Basic and Bedside Electrocardiography, 1st Edition (2009)

Appendix. Commonly Used Injectable Pharmacologic Agents

Adenosine (Adenocard): Pregnancy Category C

·         Indication: Drug of choice for the conversion of paroxysmal supraventricular tachycardia (PSVT) to normal sinus rhythm.

·         Mechanism of action: Adenosine is an atrioventricular (AV) nodal blocker and can interrupt supraventricular arrhythmias that are AV node-dependent. It also inhibits the sinus node resulting in depression of sinus node function.

·         Intravenous dose:

o    Rapid bolus of 6 mg given intravenously as quickly as possible (within 1 to 2 seconds) preferably to a proximal vein. The injection should be followed by a flush of 10 to 20 mL normal saline using a separate syringe. To enhance delivery of the pharmacologic agent to the heart, the arm should be elevated immediately after the injection especially if a distal vein is used.

o    If the supraventricular tachycardia (SVT) is not converted after 1 to 2 minutes, a higher dose of 12 mg is given.

o    If the SVT has not converted, a third and final dose of 12 mg is given.

o    A rhythm strip should always be recorded during injection, which may be useful in the diagnosis of other tachycardias other than paroxysmal SVT (PSVT).

·         Contraindications:

o    Adenosine can cause bronchoconstriction in patients with asthma or in patients with history of bronchospastic pulmonary disease.

o    Patients with sick sinus syndrome may develop pronounced bradycardia after the PSVT is terminated.

·         Other things you should know about adenosine:

o    Intravenous doses of more than 12 mg are not recommended.

o    Injection into a central IV line may result in a more pronounced effect. Consider giving a smaller initial dose of 3 mg if adenosine is injected into a central line.

o    Carbamazepine and dipyridamole potentiate the effects of adenosine. If the patient is on any of these agents, the initial dose of adenosine should also be reduced to 3 mg.

o    Methylxanthines such as caffeine and theophylline is the antidote of adenosine. The usual dose of adenosine may not be effective in patients who are on theophylline. Larger doses are necessary, but should not be given if the patient is taking theophylline for bronchospastic pulmonary disease.

o    Sixty percent of patients with PSVT will convert to normal sinus rhythm within 1 minute after an initial bolus of 6 mg and up to 92% after a 12-mg bolus.

o    The elimination half-life of adenosine is <10 seconds. Transient periods of asystole, AV block, or bradycardia frequently occur before conversion to normal sinus rhythm. The antidote for adenosine is aminophylline given intravenously. The antidote is rarely needed because the half-life of adenosine is very short.

o    When given to patients with wide complex tachycardia, adenosine can depress left ventricular function, but because of its short half-life, its effect is transient and is usually tolerable even in patients with poor left ventricular dysfunction. It receives a Class IIb recommendation by the American College of Cardiology/American Heart Association/European Society of Cardiology guidelines on supraventricular arrhythmias when given to patients with wide complex tachycardia of unknown origin.

o    Adenosine should be used cautiously in patients with severe coronary artery disease because adenosine is a potent coronary vasodilator and can cause ischemia by redistributing coronary flow to normal vessels.

o    Prolonged asystole, ventricular tachycardia, and ventricular fibrillation may occur.

o    Atrial fibrillation can occur in up to 10% of patients and may be catastrophic in a patient with Wolff-Parkinson-White (WPW) syndrome.

o    Adenosine does not convert atrial flutter or atrial fibrillation to normal sinus rhythm but can slow ventricular rate transiently, which may be useful if the diagnosis of the narrow complex tachycardia is uncertain.

Amiodarone (Cordarone): Pregnancy Category D

·         Indication: Amiodarone is indicated only for the treatment of ventricular arrhythmias. The use of amiodarone in the treatment of supraventricular arrhythmias and control of ventricular rate in atrial flutter or fibrillation is not recommended by the Food and Drug Administration (FDA) and its use is based solely on published information.

o    Ventricular arrhythmias:

§  Amiodarone IV is indicated for the treatment of ventricular tachycardia (VT) in patients with normal left ventricular systolic function and in patients with systolic dysfunction.

§  It is also indicated for the treatment of ventricular fibrillation (VF) and pulseless VT.

§  Indicated for the treatment of wide complex tachycardia of uncertain etiology.

o    Supraventricular arrhythmias:

§  Accepted as a second- or third-line agent for the termination of atrial tachycardia from enhanced automaticity including focal atrial tachycardia, multifocal atrial tachycardia, and other types of atrial tachycardia resulting from reentry that are refractory to medical therapy.

§  Although amiodarone is extensively used and is effective in controlling the ventricular rate in atrial fibrillation and converting patients with atrial fibrillation to normal sinus rhythm, it has not been approved by the FDA for these indications.

·         Mechanism of action: Amiodarone is generally a Class III antiarrhythmic agent, but exhibits all Class I to IV properties of the Vaughan Williams classification. Thus, similar to Class I agents, it is a sodium channel blocker; similar to beta blockers (Class II), it has antisympathetic properties; and similar to Class III agents, it blocks the potassium channel and therefore prolongs the duration of the action potential, slows conduction and prolongs the refractory period. It also has Class IV negative chronotropic effects on AV nodal tissues similar to calcium blockers thereby slowing AV conduction.

·         Intravenous dose:

o    Sustained VT or wide complex tachycardia of unknown origin:

§  Initial bolus: 150 mg given IV rapidly for 10 minutes (150 mg or 3 mL of amiodarone is diluted with 100 mL D5W and infused over 10 minutes equivalent to 15 mg/minute).

§  This infusion may be repeated every 10 minutes as needed.

o    Cardiac arrest from pulseless VT or VF:

§  Initial bolus: Amiodarone is given at a bigger dose of 300 mg diluted to 20 to 30 mL of saline or D5W given IV push.

§  This may be followed by supplementary boluses of 150 mg IV given by IV push every 3 to 5 minutes.

o    Next 6 hours: Follow initial bolus with an IV drip of 1 mg/minute × 6 hours (total = 360 mg). The solution is prepared by adding 900 mg of 18 mL of amiodarone to 500 mL D5W (or 450 mg in 250 mL D5W).

§  If the arrhythmia keeps recurring, an alternative is to give the solution as 150 mg IV boluses for 10 minutes every 10 to 15 minutes as needed, instead of giving the solution by IV drip.

o    Next 18 hours: Continue the IV drip to a lower dose of 0.5 mg/minute × 18 hours (total = 540 mg). The maximum total cumulative dose including dose used in resuscitation should not exceed 2.2 g in the first 24 hours.

o    After 24 hours: The intravenous dose is maintained after 24 hours:

§  The infusion is continued at 0.5 mg/minute × 24 hours. Maintenance infusion of 0.5 mg/minute can be continued for several days and if necessary up to 2 to 3 weeks.

§  If patient develops recurrence of the ventricular arrhythmia at any time during infusion, a supplemental bolus of 150 mg diluted with 100 mL D5W may be given IV over 10 minutes.

§  The maximum daily dose should not exceed 2,100 mg. Intravenous dosing should be switched to oral medication when the arrhythmia has been suppressed.

§  Doses >2,200 mg/24 hours are associated with significant hypotension.

·         Other things you should know about amiodarone:

o    Amiodarone is the preferred drug for ventricular arrhythmias and some atrial arrhythmias when there is left ventricular systolic dysfunction (ejection fraction ≤40% or when congestive heart failure is present). Amiodarone is indicated only for the treatment of VT/VF but is also effective in the following conditions:

§  It is effective in persistent VT or VF after defibrillation.

§  It is effective in stable monomorphic VT.

§  It is indicated for wide complex tachycardia that has not been diagnosed to be either VT or wide complex SVT.

§  It is effective in regular polymorphic VT (no QT prolongation).

§  It can be used as second- to third-line therapy for conversion of SVT to normal sinus rhythm when other drugs are not effective.

§  It is effective in conversion of atrial fibrillation to normal sinus rhythm.

§  It is also effective in controlling ventricular rate in atrial fibrillation especially in patients with WPW syndrome.

o    Amiodarone prolongs the QTc and is proarrhythmic. Its proarrhythmic effect however is much less than the other antiarrhythmic agents. It should not be administered with other agents that prolong the QTc.

o    The half-life of intravenous boluses varies from 4.8 to 68 hours and becomes longer as tissues become saturated. After steady state is reached, amiodarone has a long and variable half-life from 40 days to 3 to 5 months.

o    It can cause multiple organ toxicity including hepatocellular damage, hyper- or hypothyroidism, optic neuritis, and pulmonary disorders including acute respiratory distress syndrome.

o    Acute hepatocellular injury may occur with doses that are larger than recommended.

o    Its hypotensive and bradycardic effects are frequently related to the rapidity of infusion rather than the dose.

o    It is metabolized through the cytochrome P450 (CYP 450) 3A4 and 2C9 pathways and therefore has the potential for several drug-drug interactions.

§  Statins (lovastatin, atorvastatin, and simvastatin but not pravastatin or rosuvastatin) are metabolized through the CYP 450 3A4 pathway. Serum concentration of these statins can increase resulting in higher incidence of myopathy or rhabdomyolysis.

§  Calcium channel blockers such as verapamil and diltiazem are also metabolized through the CYP 450 3A4 pathway. The effects of these agents can be potentiated by amiodarone resulting in significant bradycardia.

§  CYP 450 3A4 inhibitors such as grapefruit juice, protease inhibitors, and cimetidine may increase the serum levels of amiodarone and can potentially cause amiodarone toxicity.

§  Agents that accelerate the CYP 450 3A4 metabolic pathway such as rifampin, barbiturates, and St. John's wort may decrease the blood levels of amiodarone making it subtherapeutic.

§  Amiodarone is also metabolized through the CYP 450 2C9 pathway and therefore competes with the metabolism of warfarin resulting in prolongation of the prothrombin time. The maintenance dose of warfarin should be reduced when amiodarone is started. Patients on warfarin should have prothrombin tests monitored carefully.

§  Beta blockers in combination with amiodarone can cause profound bradycardia.

§  Amiodarone can also potentiate the effect of digitalis; hence, the maintenance dose of digoxin should be reduced by half when amiodarone is given.

§  Effective plasma concentration of amiodarone is between 1 to 2 mcg/mL. The plasma concentration of amiodarone may be helpful in monitoring the efficacy but not toxicity. The effective therapeutic levels of amiodarone overlap with toxic levels and should not exceed 3 to 4 mcg/L.

Atenolol (Tenormin): Pregnancy Category D

·         Indication: Atenolol is indicated in the management of patients with angina pectoris, acute myocardial infarction, and control of hypertension. Although atenolol does not carry indication for termination of SVT or for controlling the ventricular rate in atrial flutter or fibrillation, it is frequently used for this purpose based on published information.

·         Mechanism of action: Atenolol is a synthetic selective β1 adrenergic blocking agent. When given in high doses, β1 receptor blocking agents including atenolol are not specific β1blockers but also blocks β2 receptors, which are present in bronchial and vascular smooth muscles.

·         Dose: The IV dose of atenolol for patients with acute myocardial infarction (or for the management of supraventricular arrhythmias), is 5 mg IV given slowly over 5 minutes. Injection rate should not exceed 1 mg/minute. A second dose of 5 mg is given IV after 10 minutes if the first dose was well tolerated. The blood pressure, heart rate, and electrocardiogram should be monitored during the intravenous infusion. If the intravenous dose is well tolerated, an oral dose of 50 mg is given 10 minutes after the last IV dose followed by another 50 mg 12 hours later. The maintenance dose is 50 mg twice daily or 100 mg once daily.

·         Other things you should know about atenolol:

o    Unlike metoprolol or propranolol, atenolol is primarily excreted by the kidneys (85%) and is not metabolized or is only minimally metabolized by the liver. Thus, atenolol given orally does not undergo first pass degradation by the liver. When there is renal failure, the dose should be adjusted.

o    When atenolol is given orally, only approximately 50% is absorbed. The other half is excreted unchanged in the gastrointestinal tract. This is unlike metoprolol where absorption is rapid and complete when given orally. Metoprolol is primarily metabolized in the liver and 50% of the oral dose is eliminated during first pass.

o    The elimination half-life of atenolol is approximately 7 hours, but is much longer when there is renal dysfunction.

o    Abrupt discontinuation or cessation of any beta blocker, including atenolol, in patients with known coronary disease and symptoms of angina may result in exacerbation of anginal symptoms or occurrence of acute coronary syndrome.

o    The latest 2007 focused update of the American College of Cardiology/American Heart Association 2004 guidelines raises doubt about the safety of intravenous beta blockers in acute ST elevation myocardial infarction and should not be given to patients at increased risk for cardiogenic shock (see Metoprolol).

o    Atenolol is the only beta blocker that receives a category D pregnancy risk classification by the FDA. All other beta blockers receive a category C classification. Sotalol, which also has beta blocking properties, carry a category B classification.

Atropine Sulfate: Pregnancy Category C

·         Indication: According to the 2005 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care, atropine remains the first-line drug for the treatment of acute symptomatic bradycardia. It is indicated for the treatment of acute symptomatic bradyarrhythmia due to sinus node dysfunction, AV nodal block, and increased vagal activity. It is the second drug of choice after epinephrine or vasopressin, in patients with ventricular asystole and pulseless electrical activity.

·         Mechanism of action: Atropine is an anticholinergic agent and increases ventricular rate by reversing vagally mediated mechanisms of bradycardia and hypotension.

·         Dosing:

o    Asystole: For asystole or slow pulseless electrical activity, a dose of 1.0 mg is given IV. If not effective, the dose is repeated every 3 to 5 minutes until a maximum dose of 3.0 mg is given. Complete vagal blockade occurs at a total dose of 0.04 mg/kg, which is 2.0 mg for a 50-kg and almost 3.0 mg for a 70-kg patient.

o    Bradycardia from AV block or sinus dysfunction: The initial dose is 0.5 to 1.0 mg IV every 3 to 5 minutes as needed until the maximum dose is given.

·         Other things you should know about atropine:

o    For the treatment of bradycardia, doses of <0.5 mg should not be given because small doses of atropine can cause paradoxical slowing of the heart rate. Small doses of atropine are parasympathomimetic. It stimulates the vagal nuclei, resulting in paradoxical slowing. This paradoxical effect can also occur if injected subcutaneously or intramuscularly. Atropine should always be given IV. If an IV route is not available during cardiac resuscitation, it can be given intratracheally at a dose of 2 to 3 mg diluted with 10 mL normal saline.

o    It is not effective and should not be given to patients with infranodal blocks (AV block below the level of the AV node) such as those due to Mobitz II second-degree AV block and complete AV block below the level of the AV node with wide QRS escape complexes (Class IIb recommendation).

o    Should be avoided in patients with bradycardia from hypothermia.

o    The use of atropine should not delay the insertion of transcutaneous or transvenous pacing in patients with symptomatic bradycardia with low cardiac output.

Beta Blockers: Beta Blockers are Class II Agents According to the Vaughan Williams Classification of Anti-Arrhythmic Agents

·         Beta blockers that are available intravenously include atenolol, esmolol, metoprolol, and propranolol. These different beta blockers are discussed individually in alphabetical listing.

Digoxin (Lanoxin): Pregnancy Category C

·         Indication: Control of ventricular rate in atrial fibrillation. It is also used for control of ventricular rate in atrial flutter and conversion of PSVT to normal sinus rhythm although these two indications have not been approved by the FDA.

·         Mechanism of action:

o    Digoxin inhibits sodium-potassium ATPase, which is an enzyme that regulates the exchange of sodium and potassium inside the cells. When ATPase is inhibited, sodium builds up within the cells. Sodium buildup activates the sodium-calcium exchange mechanism. Increase in calcium inside the cell activates the intracellular cytosol system to release more calcium. The increased calcium inside the cell enhances myocardial inotropicity with increased myocardial systolic contraction.

o    Digoxin also affects the cardiovascular system indirectly by its effect on the autonomic nervous system.

§  It has parasympathetic effects, which inhibits the sinus node, thus slowing the heart rate and slowing conduction at the AV node.

§  It reduces activity of the sympathetic nervous system and renin-angiotensin-aldosterone-system, thus reducing the activation of the neurohormonal system. This is mediated through baroreceptors sensitization, which causes increased afferent inhibitory activities.

·         Intravenous dose:

o    Before giving a full loading dose, first ascertain that the patient is not already on digoxin.

o    The ideal serum therapeutic level of digoxin is 0.7 to 1.1 ng/mL. The dose of digoxin that is needed to achieve this level in a 70-kg man is 0.6 to 1.0 mg (10 to 15 mcg/kg). The total dose depends on the lean body mass (and not total body weight) and renal function. Fifty percent of the total dose is given initially. Subsequent additional doses are given at 6- to 8-hour intervals.

o    Thus, if the patient weighs 70 kg, the total digitalizing dose is approximately 1.0 mg. Half the total dose or 0.5 mg, is given IV followed by another 0.25 mg IV in 6 hours and 0.25 mg IV after another 6 hours. The patient will have received the full digitalizing dose of 1.0 mg in 12 hours.

o    Digoxin is excreted primarily in the kidneys. Renal excretion is dependent on glomerular filtration. In patients with renal dysfunction, the creatinine clearance should be calculated using the Cockroft and Gault formula: Creatinine clearance for men = {(140 - age) + (weight in kg)} divided by 72 × serum creatinine (in mg/mL). The calculated renal clearance for men is multiplied by 0.85 for women.

§  If the creatinine clearance is ≥90, the normal dosage is unchanged.

§  If the creatinine clearance is 60 to 89, maintenance dose is 0.125 mg daily.

§  If the creatinine clearance is 30 to 59, 0.125 mg is given every other day.

§  If the creatinine clearance is <29, use digoxin very cautiously.

·         Other things you should know about digoxin:

o    Intramuscular injection of digoxin is very painful. Parenteral injections therefore should be limited intravenously.

o    Rapid injection or infusion can cause systemic and coronary constriction. Injection of digoxin therefore should be given slowly over 5 minutes or longer and not given as a bolus injection.

o    Serum concentrations of digoxin are not altered significantly by increase in body fat, thus lean body weight and not total body weight correlates best with the distribution space of digoxin.

o    The half-life of digoxin in patients with normal kidney function is 1.5 to 2 days. In anuric patients, it is prolonged to 3.5 to 5 days. Maintenance dosing can be given once per day.

o    Elderly patients, especially those with renal dysfunction, may be difficult to digitalize because maintenance dosing may be difficult; hence, serum digoxin level should be monitored.

o    When assessing for serum digoxin level, blood should be drawn after steady state is reached to allow proper equilibration between serum and tissue levels. Therefore, the level should be assayed just before the next daily dose. If not possible, at least 6 to 8 hours after the last dose should have elapsed regardless whether oral or IV preparation is being given. The serum level will be 10% to 25% lower after 24 hours as compared with 8 hours with once-daily dosing, but minor differences in serum level with twice-daily dosing at 8 or 12 hours after last dose.

o    The initial high levels of digoxin do not reflect the actual concentration at the site of action until a steady state of distribution occurs during chronic use. Serum level reflects pharmacologic effect when serum concentrations are in equilibrium with tissue concentrations.

o    The serum level of digoxin should not exceed 1.3 ng/mL. Higher levels may be necessary to control the ventricular rate in atrial fibrillation as compared with digoxin being given for inotropic support in heart failure; nevertheless, higher serum digoxin levels were associated with a higher mortality in the Digitalis Investigation Group study.

o    Digoxin competes with amiodarone and quinidine. These two drugs are the most significant in increasing the digoxin levels. Therefore, the dose of digoxin should generally be halved when giving digoxin in combination with these drugs. Digoxin level should be monitored.

o    Digitalis has a tendency to increase automaticity and at the same time cause AV block; thus, automatic atrial tachycardia with 2:1 AV block is usually a manifestation of digitalis toxicity. Other arrhythmias associated with digitalis include ventricular ectopy, bidirectional ventricular tachycardia, sinus dysfunction, and all degrees of AV block.

o    Digoxin is not removed by dialysis; therefore, dialysis or exchange transfusion is not effective in treating digitalis toxicity. Most of the drug is bound to tissue and does not circulate freely.

o    Digibind is the antidote for digitalis toxicity. This is given intravenously and the dose is calculated according to the serum digoxin level. Digibind should be given only for life-threatening arrhythmias such as paroxysmal atrial tachycardia with block or significant bradyarrhythmias from AV block or sinus dysfunction.

o    Digibind is excreted by the kidneys as a digoxin-Digibind complex. When there is renal failure, the Digibind-digoxin complex may not be excreted or excretion may be significantly delayed. Thus, digitalis toxicity may recur after 72 hours because the effect of Digibind in binding be effective after that time.

o    The serum level of digoxin does not reflect the digoxin level after Digibind is given. Thus it is not possible to reassess digoxin toxicity after the antidote is given.

o    Slowing of the ventricular rate in patients with heart failure is more pronounce when digoxin is combined with a beta blocker (such as carvedilol) compared with the use of either drug alone.

o    Avoid electrical cardioversion if patient is on digoxin. If cardioversion is necessary, use lower current during cardioversion.

Diltiazem (Cardizem Injectable or Lyo-Jet Syringe): Pregnancy Category C

·         Indication: Conversion of paroxysmal supraventricular tachycardia to normal sinus rhythm, control of ventricular rate in atrial flutter, or fibrillation or in patients with multifocal atrial tachycardia.

·         Mechanism of action: Diltiazem, like verapamil, is a nondihydropyridine calcium channel blocker. It increases refractoriness of the AV node and can slow down the rate of the sinus node. It is a negative inotropic agent and can decrease myocardial contractility. It relaxes vascular smooth muscle resulting in peripheral vasodilatation.

·         Intravenous dose:

o    Initial bolus of 0.25 mg/kg (approximately 15 to 20 mg for a 70-kg patient) given slowly IV over 2 minutes. If not effective, a second dose of 0.35 mg/kg (approximately 20 to 25 mg for a 70-kg patient) may be given after 15 minutes, slowly, IV. The heart rate and blood pressure should be monitored during IV infusion.

o    To prolong the half-life of diltiazem and maintain control of ventricular rate in atrial fibrillation, an intravenous drip of 5 to 15 mg/hour should be started after giving the intravenous bolus.

o    Additional small boluses of ≤5 mg may be given intermittently during infusion if ventricular rate is not optimally controlled with maintenance IV infusion.

·         Other things you should know about diltiazem:

o    Diltiazem is just as effective as verapamil in converting PSVT to normal sinus rhythm, but is less negatively inotropic and may be used cautiously in patients with left ventricular dysfunction who are not hemodynamically decompensated.

o    The elimination half life of IV diltiazem is approximately 3 to 5 hours and is shorter than verapamil. Because of the relatively short half-life, a maintenance infusion is necessary when controlling the heart rate in atrial fibrillation. The maintenance infusion dose is 5 to 15 mg/hour. While on maintenance infusion, an oral dose should be started within 3 hours after the initial IV dose so that the infusion can be discontinued within 24 hours unless the patient can not take oral medications.

o    Although IV diltiazem may be tolerable in patients with atrial arrhythmias with mild heart failure, they should not be given to patients with acutely decompensated heart failure. Oral nondihydropyridine calcium channel blockers, including oral diltiazem, should not be given when there is left ventricular dysfunction. It should not be given for wide complex tachycardia of unknown origin, sick sinus syndrome, or atrial fibrillation associated with WPW syndrome.

o    Severe bradycardia and hypotension may occur when diltiazem is combined with beta blockers.

Dobutamine (Dobutrex): Pregnancy Category B

·         Indication: Dobutamine is indicated for the treatment of heart failure. It is also used off-label for the treatment of bradyarrhythmias and heart block not responsive to atropine, especially in treatment of infranodal AV block.

·         Mechanism of action: Dobutamine is a synthetic catecholamine with predominantly β1 and slight β2 adrenergic properties and mild to moderate α properties.

·         Dosing: Given as IV infusion with an initial dose of 1 mcg/kg/minute and increased to 2.5 to 5.0 mcg/kg/minute. This can be titrated gradually every 3 minutes according to heart rate to a maximum dose of 20 mcg/kg/minute. Higher doses up to 40 mcg/kg/minute can be given but are usually associated with atrial and ventricular arrhythmias. The use of dobutamine for AV block and bradyarrhythmias should only be temporary, before a temporary pacemaker can be inserted. The drug very often comes in premix infusion of 500 mg in 250 mL D5W.

·         Other things you should know about dobutamine:

o    Dobutamine has a short elimination half-life of 2 minutes and should be given as a continuous intravenous infusion.

o    It is indicated for the treatment of patients with low cardiac output or heart failure. It is also used off-label as temporary measure for treatment of symptomatic bradyarrhythmia before a pacemaker can be inserted. It is the preferred agent in infranodal AV block with wide escape complexes, because atropine is not effective when AV block is infranodal. It can also be tried in patients with symptomatic bradyarrhythmias not responsive to atropine before a pacemaker can be inserted.

o    The chronotropic effect of dobutamine is not as potent as dopamine or isoproterenol and is more often used as an inotropic agent in acute heart failure rather than for its chronotropic effect in patients with bradyarrhythmias or AV block. If dobutamine is not effective in increasing the heart rate, isoproterenol should be given instead.

Epinephrine: Pregnancy Category C

·         Indication: Epinephrine is indicated for cardiac arrest due to VF or pulseless VT. It is also indicated for the treatment of anaphylaxis and syncope from complete heart block or hypersensitive carotid sinus and for the treatment of asthma.

·         Mechanism of action: The drug is a sympathomimetic catecholamine with α, β1, and β2-adrenergic activity. It has the most potent α-adrenergic effect resulting in intense vasoconstriction, which can result in coronary and cerebral perfusion pressure during cardiopulmonary resuscitation. It is this intense α-adrenergic effect that is useful in cardiac arrest.

·         Dose: According to the 2005 American Heart Association guidelines for cardiopulmonary resuscitation, the dose of epinephrine in cardiac resuscitation is 1 mg given by intravenous or if not possible by intraosseous administration every 3 to 5 minutes. Higher doses may be given to overcome beta blocker or calcium channel overdose. If intravenous or intraosseous administration is not possible during resuscitation, it may be given intratracheally at a dose of 2 to 2.5 mg. Higher doses of epinephrine has not been shown to be more effective than standard doses during cardiopulmonary resuscitation.

o    For anaphylaxis, the drug is given intramuscularly 0.3 mg, which may be repeated if needed. It may also be given subcutaneously at a dose of 0.2 to 1.0 mg.

o    For asthma, the drug is given subcutaneously 0.2 to 0.5 mg. If needed for severe attacks, a second and third dose may be given every 20 minutes for a maximum of three doses.

Esmolol (Brevibloc): Pregnancy Category C

·         Indication: Esmolol is indicated for the conversion of SVT to normal sinus rhythm and control of ventricular rate in patients with atrial fibrillation or atrial flutter. Also indicated for the treatment of inappropriate, noncompensatory sinus tachycardia and hypertension that occur during induction and tracheal intubation, during surgery or emergence from anesthesia and postoperative period.

·         Mechanism of action: Esmolol is a selective β1 blocker.

·         Dose: The dose of esmolol is quite complicated because the drug is very short acting and may need frequent retitration:

o    The initial IV loading dose is 0.5 mg/kg over 1 minute followed by an infusion of 50 mcg/kg/minute for 4 minutes. If effective, the infusion rate is continued. The dose can be titrated depending on the desired ventricular rate during atrial flutter or fibrillation. Thus, the maintenance infusion rate can be increased from 50 to 100 mcg/kg/minute, and after 4 or more minutes to 150 mcg/kg/minute and subsequently up to a maximum of 200 mcg/kg/minute.

o    If the first bolus is not effective, another option is to give a second bolus of 0.5 mg/kg over 1 minute and increase infusion rate by 50 mcg for an infusion rate of 100 mcg/kg/minute for 4 minutes. If effective, continue the infusion rate.

o    If not effective, give a third and final bolus of 0.5 mg/kg over 1 minute and increase infusion rate by 50 mcg for an infusion rate of 150 mcg/kg/minute for 4 minutes. The infusion rate can be increased by 50 mcg/kg/minute to a maximum of 200 mcg/kg/minute.

o    The usual maintenance infusion rate is 50 to 200 mcg/kg/minute. Maintenance infusion can be given for 24 hours if necessary; however, the patient should be monitored for hypotension and bradycardia.

o    A higher maximum maintenance infusion dose of 50 to 300 mcg/kg/minute may be given for the treatment of hypertension.

·         Other things you should know about esmolol:

o    Esmolol has a very short half-life of only 2 to 9 minutes. The drug is too short-acting, making routine use for control of ventricular rate in atrial flutter and fibrillation difficult to maintain in the medical intensive care unit, more especially when long-term control is necessary. The short half-life, however, may be advantageous to patients who develop arrhythmia during the perioperative and immediate postoperative period where immediate and short-term control is all that is needed.

o    Esmolol is also indicated for hypertension occurring during the perioperative and immediate postoperative period. For control of hypertension, a higher maintenance infusion dose of up to 250 to 300 mcg/kg/minute may be necessary (see dosing). It can also be given as treatment for noncompensatory sinus tachycardia, which, according to the judgment of the physician, may be inappropriate and needs to be controlled.

o    Dosing is not affected by hepatic or renal disease.

o    Can cause slowing of the sinus node, thus the agent should be given cautiously when there is history of sick sinus syndrome or previous bradycardia.

o    The maximum infusion dose should not exceed 200 mcg/kg/minute and the agent may be continued as an infusion up to 24 hours.

Ibutilide (Corvert): Pregnancy Category C

·         Indication: Rapid conversion of atrial flutter or atrial fibrillation to normal sinus rhythm

·         Mechanism of Action: Ibutilide is a Class III antiarrhythmic agent. Class III agents block the potassium channel and therefore prolong the duration of the action potential. Conduction is slowed and atrial and ventricular refractoriness are prolonged. The effect of ibutilide is different when compared to other Class III agents because it prolongs the action potential duration by slowing the inward flow of sodium during repolarization in contrast to most type III agents, which slow the outward flow of potassium.

·         Dosing:

o    Before converting atrial flutter or atrial fibrillation to normal sinus rhythm with ibutilide, any patient known to have the arrhythmia for more than 48 hours should first be adequately anticoagulated for at least 3 weeks before attempting conversion to normal sinus rhythm. However, if a more immediate cardioversion seems necessary, a trans-esophageal echocardiogram should be performed to exclude thrombi in the atria or left atrial appendage. Cardioversion may then be carried out under adequate anticoagulation if no thrombi are demonstrated.

o    For patients weighing ≥60 kg, the dose of ibutilide is 1 mg given intravenously for 10 minutes. For patients weighing <60 kg, the dose is 0.01 mg/kg or a maximum of 0.6 mg. One mg of ibutilide is available as a 10-mL preparation and is injected at a rate of 1 mL/minute. The 10-mL preparation (1 mg) can be injected directly IV (10 minutes) without dilution. It could also be diluted to a larger volume of 50 mL and infused intravenously for 10 minutes.

o    If the arrhythmia has not converted 10 minutes after injection, the same dose can be repeated with the same rate of administration. There is a 50% to 70% chance for atrial flutter and 30% to 50% chance for atrial fibrillation to convert to normal sinus rhythm almost immediately after the drug is administered. If the arrhythmia has not converted after the second dose, no further injections should be given.

o    For postcardiac surgery patients weighing <60 kg, 0.5 mg (0.005 mg/kg per dose) given as a single or double dose, was effective for atrial fibrillation and flutter.

·         Other things you should know about ibutilide:

o    Sustained polymorphic ventricular tachycardia (PVT) requiring cardioversion can occur in approximately 1.7% of patients receiving intravenous ibutilide. This arrhythmia can be fatal if not immediately recognized. PVT may or may not be associated with baseline QTc prolongation; the tachycardia is called torsades de pointes.

o    The initial episode of PVT can occur up to 40 minutes after initial infusion, although recurrence of PVT can occur up to 3 hours after initial infusion.

o    Sustained PVT is more common in patients with low ejection fraction or patients with history of congestive heart failure, especially where there is baseline QT prolongation. The drug, therefore, should not be given to patients who are hemodynamically unstable or in heart failure, in patients with recent myocardial infarction or angina, patients with electrolyte and blood gas abnormalities including patients with baseline QT prolongation, or those who are metabolically deranged.

o    Nonsustained PVT occurred in an additional 2.7% of patients and nonsustained monomorphic VT in 4.9%.

o    Cardiac monitoring should be continued for at least 4 hours after infusion or until QTc is back to baseline. Longer monitoring is required for patients with hepatic dysfunction. Prolongation of the QT interval is related to the dose and infusion rate. Patients developing PVT should be monitored for a longer period.

o    The hemodynamic effect of the drug is similar in patients with systolic dysfunction and those without. No significant effect in cardiac output or pulmonary wedge pressure has been noted. The drug has not been shown to increase the duration of the QRS complex.

o    When giving ibutilide, the QTc interval should preferably be <440 milliseconds and the serum potassium at least 4.0 mEq/L. Patients with QTc >440 milliseconds and potassium <4.0 mEq/L were not allowed to participate when clinical trials with ibutilide were conducted.

o    Although torsade is the most common arrhythmia associated with the drug, sinus arrest and complete asystole can occur during conversion from atrial flutter or atrial fibrillation to normal sinus rhythm especially in patients with sick sinus syndrome.

o    The drug is more effective in atrial flutter than in atrial fibrillation. Approximately 53% of patients with atrial flutter will convert with the first 1 mg dose and 70% after the second dose. In atrial fibrillation, approximately 22% will convert with the first dose and 43% after the second dose. Conversion occurred within 30 minutes after the start of infusion. This is in contrast to intravenous sotalol (1.5 mg/kg), where only 18% of patients with atrial flutter and 10% with atrial fibrillation converted during clinical trials with the drug.

o    If atrial flutter or atrial fibrillation has not converted after 90 minutes after the infusion is completed, the patient can be electrically cardioverted if appropriate. Other antiarrhythmic agents can also be started 4 hours after the infusion is completed.

o    Patients with more recent onset atrial flutter or atrial fibrillation (within 30 days) have a higher chance of conversion to normal sinus rhythm compared with patients whose arrhythmias were of longer duration. The efficacy of ibutilide has not been tested in patients with atrial flutter or atrial fibrillation longer than 90 days in duration.

Isoproterenol (Isuprel): Pregnancy Category C

·         Indication: As a temporizing measure for the treatment of heart block or symptomatic bradyarrhythmias when atropine or dobutamine has failed. It is also given as a temporizing measure for the treatment of torsades de pointes before a pacemaker can be inserted.

·         Mechanism of Action: Isoproterenol is a β-adrenergic agonist with very potent β1 and β2 properties. Similar to other β-adrenergic agents, it increases cyclic AMP by stimulating adenyl cyclase, eventually increasing intracellular calcium. It has very potent chronotropic and inotropic properties and prevents bronchospasm.

·         Dose: Given as an intravenous infusion at 2 to 10 mcg/minute titrated according to the heart rate, It is usually prepared by diluting 1 mg of isoproterenol to 500 mL D5W, resulting in a concentration of 2 mcg/mL.

·         Other things you should know about isoproterenol:

o    Isoproterenol is the drug of choice for the temporary treatment of infranodal AV block. It shortens the refractory period of the AV node and enhances AV conduction. It also increases automaticity allowing latent pacemakers to become manifest. Because of its serious side effects, it is potentially dangerous to use routinely and should be used cautiously only as a temporizing measure for the treatment of heart block and bradyarrhythmias before a temporary pacemaker can be inserted or after atropine or dobutamine has failed.

o    Isoproterenol is a very potent β1 - and β2-adrenergic agent. It increases automaticity not only of the sinus node but all cells with pacemaking potential, resulting in ectopic rhythms that may dominate over that of the sinus node. It can cause ectopic atrial tachycardia, atrial flutter, atrial fibrillation, and ventricular tachycardia or fibrillation even in patients with structurally normal hearts.

o    Isoproterenol increases inotropicity and cardiac output and markedly increases oxygen consumption. It can provoke ischemia in patients with coronary disease and can provoke arrhythmias especially in patients with left ventricular dysfunction.

o    Torsades de pointes: Isoproterenol may be used as a temporizing procedure in patients with bradycardia dependent torsades de pointes before a temporary pacemaker can be inserted.

o    Isoproterenol should be given at the lowest dose possible. Because it enhances myocardial oxygen consumption, it can expand infarct size and cause complex ventricular and supraventricular arrhythmias.

Labetalol (Normodyne): Pregnancy Category C

·         Indication: Intravenous labetalol is indicated for the emergency treatment of hypertension. It does not carry indication for the treatment of cardiac arrhythmias.

·         Mechanism: Labetalol is a nonspecific beta blocker with α1-, β1- and β2-adrenergic receptor blocking properties. In addition, it also has intrinsic sympathomimetic activity.

·         Dose: For the treatment of hypertension, 10 mg is given IV push over 1 to 2 minutes. The dose is repeated or doubled every 10 minutes if needed to a maximum dose of 150 mg. Another option is to give an initial bolus followed by an infusion of 2 to 8 mg/minute.

Lidocaine (Xylocaine HCL): Pregnancy Category B

·         Indication: For acute suppression of VT or VF.

·         Mechanism of Action: Lidocaine is Class IB antiarrhythmic agent. It blocks the sodium channel but has no effect on potassium channel. It does not prolong and may even shorten action potential duration and effective refractory period of the His-Purkinje system.

·         Dosing:

o    In cardiac arrest, an initial bolus of 1.0 to 1.5 mg/kg is given. The higher dose is given only for ventricular fibrillation or pulseless VT after defibrillation and epinephrine has failed.

o    For refractory VT or VF, an additional bolus of 0.5 to 0.75 mg/kg is given IV over 3 to 5 minutes. The rate should not exceed 50 mg/minute. Lidocaine is distributed rapidly out of the plasma in <10 minutes. The initial dose therefore is only transiently therapeutic and additional boluses have to be given repeatedly every 5 to 10 minutes, as needed, for a maximum total loading dose of 3 mg/kg over 1 hour. The loading dose should be decreased in patients with heart failure.

o    The initial loading dose is followed by an IV infusion of 1 to 4 mg/minute to maintain therapeutic blood levels. Maintenance infusion should be adjusted to a lower rate in patients with heart failure and liver disease.

o    The volume of distribution does not reach steady state until after 8 to 10 hours or even longer, up to 24 hours in patients with liver disease, heart failure, or low output states.

·         Other things you should know about lidocaine:

o    Lidocaine does not prolong action potential duration and therefore does not prolong the QT interval. The drug is useful in patients with normal or prolonged QT intervals or patients with monomorphic or polymorphic VT.

o    Is primarily indicated for patients with ischemic VT/VF and is the drug of choice for VT/VF associated with acute myocardial infarction.

o    Unlike most antiarrhythmic agents, lidocaine can be used in patients with impaired left ventricular function.

o    It is not effective in blocking the AV node and therefore is not useful in supraventricular arrhythmias. It may even enhance AV conduction, which can result in 1:1 AV conduction in atrial flutter.

o    Lidocaine as well as its metabolites undergoes degradation through the CYP 450 3A4 pathway. Continuous infusion of lidocaine at the same dose for 24 to 48 hours increases its half-life and generally leads to toxicity.

o    Symptoms of toxicity are usually from central nervous system involvement, which include seizures, dysarthria or slurred speech, muscle twitching, drowsiness, altered consciousness, or even coma.

o    Lidocaine should generally be discontinued 12 hours after the arrhythmia has been successfully suppressed unless there is an indication to infuse the medication for a longer period.

o    After the infusion is terminated, plasma levels slowly decline over several hours. If the medication is no longer needed, the medication can be discontinued outright without tapering the dose.

o    Therapeutic blood levels can be monitored, which ranges from 1.5 to 5 mcg/mL.

Magnesium Sulfate: Pregnancy Category C

·         Indication: Replacement therapy in the presence of magnesium deficiency. Also used in the treatment of torsade de pointes characterized by polymorphous VT with prolonged QT interval.

·         Mechanism of Action: Severe magnesium deficiency can cause cardiac arrhythmias including ventricular fibrillation and sudden cardiac death. Hypomagnesemia also prevents the correction of potassium deficiency.

·         Dosing:

o    For refractory VF: In emergent conditions where there is refractory VF associated with magnesium deficiency, dilute 1 to 2 g magnesium sulfate in 100 mL D5W and inject IV over 1 to 2 minutes.

o    For torsade: Even in the absence of magnesium deficiency, give a loading dose of 1 to 2 g mixed with 50 to 100 mL D5W injected IV over 5 to 60 minutes, depending on the urgency of administration. Follow with a continuous IV infusion of 0.5 to 1.0 g/hour.

o    For magnesium deficiency: Dilute 5 g in 1 L D5W, 0.9% NaCl or lactated Ringers solution and given as a continuous infusion. Maximum concentration is 4 g in 250 mL given IV over 3 hours. Dose should not exceed a total of 30 to 40 g in adults and rate should not exceed 50 mg/minute.

Metoprolol (Lopressor): Pregnancy Category C

·         Indication: Metoprolol is indicated for reduction of mortality in acute myocardial infarction. It is also indicated for angina and hypertension. It is effective as an antiarrhythmic agent in supraventricular arrhythmias and reduces incidence of ventricular tachycardia/fibrillation in patients with acute myocardial infarction.

·         Mechanism of action: Metoprolol is a cardioselective β1-adrenergic blocking agent.

·         Dose: The initial IV dose is 5 mg slowly over 5 minutes. May be repeated every 5 minutes if well tolerated for a total of three doses or 15 mg over 15 minutes. If maintenance oral dose is necessary and patient is postoperative or NPO, give IV piggyback 20 mg over 2 hours. This is equal to 50 mg of oral metoprolol. The IV dose is followed by an oral dose of 50 mg BID × 24 hours, then 100 mg BID.

·         Other things you should know about metoprolol:

o    The most recent 2007 focused update of the American College of Cardiology/American Heart Association 2004 guidelines for the management of ST elevation MI raises doubt about the safety of IV metoprolol or similar beta blockers based on the results of a large clinical trial (Clopidogrel and Metoprolol in Myocardial Infarction). Although metoprolol IV has been shown to decrease reinfarction and ventricular fibrillation in this study, there were more episodes of cardiogenic shock. Thus, the use of metoprolol IV is reasonable only when hypertension is present and the patient does not have any of the following findings:

§  Signs of heart failure

§  Low output state

§  Increased risk for cardiogenic shock (age >70 years, systolic blood pressure <120 mm Hg, sinus tachycardia >100 beats per minute, or heart rate <60 beats per minute and increased time since onset of acute MI).

§  Contraindications to beta blockade (PR >0.24 second, second- or third-degree AV block, reactive airway disease or active asthma).

o    The long-term use of beta blockers remains a Class I recommendation when given orally within 24 hours to patients who do not have contraindications and are not high risk for hypotension or cardiogenic shock.

o    In patients with left ventricular dysfunction, oral beta blocker therapy is recommended but should be gradually titrated.

Norepinephrine: Pregnancy Category C

·         Indication: Cardiac arrest and hypotension

·         Mechanism of Action: Norepinephrine is a sympathomimetic agent with both alpha and beta adrenergic activity.

·         Dosing: The initial dose is 0.5 to 1 mcg/minute given IV titrated to 8 to 30 mcg/minute. The dose is adjusted according to the blood pressure.

·         Other things you should know about norepinephrine:

o    The solution should be given IV using a large vein. Extravasation may cause sloughing and necrosis because of its α-adrenergic effect resulting in vasoconstriction. After extravasation occurs, the area should be immediately injected with 10 to 15 mL of saline containing 10 mg of phentolamine.

Procainamide: Pregnancy Category C

·         Indication: Effective for both supraventricular and ventricular arrhythmias. It is indicated for conversion of atrial flutter and atrial fibrillation to normal sinus rhythm, for control of ventricular rate in atrial fibrillation in the setting of WPW syndrome, and for stable monomorphic wide complex tachycardia that may be ventricular or supraventricular.

·         Mechanism of Action: Procainamide is a type IA antiarrhythmic agent (Class I agents inhibit the fast inward sodium channel causing a decrease in the maximum depolarization rate during phase 0 of the action potential). It decreases automaticity by decreasing the slope of spontaneous (phase 4) depolarization. Procainamide also inhibits the potassium channel and therefore prolongs the duration of the action potential. Conduction velocity in the atrium, AV node, His-Purkinje system, and ventricles is prolonged. The drug is metabolized to N-acetylprocainamide (NAPA), which is also an effective antiarrhythmic agent but has Class III effects. Class III drugs prolong the action potential duration as well as refractoriness of cardiac tissues.

·         Dosing:

o    Procainamide is given IV at an infusion rate of 20 mg/minute. The dose should not exceed 17 mg/kg. The infusion is given until the arrhythmia is suppressed or toxic complications from the drug is manifested such as widening of the QRS complex by 50% when compared with baseline, prolongation of the QT interval or hypotension occurs.

o    When more rapid infusion is needed, an alternative is to give intravenous boluses of ≤100 mg for 3 minutes every 5 minutes. The drug can also be given at a faster infusion rate of 50 mg/minute, to a total dose of 17 mg/kg during cardiac resuscitation.

o    Infusion is maintained at 1 to 4 mg/minute but should be reduced if there is renal dysfunction.

·         Other things you should know about procainamide:

o    Is effective for both atrial and ventricular arrhythmias.

o    The drug should not be given to patients with prolonged QT interval.

o    Procainamide is negatively inotropic and is proarrhythmic and should not be given to patients with congestive heart failure or patients with systolic left ventricular dysfunction (ejection fraction ≤40%).

o    Hypotension can be precipitated if the drug is injected too rapidly.

o    Unlike quinidine, another type IA antiarrhythmic agent, procainamide does not increase digoxin levels.

o    The drug is metabolized to NAPA, which is also an effective antiarrhythmic agent. When procainamide blood levels are checked, NAPA levels should be included. Therapeutic level of procainamide is 4 to 8 mcg/mL and for NAPA 7 to 15 mcg/mL.

o    The drug is mainly excreted through the kidneys unchanged with a half-life of approximately 3 hours. Excretion is delayed when there is renal dysfunction or heart failure.

o    Blood levels should be checked when there is renal dysfunction or maintenance infusion exceeds 2 mg/minute or infusion exceeds 48 hours.

o    Can cause drug induced lupus when oral therapy is continued for prolonged periods.

Propranolol (Inderal): Pregnancy Category C

·         Indication: Propranolol has approved indications for hypertension, angina pectoris, acute myocardial infarction, and treatment of cardiac dysrhythmias including conversion of SVT to normal sinus rhythm.

·         Mechanism: Propranolol is a nonselective beta blocker with β1- and β2-adrenergic blocking properties.

·         Dose: Approximately 1 to 3 mg is initially given. IV administration should not exceed 1 mg/minute. Additional doses may be repeated after 2 minutes if needed. The total IV dose should not exceed 10 mg administered in three equal parts. The total dose can also be given IV piggyback over 10 to 15 minutes. The IV dose is followed by a maintenance oral dose of 180 to 320 mg daily in divided doses.

·         Other things you should know about propranolol:

o    The elimination half-life of propranolol is 4 hours. After the initial dose, additional IV doses should not be given until after 4 hours after the last dose.

o    The drug is eliminated by hepatic metabolism.

Sotalol: Pregnancy Category B

·         Indication:

o    Sotalol is indicated in converting atrial fibrillation to normal sinus rhythm in patients with WPW syndrome when the duration of the atrial fibrillation is ≤48 hours.

o    It is also indicated for monomorphic ventricular tachycardia.

·         Mechanism of action: Sotalol is a Class III antiarrhythmic agent. Similar to amiodarone, it prolongs action potential duration and increases refractoriness of atrial and ventricular myocardium. It also has nonselective beta blocking properties.

·         Dosing: The dose is 1 to 1.5 mg/kg given IV at 10 mg/minute.

·         Other things you should know about sotalol:

o    The intravenous preparation of sotalol is not available in the United States.

o    According to the American College of Cardiology/American Heart Association/European Society of Cardiology 2006 guidelines for the management of patients with atrial fibrillation, sotalol is not effective for conversion of atrial fibrillation to sinus rhythm but is effective for maintenance of sinus rhythm and is used for preventing recurrence of atrial fibrillation after the patient has converted to normal sinus rhythm.

o    In patients with monomorphic VT, sotalol should be given only when left ventricular systolic function is preserved.

o    Sotalol has beta blocking properties. It should not be given to patients who are already on beta blockers.

o    The intravenous infusion can cause bradycardia and hypotension. Sotalol is also proarrhythmic and can cause torsade de pointes.

Vasopressin (Pitressin): Pregnancy Category C

·         Indication: VT/VF. Intended as an alternative to epinephrine during cardiac resuscitation.

·         Mechanism of action: Vasopressin is a non-adrenergic peripheral vasoconstrictor that is naturally present in the body. It is an antidiuretic hormone. The agent becomes a powerful peripheral vasoconstrictor when given in much higher doses than normally present in the body. It does not have beta adrenergic activity and directly stimulates non-adrenergic smooth muscle receptors. It mimics the positive effects but not the adverse effects of epinephrine and has a longer half-life of 10 to 20 minutes compared with epinephrine, which is 3 to 5 minutes.

·         Dosing: A one-time bolus injection of 40 units given IV during cardiac resuscitation for VT/VF. This substitutes for epinephrine during resuscitation for cardiac arrest, although epinephrine can still be given in repeated doses if necessary after 10 to 20 minutes if vasopressin is not effective.

·         Other things you should know about vasopressin:

o    Vasopressin is a powerful non-adrenergic vasoconstrictor given as a one-time dose of 40 units. It is effective even in the presence of severe acidosis, which commonly occurs during cardiac resuscitation.

o    May be effective in asystole and pulseless electrical activity

Verapamil (Isoptin): Pregnancy Category C

·         Indication: Conversion of paroxysmal supraventricular tachycardia to normal sinus rhythm, control of ventricular rate in atrial flutter, or fibrillation or in patients with multifocal atrial tachycardia.

·         Mechanism of action: Verapamil is a nondihydropyridine calcium channel blocker that increases refractoriness of the AV node. It can also slow down the rate of the sinus node. It is a negative inotropic agent and can decrease myocardial contractility resulting in heart failure in patients with left ventricular dysfunction. It is also a peripheral vasodilator and can cause hypotension.

·         Intravenous dose: The drug should not be given to patient with left ventricular dysfunction. Give slowly IV 2.5 to 5 mg over 2 minutes, longer in elderly patients, under continuous electrocardiogram and blood pressure monitoring. If not effective, and no adverse event is noted, repeat with another dose of 5 to 10 mg every 15 to 30 minutes to a maximum dose of 20 mg. Another option is to give 5-mg boluses every 15 minutes to a maximum dose of 30 mg.

·         Other things you should know about verapamil:

o    Nondihydropyridine calcium channel blockers such as verapamil and diltiazem are very effective agents in converting PSVT to normal sinus rhythm. They are the next agents that should be used for conversion of PSVT to normal sinus rhythm if adenosine is not effective or is contraindicated.

o    Verapamil is a vasodilator and is negatively inotropic. It should not be given to patients with left ventricular dysfunction or patients with congestive heart failure.

o    Verapamil should be given only to paroxysmal supraventricular tachycardia with narrow complexes or supraventricular tachycardia with wide QRS complexes with normal left ventricular function. When there is wide complex tachycardia and the diagnosis of the tachycardia is uncertain, verapamil should not be given. If the wide complex tachycardia turns out to be ventricular, the administration of verapamil may cause severe hypotension or even death.

o    Intravenous hydration and calcium chloride or calcium gluconate IV may be given to counteract the hypotensive effect of verapamil or diltiazem without diminishing its antiarrhythmic effect.