Torsades de pointes risk factors: Difference between revisions
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===Clinical Correlation === | ===Clinical Correlation === | ||
# Drugs: [[quinidine]], [[PCA]], [[norpace]], [[amiodarone]], [[phenothiazines]], [[ | # Drugs: [[quinidine]], [[PCA]], [[norpace]], [[amiodarone]], [[phenothiazines]], [[tricyclic antidepressants]], [[pentamidine]]. | ||
#* with [[quinidine]] majority of the cases occur within one week of initiation, and with therapeutic levels | #* with [[quinidine]] majority of the cases occur within one week of initiation, and with therapeutic levels | ||
# Electrolyte imbalances: [[ | # Electrolyte imbalances: [[hypokalemia]], [[hypomagnesemia]], [[hypocalcemia]] | ||
# [[CAD]] | # [[CAD]] | ||
# [[MVP]] | # [[MVP]] |
Revision as of 02:06, 15 October 2012
Torsades de pointes Microchapters |
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Torsades de pointes risk factors On the Web |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Risk Factors
Factors that are associated with an increased tendency toward torsades de pointes include:
- Familial long QT syndrome
- Class IA antiarrhythmics
- Hypomagnesemia
- Hypokalemia
- Hypoxia
- Acidosis
- Heart failure
- Left ventricular hypertrophy
- Slow heart rate
- Female gender
- Baseline electrocardiographic abnormalities
- Renal or liver failure
Clinical Correlation
- Drugs: quinidine, PCA, norpace, amiodarone, phenothiazines, tricyclic antidepressants, pentamidine.
- with quinidine majority of the cases occur within one week of initiation, and with therapeutic levels
- Electrolyte imbalances: hypokalemia, hypomagnesemia, hypocalcemia
- CAD
- MVP
- Variant angina
- Myocarditis
- Subarachnoid hemorrhage
- Congenital QT prolongation
- Liquid protein diets
- Hypothyroidism
- because of bradycardia and a prolonged QT syndrome
- Organophosphate poisoning [1] [2]