Pharmacotherapeutics for Advanced Practice A Practical Approach THIRD EDITION (2)

Document Content and Description Below

TABLE 23.2 Recommended Order of Treatment for Arrhythmias (Continued ) Order Agents Comments Sustained Ventricular Tachycardia First line Hemodynamically unstable patient: synchronized DCC (100 ... J, biphasic). Hemodynamically stable patient: IV procainamide, IV amiodarone, or IV sotalol Premedicate whenever possible when performing DCC. Correct reversible causes. Second line Hemodynamically stable patient: IV lidocaine; synchronized DCC should be considered if AAD therapy fails. Once arrhythmia acutely terminated, patient should be considered for ICD placement. If patient refuses or is not a candidate for an ICD, PO amiodarone can be considered. If frequent shocks occur in patients with an ICD, PO amiodarone and β-blocker combination therapy or sotalol monotherapy can be used. Pulseless Ventricular Tachycardia/ Ventricular Fibrillation First line Start CPR, establish an airway, and deliver one shock (biphasic defibrillator: 120–200 J; monophasic defibrillator: 360 J); immediately resume CPR for 2 min, then check rhythm. Correct reversible causes. Second line If patient remains in pulseless VT/VF, deliver one shock and then immediately resume CPR; if pulseless VT/VF persists after at least one shock and CPR, give vasopressor therapy (epinephrine 1 mg IV push/IO every 3–5 min through pulseless VT/VF episode or vasopressin 40 units IV push/IO [to replace first or second dose of epinephrine]) (give drugs during CPR; do not interrupt CPR to give drugs); immediately resume CPR for 2 min, then check pulse. Third line If patient remains in pulseless VT/VF, deliver one shock and then immediately resume CPR; if pulseless VT/ VF persists despite defibrillation, CPR and vasopressor therapy, consider AAD therapy (IV amiodarone; lidocaine may be used if IV amiodarone unavailable) (give drugs during CPR; do not interrupt CPR to give drugs); consider IV magnesium sulfate if torsades de pointes present; immediately resume CPR for 2 min, then check pulse. Bradycardia First line Patient with stable bradycardia: Close observation Patients with bradycardia and signs/symptoms of poor perfusion (e.g., altered mental status, chest pain, hypotension, shock): Immediately administer IV atropine (0.5 mg every 3 to 5 min, up to 3 mg total dose. If the atropine is ineffective, transcutaneous pacing or sympathomimetic continuous infusion (dopamine or epinephrine) should be initiated. Correct reversible causes. Second line If drug therapy and transcutaneous pacing are ineffective, transvenous pacing should be utilized. AV, atrioventricular; CPR, cardiopulmonary resuscitation; DCC, direct current cardioversion; ICD, implantable cardioverter-defibrillator; INR, International Normalized Ratio; IV, intravenous; J, joules; LV, left ventricular; LVEF, left ventricular ejection fraction; MI, myocardial infarction; NSVT, nonsustained ventricular tachycardia; PO, oral; PSVT, paroxysmal supraventricular tachycardia; PVC, premature ventricular contraction; TEE, transesophageal echocardiogram; VF, ventricular fibrillation; VT, ventricular tachycardia Arcangelo_Chap23.indd 322 10/8/2011 1:52:29 PM CHAPTER 23 | ARRHYTHMIAS 323 in those patients with risk factors for thromboembolism, a TEE-guided approach (see above) can be considered. Those patients with risk factors for thromboembolism should also be considered for at least 4 weeks of post-cardioversion anticoagulation therapy (Singer, et al., 2008). If the practitioner decides to proceed with pharmacologic cardioversion as the initial therapy, the selection of drug should be based on the patient’s LV systolic function. Pharmacologic cardioversion is most effective when initiated within 7 days of the onset of AF. The AADs with proven efficacy during this time frame include dofetilide, flecainide, ibutilide, propafenone, or amiodarone (oral or IV). The class Ia AADs, disopyramide, procainamide, and quinidine have limited efficacy or have been incompletely studied for this purpose. Sotalol is not effective for converting AF to SR. Although the use of single, oral loading doses of propafenone or flecainide is effective in restoring SR, these drugs should only be used in patients without underlying SHD. Ibutilide may also be considered in these patients. A patient’s ventricular rate should be adequately controlled with AV nodal-blocking drugs prior to administering a class Ic (or class Ia) AAD for cardioversion. In patients with SHD, propafenone, flecainide, and ibutilide should be avoided because of the increased risk of proarrhythmia. Instead, amiodarone or dofetilide should be primarily used in this patient population. In patients with AF present for more than 7 days, the only AADs with proven efficacy are dofetilide, amiodarone (oral or IV), and ibutilide. The selection of AAD therapy during this time frame should again be based on the presence of SHD (Fuster, et al., 2006). If the practitioner does not wish to proceed with cardioversion, an initial management strategy of ventricular rate control and anticoagulation is also reasonable. As previously stated, this strategy, whereby the patient is left in AF, has been shown to be an acceptable alternative to rhythm control for the chronic management of AF. The selection of an oral drug for chronic ventricular rate control is primarily based on the patient’s LV systolic function. In patients with normal LV systolic function (LVEF >40%), an oral b-blocker, diltiazem, or verapamil is preferred over digoxin (Fuster, et al., 2006). Digoxin can be added if adequate ventricular rate control cannot be achieved with one of these drugs. In patients with LVSD (LVEF of 40% or less), an oral b-blocker or digoxin is preferred because these drugs can also concomitantly be used to treat chronic HF. The nondihydropyridine CCBs should be avoided in patients with LVSD because of their potent negative inotropic effects. In patients with AF and stable HF symptoms (NYHA class II or III), the b-blockers carvedilol, metoprolol succinate, or bisoprolol should be used as first-line therapy because of their documented survival benefits in patients with HF (CIBIS II Investigators and Committees, 1999; MERIT-HF Study Group, 1999; Packer, et al., 1996). Other b-blockers should be avoided in these patients because their effects on survival in HF are unknown. Digoxin should be used as first-line therapy in patients with AF and decompensated HF (NYHA class IV) because b-blocker therapy may exacerbate HF symptoms. For patients with normal or depressed LV systolic function, oral amiodarone may also be considered if adequate ventricular rate control cannot be achieved with the use of b-blockers, nondihydropyridine CCBs, and/or digoxin (Fuster, et al., 2006). In patients with persistent AF who have no or acceptable symptoms and stable LV systolic function (LVEF greater than 40%), the goal heart rate should be less than 110 beats/minute at rest (Van Gelder, et al., 2010; Wann, et al., 2011). In patients with LVSD (LVEF of 40% or less), a stricter heart rate goal (less than 80 beats/minute) should be considered to minimize the potential harmful effects of a rapid heart rate response on ventricular function (Wann, et al., 2011). Assessing the patient’s risk of stroke becomes important for selecting the most appropriate antithrombotic regimen. The CHADS2 index is recommended for stroke risk stratification in patients with AF (Singer, et al., 2008). With this risk index, patients with AF are given 2 points if they have a history of a previous stroke or transient ischemic attack and one point each for being at least 75 years old, having hypertension, having diabetes, or having congestive HF (CHADS2 is an acronym for each of these risk factors). The points are added up, and the total score is then used to determine the most appropriate antithrombotic therapy for the patient. Patients with a CHADS2 score of at least 2 are considered to be at high risk for stroke and should receive warfarin (target INR: 2.5; range: 2.0 to 3.0). Patients with a CHADS2 score of 1 are considered to be at intermediate risk for stroke and should receive either warfarin (target INR: 2.5; range: 2.0 to 3.0) or aspirin 75–325 mg/d. However, because of its superior efficacy in preventing stroke, the use of warfarin is suggested over that of aspirin in this particular group of patients. Patients with a CHADS2 score of 0 are considered to be at low risk for stroke and should receive aspirin 75–325 mg/d. Dabigatran, an oral direct thrombin inhibitor, can also be considered as an alternative to warfarin for stroke prevention in patients with paroxysmal or persistent AF and risk factors for stroke or systemic embolism (Wann, et al., 2011). Patients with prosthetic heart valves, hemodynamically significant valvular disease, a creatinine clearance less than 15 mL/minute, or advanced liver disease are not appropriate candidates for dabigatran therapy. Please refer to Chapter 54 for a further discussion of anticoagulation in AF. Antithrombotic therapy should be considered for all patients regardless of whether a rate-control or rhythm- control strategy is initiated. In addition, antithrombotic therapy should be continued if SR is restored because of the potential for patients to have episodes of recurrent AF. Third-Line Therapy For those patients who remain symptomatic despite having adequate ventricular rate control or for those patients in whom adequate ventricular rate control cannot be achieved, it is reasonable to consider AAD therapy to maintain SR once they have been converted to SR. The selection of an AAD to maintain SR is primarily based on the presence of SHD (Wann, et al., 2011). (See Figure 23-2.) In patients without SHD, any oral class Ia, Ic, or III AAD can be used to maintain SR. Arcangelo_Chap23.indd 323 10/8/2011 1:52:29 PM 324 UNIT 4 | PHARMACOTHERAPY FOR CARDIOVASCULAR DISORDERS However, dronedarone, flecainide, propafenone, or sotalol should be considered as initial therapy in these patients because of their less toxic adverse effect profiles. Amiodarone or dofetilide can be used as alternative therapy if the patient fails or does not tolerate one of these initial AADs. In patients with any type of SHD, the class Ic AADs flecainide and propafenone should be avoided. In these patients, the selection of AAD therapy is based upon the type of SHD present. In patients with LVSD (LVEF of 40% or less), either oral amiodarone or dofetilide can be used. Both dronedarone and sotalol should be avoided in patients with LVSD because of the risk of increased mortality (dronedarone) or worsening HF (sotalol). In patients with coronary artery disease, sotalol, dofetilide, or dronedarone can be used as initial therapy. In these patients, sotalol and dronedarone should only be used if their LV systolic function is normal. Amiodarone can be considered as an alternative therapy in these patients if these AADs are not tolerated. In patients with significant LV hypertrophy, amiodarone is the drug of choice. For patients with permanent AF, a treatment strategy of ventricular rate control and anticoagulation should be used because the efficacy of AADs is extremely poor in this population. The oral drugs used for ventricular rate control are discussed in the “Second-Line Therapy” section. Patients with symptomatic episodes of recurrent AF who fail or do not tolerate at least one class I or III AAD may also be considered for radiofrequency catheter ablation (Calkins, et al., 2007). Paroxysmal Supraventricular Tachycardia (Due to Atrioventricular Nodal Reentrant Tachycardia) First-Line Therapy Hemodynamically unstable PSVT requires first-line therapy of synchronized DCC to restore SR and correct hemodynamic compromise. Unless contraindicated, patients with mild to moderate symptoms can be initially managed with vagal maneuvers (e.g., unilateral carotid sinus massage, Valsalva maneuver, facial immersion in ice water, and coughing). Figure 23-3 illustrates an algorithm for the management of PSVT due to AV nodal reentrant tachycardia. Second-Line Therapy If vagal maneuvers are unsuccessful or if PSVT recurs after successful vagal maneuvers, second-line therapy is AADs. The drug of choice for PSVT is adenosine (American Heart Association, 2010). Clinical studies have shown that adenosine is as effective as IV verapamil in initial conversion of PSVT. Adenosine does not produce hypotension to the degree that verapamil does, and it has a shorter half-life. If a total of 30 mg of adenosine does not successfully terminate PSVT, further doses of this agent are unlikely to be effective. Therefore, in patients with persistent PSVT, other AADs will need to be used. In these patients, IV diltiazem, verapamil, or a b-blocker can be used. If PSVT continues despite these treatment measures, the use of IV procainamide (LVEF >40%) or amiodarone (normal or depressed LVEF) can also be considered. Third-Line Therapy Third-line therapy focuses on the management of chronic PSVT. Chronic preventive therapy is usually necessary if the patient has either frequent episodes of PSVT that require therapeutic intervention or infrequent episodes of PSVT that are accompanied by severe symptoms. Radiofrequency catheter ablation is considered first-line therapy for most of these patients because of its effectiveness in preventing recurrence of PSVT and its relatively low complication rate. Drug therapy with oral diltiazem, verapamil, b-blockers, or digoxin can also be considered if the patient is not a candidate for or refuses to undergo radio-frequency catheter ablation. Premature Ventricular Contractions Occasional PVCs occur in most people and rarely compromise cardiac output or function. Correcting reversible causes such as an electrolyte imbalance sometimes eliminates these benign PVCs. Asymptomatic or minimally symptomatic PVCs in patients without associated heart disease carry little or no risk. PVCs in patients with heart disease were traditionally treated in the past. Decreasing the number and frequency of PVCs was thought to diminish the risk of sudden cardiac death. However, the results of the CAST showed that the use of AADs to suppress asymptomatic PVCs in patients after MI may increase mortality rates (CAST Investigators, 1989). Therefore, if patients with SHD have symptomatic PVCs, drug therapy should be limited to b-blockers. These agents have been associated with a reduction in mortality and sudden cardiac death in post-MI patients. These agents are also effective for suppressing symptomatic PVCs in patients without SHD. Asymptomatic PVCs do not require treatment. Nonsustained Ventricular Tachycardia Ventricular tachycardia that spontaneously terminates within 30 seconds is known as nonsustained VT. Given the poor survival of patients who experience cardiac arrest, it is essential to identify the most effective treatment strategies to prevent the initial episode of sustained VT or sudden cardiac death from occurring. The presence of nonsustained VT in patients without SHD is not associated with an increased risk of sudden cardiac death. Therefore, drug therapy is not necessary in these patients if they are asymptomatic. However, if these patients do become symptomatic, b-blocker therapy can be initiated. Post-MI patients (especially those with LVSD) who develop nonsustained VT are at increased risk for sudden cardiac death. For these patients, the selection of therapy is based on the patient’s LV systolic function. In post-MI patients with an LVEF greater than 35%, drug therapy is not necessary to treat the arrhythmia if they are asymptomatic. However, these patients should still chronically receive a b-blocker specifically to reduce mortality associated with the MI. b-blockers are also effective if these patients develop significant symptoms associated with the nonsustained VT. In post-MI patients with an LVEF of 35% or less, electrophysiologic testing is often Arcangelo_Chap23.indd 324 10/8/2011 1:52:29 PM CHAPTER 23 | ARRHYTHMIAS 325 performed when asymptomatic nonsustained VT occurs (Moss, et al., 1996; Buxton, et al., 1999). If sustained VT or VF is induced, an ICD is then recommended (Epstein, et al., 2008). In these patients, implantation of the ICD should be delayed until more than 40 days have elapsed since the MI occurred. If sustained VT or VF is not induced, a b-blocker or amiodarone can be initiated. Sustained Ventricular Tachycardia VT that persists for at least 30 seconds or that requires electrical or pharmacologic termination because of hemodynamic instability is known as sustained VT. Since sustained VT can degenerate into VF, the treatment goals are to terminate the VT acutely and then prevent recurrence of the arrhythmia. First-Line Therapy If the patient is hemodynamically unstable (i.e., severe hypotension, syncope, HF, or angina), immediate synchronized DCC is first-line therapy. If the patient is hemodynamically stable, IV amiodarone, IV procainamide, or IV sotalol can be considered (American Heart Association, 2010). Lidocaine can be used as alternative therapy. Synchronized DCC should be considered if AAD therapy fails. Second-Line Therapy Once the acute episode is terminated, measures should be taken to prevent recurrent episodes of VT. Based on the results of several trials, ICDs are clearly indicated as first-line therapy in patients with a history of sustained VT or VF (AVID Investigators, 1997; Connolly, et al., 2000; Kuck, et al., 2000, Epstein, et al., 2008). If the patient with an ICD experiences frequent discharges because of recurrent ventricular arrhythmias or new-onset supraventricular arrhythmias (e.g., AF), either amiodarone and a b-blocker or sotalol monotherapy can be used. For the patient who refuses or is not a candidate for an ICD, oral amiodarone should be used as an alternative therapy. Pulseless Ventricular Tachycardia/ Ventricular Fibrillation The majority of cases of sudden cardiac death can be attributed to VF. Sustained VT usually precedes VF and most commonly occurs in patients with ischemic heart disease. VF is usually not preceded by any symptoms and always results in a loss of consciousness and eventually death if not treated. Immediate treatment is essential in patients who develop VF or pulseless VT, since survival is reduced by 10% for every minute that the patient remains in the arrhythmia. It is imperative to identify and correct any potential reversible causes for the arrhythmia. For administration of drug therapy during an episode of pulseless VT/VF, while IV access is preferred, the guidelines recommend the intraosseous (IO) route as an alternative if IV access cannot be established (American Heart Association, 2010). IO access can be used not only for administration of drugs and fluids, but also for obtaining blood for laboratory monitoring. If neither IV nor IO access can be established, the endotracheal route can then be used for the administration of only certain agents (i.e., atropine, lidocaine, epinephrine, and vasopressin). Figure 23-4 illustrates an algorithm for the management of pulseless VT/VF. First-Line Therapy In patients with pulseless VT/VF, high-quality cardiopulmonary resuscitation (CPR) should be immediately initiated until a defibrillator or automated external defibrillator (AED) arrives (American Heart Association, 2010). High-quality CPR is considered to be delivery of at least 100 compressions per minute, with the depth of chest compressions being at least 2 inches. Each cycle of CPR involves delivering 30 chest compressions followed by two breaths. If a defibrillator or AED is not readily available, hands-only CPR (compressions only; no ventilations) should be provided if the bystander possesses no CPR training or is trained but lacks confidence in providing effective CPR with rescue breaths. If the bystander possesses CPR training and is confident in their ability to provide effective CPR with rescue breaths, conventional cycles of CPR (30 chest compressions followed by two breaths) should be delivered until a defibrillator or AED becomes available. Once an advanced airway (e.g., endotracheal tube) is placed, chest compressions should be delivered continuously at a rate of 100 compressions per minute without pausing for ventilation (should be provided by a separate individual at a rate of one breath every 6 to 8 seconds). Once a defibrillator or AED arrives, defibrillation should be administered immediately. With regard to defibrillation, delivery of only one shock at a time is recommended in patients with pulseless VT/VF to minimize interruptions in chest compressions (American Heart Association, 2010). For biphasic defibrillators, the dose of the shock is device-specific (usually 120 to 200 J); the maximum dose available can be used for the initial shock if the effective dose range of the defibrillator is unknown. This dose or a higher dose can then be used for any subsequent shocks that may be needed. After delivery of the initial shock in patients with pulseless VT/VF, CPR should be immediately resumed and continued for 2 minutes, after which the patient’s pulse and rhythm should be checked. Delaying pulse and rhythm checks until after this period of CPR is administered is intended to minimize interruptions in chest compressions and increase the potential for success with defibrillation. If pulseless VT/VF persists, another shock should be delivered at the appropriate dose, followed by 2 minutes of CPR. This general sequence of resuscitation and defibrillation should be followed for as long as the patient remains in pulseless VT/VF. Second-Line Therapy If pulseless VT/VF persists after delivery of at least one shock and CPR, vasopressor therapy with either epinephrine or vasopressin should be initiated (American Heart Association, 2010). One dose of vasopressin may be given to replace either the first or second dose of epinephrine. Vasopressin’s half-life Arcangelo_Chap23.indd 325 10/8/2011 1:52:29 PM 326 UNIT 4 | PHARMACOTHERAPY FOR CARDIOVASCULAR DISORDERS of approximately 10 to 20 minutes is considerably longer than the 3- to 5-minute half-life of epinephrine, which suggests that its vasopressor effects may be more sustained than those of epinephrine during cardiac arrest. Unlike epinephrine, vasopressin also maintains its vasoconstrictive effects under acidotic and hypoxic conditions, which suggests that this agent may continue to work during prolonged cardiac arrest situations. The recommended dosage of epinephrine for pulseless VT/ VF is 1 mg given IV push/IO every 3 to 5 minutes throughout the duration of the pulseless VT/VF episode. The recommended dosage of vasopressin for pulseless VT/VF is 40 units IV push/IO for one dose only. Third-Line Therapy If pulseless VT/VF persists despite the use of defibrillation, CPR, and vasopressor therapy, AAD therapy can be considered. IV amiodarone is recommended as first-line AAD therapy for the treatment of pulseless VT/VF (American Heart Association, 2010). This agent has been shown to be safe and effective in the management of both in-hospital and outof-hospital pulseless VT/VF (Dorian, et al., 2002; Kudenchuck, et al., 1999). Compared to lidocaine, IV amiodarone has been associated with a significantly higher rate of survival to hospital admission in patients with out-of-hospital cardiac arrest due to VF (Dorian, et al., 2002). Therefore, lidocaine should only be considered for the treatment of pulseless VT/VF if IV amiodarone is not available (American Heart Association, 2010). IV procainamide is no longer recommended for pulseless VT/VF. IV magnesium sulfate can be considered if TdP is present or suspected. If the patient is resuscitated from the pulseless VT/VF episode, measures should be taken to prevent recurrent episodes of cardiac arrest. Based on the results of several trials, ICDs are clearly indicated as first-line therapy in patients with a history of sustained VT or VF (AVID Investigators, 1997; Connolly, et al., 2000; Kuck, et al., 2000; Epstein, et al., 2008). If patients with an ICD experience frequent discharges because of recurrent ventricular arrhythmias or new-onset supraventricular arrhythmias (e.g., AF), either amiodarone and a b-blocker or sotalol monotherapy can be used. For patients who refuse or are not candidates for an ICD, oral amiodarone should be used as an alternative therapy. Bradycardia If patients with bradycardia present with signs and symptoms of adequate perfusion, only close observation is required. If patients with bradycardia develop signs or symptoms of poor perfusion (e.g., altered mental status, chest pain, hypotension, shock), IV atropine (0.5 mg every 3 to 5 minutes, up to 3 mg total dose) should be immediately administered (American Heart Association, 2010). If atropine is not effective, either transcutaneous pacing or a continuous infusion of a sympathomimetic agent, such as dopamine (2 to 10 mcg/ kg/min) or epinephrine (2 to 10 mcg/min) (i.e., dopamine or epinephrine) should be initiated. If symptomatic bradycardia persists despite any of these measures, transvenous pacing should be utilized. Figure 23-5 illustrates an algorithm for the management of bradycardia. Special Population Considerations Pediatric The epidemiology of arrhythmias is different between adults and children. Adults have arrhythmias primarily of a cardiac origin, whereas children have arrhythmias primarily of a respiratory origin. Tachyarrhythmias occasionally compromise infants and young children. PSVT is the most common arrhythmia in young children. It typically occurs during infancy or in children with congenital heart disease. PSVT with ventricular rates exceeding 180 to 220 beats/minute can produce signs of shock. If signs of shock appear, synchronized cardioversion or administration of adenosine can be done in an emergency. Common causes of PSVT in young children and infants are congenital heart disease (preoperative) such as Ebstein’s anomaly, transposition of the great arteries, or a single ventricle. Postoperative PSVT also can occur after atrial surgery for correction of congenital defects of the heart. Other common causes of PSVT in children are drugs such as sympathomimetics (cold medications, theophylline, b-agonists). WPW syndrome and hyperthyroidism also can cause PSVT. Common causes of AF and atrial flutter in children are intra-atrial surgery, Ebstein’s anomaly, heart disease with dilated atria (aortic valve regurgitation), cardiomyopathy, WPW syndrome, sick sinus syndrome, and myocarditis. Bradycardia is a common arrhythmia in seriously ill infants or children. It is usually associated with a fall in cardiac output and is an ominous sign, suggesting that cardiac arrest is imminent. The first-line therapy for this arrhythmia in infants and young children is administration of oxygen, support respiration, epinephrine and, possibly, atropine. Pulseless VT and VF are treated much the same way as in adults; however, vasopressin is not currently recommended for children (American Heart Association, 2010). The recommended dose of epinephrine for a child with pulseless VT/VF is 0.01 mg/kg IV/IO, administered as 0.1 mL/kg of a 1:10,000 dilution. If IV/IO access cannot be established, epinephrine can be administered endotracheally (0.1 mg/kg administered as 0.1 mL/kg of a 1:1,000 dilution). Geriatric With aging, body fat increases, lean body tissue decreases, and hepatic and renal system changes set the stage for potential overdosage and toxicity, particularly in the case of AADs. Similarly, declining function affects the amount and dosage of the drug prescribed as well as the occurrence of adverse effects. Cardiac disease and chronic conditions such as HF exacerbate the decline in organ function. Together, these factors can increase the risk of an adverse effect from the AADs the practitioner prescribes. For example, digoxin toxicity is relatively common in elderly patients who are not receiving a reduced dosage to accommodate for the reduced renal function. The practitioner must always assess the patient’s baseline renal function (to identify abnormalities in the blood urea nitrogen and serum creatinine) and baseline hepatic function (to identify impairment in liver function). These two tests are important in prescribing the proper dosage of many of the AADs discussed in this chapter. Arcangelo_Chap23.indd 326 10/8/2011 1:52:30 PM CHAPTER 23 | ARRHYTHMIAS 327 Signs and symptoms of adverse effects of many drugs are confusion, weakness, and lethargy. These signs and symptoms are often attributed to senility or disease. Therefore, it is important for the practitioner to take a thorough drug history and to document accurately the dosages and frequencies prescribed in the patient record. If the practitioner merely attributes confusion to old age, the patient may continue to receive the drug while actually experiencing drug toxicity. Furthermore, the practitioner may add another drug to treat the complications caused by the original AAD, compounding the issue of polypharmacy and excessive medication. In elderly patients taking AADs, the practitioner must be particularly alert to adverse effects from diuretics, digoxin, sleeping aids, and nonprescription drugs. AADs sometimes require accurate and timely dosing. If an elderly patient forgets to take a dose or cannot remember when he or she took the last dose, undermedication or overmedication may occur. This can be dangerous when AADs are prescribed. Many of the elderly have multiple prescriptions, even for the same medication, and therefore take an overdose of the drug. Consequently, it is essential to review medications with elderly patients and make sure they understand and can follow a safe drug therapy regimen. MONITORING PATIENT RESPONSE The goals of AAD therapy are to restore SR and prevent recurrences of the original arrhythmia or development of new arrhythmias. Evaluating the outcomes of AAD therapy requires the practitioner to schedule regular follow-up visits after initial treatment of the arrhythmia. The outcomes to be closely monitored include impulse generation and conduction from the SA node to the AV node, time interval for conduction, heart rate within a normal range that is age-specific, and patterns of AV and ventricular conduction. Data to be monitored to evaluate therapeutic outcomes vary from the simple to complex. The patient may monitor some of them and needs to be taught the signs and symptoms to look for and the expectations from the therapeutic regimen. Patients with arrhythmias may be monitored on a regular or periodic basis with 12-lead ECG, 24-hour Holter monitors, electrophysiologic testing, monitoring of vital signs (blood pressure, pulse rate), echocardiograms for cardiac function, electrolytes, and serum drug levels. In addition, the patient needs to self-monitor for symptoms such as lightheadedness, dizziness, syncopal episodes, palpitations, chest pain, shortness of breath, or weight gain. Other clinical outcomes to be monitored are those that affect quality of life, such as activity tolerance, organ perfusion, cognitive function, fear, anxiety, and depression. PATIENT EDUCATION Drug Information Included in the therapeutic plan for arrhythmia is patient education. Learning outcomes can be evaluated by monitoring compliance with the medication regimen, recurrences of arrhythmia, adverse effects, weight gain, blood pressure, heart rate, and emergency department visits or hospitalizations. AADs have narrow therapeutic windows. Toxicity is common at normal dosages. Consequently, patient education is essential for providing maximal benefits and avoiding adverse effects and accidental overdosing or underdosing. The patient, family, and significant others should be taught the basics, such as the name of the drug (both the generic and trade name), the dose, the frequency and timing of the dose, and the reason the drug is needed. This may avoid duplicate prescribing and administration of AADs. The patient should communicate, either verbally or in writing, the names and dosages of these drugs to all other health care providers and should wear a medical identification device listing all medications. In addition, the patient should inform his or her health care provider when any new prescription, over-the-counter, or complementary or alternative medications are started so that potential drug interactions can be minimized or avoided. The practitioner should provide written instructions for the medication regimen. Providing instructions in large print and simple language may be helpful to patients who have difficulty with memory, hearing, or vision. Instructions should include what to do when the patient misses a dose of medication, has an adverse response to the medication, or wants to stop taking the drug. If b-blockers are prescribed, the patient should be warned that abrupt discontinuation may result in rebound angina, an increased heart rate, and hypertension. The symptoms associated with these adverse effects also should be identified. The practitioner can also teach the patient or caregiver how to take blood pressure and pulse readings, how to interpret the readings, and how to recognize and respond to signs and symptoms of hypotension, dizziness, chest pain, shortness of breath, peripheral edema, or palpitations. The patient should take his or her weight each day and call the practitioner if weight gain of over 2 pounds occurs. If the patient has difficulty learning these monitoring techniques or cannot perform them, he or she may need to schedule regular follow-up appointments for monitoring. Patients with AF or atrial flutter should know the signs and symptoms of a stroke. In today’s health care environment, the insurance plan’s pharmacy provider sometimes makes substitutions with generics or less expensive brands of medications. To prevent harmful drug effects, the patient needs to be aware of this practice and should be cautioned not to change brands of the prescribed AAD or anticoagulant without the approval of the practitioner. An important teaching point from an ethical and legal perspective is to warn the patient to avoid hazardous activities such as driving, using electrical tools, climbing ladders, or any activity that would put the patient or others in harm’s way until the effects of the drug are demonstrated. Patients with an ICD should refrain from driving for at least 6 months after either implantation of the device or an appropriate discharge from the device for a ventricular arrhythmia. Documentation of patient teaching on risks, benefits, lifestyle modification, and safety issues with AAD treatment should always be entered in Arcangelo_Chap23.indd 327 10/8/2011 1:52:30 PM 328 UNIT 4 | PHARMACOTHERAPY FOR CARDIOVASCULAR DISORDERS the patient’s record. Documenting a review of this information on a follow-up visit aids health care providers who follow up on the patient’s progress in the future. Nutrition Clear instructions should be given to avoid alcohol, excessive salt intake, and caffeine during treatment for arrhythmias. Many AADs may cause periods of hypotension resulting in dizziness, or the dose of the drug may need to be regulated, especially in the initial weeks. Complementary and Alternative Medications The practitioner must emphasize to the patient the importance of reporting the use of any of these agents so that interactions with AAD therapy can be minimized or avoided. While the information regarding potential interactions between AADs and specific complementary and alternative medications is relatively sparse, there are a few notable interactions of which practitioners should be aware. Patients taking AADs should avoid licorice root. Licorice has mineralocorticoid effects, which can promote hypokalemia. In patients taking digoxin, the presence of hypokalemia may predispose the patient to digoxin toxicity. In patients taking other AADs, the presence of hypokalemia may promote the development of atrial or ventricular arrhythmias. In addition, certain licorice preparations have been shown to cause a prolonged QT interval, which may be additive in patients receiving class Ia or III AADs. This interaction could lead to TdP. The use of Siberian ginseng or oleander should also be avoided in patients receiving digoxin, as digoxin toxicity may result. The use of St. John’s wort may decrease digoxin concentrations; therefore, digoxin concentrations should be closely monitored when concomitant therapy is used. St. John’s wort may also decrease plasma concentrations of amiodarone and dronedarone, which may predispose the patient to arrhythmia recurrence. Consequently, the use of St. John’s wort in patients receiving amiodarone or dronedarone should be avoided. Patients with a history of atrial or ventricular arrhythmias should also be instructed to avoid the use of any medication containing ephedra (e.g., Ma Huang) because it can promote the development of arrhythmias. BIBLIOGRAPHY *Starred references are cited in the text. *2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care science. (2010). Circulation, 122(Suppl 3), S1–S933. *The Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) Investigators. (2002). A comparison of rate control and rhythm control in patients with atrial fibrillation. New England Journal of Medicine, 347, 1825–1833. *Anderson, J. L., Lutz, J. R., & Allison, S. B. (1983). Electrophysiologic and antiarrhythmic effects of oral flecainide in patients with inducible ventricular tachycardia. Journal of the American College of Cardiology, 2, 105–114. *Antiarrhythmics Versus Implantable Defibrillators (AVID) Investigators (1997). A comparison of antiarrhythmic-drug therapy with implantable defibrillators in patients resuscitated from near-fatal ventricular arrhythmias. New England Journal of Medicine, 337, 1576–1583. *Bardy, G. H., Lee, K. L., Mark, D. B., et al. (2005). Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure. New England Journal of Medicine, 352, 225–237. *Buchanan, L. V., Turcotte, U. M., Kabell, G. G., & Gibson, J. K. (1993). Antiarrhythmic and electrophysiologic effects of ibutilide in a chronic canine model of atrial flutter. Journal of Cardiovascular Pharmacology, 33, 10–14. *Buxton, A. E., Lee, K. L., Fisher, J. D., et al. (1999). A randomized study of the prevention of sudden death in patients with coronary artery disease. New England Journal of Medicine, 341, 1882–1890. Cairns, J. A., Connolly, S. J., & Roberts, R. (1997). Randomized trial of outcome after myocardial infarction in patients with frequent or repetitive ventricular premature depolarizations: CAMIAT. Lancet, 349, 675–682. *Calkins, H., Brugada, J., Packer, D.L., et al. (2007). HRS/EHRA/ECAS expert consensus statement on catheter and surgical ablation of atrial fibrillation: Recommendations for personnel, policy, and follow-up. Heart Rhythm, 4, 816–861. *Cardiac Suppression Trial Investigators. (1989). Preliminary report: Effect of encainide and flecainide on mortality in a randomized trial of arrhythmia suppression after myocardial infarction. New England Journal of Medicine, 321, 406–412. *Carlsson, J., Miketic, S., Windeler, J., et al. (2004). Randomized trial of rate-control versus rhythm-control in persistent atrial fibrillation: The Strategies of Treatment of Atrial Fibrillation (STAF) study. Journal of the American College of Cardiology, 41, 1690–1696. *CIBIS II Investigators and Committees. (1999). The Cardiac Insufficiency Bisoprolol Study II (CIBIS-II): A randomised trial. Lancet, 353, 9–13. *Connolly, S., Gent, M., Roberts, R. S., et al. (2000). Canadian Implantable Defibrillator Study (CIDS): A randomized trial of the implantable cardioverter defibrillator versus amiodarone. Circulation, 101, 1297–1302. *Connolly, S. J., Dorian, P., Roberts, R. S., et al. (2006). Comparison of beta-blockers, amiodarone plus beta-blockers, or sotalol for prevention of shocks from implantable cardioverter defibrillators: The OPTIC study. Journal of the American Medical Association, 295, 165–171. Dager, W. E., Sanoski, C. A., Wiggins, B. S., & Tisdale, J. E. (2006). Pharmacotherapy considerations in advanced cardiac life support. Pharmacotherapy, 26, 1703–1729. *Dorian, P., Cass, D., Schwartz, B., et al. (2002). Amiodarone as compared with lidocaine for shock-resistant ventricular fibrillation. New England Journal of Medicine, 346, 884–890. *Duff, H. J., Roden, D., & Primm, R. K. (1983). Mexiletine in the treatment of resistant ventricular arrhythmias: Enhancement of efficacy and reduction of dose-related side effects by combination with quinidine. Circulation, 67, 1124–1128. *Epstein, A. E., DiMarco, J. P., Ellenbogen, K. A., et al. (2008). ACC/AHA/ HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices). Journal of the American College of Cardiology, 51, e1–e62. *Fuster, V., Rydén, L. E., Cannom, D. S., et al. (2006). ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Atrial Fibrillation). Journal of the American College of Cardiology, 48, e149–e246. *Goldschlager, N., Epstein, A. E., Naccarelli, G., et al. (2007). A practical guide for clinicians who treat patients with amiodarone. Heart Rhythm, 4, 1250–1259. *Hohnloser, S. H., Crijns, H. J., van Eickels, M., et al. (2009). Effect of dronedarone on cardiovascular events in atrial fibrillation. New England Journal of Medicine, 360, 668–678. Arcangelo_Chap23.indd 328 10/8/2011 1:52:30 PM CHAPTER 23 | ARRHYTHMIAS 329 *Hohnloser, S. H., Kuck, K. H., & Lilienthal, J. (2000). Rhythm or rate control in atrial fibrillation—Pharmacological Intervention in Atrial Fibrillation (PIAF): A randomised trial. Lancet, 356, 1789–1794. Julian, D. G., Camm, A. J., & Fragnin, G. (1997). Randomized trial of effect of amiodarone on mortality inpatients with left ventricular dysfunction after recent myocardial infarction: EMIAT. Lancet, 349, 667–674. *Kennedy, H. L., Brooks, M. M., & Barker, A. H. (1994). Beta blocker therapy in the Cardiac Arrhythmia Suppression Trial. American Journal of Cardiology, 74, 674–680. *Køber, L., Bloch-Thomsen, P. E., Møller, M., et al. (2000). Danish Investigations of Arrhythmia and Mortality on Dofetilide (DIAMOND) Study Group. Effect of dofetilide in patients with recent myocardial infarction and left-ventricular dysfunction: A randomised trial. Lancet, 356, 2052–2058. *Køber, L., Torp-Pedersen, C., McMurray, J. J., et al. (2008). Increased mortality after dronedarone therapy for severe heart failure. New England Journal of Medicine, 358, 2678–2687. *Kuck, K. H., Cappato, R., Siebels, J., et al. (2000). Randomized comparison of antiarrhythmic drug therapy with implantable defibrillators in patients resuscitated from cardiac arrest: The Cardiac Arrest Study Hamburg (CASH). Circulation, 102, 748–754. *Kudenchuck, P. J., Cobb, L. A., Copass, M. K., et al. (1999). Amiodarone for resuscitation after out-of-hospital cardiac arrest due to ventricular fibrillation. New England Journal of Medicine, 341, 871–879. *Lichstein, E., Morganroth, J., Harrist, R., & Hubble, M. S. (1983). Effect of propranolol on ventricular arrhythmia: The beta blocker heart attack trial experience. Circulation, 67 (Suppl. I), 5–10. *MERIT-HF Study Group (1999). Effect of metoprolol CR/XL in chronic heart failure: Metoprolol CR/XL Randomized Intervention Trial in Congestive Heart Failure (MERIT-HF). Lancet, 353, 2001–2007. *Miller, M. R., McNamara, R. L., Segal, J. B., et al. (2000). Efficacy of agents for pharmacological conversion of atrial fibrillation and subsequent maintenance of sinus rhythm: A meta-analysis of clinical trials. Journal of Family Practice, 49, 1033–1046. *Moss, A. J., Hall, W. J., Cannom, D. S., et al. (1996). Improved survival with an implanted defibrillator in patients with coronary disease at high risk for ventricular arrhythmia. New England Journal of Medicine, 335, 1933–1940. *Moss, A. J., Zareba, W., Hall, W. J., et al. (2002). Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction. New England Journal of Medicine, 346, 877–883. *Opolski, G., Torbicki, A., Kosior, D. A., et al. (2004). Rate control vs rhythm control in patients with nonvalvular persistent atrial fibrillation: The results of the Polish How to Treat Chronic Atrial Fibrillation (HOT CAFE) Study. Chest, 126, 476–486. *Oral, H., Souza, J. J., Michaud, G. F., et al. (1999). Facilitating transthoracic cardioversion of atrial fibrillation with ibutilide pretreatment. New England Journal of Medicine, 340, 1849–1854. *Pacifico, A., Hohnloser, S. H., Williams, J. H., et al. (1999). Prevention of implantable-defibrillator shocks by treatment with sotalol: Sotalol Implantable Cardioverter-Defibrillator Study Group. New England Journal of Medicine, 340, 1855–1862. *Packer, M., Bristow, M. R., Cohn, J. N., et al. (1996). The effect of carvedilol on morbidity and mortality in patients with chronic heart failure. New England Journal of Medicine, 334, 1349–1355. *Phillips, B. G., Gandhi, A. J., Sanoski, C. A., et al. (1997). Comparison of intravenous diltiazem and verapamil for the acute treatment of atrial fibrillation and flutter. Pharmacotherapy, 17, 1238–1245. *Roy, D., Talajic, M., Dorian, P., et al. (2000). Amiodarone to prevent recurrence of atrial fibrillation. New England Journal of Medicine, 342, 913–920. *Roy, D., Talajic, M., Nattel, S., et al. (2008). Rhythm control versus rate control for atrial fibrillation and heart failure. New England Journal of Medicine, 358, 2667–2677. *Sanoski, C. A., & Bauman, J. L. (2002). Clinical observations with the amiodarone/warfarin interaction: Dosing relationships with long-term therapy. Chest, 121, 19–23. *Singer, D. E., Albers, G. W., Dalen, J. E., et al. (2008). Antithrombotic therapy in atrial fibrillation: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th ed.). Chest, 133, 546S–592S. *Singh, B. N., Connolly, S. J., Crijns, H. J., et al. (2007). Dronedarone for maintenance of sinus rhythm in atrial fibrillation or flutter. New England Journal of Medicine, 357, 987–999. *Singh, S., Zoble, R. G., Yellen, L., et al. (2000). Efficacy and safety of oral dofetilide in converting to and maintaining sinus rhythm in patients with chronic atrial fibrillation or atrial flutter: The Symptomatic Atrial Fibrillation Investigative Research on Dofetilide (SAFIRE-D) Study. Circulation, 102, 2385–2390. *Slavik, R. S., Tisdale, J. E., & Borzak, S. (2001). Pharmacological conversion of atrial fibrillation: A systematic review of available evidence. Progress in Cardiovascular Diseases, 44, 121–152. *Stambler, B. S., Wood, M. A., Ellenbogen, K. A., et al. (1996). Efficacy and safety of repeated intravenous doses of ibutilide for rapid conversion of atrial flutter or fibrillation. Circulation, 94, 1613–1621. Stroke Prevention in Atrial Fibrillation Investigators. (1991). Stroke prevention in atrial fibrillation study: Final report. Circulation, 84, 527–539. *Teo, K. K., Yusuf, S., & Furberg, C. D. (1993). Effects of prophylactic antiarrhythmic drug therapy in acute myocardial infarction: An overview of results from randomized controlled trials. Journal of the American Medical Association, 270, 1589–1595. *Van Gelder, I. C., Groenveld, H. F., Crijns H. J. G. M., et al. (2010). Lenient versus strict rate control in patients with atrial fibrillation. New England Journal of Medicine, 362, 1363–1373. *Van Gelder, I. C., Hagens, V. E., Bosker, H. A., et al. (2002). The Rate Control Versus Electrical Cardioversion for Persistent Atrial Fibrillation Study Group. A comparison of rate control and rhythm control in patients with recurrent persistent atrial fibrillation. New England Journal of Medicine, 347, 1834–1840. *Vaughan Williams, E. M. (1984). A classification of antiarrhythmic actions reassessed after a decade of new drugs. Journal of Clinical Pharmacology, 24, 129–147. *Volgman, A. S., Winkel, E. M., Pinski, S. L., et al. (1998). Conversion efficacy and safety of intravenous ibutilide compared with intravenous procainamide in patients with atrial flutter or fibrillation. Journal of the American College of Cardiology, 31, 1414–1419. *Vukmir, R. B., & Stein, K. L. (1991). Torsades de pointes therapy with phenytoin. Annals of Emergency Medicine, 20, 198–200. *Wann, L. S., Curtis, A. B., Ellenbogen, K. A., et al. (2011). 2011 ACCF/ AHA/HRS focused update on the management of patients with atrial fibrillation (update on dabigatran): A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation, 123, 1144–1150. *Wann, L. S., Curtis, A. B., January, C. T., et al. (2011). 2011 ACCF/AHA/ HRS focused update on the management of patients with atrial fibrillation (updating the 2006 guidelines): A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation, 123, 104–123. *Wit, A. L., Rosen, M. R., & Hoffman, B. F. (1974). Electrophysiology and pharmacology of cardiac arrhythmias: Relationship of normal and abnormal electrical activity of cardiac fibers to the genesis of arrhythmias. American Heart Journal, 88, 664–670, 798–806. *Wyse, D. G., Kellen, J., & Rademaker, A. W. (1988). Prophylactic versus selective lidocaine for early ventricular arrhythmias of myocardial infarction. Journal of the American College of Cardiology, 12, 507–513. *Wyse, D. G., Waldo, A. L., DiMarco, J. P., et al. (2002). A comparison of rate control and rhythm control in patients with atrial fibrillation. New England Journal of Medicine, 347, 1825–1833. Zipes, D. P., Camm, A. J., Borggrefe, M., et al. (2006). ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: A report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death). Journal of the American College of Cardiology, 48, e247–e346. Arcangelo_Chap23.indd 329 10/8/2011 1:52:30 PM Arcangelo_Chap23.indd 330 10/8/2011 1:52:30 PM 5 UNIT Pharmacotherapy for Respiratory Disorders Arcangelo_Chap24.indd 331 10/8/2011 1:52:50 PM CHAPTER 332 Virginia P. Arcangelo fall and spring, and coronavirus (10% to 15%), which is most prevalent during the winter. The respiratory syncytial virus, influenza virus, parainfluenza virus, and adenovirus are also responsible, but the rhinovirus is the single most pervasive cause of colds. The rhinovirus is a single-stranded ribonucleic acid virus that replicates well at 95°F (35°C) or below but poorly at 99 to 100°F (37.2 to 37.8°C), which is probably why it causes URIs and not pneumonia. Predisposition to viral infections can be attributed to many factors, including frequent exposure to viral infectious agents; in children, the age of the child; and the inability to resist invading organisms because of allergies, malnutrition, immune deficiencies, physical abnormalities, or other comorbid conditions. Some experts propose a relationship between the host response to the virus and the production of cold symptoms. Studies show that common colds are more frequent or more severe in those under increased stress, probably as a result of stress weakening the immune system. PATHOPHYSIOLOGY If the protective barriers of the upper respiratory tract (i.e., cough, gag, and sneeze reflexes, lymph nodes, immunoglobulin [Ig] A antibodies, and rich vasculature) fail, viral pathogens trigger an acute inflammatory reaction with release of vasoactive mediators and increased parasympathetic stimuli. This produces congestion and rhinorrhea. Rhinoviruses grow in the upper airway, and attach and gain entry to host cells by binding to an intracellular adhesion molecule. Infection begins in the adenoidal area and spreads to the ciliated epithelium in the nose. Rhinoviruses are hardy and remain infectious for at least 3 hours after drying on hard surfaces such as telephones or countertops, but they do not last as long on porous surfaces such as tissues. Transmission of the virus has been attributed to three methods: airborne transmission by small particles (droplets), airborne transmission by large particles, and direct contact. Large particle transmission is not efficient and requires prolonged exposure. The major means of transmission is by direct contact from a donor’s nose to a donor’s hand, and from there to the recipient’s hand and subsequently to the nose or eye. Although conjunctival cells are not thought to harbor Upper Respiratory Infections Upper respiratory tract infections (URIs), including the common cold and sinusitis, are some of the most common problems seen in primary care. URIs are usually self-limiting, minor illnesses that account for half or more of all acute illnesses. It is difficult to differentiate the common cold from sinusitis or allergic rhinitis. (See Chapter 47.) URIs share common symptoms, such as nasal discharge, nasal congestion, tenderness over the sinuses, fever, headache, malaise, sore throat and myalgias, sneezing, a full feeling around the eyes and ears, and coughing. Symptoms may present individually or in combination, and it is difficult to determine whether the cause is viral or bacterial. URIs can progress to acute or chronic complications. In children especially, URIs may progress to otitis media. In 5% to 10% of cases, the viral or bacterial cause may travel, causing sinusitis and bronchitis. There is an enormous economic burden associated with URIs. COMMON COLD Acute infectious rhinitis (coryza), or the common cold, is a viral URI. One of the most common infections, it is self-limiting. Coryza is an acute inflammation of the mucous membranes of the respiratory passages, particularly of the nose, sinuses, and throat, and is characterized by sneezing, rhinorrhea (watery nasal discharge), and coughing. The common cold has a short duration. Approximately 100 million colds occur annually in the United States, resulting in approximately 26 million days off from school, 23 million absent days from work, 27 million visits to a primary care provider, and 250 million days of restricted activities. Nearly $1 billion is spent on cold remedies and $1.5 billion on analgesics. Adults average three colds per year. Children average six episodes per year, and the common cold is more common in children who attend day care or preschool (where they are in contact with other children and groups that may spread disease) than in those who spend more time at home and have less contact with crowds. Exposure to smoke is also a predisposing factor. CAUSES The pathogens most frequently associated with common colds are rhinovirus (30% to 40% of cases), especially during the 24 Arcangelo_Chap24.indd 332 10/8/2011 1:52:50 PM CHAPTER 24 | UPPER RESPIRATORY INFECTIONS 333 rhinovirus, it probably can be passed through the tear duct into the nose. Incubation of the rhinovirus is 1 to 10 days. Onset of signs and symptoms occurs 1 to 2 days after viral infection, and they peak in approximately 2 to 4 days. The virus may remain present for a week or longer after the onset of symptoms. A cough may persist after other symptoms resolve. DIAGNOSTIC CRITERIA Diagnostic tests have no cost/benefit effect in diagnosing the common cold. Symptoms consist primarily of clear nasal discharge, sneezing, nasal congestion, cough, low-grade fever (below 102°F [38.9°C]), scratchy or sore throat, mild aches, chills, headache, watery eyes, tenderness around the eyes, full feeling in the ears, and fatigue. In children, the presentation could also include nasal blockage, fever with seizures, anorexia, vomiting, diarrhea, and abdominal pain. Symptoms usually resolve in approximately 1 week, but they may linger for 2 weeks. INITIATING DRUG THERAPY Mistreatment of the common cold by clinicians is common for two reasons: • It is difficult to determine whether the cause is viral or bacterial. • Patients often have preconceived notions and demand antibiotics for their URI even though it is simply the common cold, which is caused by a virus. There is no cure for the common cold. Treatment is geared toward minimizing symptoms (Table 24.1). Nonpharmacologic alternatives to treating the common cold are the first line of treatment. For example, rest allows the body to gain strength and be more effective in defending itself against the pathogen. The body can then dictate the increase in activities. An alternative to decongestants and expectorants is increasing water or juice intake. This assists in liquefying tenacious secretions, making expectoration easier, soothing scratchy, sore throats, and relieving dry skin and lips. Saline gargles also are effective for soothing sore throats. Coughing caused by chest congestion can cause a muscular chest pain. Menthol rubs can soothe this ache and open airways for some congestion relief. Menthol lozenges also have been effective in soothing scratchy throats and clearing nasal passages. Saline nasal flushes are also effective for clearing nasal passages without the rebound side effect. Petrolatum-based ointments for raw and macerated skin around the nose and upper lip ease the drying effects of dehydration and the use of multiple tissues. (See Table 24.1.) Other measures, such as drinking chicken soup, taking a hot shower, or using a room humidifier, may prove helpful. TABLE 24.1 Alternative Therapies for Cold Symptoms Symptoms Nonpharmacologic Pharmacologic Alternative Therapy Any cold symptoms Eat proper diet, rest, drink fluids. Echinacea (prevention) Zinc lozenges (decreased duration of symptoms) Rhinorrhea Use disposable paper tissues. Anticholinergic nasal spray Nasal obstruction Decrease ingestion of milk products. Children: saline nose drops by bulb syringe Bayberry tea Inhale warm, moist heat, such as showers. Apply topical decongestants. Increase fluid intake. If nasal obstruction is still a problem after 3 d, take oral decongestants unless contraindicated by hypertension or coronary artery disease. Serous otitis media or sensation of fullness in ears Decongestants (oral) Headache, sore throat, malaise, myalgia, fever Gargle with salt water, drink plenty of fluids, suck on menthol lozenges. Nonsteroidal anti-inflammatory drugs Chaparral, aromatherapy rubs, boneset Chest congestion Drink fluids, have menthol rubs, and humidify room air. Expectorants Sneezing and watery eyes Humidify room air. Two schools of thought: antihistamine of choice, but critics say antihistamines not needed in treating colds, especially in children Cough Humidify room air. Antitussives, naproxen Vicks VapoRub on the soles of feet covered by socks at bedtime Arcangelo_Chap24.indd 333 10/8/2011 1:52:50 PM 334 UNIT 5 | PHARMACOTHERAPY FOR RESPIRATORY DISORDERS Inhaling warm, moist heat helps raise the temperature of the nasal mucosa to at least 98.6°F (37°C), a temperature at which the virus does not replicate so readily. Applying Vicks VapoRub on the soles of the feet and then putting on socks may help with a persistent night-time cough. Goals of Drug Therapy The main goals of treatment for the common cold are relief of symptoms, reduction of the risk for complications, and prevention of spread to others (Box 24.1). Polypharmacy is often used to treat intolerable symptoms. Decongestants Mechanism of Action Decongestants are sympathomimetic agents that stimulate alpha- and beta-adrenergic receptors, causing vasoconstriction in the respiratory tract mucosa and thereby improving ventilation (Table 24.2). Decongestants come in topical or oral preparations. Topical decongestants in the form of nasal sprays slow ciliary motility and mucociliary clearance. Topical agents have little systemic absorption. However, topical decongestants should not be used for more than 3 days because prolonged use can cause rhinitis medicamentosa (rebound congestion), which is characterized by severe nasal edema, rebound congestion, and increased discharge due to decreased receptor sensitivity. Oral decongestants are frequently used and are sold over the counter (OTC) alone or in combination with other drugs. A common example of a combination preparation is an antihistamine and a decongestant. The most common oral decongestant is pseudoephedrine (Sudafed, others). Oral decongestants have the same mode of action as topical agents but can cause more systemic responses. Decongestants assist in clearing nasal obstruction. Their use may be encouraged to prevent sinusitis and eustachian tube blockage. Contraindications Decongestants are contraindicated in patients with narrowangle glaucoma, hypertension, and severe coronary artery disease. Caution is recommended in patients with hyperthyroidism, diabetes, and prostatic hypertrophy (causes difficulty with urination). Adverse Events Adverse events include increased blood pressure, increased heart rate, palpitations, headache, dizziness, gastrointestinal (GI) distress, and tremor. These reactions are especially seen at doses above 210 mg. Interactions Decongestants interact with appetite suppressants, monoamine oxidase (MAO) inhibitors (hypertensive crisis), and beta- adrenergic agents (bradycardia and hypertension). Decongestants are less effective when taken with drugs that acidify the urine and more effective when taken with drugs that alkalize the urine. Expectorants One of the most important nondrug considerations in treating coughs is discovering its cause, because the prolonged use of OTC expectorants or other cough products may mask symptoms of a serious underlying disorder. The drug should not be used for more than a week. If the cough persists, additional measures may be investigated. Mechanism of Action Expectorants, including water, increase the output of respiratory tract fluid by decreasing the adhesiveness and surface tension of the respiratory tract and by facilitating removal of viscous mucous. (See Table 24.2.) The effect is noted within 1 to 2 hours. Adverse Events Adverse events include drowsiness, headache, and GI symptoms. Antitussives Cough is a frequent complaint of a person with an URI. Cough can be stimulated from congestion or can occur as a result of postnasal drip. There are many cough suppressants available, but studies have shown minimal benefit with the common cold. • Avoid touching face with hands. • Wash hands frequently. • Avoid people with colds or URIs. • Avoid crowded areas during peak URI/flu season. • Stop smoking. • Avoid excessive intake of alcohol. • Avoid second-hand smoke. • Avoid excessive dry heat. • Use disposable tissues and dispose of them properly. • Obtain influenza vaccine, if recommended. • Eat a nutritious diet. • Get adequate rest and sleep. • Avoid or reduce stress. • Exercise regularly. • Increase humidity in the house, especially during winter months. • Maintain good oral hygiene. • Avoid certain environmental irritants and allergens (dust, chemicals, smoke, and animal dander) when possible. • Use central ventilation fans/air conditioning with microstatic air filters. BOX 24.1 Preventing Upper Respiratory Infections Arcangelo_Chap24.indd 334 10/8/2011 1:52:50 PM CHAPTER 24 | UPPER RESPIRATORY INFECTIONS 335 TABLE 24.2 Overview of Agents for Upper Respiratory Infections Generic (Trade) Name and Dosage Selected Adverse Events Contraindications Special Considerations Decongestants oxymetazoline hydrochloride (Afrin) ≥6 y: 2–3 sprays bid 2–6 y (use children’s spray): 2–3 sprays bid Palpitations, headaches These drugs may cause rebound congestion. Use only 2 to 3 days, then switch to oral decongestants. phenylephrine hydrochloride (Neo-Synephrine) Adults: 1 spray q3–4h as needed Palpitations, headaches Not recommended for children These drugs may cause rebound congestion. Use only 2 to 3 days, then switch to oral decongestants. pseudoephedrine (Sudafed, Benylin decongestant) Adults: short acting: 60 mg q4–6h; long acting: 120 mg q12h Children 7–12 y: short acting: 30 mg q4–6h Children 3–6 y: 15 mg q4–6h Palpitations, headaches, increased blood pressure, dizziness, GI upset, tremor Hypertension, coronary artery disease Give at least 2 h before bedtime. Do not crush, break, or chew tablets. Expectorants guaifenesin (Antitussin, Mucinex, Robitussin, Uni-Tussin) Adults: short acting: 200–400 mg q4h long acting: 600–1,200 mg q12h Children 7–12 y: short acting: 100–200 mg q4h long acting: 600 mg q12h Children 2–6 y: 50–100 mg q4h GI upset, drowsiness, headache, rash, dizziness Breast-feeding mothers, pregnancy category C Not given for prolonged time if cough persists or accompanied by high fever Humibid sprinkles may be swallowed whole or opened and sprinkled on soft food. Antitussives dextromethorphan (Benylin—15 mg/5 mL) 10 mL q6–8h (Delsym—30 mg/5 mL) Adults: 10 mL q12h Children 2–5 y: 2.5 mL q12h 6–12 y: 5 mL q12h benzonatate (Tessalon) 100–200 mg tid Not for ≤ 10 years old Drowsiness, palpitations, excitability in children Drowsiness, headache, GI upset, confusion Hypertension, diabetes, asthma Pregnancy category C None Narcotic Antitussives codeine phosphate 10 mg, guaifenesin 300 mg tablets and liquid (Brontex) Adults: 20 mL q4h Children 6–12 y: 10 mL q4h Lightheadedness, dizziness, sedation, sweating, nausea, vomiting Known addiction, cautious use in asthmatics, COPD, cardiac disease, seizure disorders, renal/hepatic impairment, BPH, head injuries, hypothyroidism, and pregnancy Increased CNS depression if used with alcohol or other narcotics Usually used with antihistamines, expectorants, decongestants, or analgesics Controlled substance (Drug Enforcement Agency number required for prescription) Phenergan with codeine (codeine 10 mg and promethazine 6.25 mg/5 mL) Adults: 5 mL Children: 2–5 y: 1.25–2.5 mL q4h 6–12 y: 2.5–5 mL q4h Same as above Same as above Same as above (continued ) Arcangelo_Chap24.indd 335 10/8/2011 1:52:50 PM 336 UNIT 5 | PHARMACOTHERAPY FOR RESPIRATORY DISORDERS TABLE 24.2 Overview of Agents for Upper Respiratory Infections (Continued ) Generic (Trade) Name and Dosage Selected Adverse Events Contraindications Special Considerations codeine 10 mg, guaifenesin 100 mg/5 mL (Robitussin AC) or codeine 10 mg, pseudoephedrine 30 mg, and guaifenesin 100 mg/5 mL (Tussar SF) Adults: 10 mL q4h to maximum of 40 mL/d Same as above Children: not recommended Same as above hydrocodone (in combination with other agents) 5 mg up to 4 qid Same as above Known addiction; cautious use in asthmatics, COPD, cardiac disease, seizure disorders, renal/hepatic impairment, BPH, head injuries, hypothyroidism, and pregnancy Same as above hydrocodone 2.5 mg, guaifenesin 100 mg, pseudoephedrine 30 mg/ 5 mL (Duratuss HD) Same as above Same as above Same as above Adults: 10 mL q4–6h Children 6–12 y: 5 mL q2–6h Maximum of 4 doses/d hydrocodone 5 mg and homatropine 1.5 mg (Hycodan tablets and syrup) Same as above Same as above Same as above Adults: 1 tablet or 5 mL q4–6h Children: 6–12 y: ½ tablet or 2.5 mL q4–6h hydrocodone 5 mg and guaifenesin 100 mg/5 mL (Hycotuss) Adults: 5 mL after meals and hs Children: 6–12 y: 2.5–5 mL after meals and hs Same as above Same as above Same as above hydrocodone 10 mg and chlorpheniramine maleate 8 mg/5 mL (Tussionex) Adults: 5 mL q12h Children: 6–12 y: 2.5 mL q12h Same as above Same as above Same as above hydrocodone 5 mg guaifenesin 100 mg per 5 mL (Vicodin Tuss) Adults: 5 mL at meals and hs Children 6–12 y: 2.5 mL at meals and hs Same as above Same as above Same as above Combination Products—Non-Narcotic dextromethorphan hydrobromide 10 mg, brompheniramine maleate 2 mg, pseudoephedrine 30 mg/5 mL (Bromfed-D, Dimetane-DX) Adults: 10 mL q4h Children: 2–5 y: 2.5 mL q4h 6–12 y: 5 mL q4h Drowsiness, sedation, nausea, dizziness, palpitations, increased blood pressure, excitation in children, constipation Asthma, lower respiratory disorders, neonates, severe hypertension, severe cardiovascular disease, within 14 d of monoamine oxidase inhibitors, nursing mothers; use cautiously in patients with history of urinary obstruction, mild hypertension, and hyperthyroidism These drugs are combination antitussives, antihistamines, and sympathomimetics. Used for cough and congestion Pregnancy category C Not recommended for children <2 y These drugs are sold over the counter. [Show More]

Last updated: 3 years ago

Preview 1 out of 339 pages