TABLE 241 Common Dysrhythmias of Digoxin Toxicity Approximate Incidence

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Reentrant SVT can occur in a normal heart or in association with rheumatic heart disease, acute pericarditis, myocardial infarction, mitral valve prolapse, or one of the preexcitation syndromes.

SVT often causes a sensation of palpitations and light-headedness. In patients with coronary artery disease, anginal chest pain and dyspnea may occur from the rapid heart rate. Frank heart failure and pulmonary edema may occur in patients with poor left ventricular function. The decrease in diastolic filling period and subsequent decrease in cardiac output cannot be tolerated in the patient with left ventricular failure.

Treatment Ectopic SVT due to digoxin toxicity is treated as follows:

1. Discontinuation of the digoxin.

2. As long as there is not a high-grade AV block, correction of any existing hypokalemia to bring serum potassium into the high-normal range in an effort to reduce atrial ectopy is indicated.

3. Digoxin-specific antibody fragments (Fab) should be considered for patients with hemodynamic deterioration or serious ventricular dysrhythmias due to digoxin toxicity.

4. Either phenytoin, lidocaine, or magnesium given intravenously can reduce atrial ectopy. Published reports are not methodologically adequate for determination of the response rate, risks, and benefits of each agent, so the choice is often guided by personal preference. Historically, phenytoin has been the most commonly used drug, but its response rate has not been impressive and toxic side effects are common with full loading doses (15 to 18 mg/kg IV). Lidocaine has not been considered a useful agent for this dysrhythmia, but a recent report indicates some benefit. Recent studies indicate that magnesium sulfate 1 g IV impressively reduces atrial ectopy due to digoxin toxicity, and perhaps this agent has a greater effect than phenytoin or lidocaine.

5. Cardioversion is not effective and is potentially hazardous.

Reentrant SVT can be converted by impeding conduction through one limb of the reentry circuit; sustained reentry is then impossible and extinguishes, allowing sinus rhythm to resume ventricular pacing. Since it is usually impossible to differentiate ectopic from reentrant SVT clinically, treatment should be the same.

1. Maneuvers that increase vagal tone have been shown to slow conduction and prolong the refractory period in the AV node. These maneuvers can be done by themselves or after administration of drugs.

a. Carotid sinus massage. This attempts to massage the carotid sinus and its baroreceptors against the transverse process of C6. Massage should be done for 10 s at a time, first attempted on the side of the nondominant cerebral hemisphere, and should never be done simultaneously on both sides. In addition, bruits should be discovered prior to the procedure. Prolonged AV block during carotid massage may occur in patients with AV node disease or who are on digoxin. Patients with carotid artery stenosis may develop cerebral ischemia or infarction from overvigorous carotid massage.

b. Facial immersion in cold water for 6 to 7 s with the nostrils held closed ("diving reflex"). This maneuver is particularly effective in infants. The parents usually have more vagal tone than the infant so this must be approached carefully.

c. The Valsalva maneuver. Done in the supine position, it appears to be the most effective vagal maneuver for the conversion of reentrant SVT. For maximal effectiveness, the strain phase must be adequate (usually at least 10 s) with slowing or conversion seen during the release phase.

2. Administration of adenosine. An ultra-short-acting (20 s) agent, adenosine produces AV block and has been observed to convert over 90 percent of reentrant SVT. The initial dose is a 6-mg rapid IV bolus. This must be given in a large vein, preferably in the antecubital space. If no effect is seen within 2 min, a second dose of 12 mg can be given. There is no proven benefit to repeated doses or administration of more than 20 mg. Half or more of patients experience distressing albeit transient side effects of facial flushing or chest pain. This should obviously be discussed with the patient when possible. Because adenosine possesses no sustained antiarrhythmic effect, subsequent ectopic beats are able to initial the dysrhythmia again, and early recurrences of SVT are seen in up to 25 percent of patients. The major advantage of adenosine is its ultrashort effect and its lack of hypotensive or myocardial depressive activity. Adenosine is also safe and effective in unstable patients (chest pain and/or hypotension) with reentrant SVT. It is safer in pregnancy. In addition, it is not contraindicated in the presence of Wolff-Parkinson-White syndrome.

3. Verapamil, 0.075 to 0.15 mg/kg (3 to 10 mg) IV over 15 to 60 s, with a repeat dose in 30 min if necessary. Studies have found that more than 90 percent of adults with reentrant SVT will respond within 1 to 2 min to verapamil. In patients with a normal blood pressure, intravenous verapamil is almost always associated with a decrease in blood pressure, even following successful conversion of SVT. The falls in systolic and mean arterial pressures are around 20 and 10 mmHg, respectively. The drop in blood pressure due to verapamil can be prevented and/or treated with intravenous calcium without reducing the antiarrhythmic action of verapamil. While the use of different calcium doses and salts has been reported, 90 mg of elemental calcium given intravenously over 3 to 6 min appears safe and effective (90 mg elemental calcium = 10 mL calcium gluconate 10% solution = 3.3 mL calcium chloride 10% solution). Whenever verapamil is used intravenously, calcium should be readily available. Intravenous verapamil is generally considered to be contraindicated in the hypotensive patient. Studies of intravenous verapamil in hypotensive patients with SVT report an excellent conversion rate (80 percent or better), the ventricular rate almost always slows, and rarely does the systolic blood pressure decrease without a change in ventricular rate. I would consider cardioversion a better approach to the hypotensive patient with SVT.

4. Diltiazem 20 mg (0.25 mg/kg) IV over 2 min. This is reported to be 75 to 100 percent effective in converting reentrant SVT.

5. Parasympathetic tone can be increased with edrophonium. A standard treatment protocol is a 1-mg IV test dose, a wait of 3 to 5 min, followed by 5 to 10 mg IV over 60 s. Historically, edrophonium does not have the 90 percent response rate seen with verapamil. I have not used this drug for the last 12 years but have noted that, most likely, it was the profound vomiting that caused the conversion rather than the direct effect of the drug.

6. Vagal tone can be enhanced by pharmacologically evaluating blood pressure with a pure peripheral vasoconstrictor; do not use agents with b-adrenergic activity. This method should be combined with carotid sinus massage. Blood pressure should be monitored frequently, and diastolic pressure should not be allowed to exceed 130 mmHg. This method should not be used if hypertension is already present.

a. Metaraminol 200 mg/500 mL D5W or norepinephrine 4 mg/500 mL D5W can be infused at rates of 1 to 2 mL/min and titrated until the rhythm converts.

b. Methoxamine or phenylephrine 0.5 to 1.0 mg IV over 2 to 3 min, with repeat doses as required.

7. Esmolol is an intravenous b-adrenergic blocker with an ultrashort duration of activity that can be titrated to effect. This agent can be used to control the ventricular rate in most tachycardias of supraventricular origin and is capable of converting about half of reentrant SVT. Esmolol is given as a bolus dose of 300 pg/kg over 60 s, followed by an infusion starting at 50 pg/kg per min. If there is an inadequate response after 2 to 5 min, a repeat bolus of 300 pg/kg should be given and increases in the infusion rate in increments of 50 pg/kg per min. should be made. The maximal recommended infusion rate is 300 pg/kg per min., although most patients respond to rates of 200 pg/kg per min. or less. With aggressive dosing regimens, hypotension occurs in about half of patients but can be quickly reversed by halting the infusion.

8. Propranolol 0.5 to 1.0 mg IV slowly over 60 s, repeated every 5 min, until the rhythm converts or the total dose reaches 0.1 mg/kg. Overall, propranolol has about a 50 percent success rate in converting reentrant SVT: about 80 percent with AV nodal reentry and 15 to 20 percent with accessory tract retrograde reentry.

9. Digoxin 0.5 mg IV with repeat doses of 0.25 mg in 30 to 60 min until a response occurs or the total dose reaches 0.02 mg/kg. The chief drawback of digoxin has been its long onset of action and potential hazard in patients with accessory (bypass) tracts who develop either atrial fibrillation or flutter.

10. External noninvasive pacing has been used in a limited number of patients to terminate reentrant SVT. Asynchronous pacing with 2 to 10 external pulses at a rate 240 to 280 (typically 40 faster than the SVT rate) with an impulse amplitude of 120 mA is effective in young, hemodynamically stable adults. Most pacing units in the ED do not pace at 240 to 280 beats per min. Some automatic internal cardiac defibrillators (AICDs) have overdrive pacing capability.

11. Synchronized cardioversion should be done in any unstable patient with hypotension, pulmonary edema, or severe chest pain. The dose required is usually small, less than 50 J.

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