It’s 3 AM on Medical South. The night is progressing quietly when suddenly you hear the nurse’s aide frantically yelling. “Call a code blue!” Immediately, your stomach begins to turn inside out and your heart begins to race. Sound familiar?

Quite often, the main fear experienced by nurses is related to the administration of emergency drugs. Familiarity with the Advanced Cardiac Life Support (ACLS) emergency drug therapy guidelines for treatment of cardiac dysrhythmias can diminish that apprehension. The American Heart Association (AHA) has formulated algorithms — protocols that prioritize treatment modalities for life-threatening cardiac dysrhythmias.

During a code, drug therapy is usually not your first priority. It’s essential that first responders to a code use their CPR skills. The AHA emergency cardiac care approach utilizes the mnemonic “ABCD/ABCD” along with “assess, manage, and go no further.” The mnemonic reminds you of Airway, Breathing, Circulation, Defibrillation, and Differential Diagnosis. “Assess, manage, and go no further” reminds you to treat as you find. For example, if the airway is obstructed, open the airway before attempting ventilations. Drug therapy should only be implemented after the primary and secondary ABCD surveys, accurately assessing cardiac rhythm, and assessing patient clinical status. In the event that emergency cardiac drug therapy is necessary, nurses will probably encounter the following drugs during one code or another. Practices that guide the use of emergency drugs are evidence-based, derived from the American Heart Association, and can be found at http://circ.ahajournals.org/content/vol112/22_suppl.

Most frequently encountered drugs

Epinephrine is a catecholamine that increases heart rate, myocardial contractility, vascular resistance, and automaticity of the heart.

Providers directing code teams prescribe this agent for patients sustaining ventricular fibrillation, pulseless ventricular tachycardia, asystole, and pulseless electrical activity (PEA). The usual dose of epinephrine is 1 mg IV push (IVP) with repeated doses every three to five minutes according to patient response. Follow each dose with 20 mL normal saline (NS) IV flush. Epinephrine is most commonly supplied on code carts in prefilled 10 mL syringes (10 mL = 1 mg, if a 1:10,000 dilution is used). AHA guidelines recommend the use of a continuous infusion of epinephrine (2 mcg/min to 10 mcg/min) in symptomatic bradycardia or hypotension after atropine, and while awaiting transcutaneous pacing, or if transcutaneous pacing has failed.

Atropine is an anticholinergic drug that has a direct vagolytic effect. By stimulating sinoatrial (SA) node automaticity and atrioventricular (AV) conduction, this agent augments heart rate, systemic vascular resistance, and blood pressure.

Atropine is used to treat patients with symptomatic sinus bradycardia and AV blocks. Atropine will not be effective against second-degree AV block Mobitz Type II nor third degree AV block with wide QRS complexes. Atropine is the second drug of choice (after epinephrine or vasopressin) for asystole. It is also given to patients in PEA, after other therapeutic modalities and epinephrine have failed if they experience absolute bradycardia; a heart rate is less than 60.

For asystole or PEA, give atropine 1 mg IVP every three to five minutes up to a maximum of 3 doses or 3 mg. In symptomatic bradycardia, the dose is 0.5 mg to 1 mg IVP, repeated every three to five minutes as needed up to a total dose of 3 mg. Follow each dose with 20 mL NS IV flush. Atropine is most commonly supplied in prefilled syringes with 1 mg in 10 mL.

When administering atropine, remember the following points. First, your patient’s pupils will become dilated; therefore, pupil checks have no clinical significance. Second, because atropine may produce tachycardia, exercise caution with patients whose ECGs reveal acute changes of ischemia or injury due to increased oxygen demand. Third, atropine is contraindicated in patients who have received heart transplants because the vagus nerve is severed during transplantation making atropine ineffective in this situation. Finally, watch for side effects like tachydysrhythmias, delirium, flushed skin, ataxia, blurred vision, and coma. Use atropine cautiously because the increase in heart rate may worsen ischemia or increase the infarcted area of an MI.

Amiodarone is an antidysrhythmic that alters the function of all cardiac tissue. SA nodal firing and AV nodal conduction time are slowed. The refractory period is prolonged in the atria, AV node, and ventricles. Amiodarone is indicated for shock-refractory ventricular fibrillation and pulseless ventricular tachycardia. It is used to treat wide-complex tachydysrhythmias and as an adjunct to electrical cardioversion of paroxysmal supraventricular tachycardia (PSVT). Amiodarone is acceptable for termination of atrial tachycardia with preserved or impaired left-ventricular function. This drug may be used for rate control of atrial fibrillation or atrial flutter when other therapies have failed.

The usual dose of amiodarone for ventricular fibrillation and pulseless ventricular tachycardia is 300 mg IVP. If there is no response in three to five minutes, consider a second dose of 150 mg IVP. The maximum cumulative dose of amiodarone is 2.2 g IV in 24 hours. The usual dose of amiodarone for stable wide-complex tachycardia is 150 mg IV over ten minutes. Additional infusions of 150 mg may be given every ten minutes as needed up to the maximum of 2.2 g in 24 hours. Follow a successful bolus of amiodarone with a maintenance infusion of 540 mg over 18 hours (0.5 mg/min).

Amiodarone may produce vasodilation and hypotension. This drug may produce negative inotropic effects and may prolong the QT interval. Do not routinely administer amiodarone with procainamide or other drugs that prolong the QT interval. Use amiodarone with caution in the patient with renal failure. Terminal elimination is extremely long. Amiodarone’s half-life lasts up to 40 days.

Adenosine is an antidysrhythmic that works by slowing the initiation of SA node impulses and blocking AV conduction reentry. This action produces a decrease of reentry dysrhythmias such as PSVT.

Adenosine is indicated for the treatment of PSVT, and it is the drug of choice for most narrow-complex tachycardias. It does not convert atrial fibrillation or atrial flutter, but may be used as a diagnostic tool by producing transient AV block that clarifies the underlying rhythm. Adenosine is not used for wide-complex tachycardia of uncertain origin. ACLS guidelines recommend cardioversion for unstable wide-complex tachycardia of unknown type. The pharmacological treatment after cardioversion is amiodarone or procainamide.

The usual dose of adenosine is 6 mg given rapidly IVP over one to three seconds followed by 20 mL NS IV flush and elevation of the arm with the IV access. The second dose is 12 mg given one to two minutes later if there is no response to the first dose. The 12 mg dose may be repeated one more time after one to two minutes, if needed. The maximum dose is 30 mg. An important fact to keep in mind regarding adenosine is that it has an extremely short half-life (<10 seconds) and must be administered rapidly (in one to three seconds) through the IV port closest to the heart. After administration, adenosine should be quickly followed by a normal saline flush. A stopcock setup with normal saline already attached to the IV site is recommended.

Because adenosine slows AV conduction, it is contraindicated in patients with second- or third-degree AV blocks who do not have artificial pacemakers. In addition, adenosine is contraindicated in patients taking theophylline derivatives, carbamazepine (Tegretol), or dipyridamole (Persantine). These drugs may interfere with the action of adenosine; therefore, other drugs should be considered.

When administering adenosine, you must observe the cardiac monitor closely for momentary periods of asystole, sinus bradycardia, or ventricular ectopy. Your patient may also experience periods of dyspnea, chest pain, or flushing. These symptoms are usually short-lived and generally disappear within a minute. However, emergency equipment should be immediately available should resuscitation become necessary.

Other emergency agents

Vasopressin is a hormone that promotes reabsorption of water in the kidneys and causes peripheral vasoconstriction. If ventricular fibrillation or pulseless ventricular tachycardia persists after delivery of 1 or 2 shocks plus CPR, one dose of vasopressin may replace either the first or second dose of epinephrine. In asystole or pulseless electrical activity, vasopressin may also be given to replace the first or second dose of epinephrine. The dose of vasopressin is 40 units and is usually administered IVP; however, vasopressin may also be given through the endotracheal tube at the same dose. Vasopressin is usually supplied in crash carts as a 20 unit vial. You will need 2 vials to equal 40 units. Because vasopressin is a potent peripheral vasoconstrictor and may provoke or worsen cardiac ischemia, it is not recommended for use in responsive patients with coronary artery disease.

Dopamine, commonly used after establishing a normal sinus rhythm and prior to transferring the patient to a critical care unit, is an inotropic vasoactive agent. This drug is always administered via IV drip with a usual concentration of 400 mg in 250 mL D5W. Its actions are dose-related, and it is titrated to effect. In low doses (1 mcg/kg/min to 5 mcg/kg/min), dopamine dilates renal arteries, improves renal perfusion, and increases urine output. In doses of 5 mcg/kg/min to 10 mcg/kg/min, it augments cardiac output by increasing heart rate, myocardial contractility, and cardiac output, and at 10 mcg/kg/min to 20 mcg/kg/min, it raises blood pressure by causing peripheral vasoconstriction. If doses greater than 20 mcg/kg/min are needed to maintain an adequate blood pressure, norepinephrine should be administered simultaneously.

Although dopamine is generally considered to be a safe drug, monitor blood pressure frequently and take the following precautions. First, monitor the patient for supraventricular or ventricular dysrhythmias. Second, if your patient is receiving a monoamine oxidase (MAO) inhibitor, which can potentiate the action of dopamine, give only about one tenth of the usual dopamine dose. Third, closely observe the IV site because there is a high potential for subcutaneous tissue necrosis if infiltration occurs. Fourth, never use the infusion line to give alkaline medications such as sodium bicarbonate (NaHCO3) because an alkaline solution will inactivate dopamine. Fifth, use dopamine with caution on a hypovolemic patient, or a patient with an ischemic heart. Finally, gradually taper the infusion when discontinuing because sudden drops in dosage are likely to produce a hypotensive crisis.

Procainamide is an antidysrhythmic that decreases electrical conduction velocity and automaticity in both the atrium and ventricles. It is indicated for stable wide-complex tachycardia, and atrial fibrillation with rapid rate in Wolff-Parkinson-White syndrome. A usual loading dose is 20 mg/min to 30 mg/min to a maximum dose of 17 mg/kg (or 1,000 mg) IV, followed by a continuous IV infusion at 1 mg/min to 4 mg/min. Remember to discontinue the loading dose as soon as it is effective and begin the continuous infusion to avoid toxicity. Closely monitor patients receiving this drug for changes in blood pressure and adverse reactions, such as widening of the QRS complex, lengthening of the PR and QT intervals, and hypotension. If the QRS complex widens by greater than 50% of the pre-drug administration width, discontinue the medication.

Diltiazem is a calcium channel blocker used in ACLS algorithms to control the ventricular rate in atrial fibrillation and atrial flutter. Diltiazem may terminate reentry dysrhythmias that require AV nodal conduction for their continuation. Diltiazem is used after adenosine to treat refractory PSVT in patients with narrow QRS complexes and adequate blood pressure. The dose of diltiazem is 0.25 mg/kg to 0.35 mg/kg IV over 2 minutes and may be repeated in 15 minutes. Maintenance infusion is 5 mg/hr to 15 mg/hr titrated to the desired heart rate. Hypotension is a serious potential adverse reaction and requires that you closely monitor your patient’s blood pressure during therapy.

Verapamil is a commonly used calcium channel blocker for the treatment of PSVT and other narrow complex tachycardias after adenosine has proven to be ineffective. The usual dose is 2.5 mg to 5 mg IV; the second dose is 5 mg to 10 mg given after 15 to 30 minutes to a total of 20 mg. An alternative dosing regimen is to give a 5 mg. bolus every 15 minutes to a total dose of 30 mg. Administer slowly over a period of one to three minutes, closely monitoring for hypotension. Patients who are unstable with tachydysrhythmias should be cardioverted before instituting this drug therapy. Verapamil should be avoided in wide-QRS complex tachycardias because ventricular failure may become worse due to negative inotropic effects.

Magnesium sulfate (MgSO4) is an electrolyte that regulates the movement of calcium in and out of cells. Because calcium is necessary for cardiac contraction, deficiencies in magnesium disrupt the function of calcium, which can cause cardiac dysrhythmias such as refractory ventricular fibrillation and torsade de pointes, a form of ventricular tachycardia. Magnesium sulfate is recommended for treatment of torsade de pointes with or without cardiac arrest.

When MgSO4 is administered in a code blue situation, the usual dose is 1 gm to 2 gms in 10 mL D5W given IV over one to two minutes for an unstable patient. MgSO4 may also be given prophylactically for the acute MI patient with confirmed hypomagnesemia to decrease ventricular ectopy; this dose is 1 gm to 2 gms in 100 mL of D5W over 50 to 60 minutes followed by a 24-hour infusion of 0.5 gm/hour to 1 gm/hour. Rapid administration can produce significant hypotension and asystole, as well as a prolonged PR interval and a widened QRS complex. Patients may also develop flushing, respiratory depression, heart blocks, and loss of deep tendon reflexes. The treatment for MgSO4 toxicity is calcium gluconate.

Calcium chloride is an electrolyte that increases the force of myocardial contractions when an orderly, but ineffectual rhythm has been established; it is also indicated for hyperkalemia, hypocalcemia, or calcium channel blocker toxicity. Calcium should not be used routinely in an arrest situation. The dose is 8 mg/kg to 16 mg/kg of a 10% solution; generally, 1 gm (10 mL) is given IVP. Do not mix with sodium bicarbonate. Precaution must be taken with patients who are digitalized because calcium increases ventricular irritability and may precipitate digoxin toxicity.

Oxygen is a drug and an essential component in the positive outcome of cardiopulmonary resuscitation. Oxygen should be administered to all patients with chest pain that might be of cardiac origin or due to hypoxemia, as well as to all patients in cardiac arrest. During an arrest situation, deliver oxygen via a positive pressure ventilation device such as a bag-valve-mask as soon as it is available, then intubate and use 100% oxygen.

Lidocaine is no longer given for ventricular fibrillation or pulseless ventricular tachycardia until after defibrillation, epinephrine or vasopressin, and if amiodarone is not available. Lidocaine suppresses automaticity and excitability of the HIS-Purkinje system during diastole. Through critical appraisal and expert discussion, lidocaine has now been classified as an “indeterminate” ACLS recommendation. It does no harm and has no benefit.

The usual dose of lidocaine for ventricular fibrillation is 1 mg/kg to 1.5 mg/kg IVP, may repeat every three to five minutes to a maximum of 3 mg/kg. The dose for ventricular tachycardia is 1 mg/kg to 1.5 mg/kg IVP with doses of 0.5 mg/kg to 0.75 mg/kg repeated every five to ten minutes up to a maximum dose of 3 mg/kg. Following a successful lidocaine bolus, institute a continuous IV infusion (2 Gm in 500 mL D5W) at 2 mg/min to 4 mg/min. Prophylactic lidocaine with acute myocardial infarction is no longer recommended.

Administer lidocaine with caution in patients with conduction disturbances, avoiding it altogether for patients in third-degree heart block with ventricular escape patterns. Large doses may depress the sinus node and produce heart blocks. Also, you might want to reduce the dosage for those who have impaired hepatic function, pulmonary edema, and shock or who are over the age of 70. Be alert for signs and symptoms of toxicity, which may include drowsiness, disorientation, tinnitus, paresthesias, and seizures. If toxicity is suspected, stop the drip, hang a normal saline IV, and promptly notify the physician.

Sodium bicarbonate is not recommended for routine use in cardiac arrest patients and should only be administered when there is documented hyperkalemia, metabolic acidosis, or tricyclic antidepressant drug overdose. The best way to correct hypercarbic acidosis is through aggressive CPR and ventilation. Sodium bicarb is usually supplied in a 50 cc syringe containing 40 mEq. An initial dose is 1 mEq/kg IV over one to two minutes, which can be repeated in 10 minutes at 0.5 mEq/kg or until a more appropriate dosage can be calculated from arterial blood gas findings.

Administration

Medications are given primarily intravenously during a code. Be prepared to administer a 20 mL bolus of IV fluid or saline flush and elevate the arm after each IV medication. This will enhance delivery of medications to the central circulation. However, certain drugs, such as epinephrine, atropine, lidocaine, and vasopressin, may be given via the endotracheal tube in the absence of IV access. When administering via the ET route, the dose should usually be 2 to 2.5 times the normal IV dose. Dilution with water instead of normal saline may achieve improved drug absorption with epinephrine and lidocaine. Medication should be diluted in 5 mL to 10 mL of normal saline, instilled into the tube, and followed by positive pressure ventilations to promote bronchial absorption.

Golden rules

A code situation is stressful but following these few guidelines can ensure that drug administration is safe, orderly, accurate, and appropriate.

Treat the patient and not the monitor. Continual assessment of your patient’s clinical status promotes appropriate and effective treatment. For example: Are ventilations adequate? Does the patient with ventricular tachycardia on the monitor have a pulse? Is the team looking for the cause of the arrest and treating it?

Organize the code. Everyone should have a role and stick to it — for example, medication nurse, recording nurse, and patient care nurse. Locate medications and learn how to use equipment before the code. Practice setting up oxygen and suction apparatus and become familiar with using the defibrillator/monitor or AED to quickly establish the patient’s rhythm. Participate in mock codes.

Document accurately. Record the events leading up to the code, when CPR was begun, and when defibrillation was performed. Clearly identify rhythms, their treatment, medications, and the patient’s responses. Record vital signs frequently. Sign the code form legibly and include the names of key code members, if that is the policy at your institution.

Take care of the family. Remember that the patient’s family and significant others will be terrified about the outcome in the event of a cardiac emergency. Assign a support person such as a psychiatric liaison or staff nurse, chaplain, or social worker, to stay with family/significant others especially if they are present during resuscitation; and the patient’s physician will need to speak with them as soon as possible. Families appreciate knowing, in gentle language, what is going on during the code. Be prepared by learning respective, effective techniques for talking with the patient’s family/significant others about the resuscitation and its outcome.

Support the team. The code and patient care team members need varying levels of support depending on the patient and the particular circumstances. Learning about effective debriefing and implementing it following resuscitation will facilitate competent performance in future emergency situations.

Emergency drug therapy plays a key role in the survival of code blue patients. Nurses in clinical areas need to be competent in BLS and familiar with emergency drugs and their use in accordance with ACLS protocols.