Clomiphene

Helen W. Boucher, M.D., F.A.C.P.

• Assistant Professor of Medicine
• Tufts University School of Medicine
• Director
• Fellowship Program
• Division of Geographic Medicine and
• Infectious Diseases
• Tufts Medical Center
• Boston, Massachusetts

More recently womens health grand rapids cheap 100 mg clomiphene mastercard, the mortality rate has declined; nevertheless women's health center towson md clomiphene 50 mg online, triple-valve replacement should be avoided if possible womens health 21 day bikini body cheap clomiphene 100 mg line. Patients who survive triple-valve replacement surgery usually experience substantial clinical improvement during the early postoperative period breast cancer diagnosis buy clomiphene 50 mg lowest price, and postoperative catheterization studies show marked reductions in pulmonary arterial and capillary pressures menstrual gas clomiphene 100 mg buy online. However, some patients die of arrhythmias or congestive heart failure in the late postoperative period despite three normally functioning prostheses. The cause of cardiac failure in this situation is unknown, but may be related to intraoperative myocardial ischemia, microemboli from the multiple prostheses, or continued subclinical episodes of rheumatic myocarditis. When multiple prosthetic valves must be inserted, it is logical to select two bioprostheses or two mechanical prostheses for the left side of the heart. If the patient is to be exposed to the hazards of anticoagulants for one mechanical prosthesis, it seems unreasonable to add the potential risks of early failure of a bioprosthesis. However, if two mechanical prostheses are selected for the left side of the heart, the use of a bioprosthesis in the tricuspid position is suggested. The major differences are related to the risk of thromboembolism (higher with mechanical valves) and the risk of structural deterioration of the prosthesis (higher with bioprostheses). The bileaflet valves are the most commonly implanted mechanical valves because of their low bulk and flat profile and superior hemodynamics. Jude Medical, West Berlin, New Jersey) is coated with pyrolytic carbon and has two semicircular discs that pivot between open and closed positions without the need for supporting struts. C, Caged ball valve (Starr-Edwards, Edwards Lifesciences Corporation, Irvine, Calif). E, Stented pericardial bioprosthesis (Carpentier-Edwards Magna, Edwards Lifesciences). Thrombogenicity in the mitral position may be less than that associated with other prosthetic valves, although, as with other mechanical prostheses, life-long anticoagulation is needed. Jude valve, the CarboMedics prosthesis (Sorin Group, Milan, Italy), also is a bileaflet valve composed of pyrolytic carbon with a titanium housing that can be rotated to avoid interference with disc excursion by subvalvular tissue. An example of a tilting disc valve in current use is the MedtronicHall valve (Medtronic, Minneapolis), which has a Teflon sewing ring and titanium housing; its thin, carbon-coated pivoting disc has a central perforation that allows improved hemodynamics. Thrombogenicity appears to be low (less than one episode/100 patient-years in the mitral position), and mechanical performance is excellent over the long term. Mechanical valves, both bileaflet and tilting disc, are associated with small (5 to 10 mL/beat) obligatory (normal) regurgitation. Production of the Starr-Edwards caged ball valve was discontinued in 2007, but patients in whom this valve was implanted are still encountered frequently in clinical practice. The poppet is made of silicone rubber, the cage of Stellite alloy, and the sewing ring of Teflon and polypropylene cloth. In a small number of patients, this valve induces hemolysis, which may be greatly exaggerated and become clinically important if a perivalvular leak develops. When they are of small size, Starr-Edwards valves may cause mild obstruction, and the incidence of thromboembolism is slightly higher than with the tilting disc or bileaflet valve. Without anticoagulants and aspirin, the incidence of thromboembolism is three to six times higher than when proper doses of these medications are administered. This may be a fatal event, but when nonfatal, it interferes with prosthetic valve function. However, the addition of aspirin, 75 to 100 mg daily, together with warfarin reduces the risk of thromboembolism and is indicated in all patients with prosthetic valves. The antithrombin agent dabigtran is contraindicated for thromboembolic prophylaxis in patients with mechanical valves309-311; the new anti-Xa anticoagulants have not yet been tested in this situation and should not be used until evidence of safety and efficacy has been accumulated. Prosthetic valve thrombosis should be suspected from the sudden appearance of dyspnea and muffled sounds or new murmurs on auscultation. Valve thrombosis, a particularly hazardous complication, occurs at an incidence of approximately 0. All mechanical prosthetic valves have an excellent record of durability, up to 40 years for the Starr-Edwards valve and more than 25 years for the St. Thrombosis and thromboembolism risks are greater with any mechanical valve in the mitral than in the aortic position, and higher doses of warfarin are generally recommended for mitral prostheses. The incidence of thrombosis with mechanical prostheses in the tricuspid position is high, so bioprostheses are preferred at this site. The incidence of embolization in patients who have experienced repeated emboli from a prosthetic valve despite anticoagulants may be reduced by replacement with a tissue valve. Mechanical prostheses regularly cause mild hemolysis, but this is not severe enough to be of clinical importance unless the patient develops paraprosthetic regurgitation. It then accelerates and, by 15 years postoperatively, the actuarial freedom from bioprosthetic primary tissue failure has ranged from 30% to 60% in several series. By contrast, stented pericardial valves have a lower rate of primary tissue failure, with 86% free of structural deterioration at 12 years. Prosthetic valve endocarditis is a serious, often grave, illness, with the risk of endocarditis highest in the first few months after valve implantation (see Chapter 64). Structural valve deterioration is more frequent in patients with bioprostheses in the mitral than in the aortic position, presumably because of the higher closing pressure. Valve failure is prohibitively rapid in children and in adults younger than 35 to 40 years. On the other hand, degeneration is rare when these valves are implanted into patients older than 70 years. Bioprostheses also have been reported to have extremely limited durability in patients with chronic renal failure, but recent studies have called this into question (see later). Other factors that increase the likelihood of bioprosthetic valve deterioration include abnormalities of calcium metabolism and, possibly, hypercholesterolemia and pregnancy. Fortunately, tissue valves usually do not fail suddenly, as is often the case with structural failure or thrombosis of mechanical prostheses. Re-replacement of a bioprosthetic valve should be carried out when significant and/or progressive structural deterioration is evident or when standard criteria for intervention for native valve disease are met. The second operation, when carried out on an elective basis, may be associated with a surgical mortality rate that is two to three times higher than with the initial valve replacement. Stented Bioprosthetic Valves A stented tissue valve consists of three tissue leaflets mounted on a ring with semirigid stents that facilitate implantation and maintain the three-dimensional relationship between the leaflets. Stented porcine aortic heterografts were developed for the mitral and aortic positions and have been in wide clinical use since 1965. Over the past 49 years, stented bioprosthetic valve design has improved to maximize orifice area by reconfiguration of the sewing ring and stents and improve durability by the use of other biologic tissues, improved fixation techniques, and anticalcification treatments. In the United States, the number of bioprostheses implanted each year greatly exceeds the number of mechanical valves. This is not a uniform practice, particularly for aortic bioprostheses,316 but is more uniform in the mitral position. When implanted in the mitral position in patients who are in sinus rhythm, do not have heart failure or thrombus in the left atrium or the left atrial appendage, and do not have a history of embolism preoperatively, anticoagulants are not needed after the first 3 postoperative months. After 3 months in either the aortic or mitral position, the thromboembolic rate also is approximately one or two episodes/100 patient-years,1,306,307 although one study suggested higher risk up to 6 months postoperatively. Jude or other mechanical valves who are receiving anticoagulants and are therefore at increased risk for hemorrhage. It is unlikely that any mitral valve replacement can be associated with a thromboembolic rate much below 0. This risk scenario negates the principal advantage of the tissue valves, and mechanical prostheses appear to be preferable to bioprostheses in these patients. A baseline echocardiographic study is recommended 2 to 4 weeks after hospital discharge for valve replacement. After 5 years, annual echocardiography is reasonable, even in the absence of clinical findings, to evaluate for bioprosthetic valve deterioration. However, in randomized studies, there was no benefit of homografts compared with other tissue valves in outcome after endocarditis. In children and adolescents, available evidence indicates that the autograft grows along with the patient. The risk of endocarditis is very low, anticoagulants are not required, and perhaps most important long-term survival appears to be excellent,320,321 but the durability of the autograft after two decades may be in question. The pulmonary artery tissue adapts to the aortic pressure and usually does not dilate. However, concern has been raised about this procedure in patients with bicuspid valves and dilated aortic roots, because the implanted pulmonary artery tissue exposed to the higher aortic pressures also may undergo degenerative changes, leading to significant dilation of the autograft. A subcoronary technique, in which the pulmonary autograft is inserted without a root replacement, may circumvent this problem, but late dilation of the autograft remains a concern. The most commonly used prosthetic valves-mechanical prostheses and stented porcine or pericardial xenografts-have an effective in vitro orifice size that is smaller than the normal valve at the same site. Although all prosthetic valves are inherently mildly stenotic, postoperative hemodynamic measurements show reasonably good function, with effective mitral valve orifice areas averaging 1. Aortic valve effective orifice areas and transvalvular gradients depend on valve size and type and have been detailed in published tables of normal values and guidelines. Stentless Bioprosthetic Valves Because the stent adds to the obstruction, thereby increasing stress on the leaflets, stentless valves have been developed for the aortic position and are especially useful for patients with small aortic roots. They are sterilized with antibiotics and cryopreserved for long periods at -196° C. They are inserted directly, usually in the aortic position, without being placed into a prosthetic stent. In the aortic position, the isolated valve is implanted in the subcoronary position or the valve and a portion of attached aorta are implanted as a root replacement, with reimplantation of the coronary arteries into the graft. Homograft hemodynamics are superior to those of stented porcine valves and similar to those of stentless porcine valves. In addition, the homograft valve and root are prone to severe calcification, making reoperation difficult. One possible advantage of homografts is in the avoidance of early endocarditis, and homografts are commonly used in the treatment of aortic valve endocarditis, particularly complex aortic root Most comparisons of mechanical and bioprosthetic valves indicate similar overall results in terms of early and late mortality, prosthetic valve endocarditis and other complications, and the need for reoperation, at least for the first 5 years postoperatively. SelectionofanArtificialValve 1509 the major task in selecting an artificial valve is to weigh the advantage of durability and the disadvantages of the risks of thromboembolism and anticoagulant treatment inherent in mechanical prostheses on the one hand with the advantage of low thrombogenicity and the disadvantage of abbreviated durability of bioprostheses on the other. Much of the increased mortality in patients receiving a tissue valve is because of reoperation, which is associated with approximately twice the mortality of the initial procedure. As surgical risk declines, however, this balance may change, and this concern is not applicable in older patients who are unlikely to require a second valve replacement. The option of valve-in-valve transcatheter valve replacement for prosthetic valve dysfunction330-332 also may tilt the balance toward a bioprosthetic valve (see Chapter 56). With mitral valve replacement, the prosthetic valve type does not influence survival nor the probability of developing other valve-related complications, including endocarditis, valve thrombosis, and systemic embolism, although anticoagulant-related bleeding is higher in patients receiving mechanical valves. Patients with mechanical valves also have a higher incidence of paravalvular regurgitation in the mitral position, and a trend for this complication in the aortic position has been noted. The higher survival rates with mechanical than with bioprosthetic valves have been confirmed in several studies. Women with artificial valves can tolerate the hemodynamic burden of pregnancy well, but the hypercoagulable state of pregnancy increases the risk of thromboembolism in pregnant patients with mechanical prostheses (see Chapter 78). There is also a risk of fetal malformation caused by the probable teratogenic effect of warfarin. Although these problems represent rationales for the use of tissue valves in all women of childbearing age, their limited durability in young adults makes their use unacceptable. Therefore, every effort should be made to defer valve replacement until after childbirth. Women of childbearing potential who have a mechanical prosthesis should be counseled against pregnancy. When a woman who already has a mechanical prosthetic valve becomes pregnant, the risk of fetal defects with oral anticoagulants must be balanced against the risk of inadequate anticoagulation if oral therapy is interrupted. The management of anticoagulation in pregnant women with mechanical valves is controversial. All agree that the goal is continuous, effective, monitored anticoagulation and avoidance of fetal defects. In pregnant patients who receive warfarin, oral therapy is discontinued at week 36 of gestation and replaced with continuous intravenous unfractionated heparin. Heparin should be discontinued at the onset of labor but may be restarted, along with warfarin, several hours after delivery. When noncardiac surgery is required for patients with prosthetic valves who are receiving anticoagulants, the risk depends on the valve type, location, and associated risk factors. B, Freedom from valve-related complications after mechanical versus bio- prosthetic mitral valve replacement. The use of subcutaneous low-molecular-weight heparin in this situation has been advocated by some experts, but this topic represents another area of controversy. The high incidence of bioprosthetic valve failure in children and adolescents almost prohibits their use in these groups. In young adults between the ages of 25 and 35 years, the failure of bioprosthetic valves is somewhat higher than in older adults; this serves as a relative, but not an absolute, contraindication to their use in this age group. Jude valve), with its favorable hemodynamics and established durability, is preferred despite the disadvantages inherent in the need for anticoagulants in this age group. However, several studies have reported no difference in survival of patients with a bioprosthesis or a mechanical valve, coupled with an unacceptably high rate of stroke and major bleeding in patients with the mechanical valves. Current guidelines no longer recommend mechanical valves for these patients, but this clearly is an area in which physician judgment is important for individual patients. The risk of thrombosis for all valves is highest in the tricuspid position because of the lower pressures and velocity of blood flow. This complication appears to be highest for tilting disc valves, intermediate for caged ball valves, and lowest for bioprostheses, which are the valves of choice as tricuspid replacements. Fortunately, bioprostheses exhibit a much slower rate of mechanical deterioration in the tricuspid position than in the mitral or aortic positions. Bosse Y, Mathieu P, Pibarot P: Genomics: the next step to elucidate the etiology of calcific aortic valve stenosis.

Because of potential toxicity in various organ systems breast cancer in men statistics order clomiphene with mastercard, special multidisciplinary amiodarone clinics have been used by some in an attempt to prevent adverse outcomes when the drug is used pregnancy 13 weeks generic 50 mg clomiphene free shipping. Important interactions with other drugs occur pregnancy 5 weeks ultrasound photos order generic clomiphene online, and when given concomitantly with amiodarone menopause gastro symptoms buy clomiphene australia, the doses of warfarin pregnancy line order 100 mg clomiphene overnight delivery, digoxin, and other antiarrhythmic drugs should be reduced by a third to a half and the patient observed closely. Drugs with synergistic actions, such as beta blockers or calcium channel blockers, must be given cautiously. The safety of amiodarone during pregnancy has not been established, and it should be used in pregnant patients only if no alternatives exist. Like amiodarone, dronedarone alters the activity of multiple cardiac ion channels (see Tables 35-1, 35-2, 35-3, and 35-5). It is a more potent blocker of the rapid sodium current than amiodarone is and exhibits similar effects on the L-type calcium current. Blockade of both the rapid and slow components of the delayed rectifier potassium current by dronedarone is also similar to that by amiodarone, whereas its effect on the atrial acetylcholine-activated potassium current and antiadrenergic effects (via noncompetitive binding) are significantly more potent than that of amiodarone. Dronedarone has little effect on cardiac performance except in patients with compromised ventricular systolic function and should not be used in those with clinical signs of heart failure. Dronedarone is 70% to 90% absorbed after oral administration, with peak plasma concentrations being achieved in 3 to 4 hours; absorption is enhanced by food (see Table 35-4). Unlike the very long half-life of amiodarone, the elimination half-life of dronedarone is 13 to 19 hours, with 85% of the drug being excreted unchanged in feces and the remainder in urine. There is little warfarin interaction, but dronedarone increases serum levels of dabigatran. Although it can increase the strength of contraction by prolonging repolarization, which occurs maximally at slow heart rates, the negative inotropic effects predominate. In patients with reduced cardiac function, sotalol can decrease the cardiac index, increase filling pressure, and precipitate overt heart failure. Therefore, it must be used cautiously in patients with marginal cardiac compensation but is well tolerated in those with normal cardiac function. Sotalol is completely absorbed and not metabolized, thus making it 90% to 100% bioavailable. It is not bound to plasma proteins, is excreted unchanged primarily by the kidneys, and has an elimination half-life of 10 to 15 hours (see Table 35-4). Over the dose range of 160 to 640 mg, sotalol displays dose proportionality with plasma concentration (usually in the range of 2. The standard recommended dose is 400 mg every 12 hours with food (see Table 35-4). Dronedarone is indicated to facilitate cardioversion of atrial flutter or fibrillation or to maintain sinus rhythm after restoration of sinus rhythm. Patients taking dronedarone should be evaluated periodically to ensure that permanent fibrillation or heart failure has not developed. A transient, predictable increase in serum creatinine, without adversely affecting actual glomerular filtration or other measures of renal function, occurs with standard dosing and is not a reason to alter the dose or to discontinue use of the drug. Rash, photosensitivity, nausea, diarrhea, dyspepsia, headache, and asthenia have occurred in treated patients at higher frequency than in controls. Absence of the iodine molecule appears to account for the lower prevalence of lung and thyroid toxicity in dronedarone-treated patients than in those taking amiodarone. Dronedarone should not be used during pregnancy (category X, evidence or risk of fetal harm) and is possibly unsafe for breast feeding. Bretylium Tosylate Bretylium is a quaternary ammonium compound that had been used parenterally in patients with life-threatening ventricular tachyarrhythmias. Because of poor efficacy, it is no longer manufactured or available in the United States. Sotalol Sotalol is a nonspecific beta adrenoceptor blocker without intrinsic sympathomimetic activity that prolongs repolarization. Both the d- and l-isomers have similar effects on prolonging repolarization, whereas the l-isomer is responsible for almost all the beta-blocking activity (see Tables 35-1, 35-2, 35-3, and 35-5). Action potential prolongation is greater at slower rates (reverse use dependence). Resting membrane potential, action potential amplitude, and Vmax are not significantly altered. Doses exceeding 320 mg/day can be used in patients when the potential benefits outweigh the risk for proarrhythmia. It appears to be more effective than conventional antiarrhythmic drugs and may be comparable to amiodarone in the treatment of patients with ventricular tachyarrhythmias, as well as in prevention of recurrences of atrial fibrillation after cardioversion. It has been used successfully to decrease the incidence of atrial fibrillation after cardiac surgery. Overall, new or worsened ventricular tachyarrhythmias occur in approximately 4% of patients; this response is the result of torsades de pointes in around 2. Other adverse effects commonly seen with other beta blockers also apply to sotalol. Ibutilide Ibutilide is an agent released for acute termination of episodes of atrial flutter and fibrillation (see Chapter 37). Ibutilide is administered intravenously and has a large volume of distribution (see Table 35-4). Clearance is 700 V predominantly renal, with a drug half-life averaging 6 hours, but with considerable interpatient variability. Significant drug-drug interactions have been reported in patients taking dofetilide; cimetidine, verapamil, ketoconazole, and trimethoprim, alone or in combination with sulfamethoxazole, cause a significant elevation in the dofetilide serum concentration and should not be used with this drug. Ibutilide is given as an intravenous infusion of 1 mg over a 10-minute period (see Table 35-4). A second 1-mg dose may be given after the first dose is finished if the arrhythmia persists. Patients must have continuous electrocardiographic monitoring throughout the dosing period and for 6 to 8 hours thereafter because of the risk for ventricular arrhythmias. Pretreatment with intravenous magnesium may decrease the risk for ventricular arrhythmias and enhance efficacy in treating some atrial arrhythmias. Ibutilide is indicated for termination of an established episode of atrial flutter or fibrillation. It should not be used in patients with frequent short paroxysms of atrial fibrillation because it merely terminates episodes and is not useful for long-term prevention. Patients whose condition is hemodynamically unstable should proceed to direct-current cardioversion. Ibutilide has been used safely and effectively in patients who were already taking amiodarone or propafenone but should be used with caution in these cases. Ibutilide has been administered at the time of transthoracic electrical cardioversion to increase the likelihood of termination of atrial fibrillation. In one study, all 50 patients given ibutilide before attempted electrical cardioversion achieved sinus rhythm, whereas only 34 of 50 who did not receive the drug converted to sinus rhythm. Of note, all 16 patients who did not respond to electrical cardioversion without ibutilide were successfully electrically cardioverted to sinus rhythm when a second attempt was made after ibutilide pretreatment. Ibutilide prolongs accessory pathway refractoriness and can temporarily slow the ventricular rate during preexcited atrial fibrillation. This effect develops within the first 4 to 6 hours of dosing, after which the risk is negligible. Thus, patients in whom the drug is used must undergo electrocardiographic monitoring for up to 8 hours after dosing. This requirement can make the use of ibutilide in emergency departments or private offices problematic. The safety of ibutilide during pregnancy has not been well studied, and its use in this setting should be restricted to patients in whom no safer alternative exists. Oral dofetilide is indicated for prevention of episodes of supraventricular tachyarrhythmias, particularly atrial flutter and fibrillation. Because the risk for torsades de pointes is highest at the time of drug initiation, it should be used continuously and not as intermittent outpatient dosing. Its use in pregnancy has not been studied extensively, and it should probably be avoided in this setting if possible. Nifedipine and other dihydropyridine agents exhibit minimal electrophysiologic effects at clinically used doses; these drugs are not discussed here. L in all cardiac fibers, verapamil reduces the plateau height of the action potential, slightly shortens muscle action potential, and slightly prolongs Purkinje fiber action potential (see Tables 35-1, 35-2, 35-3, and 35-5). It does not appreciably affect the action potential amplitude, V max of phase 0, or resting membrane voltage in cells that have fast-response characteristics related to I Na. Verapamil suppresses slow responses elicited by various experimental methods, as well as sustained triggered activity and early and late afterdepolarizations. Verapamil slows activation of the slow channel and delays its recovery from inactivation. The l-isomer blocks the slow inward current carried by calcium, as well as other ions, traveling through the slow channel. Verapamil may also cause other effects that indirectly alter cardiac electrophysiology, such as decreasing platelet adhesiveness or reducing the extent of myocardial ischemia. This effect is more prominent in the atria than in the ventricles-30% increase in the atrial refractory period versus 20% in the ventricle. Dofetilide is more effective than quinidine at converting atrial fibrillation to sinus rhythm. Orally administered dofetilide is absorbed well, and more than 90% is bioavailable. The spontaneous sinus rate may decrease slightly, an effect only partially reversed by atropine. More commonly, the sinus rate does not change significantly because verapamil causes peripheral vasodilation, transient hypotension, and reflex sympathetic stimulation, which mitigates any direct slowing effect that verapamil exerts on the sinus node. If verapamil is given to a patient who is also receiving a beta blocker, the sinus node discharge rate may slow because reflex sympathetic stimulation is blocked. Verapamil does not exert a significant direct effect on atrial or ventricular refractoriness or on the anterograde or retrograde properties of accessory pathways. However, reflex sympathetic stimulation after intravenous verapamil administration may increase the ventricular response over the accessory pathway during atrial fibrillation in patients with Wolff-ParkinsonWhite syndrome, sometimes dangerously so. Because verapamil interferes with excitation-contraction coupling, it inhibits vascular smooth muscle contraction and causes marked vasodilation in coronary and other peripheral vascular beds. The reflex sympathetic effects of verapamil may reduce its marked negative inotropic action on isolated cardiac muscle, but the direct myocardial depressant effects of verapamil may predominate when the drug is given in high doses. In patients with well-preserved left ventricular function, combined therapy with propranolol and verapamil appears to be well tolerated, but beta blockade can accentuate the hemodynamic depressant effects produced by oral verapamil. Patients with reduced left ventricular function may not tolerate the combined blockade of beta receptors and calcium channels; thus, in these patients, verapamil and propranolol should be used in combination either cautiously or not at all. Verapamil reduces myocardial oxygen demand while decreasing coronary vascular resistance. Peak alterations in hemodynamic variables occur 3 to 5 minutes after completion of a verapamil injection, with the major effects dissipating within 10 minutes. Systemic resistance and mean arterial pressure decrease, as does left ventricular dP/dtmax, and left ventricular end-diastolic pressure increases. Heart rate, cardiac index, and mean pulmonary artery pressure do not change significantly in individuals with normal resting left ventricular systolic function. Thus the afterload reduction produced by verapamil significantly counterbalances its negative inotropic action, so the cardiac index may not be reduced. In addition, when verapamil slows the ventricular rate in a patient with tachycardia, hemodynamics may also improve. Nevertheless, caution should be exercised in giving verapamil to patients with severe myocardial depression or those receiving beta blockers or disopyramide because hemodynamic deterioration may progress in some patients. After oral administration, absorption is almost complete, but its overall bioavailability of 20% to 35% suggests substantial first-pass metabolism in the liver, particularly of the l-isomer. Norverapamil is a major metabolite that may contribute to the electrophysiologic actions of verapamil. With diltiazem, the percentage of heart rate reduction in atrial fibrillation is related to its plasma concentration. The initial effect achieved with the first bolus injection, such as slowing of the ventricular response during atrial fibrillation, can be maintained by continuous infusion of the drug at a rate of 0. Significant hypotension resulting from intravenous diltiazem can be countered by volume expansion or the judicious use of a pure vasoconstrictor agent such as phenylephrine. Various 35 long-acting preparations (once daily) are available for verapamil and diltiazem. Assuming that the patient is stable, verapamil should definitely be tried before termination is attempted by digitalis administration, pacing, electrical direct-current cardioversion, or acute blood pressure elevation with vasopressors. Although intravenous verapamil has been given along with intravenous propranolol, this combination should be used only with great caution because of combined adverse hemodynamic effects. In addition, verapamil may prevent early recurrence of atrial fibrillation after electrical cardioversion. Atrial fibrillation may develop in some patients with atrial flutter after verapamil administration. As noted earlier, in patients with preexcited ventricular complexes during atrial fibrillation associated with Wolff-Parkinson-White syndrome, intravenous verapamil may accelerate the ventricular response; therefore the intravenous route is contraindicated in this situation. Verapamil must be used cautiously in patients with significant hemodynamic impairment or in those receiving beta blockers, as noted earlier. Hemodynamic collapse has been noted in infants, and verapamil should be used cautiously in children younger than 1 year. Verapamil should also be used with caution in patients with sinus node abnormalities because marked depression of sinus node function or asystole can result in some of these patients. Intravenous isoproterenol, calcium, glucagon, dopamine, or atropine, which may be only partially effective, or temporary pacing may be necessary to counteract some of the adverse effects of verapamil.

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Disruption menstruation definition purchase 25 mg clomiphene mastercard, platelet aggregation menstruation and breastfeeding generic 25 mg clomiphene with visa, and thrombosis are associated with markers of inflammation and various conventional risk factors for coronary atherosclerosis women's health on birth control clomiphene 25 mg order fast delivery, such as cigarette smoking and hyperlipidemia menopause young living clomiphene 100 mg buy low price. Some of the less common women's health kindle clomiphene 100 mg order mastercard, nonatherosclerotic coronary artery abnormalities have specific pathologic features as well. Experimental data have also suggested increased susceptibility to poten36 sec tially lethal ventricular arrhythmias in patients with left ventricular hypertrophy and ischemia and reperfusion. Lev disease, Lenègre disease, ischemic injury caused by small144 sec Spontaneous vessel disease, and numerous infiltrative or inflamreversion A matory processes can result in such changes. Closed arrows indicate the site of spasm before and after nitroglycerin; the open arrow indicates a lower grade distal lesion. In one study, 72% of men in the 25- to secondary cardioneuropathy) or may be primary, as in a selective 44-year age group who died suddenly (24 hours) with no previous cardiac viral neuropathy. Secondary involvement can be a conseclinical history of coronary heart disease had scars of large (63%) or quence of ischemic neural injury in coronary heart disease and has small (<1-cm cross-sectional area, 9%) areas of healed myocardial been proposed to result in autonomic destabilization, thereby enhancnecrosis. The incidence of acute myocardial infarction is considerably ing the propensity to arrhythmias. Nerve sprouting may be imporlower, with cytopathologic evidence of recent myocardial infarction tant. This estia clinical technique for imaging of cardiac neural fibers suggests a mate corresponds well with the results of studies of out-of-hospital changing pattern over time after myocardial infarction. Viral, neurocardiac arrest survivors, who were found to have an incidence of new toxic, and hereditary causes. Even though there is an association MechanismsandPathophysiology between elevations in troponin levels during chest pain syndromes Electrical mechanisms of cardiac arrest are divided into tachyarand risk for subsequent cardiac death and although increases in troponin levels are seen in a substantial proportion of cardiac arrest rhythmic and bradyarrhythmic-asystolic events. No close correlation has been found a mechanical event because of complete absence of electrical activbetween increased heart weight and the severity of coronary heart ity (asystole). Risk for hypertrophy-associated adequately perfuse and maintain consciousness, which usually Spontaneous spasm Cardiac Arrest and Sudden Cardiac Death 838 requires a heart rate of less than 20 beats/min. The risk for cardiac arrest is conditioned by the presence of structural abnormalities and modulated by functional variations. The specialized conducting tissue is more resistant to acute ischemia than working myocardium is, and therefore the electrophysiologic consequences are less intense and delayed in onset in specialized conduction tissue. Reperfusion of ischemic areas can occur by three mechanisms: (1) spontaneous thrombolysis, (2) collateral flow from other coronary vascular beds to the ischemic bed, and (3) reversal of vasospasm. Some mechanisms of reperfusion-induced arrhythmogenesis appear to be related to the duration of ischemia before reperfusion. Experimentally, there is a window of vulnerability beginning 5 to 10 minutes after the onset of ischemia and lasting up to 20 to 30 minutes. Within the first minutes after experimental coronary ligation, there is a propensity to ventricular arrhythmias that abates after 30 minutes and reappears after several hours (see Chapter 33). The initial 30 minutes of arrhythmias is divided into two periods, the first of which lasts for approximately 10 minutes and is presumably directly related to the initial ischemic injury. The second period (20 to 30 minutes) may be related either to reperfusion of ischemic areas or to the evolution of different injury patterns in epicardial and endocardial muscle. Multiple mechanisms of reperfusion arrhythmias have been observed experimentally, including slow conduction and reentry and afterdepolarizations and triggered activity. At the level of the myocyte, the immediate consequences of ischemia, which include alterations in cell membrane physiology, with efflux of K+, influx of Ca2+, acidosis, reduction of transmembrane resting potentials, and enhanced automaticity in some tissues, are followed by a separate series of changes during reperfusion. Those of particular interest are the possible continued influx of Ca2+, which may produce electrical instability; responses to alpha or beta adrenoceptor stimulation, or both; and afterdepolarizations as triggering responses for Ca2+-dependent arrhythmias. Other possible mechanisms studied experimentally include the formation of superoxide radicals in reperfusion arrhythmias and differential responses of endocardial and epicardial muscle activation times and refractory periods during ischemia or reperfusion. Its activation results in a strong efflux of K+ ions from myocytes and markedly shortening of the time course of repolarization, which leads to slow conduction and ultimately to inexcitability. The fact that this response is more marked in epicardium than in endocardium leads to a prominent dispersion of repolarization across the myocardium during transmural ischemia. At an intercellular level, ischemia alters the distribution of connexin 43, the primary gap junction protein between myocytes. Tissue healed after previous injury appears to be more susceptible to the electrical destabilizing effects of acute ischemia, as is chronically hypertrophied muscle. Some data suggest that remodeling-induced local stretch, regional hypertrophy, or intrinsic cellular alteration may contribute to this vulnerability. Of more direct clinical relevance is the suggestion that potassium depletion by diuretics and clinical hypokalemia may make ventricular myocardium more susceptible to potentially lethal arrhythmias. The association of metabolic and electrolyte abnormalities and neurophysiologic and neurohumoral changes with lethal arrhythmias emphasizes the importance of integrating changes in the myocardial substrate with systemic influences. Most direct among myocardial metabolic changes in response to ischemia are local acute increase in interstitial K+ levels to values exceeding 15 mM, a decrease in tissue pH to below 6. Other metabolic changes, such as elevation of cyclic adenosine monophosphate levels, accumulation of free fatty acids and their metabolites, formation of lysophosphoglycerides, and impaired myocardial glycolysis, have also been suggested as myocardial-destabilizing influences. However, the specific mechanisms by which these lesions lead to potentially lethal disturbances in electrical stability are not simply the consequence of steady-state reductions in regional myocardial blood flow in association with variable demands (see Chapter 41). However, the dynamic nature of the pathophysiologic mechanism of coronary events has led to the recognition that superimposed acute lesions create a setting in which alterations in the metabolic or electrolyte state of the myocardium are the common circumstance leading to disturbed electrical stability. Neurogenic influences may play a role but do not appear to be a sine qua non for the production of spasm. Vessel susceptibility and humoral factors, particularly those related to platelet activation and aggregation, also appear to be important mechanisms. Inflammatory responses in atherosclerotic plaque are now viewed as the condition leading to lesion progression, including erosion, disruption, platelet activation, and thrombosis. The rapid initiation of lethal arrhythmias, the spontaneous thrombolysis, a dominant role of spasm induced by platelet products, or a combination of these factors may explain this observation. The triggering event may be electrophysiologic, ischemic, metabolic, or hemodynamic. The endpoint of their interaction is disorganization of patterns of myocardial activation into multiple uncoordinated reentrant pathways. Clinical, experimental, and pharmacologic data have suggested that triggering events in the absence of myocardial instability are unlikely to initiate lethal arrhythmias. Recurrence rates decreased subsequently, probably in part the result of long-term interventions. However, it is not known whether the decrease resulted from a change in the natural history, changes in preventive strategies for the underlying disease, or long-term interventions for control of arrhythmic risk. Asystolic arrest is more common in severely diseased hearts and in patients with a number of endstage disorders, cardiac and noncardiac. These mechanisms may result, in part, from diffuse involvement of subendocardial Purkinje fibers in advanced heart disease. The common denominator in both is the presence of organized cardiac electrical activity in the absence of effective mechanical function. The primary form is the more familiar; in this form none of these obvious mechanical factors is present, but ventricular muscle fails to produce an effective contraction despite continued electrical activity. It usually occurs as an end-stage event in advanced heart disease, but it can occur in patients with acute ischemic events or, more commonly, after electrical resuscitation from prolonged cardiac arrest. Although it is not thoroughly understood, it appears that diffuse disease, metabolic abnormalities, or global ischemia provides the pathophysiologic substrate. Although several studies have reported that 12% to 46% of fatalities occur in patients who had seen a physician 1 to 6 months before death, such visits are more likely to presage myocardial infarction or nonsudden death, and most complaints responsible for these visits are not heart related. The symptoms that occur within the last hours or minutes before cardiac arrest are more specific for heart disease and may include symptoms of arrhythmias, ischemia, and heart failure. Nonetheless, many have elevations in enzyme levels along with nonspecific electrocardiographic changes suggesting myocardial damage, which may be caused by transient ischemia as a triggering event or be a consequence of the loss of myocardial perfusion during the cardiac arrest. The former supports the concept of transient pathophysiologic changes (such as a transient platelet plug) associated with acute coronary syndromes as the trigger for cardiac arrest. The recurrence rate is low in survivors of out-of-hospital cardiac arrest caused by documented transmural myocardial infarction. In the period of 1 hour or less between acute changes in cardiovascular status and the cardiac arrest itself is defined as the "onset of the terminal event. Alterations in autonomic nervous system activity may also contribute to onset of the event. Studies of short-term variations in heart rate variability or related measures have identified changes that correlate with the occurrence of ventricular arrhythmias. Although these physiologic properties may be associated with transient electrophysiologic destabilization of the myocardium, the extent to which they are paralleled by clinical symptoms or events has been less well documented. CardiacArrest Cardiac arrest is characterized by abrupt loss of consciousness caused by lack of adequate cerebral blood flow as a result of failure of cardiac pump function. It almost always leads to death in the absence of a successful intervention, although spontaneous reversions occur rarely. Mechanical mechanisms include rupture of the ventricle, cardiac tamponade, acute mechanical obstruction to flow, and acute disruption of a major blood vessel. Closely related to the potential for successful resuscitation is the decision regarding whether to attempt to resuscitate. Although 41% of the patients had suffered an acute myocardial infarction, 73% had a history of congestive heart failure and 20% had experienced previous cardiac arrests. The mean age of 70 years may have influenced the outcome statistics, but patients with high-risk complicated myocardial infarction and those with other high-risk markers heavily influenced the population of patients at risk for in-hospital cardiac arrest. Non­cardiac-related clinical diagnoses were dominated by renal failure, pneumonia, sepsis, diabetes, and a history of cancer. Adverse risks were age older than 70 years, previous stroke or renal failure, and heart failure on admission. Better outcomes were predicted by previous angina pectoris or admission because of ventricular arrhythmias. Strategic factors affecting survival after in-hospital cardiac arrest include the location in the hospital, the type of hospital, daytime and evening events versus night and weekend events, and a rapid time to performance of defibrillation. However, the proportion maintained on mechanical ventilators at the time of arrest did increase from 67. The fraction of out-of-hospital cardiac arrest survivors who are discharged from the hospital alive may now equal or exceed the fraction of in-hospital cardiac arrest victims who are discharged alive, and the postdischarge mortality rate for in-hospital cardiac arrest survivors is higher than that for out-of-hospital cardiac arrest survivors; these are telling clinical statistics. They emphasize the success of preventive measures for cardiac arrest in low-risk in-hospital patients, a finding indicating that these statistics are dominated by higher risk patients. However, other data demonstrate that survival after in-hospital cardiac arrest is lower for events that occur during weeknights and weekends than during the daytime and evening hours during the week125 and that more rapid times to defibrillation are advantageous. Among elderly persons, outcomes after community-based responses to out-of-hospital cardiac arrest are not as good as for younger victims. In one study comparing persons younger than 80 years (mean age, 64 years) with those in their 80s and 90s, the survival rate to hospital discharge in the younger group was 19. ArrhythmiAs, sudden deAth, And syncope 17%, respectively), but the frequency of ventricular tachyarrhythmias versus nonshockable rhythms was lower in elderly persons. Overall, advanced age is only a weak predictor of an adverse outcome and should not be used in isolation as a reason to not resuscitate. Longterm neurologic status and length of hospitalization were similar in older and younger surviving patients. ProgressiontoBiologicDeath the time course for progression from cardiac arrest to biologic death is related to the mechanism of the cardiac arrest, the nature of the underlying disease process, and the delay between onset and resuscitative efforts. The onset of irreversible brain damage usually begins within 4 to 6 minutes after loss of cerebral circulation, and biologic death follows quickly in unattended cardiac arrest. In large series, however, it has been demonstrated that a limited number of victims can remain biologically alive for longer periods and may be resuscitated after delays in excess of 8 minutes before beginning basic life support and in excess of 16 minutes before advanced life support. Despite these exceptions, it is clear that the probability of a favorable outcome-survival neurologically intact-deteriorates rapidly as a function of time after cardiac arrest. Younger patients with less severe cardiac disease and the absence of coexistent multisystem disease have a higher probability of a favorable outcome after such delays. Irreversible injury to the central nervous system usually occurs before biologic death, and the interval may extend days to weeks and occasionally result in very prolonged persistent vegetative states in patients who are resuscitated during the temporal gap between brain damage and biologic death. Thus there is a longer interval between the onset of cardiac arrest and the end of the period that allows successful resuscitation. Such patients, whether in an in-hospital or outof-hospital environment, have a poor prognosis because of advanced heart disease or coexistent multisystem disease. They tend to respond poorly to interventions, even if the heart is successfully paced. Although a small subgroup of patients with bradyarrhythmias 841 associated with electrolyte or pharmacologic abnormalities may respond well to interventions, most progress rapidly to biologic death. The infrequent cardiac arrests caused by mechanical factors such as tamponade, structural disruption, and impedance to flow by major thromboembolic obstructions to right or left ventricular outflow are reversible only in patients in whom the mechanism is recognized and an intervention is feasible. Most of these events lead to rapid biologic death, although prompt relief of tamponade-induced cardiac arrest will save some lives. The mean age of this group was 43 years, and 46% had had no previous history of presyncope or syncope. Cardiac Arrest and Sudden Cardiac Death SurvivorsofCardiacArrest Hospital Course Cardiac arrests during the acute phase of myocardial infarction are classified as primary (electrical event not associated with hemodynamic dysfunction) or secondary (electrical event linked to hemodynamic dysfunction). Management after secondary cardiac arrest in patients with myocardial infarction is dominated by the hemodynamic status of the patient. Survivors of out-of-hospital cardiac arrest may have repetitive ventricular arrhythmias during the initial 24 to 48 hours of hospitalization. These arrhythmias have variable responses to antiarrhythmic therapy, depending on hemodynamic status. The overall rate of recurrent cardiac arrest is low, 10% to 20%, but the mortality rate in patients who have recurrent cardiac arrests is approximately 50%. Only 5% to 10% of in-hospital deaths after out-of-hospital resuscitation are caused by recurrent cardiac arrhythmias. The most common causes of death in hospitalized survivors of out-of-hospital cardiac arrest are noncardiac events related to central nervous system injury, including anoxic encephalopathy and sepsis related to prolonged intubation and hemodynamic monitoring lines. Fifty-nine percent of deaths during the index hospitalization after out-of-hospital resuscitation have been reported to be from these causes. Approximately 40% of those who arrive at the hospital in coma never awaken after admission to the hospital and die after a median survival of 3.

Rates lower than 60 beats/minute are considered to be bradycardia menopause increased libido 25 mg clomiphene purchase visa, and rates higher than 100 beats/minute are considered to be tachycardia menstruation vs pregnancy order clomiphene online pills. Arrhythmias resulting in bradycardia or tachycardia can be thought of as specific disorders of each of these components menopause longer periods 50 mg clomiphene buy visa. For example pregnancy 01 cheap clomiphene 50 mg fast delivery, the response to carotid sinus massage may be slightly different from what is listed breast cancer 101 cheap clomiphene 100 mg line. Acute therapy to terminate a tachycardia may be different from chronic therapy to prevent recurrence. Some of the exceptions are indicated in the footnotes; the reader is referred to text for a complete discussion. P waves initiated by sinus node discharge may not be precisely regular because of sinus arrhythmia. Carotid sinus massage and Valsalva or other vagal maneuvers gradually slow sinus tachycardia, which then accelerates to its previous rate on cessation of the enhanced vagal tone. More rapid sinus rates can fail to slow in response to a vagal maneuver, particularly those driven by high adrenergic tone. Specific Arrhythmias: Diagnosis and Treatment Clinical Features Sinus tachycardia is common in infancy and early childhood and is the normal reaction to various physiologic Atrial rate greater or pathophysiologic stress, such as fever, hypotension, than ventricular rate In postural orthostatic tachycardia syndrome, a tients with supraventricular arrhythmias-executive summary: A report of the American College of related syndrome consisting of orthostatic hypotension Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society and sinus tachycardia, the cause of the orthostatic of Cardiology Committee for Practice Guidelines [Writing Committee to Develop Guidelines for the decrease in blood pressure is not hypovolemia or drugs. The maximum heart rate achieved during strenuous physical activity varies widely but decreases with age. The P-P interval can vary slightly from cycle to cycle, especially at slower rates. P waves have a normal contour, a larger amplitude can develop, and the wave can become peaked. The most common reversible causes include hyperthyroidism, anemia, infection or inflammation, and hypovolemia. Elimination of tobacco, alcohol, caffeine, or other stimulants, such as the sympathomimetic agents in nose drops and cold medications, may be helpful. Beta blockers and nondihydropyridine calcium channel blockers (verapamil and diltiazem), fluid replacement in a hypovolemic patient, or fever reduction in a febrile patient can help slow the sinus nodal discharge rate. Treatment of inappropriate sinus tachycardia requires beta blockers or calcium channel blockers, alone or in combination. After three spontaneous sinus-initiated beats, premature stimulation of the high right atrium (S2, S3) initiates a sustained tachycardia at a cycle length of 450 milliseconds that has the identical high-low atrial activation sequence characteristic of sinus node discharge. V diagnosis of prematurity difficult, differences in the contour of the P waves are usually apparent and indicate a different focus of origin. The length of the pause that follows any premature complex or series of premature complexes is determined by the interaction of several factors. Reset (noncompensatory pause) occurs when the A1-A 2 interval plus the A 2-A 3 interval is less than two times the A1-A1 interval and the A 2-A 3 interval is greater than the A1-A1 interval. Often when this happens, the interval between the A 3 and the next sinus-initiated P wave exceeds the A1A1 interval. ArrhythmiAs, sudden deAth, And syncope PrematureAtrialComplexes Premature complexes are among the most common causes of an irregular pulse and palpitations. Premature complexes are common in normal hearts and increase in frequency with age. Although the contour of a premature P wave can resemble that of a normal sinus P wave, it generally differs. An interpolated atrial or ventricular premature complex of any type represents the only type of premature systole that does not actually replace the normally conducted beat. Because the right bundle branch at long cycles has a longer refractory period than the left bundle branch does, aberration with a right bundle branch block pattern at slow rates occurs more commonly than aberration with a left bundle branch block pattern. At shorter cycles, the refractory period of the left bundle branch Three types of atrial tachycardia have been distinguished experimentally- automatic, triggered, and reentrant. For example, adrenergic stimulation can initiate automatic and triggered atrial tachycardias, and burst pacing may initiate triggered and microreentrant atrial tachycardias. Therefore, because it determines the approach to mapping and management, atrial tachycardias are more broadly characterized clinically as being focal (originating from a small area of the atrium with atrial excitation emanating from this focus) or macroreentrant (a relatively large reentrant circuit using conduction barriers to create the circuit). AtrialTachycardias Atrial Flutter and Other Macroreentrant Atrial Tachycardias Atrial flutter is the prototypic macroreentrant atrial rhythm. The typical atrial flutter is a reentrant rhythm in the right atrium that is constrained anteriorly by the tricuspid annulus and posteriorly by the crista terminalis and eustachian ridge. The flutter can circulate in a counterclockwise direction around the tricuspid annulus in the frontal plane (typical flutter, counterclockwise flutter) or in a clockwise direction (atypical, clockwise, or reverse flutter). Rarely, intra-isthmus flutter can occur when the reentrant circuit is isolated to the cavotricuspid isthmus rather than rotating around the entire tricuspid annulus; this typically occurs after ablation in this region (usually done as treatment of typical flutter). Other forms of atrial flutter are now recognized as distinct types and include atrial macroreentry caused by incisional scars from previous atrial surgery, previous atrial ablation, mitral annular flutter, idiopathic fibrosis in areas of the atrium, or other anatomic or functional barriers to conduction in the atria. Because the barriers that constrain these atrial flutters are variable, the electrocardiographic pattern of these so-called atypical atrial flutters can be varied. Sometimes, flutter wave morphology changes during the same episode of flutter, which indicates multiple circuits or nonfixed conduction barriers. The ratio of flutter waves to conducted ventricular complexes is most often an even number. However, these tachycardias frequently have a flutter rate similar to that of typical flutter (250 to 390 beats/min). Table 37-2 shows common electrocardiographic findings with the different types of macroreentrant atrial flutter. After extensive left atrial ablation for atrial fibrillation, the electrocardiographic pattern of even typical flutter can appear "atypical" (not have the typical appearance described before) because of the altered left atrial activation as a result of altered conduction secondary to the left atrial ablation. ArrhythmiAs, sudden deAth, And syncope Electrocardiographic Recognition the atrial rate during typical atrial flutter is usually 250 to 350 beats/ minute, although it is occasionally slower, particularly when the patient is treated with antiarrhythmic drugs, which can reduce the rate to about 200 beats/minute. If such slowing occurs, the ventricles can respond in a 1:1 fashion to the slower atrial rate. When the flutter waves are upright from clockwise rotation, they are often notched. It can occur as a result of atrial dilation from septal defects, pulmonary emboli, mitral or tricuspid valve stenosis or regurgitation, heart failure, previous extensive atrial ablation, and aging, but it can also occur without underlying heart disease. Toxic and metabolic conditions that affect the heart, such as thyrotoxicosis, alcoholism, and pericarditis, can cause atrial flutter. When it follows reparative surgery for congenital heart disease, most patients will be able to have both typical flutter and atypical flutter involving the atriotomy, which often occurs years after the surgery. Atrial flutter usually responds to carotid sinus massage with a decrease in the ventricular rate in stepwise multiples and returns in reverse manner to the former ventricular rate at the termination of carotid massage. In counterclockwise atrial Cardioversion (see Chapter 35) is commonly the initial treatment of choice for atrial flutter because it promptly and effectively restores sinus rhythm. If the electrical shock results in atrial fibrillation, a second shock at a higher energy level is used to restore sinus rhythm, or depending on clinical circumstances, the atrial fibrillation can be left untreated and can revert to atrial flutter or sinus rhythm. The short-acting antiarrhythmic medication ibutilide can also be given intravenously to convert atrial flutter. Ibutilide appears to successfully cardiovert approximately 60% to 90% of episodes of atrial flutter. Other medications, such as procainamide or amiodarone, can be given to convert atrial flutter chemically, but they are generally less effective than ibutilide. Rapid atrial pacing with a catheter in the esophagus or the right atrium can effectively terminate typical and some forms of atypical atrial flutter in most 754. This tachycardia uses a reentrant circuit established by the atriotomy on the lateral atrial wall. Because ablation is highly effective for typical flutter and because of the high relapse rate after cardioversion, ablation is the preferred approach for stable patients who do not require immediate cardioversion. Although the risk for thromboembolism is lower than that for atrial fibrillation, patients with atrial flutter do appear to have a risk for thromboembolism immediately after conversion to sinus rhythm. In general, indications for anticoagulation in patients with atrial flutter are similar to those in patients with atrial fibrillation. As a general rule, atrial flutter is much more difficult to rate-control than atrial fibrillation is. To slow the ventricular response, verapamil (see Chapter 35), given as an initial bolus of 2. Esmolol, a betaadrenergic blocker with a 9-minute elimination half-life, or other intravenous beta blockers can be used to slow the ventricular rate. If the use of calcium channel blockers and beta blockers in combination is insufficient, digoxin can be added. The dose of digitalis necessary to slow the ventricular response varies and at times can result in toxic levels because it is often difficult to slow the ventricular rate during atrial flutter. Intravenous administration of amiodarone can slow the ventricular rate as effectively as digoxin can. Side effects of these drugs, especially proarrhythmic responses, must be carefully considered (see Chapter 35). Treatment of the underlying disorder, such as thyrotoxicosis, is sometimes necessary to effect conversion to sinus rhythm. In many cases, atrial flutter can continue (or even become more persistent) while taking antiarrhythmic drugs, and the flutter rate will slow. Prevention of recurrent atrial flutter is frequently difficult to achieve medically but should be approached as outlined for atrial fibrillation (see Chapters 35 and 38). Catheter ablation should be considered in patients with symptomatic or recurrent atrial flutter. Catheter ablation of typical flutter (counterclockwise and clockwise) is a highly effective cure and has a long-term success rate of 90% to 100%. Because ablation of atrial flutter is so effective and poses little risk, it can be offered as an alternative to drug therapy. Ablation of other forms of macroreentrant atrial tachycardia is also effective, although success rates are somewhat lower and more variable. Increasing evidence has indicated that the risk for emboli in patients with atrial flutter may be more significant than once thought. Consequently and because many patients with atrial flutter also have atrial fibrillation, anticoagulation is usually warranted. However, carefully controlled studies to determine the degree of embolic risk in patients with only atrial flutter are lacking. Long-term anticoagulation, as for atrial fibrillation, should probably be considered until more definitive data are available. At onset there may be some warming up of the rate that results in a slight increase in the heart rate over the initial several complexes. Frequently, atrial tachycardias occur in short, recurrent bursts with spontaneous terminations. In nearly half the cases of atrial tachycardia with block, the atrial rate is irregular. Characteristic isoelectric intervals between P waves, in contrast to atrial flutter, are usually present in all leads. It should be performed cautiously in patients with digitalis toxicity because serious ventricular arrhythmias can result. On occasion, carotid sinus massage or adenosine can terminate some forms of atrial tachycardia. Inducibility can be variable, depending on the B mechanism of the atrial tachycardia. Analysis of P wave configuration during tachycardia indicates that a positive or biphasic P wave in V1 predicts a left atrial focus Chaotic Atrial Tachycardia. Chaotic (sometimes called multifocal) whereas a negative P wave in V1 predicts a right atrial focus. It can also occur with digitalis intoxication, often precipitated by potassium depletion. The signs, symptoms, and prognosis are usually related to the underlying cardiovascular status and the rate of the tachycardia. Atrial tachycardias frequently occur in short recurrent bursts but on occasion can be incessant. In some patients, exercise or stress can provoke the tachycardia; in others, the tachycardia may be positional. This tachycardia occurs commonly in older patients with chronic obstructive pulmonary disease and congestive heart failure and may eventually develop into atrial fibrillation. Digitalis appears to be an unusual cause, and theophylline administration has been implicated. Antiarrhythmic agents are frequently ineffective in slowing either the rate of the atrial tachycardia or the ventricular response. Beta adrenoceptor blockers should be avoided in patients with bronchospastic pulmonary disease but can be effective if tolerated. Thus, no universally acceptable nomenclature exists, but rather descriptive labels for specific arrhythmias, as used throughout this chapter. The R-R interval can shorten over the course of the first few beats at the onset or lengthen during the last few beats preceding termination of the tachycardia. If conduction over the reentrant pathway reverses direction a necessary link between the fast and slow pathways. In the left example, reentrant excitation is drawn with retrograde atrial activity H1-H2) interval. In the right example, atrial activity occurs slightly later than ventricular activity because of retrograde conduction delay. The tachycardia is caused by reentry within the sinus node, which then conducts the impulse to identical paced rates or by a sudden jump in the rest of the heart. Tachycardia is caused by reentry within the atrium, which the A-H interval during atrial pacing at a then conducts the impulse to the rest of the heart.

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