RT Book, Section A1 Ferry, David R. SR Print(0) ID 1128945305 T1 Medication and Electrolyte Effects; Miscellaneous Conditions T2 ECG in 10 Days, 2e YR 2007 FD 2007 PB McGraw-Hill Education PP New York, NY SN 9780071465625 LK accesscardiology.mhmedical.com/content.aspx?aid=1128945305 RD 2024/03/29 AB Medication effectsDigoxin (Day 9-01)Digoxin has a narrow therapeutic to toxic ratio, and is potent stimulator of arrhythmias.At therapeutic levels, digoxin frequently causes nonspecific ST changes with "scooping" of the ST segment and shortening of the QT interval.Digoxin causes SA nodal suppression and AV block.Digoxin can cause virtually any arrhythmia, but, because of its ability to enhance automaticity, ectopic arrhythmias are commonly encountered in digoxin toxicity.The commonest arrhythmia manifested by digoxin toxicity is multiform PVCs. (Day 9-02)The two most specific arrhythmias are accelerated junctional rhythm and atrial tachycardia with AV block. (Day 9-03) (Day 9-04)Sotalol and amiodarone (Day 9-05)These agents slow conduction in general and result in bradycardia and prolongation of the PR, QRS, and QT intervals.Sotalol also has significant beta blocking properties, which exacerbates the bradyarrhythmic effects.Sotalol can also prolong the QT interval and cause torsades de pointe.Quinidine and other Class IA agents (see long QT below)These agents are less frequently used than previously because of side effects, proarrhythmic potential, and possibly increased mortality.Quinidine prolongs the QRS duration and QT interval, and may cause torsades de pointe. (Day 6-11)Verapamil and diltiazemThese agents can cause sinus bradycardia, varying amounts of AV block, and, in toxic doses, intraventricular conduction defects. (Day 9-06)Their effects are additive with beta blockers. DAY 9-01 DAY 9-02 DAY 9-03 DAY 9-04 DAY 9-05 DAY 9-06 Electrolyte abnormalitiesHypokalemiaHypokalemia potentiates a variety of arrhythmias, including VT and torsade de pointes.Hypokalemia is associated with ST segment depression, a prolonged QT interval, and a prominent U wave. (Day 9-07) (Day 9-08)HyperkalemiaHyperkalemia is manifested by peaked T waves, loss of obvious P waves or prolongation of the PR segment, and prolongation of the QRS complex. (Day 9-09) (Day 9-10)When potassium levels reach 8–9 mmol/l, the ECG may resemble a sine wave; further elevation may cause asystole. (Day 9-11) (Day 9-12)Hypocalcemia is manifested by prolongation of the QT interval; the ST segment is usually flat and the T wave is not distorted (see figure). (Day 9-13)Hypercalcemia is associated with a short QT interval.QT prolongation and U wave abnormalitiesA rough indicator of QT prolongation is that the QT interval should not exceed one half of the surrounding R-R interval.Congenital long QT syndromesThere are at least five forms of congenital long QT syndromes, two of which are:Jervell and Lange-Nielsen syndrome is an autosomal recessive disorder associated with deafness.Romano-Ward is an autosomal dominant disorder.Acquired long QT syndromesNon-drug causes of long QT interval include ischemia, central nervous system (CNS) lesions, and significant bradyarrhythmias. (Day 9-14) (Day 9-15)Many drugs can prolong the QT interval, including the Class IA, IC, and III antiarrhythmic agents, erythromycin, some antihistamines, and some psychiatric drugs.U wave abnormalitiesProminent U waves are seen with hypokalemia, digoxin, LVH, and amiodarone (see previous page)Negative U waves are encountered in hypertension (HTN), aortic and mitral disease, and ischemia. DAY 9-07 DAY 9-08 DAY 9-09 DAY 9-10 DAY 9-11 DAY 9-12 DAY 9-13 DAY 9-14 DAY 9-15 Causes of tall R waves in V1Right ventricular hypertrophy (RVH) (Day 9-16)Posterior MI (Day 9-17)RBBB (Day 9-18)Wolff-Parkinson-White (WPW) (Day 9-19)Hypertrophic obstructive cardiomyopathy (HOCM) with ...