>1px alt=gallery>1px alt=gallery>1px alt=gallery>1px alt=gallery>1px alt=gallery>1px alt=gallery>1px alt=gallery>1px alt=gallery>1px alt=gallery>1px alt=gallery>1px alt=gallery>1px alt=gallery>1px alt=gallery>1px alt=gallery>1px alt=gallery>1px alt=gallery>1px alt=gallery>1px alt=gallery>1px alt=gallery>1px alt=gallery>1px alt=gallery>1px alt=gallery>1px alt=gallery>1px alt=gallery>1px alt=gallery>1px alt=gallery>1px alt=gallery>Nude Latinas Fake Pictures erotic wives fiction sex * * * * * Jane first saw the silent man with the shaved head at her own engagement party at her fianceyes enthralled to his thin muscular body for a long time. Arthur Stoddard and Jane Betts had been standing in the midst of family, friends, well-wishers, co-workers and everyone else's significant others, while "dark eyes" seemed to skirt the edge of the room nodding an occasional brief exchange with some other person. Yet, whenever Jane glanced back toward him, his deep, dark eyes consistently returned her questioning look with an obviously covetous answer. Nickie was attractive. Men looked at her. She could pull easily. Pulling the right man was another matter. She hadnbody gave wetness to his touch as the sky rained on the willing earth. His initial penetration was the nicest pain she had ever felt. She loved the sounds that he made as he climaxed. She went out with him for a year until she found out about his other dalliances " with her classmates. What particularly pissed her off was when " in the student bar " she overheard Helen boasting about the orgasms she had with him. Nickie had never been given this privilege. Downstairs, a key scraped in the lock, the front door swung open and John Walker slipped quietly into his house. He was so glad the party ended earlier than he had thought and he was certain Justine would be happy to get off earlier than she thought. He rubbed his tired eyes and looked into the empty living room. There was no sign of her and the television was still on. That was odd. Justine was the most responsible teenager he knew; he never came home to a mess and she took care of his two daughters beautifully. Yet why would that take a half hour' Renee sat down in her chair at the office and started addressing the issue with Dina and Jennifer again. "Didn't I warn you guys'" Renee said. Dina and Jennifer cried out that they could do whatever they want in the team. Renee got so angry with them that she suspended both of them for misconduct. That really got Dina and Jennifer angry. Just as Renee was about to get up and change for practice, Dina pushed her back into the office as Renee was about to walk by them. "I brought the antidote," Candice said, reaching into her satchel and pulling out the jar of goo that Lovelle had used on Harriet. "Oh God, I'm going to be in so much trouble if the other girls find out." "It was the context. Bill had...oh never mind. I'll catch you two up on the joke later. Lets go eat first. I'm starved." "Hell no I ain't stopping', I've still got four more inches for you." Her lover said as he forced himself even further into her. Ruth Eleanor smiled. "Was I'" It seemed to take forever for the station to get to the main competition. My friends were so excited, secretly I was too, but I held the cynical thought that this is going to be complete pants. It's a fake, I kept saying that and all my friends cried me down. Then there was a drum role and a hush came over everyone then someone shouted 'About time' and the rest of the crowed screamed and yelled and all hell broke loose. Finally the crowd calmed down. The DJ droned on and on ... then finally when it was clear the crowed was about to lynch him he got round to announcing the winner. The drum role was played again ... then 'Sarah Bradshaw' was shouted out. Everything around me went silent then a piercing scream from Jenny broke the silence and possibly my eardrum. The DJ asked if the winner was there and my friends all screamed that she was. They started to drag me and I didn't understand why. 'You won', 'It was your name', 'Sarah it's you'. Slowly it began to dawn on me that I had won. I made my way with my friends to the front of the crowd, still convinced that it was some big hoax. But... "Those are really pretty! If I had known, I would have bought you some in the store! Turn around so I can see them!" (Whew! Past that hurdle!). And then he pulls me to him and gives me a little kiss on the stomach! David swallowed. All the way home I fantasized about how Joseph would look without his clothes. It never occurred to me that he wouldn't show up. His kiss had told me that he would. He arrived about forty-five minutes after I pulled into my drive. I was already ready. His knock on my door sent shivers down me, but not down my spine. My twat was quivering. I couldn't wait to feel him inside me. This gave me a great opportunity to lead her on. I turned and watched the television. The woman was giving the main character a blowjob, while he tongued the other man. My hands caressed my nipples through the soft silk. I became engrossed in the movie. Watching the three bodies intertwine, imagining I was part of them. My nipples became hard, as I rubbed and pinched them. My cock was so hard now " I could feel it rub against the panties. I so wanted to touch it. 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The intrinsic pacemaker rate is highest in the sinoatrial node, which dominates the lower, slower latent cardiac pacemakers. Sinus rhythm varies remarkably on short-term and long-term recordings.Respiratory sinus arrhythmia, mediated by oscillations in vagal tone, is particularly common in young persons. The oscillations are dampened but do not entirely disappear with age. Exercise and emotion are potent accelerators of sinus rhythm through sympathetic neural and catecholamine drive. Resting sinus rates of 60 to 100 beats/min classically represent the limits of normal, but much slower sinus rates occur in young persons, particularly those trained as athletes . Thus, resting rates 100 beats/min. Normal persons have a marked diurnal variation in heart rate, with lowest rates just before early morning awakening, when sinus acceleration is substantial . Absolute regularity of sinus rhythm is pathologic and occurs with autonomic denervation (eg, in advanced diabetes).PathogenesisBradyarrhythmias arise through abnormalities of intrinsic automatic behavior or conduction, principally within the atrioventricular node and the His-Purkinje's network. Tachyarrhythmias may arise by altered automaticity, reentry, or triggered automaticity, which have been identified electrophysiologically but can rarely be differentiated clinically. Most clinically significant tachyarrhythmias are probably due to reentry.Some arrhythmias cause few or no symptoms but are associated with an adverse prognosis. Much evidence suggests that prognosis is not necessarily improved by their suppression. Other arrhythmias, although symptomatic, are benign. The nature and severity of underlying heart disease are often of greater prognostic significance than is the arrhythmia itself.Symptoms and SignsThere is a wide variation in patient awareness of arrhythmias, either as palpitations or through the more serious symptoms of hemodynamic upset.Palpitations (awareness of the heartbeat) are often disagreeable and may arise equally from increased force of contraction and from rhythm disturbance. They should be investigated to define the cause and to allay anxiety.Arrhythmias that cause hemodynamic upset are usually sustained bradycardias or tachycardias and may be life threatening. Resulting dizziness and syncope are common and may disqualify patients from driving or from certain occupations (eg, airline pilot, railroad engineer). These arrhythmias require urgent attention and, often, hospitalization.DiagnosisThe history usually provides sufficient information for establishing a working diagnosis. Patients are relatively reliable in their detection of the fast, completely irregular palpitations of paroxysmal atrial fibrillation (AF) and will tap out regular tachyarrhythmias to within 10 beats/min. The history should differentiate brief arrhythmic episodes (eg, ectopic beats, second-degree atrioventricular block) from sustained events. The onset and offset characteristics and any other symptoms should be obtained. It is a widely held but erroneous belief that a well-tolerated tachyarrhythmia must be a supraventricular tachycardia rather than a ventricular tachycardia (VT) and vice versa.If examined during an arrhythmia, the peripheral pulse (reflecting ventricular activation) and the jugular venous pulse (JVP--reflecting atrial and ventricular activation) are important for diagnosis and can positively identify VT (if atrioventricular dissociation is present) from other sustained regular tachycardias, AF, atrial flutter, atrial and ventricular ectopic beats (VEBs), and second-degree and third-degree heart block.Whereas the history should give a working diagnosis, and pulse and JVP examination during an arrhythmia may give an accurate diagnosis, the ECG remains the major diagnostic procedure. The surface ECG represents the net electrical forces of myocardial depolarization. Although each cardiac cell oscillates over a potential difference of about 90 to 100 mV, ECG signals at the body surface are typically only 1 mV in amplitude. Activation of small structures (eg, sinoatrial node, atrioventricular node, His bundle) is not seen.The standard 12-lead ECG is crucial for the characterization and diagnosis of the various sustained tachycardias. However, it provides only a brief sample of cardiac rhythm, particularly when recorded by simultaneous multichannel recorders.Ambulatory ECG monitoring is the most powerful method of capturing arrhythmic events, and its value is enhanced by keeping a diary of associated symptoms. ECG recorders are of many types, eg, those that log a continuous 24 h (Holter 24 h) or those activated by the patient or by automatic detection of an arrhythmic episode. Solid-state recorders can eliminate the vagaries of mechanical tape transport systems. Ambulatory ECG monitoring is less useful when arrhythmias are infrequent. Patients with suspected life-threatening rhythm disturbances should be hospitalized for monitoring to avoid a fatal out-of-hospital event.Invasive electrophysiologic studies are indicated when spontaneous arrhythmias are infrequent and when a serious sustained arrhythmia is suspected. Using programmed stimulation techniques, reentrant arrhythmias can be initiated and terminated. However, automatic and triggered automatic arrhythmias often are unresponsive to these techniques. Most clinical arrhythmias of importance (VT, atrioventricular nodal reentry tachycardia, reciprocating tachycardias of the preexcitation syndromes) are reentrant.Signal averaging of the surface ECG can noninvasively detect areas of slowed ventricular activation that are part of the substrate for VT. These are reflected by low-voltage post-QRS potentials. Normally obscured by ambient noise, they are exposed by averaging and amplification. Signal-averaged late potentials in survivors of acute MI have been correlated with an increased risk of sudden death and a propensity to VT Signal averaging does not help select appropriate therapy but identifies patients who warrant further investigation; it plays no role in the investigation of narrow QRS tachycardias .TreatmentReassurance is important. Most cardiac arrhythmias cause no symptoms, have no hemodynamic importance, and have no prognostic significance but may cause anxiety in a patient who becomes aware of them. Some patients with benign arrhythmias remain disabled despite reassurance. Behavior modification therapy often helps when reassurance has failed. In rare cases, a precipitating factor may be identified and modified (eg, excessive intake of caffeine or alcohol).Drug treatment: Antiarrhythmic drug therapy is the mainstay of management for most important arrhythmias. There is no universally effective drug; all have important safety limitations and can aggravate or promote arrhythmias (arrhythmogenesis, proarrhythmia). Drug selection is difficult and often involves trial and error.Antiarrhythmic drug actions based on cellular electrophysiologic effects have been classified by Vaughan Williams. This classification is recognized internationally and provides a general logic for grouping drugs, although its usefulness for prescribing is limited.Class I drugs are Na channel blockers, including older antiarrhythmic drugs (eg, quinidine). All reduce the maximal rate of depolarization of the action potential and thereby slow conduction. They are very effective in suppressing VEBs but, to a varying degree, depress left ventricular performance, and all have been associated with proarrhythmia. They are subclassified based on the kinetics of their receptor effects: class Ia--drugs with intermediate onset and offset; class Ib--drugs with short effects; and class Ic--drugs with prolonged effects.Quinidine (class Ia) prolongs action potential and refractoriness (seen on ECG as QT prolongation). This broad-spectrum drug is effective for the suppression of VEBs and VT and for the control of narrow QRS tachycardias, including atrial flutter and fibrillation. It is one of the few drugs that may convert AF to sinus rhythm. Elimination half-life (t1/2) is 6 to 7 h. If an initial test dose of quinidine sulfate is tolerated, the maintenance dosage is usually 200 to 400 mg po q 4 to 6 h. The target plasma concentration is 2 to 6 140 msec (unless there is preexisting bundle branch block) and QT is 550 msec. About 30% of patients develop adverse reactions. GI problems (diarrhea, colic, flatulence) are most common, but fever, thrombocytopenia, and liver function abnormalities also occur. Quinidine syncope is a potentially dangerous idiosyncratic and unpredictable effect caused by torsade de pointesProcainamide (class Ia) has much less effect than quinidine on refractoriness. The main metabolite, N-acetyl procainamide, also has antiarrhythmic effects and contributes to procainamide's efficacy and toxicity. It can be given cautiously IV as 100 mg over 1 to 2 min repeated q 5 min to a usual maximum total dose of 600 mg (rarely up to 1 g) while monitoring BP and ECG. Oral procainamide has a short elimination t1/2 ( 12 mo) develop serologic abnormalities (notably a positive antinuclear factor test), and up to 40% have symptoms and signs of hypersensitivity (arthralgia, fever, pleural effusions).Disopyramide (class Ia) produces little change in the refractory period. It has an elimination t1/2 of 5 to 7 h. The target plasma concentration is 3 to 6 Lidocaine (class Ib) has substantial first-pass hepatic metabolism. It produces minimal myocardial depression and has little effect on the sinus node, atria, or atrioventricular node but acts powerfully on His-Purkinje's and ventricular myocardial tissue. It can suppress the ventricular arrhythmias that complicate MI (VEBs, VT) and reduce the incidence of primary ventricular fibrillation (VF) when given prophylactically in early acute MI. However, asystolic events are increased, suggesting sinoatrial and atrioventricular nodal effects. Lidocaine's elimination t1/2 is 30 to 60 min. The target plasma concentration is 2 to 5 mg/L. It is used only parenterally. The usual regimen is 100 mg IV over 2 min followed by 50 mg IV 5 min later if the arrhythmia has not reverted. An infusion of 4 mg/min (2 mg/min in patients > 65 yr) should then be started. If it is continued for > 12 h, toxic levels may be reached. Concomitant -blocker therapy increases the risk of toxicity, and the lidocaine dose should be halved. Adverse effects are neurologic (tremor, convulsions) rather than cardiac. Drowsiness, delirium, and paresthesias may occur with too-rapid administration.Mexiletine (class Ib) is an analog of lidocaine with similar electrophysiologic actions, but it has little or no first-pass hepatic metabolism. Mexiletine can suppress symptomatic ventricular arrhythmias, including VT, but has little or no role in the management of narrow QRS (supraventricular) arrhythmias. Mexiletine's elimination t1/2 is 6 to 12 h, and the target plasma concentration is 1 to 2 Tocainide (class Ib) is another congener of lidocaine, with little or no first-pass hepatic metabolism. Elimination t1/2 is 11 to 15 h, and the target plasma concentration is 4 to 10 Phenytoin is variably classified but probably belongs to class lb. It was used extensively for arrhythmia management, particularly for suppressing the ventricular arrhythmias of digitalis toxicity, until the advent of newer drugs and the decline of digoxin toxicity (which may be better treated by digoxin immune Fab). It has a long elimination t1/2 (22 h). Adverse effects include gingival hyperplasia and blood dyscrasias.Class Ic drugs are among the most powerful antiarrhythmics but have been associated with a significant risk of proarrhythmia and depression of cardiac contractility. These adverse effects are uncommon in patients with hemodynamically normal hearts (eg, Wolff-Parkinson-White (WPW) syndrome) but important in patients with extensive cardiac damage subject to life-threatening ventricular tachyarrhythmias. Class Ic drugs are used in these latter patients only when the arrhythmia is unresponsive to other therapy.Class Ic drugs are proving highly effective for the medical cardioversion of AF and for the prophylaxis of AF attacks. These indications have become the principal application for these drugs, particularly because proarrhythmic risks in this context seem relatively low.Flecainide is a powerful class Ic antiarrhythmic. It has a profound effect on the Na channel, so conduction is markedly slowed but refractoriness is little affected. Left ventricular performance may be depressed. Flecainide can control symptomatic VEBs, VT, and the reciprocating tachycardias of the WPW syndrome. Elimination t1/2 is 12 to 27 h, and the target plasma concentration is 0.2 to 1 Propafenone (class Ic) has effects similar to those of flecainide and is probably similarly proarrhythmic. The elimination t1/2 is 6 to 7 h. The target plasma concentration is 5 to 8 Class II drugs ( -blockers) may be the least toxic and most powerful drugs available, yet their antiarrhythmic effects are often overlooked. Whereas relatively few arrhythmias are primarily caused by sympathetic overactivity, most are modulated by autonomic tone. -Blockers have poor efficacy in conventional antiarrhythmic tests (eg, VEB suppression), but they raise the threshold to VF and may be potent preventers of VF. -Blockers are 1-selective or nonselective, may have intrinsic sympathomimetic activity (ISA), and are lipophilic or hydrophilic. These differences seem of little antiarrhythmic relevance, although ISA may reduce antiarrhythmic potency. In general, -blockers are well tolerated but may depress left ventricular function, particularly in antiarrhythmic doses. They are contraindicated in bronchospastic airway disease and should be used cautiously in other lung diseases. GI disturbances, insomnia, and nightmares may occur. Lassitude is common on initiating therapy but rarely persists.Class III drugs interfere with the K channel to alter the plateau phase of the action potential and increase refractoriness. Conduction velocity is little affected, but, theoretically, the discharge rate of automatic foci is reduced. These drugs can be proarrhythmic.Amiodarone is a powerful class III antiarrhythmic. It has few cardiovascular adverse effects and, perhaps through its modest vasodilator action, produces little or no left ventricular depression. Sinoatrial node activity is little affected. Amiodarone, by prolonging refractoriness, may create homogeneous conditions of repolarization throughout the heart. The QT interval on ECG is prolonged, and no upper safe limit to this effect has been suggested. The elimination t1/2 is > 50 days, with substantial delay in onset of action. Initial loading doses of 600 to 1200 mg/day po for 7 to 10 days have been advocated but with little evidence of faster onset. Oral maintenance doses should be the minimum needed to control arrhythmias, ideally 5 yr and may be fatal. Serial pulmonary function testing may detect pulmonary fibrosis early, allowing discontinuation of amiodarone. Other complications include photosensitive dermatitis, hepatic abnormalities, peripheral neuropathy, corneal microdeposits (occur in almost all treated patients, do not seriously affect vision, and are reversible on stopping therapy), hypothyroidism (usually not serious; thyroid hormone replacement can be given while amiodarone dosing continues), and hyperthyroidism (more difficult to manage; usually necessitates stopping amiodarone). Torsade de pointes is rarely produced by amiodarone but can be life threatening. Unless no alternative exists, amiodarone should not be given to children.Racemic (D-L) sotalol has class II and III antiarrhythmic properties, but, although measurable class III effects (QT prolongation, refractory period change) are detectable in clinical use, they are largely masked by the drug's -blocking properties. Most class III activity resides in the D-isomer. Sotalol is given as 80 to 160 mg po q 12 h. It depresses left ventricular performance and has been associated with proarrhythmia. The usual contraindications for -blockers apply to its use. In studies of D-sotalol, mortality was increased. Only racemic sotalol is available for clinical use.Ibutilide is a newly approved class III drug (prolongs repolarization) that differs markedly from amiodarone and sotalol. It achieves its effect by activating a slow inward Na current rather than by blocking outward K currents. Ibutilide can acutely terminate AF (about 40% success) and atrial flutter (about 65% success). Ibutilide is given IV over 10 min as a 1-mg infusion for patients >= 60 kg or as 0.01 mg/kg for smaller patients. A dose identical to the first may be given after 10 min if the first infusion is unsuccessful. Torsade de pointes has developed in 2% of patients. Ibutilide should therefore be used in well-monitored situations and by staff familiar with the management of torsade de pointes.Bretylium also has antisympathetic (class II) and class III actions. It may cause marked hypotension and is indicated only for the management of potentially lethal refractory ventricular tachyarrhythmias (intractable VT, recurrent VF). Bretylium usually is effective within 30 min of injection. The target plasma concentration is 1 to 1.5 Class IV drugs are Ca blockers (Ca entry blockers). Nifedipine, similar to other dihydropyridines, has almost no electrophysiologic effects, but verapamil and diltiazem influence atrioventricular nodal electrophysiology and may alter that of Ca-dependent ischemic cells.Verapamil acts principally on the atrioventricular node, slowing conduction. Used IV, it has a place in the acute management of narrow QRS tachycardias, which involve the atrioventricular node. Reportedly, termination rates approach 100% with doses of 5 to 15 mg IV over 10 min. However, if verapamil is given to patients in VT, serious adverse reactions, including VF, intractable hypotension, and death, may occur. Thus, verapamil is contraindicated for broad QRS tachycardias. Verapamil 40 to 120 mg po tid is widely prescribed for arrhythmia prophylaxis, but the substantial first-pass hepatic metabolism may limit its clinical use.Diltiazem has a similar electrophysiologic profile to verapamil. It has a long t1/2 (making it less acceptable as IV therapy for narrow QRS tachycardia) but has little or no first-pass hepatic metabolism, making it better suited for chronic arrhythmia prophylaxis.Drugs not covered by the Vaughan Williams classification are also used. Digoxin shortens atrial and ventricular refractory periods and prolongs conduction in the atrioventricular node. The target plasma concentration is 0.8 to 1.6 ng/mL. Part or all of the 1-mg digitalizing dose may be administered slowly IV and under ECG control, with full resuscitative facilities available. Maintenance is 0.125 to 0.25 mg/day po, depending on body weight and renal function. Although uncommon, digoxin toxicity is manifested by anorexia, nausea, vomiting, and often serious arrhythmias (VEBs, atrial ectopic beats, occasionally paroxysmal atrial tachycardia with block) or second-degree or third-degree atrioventricular block. Treatment of serious digoxin toxicity using digoxin immune Fab is safer and more logical than using an antiarrhythmic drug; in other situations, stopping therapy for 48 h and resuming with a lower dose is usually satisfactory. Digoxin is contraindicated in patients with antegrade conduction over an accessory pathway (manifest WPW syndrome) because, in the event of AF, excessive ventricular responses may occur through facilitation of the accessory pathway. Digoxin can be used prophylactically in infants and children 10 yr with WPW (see below).Adenosine is a purine nucleoside that acts through extracellular adenosine receptors to slow or block atrioventricular nodal conduction. It can terminate arrhythmias that involve the atrioventricular node. Adenosine may be safer than verapamil for this purpose because of its extremely short duration of action. It is rapidly metabolized after administration. The dose is 6 mg followed by up to 12 mg by rapid IV injection. Short-lived adverse effects (dyspnea, chest discomfort, flushing) occur in 30 to 60% of patients. Adenosine may cause bronchospasm and should not be used in asthmatic patients.Pacemakers: Technical advances have been dramatic. Sophisticated pacing modalities and programmability are common. Low-energy circuitry and new battery designs have increased device longevity. Screening of devices and interference-resistant circuitry have almost eliminated the risk that automobile distributors, radar antennae, microwave devices, and airport security detectors once posed in suppressing pacemaker function. MRI and operative diathermy may, however, interfere with pacemakers and should be avoided. Cellular telephones are a source of electromagnetic emissions; pacemaker patients should avoid using such devices in proximity to the pacemaker generator.Two important pacemaker developments are corticosteroid-eluting leads and mode switching. Use of the former reduces pacing threshold with increased pacemaker longevity. The latter is proving important for patients with atrioventricular nodal conduction disorders (natural or iatrogenic) in whom occasional disturbances of sinus rhythm occur. A mode-switching DDDR pacemaker (for the international coding of pacemakers and implantable devices, can detect atrial arrhythmias such as AF and automatically operate as a VVIR pacemaker until sinus rhythm returns.Antibradycardia pacemakers are important for symptomatic bradyarrhythmias, which may be caused by atrioventricular block, sinoatrial node depression, sinoatrial conduction block, or infra-His block. The severity depends on the rate and reliability of the escape pacemaker. Dangerous bradycardias are optimally treated with pacemakers. A simple VVI pacemaker may be adequate for transient or infrequent bradyarrhythmia. for frequent or persistent bradyarrhythmia, prolonged dependence on ventricular pacing may warrant use of a rate-responsive demand unit (VVIR or DDDR) or, if no atrial or sinus node abnormalities are present, a dual-chamber system (DDD).Antitachycardia pacemakers offer automatic arrhythmia termination by programmed stimulation. These implantable devices, which may be no larger than conventional pacemakers, deliver a series of preprogrammed pacing sequences when an arrhythmia occurs. Current antitachycardia pacemakers should not be used for VT (although it may respond) because they may precipitate VF; units with backup defibrillation capability should be used in this context. Indications include the reciprocating tachycardias of WPW syndrome, preferably when there is slow or no antegrade conduction over the accessory pathway (lest AF be precipitated and conducted rapidly to the ventricles), and atrioventricular nodal reentry tachycardia (see below). Other treatment modalities, especially radiofrequency ablation, are superseding antitachycardia pacing therapy.Implantable cardioverter defibrillators (ICDs) use relatively low energy shocks ( 200 shocks and provide arrhythmia surveillance for >= 5 yr. Implantation formerly involved a limited thoracotomy, but now > 95% of systems use transvenous electrodes.In modern ICDs, backup antibradycardia pacing and telemetry facilities are available. Current indications for ICD use include resuscitated sudden death (except in the first few hours of acute MI) and medically intractable life-threatening VT. Defibrillators do not prevent symptomatic arrhythmias and may be combined with suppressive antiarrhythmic therapy. Randomized controlled studies of ICD therapy are scarce. Two studies involved highly selected high-risk patients (sudden cardiac death survivors); in both, total mortality was reduced with the ICD vs. the best medical therapy. However, the ICD is not without problems: it offers palliation rather than cure. Patients experience shocks, some of which may be inappropriate responses to other arrhythmias such as AF. ICDs are also expensive and must be used responsibly.Antitachycardia pacing is a further ICD development. Many episodes of VT are based on reentry and can be terminated by various overdrive pacing sequences. Until the advent of ICD, which offers backup defibrillation in the event of provoking VF, this therapy had not been exploited. Follow-up and programming these devices require a specialist.Radiofrequency (RF) ablation: RF ablation has revolutionized the approach to many types of arrhythmias. RF lesions are created by gentle heating (typically to 60RF ablation is remarkably safe. Deaths have occurred principally through cardiac perforation and tamponade (death, 1/2000; tamponade, 1/2400).Surgery: The anatomic basis of WPW syndrome and its arrhythmias is well understood. After accurate localization by catheter or epicardial mapping, the accessory pathway may be destroyed by surgery (success, > 95%; operative mortality, 0.1%) using an epicardial or endocardial approach. However, RF ablation has made surgery for WPW almost obsolete.Postinfarction VT usually originates in the subendocardium, which, when localized by intraoperative mapping, can be removed by procedures such as endocardial resection. Surgery has an operative mortality of 5 to 25% depending on preoperative status, but survivors have a 90% arrhythmia-free 1-yr survival.Dr. Guillermo Pecci Saavedra M.D., Ph.D. Mt. Sinai School of MedicineNew York, N.Y., U.S.Ahttp://chronic-sinus.healthblogger.net/21966/ Mon, 07 Aug 2006 06:11:25 -0500 acid reflux bad breath http://chronic-sinus.healthblogger.net/21966/ acid reflux bad breathAn overview of some of the causes and treatments of halitosis, bad breath, including gingivitis, periodontitis, stomach problems. 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