be closely packed, and therefore could affect the melting temperature of the membrane or of the fat.
trans
A trans configuration, by contrast, means that the next two carbon atoms are bound to opposite sides of the double bond. As a result, they do not cause the chain to bend much, and their shape is similar to straight saturated fatty acids.

In most naturally-occurring unsaturated fatty acids, each double bond has 3n carbon atoms after it, for some n, and all are cis bonds. Most fatty acids in the trans configuration (trans fats) are not found in nature and are the result of human processing (e.g., hydrogenation).

The differences in geometry between the various types of unsaturated fatty acids, as well as between saturated and unsaturated fatty acids, play an important role in biological processes, and in the construction of biological structures (such as cell membranes).

Nomenclature

There are several different ways to make clear where the double bonds are located in molecules. For example:

  • cis/trans-Delta-x or cis/trans-Δx: The double bond is located on the xth carbon-carbon bond, counting from the carboxylic acid end. The cis or trans notation indicates whether the molecule is arranged in a cis or trans conformation. In the case of a molecule’s having more than one double bond, the notation is, for example, cis,cis-Δ9,Δ12.
  • Omega-x or ω-x : A double bond is located on the xth carbon-carbon bond, counting from the ω, (methyl carbon) end of the chain. Sometimes, the symbol ω is replaced with a lowercase letter n, making it n-6 or n-3.
  • In IUPAC nomenclature, a systematic naming system for all chemical compounds, counting is begins from the carboxylic acid end and cis double bonds are labelled Z and trans double bonds are labelled E. (See IUPAC nomenclature of organic chemistry for details.)

Examples of unsaturated fatty acids

Common name Chemical structure ω    Δ Abbr.
Myristoleic acid: CH3(CH2)3CH=CH(CH2)7COOH ω-5 cis-Δ5 C14:1
Palmitoleic acid: CH3(CH2)5CH=CH(CH2)7COOH ω-7 cis-Δ7 C16:1
Oleic acid: CH3(CH2)7CH=CH(CH2)7COOH ω-9 cis-Δ9 C18:1
Linoleic acid: CH3(CH2)4CH=CHCH2CH=CH(CH2)7COOH ω-6 cis, cis-Δ6, Δ9 C18:2
Alpha-linolenic acid: CH3CH2CH=CHCH2CH=CHCH2CH=CH(CH2)7COOH ω-3 cis, cis, cis-Δ3, Δ6, Δ9 C18:3
Arachidonic acid CH3(CH2)4CH=CHCH2CH=CHCH2CH=CHCH2CH=CH(CH2)3COOHNIST ω-6 cis, cis, cis, cis-Δ6, Δ9, Δ12, Δ15 C20:4
Eicosapentaenoic acid CH3CH2CH=CHCH2CH=CHCH2CH=CHCH2CH=CHCH2CH=CH(CH2)3COOH ω-3 cis, cis, cis, cis, cis-Δ3, Δ6, Δ9, Δ12, Δ15 C20:5
Erucic acid: CH3(CH2)7CH=CH(CH2)11COOH ω-9 cis-Δ9 C22:1
Docosahexaenoic acid CH3CH2CH=CHCH2CH=CHCH2CH=CHCH2CH=CHCH2CH=CHCH2CH=CH(CH2)2COOH ω-3 cis, cis, cis, cis, cis, cis-Δ3, Δ6, Δ9, Δ12, Δ15, Δ18 C22:6

Myristoleic is omega-5 fatty acid, palmitoleic is omega-7 fatty acid, and oleic and erucic acid are omega-9 fatty acids. Stearic and oleic acid are both C18 fatty acids. They differ only in that stearic acid is saturated with hydrogen, whereas oleic acid is an unsaturated fatty acid with two fewer hydrogens.

Omega-3 fatty acid

Docosahexaenoic acid (DHA), and eicosapentaenoic acid (EPA) are examples of long chain omega-3 fatty acids (LCn3) in fish oil. Alpha-linolenic is a long chain omega-3 fatty acid from plants. LCn3 may benefit health.

Omega-6 fatty acid

Linoleic acid and arachidonic acid are omega-6 fatty acids. These fatty acids may be harmful.

Essential fatty acids

Main article: Essential fatty acid

The human body can produce all but two of the fatty acids it needs. These two, linoleic acid (LA) and alpha-linolenic acid (LNA), are widely distributed in plant oils. In addition, fish oils contain the longer-chain omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). Other marine oils, such as from seal, also contain significant amounts of docosapentaenoic acid (DPA), which is also an omega-3 fatty acid. Although the body to some extent can convert LA and LNA into these longer-chain omega-3 fatty acids, the omega-3 fatty acids found in marine oils help fulfil the requirement of essential fatty acids (and have been shown to have wholesome properties of their own).

Since they cannot be made in the body from other substrates and must be supplied in food, they are called essential fatty acids. Mammals lack the ability to introduce double bonds in fatty acids beyond carbons 9 and 10. Hence linoleic acid and linoleinic acid are essential fatty acids for humans.

In the body, essential fatty acids are primarily used to produce hormone-like substances that regulate a wide range of functions, including blood pressure, blood clotting, blood lipid levels, the immune response, and the inflammation response to injury infection.

Essential fatty acids are polyunsaturated fatty acids and are the parent compounds of the omega-6 and omega-3 fatty acid series, respectively. They are essential in the human diet because there is no synthetic mechanism for them. Humans can easily make saturated fatty acids or monounsaturated fatty acids with a double bond at the omega-9 position, but do not have the enzymes necessary to introduce a double bond at the omega-3 position or omega-6 position.

The essential fatty acids are important in several human body systems, including the immune system and in blood pressure regulation, since they are used to make compounds such as prostaglandins. The brain has increased amounts of linolenic and alpha-linoleic acid derivatives. Changes in the levels and balance of these fatty acids due to a typical Western diet rich in omega-6 and poor in omega-3 fatty acids is alleged to be associated with depression and behavioral change, including violence. The actual connection, if any, is still under investigation. Further, changing to a diet richer in omega-3 fatty acids, or consumption of supplements to compensate for a dietary imbalance, has been associated with reduced violent behavior[1] and increased attention span, but the mechanisms for the effect are still unclear. So far, at least three human studies have shown results that support this: two school studies[2] as well as a double blind study in a prison.[1][3][4]

Fatty acids play an important role in the life and death of cardiac cells because they are essential fuels for mechanical and electrical activities of the heart. [5] [6] [7] [8]

Trans fatty acids

Main article: Trans fat

A trans fatty acid (commonly shortened to trans fat) is an unsaturated fatty acid molecule that contains a trans double bond between carbon atoms, which makes the molecule less ‘kinked’ in comparison to fatty acids with cis double bonds. These bonds are characteristically produced during industrial hydrogenation of plant oils. Research suggests that amounts of trans fats correlate with circulatory diseases such as atherosclerosis and coronary heart disease more than the same amount of non-trans fats, for reasons that are not well understood.

Free fatty acids

Fatty acids can be bound or attached to other molecules, such as in triglycerides or phospholipids. When they are not attached to other molecules, they are known as “free” fatty acids.

The uncombined fatty acids or free fatty acids may come from the breakdown of a triglyceride into its components (fatty acids and glycerol).

Free fatty acids are an important source of fuel for many tissues since they can yield relatively large quantities of ATP. Many cell types can use either glucose or fatty acids for this purpose. In particular, heart and skeletal muscle prefer fatty acids. The brain cannot use fatty acids as a source of fuel; it relies on glucose, or on ketone bodies. Ketone bodies are produced in the liver by fatty acid metabolism during starvation, or during periods of low carbohydrate intake.

Fatty acids in dietary fats

The following table gives the fatty acid and cholesterol composition of some common dietary fats.[9] [10]

Saturated Monounsaturated Polyunsaturated Cholesterol Vitamin E
g/100g g/100g g/100g mg/100g mg/100g
Animal fats
Lard 40.8 43.8 9.6 93 0.00
Butter 54.0 19.8 2.6 230 2.00
Vegetable fats
Coconut oil 85.2 6.6 1.7 0 .66
Palm oil 45.3 41.6 8.3 0 33.12
Cottonseed oil 25.5 21.3 48.1 0 42.77
Wheat germ oil 18.8 15.9 60.7 0 136.65
Soya oil 14.5 23.2 56.5 0 16.29
Olive oil 14.0 69.7 11.2 0 5.10
Corn oil 12.7 24.7 57.8 0 17.24
Sunflower oil 11.9 20.2 63.0 0 49.0 
Safflower oil 10.2 12.6 72.1 0 40.68
Rapeseed/Canola oil 5.3 64.3 24.8 0 22.21

Acidity

Short chain carboxylic acids such as formic acid and acetic acid are miscible with water and dissociate to form reasonably strong acids (pKa 3.77 and 4.76, respectively). Longer-chain fatty acids do not show a great change in pKa. Nonanoic acid, for example, has a pKa of 4.96. However, as the chain length increases the solubility of the fatty acids in water decreases very rapidly, so that the longer-chain fatty acids have very little effect on the pH of a solution. The significance of their pKa values therefore has relevance only to the types of reactions in which they can take part.

Even those fatty acids that are insoluble in water will dissolve in warm ethanol, and can be titrated with sodium hydroxide solution using phenolphthalein as an indicator to a pale-pink endpoint. This analysis is used to determine the free fatty acid content of fats, i.e., the proportion of the triglycerides that have been hydrolyzed.

Reaction of fatty acids

Fatty acids react just like any other carboxylic acid, which means they can undergo esterification and acid-base reactions. Reduction of fatty acids yields fatty alcohols. Unsaturated fatty acids can also undergo addition reactions, most commonly hydrogenation, which is used to convert vegetable oils into margarine. With partial hydrogenation, unsaturated fatty acids can be isomerized from cis to trans configuration. In the Varrentrapp reaction certain unsaturated fatty acids are cleaved in molten alkali, a reaction at one time of relevance to structure elucidation.

Auto-oxidation and rancidity

Main article: Rancidification

Fatty acids at room temperature undergo a chemical change known as auto-oxidation. The fatty acid breaks down into hydrocarbons, ketones, aldehydes, and smaller amounts of epoxides and alcohols. Heavy metals present at low levels in fats and oils promote auto-oxidation. Fats and oils often are treated with chelating agents such as citric acid.

References

  1. ↑ 1.0 1.1 C. Bernard Gesch, CQSW Sean M. Hammond, PhD Sarah E. Hampson, PhD Anita Eves, PhD Martin J. Crowder, PhD (2002). “Influence of supplementary vitamins, minerals and essential fatty acids on the antisocial behaviour of young adult prisoners”. The British Journal of Psychiatry. 181: 22–28. Retrieved 2006-06-27.
  2. ↑ Alexandra J. Richardson and Paul Montgomery (2005). “The Oxford-Durham study: a randomized controlled trial of dietary supplementation with fatty acids in children with developmental coordination disorder”. Pediatrics. 115 (5): 1360–1366. doi:10.1542/peds.2004-2164. |access-date= requires |url= (help)
  3. ↑ Lawrence, Felicity (2004). Kate Barker, ed. Not on the Label. Penguin. p. 213. ISBN 0-14-101566-7.
  4. ↑ “Using Fatty Acids for Enhancing Classroom Achievement”. Unknown parameter |accessyear= ignored (|access-date= suggested) (help); Unknown parameter |accessmonthday= ignored (help)
  5. ↑ “External blockade…by polyunsaturated fatty acids”. pubmed. Retrieved 2007-01-18. – see page 1 of this link
  6. ↑ “Antiarrythmic effects of omega-3 fatty acids”. pubmed. Retrieved 2007-01-18.
  7. ↑ “Alpha-linolenic acid, cardiovascular disease and sudden death”. pubmed. Retrieved 2007-01-18.
  8. ↑ “Omega-3 and health”. pubmed. Retrieved 2007-01-18.
  9. ↑ Food Standards Agency (1991). “Fats and Oils”. McCance & Widdowson’s The Composition of Foods. Royal Society of Chemistry.
  10. ↑ Ted Altar. “More Than You Wanted To Know About Fats/Oils”. Sundance Natural Foods Online. Retrieved 2006-08-31.

See also

ar:حمض دهني cs:Mastná kyselina da:Fedtsyre de:Fettsäure eo:Grasacido ko:지방산 hr:Masne kiseline id:Asam lemak it:Acidi grassi he:חומצת שומן lv:Taukskābe hu:Zsírsav mk:Масна киселина nl:Vetzuur no:Fettsyre sl:Maščobna kislina fi:Rasvahappo sv:Fettsyra th:กรดไขมัน uk:Жирні кислоти

Template:WH Template:WS Template:Jb1

Specific recommendation

Specific recommendation

Management of patients with Polymorphic Ventricular arrhythmia

Management of patients with Polymorphic Ventricular arrhythmia

 
 
 
Polymorphic Ventricular arrhythmia
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Underlying etiology
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Acute ischemia
 
External precipitating factors
 
Polymorphic Ventricular Arrhythmia triggered by unifocal PVC
 
Acquired long QT
 
 
 
 
 
 
 
Primary electrical disease
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Approach to STEMI
 
Treatment of underlying condition (Class I)
 
Catheter ablation (Class IIa)
 
 
Remove precipitating factors (Class I)
  • Mg++/K+ i.v.(Class I)
  • Isoproterenol (Class I)
  • Pacing (Class I)
    •  
     
     
    		Brugada, Early repolarization syndrome
     
    		Idiopathic VF
     
    		Long QT, CPVT
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
    		Recurrent Ventricular arrhythmia
     
     
     
    		Recurrent Ventricular arrhythmia
     
    		Recurrent Ventricular arrhythmia
     
     
    		Isoproterenol (Class IIa)
     
    		Isoproterenol (Class IIa)
  • Quinidine (Class IIa)
  • Verapamil (Class IIa
  • Catheter ablation of PVC triggers (Class IIa)
    •  
    		Beta-blocker (Class I)
  • Pacing (Class I)
  • Mg++/K+ i.v (Class I)
  • Antiarrhythmic drugs according to underlying disease (Class 2a)
  • Autonomic modulation (Class 2a)
    •  
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
    		Deep sedation/ intubation (Class IIa)
     
    		Deep sedation/ intubation (Class IIa)
  • Mechanical circulatory support (Class IIb)
    •  
    		Deep sedation/ intubation (Class IIa)
  • Mechanical circulatory support (Class IIb)
    •  
     
    		Recurrent ventricular arrhythmia
     
    		Recurrent ventricular arrhythmia
     
    		Recurrent ventricular arrhythmia
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
    		Deep sedation/ intubation (Class IIa)
     
    		Deep sedation/ intubation (Class IIa)
  • Mechanical circulatory support (Class IIb)
    •  
    		Deep sedation/ intubation (Class IIa)
  • Mechanical circulatory support (Class IIb)
    •  
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
    The above algorithm adopted from 2022 ESC Guideline[38]
    A patient having his blood pressure taken by a doctor.

    Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]


    A patient is any person who receives medical attention, care, or treatment. The person is most often ill or injured and in need of treatment by a physician or other medical professional. Health consumer, health care consumer or client are other names for patient, usually used by governmental agencies, insurance companies, and/or patient groups (who may object to some implications of the word ‘patient’).

    Etymology

    The word patient is derived from the Latin word patiens, the present participle of the deponent verb pati, meaning “one who endures” or “one who suffers”.

    Patient is also the adjective form of patience. Both senses of the word share a common origin.

    In itself the definition of patient doesn’t imply suffering or passivity but the role it describes is often associated with the definitions of the adjective form: enduring trying circumstances with even temper. Some have argued recently that the term should be dropped, because it underlines the inferior status of recipients of health care. [1]

    Pediatric polysomnography patient at the
    Children’s Hospital in Saint Louis, USA

    .

    For them, “the active patient is a contradiction in terms, and it is the assumption underlying the passivity that is the most dangerous”. Unfortunately none of the alternative terms seem to offer a better definition.

    • Client, whose Latin root cliens means “one who is obliged to make supplications to a powerful figure for material assistance“, carries a sense of subservience.
    • Consumer suggest both a financial relationship and a particular social/political stance, implying that health care services operate exactly like all other commercial markets. Many reject that term on the grounds that consumerism is an individualistic concept that fails to capture the particularity of health care systems.

    Outpatient vs inpatient

    An outpatient is a patient who only comes to a hospital or doctor for diagnosis and/or therapy and then leaves again.

    An inpatient on the other hand is ‘admitted’ to the hospital and stays overnight or for an indeterminate time, usually several days or weeks (though some cases, like coma patients, have stayed in hospitals for decades).

    See also

    References

    1. ↑ Neuberger, J. (1999). “Let’s do away with “patients““. British Medical Journal. 318: 1756–8.


    cs:Pacient da:Patient de:Patient eu:Paziente id:Pasien he:חולה lv:Pacients nl:Patiënt qu:Hampina sk:Pacient fi:Potilas sv:Patient th:ผู้ป่วย

    Template:WikiDoc Sources

    Management of sustained monomorphic ventricular tachycardia

    Management of sustained monomorphic ventricular tachycardia

    Recommendations for acute management of sustained VT
    DC cardiovertion (Class I, Level of Evidence B):

    ❑ DC cardioversion is recommended as the first-line therapy for hemodynamically not-tolerated sustained monomorphic ventricular tachycardia

    DC cardiovertion (Class I, Level of Evidence C) :

    ❑ DC cardioversion is recommended as the first-line treatment for patients presenting with tolerated sustained monomorphic VT when anesthetic/sedation risk is low

    Supraventricular tachycardia (Class IIa, Level of Evidence C)

    ❑ In patients presenting with a regular hemodynamically tolerated wide QRS complex tachycardia suspected for supraventricular tachycardia, administration of adenosine or vagal maneuvers should be considered

    Procainamide (Class IIa, Level of Evidence B)

    ❑In patients presenting with a hemodynamically tolerated sustained monomorphic VT and presence of structural heart disease, intravenous procainamide should be considered

    Flecainide, ajmaline, sotalol (Class IIb, Level of Evidence B)

    ❑In patients presenting with a hemodynamically tolerated sustained monomorphic VT in the absence of significant structural heart disease, flecainide, ajmaline, or sotalol may be considered

    Verapamil (Class III, Level of Evidence B)

    ❑Intravenous verapamil is not recommended in wide QRS complex tachycardia of unknown mechanism

    The above table adopted from 2022 ESC Guideline[38]
    Management of electrical storm

    Management of electrical storm

    Recommendations for management of electrical storm
    Sedation (Class I, Level of Evidence C):

    ❑ Mild to moderate sedation is recommended in patients with the electrical storm to reduce psychological distress and reduce sympathetic tone

    Strucrural heart disease (Class I, Level of Evidence B) :

    ❑ Antiarrhythmic therapy with beta-blockers (non-selective preferred) in combination with intravenous amiodarone is recommended in patients with structural heart disease and electrical storm unless contraindicated
    ❑Catheter ablation is recommended in patients presenting with incessant VT or electrical storm due to sustained monomorphic VT refractory to antiarrhythmic drugs

    Torsades depointes (Class I, Level of Evidence C)

    ❑ Intravenous magnesium with supplementation of potassium is recommended in patients with TdP
    ❑Isoproterenol or transvenous pacing to increase heart rate is recommended in patients with acquired LQT syndrome and recurrent TdP despite correction of precipitating conditions and magnesium

    Procainamide (Class IIa, Level of Evidence B)

    ❑In patients presenting with a hemodynamically tolerated sustained monomorphic VT and presence of structural heart disease, intravenous procainamide should be considered

    Intubation (Class IIa, Level of Evidence C)

    ❑Deep sedation/intubation should be considered in patients with an intractable electrical storm non-responsive drug treatment

    ❑Catheter ablation should be considered in patients with recurrent episodes of VT/VF triggered by a similar PVC, refractory to medical treatment or coronary revascularization

    Quinidine (Class IIb, Level of Evidence C)

    ❑Quinidine may be considered in patients with coronary artery disease and electrical storm due to recurrent VT refractory to other antiarrhythmic drugs

    Refractory electerical storm (Class IIb, Level of Evidence C)

    ❑Autonomic modulation may be considered in patients with electrical storm refractory to medical therapy and in whom catheter ablation is ineffective or not possible
    ❑ Mechanical circulatory support may be considered in the management of drug-refractory electrical storm and [[cardiogenic shock]]

    The above table adopted from 2022 ESC Guideline[38]
    Recommendations for treatment with heart failure medication

    Recommendations for treatment with heart failure medication

    Class I
    “Optimal medical treatment including ACE-I/ARB/ ARNIs, mineralocorticoid receptor antagonist, beta-blockers, and SGLT2 inhibitors is indicated in all heart failure patients with reduced EF‘ (Level of Evidence A)”
    The above table adopted from 2022 ESC Guideline[38]

    Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Lakshmi Gopalakrishnan, M.B.B.S. [2], Mitra Chitsazan, M.D.[3] Seyedmahdi Pahlavani, M.D. [4] Syed Hassan A. Kazmi BSc, MD [5] Edzel Lorraine Co, D.M.D., M.D. [6]

    Synonyms and keywords: CHF; pump failure; left heart failure; chronic heart failure; acute heart failure; LV dysfunction; LV failure; impaired filling; reduced cardiac output; HFpEF; HFrEF; heart failure preserved ejection fraction; heart failure reduced ejection fraction; decompensated heart failure; acute decompensated heart failure; ADHF

    Overview

    Classification

    Pathophysiology

    Systolic dysfunction | Diastolic dysfunction | HFpEF | HFrEF

    Causes

    Differentiating Chronic Heart Failure from other Diseases

    Epidemiology and Demographics

    Risk Factors

    Natural History, Complications and Prognosis

    Diagnosis

    Clinical Assessment | History and Symptoms | Physical Examination | Laboratory Findings | Electrocardiogram | Chest X Ray | Echocardiography | Cardiac MRI | Exercise Stress Test | Myocardial Viability Studies | Cardiac Catheterization | Invasive hemodynamic monitoring

    Treatment

    Treatment of Heart failure with reduced ejection fraction

    Pharmacological treatments for patients with heart failure with reduced ejection fraction:

    Guideline-recommended medical therapy (GDMT) for heart failure with reduced ejection fraction (HFrEF) can be suggested by the Heart Failure Educational Decision Aid medication optimization algorithm[1].

    Cardiac rhythm management for patients with heart failure with reduced ejection fraction: Antiarrhythmic drugs | Implantable cardioverter defibrillator | Cardiac resynchronization therapy
    Nutritional supplements and hormonal therapies
    Exercise training
    Drugs to avoid
    Drug interactions
    Treatment of underlying causes
    Treatment of associated conditions

    Treatment of Heart failure with preserved ejection fraction

    Management of Acute heart failure

    Management of Advanced heart failure

    Ultrafiltration | Mechanical circulatory support | Heart transplantation

    ACC/AHA Guideline Recommendations

    Hospitalized Patients

    Patients With a Prior MI

    Sudden Cardiac Death Prevention

    Stage A: Patients at High Risk for Developing Heart Failure

    Treatment of Hypertension | Treatment of Diabetes Mellitus | Management of Metabolic Syndrome | Management of Atherosclerotic Disease | Control of Conditions That May Cause Heart Failure | ACC/AHA Guideline Recommendations

    Stage B: Patients with Cardiac Structural Abnormalities

    Stage C: Patients with Current or Prior Heart Failure Symptoms

    Stage D: Patients with Refractory End-stage Heart Failure

    Implementation of Practice Guidelines

    End-Of-Life Considerations

    Specific Groups

    Special Populations | Patients who have concomitant disorders | Obstructive Sleep Apnea in the Patient with CHF

    References

    1. ↑ Dorsch, Michael P.; Sifuentes, Aaron; Cordwin, David J.; Kuo, Rachel; Rowell, Brigid E.; Arzac, Juan J.; DeBacker, Ken; Guidi, Jessica L.; Hummel, Scott L.; Koelling, Todd M. (April 2023). “A Computable Algorithm for Medication Optimization in Heart Failure With Reduced Ejection Fraction”. JACC: Advances: 100289. doi:10.1016/j.jacadv.2023.100289. ISSN 2772-963X.

    Template:WikiDoc Sources

    Notes

    Notes

    use of beta blockers lessened mortality rate.[50]

    • Prophylactic use of Higher dose amiodarone after MI increase mortality, whereas moderate dose amiodarone was not superior to placebo.[51]


     
     
     
     
     
     
     
     
     
     
    		Sustained monomorphic VT
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
    		Hemodynamic stability
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
    		Stable
     
     
     
     
     
     
     
     
     
     
     
    		Unstable
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
    		12-Lead ECG, history, physical exam
     
     
     
     
     
     
     
     
     
     
     
    		Dirrect current cardioversion,ACLS
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
    		Notifying disease causing VT
     
     
     
    		Cardioversion(class1)
     
     
     
     
     
     
     
    		VT termination
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
    		Structural heart disease
     
     
     
    		Intravenous procainamide (class2a)
     
     
     
     
     
    		Yes, therapy of underlying heart disease
     
    		NO, cardioversion (class1)
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
    		NO, Ideopathic VT
     
     
     
    		Intravenous amiodarone or sotalole (class2b)
     
     
     
     
     
     
     
     
    		VT termination
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
    		Verapamil sensitive VT: Verapamil outflow tract VT: betablocker (class2a)
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
    		Effective
     
    		Non effective: cardioversion
     
     
     
     
     
     
     
     
    		Yes,therapy of underlying heart disease
     
    		NO, Sedation ,anesthesia, reassessing antiarrhythmic therapy, repeating cardioversion
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
    		Therapy to prevent recurrence of VT
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
    		No VT termination
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
    		Catheter ablation (class1)
     
     
    Catheter ablation (class1)
     
    		Verapamil , betablocker (class2a)
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
     
    The above algorithm adopted from 2017 AHA/ACC/HRS Guideline
    Comments

    Comments




    Recommendations for treatment of recurrent ventricular tachycardia in ischemic heart disease
    Medications (Class I, Level of Evidence B):

    ❑ In patients with IHD and recurrent symptomatic ventricular tachycardia and frequent ICD shocks despite programming, betablocker, sotalol, amiodarone is recommended for supression of arrhythmia
    ❑ In patients with period MI and presence of VT storm refractory to amiodarone or other antiarrhythmic drugs, catheter ablation is recommended

    Catheter ablation (Class IIb, Level of Evidence C) :

    ❑ Catheter ablation can be the first line therapy for recurrent sustained monomorphic VT in IHD

    (Class III, Level of Evidence C)

    ❑ Class IC antiarrhythmic drugs (flecainide, propafenone ) is harmful for supression of ventricular tachycardia in patients with perior MI
    ❑ In patients with incessant VT/VF, after controlling tachyarrhythmia ICD should be implanted due to avoiding of repeated ICD shocks
    ❑ In patients with recurrent monomorphic VT , only revascularization is ineffective for preventing of tachyarrhythmia

    The above table adopted from 2017 AHA/ACC/HRS Guideline[2]
    Message

    Message

    Recommendations for treatment of recurrent ventricular tachycardia in non-ischemic heart disease
    Amiodarone, sotalol (Class IIa, Level of Evidence B):

    ❑ Amiodarone or sotalol is recommended in the presensence of recurrent ventricular arrhythmia and frequent ICD shocks despite optimal programming or beta blocker therapy

    Catheter ablation (Class IIa, Level of Evidence B) :

    ❑ In the setting of frequent ventricular arrhythmia despite optimal ICD programming or failed antiarrhythmic medications, catheter ablation is recommended

    The above table adopted from 2017 AHA/ACC/HRS Guideline[2]
    References

    References

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    2. ↑ 2.0 2.1 2.2 Al-Khatib, Sana M.; Stevenson, William G.; Ackerman, Michael J.; Bryant, William J.; Callans, David J.; Curtis, Anne B.; Deal, Barbara J.; Dickfeld, Timm; Field, Michael E.; Fonarow, Gregg C.; Gillis, Anne M.; Granger, Christopher B.; Hammill, Stephen C.; Hlatky, Mark A.; Joglar, José A.; Kay, G. Neal; Matlock, Daniel D.; Myerburg, Robert J.; Page, Richard L. (2018). “2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death”. Circulation. 138 (13). doi:10.1161/CIR.0000000000000549. ISSN 0009-7322.
    3. ↑ Kudenchuk, Peter J.; Brown, Siobhan P.; Daya, Mohamud; Rea, Thomas; Nichol, Graham; Morrison, Laurie J.; Leroux, Brian; Vaillancourt, Christian; Wittwer, Lynn; Callaway, Clifton W.; Christenson, James; Egan, Debra; Ornato, Joseph P.; Weisfeldt, Myron L.; Stiell, Ian G.; Idris, Ahamed H.; Aufderheide, Tom P.; Dunford, James V.; Colella, M. Riccardo; Vilke, Gary M.; Brienza, Ashley M.; Desvigne-Nickens, Patrice; Gray, Pamela C.; Gray, Randal; Seals, Norman; Straight, Ron; Dorian, Paul (2016). “Amiodarone, Lidocaine, or Placebo in Out-of-Hospital Cardiac Arrest”. New England Journal of Medicine. 374 (18): 1711–1722. doi:10.1056/NEJMoa1514204. ISSN 0028-4793.
    4. ↑ Mazzanti, Andrea; Maragna, Riccardo; Faragli, Alessandro; Monteforte, Nicola; Bloise, Raffaella; Memmi, Mirella; Novelli, Valeria; Baiardi, Paola; Bagnardi, Vincenzo; Etheridge, Susan P.; Napolitano, Carlo; Priori, Silvia G. (2016). “Gene-Specific Therapy With Mexiletine Reduces Arrhythmic Events in Patients With Long QT Syndrome Type 3”. Journal of the American College of Cardiology. 67 (9): 1053–1058. doi:10.1016/j.jacc.2015.12.033. ISSN 0735-1097.
    5. ↑ Watanabe, Hiroshi; Chopra, Nagesh; Laver, Derek; Hwang, Hyun Seok; Davies, Sean S; Roach, Daniel E; Duff, Henry J; Roden, Dan M; Wilde, Arthur A M; Knollmann, Björn C (2009). “Flecainide prevents catecholaminergic polymorphic ventricular tachycardia in mice and humans”. Nature Medicine. 15 (4): 380–383. doi:10.1038/nm.1942. ISSN 1078-8956.
    6. ↑ Scirica, Benjamin M.; Braunwald, Eugene; Belardinelli, Luiz; Hedgepeth, Chester M.; Spinar, Jindrich; Wang, Whedy; Qin, Jie; Karwatowska-Prokopczuk, Ewa; Verheugt, Freek W.A.; Morrow, David A. (2010). “Relationship Between Nonsustained Ventricular Tachycardia After Non–ST-Elevation Acute Coronary Syndrome and Sudden Cardiac Death”. Circulation. 122 (5): 455–462. doi:10.1161/CIRCULATIONAHA.110.937136. ISSN 0009-7322.
    7. ↑ Zareba, Wojciech; Daubert, James P.; Beck, Christopher A.; Huang, David T.; Alexis, Jeffrey D.; Brown, Mary W.; Pyykkonen, Kathryn; McNitt, Scott; Oakes, David; Feng, Changyong; Aktas, Mehmet K.; Ayala-Parades, Felix; Baranchuk, Adrian; Dubuc, Marc; Haigney, Mark; Mazur, Alexander; McPherson, Craig A.; Mitchell, L. Brent; Natale, Andrea; Piccini, Jonathan P.; Raitt, Merritt; Rashtian, Mayer Y.; Schuger, Claudio; Winters, Stephen; Worley, Seth J.; Ziv, Ohad; Moss, Arthur J.; Zareba, W.; Pyykkonen, K.; Buttaccio, A.; Perkins, E.; DeGrey, D.; Robertson, S.; Moss, A.J.; Brown, M.; Lansing, R.; Oberer, A.; Polonsky, B.; Ross, V.; Papernov, A.; Schleede, S.; Beck, C.; Oakes, D.; Feng, C.; McNitt S, S.; Hall, W.J.; Zareba, W.; Moss, A.; Daubert, J.; Beck, C.; Brown, M.; Huang, D.; Winters, S.; Schuger, C.; Haigney, M.; Piccini, J.; Alexis, J.; Chen, L.; Miller, A.; Richeson, J.F.; Rosero, S.; Huang, D.; Kutyifa, V.; Shah, A.; Lamas, G.; Cohn, F.; Harrell, F.; Piña, I.; Poole, J.; Sullivan, M.; Lathrop, D.; Geller, N.; Boineau, R.; Trondell, J.; Cooper, L.; Itturiaga, E.; Boineau, R.; Gottlieb, C.; Greer, S.; Perzanowski, C.; McPherson, C.; Hedgepeth, C.; Assal, C.; Salam, T.; Woollett, I.; Tomassoni, G.; Ayala-Paredes, F.; Russo, A.; Punnam, S.; Sangrigoli, R.; Sloan, S.; Kutalek, S.; Piccini, J.; Sun, A.; Lustgarten, D.; Monir, G.; Haithcock, D.; Sorrentino, R.; Cannom, D.; Kluger, J.; Schuger, C.; Varanasi, S.; Rashtian, M.; Philippon, F.; Berger, R.; Mazzella, M.; Lessmeier, T.; Silver, J.; Worley, S.; Bernabei, M.; Esberg, D.; Dixon, M.; LeLorier, P.; Greenberg, Y.; Essebag, V.; Venkataraman, G.; Shinn, T.; Dubuc, M.; Winters, S.; Turitto, G.; Henrikson, C.; Mirro, M.; Raitt, M.; Baranchuk, A.; O’Neill, G.; Lockwood, E.; Vloka, M.; Hurwitz, J.; Mead, R.H.; Somasundarum, P.; Aziz, E.; Rashba, E.; Budzikowski, A.; Cox, M.; Natale, A.; Chung, E.; Ziv, O.; McGrew, F.; Tamirisa, K.; Greenspon, A.; Estes, M.; Taylor, S.; Janardhanan, R.; Mitchell, L.B.; Burke, M.; Attari, M.; Mikaelian, B.; Hsu, S.; Conti, J.; Mazur, A.; Shorofsky, S.; Rosenthal, L.; Sakaguchi, S.; Wolfe, D.; Flaker, G.; Saba, S.; Aktas, M.; Mason, P.; Shalaby, A.; Musat, D.; Abraham, R.; Ellenbogen, K.; Fellows, C.; Venkataraman, G.; Kavesh, N.; Thomas, G.; Hemsworth, D.; Williamson, B. (2018). “Ranolazine in High-Risk Patients With Implanted Cardioverter-Defibrillators”. Journal of the American College of Cardiology. 72 (6): 636–645. doi:10.1016/j.jacc.2018.04.086. ISSN 0735-1097.
    8. ↑ Reiter, Michael J.; Reiffel, James A. (1998). “Importance of beta blockade in the therapy of serious ventricular arrhythmias”. The American Journal of Cardiology. 82 (4): 9I–19I. doi:10.1016/S0002-9149(98)00468-8. ISSN 0002-9149.
    9. ↑ “Effect of metoprolol CR/XL in chronic heart failure: Metoprolol CR/XL Randomised Intervention Trial in Congestive Heart Failure (MERIT-HF)”. Lancet. 353 (9169): 2001–7. June 1999. PMID 10376614.
    10. ↑ Kontos, Michael C.; Diercks, Debra B.; Ho, P. Michael; Wang, Tracy Y.; Chen, Anita Y.; Roe, Matthew T. (2011). “Treatment and outcomes in patients with myocardial infarction treated with acute β-blocker therapy: Results from the American College of Cardiology’s NCDR®”. American Heart Journal. 161 (5): 864–870. doi:10.1016/j.ahj.2011.01.006. ISSN 0002-8703.
    11. ↑ Hirsowitz, Geoffrey; Podrid, Philip J.; Lampert, Steven; Stein, Joseph; Lown, Bernard (1986). “The role of beta blocking agents as adjunct therapy to membrane stabilizing drugs in malignant ventricular arrhythmia”. American Heart Journal. 111 (5): 852–860. doi:10.1016/0002-8703(86)90633-2. ISSN 0002-8703.
    12. ↑ Bardy, Gust H.; Lee, Kerry L.; Mark, Daniel B.; Poole, Jeanne E.; Packer, Douglas L.; Boineau, Robin; Domanski, Michael; Troutman, Charles; Anderson, Jill; Johnson, George; McNulty, Steven E.; Clapp-Channing, Nancy; Davidson-Ray, Linda D.; Fraulo, Elizabeth S.; Fishbein, Daniel P.; Luceri, Richard M.; Ip, John H. (2005). “Amiodarone or an Implantable Cardioverter–Defibrillator for Congestive Heart Failure”. New England Journal of Medicine. 352 (3): 225–237. doi:10.1056/NEJMoa043399. ISSN 0028-4793.
    13. ↑ Thomas, Kevin L.; Al-Khatib, Sana M.; Lokhnygina, Yuliya; Solomon, Scott D.; Kober, Lars; McMurray, John J.V.; Califf, Robert M.; Velazquez, Eric J. (2008). “Amiodarone use after acute myocardial infarction complicated by heart failure and/or left ventricular dysfunction may be associated with excess mortality”. American Heart Journal. 155 (1): 87–93. doi:10.1016/j.ahj.2007.09.010. ISSN 0002-8703.
    14. ↑ 14.0 14.1 14.2 Claro, Juan Carlos; Candia, Roberto; Rada, Gabriel; Baraona, Fernando; Larrondo, Francisco; Letelier, Luz M (2015). “Amiodarone versus other pharmacological interventions for prevention of sudden cardiac death”. Cochrane Database of Systematic Reviews. doi:10.1002/14651858.CD008093.pub2. ISSN 1465-1858.
    15. ↑ Kudenchuk, Peter J.; Cobb, Leonard A.; Copass, Michael K.; Cummins, Richard O.; Doherty, Alidene M.; Fahrenbruch, Carol E.; Hallstrom, Alfred P.; Murray, William A.; Olsufka, Michele; Walsh, Thomas (1999). “Amiodarone for Resuscitation after Out-of-Hospital Cardiac Arrest Due to Ventricular Fibrillation”. New England Journal of Medicine. 341 (12): 871–878. doi:10.1056/NEJM199909163411203. ISSN 0028-4793.
    16. ↑ Epstein, Andrew E.; Olshansky, Brian; Naccarelli, Gerald V.; Kennedy, John I.; Murphy, Elizabeth J.; Goldschlager, Nora (2016). “Practical Management Guide for Clinicians Who Treat Patients with Amiodarone”. The American Journal of Medicine. 129 (5): 468–475. doi:10.1016/j.amjmed.2015.08.039. ISSN 0002-9343.
    17. ↑ Waldo AL, Camm AJ, deRuyter H, Freidman PL, MacNeil DJ, Pitt B, Pratt CM, Rodda BE, Schwartz PJ (May 1995). “Survival with oral d-sotalol in patients with left ventricular dysfunction after myocardial infarction: rationale, design, and methods (the SWORD trial)”. Am J Cardiol. 75 (15): 1023–7. doi:10.1016/s0002-9149(99)80717-6. PMID 7747682.
    18. ↑ Page, Richard L (2000). “Effects of antiarrhythmic medication on implantable cardioverter-defibrillator function”. The American Journal of Cardiology. 85 (12): 1481–1485. doi:10.1016/S0002-9149(00)00799-2. ISSN 0002-9149.
    19. ↑ 19.0 19.1 Buxton, Alfred E.; Marchlinski, Francis E.; Doherty, John U.; Flores, Belinda; Josephson, Mark E. (1987). “Hazards of intravenous verapamil for sustained ventricular tachycardia”. The American Journal of Cardiology. 59 (12): 1107–1110. doi:10.1016/0002-9149(87)90857-5. ISSN 0002-9149.
    20. ↑ Gill, Jaswinder S.; Ward, David E.; Camm, A. John (1992). “Comparison of Verapamil and Diltiazem in the Suppression of Idiopathic Ventricular Tachycardia”. Pacing and Clinical Electrophysiology. 15 (11): 2122–2126. doi:10.1111/j.1540-8159.1992.tb03033.x. ISSN 0147-8389.
    21. ↑ Badhwar, Nitish; Scheinman, Melvin M. (2007). “Idiopathic Ventricular Tachycardia: Diagnosis and Management”. Current Problems in Cardiology. 32 (1): 7–43. doi:10.1016/j.cpcardiol.2006.10.002. ISSN 0146-2806.
    22. ↑ 22.0 22.1 Cooper, Howard A.; Dries, Daniel L.; Davis, C. E.; Shen, Yuan Li; Domanski, Michael J. (1999). “Diuretics and Risk of Arrhythmic Death in Patients With Left Ventricular Dysfunction”. Circulation. 100 (12): 1311–1315. doi:10.1161/01.CIR.100.12.1311. ISSN 0009-7322.
    23. ↑ Yan, Gan-Xin; Antzelevitch, Charles (1998). “Cellular Basis for the Normal T Wave and the Electrocardiographic Manifestations of the Long-QT Syndrome”. Circulation. 98 (18): 1928–1936. doi:10.1161/01.CIR.98.18.1928. ISSN 0009-7322.
    24. ↑ Tzivoni, D; Banai, S; Schuger, C; Benhorin, J; Keren, A; Gottlieb, S; Stern, S (1988). “Treatment of torsade de pointes with magnesium sulfate”. Circulation. 77 (2): 392–397. doi:10.1161/01.CIR.77.2.392. ISSN 0009-7322.
    25. ↑ Cohn, Jay N.; Kowey, Peter R.; Whelton, Paul K.; Prisant, L. Michael (2000). “New Guidelines for Potassium Replacement in Clinical Practice”. Archives of Internal Medicine. 160 (16): 2429. doi:10.1001/archinte.160.16.2429. ISSN 0003-9926.
    26. ↑ Goyal, Abhinav; Spertus, John A.; Gosch, Kensey; Venkitachalam, Lakshmi; Jones, Philip G.; Van den Berghe, Greet; Kosiborod, Mikhail (2012). “Serum Potassium Levels and Mortality in Acute Myocardial Infarction”. JAMA. 307 (2): 157. doi:10.1001/jama.2011.1967. ISSN 0098-7484.
    27. ↑ Antman, Elliott M (2002). “Early administration of intravenous magnesium to high-risk patients with acute myocardial infarction in the Magnesium in Coronaries (MAGIC) Trial: a randomised controlled trial”. The Lancet. 360 (9341): 1189–1196. doi:10.1016/S0140-6736(02)11278-5. ISSN 0140-6736.
    28. ↑ Leaf, Alexander; Kang, Jing X.; Xiao, Yong-Fu; Billman, George E. (2003). “Clinical Prevention of Sudden Cardiac Death by n-3 Polyunsaturated Fatty Acids and Mechanism of Prevention of Arrhythmias by n-3 Fish Oils”. Circulation. 107 (21): 2646–2652. doi:10.1161/01.CIR.0000069566.78305.33. ISSN 0009-7322.
    29. ↑ Marchioli, Roberto; Barzi, Federica; Bomba, Elena; Chieffo, Carmine; Di Gregorio, Domenico; Di Mascio, Rocco; Franzosi, Maria Grazia; Geraci, Enrico; Levantesi, Giacomo; Maggioni, Aldo Pietro; Mantini, Loredana; Marfisi, Rosa Maria; Mastrogiuseppe, G.; Mininni, Nicola; Nicolosi, Gian Luigi; Santini, Massimo; Schweiger, Carlo; Tavazzi, Luigi; Tognoni, Gianni; Tucci, Corrado; Valagussa, Franco (2002). “Early Protection Against Sudden Death by n-3 Polyunsaturated Fatty Acids After Myocardial Infarction”. Circulation. 105 (16): 1897–1903. doi:10.1161/01.CIR.0000014682.14181.F2. ISSN 0009-7322.
    30. ↑ “n–3 Fatty Acids and Cardiovascular Outcomes in Patients with Dysglycemia”. New England Journal of Medicine. 367 (4): 309–318. 2012. doi:10.1056/NEJMoa1203859. ISSN 0028-4793.
    31. ↑ LaRosa, John C.; He, Jiang; Vupputuri, Suma (1999). “Effect of Statins on Risk of Coronary Disease”. JAMA. 282 (24): 2340. doi:10.1001/jama.282.24.2340. ISSN 0098-7484.
    32. ↑ Tavazzi L, Maggioni AP, Marchioli R, Barlera S, Franzosi MG, Latini R, Lucci D, Nicolosi GL, Porcu M, Tognoni G (October 2008). “Effect of rosuvastatin in patients with chronic heart failure (the GISSI-HF trial): a randomised, double-blind, placebo-controlled trial”. Lancet. 372 (9645): 1231–9. doi:10.1016/S0140-6736(08)61240-4. PMID 18757089.
    33. ↑ Cohn JN, Johnson G, Ziesche S, Cobb F, Francis G, Tristani F, Smith R, Dunkman WB, Loeb H, Wong M (August 1991). “A comparison of enalapril with hydralazine-isosorbide dinitrate in the treatment of chronic congestive heart failure”. N Engl J Med. 325 (5): 303–10. doi:10.1056/NEJM199108013250502. PMID 2057035.
    34. ↑ “The Cardiac Insufficiency Bisoprolol Study II (CIBIS-II): a randomised trial”. Lancet. 353 (9146): 9–13. January 1999. PMID 10023943.
    35. ↑ Dargie HJ (May 2001). “Effect of carvedilol on outcome after myocardial infarction in patients with left-ventricular dysfunction: the CAPRICORN randomised trial”. Lancet. 357 (9266): 1385–90. doi:10.1016/s0140-6736(00)04560-8. PMID 11356434.
    36. ↑ Hjalmarson A, Goldstein S, Fagerberg B, Wedel H, Waagstein F, Kjekshus J, Wikstrand J, El Allaf D, Vítovec J, Aldershvile J, Halinen M, Dietz R, Neuhaus KL, Jánosi A, Thorgeirsson G, Dunselman PH, Gullestad L, Kuch J, Herlitz J, Rickenbacher P, Ball S, Gottlieb S, Deedwania P (March 2000). “Effects of controlled-release metoprolol on total mortality, hospitalizations, and well-being in patients with heart failure: the Metoprolol CR/XL Randomized Intervention Trial in congestive heart failure (MERIT-HF). MERIT-HF Study Group”. JAMA. 283 (10): 1295–302. doi:10.1001/jama.283.10.1295. PMID 10714728.
    37. ↑ Pitt B, Zannad F, Remme WJ, Cody R, Castaigne A, Perez A, Palensky J, Wittes J (September 1999). “The effect of spironolactone on morbidity and mortality in patients with severe heart failure. Randomized Aldactone Evaluation Study Investigators”. N Engl J Med. 341 (10): 709–17. doi:10.1056/NEJM199909023411001. PMID 10471456.
    38. ↑ 38.0 38.1 38.2 38.3 Zeppenfeld K, Tfelt-Hansen J, de Riva M, Winkel BG, Behr ER, Blom NA, Charron P, Corrado D, Dagres N, de Chillou C, Eckardt L, Friede T, Haugaa KH, Hocini M, Lambiase PD, Marijon E, Merino JL, Peichl P, Priori SG, Reichlin T, Schulz-Menger J, Sticherling C, Tzeis S, Verstrael A, Volterrani M (August 2022). “2022 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death”. Eur Heart J. doi:10.1093/eurheartj/ehac262. PMID 36017572 Check |pmid= value (help).
    39. ↑ Zipes, Douglas P.; Camm, A. John; Borggrefe, Martin; Buxton, Alfred E.; Chaitman, Bernard; Fromer, Martin; Gregoratos, Gabriel; Klein, George; Moss, Arthur J.; Myerburg, Robert J.; Priori, Silvia G.; Quinones, Miguel A.; Roden, Dan M.; Silka, Michael J.; Tracy, Cynthia (2006). “ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death”. Circulation. 114 (10). doi:10.1161/CIRCULATIONAHA.106.178233. ISSN 0009-7322.
    40. ↑ Sasson, Comilla; Rogers, Mary A.M.; Dahl, Jason; Kellermann, Arthur L. (2010). “Predictors of Survival From Out-of-Hospital Cardiac Arrest”. Circulation: Cardiovascular Quality and Outcomes. 3 (1): 63–81. doi:10.1161/CIRCOUTCOMES.109.889576. ISSN 1941-7713.
    41. ↑ Connolly, S (2000). “Meta-analysis of the implantable cardioverter defibrillator secondary prevention trials”. European Heart Journal. 21 (24): 2071–2078. doi:10.1053/euhj.2000.2476. ISSN 0195-668X.
    42. ↑ Spaulding, Christian M.; Joly, Luc-Marie; Rosenberg, Alain; Monchi, Mehran; Weber, Simon N.; Dhainaut, Jean-François A.; Carli, Pierre (1997). “Immediate Coronary Angiography in Survivors of Out-of-Hospital Cardiac Arrest”. New England Journal of Medicine. 336 (23): 1629–1633. doi:10.1056/NEJM199706053362302. ISSN 0028-4793.
    43. ↑ Zanuttini, Davide; Armellini, Ilaria; Nucifora, Gaetano; Carchietti, Elio; Trillò, Giulio; Spedicato, Leonardo; Bernardi, Guglielmo; Proclemer, Alessandro (2012). “Impact of Emergency Coronary Angiography on In-Hospital Outcome of Unconscious Survivors After Out-of-Hospital Cardiac Arrest”. The American Journal of Cardiology. 110 (12): 1723–1728. doi:10.1016/j.amjcard.2012.08.006. ISSN 0002-9149.
    44. ↑ Dumas, Florence; Bougouin, Wulfran; Geri, Guillaume; Lamhaut, Lionel; Rosencher, Julien; Pène, Frédéric; Chiche, Jean-Daniel; Varenne, Olivier; Carli, Pierre; Jouven, Xavier; Mira, Jean-Paul; Spaulding, Christian; Cariou, Alain (2016). “Emergency Percutaneous Coronary Intervention in Post–Cardiac Arrest Patients Without ST-Segment Elevation Pattern”. JACC: Cardiovascular Interventions. 9 (10): 1011–1018. doi:10.1016/j.jcin.2016.02.001. ISSN 1936-8798.
    45. ↑ Somberg, John C; Bailin, Steven J; Haffajee, Charles I; Paladino, Walter P; Kerin, Nicholas Z; Bridges, Duane; Timar, Sandor; Molnar, Janos (2002). “Intravenous lidocaine versus intravenous amiodarone (in a new aqueous formulation) for incessant ventricular tachycardia”. The American Journal of Cardiology. 90 (8): 853–859. doi:10.1016/S0002-9149(02)02707-8. ISSN 0002-9149.
    46. ↑ Gorgels, Anton P.M.; van den Dool, Adri; Hofs, Anton; Mulleneers, Rob; Smeets, Joep L.R.M.; Vos, Marc A.; Wellens, Hein J.J. (1996). “Comparison of procainamide and lidocaine in terminating sustained monomorphic ventricular tachycardia”. The American Journal of Cardiology. 78 (1): 43–46. doi:10.1016/S0002-9149(96)00224-X. ISSN 0002-9149.
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    49. ↑ Hassan, T B (2002). “A randomised trial to investigate the efficacy of magnesium sulphate for refractory ventricular fibrillation”. Emergency Medicine Journal. 19 (1): 57–62. doi:10.1136/emj.19.1.57. ISSN 1472-0205.
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    51. ↑ Elizari, M (2000). “Morbidity and mortality following early administration of amiodarone in acute myocardial infarction”. European Heart Journal. 21 (3): 198–205. doi:10.1053/euhj.1999.1687. ISSN 0195-668X.
    52. ↑ Kettering, Klaus; Mewis, Christian; Dornberger, Volker; Vonthein, Reinhard; Bosch, Ralph F.; Kuhlkamp, Volker (2002). “Efficacy of Metoprolol and Sotalol in the Prevention of Recurrences of Sustained Ventricular Tachyarrhythmias in Patients with an Implantable Cardioverter Defibrillator”. Pacing and Clinical Electrophysiology. 25 (11): 1571–1576. doi:10.1046/j.1460-9592.2002.01571.x. ISSN 0147-8389.
    53. ↑ 53.0 53.1 Connolly, Stuart J. (2006). “Comparison of β-Blockers, Amiodarone Plus β-Blockers, or Sotalol for Prevention of Shocks From Implantable Cardioverter Defibrillators<SUBTITLE>The OPTIC Study: A Randomized Trial</SUBTITLE>”. JAMA. 295 (2): 165. doi:10.1001/jama.295.2.165. ISSN 0098-7484.
    54. ↑ Tung, Roderick; Vaseghi, Marmar; Frankel, David S.; Vergara, Pasquale; Di Biase, Luigi; Nagashima, Koichi; Yu, Ricky; Vangala, Sitaram; Tseng, Chi-Hong; Choi, Eue-Keun; Khurshid, Shaan; Patel, Mehul; Mathuria, Nilesh; Nakahara, Shiro; Tzou, Wendy S.; Sauer, William H.; Vakil, Kairav; Tedrow, Usha; Burkhardt, J. David; Tholakanahalli, Venkatakrishna N.; Saliaris, Anastasios; Dickfeld, Timm; Weiss, J. Peter; Bunch, T. Jared; Reddy, Madhu; Kanmanthareddy, Arun; Callans, David J.; Lakkireddy, Dhanunjaya; Natale, Andrea; Marchlinski, Francis; Stevenson, William G.; Della Bella, Paolo; Shivkumar, Kalyanam (2015). “Freedom from recurrent ventricular tachycardia after catheter ablation is associated with improved survival in patients with structural heart disease: An International VT Ablation Center Collaborative Group study”. Heart Rhythm. 12 (9): 1997–2007. doi:10.1016/j.hrthm.2015.05.036. ISSN 1547-5271.
    55. ↑ Echt, Debra S.; Liebson, Philip R.; Mitchell, L. Brent; Peters, Robert W.; Obias-Manno, Dulce; Barker, Allan H.; Arensberg, Daniel; Baker, Andrea; Friedman, Lawrence; Greene, H. Leon; Huther, Melissa L.; Richardson, David W. (1991). “Mortality and Morbidity in Patients Receiving Encainide, Flecainide, or Placebo”. New England Journal of Medicine. 324 (12): 781–788. doi:10.1056/NEJM199103213241201. ISSN 0028-4793.
    56. ↑ Brugada, Josep; Aguinaga, Luis; Mont, Lluı́s; Betriu, Amadeu; Mulet, Jaume; Sanz, Ginés (2001). “Coronary artery revascularization in patients with sustained ventricular arrhythmias in the chronic phase of a myocardial infarction: effects on the electrophysiologic substrate and outcome”. Journal of the American College of Cardiology. 37 (2): 529–533. doi:10.1016/S0735-1097(00)01133-5. ISSN 0735-1097.
    57. ↑ Berntsen, R. F.; Gunnes, P.; Lie, M.; Rasmussen, K. (1993). “Surgical revascularization in the treatment of ventricular tachycardia and fibrillation exposed by exercise-induced ischaemia”. European Heart Journal. 14 (10): 1297–1303. doi:10.1093/eurheartj/14.10.1297. ISSN 0195-668X.
    58. ↑ Naruse, Yoshihisa; Sekiguchi, Yukio; Nogami, Akihiko; Okada, Hiroyuki; Yamauchi, Yasuteru; Machino, Takeshi; Kuroki, Kenji; Ito, Yoko; Yamasaki, Hiro; Igarashi, Miyako; Tada, Hiroshi; Nitta, Junichi; Xu, Dongzhu; Sato, Akira; Aonuma, Kazutaka (2014). “Systematic Treatment Approach to Ventricular Tachycardia in Cardiac Sarcoidosis”. Circulation: Arrhythmia and Electrophysiology. 7 (3): 407–413. doi:10.1161/CIRCEP.113.000734. ISSN 1941-3149.
    59. ↑ Dinov, Borislav; Fiedler, Lukas; Schönbauer, Robert; Bollmann, Andreas; Rolf, Sascha; Piorkowski, Christopher; Hindricks, Gerhard; Arya, Arash (2014). “Outcomes in Catheter Ablation of Ventricular Tachycardia in Dilated Nonischemic Cardiomyopathy Compared With Ischemic Cardiomyopathy”. Circulation. 129 (7): 728–736. doi:10.1161/CIRCULATIONAHA.113.003063. ISSN 0009-7322.

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