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PHARMACOLOGIC TREATMENTS

232

What can happen

Adverse cardiovascular effects of magnesium sulfate include diaphoresis, flushing, depressed cardiac function, bradycardia, hypotension, and circulatory collapse. (See Noncardiac adverse effects of magnesium sulfate.)

How you intervene

Keep the following points in mind when caring for a patient receiving magnesium sulfate:

Monitor the patient’s heart rate, blood pressure, ventilatory rate, ECG, urine output, deep tendon reflexes, and mental status.

Remember that magnesium sulfate should be avoided in patients with renal disease. Use it cautiously in patients with renal insufficiency and in those taking digoxin.

Monitor closely for signs and symptoms of hypermagnesemia, such as hypotension, AV block, central nervous system depression, depressed or absent deep tendon reflexes, muscle weakness or paralysis, and respiratory arrest.

Have I.V. calcium available to counteract the effects of hypermagnesemia.

Have intubation equipment and a mechanical ventilator available.

Magnesium sulfate is contraindicated in heart block and in patients with myocardial damage.

Teaching about antiarrhythmics

Here are some important points to emphasize when teaching your patient about antiarrhythmic drugs:

Take the drug exactly as prescribed. Don’t stop taking the drug without consulting your practitioner.

Call the practitioner if you experience chest pain, shortness of breath, cough, palpitations, dizziness, fatigue, a weight gain of more than 2 lb (0.9 kg) per day, a very fast or slow heart rate, or a change in the regularity of the heartbeat or if you notice persistent changes you feel might be related to drug therapy.

See your practitioner for regular checkups, as scheduled. Periodic physical examinations, ECGs, chest X-rays, and laboratory studies will help evaluate the effectiveness of therapy.

Use herbal preparations with care. Some preparations can cause life-threatening interactions.

Avoid administering magnesium sulfate to patients with renal disease.

Noncardiac adverse effects of magnesium sulfate

In addition to adverse cardiovascular effects of magnesium sulfate, other adverse effects include:

Central nervous system—drowsiness, depressed reflexes, flaccid paralysis, hypothermia

Respiratory—respira- tory paralysis

Other—hypocalcemia.

TEACHING ABOUT ANTIARRHYTHMICS

233

 

That’s a wrap!

Pharmacologic treatments review

Antiarrhythmic drugs

Classified according to effect on the cell’s electrical activity (action potential) and mechanism of action

Class Ia antiarrhythmics

Are called sodium channel blockers

Reduce excitability of cardiac cells and decrease contractility

Have anticholinergic and proarrhythmic effects

Show widened QRS complex and prolonged QT intervals on ECG

Quinidine

Used for supraventricular and ventricular arrhythmias

Procainamide hydrochloride

Used for supraventricular and ventricular arrhythmias

Class Ib antiarrhythmics

Suppress ventricular ectopy

Slow phase 0 depolarization

Shorten phase 3 repolarization and action potential

Lidocaine hydrochloride

Former drug of choice for suppressing ventricular arrhythmias

Class Ic antiarrhythmics

Slow conduction

Flecainide acetate

Used for paroxysmal atrial fibrillation or flutter in patients without structural heart disease and with life-threatening ventricular arrhythmias; prevents supraventricular tachycardia

Propafenone hydrochloride

Used only for life-threatening ventricular arrhythmias

Class II antiarrhythmics

Are called beta-adrenergic blockers

Block sympathetic nervous system beta receptors and decrease heart rate

Used to treat supraventricular and ventricular arrhythmias

Include acebutolol, propranolol, esmolol, and sotalol

Class III antiarrhythmics

Are called potassium channel blockers

Block potassium movement during phase 3

Increase the duration of the action potential

Prolong the effective refractory period

Show prolonged PR and QT intervals and widened QRS complex on ECG

Amiodarone

Used for supraventricular arrhythmias, PSVT caused by accessory pathway conduction (as in Wolff-Parkinson-White syndrome), and ventricular arrhythmias

PHARMACOLOGIC TREATMENTS

234

Pharmacologic treatments review (continued)

Ibutilide fumarate

Rapidly converts recent-onset atrial fibrillation or flutter

Dofetilide

Used for maintenance of normal sinus rhythm in patients with atrial fibrillation or flutter lasting longer than 1 week who have been converted to normal sinus rhythm

Used to convert atrial fibrillation and flutter to normal sinus rhythm

Class IV antiarrhythmics

Are called calcium channel blockers

Prolong conduction time and refractory period in the AV node

Decrease contractility

Show PR interval prolonged on ECG

Verapamil

Used for PSVT and to slow ventricular response in atrial fibrillation and flutter

Diltiazem

Used for PSVT and atrial fibrillation or flutter

Unclassified antiarrhythmics

Also called miscellaneous antiarrhythmics

Adenosine

Slows AV node conduction and inhibits reentry pathways

Used to treat PSVT

Atropine

Anticholinergic drug that blocks vagal effects on the SA and AV nodes

Used to treat symptomatic bradycardia and asystole

Digoxin

Enhances vagal tone and slows conduction through the SA and AV nodes

Shows ST-segment depression opposite the QRS deflection on ECG; P wave may be notched

Used to treat PSVT and atrial fibrillation and flutter

Epinephrine

Catecholamine that acts on alphaadrenergic and beta-adrenergic receptor sites of the sympathetic nervous system

Used for symptomatic bradycardia and to restore cardiac rhythm in cardiac arrest

Magnesium sulfate

Decreases cardiac cell excitability and conduction; slows conduction through the AV node and prolongs the refractory period

Used to treat ventricular arrhythmias

TEACHING ABOUT ANTIARRHYTHMICS

235

 

Quick quiz

1. Antiarrhythmic drugs that depress the rate of depolarization belong to class:

A.I.

B.II.

C.III.

D.IV.

Answer: A. Class I antiarrhythmic drugs block sodium influx during phase 0, depressing the rate of depolarization.

2. The drug that blocks vagal stimulation and increases the heart rate is:

A.magnesium sulfate.

B.diltiazem.

C.verapamil.

D.atropine.

Answer: D. Atropine blocks vagal effects on the SA node, enhances conduction through the node, and speeds the heart rate. The drug is used to treat symptomatic bradycardia.

3. The class III antiarrhythmic drug used for the rapid conversion of recent-onset atrial fibrillation or flutter to sinus rhythm is:

A.digoxin.

B.ibutilide fumarate.

C.procainamide.

D.verapamil.

Answer: B. Ibutilide fumarate increases atrial and ventricular refractoriness and is used for the rapid conversion of recent-onset atrial fibrillation or flutter.

4.A drug known for lowering the resting heart rate is:

A.quinidine.

B.amiodarone.

C.propranolol.

D.lidocaine.

Answer: C. Beta-adrenergic blockers, such as propranolol, block sympathetic nervous system beta-adrenergic receptors and lower heart rate, contractility, and conduction.

PHARMACOLOGIC TREATMENTS

236

Scoring

If you answered all four questions correctly, just say “wow”! You’re the antiarrhythmic drug czar.

If you answered three questions correctly, great job! You’re the deputy antiarrhythmic drug czar.

If you answered fewer than three questions correctly, don’t fret. Get into the rhythm of antiarrhythmics by reviewing this chapter again.

Part IV The 12-lead ECG

11

Obtaining a 12-lead ECG

239

12

Interpreting a 12-lead ECG

255

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