Use of procainamide in patients with the Wolff-Parkinson-White syndrome to disclose a short refractory period of the accessory pathway purchase atarax 10 mg amex. Value of noninvasive techniques in the Wolff-Parkinson-White syndrome with particular reference to exercise testing discount 25 mg atarax with visa. Evaluation of noninvasive tests for identifying patients with preexcitation syndrome at risk of rapid ventricular response buy atarax with paypal. Importance of initial length of effective refractory period of the accessory pathway. Procainamide infusion test: inability to identify patients with Wolff-Parkinson-White syndrome who are potentially at risk of sudden death. Effect of isoproterenol on the anterograde refractory period of the accessory pathway in patients with the Wolff-Parkinson-White syndrome. Refractory periods of the accessory pathway in the Wolff- Parkinson-White syndrome. Syncope in the Wolff-Parkinson-White syndrome: incidence and electrophysiologic correlates. Transient entrainment and interruption of the atrioventricular bypass pathway type of paroxysmal atrial tachycardia. Electrophysiologic demonstration of bilateral anomalous pathways in a patient with Wolff-Parkinson-White syndrome (type B preexcitation). Quintuple pathways participating in three distinct types of atrioventricular reciprocating tachycardia in a patient with Wolff-Parkinson-White syndrome. Characteristics of atrioventricular conduction and the spectrum of arrhythmias in Lown-Ganong-Levine syndrome. One to one atrioventricular conduction during atrial pacing at rates of 300/minute in absence of Wolff-Parkinson-White Syndrome. Analysis of anterograde and retrograde fast pathway properties in patients with dual atrioventricular nodal pathways: observations regarding the pathophysiology of the Lown-Ganong-Levine syndrome. Enhanced atrioventricular nodal conduction in man: electrophysiologic effects of pharmacologic autonomic blockade. Cycle length in atrioventricular nodal reentrant paroxysmal tachycardia with observations on the Lown-Ganong-Levine syndrome. Comparison of the ventricular response during atrial fibrillation in patients with enhanced atrioventricular node conduction and Wolff-Parkinson-White syndrome. Nouvelles recherches sur les connections supericures de la branche du faisceau de His-Tawara avec cloison interventriculaire. Radiofrequency catheter ablation of right atriofascicular (Mahaim) accessory pathways guided by accessory pathway activation potentials. Supraventricular tachycardia associated with nodoventricular and concealed atrioventricular bypass tracts. Catheter ablation of Mahaim fibers with preservation of atrioventricular nodal conduction. Electrocardiogram in patients with fasciculoventricular pathways: a comparative study with anteroseptal and midseptal accessory pathways. Radiofrequency catheter ablation of atriofascicular and nodoventricular Mahaim tracts. Paroxysmal tachycardia with atrioventricular dissociation in a patient with a variant of pre-excitation syndrome. His-ventricular dissociation in a patient with reciprocating tachycardia and a nodoventricular bypass tract. These and other observations concerning mechanism are discussed in detail later in this chapter. Over the past four decades, electrophysiologic studies have been responsible for a greater understanding of ventricular arrhythmias. This has led to major advances in their pharmacologic and nonpharmacologic therapy. It is imperative that clinicians and clinical investigators recognize that the study of ventricular arrhythmias is still evolving. The role of electrophysiologic studies in evaluating nonsustained and/or polymorphic arrhythmias associated with metabolic disorders, drug toxicity, cardiomyopathy, and so on is not yet established. A discussion of our current level of understanding of this issue is included and detailed later. Definitions of Ventricular Tachycardias The definitions employed by electrophysiology laboratories are arbitrary but provide a useful framework for both the clinician and the electrophysiologist to distinguish “pathologic” responses from “normal” expected 1 2 3 responses. This is a fairly common mechanism of sudden cardiac 6 7 8 death recorded by Holter monitor. Duration Most laboratories consider a tachycardia sustained if it lasts ≥30 seconds. Repetitive polymorphic responses are also very common (up to 50%), particularly when multiple (≥3) extrastimuli are used with extremely short coupling intervals (<180 msec). The clinical significance of induced nonsustained polymorphic tachycardia is questionable and requires further evaluation to determine its relevance (to be discussed in subsequent paragraphs). They reported good sensitivity and specificity, but I have not found it significantly better than V1–2 criteria. Furthermore, A-V dissociation can be seen with supraventricular rhythms, fusion complexes can result from two ventricular ectopic foci, and morphologic and/or axis characteristics established for patients with normal P. In the absence of pre-excitation a supraventricular impulse must pass through the His bundle and the specialized ventricular conducting system before initiating depolarization of the ventricles. This may result because no engagement of the His–Purkinje system by the ventricular impulse occurs (probably uncommon), or because retrograde His bundle activation occurs during ventricular activation and is obscured by the large ventricular deflection in the His bundle recording. His deflections can usually be observed if attention is given to catheter position. One may identify His bundle activity before ventricular activation (in this instance, the H-V interval is shorter than normal; e. If His bundle deflections are not seen, one must differentiate the absence of retrograde activation of the His– Purkinje P. This can be fortuitously observed if a sinus impulse conducts antegradely to the His bundle producing a clear His deflection. In these instances, linking of the His bundle potential to atrial activation proves that they are due to antegrade depolarization and are unrelated to the tachycardia. Retrograde block in the A-V node is present because atrial activation is dissociated from the tachycardia. It is often difficult to determine whether the recorded His deflection is antegrade or retrograde—or for that matter whether an apparent His bundle deflection is really a right bundle branch potential. Two techniques that may be used to clarify the situation are (a) recording right and left bundle branch potentials to demonstrate that their activation begins before His bundle activation and (b) His bundle pacing producing a longer H-V interval than the one noted during the tachycardia. Both of these are extremely difficult to do but can help define the mechanism of His bundle activation and the tachycardia origin. The simplest methods for verifying proper catheter position include the following: (a) the immediate appearance of His bundle deflections on termination of the tachycardia, or conversely, disappearance of the His bundle deflection on initiation of the tachycardia, without catheter manipulation; (b) spontaneously occurring or induced supraventricular capture of the His–Purkinje system (with or without ventricular capture) during the tachycardia with the sudden appearance of His bundle deflections; and (c) in the presence of supraventricular capture, H-V intervals comparable to those during sinus rhythm (Figs.

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When it was more visible generic 25mg atarax, they had to focus on whether the condition could be hidden atarax 10 mg. Three strategies are used to manage stigma: avoid hurtful situations buy discount atarax online, pass as normal, 116 and appropriate a philosophy to help cope with the stigma (Figure 8. The stigma, level of shame, and embarrassment attached to incontinence is higher than that for depression and cancer [18]. This is not surprising as bladder and bowel continence is an adjustment to the social norm, especially in Western cultures, which have developed acceptable rules and behavior for bladder and bowel emptying [19–21]. Our society places a significant emphasis on sanitation and personal hygiene [23]. Discussions of personal hygiene and/or elimination are not part of social conversations, especially in Western cultures. During toilet training, children are inoculated with all the cultural norms and expectations concerning elimination of urine and stool [24]. If incontinence occurs in adulthood, persons revive those childhood beliefs and begin to internalize their condition causing a decrease in self-esteem and feelings of shame and of not being “normal” [10]. These barriers are shared by the public as well as by many health-care providers and may contribute to the burden of caregiving [25]. Self-stigma Harsh or unjustified beliefs about Belief that they are the only person with the problem. Avoidance of incontinence is a strategy many use and is a worldwide coping measure. More than 80% of all respondents stated they agreed with the following statements: Accidental loss of urine is a common problem that every woman faces. Persons with incontinence experience insensitive language and loss of freedom and endure questions of a sensitive nature. Latina women maintained more secrecy around this issue, even among family members. Similar perceptions are reported by persons who experience fecal or anal incontinence. The analysis resulted in four different themes: self-affirmation, guilt and shame, 118 limitations in life, and personal approach. Ignorance and lack of tolerance by and of others is common, leading frequently to anger and withdrawal. The stigma associated with incontinence is similar to the stigma in other conditions and is associated with public ignorance and lack of awareness. The shame, embarrassment, and stigma associated with these conditions pose significant barriers to seeking professional treatment, resulting in many persons who suffer from these conditions living in silence [12,29]. The traditional medical model of care is very much focused at “treatment” but does not empower the sufferer to actually develop strategies to cope with what is often a lifelong condition. Society also ignores the presence of a taboo by refusing to acknowledge or address it; the taboo is stigmatized [31]. It is possible to understand the long- standing stigma surrounding unexpected loss of urine and feces by considering the potential health consequence of incontinence on society [9]. Epidemiological and clinical studies of individuals with incontinence indicate that the condition has a considerable impact on overall QoL and well-being. The inability to control urine or feces is one of the most unpleasant and distressing symptoms a person can experience, causing stigmatization and denial of the condition [12]. Emotional well-being is impaired, probably as a result of social isolation and feelings of stigmatization produced by the incontinence. Society does not know how to respond to persons with incontinence, so avoidance is the norm. This public stigma affects treatment-seeking attitudes through internationalization of messages [32]. Urologic and gastrointestinal symptoms are associated with feelings of stigma, making it challenging for individuals to talk with doctors about their condition [33,34]. To avoid embarrassment, persons with incontinence turn to “self-management” rather than “seeking help” from a doctor or nurse. Unfortunately, factors that promote care-seeking behavior for incontinence issues remain less researched and are complex and multifactorial [8]. Older adults may be keen to seek help if they are concerned that a health issue such as how incontinence impacts on their ability to remain independent and living in the community [21]. In certain parts of the world, the gender of the person with incontinence may be a factor in help-seeking behavior and the gender of the health-care provider may be a barrier. A known barrier is terminology for incontinence as how patients relate their condition may not match health-care professional’s medical assessment. Barriers to seeking help for continence issues that have been frequently identified in the literature include embarrassment, social stigma, and the mistaken belief that incontinence is inevitable, untreatable, and/or a normal part of aging. The authors of a Swedish study suspected that lack of knowledge, worries about different procedures, and negative expectations may be important factors in reducing the desire to seek treatment among even those most severely affected [36]. Men reported feeling stigmatized for being seen making frequent trips to the bathroom and feared being viewed as impotent. Women feared being stigmatized based on having an unclean body and a compromised social identity. Like others, Hispanic individuals wanted to keep urinary symptoms a secret from others. The further the person is connected from the sufferer, the more negative attitudes become. As the condition becomes more severe, the more obvious it becomes to others, and often, therefore, the more the person is likely to be stigmatized [12,21]. In addition, attitudes and reactions of both the person with incontinence and those in society who interact with that person may vary according to the age of the person. At the extreme is the newborn child, where incontinence is regarded as a norm, through to childhood bedwetting, all the way to a frail old person in a nursing home. Depending on the age, sex, and social situation of the person, the reaction may well be different. It is important to understand how attitudes and stigma changed for these conditions. An important component is breaking the cycle of public and personal ignorance through education and public awareness programs [8,29]. For this to be successful, there needs to be a partnership between health- care professionals, governments, and industry groups with a vested interest to work together to break the cycle of ignorance and negative attitude. Central to this is the availability of funds, either in allocated dollars or “in kind” (e. A group of experts [9] conducted a systematic review of existing evidence, collated qualitative data, and used expert consensus to develop an internationally applicable service specification for continence care around the world. This service can be tackled locally and internationally in order to raise awareness of incontinence, bring a greater opportunity to incontinence management, and improve the plight of hundreds of millions of people around the world.

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Similarly order atarax 25 mg visa, the appearance of a spontaneous sustained tachycardia in a patient who has only had asymptomatic nonsustained arrhythmias need not represent a proarrhythmic effect buy discount atarax 10 mg online. Electrophysiologic Studies and Proarrhythmia One of the major questions frequently posed to electrophysiologists is whether or not electrophysiologic testing can predict the proarrhythmic effect of antiarrhythmic agents generic atarax 10 mg free shipping. Preliminary data from our institution suggest that in most patients none of these is in fact true. We have evaluated the patients resuscitated from cardiac arrest who had the arrest while taking Class lA antiarrhythmic agents. Thus, cardiac arrest while on a Class 1 agent, even if no inducible arrhythmia is present following drug withdrawal, suggests a substrate for arrhythmias and/or triggering mechanism (e. Thus, the presence of a new tachycardia induced while on a drug should not be interpreted as being proarrhythmic; it may simply mean a variability of response to programmed stimulation. This is particularly true because most investigators fail to complete the stimulation protocol from both sites before testing an antiarrhythmic drug. The failure to do so often prevents them from observing multiple distinct morphologic tachycardias at different cycle lengths during control. Having a faster poorly tolerated tachycardia while on an antiarrhythmic agent does not really suggest a proarrhythmic effect. While the induction of a nontolerated tachycardia has been suggested as a predictor of a nontolerated recurrence,188 this is not necessarily so. Moreover, since people who have nontolerated tachycardias induced more commonly present with cardiac arrest, the induction of a nontolerated tachycardia on a drug should not and cannot be interpreted as proarrhythmic. Those presenting with cardiac arrest had recurrent cardiac arrest in 25% of individuals in whom the drug slowed the tachycardia in the laboratory. It has been stated widely that a tachycardia that is easier to induce means a proarrhythmic effect of the drug. As stated earlier in this chapter, we have never found the relative ease of induction or the absolute number of extrastimuli used to be of value in predicting recurrence (Figs. Thus, I believe that there are no hard data to support that the relative ease of induction or number of extrastimuli has any role in predicting a proarrhythmic effect. Finally, inducing a tachycardia that is harder to terminate has nothing to do with proarrhythmia. That may have something to do with termination of the arrhythmia, but it has nothing to do with the development of an arrhythmia. As previously discussed in Chapter 11, it is well known that drugs that slow conduction can make it more difficult to terminate an arrhythmia, either by preventing extrastimuli from reaching the circuit at an appropriate time interval or by accelerating arrhythmias by less clearly defined mechanisms. Therefore, in my opinion, electrophysiologic testing cannot be used to predict the type of recurrence or the frequency of recurrence. While slow tachycardias that are induced in the laboratory appear to be associated with slow recurrences, the spontaneous presentation of a slow tachycardia is a more important predictor of type of recurrence. A classification of antiarrhythmic actions reassessed after a decade of new drugs. The differential effect of quinidine and pyrilamine on the myocardial action potential at various rates of stimulation. Effect of lidocaine and quinidine on steady-state characteristics and recovery kinetics of (dV/dt)max in guinea pig ventricular myocardium. Interval-dependent effects of small antiarrhythmic drugs on excitability of guinea-pig myocardium. Importance of physico-chemical properties in determining the kinetics of the effects of Class I antiarrhythmic drugs on maximum rate of depolarization in guinea- pig ventricle. Kinetics of onset of rate-dependent effects of Class I antiarrhythmic drugs are important in determining their effects on refractoriness in guinea-pig ventricle, and provide a theoretical basis for their subclassification. Time- and voltage-dependent interactions of antiarrhythmic drugs with cardiac sodium channels. Antiarrhythmic agents: the modulated receptor mechanism of action of sodium and calcium channel-blocking drugs. Block of inactivated sodium channels and of depolarization-induced automaticity in guinea pig papillary muscle by amiodarone. The effects of antiarrhythmic drugs, stimulation frequency, and potassium-induced resting membrane potential changes on conduction velocity and dV/dtmax in guinea pig myocardium. Effect of procainamide on transmembrane action potentials in guinea-pig papillary muscles as affected by external potassium concentration. The influence of pH on the electrophysiological effects of lidocaine in guinea pig ventricular myocardium. Depressant effects of fast sodium channel blockade on the electrical activity of ischaemic canine ventricle: mediation by the sympathetic nervous system. The effect of procaine amide on components of excitability in long mammalian cardiac Purkinje fibers. The effects of procainamide on conduction in anisotropic canine ventricular myocardium. Effects of digitalis on the human sick sinus node after pharmacologic autonomic blockade. Clinical effects of digoxin on sinus node and atrioventricular node function after pharmacologic autonomic blockade. The direct electrophysiologic effects of disopyramide phosphate in the transplanted human heart. The electrophysiological effects of intramuscular guinidine on the atrioventricular conducting system in man. Comparison of the antiarrhythmic efficacy of disopyramide and mexiletine against stimulus-induced ventricular tachycardia. Effects of intravenous and oral disopyramide on paroxysmal atrioventricular nodal tachycardia. Effect of procainamide, mexilitine, and propranolol on ventricular activation time recorded at cardiac mapping in chronic canine myocardial infarction. Electrophysiologic effects of procainamide on sinus function in patients with and without sinus node disease. Electrophysiologic effects of disopyramide phosphate in patients with Wolff-Parkinson-White syndrome. Comparative electrophysiologic effects of intravenous and oral procainamide in patients with sustained ventricular arrhythmias. Effect of procainamide and N-acetylprocainamide on atrial flutter: studies in vivo and in vitro. Effect of propafenone in the Wolff-Parkinson-White syndrome: electrophysiologic findings and long-term follow-up. Suppression of incessant supraventricular tachycardia by intravenous and oral encainide. Clinical usefulness of flecainide acetate in the treatment of paroxysmal supraventricular arrhythmias.

W. Fabio. Rogers State University.

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