By L. Akascha. Southeastern University. 2019.

Such types of intra-atrial delays appear to be substrates for intra-atrial reentry (Chapters 8 cheap betoptic 5ml otc, 9) proven betoptic 5 ml. Interatrial and intra-atrial dissociation have been observed during atrial tachyarrhythmias betoptic 5ml with amex, particularly atrial flutter and fibrillation. In such instances, all or some part of the atrium manifests one rhythm while the remainder is activated differently. Atrioventricular Node The A-V node accounts for the major component of time in normal A-V transmission. The range of normal A-H time during sinus rhythm is broad (60 to 125 msec), and it can be profoundly influenced by changes in autonomic tone. Thus, 11 measurements of A-V nodal function over periods of time may not be reproducible. Delay in the A-V node is by far the most common source of prolonged A-V conduction (first-degree A-V block) 12 (Fig. From another viewpoint, most patients (≥95%) with a total P-R interval greater than 300 msec have some degree of A-V nodal delay. It is worth reemphasizing that A-V conduction can vary greatly with changes in the P. On the other hand, clinical states with heightened sympathetic tone are accompanied by decreased A-V nodal and conduction time and refractoriness at any paced rate. Second-degree block that is due to intermittent failure of conduction through the A-V node is very common in a wide variety of circumstances. Type I second- degree block may be a manifestation of a pathologic process, or it may be a physiologic response within normal limits. This type of block may occur in the setting of any acquired or congenital disease of the A-V node, especially inferior wall myocardial infarction. It can also be precipitated by drugs such as digitalis, beta blockers, calcium channel blockers, or amiodarone. In addition, it may be seen in the young, healthy heart at rest in the presence of high levels of resting vagal tone, a state that is particularly common in well-trained endurance athletes. Furthermore, Type I second-degree block can be precipitated in almost all subjects by incremental atrial pacing (Chapter 2) and in an analogous fashion may be seen during atrial tachycardia. Note the progressively decreasing A-A intervals followed by a pause and then resumption of the pattern. Hr are retrograde His bundle potentials associated with fascicular depolarizations (Chapter 7), another manifestation of digitalis intoxication. It is not uncommon to observe (a) the A-H interval stabilize for several beats, especially during long Wenckebach cycles (11 to 10, etc. Typical Wenckebach periodicity is more frequently observed during pacing-induced second-degree A-V block (Fig. In patients with dual A-V nodal pathways, Wenckebach cycles are almost always atypical. The greatest jump in A-H occurs when block in the fast pathway occurs, whichever complex this may be. In patients with A-V nodal reentry, Wenckebach cycles may be terminated by A- V nodal echoes or the development of supraventricular tachycardia (Chapter 8). These should really not be called Wenckebach cycles because there is no blocked paced impulse. Progressive prolongation of the A-H (and P-R) intervals occurs until the third atrial deflection A is not followed by a His bundle or a ventricular depolarization. Note that there is little alteration in the A-H interval before the fourth A not conducting. The true nature of the arrhythmia, however, is revealed by the first conducted A after the pause, which is associated with substantial shortening of the A-H interval to 200 msec. The paced cycle length is 350 msec, and each atrial depolarization A is followed by a progressively lengthening A-H interval (at decreasing increments) until the fourth A is not followed by a His bundle deflection. Alternative atrial depolarization A is not followed by either a His bundle or a ventricular depolarization. Second-degree A-V block in the A-V node can often be partially or completely reversed by altering autonomic tone. Hence, exercise (or other measures to increase sympathetic tone) or the administration of atropine (to decrease vagal tone) may produce reversion to 1:1 conduction. In such cases spontaneous progression to third-degree block (complete A-V block) may occur. More than likely, in most instances, failure of conduction to improve following atropine or isoproterenol suggests block is probably high in the His bundle. In general, Type I second-degree A-V nodal block is usually well tolerated from a hemodynamic standpoint, and it seldom if ever merits pacemaker therapy on symptomatic grounds. Since the impaired function of the A-V node is present, the A-H, and hence, P-R, of the conducted beats is almost always prolonged. Two-to-one block with P-R ≤160 msec should suggest an intra- or infra-His site of block. Improvement of conduction by atropine, beta agonists, or exercise suggests an A-V nodal site of block. However, as stated above, if structure disease of the A-V node is present, improvement of A-V node conduction under these conditions may be small or inapparent. Third-degree (complete) heart block occurring in the A-V node is relatively common. Most cases of congenital 16 complete heart block are localized to the A-V node (Fig. This is also the site of block in digitalis intoxication or when block is produced by beta blockers and/or calcium blockers. By definition, the atrial deflection is not followed by a His bundle deflection, but the escape ventricular deflection may or may not be preceded by one. It should be emphasized that 20% to 50% of adults with chronic complete block in 18 19 the A-V node have wide complexes. His bundle escape rhythms typically have a rate of 45 to 60 beats per minute (bpm), and they are variably responsive to alterations in autonomic tone or manipulation of the autonomic nervous system by pharmacologic agents (e. Use of closely spaced electrodes and careful mapping may locate a His bundle potential, which may be in an unusual position.

Expanded paper towel test: An objective test of urine loss for stress incontinence cheap betoptic 5 ml free shipping. Hence 5 ml betoptic overnight delivery, free uroflowmetry (spontaneous or no- catheter uroflowmetry) should never be used as a single test but always combined with clinical information (e discount betoptic 5ml without prescription. Urodynamic observations may occur in the absence or presence of symptoms and signs. The French Committee of Female Urology and Urogynecology (2007) recommends evaluation of bladder emptying by uroflowmetry and measurement of postvoid residual urine in all patients prior to surgery [4]. Such measurement objectively determines the volume of urine expelled from the bladder per time sequence and quantifies micturition. Moreover, if this volume–time equation is drawn as a curve, the measurement of urinary flow also gives information on how urine evacuation exactly proceeds. Objective and quantitative data, which primarily help in the understanding of voiding symptoms, are provided by measurement of urinary flow. As with all investigations, the diagnostic value of uroflowmetry depends on the way the test is performed, the quality of the measuring equipment, and the knowledge of the individual who interprets the measurement. However, uroflowmetry can only objectively investigate symptoms related to voiding but cannot explain symptoms related to urinary storage. Additionally, uroflowmetry cannot qualify or quantify voiding in women with urinary retention. In daily life, the individual is usually the only observer of her urinary flow, and the interpretation of subjective observations may need to be objectively confirmed and quantified by flow measurements. There may appear a discrepancy between subjective reporting and objective findings of urinary flow. Long or everlasting uroflow abnormalities might not be realized as abnormal because a comparison with normal voiding is lacking in those individuals. Furthermore, most women void in privacy and have little opportunity to compare voiding patterns [6]. In contrast, continuous flow is when the individual reports emptying the bladder without pauses during a single voiding attempt. Some were based on the principle of voiding distance [8,9], audio [10], weight [11], variations of a constant magnetic field [12], rotating disk, measurement of size and velocity of drops [13], and air displacement [14]. Gravimetric meters therefore measure accumulated mass, and mass flow rate is obtained by differentiation. Nowadays, most of the uroflowmeters use this principle of uroflow measurement that is considered as the most precise measurement technique. The output signal is proportional to the accumulated volume and the volumetric flow rate is obtained by differentiation. The power required to keep the disk rotating at a constant speed is proportional to the mass flow rate of the fluid. There are differences in accuracy and precision of the flow rate signals that are dependent on the type of the uroflowmeter, internal signal processing, the proper use, and calibration of the flowmeter. The desired and actual accuracy of uroflowmetry should be assessed in relation to the potential information that could be obtained from the measurement of urinary stream compared to the information actually abstracted for clinical and research purposes. Some relevant aspects of the physiological and physical information contained in the urinary stream are outlined in the report. As most uroflowmeters are mass flowmeters using the gravimetric method, variations in the specific gravity of the fluid have a direct influence on the measured flow rate. For example, urine of high concentration increases apparent flow rate by up to 3%. Since the overall accuracy of flow rate signals is not better than ±5%, it is not important to report Qmax to a resolution better than a full milliliter per second. The mechanical properties of a relaxed bladder outlet are usually constant, and the properties can be defined by the relationship between the cross- sectional area of the urethral lumen and the intraurethral pressure at the flow controlling zone. Below the minimum urethral opening pressure, the urethral lumen is closed and urine remains in the bladder; the lumen then widely opens with little additional pressure increase and urinary flow starts to emerge. The interpretation of uroflow curves can be performed by measuring several parameters and by gross interpretation of the flow curve itself. When voiding is completed without interruption, voiding time is equal to flow time. The average flow should be interpreted with caution if the flow is interrupted or there is terminal dribbling. When the bladder outlet is completely relaxed and the woman voids without straining, the shape of the curve is only determined by the kinetics of the detrusor contraction that reflects the properties of slow contracting detrusor smooth muscle cells; therefore, flow rate should not have rapid variations. The continuous uroflow curve is defined either as a smooth arc-shaped curve or as fluctuating when there are multiple peaks during a period of continuous urine flow (Figure 31. It is a widespread assumption that micturition of a healthy, asymptomatic woman is always associated with a normal flow pattern. These women voided with a bell-shaped flow curve in 50%, 65%, 57%, and 50%, respectively. Women who strained during voiding (a major component of dysfunctional voiding) managed to void a bell-shaped flow curve in 46%, 60%, 70%, and 100%, respectively. Decrease of detrusor contraction power (detrusor underactivity) and/or increased urethral pressure will both result in decreased Qmax and Qave as well as a smooth, flat curve. The magnitude of Qmax is determined by the residual urethral diameter at the level of obstruction. Fluctuations in detrusor contractility, straining, or intermittent sphincter activity during voiding may result in complex flow patterns (Figures 31. Rapid changes in urinary flow rate may be due to sphincter/pelvic floor contractions, mechanical compression of the urethral lumen or interference at the meatus, or changes in the driving energy—as with straining. Rapid changes may also be due to artifacts caused by interference between the stream and the collecting device, movement of the stream across the surface of the funnel, or patient movements. If fast variations of urinary flow have been observed, patients should be asked whether this voiding pattern reflects normal voiding at home or they have strained or emptied their bladder next to the collecting device. A visual control with regard to urine remnants next to the flowmeter is useful in cases of suspected voiding next to the uroflowmeter.

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Because the diastolic interval influences the response of both His–Purkinje system and ventricular refractoriness to single extrastimuli cheap 5ml betoptic, what is the cause of the “quantitative” differences? Demonstration of the effects of the diastolic interval on refractoriness of ventricular muscle requires short coupling intervals betoptic 5ml on-line. In 1987 Marchlinski88 demonstrated that very short drive cycle lengths and coupling intervals produce oscillations of ventricular refractoriness analogous to that shown for the His–Purkinje system buy 5 ml betoptic otc. Thus, the diastolic interval appears to be the major determinant of the refractory period following extrastimuli in both structures. Differences in the basic action potentials of ventricular muscle and His–Purkinje fibers are responsible for the apparent differences in their response to changes in cycle length and premature stimulation. A–C: The stimulus-to- stimulus intervals (in milliseconds) are shown along the top of action potentials. Effects of sudden cycle length alteration on refractoriness of human His–Purkinje system and ventricular myocardium. During a paced cycle length of 400 msec, refractoriness was determined to be 220 msec. A: Double extrastimuli (S2 and S3) are delivered with an S1-S2 coupling interval equal to 260 msec (diastolic interval of 40 msec). This results in shortening the refractory period of S2 to 180 msec compared to the drive cycle length. Refractoriness of S3 now depends on previous diastolic interval (80 msec), as well as a refractory period of S2 (which is shorter than the refractory period of S1). This results in a refractory period of S3 at an S1-S2 = S2-S3 of 260 msec that is 195 msec. This compares to a refractory period of 220 msec during the drive and a ventricular refractory period of S2 of 180 msec. Shortening of ventricular refractorines with extrastimuli: Role of the degree of prematurity and number of extrastimuli. A wide range of normal values has been reported for refractory periods (Table 2-5). The data would be more meaningful if they were all obtained at comparable cycle lengths using the same stimulus strength and pulse width. In these different laboratories, stimulus strengths vary from twice threshold to 5 mA, and pulse widths vary from 1 to 2 msec; both of these factors can alter the so-called normal value. As noted previously, strength–interval curves may be the best way to determine atrial and ventricular refractoriness. Another factor affecting the validity of such “normal” data is that A-V nodal conduction and refractoriness are both markedly affected by autonomic tone, an impossible factor to control except by autonomic blockade, which is not done routinely. Although atrial, ventricular, and His–Purkinje refractory periods appear relatively independent of autonomic tone and are therefore relatively stable, A-V nodal refractory periods are labile and can vary significantly during the course of a single study. Although it is difficult to assess the clinical significance of his findings, Prystowsky has shown that enhanced parasympathetic tone shortens atrial refractoriness and prolongs right ventricular refractoriness. The effect of drive cycle length on ventricular refractoriness in any given patient may represent a means of discriminating between abnormal and normal refractoriness when the absolute value of a single refractory period determination is borderline. Dispersion of Refractoriness Dispersion of ventricular refractory periods has been suggested as an indicator of an arrhythmogenic substrate based on animal experiments. For example, ischemic tissue appears to have longer refractory periods than nonischemic tissue. We recently evaluated whether or not dispersion of refractoriness is a measurable entity that has clinical relevance in humans. In a small number of patients, we evaluated differences in dispersion of refractoriness during atrial pacing and ventricular pacing at 600 and 400 msec. We also assessed the difference in dispersion of refractoriness when refractory periods are determined at both twice threshold and at 10 mA (in our experience this is always on the steep portion of the strength–interval curve). Thus, we evaluated both dispersion of refractoriness and dispersion of recovery (local activation plus local refractoriness) at each site. In five patients, we studied the effect of drive cycle length on dispersion of refractoriness. At a paced cycle length of 600 msec, the dispersion of refractoriness was 66 ± 41 msec, and it was similar at a paced cycle length of 400 msec at 65 ± 45 msec. Total dispersion of recovery was 89 ± 40 msec at a paced cycle length of 600 and 88 ± 38 msec at a paced cycle length of 400 msec. Of note, the maximum dispersion at any two adjacent sites of refractoriness was 33 ± 12 msec, and for total recovery it was 41 ± 15 msec. Thus, in our studies,43 cycle lengths from 600 to 400 msec did not alter dispersion of refractoriness, as seen in experimental studies. In these patients we found no significant difference in dispersion of refractoriness. The dispersion of refractoriness was 62 msec at twice threshold and 50 msec at 10 mA, and the total recovery was 79 msec at twice threshold and 68 msec at 10 mA. A limitation of these preliminary data is that in these patients, dispersion measurement methods were mixed, some having twice threshold and 10 mA performed at sinus rhythm and some during a different ventricular-paced cycle length. The difference between this study and our data43 probably relates to the fact that we could not compare very slow rates with faster rates and only studied rates of 100 and 150 bpm in detail. Moreover, the effect of chronic bradycardia and subsequent ventricular enlargement may play an important role in refractory period measurements. Other workers have looked at the effect of site of pacing on refractoriness, considering, for example, whether atrial pacing differed from ventricular pacing. In contrast, when we compared dispersion of refractoriness and recovery from multiple left ventricular sites measured during atrial pacing and ventricular pacing at the stimulation site in five patients, we found no significant difference in dispersion of refractory periods of total recovery times. The difference between these results is unclear, although the small number of pacing sites in the study by Friehling et al. Our data on normal left ventricular dispersion of refractoriness and total recovery time serve as a reference for evaluating the role of dispersion refractoriness and/or recovery in arrhythmogenesis. The signals recorded are quite comparable to intracellular microelectrode recording, and if properly done are stable for a few hours. Thus, the value of this technique in abnormal tissue or in the presence of Na channel blockers is uncertain. Patterns of Response to Atrial Extrastimuli Several patterns of response to programmed atrial extrastimuli are characterized by differing sites of conduction delay and block and the coupling intervals at which they occur. Although it has been stated that any prolongation of His–Purkinje conduction is an abnormal response, it is not. Previous studies demonstrated that 15% to 60% of normal patients can show some prolongation of the H-V interval in response to atrial extrastimuli.

Vaginal Bleeding Withdrawal of maternal hormonal supply may cause slight Epstein Pearls vaginal bleeding on third day quality betoptic 5 ml. It disappears by seventh day Lateral to the midline of the hard palate may be seen whit- and is harmless buy 5ml betoptic mastercard. Subconjunctival Hemorrhage A neonate may show a subconjunctival hemorrhage close Sucking Callosities to the outer canthus purchase 5 ml betoptic mastercard. It subsides in a matter of few days Tese signify attempts of the baby at sucking during intra- without any intervention. Natal (Congenital) Teeth Rarely the newborn may be born with one or two already Physiological Mastitis erupted teeth (Fig. Tese need not be extracted Bilateral swelling of the breasts, which is hormonally induced, unless they interfere with breastfeeding or they are loose. Also termed congenital teeth, the condition is of some other manifestations of the disease. Extraction is indicated if teeth are loose or if they recognized—false frst: False in which hernia occurs into interfere with feeding. It occurs in 25–50% of Oriental infants which Already dealt with under “Birth injuries” in this very is 6–10 times higher than the incidence in the whites. Unlike paraumbilical or inguinal hernia, it seldom causes strangulation or incarcination. Te term refers to sudden, involuntary, jerky diaphragmatic contractions, causing abrupt inspiratory episodes against a Hydrocele closed or closing glottis. It occurs intermittently after feeds Noncommunicating hydrocele, more often on the right in normal infants and is of no signifcance. If the attacks are prolonged, discomfort, fatigue and malnutrition may side, presenting with a well transilluminated scrotal swell- develop. It usually disappears nostril, orbital pressure, carotid sinus pressure, induction spontaneously by 6 months of age. In case of its persis- of vomiting and therapy with drugs such as chlorpromazine tence beyond one year of age, herniotomy is needed. Nonretractable Prepuce Nasolacrimal Duct Blockade (Physiological Phimosis) A proportion (2%) of the newborn may have persistent Many male newborns may have a prepuce that is adherent watery discharge and even conjunctivitis (usually unilat- to the underlying glans. Te condition should be consid- the nasolacrimal duct and clears spontaneously by 1–3 ered pathological only if the difculty in retracting the pre- months. All that is needed is frequent wash of the eye with puce over the glans is persistent beyond 3 years of age and a moist sterile swab and gentle massage of the skin over causes bulging of the foreskin on passing urine. In the presence of an infection, antimi- Mothers need to be advised not to attempt to forcibly crobial eye drops may be indicated. Hymenal Tags About 60% of normal baby girls show mucosal tags at the Umbilical Hernia (Fig. Such a baby measures 46 cm or less z Buccal pad of fat is prominent in length (crown-heel) and has head circumference of 32 cm z Excessive lanugo hair present all over the body or less. Bright light is supposed to z Retinopathy of prematurity (earlier termed retrolental fbropla- act by producing chemically excited state and generating sias) (Fig. Ponderal and thin, skin losing its normal elasticity and hanging in index* is below 2 against the normal of over 2. An artist’s depiction labia minora and clitoris are edematous so that labia majora are widely of the condition developing in a premature infant’s eye as a result of placed and not covering labia minora. Maternal malnutrition, heart disease, tuberculosis, renal disease and bronchial pregnancy-induced hypertension and other diseases asthma, etc. Since cell population is reduced, adverse infuence early during gestation, reducing growth potential is considerably afected, resulting in both cell number and cell size. Incidence of accompanying congenital malformations Twin pregnancy: After 35 weeks of gestation, the is high. Te early in embryonic life causing hypoplastic type of magnitude of infants in developing world is enormous. Out of a total of 22 million such infants in the world, 21 Placental dysfunction:Maternal problems such as toxe- million belong to the developing countries. India’s share mias of pregnancy and hypertension may be responsi- is quite substantial—7–10 million. Birth (perinatal) asphyxia as a result of cerebral anoxia Hypothermia Prevention Hypoglycemia Female literacy and formal education:A well-informed, Polycythemia from chronic hypoxia educated mother is likely to have better health before and Food intolerance during pregnancy, avoid harmful agents and infuences Permanent retardation in linear growth and psycho- during pregnancy and show better reproductive perfor- motor development. Management is dictated by Maternal infections: Malaria, urinary tract infection this decision. Early feeding not only prevents hypoglycemia, but also To prevent hypothermia in the neonates. Prognosis Prompt and systematic resuscitation whenever indi- Intrauterine growth retardation infants are easy to feed cated. Clean hands: Hand hygiene, using sterile gloves z Detailed examination done and recorded. Clean cord tie: Clean and sterile ties/clamp passing urine 6–8 times/24 hours and sleeping well for 2–3 hours 4. Care in First Few Hours z Health education to mothers—proper mother care techniques like feeding, bathing, infection and prevention measures, etc. Warm chain z Proper discharge slip has been prepared and handed over to Exclusive breastfeeding, initiated within half-one hour parents. Before discharge, certain criteria Management of common problems of neonates must be met (Box 17. Early detection of high-risk cases and management Follow-up Safe and suitable referral to special care/intensive care centers. First follow-up visit—normal at 6 weeks when check-up as well as immunization can be given. Tis has a bearing on management, including tion is supine position rather than prone position. Since the dates z Rooming-in (bedding-in): Mother should be of last menstruation are frequently not forthcoming from encouraged to indulge in rooming-in, i. Yet another method umbilical stump is shed and the local area becomes of determining the gestational age is fetal ultrasonographic clean. Te expanded new Ballard scoring system (that in- sponging may be given after 24 hour of birth. Female: Widely separated labia majora with exposed labia minora and clitoris Discharge and Follow-up z Breast nodule: Less than 5 mm diameter All normal newborns need to stay in the hospital for a z Ear cartilage: Defcient with poor elastic recoil z Scalp hair: Wooly (fne) or fuzzy (fufy).

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Tachyarrhythmias that are believed to be due to early afterdepolarization are bradycardia dependent discount 5ml betoptic free shipping, and although they can be initiated in the experimental laboratory buy 5 ml betoptic with visa, they are not well suited for study by programmed stimulation cheap betoptic 5 ml overnight delivery, which automatically necessitates a relative “tachycardic” 125 126 129 130 state. As such I do not believe this mode of stimulation can distinguish triggered activity from reentrant rhythms. Some even report the results in patients who have never had a sustained arrhythmia, but who might be at risk for its occurrence. As mentioned earlier in this chapter, the anatomic and 22 23 32 89 95 electrophysiologic substrates of these arrhythmias differ. Therefore, sensitivity and specificity should only be applied to the use of programmed stimulation for a single arrhythmia type. In addition to the type of arrhythmia and the underlying anatomic substrate, specific features of the methodology of programmed stimulation can influence the ability to initiate the tachycardia. They include distance from the origin of the arrhythmia, refractoriness at the site of stimulation, and conduction to the potential site of the tachycardia circuit or focus. Thus, although some generalities exist regarding the effects of increasing number of extrastimuli, altering drive cycle lengths, and increasing current, the investigator must interpret the response to programmed stimulation in light of the specific arrhythmia being evaluated or whether stimulation is being used for risk stratification postmyocardial infarction. In general, the greater the number of extrastimuli employed, the increased sensitivity of induction of any arrhythmia; however, this is associated with a decreasing specificity of the technique (Fig. The various modes of initiation are shown on the horizontal axis from least to most aggressive, and the percentage of inducibility rate is shown on the vertical axis. It can be seen that the more aggressive the stimulation, the higher the sensitivity but the lower the specificity. A protocol involving three extrastimuli at twice diastolic threshold gives the best balance of sensitivity and specificity. Importantly, the initiating stimulus is associated with marked latency, compatible with local conduction delay at the stimulus site. Thus, in patients without a prior history of sustained ventricular arrhythmias, we try to avoid using coupling intervals <180 msec. It is clear that using three right ventricular extrastimuli there is approximately a 90% sensitivity. More aggressive modes of stimulation from the right or left ventricle add little to improve the sensitivity. By Baysean analysis, this response is more likely to have clinical significance in a patient population in whom similar arrhythmias are present. Despite this, one should always be circumspect when interpreting a polymorphic tachycardia as a clinically significant arrhythmia because, as noted previously, comparable arrhythmias can be induced in patients without any history of arrhythmia. The last two coupling intervals are 160 and 140 msec, respectively, and are associated with local conduction delay (i. It should be noted that the clinical significance of the induction of any arrhythmia, P. This is a reason for using multiple stimulation sites and drive cycle lengths (see below). When cardiac arrest is the presenting syndrome, we would not deliver more than three extrastimuli, because the additional extrastimuli would be more likely to induce polymorphic tachycardias than a uniform one (10:1), which if acted on would lead to the treatment of “nonspecific responses” in some individuals. It is important that the induced arrhythmia be comparable to the spontaneous arrhythmia to ensure specificity of programmed stimulation. It is important that repetition of “critical” coupling intervals or the entire protocol is employed in order to define a true negative study. Top: Spontaneous left bundle branch block tachycardia with left inferior axis is shown. In 10% to 15%, induction can be accomplished either during sinus rhythm or ventricular pacing. B: A single extrastimulus at the same coupling interval induces a left bundle branch block tachycardia. The cycle length used can influence the number of extrastimuli required for induction. Unfortunately, one cannot predict which cycle length will facilitate induction of the clinically relevant tachycardia. In our laboratory, we routinely use drive cycle lengths of 600 and 400 msec in all patients as well P. Additional cycle lengths may be employed if stimulation at these drive cycle lengths fails to initiate tachycardia. B: During ventricular pacing, a single extrastimulus delivered at a longer coupling interval induces the same tachycardia. Refractory periods were measured at a drive cycle length of 600 msec in 107 patients in the ventricular tachycardia group and in 57 patients in the cardiac arrest group. Refractory periods were measured at a drive cycle length of 500 msec in six patients in the ventricular tachycardia group and in two patients in the cardiac arrest group. Role of triple extrastimuli during electrophysiologic study of patients with documented sustained ventricular tachyarrhythmias. Role of triple extrastimuli during electrophysiologic study of patients with documented sustained ventricular tachyarrhythmias. Multiple Sites of Stimulation Studies have demonstrated that using at least two sites of stimulation enhances the ability to initiate 1 42 140 156 tachycardias. If three extrastimuli are delivered only from the right ventricular apex, 10% to 20% of patients will require the use of a second right ventricular or left ventricular site for initiation of 156 sustained (Fig. Thus, the inducibility appears related to the relationship of the wavefront of activation from the site of stimulation and the mechanism at the tachycardia origin. To determine the influence of stimulation site on the mode of induction and to allow for the safest stimulating protocol to induce the tachycardia (least number of extrastimuli), I recommend alternating stimulation from the right ventricular apex and outflow tract at each specified cycle length and number of extrastimuli. Role of Increasing Current Several investigators have evaluated the use of increasing current (5 to 20 mA) in the induction of sustained ventricular P. Moreover, only a small increment in sensitivity of 158 initiating a uniform sustained tachycardia occurs with increased current. Even when used, the increased current may either facilitate or inhibit induction of certain 158 tachycardias. The mechanism by which increased current seems to facilitate tachycardia is by shortening the measured local refractoriness; however, the mechanism by which induction is prevented is unknown.

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When subsequent beats are added to the drive train at the same cycle length generic betoptic 5ml online, no increase in return cycle is noted generic betoptic 5ml on line. However cheap betoptic 5 ml free shipping, the return cycle increases to 520 msec following the nth + 1 beat ( middle panel) and continues to increase with each incremental beat until the tachycardia terminates following the sixth paced beat. Comparison of resetting and entrainment of uniform sustained ventricular tachycardia; further insights into the characteristics of the excitable gap. The ability to demonstrate surface electrocardiographic fusion and thus fulfill two of the proposed criteria for “entrainment” depends on enough of the ventricular myocardium being depolarized by both the stimulated and tachycardia wavefronts so that the presence of both wavefronts can be recognized (i. This is an identical situation to that described earlier (see the section entitled Resetting with Fusion). Surface electrocardiographic fusion is, therefore, not necessary to define the presence of entrainment. Entrainment of ventricular tachycardia: explanation for surface electrocardiographic phenomena by analysis of electrograms recorded within the tachycardia circuit. The stimulated impulse would also conduct orthodromically; thus, resumption of the tachycardia would occur with the presystolic electrogram orthodromically activated. Therefore, the last stimulus of the train activates the presystolic electrogram antidromically to produce retrograde capture and simultaneously conducts orthodromically through the circuit. Local fusion and, hence, the possibility of fusion (albeit nonrecognized) outside the circuit can only occur if the presystolic electrogram is activated orthodromically. In all such cases, the return cycle measured at this local electrogram will equal the paced cycle. If pacing is performed at a shorter cycle length, then the paced impulse can penetrate the circuit antidromically and retrogradely capture the presystolic electrogram so that no exit from the tachycardia circuit is possible. When pacing is stopped, the impulse that conducts antidromically also conducts orthodromically to reset the reentrant circuit with orthodromic activation of the presystolic electrogram. An example of entrainment during right ventricular pacing at a cycle length of 310 msec is shown in the upper right panel. Note that the initial components of the presystolic left ventricular electrogram (denoted by the black arrows) remain unchanged during entrainment when compared with their morphology during tachycardia. The systolic component of this electrogram (small red asterisk) is altered at the lower right during pacing at a shorter cycle length (260 msec) the initial component of the left ventricular electrogram changes (red arrow). Also note that the left ventricular electrogram recorded during entrainment is almost identical to the electrogram recorded during right ventricular pacing in sinus rhythm (lower left). The orthodromic activation time to the presystolic electrogram (green arrow) remains unchanged. Entrainment of ventricular tachycardia: explanation for surface electrocardiographic phenomena by analysis of electrograms recorded within the tachycardia circuit. This should be classified inapparent fusion and is depicted in the right-hand panel of Figure 11-178. This can be detected only by analyzing whether or not the presystolic electrogram is orthodromically or antidromically activated. Thus, one can demonstrate two pathways of conduction to the presystolic electrogram: one that has a more prolonged conduction time—that is, the orthodromic pathway in the circuit—and one that results in antidromic capture of that electrogram. Thus, stimulation from the same site in the heart can manifest two activation times to the same point in the reentrant circuit. This has led to the concept that the orthodromic limb of the circuit exhibits a long 1 122 319 326 327 337 342 343 conduction time. During orthodromic activation, the stimulus to local electrogram interval is greater than during antidromic capture (Fig. Note that in Figure 11-180 the interval from the stimulus to local presystolic electrogram remains flat over a period of cycle lengths during both orthodromic and antidromic activation, suggesting that no decremental conduction was present. Although others have “demonstrated” the so- 326 327 335 342 343 called “decremental properties” in the orthodromic limb, , , , , this concept is misleading. Slowing is secondary to interval-dependent conduction delay through tissue that has only partially recovered excitability when the ( n + 1)th stimulus reached the circuit. As noted earlier one can observe a flat resetting curve in response to single extrastimuli, yet when rapid pacing is initiated, following the first extrastimulus producing resetting ( nth stimulus) the subsequent stimuli can occur during the relative refractory period of the excitable gap and prolong the return cycle. This prolonged stimulus to presystolic electrogram compared to a single extrastimulus does not imply decremental properties analogous to that of the A-V node (Fig. If it arrives at a fully excitable state, the stimulus to local electrogram will be the same as observed using a single extrastimulus regardless of the cycle length of pacing. This is demonstrated in analog records in Figure 11-176 and in graphic representation in Figure 11-180. The prolongation of the stimulus to local electrogram interval at shorter cycle length means that the ( n + 1)th stimulus has encountered partially excitable tissue in the reentrant circuit. The circles represent sites within the reentrant circuit just proximal to the exit site from the presystolic electrogram is recorded. Note the premature penetration of the stimulus into the entrance of the tachycardia circuit so that the tachycardia is advanced to the paced cycle length. During entrainment, collision occurs between the entrance and exit of the tachycardia circuit. The presystolic electrogram is activated by the wavefront entering the circuit and propagating antegradely (orthodromically). Thus, the initial morphology of this electrogram does not change during pacing, and the impulse can exit to produce a fusion complex. However, as depicted in the panel on the right, during pacing at a shorter cycle length, retrograde collision between the stimulated wavefront and the previous tachycardia (or stimulated wavefront) occurs before the point at which the tachycardia can exit the reentrant circuit. The solid electrogram recorded from the reentrant circuit is now activated in a retrograde fashion and is therefore changed in morphology. The open electrogram, however, is still activated in an antegrade fashion (with no change in its initial morphology). Because the presystolic solid electrogram is captured retrogradely, the preceding impulse with which it collides can never exit the circuit; therefore, fusion is impossible during entrainment with retrograde capture of the presystolic electrogram. Entrainment of ventricular tachycardia: explanation for surface electrocardiographic phenomena by analysis of electrograms recorded within the tachycardia circuit. Conversely, however, the absence of a change in morphology of the presystolic electrogram recorded from the tachycardia circuit did not always predict the presence of surface electrocardiographic fusion.

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In patients who have pre-existent antegrade bundle branch block generic 5 ml betoptic otc, retrograde block in the same bundle branch is common order betoptic 5 ml mastercard. In fact buy generic betoptic 5 ml on line, when pacing is instituted from the ipsilateral ventricle, the V-H interval is usually so long that retrograde Hs, if seen, are usually observed after the local ventricular electrogram. Once a retrograde His bundle deflection is seen, progressive prolongation of His–Purkinje conduction (S2-H2) occurs as the S1-S2 interval decreases. In most cases, the increase in S2-H2 remains relatively constant for each 10-msec decrement in S1-S2, giving rise to a fixed slope of S2-H2/S1-S2. His–Purkinje refractoriness depends markedly on the cycle length; consistent shortening of S2-H2 at any given S1-S2 is noted at decreasing basic drive cycle lengths (S1- S1). Measurement of retrograde A-V nodal conduction time is best taken from the end of the His bundle deflection to the onset of atrial depolarization. In most instances, once a retrograde His bundle deflection appears, the S1-H2 curve becomes almost horizontal (Fig. This response results in a relatively constant input into the A-V node and consequently a fixed retrograde A-V nodal conduction time (H2-A2) (Figs. Occasionally, the increases in S2-H2 greatly exceed the decreases in S1-S2, giving rise to an ascending limb on the S1-H2 curve. During the ascending limb, retrograde A-V nodal conduction improves (shorter H2-A2) because A-V nodal input is less premature (shorter S1-H2). The retrograde His deflection as seen on the drive beat (S1H1 = 15 msec) allows one to assess the sites of delay during progressively premature S1 S2. The left ventricular electrogram is being paced (S1S1) at a basic cycle length of 600 msec. A: At a coupling interval (S1 S2) of 425 msec, no retrograde His–Purkinje delay (S2 H2) is seen. B, C: At closer coupling intervals, S2 H2 prolongs without concomitant local ventricular conduction delay. As S1-S2 is decreased further, either block within the His–Purkinje system appears (Fig. Inasmuch as the slopes of retrograde His–Purkinje delay are parallel at different cycle lengths, (top) the curves of resultant minimal outputs (S1-H2) are also parallel. The general pattern, however, remains the same, with an almost linear increase in S2-H2 intervals as S1-S2 is decreased (Fig. The curves for S2-H2 versus S1-S2 are shifted to the left, and the curves relating S1-S2 versus S1-H2 are shifted down. In summary, using His bundle electrograms and right bundle deflections, it is possible to carefully analyze the sequence of retrograde activation from ventricle to atrium. With more premature ventricular extrastimuli, the initial delay occurs in the His–Purkinje system. Delay and block can occur in the A-V node, but this is usually less common than that in the His–Purkinje system. Repetitive Ventricular Responses Three types of extra beats may occur in response to ventricular stimulation, and they should be recognized as normal variants. The most common type of repetitive response, which occurs in approximately 50% of normal individuals, is termed bundle branch reentry, which is a form of macroreentry using the His–Purkinje system and ventricular muscle. At this point, the retrograde His deflection is usually observed following the local ventricular electrogram. Further decrease in the coupling intervals produces an increase in retrograde His–Purkinje conduction. This is true even if stimulation is carried out from the right ventricular outflow tract. Retrograde atrial activation, if present, follows the His deflection, and the H-V interval usually approximates that during antegrade conduction. However the H-V interval may be shorter or greater than the H-V interval during antegrade conduction. The H-V interval depends on (a) the site of His bundle recording relative to the turnaround point (Fig. The H-V interval of the bundle branch reentrant beat, therefore, reflects the interplay of these factors. A ventricular extrastimulus is delivered at V2 (asterisk), which blocks in the right bundle. A: At a premature ventricular coupling interval of 250 msec, retrograde His–Purkinje delay is manifested by prolongation of the V-H to 140 msec. The H-V interval during this complex is 165 msec (15 msec greater than during sinus rhythm). Electrophysiologic features that suggest that this extra beat is in fact due to bundle branch reentry follow: 1. The extra response is always preceded by a retrograde His deflection and is abolished when retrograde block below the His bundle recording site is achieved, a phenomenon that may occur with simultaneous right and left ventricular stimulation (Fig. Moreover, pre-excitation of the His bundle to produce block below the His bundle also prevents the repetitive response (Fig. Although the H-V interval preceding the extra beat usually approximates the H-V interval of sinus beats, a reciprocal relationship exists between the V2-H2 and H2-V3 intervals. Thus, at the onset of reentry, shorter V2-H2 intervals are associated with longer H2-V3 intervals. Progressive shortening of the coupling intervals results in longer V2-H2 intervals, which are then followed by shorter H2-V3 intervals. These types of repetitive responses can be noted during atrial fibrillation or in the absence of A-V conduction (Fig. Repetitive responses to ventricular extrastimuli: incidence, mechanism, and significance. The only factor influencing the ability to demonstrate bundle branch reentry is the presence of antegrade bundle branch block during sinus rhythm. Ventricular extrastimuli can conduct up the slowly conducting fascicle and down the “good” fascicle, giving rise to an extra beat that looks almost identical to the sinus complex. Atrial premature beats can also produce such repetitive responses by causing transient block in the slowly conducting fascicle. Conduction proceeds over the “good” fascicle and can return up the blocked fascicle if it has recovered. This often results in sustained reentry, producing a hemodynamically untolerated ventricular tachycardia.

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