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Day 9: Medication and Electrolyte Effects; Miscellaneous Conditions

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  1. Medication effects

    1. Digoxin (Day 9-01)

      1. Digoxin has a narrow therapeutic to toxic ratio, and is potent stimulator of arrhythmias.

      2. At therapeutic levels, digoxin frequently causes nonspecific ST changes with "scooping" of the ST segment and shortening of the QT interval.

      3. Digoxin causes SA nodal suppression and AV block.

      4. Digoxin can cause virtually any arrhythmia, but, because of its ability to enhance automaticity, ectopic arrhythmias are commonly encountered in digoxin toxicity.

      5. The commonest arrhythmia manifested by digoxin toxicity is multiform PVCs. (Day 9-02)

      6. The two most specific arrhythmias are accelerated junctional rhythm and atrial tachycardia with AV block. (Day 9-03) (Day 9-04)

    2. Sotalol and amiodarone (Day 9-05)

      1. These agents slow conduction in general and result in bradycardia and prolongation of the PR, QRS, and QT intervals.

      2. Sotalol also has significant beta blocking properties, which exacerbates the bradyarrhythmic effects.

      3. Sotalol can also prolong the QT interval and cause torsades de pointe.

    3. Quinidine and other Class IA agents (see long QT below)

      1. These agents are less frequently used than previously because of side effects, proarrhythmic potential, and possibly increased mortality.

      2. Quinidine prolongs the QRS duration and QT interval, and may cause torsades de pointe. (Day 6-11)

    4. Verapamil and diltiazem

      1. These agents can cause sinus bradycardia, varying amounts of AV block, and, in toxic doses, intraventricular conduction defects. (Day 9-06)

      2. Their effects are additive with beta blockers.

     

    DAY 9-01

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    DAY 9-02

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    DAY 9-03

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    DAY 9-04

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    DAY 9-05

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    DAY 9-06

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  2. Electrolyte abnormalities

    1. Hypokalemia

      1. Hypokalemia potentiates a variety of arrhythmias, including VT and torsade de pointes.

      2. Hypokalemia is associated with ST segment depression, a prolonged QT interval, and a prominent U wave. (Day 9-07) (Day 9-08)

    2. Hyperkalemia

      1. Hyperkalemia 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)

      2. 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)

    3. 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)

    4. Hypercalcemia is associated with a short QT interval.

  3. QT prolongation and U wave abnormalities

    1. A rough indicator of QT prolongation is that the QT interval should not exceed one half of the surrounding R-R interval.

    2. Congenital long QT syndromes

      1. There are at least five forms of congenital long QT syndromes, two of which are:

        1. Jervell and Lange-Nielsen syndrome is an autosomal recessive disorder associated with deafness.

        2. Romano-Ward is an autosomal dominant disorder.

    3. Acquired long QT syndromes

      1. Non-drug causes of long QT interval include ischemia, central nervous system (CNS) lesions, and significant bradyarrhythmias. (Day 9-14) (Day 9-15)

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