Sublingual nitroglycerin (0.3 to 0.8 mg) and the translingual aerosol spray (0.4-mg metered dose) preparations are indicated for patients experiencing an acute anginal attack who have a systolic blood pressure above 90 mm Hg. The patient is taught to sit or lie down and moisten 1 sublingual nitroglycerin tablet with saliva and then place it under the tongue to allow it to dissolve slowly. If the chest pain is not relieved, sublingual nitroglycerin may be repeated at 3- to 5-minute intervals—as long as the patient’s systolic blood pressure remains above 90 mm Hg—until a total of 3 tablets have been taken. Patients prescribed the translingual aerosol preparation should be reminded that the spray should not be inhaled. Instead, it should be sprayed onto or under the tongue. The patient should be instructed not to swallow for approximately 10 seconds to allow absorption of the drug. As with sublingual nitroglycerin, up to 3 doses may be taken within 15 minutes. If pain persists despite 3 doses of the sublingual or aerosol forms, further interventions are necessary in an emergency or critical care setting. An ambulance should be called if the patient is outside the hospital, and blood pressure and heart rate must be monitored closely. Hypotension is a common adverse effect, especially the first time a patient takes nitroglycerin. Tachycardia, an abnormally high heart rate in adults (>100 beats/min), or uncommonly bradycardia, a slow heart rate, also may occur. Patients who take sublingual or translingual aerosol spray nitroglycerin while wearing a nitroglycerin patch may be at higher risk for hypotension. This situation warrants caution. However, individuals who take daily nitroglycerin can develop tolerance to the drug, which can provide some protection against hypotension. If hypotension persists or worsens, the nitroglycerin patch may need to be removed. To prevent arcing and the potential for skin burns, the nitroglycerin patch must be removed prior to cardioversion or defibrillation.

IV nitroglycerin is reserved for patients with unstable angina or AMI. A continuous infusion is usually initiated at a rate of 5 mcg/min and titrated by 5 mcg/min every 3 to 5 minutes based on chest pain and blood pressure response. Maximum rate of titration is 20 mcg/min every 3 to 5 minutes. Continuous blood pressure and heart monitoring are required because hypotension is a common adverse effect. Hypotension usually is treated by reducing or discontinuing the nitroglycerin infusion (see Chapter 37) and by placing the patient in a supine position with legs elevated if tolerated.

In symptomatic bradycardia, atropine is administered IV in 0.5-mg doses at 3- to 5-minute intervals until the desired heart rate is achieved or until 0.04 mg/kg (not more than 3 mg) is given. Dosing in this manner may be repeated every 3 to 5 minutes up to a limit of 0.04 mg/kg (usually not more than 3 mg IV).

The adult IV atropine dose should never be less than 0.5 mg. Doses below 0.5 mg may produce a paradoxical bradycardia; at doses of 0.04 mg/kg or greater, vagal activity is considered completely blocked, and further atropine administration may have no benefit. However, in the case of organophosphate insecticide or nerve agent poisoning, very high doses of atropine may be necessary to counteract the pathophysiologic effects of these toxins. Therefore the typical dosing range and limits do not apply under these circumstances.

If venous access is not available in an emergency situation, atropine sulfate should be administered through the intraosseous (IO) route. As a last resort, atropine may be given via the endotracheal tube (ETT) route if venous or IO access cannot be achieved. The dose for endotracheal administration is 2 to 2.5 times the venous dose, diluted with normal saline or sterile water. Accordingly, 2 to 3 mg of atropine would be diluted in 10 mL of normal saline or sterile water and instilled deep into the ETT via a feeding tube attached to a syringe. After endotracheal administration, the patient should be ventilated vigorously with a bag-valve device to enhance absorption of the drug.

Continuous cardiac and blood pressure monitoring is essential for the patient who receives atropine sulfate. Significant adverse effects include cardiac dysrhythmias, tachycardia, myocardial ischemia, restlessness, anxiety, mydriasis, thirst, and urinary retention. See Chapter 16 for more information on atropine and other anticholinergics.

Nursing considerations include continuous cardiac monitoring and frequent assessment of vital signs. Adenosine is inhibited by methylxanthines such as caffeine and theophylline, so higher doses may be needed. Although usually transient, ventricular ectopy, bradycardia, flushing, chest pain, and dyspnea may occur. In addition, a short period of asystole may follow injection of adenosine (up to 15 seconds). Spontaneous cardiac activity typically resumes. Adenosine is contraindicated in patients with poison- or drug-related tachycardia, second- and third-degree heart block, and in patients with sick sinus syndrome except those with functioning pacemakers. If the tachycardia originated in the ventricles, the patient could deteriorate and become hypotensive after adenosine administration. See Chapter 37 for more information on antidysrhythmic drugs.

The usual initial bolus dose of IV diltiazem is 0.25 mg/kg given over 2 minutes. If the supraventricular tachycardia does not convert to a normal sinus rhythm in 15 minutes, a second IV bolus of 0.35 mg/kg over 2 minutes may be necessary. For ongoing control of the ventricular rate in patients with atrial fibrillation or flutter, a continuous infusion of diltiazem is indicated at a dose range of 5 to 15 mg/hour, titrated according to the desired heart rate.

The nurse must carefully monitor blood pressure and heart rate and rhythm after administering IV diltiazem. Arrhythmias, bradycardia, heart block, and hypotension may develop. Diltiazem can elevate serum digoxin levels, predisposing the patient to digitalis toxicity. Simultaneous use of calcium channel blockers and beta blockers is contraindicated because their negative inotropic and negative chronotropic effects are synergistic, causing myocardial depression and bradycardia. Other contraindications include preexisting heart failure, Wolff-Parkinson-White syndrome, and heart block or sick sinus syndrome in the patient without a pacemaker.

Amiodarone is especially good for patients with impaired heart function who have atrial and ventricular dysrhythmias. It has been found to be more effective and to have fewer proarrhythmic properties than other agents with similar actions.

For patients who have a pulse (i.e., those not in cardiac arrest), amiodarone 150 mg IV is given over 10 minutes, followed by a continuous infusion of 1 mg/min for 6 hours, then 0.5 mg/min over 18 hours as a maintenance infusion. For patients in cardiac arrest because of pulseless ventricular tachycardia or ventricular fibrillation, a dose of 300 mg diluted in 20 to 30 mL D₅W is given as a rapid infusion followed by a continuous infusion as described earlier. Additional doses of 150 mg may be given by rapid infusion if ventricular fibrillation or ventricular tachycardia recurs. The maximum daily dose is 2.2 g per 24-hour period.

Significant adverse effects include hypotension and bradycardia, therefore the nurse should slow the infusion rate to prevent or treat these effects and should be prepared to administer IV fluids, vasopressors, and agents to increase heart rate. A temporary pacemaker may be needed. Amiodarone has a very long half-life. It should not be given concurrently with pharmacologic drugs that prolong QT interval on electrocardiography (ECG), such as procainamide.

Important nursing considerations for the patient receiving lidocaine include continuous cardiac monitoring and assessment for signs and symptoms of lidocaine toxicity (e.g., confusion, drowsiness, hearing impairment, cardiac conduction defects, myocardial depression, muscle twitching, and seizures). Because lidocaine is metabolized by the liver, patients with hepatic impairment, heart failure, shock, and advanced age (>70 years) are at higher risk for toxicity. In these patients, the lidocaine dose may need to be reduced by as much as 50% (see Chapter 37). Lidocaine is contraindicated as a prophylactic agent to prevent ventricular dysrhythmias following AMI.

The nurse must monitor vital signs and the ECG with particular attention to heart rate and rhythm, blood pressure, and the width of the QRS complex. Procainamide administration can cause severe hypotension. Heart block, rhythm disturbances, and cardiac arrest can also occur. Procainamide is contraindicated in patients with torsades de pointes, an unusual polymorphic ventricular tachycardia often associated with a prolonged QT interval. Procainamide is eliminated via the kidneys, therefore patients with renal failure are at higher risk of adverse effects and often require a lower dosage.

The primary indications for emergency administration of magnesium sulfate are refractory ventricular tachycardia, refractory ventricular fibrillation, cardiac arrest associated with hypomagnesemia (low serum magnesium level), and life-threatening ventricular dysrhythmias from digitalis toxicity. It is also the drug of choice for the treatment of torsades de pointes.

Magnesium is administered by diluting 1 to 2 g (2 to 4 mL of a 50% solution) in 10 mL of D₅W. For cardiac arrest caused by hypomagnesemia or torsades de pointes, magnesium is given by direct IV push or via the IO route over 5 to 20 minutes. For patients experiencing torsades de pointes who are not in cardiac arrest, a magnesium infusion of 1 to 2 g diluted in 50 to 100 mL of D₅W can be given IV/IO over 5 to 60 minutes followed by a continuous infusion of 0.5 to 1 g/h.

Although magnesium toxicity is rare, the nurse should monitor the patient’s response to magnesium administration. Hypotension is the most common adverse effect when magnesium is given by rapid IV push. Other effects include mild bradycardia, flush, and sweating. True hypermagnesemia can cause diarrhea, respiratory depression, deep tendon reflex impairment, flaccid paralysis, and circulatory collapse. Because magnesium is eliminated via the kidneys, it should be administered with caution in patients with renal impairment.

For profound bradycardia or hypotension, an epinephrine infusion may be ordered at 0.1 to 0.5 mcg/kg/min. For asystole, pulseless ventricular tachycardia, and ventricular fibrillation, epinephrine is administered in 1-mg doses (1:10,000 solution) IV/IO every 3 to 5 minutes until the desired clinical response—usually return of effective cardiac activity—is achieved. Epinephrine also may be given via the ETT route in doses of 2 to 2.5 mg diluted in 10 mL of normal saline.

Nursing implications for patients receiving epinephrine include constant cardiac and hemodynamic monitoring. Epinephrine can cause myocardial ischemia and cardiac dysrhythmias. It should never be administered in the same site as an alkaline solution, such as with sodium bicarbonate, because alkaline solutions inactivate epinephrine. In addition, the presence of metabolic or respiratory acidosis decreases the effectiveness of epinephrine. All efforts should be made to correct acid-base imbalances in the patient. More drug information about epinephrine and other adrenergic drugs can be found in Chapter 12.