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D. Dennis. Prairie View A & M University.

Over the last 15 years discount clomid 100 mg amex, the evolution of the techniques has In 1975 buy clomid in united states online, Juri published a large axial pedicle flap model been undeniable purchase clomid with a mastercard. Brandy realized consecutive wide reducing allowing extensive coverage of the frontal region but with an procedures of bald areas [13]. Ciotti formed in two steps, which was then refined by Dardour with were progressively abandoned in the 1990s in favor of mini the concept of “scalp lifting” [14–16] (Fig. In 1992, Fréchet proposed a technique of scalp extension, Large cylindrical grafts performed during transplantation patenting an apposite elastomer [19, 20]. Its main aesthetic posterior branch of the temporal artery, and is 25 cm long and 3. This is a Juri flap based on a temporal artery that is microanastomosed onto the contralateral temporal artery. Ciotti 5 Surgical Anatomy of the Scalp This space is traversed by emissary veins that run from the subcutaneous layer of the scalp to the intracranial venous The scalp consists of five layers: skin, subcutaneous tissue, sinuses. The laxity of this layer explains the mobility of the galea, loose areolar tissue, and pericranium. The skin of the scalp is the thickest skin of the body, rang- This space is considered the “danger zone” of the scalp ing from 8 mm in the occipital region to 3 mm in the anterior because hematoma or infection can easily spread through it, and temporal regions. It consists of The innermost layer of the scalp, the pericranium, is adipose tissue and fibrous connective tissue organized in firmly connected to the outer table of the skull. It has a quadrilat- consists of a superficial layer that adheres to the lateral eral shape, and therefore has a superficial and a deep face border of the zygomatic arch, and a deep layer that adheres and four margins, anterior, posterior and two laterals. The superfi- The superficial face is firmly connected to the overlying cial temporal adipose tissue is located between the two structures through the septa that pass across the subcutane- layers. The deep face is separated from the pericranium by a deep layer of avascular connective tissue. The scalp is highly vascularized by four main arteries and It originates from the anterior margin of the galea and runs smaller vessels. The main arteries are the occipital and super- anteriorly and downward until the deep face of the skin in ficial temporal arteries on each side. The smaller vessels of correspondence with the eyebrows, glabella, and superior the scalp are the posterior auricular artery, small branches of portion of the dorsum of nose, where it inserts. It interdigi- the posterior auricular artery, small branches of the external tates with fibers from the procerus, corrugator supercilii, and carotid artery, and supraorbital and supratrochlear vessels. The frontalis muscle, by contract- These vessels are contained in the subcutaneous layer and ing, moves the scalp forward and causes frowning. Its fibers run obliquely, medially, and downward to insert on the posterior nuchal line and the mastoid process. The occipital artery arises from the external carotid artery The anterosuperior auricular muscle is located in the tem- above the origin of the lingual artery and runs posteriorly, poral region, forward and superiorly to the auricula. It origi- upward, and outward, passing beneath the posterior belly of nates from the lateral margin of the galea and inserts on the the digastric muscle and then in the groove of the mastoid lateral face of the auricula in correspondence with the helix, process. It pierces the fascia connecting the cranial attach- the spine of the helix, and the anterosuperior part of the con- ment of the trapezius and sternocleidomastoid muscles, and vexity of the concha. Along its course it posterior, between which runs the parietal branch of the ante- divides into the following branches: rior superficial temporal artery. The frontalis, occipitalis, and anterosuperior auricular • Muscular branches for the sternocleidomastoid, digastric, muscles are intrinsic muscles and belong to the group of stylohyoid, splenius, and longissimus capitis muscles mimic muscles. The superficial portion anastomoses Its terminal branches are: with the transverse cervical artery. The deep portion anastomoses with the vertebral and deep cervical arteries • Frontal (anterior) branch, which supplies the frontal region • Meningeal branches, which enter the skull through the • Parietal (posterior) branch, which supplies the skin and jugular foramen and condyloid canal, to supply the dura the epicranial aponeurosis of the parietal region mater in the posterior fossa The terminal branches of the occipital artery are the 6. These branches, with a tortuous course, anastomose to the contra- The supratrochlear and supraorbital arteries supply the ante- lateral occipital branches and the branches of the superficial rior region of the scalp. The supraorbital artery passes between the superior rectus muscle and levator palpebrae superioris muscle, to the apex of the orbit. The posterior auricular artery arises above the posterior belly The supratrochlear artery is one of the terminal branches of the digastric muscle, and ascends in the groove between of the ophthalmic artery. It enters the facial canal through the The supratrochlear and supraorbital arteries anastomose stylomastoid foramen and supplies the mastoid cells, the sta- in the frontoparietal subcutaneous layer of the scalp. The extracranial venous circulation is connected to the intracranial venous circulation through several emissary The superficial temporal artery is the most important vessel veins. The emissary veins, after passing through the cranial of the scalp because of its length and surface supply. The venous system of the in the substance of the parotid gland, behind the neck of the scalp follows the arterial one. In the temporal The frontal, supraorbital, and nasofrontal veins unite region, beneath the skin, it divides into a frontal and a pari- superficially at the medial angle region of the eye to form the etal branch. When it passes anterior to the tragus it is only angular vein, which runs obliquely downward and backward covered by the skin, and its pulse is palpable (pulsatility). It with a linear course, receiving numerous branches to become is accompanied by the corresponding vein and the auriculo- the anterior facial vein. Its collateral branches are: The union of the superficial temporal vein and the middle temporal vein, anterior to the auricle, forms the posterior • Parotid branches for the parotid gland facial vein. Its area corresponds to that of the superficial tem- • Transverse facial artery poral artery. The frontal nerve, the largest terminal branch of the ophthalmic nerve, enters the The scalp has numerous sensitive nerves. The supraorbital orbital cavity through the superior orbital fissure, external to and supratrochlear nerves, terminal branches of the ophthal- the tendinous ring (annulus of Zinn). It runs along the apex mic division of the fifth cranial nerve, innervate the anterior of the orbital cavity in close contact with the periosteum, From the ophthalmic division of trigeminal nerve (V1) Supraorbital nerve Supratrochlear nerve Auricular branch of vagus nerve (X) Palpebral branch of lacrimal nerve Infratrochlear nerve External nasal branch of anterior ethmoidal nerve From the maxillary Medial branches division of trigeminal of posterior divisions nerve (V2) of cervical spinal nerves Zygomaticofacial nerve Greater occipital nerve (C2) Zygomaticotemporal Third occipital nerve (C3) nerve Spinal nerves C4, C5, C6, C7 Infraorbital nerve and C8 From the mandibular Branches of cervical plexus division of trigeminal Lesser occipital nerve (V3) nerve (C2,C3) Mental nerve Great auricular Buccal nerve nerve (C2, C3) Transverse cervical (or Auriculo-temporal nerve cutaneous cervical) nerve (C2, C3) Posterior divisions of cervical spinal nerves Ophtalmic nerve (V1) Auricular branch of vagus nerve to the external acoustic Trigeminal meatus and small area of nerve (V) Maxillary nerve (V2) postero-medial aspect of the auricula Mandibular nerve (V3) Branches of cervical plexus Fig. Along its course dible, and reaches the parotid lodge, passing through the on the orbital margin it divides into the supratrochlear, fron- parotid gland. It turns superiorly, outward, between the external auditory The supratrochlear branch is the smallest and most medial meatus and the superficial temporal vessels, spreading of these three nerves. It exits from the orbital cavity above branches to the skin of the temporal region and the anterior the pulley of the superior oblique muscle, and supplies the part of the auricle [21–23]. The frontal branch, which is intermediate and outside the orbit, surrounds the orbital margin of the frontal bone and 8 First Visit and Patient Selection ascends to supply the skin of the frontal region. The supraorbital branch is the largest and most lateral of The first doctor-patient approach aims at giving both of them the branches of the frontal nerve. For the doctor it is important to evaluate the orbital foramen of the frontal bone along with the supraor- psychological aspects of the patient, determine the motiva- bital artery. Along its course it gives off numerous ascending tions behind the surgical operation, and discuss the possible branches that extend to the scalp. As a consequence, the surgeon must suggest ous branches for the forehead and the scalp, the supraorbital the best strategy without promising miraculous results.

Thus discount 25mg clomid otc, patients are advised to adopt a position where the knees are above the hips with feet flat on the floor trusted clomid 25 mg. There are now several devices available to enable a squatting position to be adopted on a pedestal toilet buy clomid 50mg with visa. The mechanism of each type of laxative will help to determine the most appropriate type of laxative for the patient’s symptoms (Table 63. Bulk Laxatives/Fiber Undigestible fiber is an important part of our diet to provide stool bulk. Bulk-forming laxatives attract water, forming larger and softer stool, which in turn causes colonic distension, stimulating peristalsis and effective propulsion of stool along the colon to rectum. Systematic review has reported that bulking agents induce an average increase of 1. Lactulose (semisynthetic disaccharide, poorly absorbed sugar), macrogols (inert polymers of ethylene glycol), or magnesium salts retain fluid in the colonic lumen causing osmotic diarrhea. Absorption of magnesium is limited but caution must be exercised in patients with impaired renal function [58]. Lactulose is less effective than macrogols [59] and its use may be limited due to flatulence and bloating caused by bacterial fermentation. Stimulant Laxatives Diphenylmethane derivatives such as bisacodyl, sodium picosulphate and anthraquinone derivatives such as senna are stimulant laxatives, which act on the enteric nervous system to increase intestinal motility but may cause abdominal cramps as a consequence. Long-term use of anthraquinone-derived stimulants can generate brown discoloration of mucosa known as pseudomelanosis coli. Parasympathomimetics such as neostigmine enhance parasympathetic activity in the gut and increase intestinal activity. Neostigmine can be used in selected cases for the treatment of pseudoobstruction that has failed to settle with conservative management [60]. Efficacy of the treatment should be reviewed after a 4-week trial of the medication. Headache, nausea, and diarrhea were more common side effects with prucalopride compared to placebo [55]. A smaller study comparing efficacy of prucalopride on patients with different subtypes of constipation showed that all categories of constipation may respond to prucalopride [65]. It is thought that by increasing the intestinal secretions, small bowel motility is increased, thereby increasing the passage of stool [66–68]. There are limited but supportive data on safety and efficacy of use of lubiprostone in the elderly population [71], constipated patients with Parkinson’s disease [72], and treatment of opioid-induced constipation [73]. Treatment of Irritable Bowel Syndrome with Constipation It is important to identify symptoms that are affecting the individual patient and tailor the treatment accordingly [10,49]. To treat their constipation, bulk-forming laxative, such as soluble fiber (ispaghula husk or oats), or osmotic laxatives (macrogol) are recommended. Biofeedback Biofeedback is based on behavior modification and operant conditioning [80]. It teaches patients how to control a physiological function that is not usually under conscious control by using an instrument that provides visual and/or auditory feedback of an action. This therapy has been reported to be effective in both constipation and incontinence [81]. Gut-directed biofeedback involves patients being taught to defecate successfully using bracing of the abdominal wall muscles and effective relaxation of the pelvic floor muscles [85]. This may be enhanced by use of a water-filled rectal balloon, which patients attempt to expel [86]. Patients are enabled to recognize the sensations associated with relaxation of the pelvic floor and anus together with correct use of abdominal muscles to create an effective pushing force and thus learn to defecate effectively. Patients may also be given basic instruction on gut anatomy and function to enhance their understanding, as well as behavioral advice about frequency and length of toilet visits, posture on the toilet, and dietary habits [87]. Biofeedback has been shown to be more effective than laxatives [93], relaxation training [89], and placebo [90]. A systematic review of seven trials, with a total of 413 participants, concluded that biofeedback conferred a sixfold increase in the odds of treatment success [84]. There is some evidence that evacuating regularly may also stimulate gut transit and so improve symptoms [86]. Whereas short-term results may vary from 60% to 90% improvement [94], long-term studies report sustained improvement in around 50% of patients [95]. As the treatment involves dedicated sessions with a single clinician, the development of that therapeutic relationship may also contribute to improvements in quality of life. Psychological Therapy Psychological therapies can improve symptoms without interacting with pharmacological treatments [96]. Additionally, they can improve patient’s ability to cope with the symptoms thus improving quality of life. Discussion of symptoms with a supportive health-care professional who listens and responds appropriately can reduce feelings of isolation and shame. Some patients need more formalized psychological interventions, including counseling and cognitive behavioral therapy. Rectal Irrigation Rectal irrigation was originally used in clinical practice for children with spina bifida [97]. Indications were extended to adults with neurogenic bowel dysfunction after conservative management had failed [98]. It is now used in a wider variety of conditions such as rectocele, obstructed defecation, and other functional bowel problems [99]. Several products are available on the market; hence, the product can be chosen to suit individual patient’s needs. They are designed to be used while sitting on the toilet to avoid accidents when transferring. The larger systems allow irrigation with a cone or balloon catheter, enabling instillation of larger quantities of water, used in patients with slow transit constipation or neurological abnormalities (Aquaflush Quick, Qufora, Peristeen). In long-term follow-up of 169 patients over 56 months, rectal irrigation was found to be effective in 44% of patients with fecal incontinence and 62% of patients with defecatory disorders [24]. Collins and Norton retrospectively assessed 50 consecutive patients using the mini system and found that 62% improved or their symptoms completely resolved [102]. Absolute contraindications include stenosis, colorectal cancers, acute diverticulitis, and active inflammatory bowel disease. Most complications reported are minor and include abdominal cramps, minor anal bleeding, and leakage of irrigant after completion [99]. Introduction of a medical device and administration of water carry a risk of bowel perforation. In a consensus review of best practice, the perforation risk was estimated at 1 per 50,000 and was thought to be noncumulative [103]. For this reason, it is important that irrigation is taught by qualified experienced clinicians. It is postulated that stimulation of the tibial nerve in turn stimulates the sacral nerves thus neuromodulating bowel motility and/or sphincter function.

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Validation that the “spike” that is recorded between atrium and ventricle is indeed due to activation over a bypass tract is required safe 25mg clomid. Bypass tract potentials should be manifested as a sharp spike 10 to 30 msec before the onset of the delta wave during antegrade recordings buy 25 mg clomid with amex. Validation that the spike is indeed recording bypass tract potentials and not a component of atrial and/or ventricular electrograms is critical and buy clomid pills in toronto, in our opinion, has been lacking in many of the examples that have been reported. Thus, initially one must record a sharp rapid deflection between the atrial and ventricular electrograms at the earliest site of retrograde atrial activation during reciprocating tachycardia, right ventricular pacing, as well as during sinus rhythm. Proof that the electrogram is not part of the atrial electrogram requires its persistence with elimination of the atrial electrogram during retrograde block. Both criteria should be met; however, in most reported cases, validation has 110 not been attempted or satisfactorily accomplished. All but one of the proposed criteria was seen in response to atrial and ventricular stimulation. The only observation they never made was block between the first and second components of the atrial electrogram simulating block between the atrium and the bypass tract. This latter observation has never been convincingly demonstrated in our laboratory. Although bypass tract recordings can be obtained and may serve as a marker for a catheter ablation of the bypass tracts, proof that the electrical signal interpreted as a bypass tract potential is a bypass tract potential, in my opinion, is rarely achieved. Most often it is not possible to distinguish a component of the atrial or ventricular electrogram from a bypass tract potential. The first two complexes manifest left anterior hemiblock and have V-A intervals of 150 msec. The next two complexes have left anterior hemiblock, and the V-A interval returns to 150 msec. Note the sharp spike of the bypass tract potential is observed on the unipolar and bipolar signals and precedes the local ventricular electrogram and the delta wave. This was recorded with a standard quadripolar catheter with electrodes spaced at 5 mm. This is consistent with that signal being a recording of a left posterior bypass tract which was located in a coronary sinus diverticulum. Schema of pacing maneuvers to prove a signal is a bypass tract potential using the second component of a split atrial electrogram to mimic a bypass tract potential. Assessment of pacing maneuvers used to validate anterograde accessory pathway potentials. Therefore, demonstration that the bypass tract plays a critical role in the genesis of the arrhythmia is imperative and is essential for appropriate therapy, especially catheter ablation or surgery. If the propensity to develop atrial fibrillation was based solely on primary intra-atrial pathophysiology, ablation of the bypass tract could cure circus movement tachycardia but would fail to prevent recurrences of atrial fibrillation later in life. Atrial tachycardia must be distinguished from antidromic tachycardia, or more accurately, “preexcited circus movement tachycardia. During atrial pacing the atrial electrogram is (A and A′) with an isoelectric interval of 35 msec. The shortest coupled atrial extrastimulus that captured produced an increase in A-A′ to 80 msec. Assessment of pacing maneuvers used to validate anterograde accessory pathway potentials. Assessment of pacing maneuvers used to validate anterograde accessory pathway potentials. During atrial pacing (S1-S1) at a cycle length of 500 msec an atrial extrastimulus (S2) was delivered, which depolarizes both components of the split electrogram mimicking block between the accessory pathway and the ventricle. Assessment of pacing maneuvers used to validate anterograde accessory pathway potentials. Assessment of pacing maneuvers used to validate anterograde accessory pathway potentials. The observations 32 38 102 103 104 111 indicating the presence of a bypass tract are well-described , , , , , and include: 1. The amount of A-V delay allows the bypass tract to recover and an atrial echo (Ae) results from retrograde conduction over the bypass tract. That impulse conducts slowly through the A-V node (A-H 300 msec) but blocks below the recorded His bundle deflection. Thus, during rapid tachycardias, a single right ventricular stimulus might not reach a left lateral bypass tract in time to preexcite the atrium. This is shown in Figure 10-84, in which the first of two ventricular extrastimuli fails to affect retrograde atrial activation while the second can terminate the tachycardia. This early activation of the atrium then resets the tachycardia with a longer A-H and a delay in the return cycle. The ability to preexcite the atria when the His bundle is refractory with the same atrial activation sequence as seen during the orthodromic tachycardia confirms the presence of functioning posteroseptal bypass tract. The tachycardia terminates by retrograde block in the bypass tract when the His is refractory. This confirms the necessary participation of the bypass tract in the tachycardia circuit. Only conditions 2, 3, 5, 6, and 7 absolutely demonstrate participation of the bypass tract in the reentrant circuit, because they demonstrate requirement of the ventricle in the tachycardia circuit. Atrial preexcitation alone is compatible with the presence of a bypass tract if the atrial activation sequence of the preexcited atrial activation is identical to that of the atrial activation sequence seen during tachycardia. Although this supports the involvement of a bypass tract in the reentrant circuit, atrial tachycardia or intra-atrial reentry conceivably could occur at the site of the atrial insertion of the bypass tract. Then, retrograde atrial activation during ventricular preexcitation would look identical to that of the atrial tachycardia. However, if atrial tachycardia were present, there would be a V-A-A-V return cycle. The V-A-V return cycle with a constant V-A excludes atrial tachycardia and makes the diagnosis of orthodromic tachycardia. Condition 1 is compatible with the presence of a bypass tract but does not demonstrate its requirement to maintain the tachycardia, because it is theoretically possible, although highly unlikely, that retrograde atrial activation over a bypass tract may be an unrelated epiphenomenon to another tachycardia mechanism. For example, we have seen ventricular tachycardia with retrograde atrial activation over a bypass tract. In this instance, ventricular tachycardia certainly does not require the bypass tract for its persistence. These are theoretical possibilities; however, in the vast majority of cases, all the conditions mentioned are useful in diagnosing the presence of a bypass tract. The first ventricular extrastimulus fails to affect the tachycardia with the antegrade His and retrograde atrial activation over the bypass tract being unaltered. The second extrastimulus, which is introduced earlier in the cardiac cycle, conducts over the bypass tract retrogradely. The inability of a right ventricular extrastimulus to affect circus movement tachycardia demonstrates the lack of requirement of the right ventricle in tachycardias using a left-sided bypass tract.

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The increasing curve may represent progressive conduction delay of the paced impulse between the pacing site and the reentrant circuit purchase clomid pills in toronto. This is highly unlikely because the shortest return cycles are virtually identical when the response to single and double extrastimuli from the same site are compared generic 25mg clomid otc. Because shortest 315 316 317 return cycles in response to single and double extrastimuli are identical buy cheap clomid 50 mg on line, this mechanism is unlikely. The first extrastimulus is fixed at a coupling interval of 300 msec in all panels. A: The second extrastimulus fails to reset a tachycardia at a coupling interval of 295 msec. B: At a coupling interval of 270 msec, resetting of the tachycardia is seen with a return cycle of 355 msec. C: As the coupling interval of the second extrastimulus is decreased to 240 msec, the return cycle increases to 380 msec. Resetting response patterns during sustained ventricular tachycardia: relationship to the excitable gap. The delay may be due to a variable site of entrance determined by the tail of refractoriness in the reentrant circuit or conduction delay surrounding the circuit. In these cases, late coupled extrastimuli would enter the reentrant pathway more distally, producing shorter return cycles than early coupled extrastimuli. Thus, the more premature impulse would have to proceed over a longer pathway within the reentrant circuit, resulting in a longer return cycle and an increasing response. Because double extrastimuli, which are relatively more premature at the site of the reentrant P. In this case, progressively more premature stimuli encounter increasingly refractory tissue producing increasing conduction delays and longer return cycles at shorter coupling intervals. This interval-dependent conduction delay may be due to either encroachment on Phase 3 of the action potential or caused by nonuniform anisotropic conduction. B: As the coupling interval of the extrastimulus is decreased to 170 msec, the return cycle remains fixed at 430 msec. Therefore, a flat response pattern having a duration of 30 msec was demonstrated with single extrastimuli. C: Double extrastimuli are delivered with the coupling interval of the first extrastimulus fixed at 220 msec, 20 msec above that which caused resetting with single extrastimuli. Beginning at an S1 and S2 interval of 310 msec, resetting is seen with a return cycle of 430 msec. D: The return cycle remains essentially fixed as the S1S2 is decreased to 240 msec. E: As the S1S2 is further decremented below 240 msec, the return cycle increases until, at an S1S2 of 180 msec, the return cycle had increased to 480 msec. The resetting response of ventricular tachycardia to single and double extrastimuli: implications for an excitable gap. As shown in Figure 11-163, in some cases a flat curve may be seen with single extrastimuli, and it is only by using double extrastimuli that an increasing component of the resetting response curve can be observed. This further demonstrates that double extrastimuli more fully characterize the excitable gap than single extrastimuli. In this example, single extrastimuli produce a flat response, while double extrastimuli produce a flat response followed by an increasing response, and finally, termination of the tachycardia. The entire excitable gap demonstrated in Figure 11-164 was 155 msec and occupied 35% of the tachycardia cycle length. The resetting response of ventricular tachycardia to single and double extrastimuli: implications for an excitable gap. Moreover, in all cases in which single extrastimuli reset the tachycardia, double extrastimuli delivered from the same site produced an identical or expected resetting curve. Thus, if single extrastimuli produce a flat curve, double extrastimuli produce a flat or a flat plus increasing curve, depending on whether or not the second extrastimulus encroaches on refractory components of the excitable gap. If single extrastimuli exhibit an increasing or mixed curve, double extrastimuli also exhibit an increasing or mixed curve, respectively. Although the type of curve is unrelated to tachycardia cycle length, the absolute duration of the curve does seem to relate to tachycardia cycle length. This mechanism has no fully excitable gap and would 341 not be possible to reset by stimulation performed at a distant site. The proposed mechanisms for the three types of curves observed in our patients are schematically shown in Figure 11-165. The flat curves with return cycles less than the tachycardia cycle length and the mixed or smoothly increasing curve have never been documented in triggered activity that is due to late afterdepolarizations. In triggered activity, extrastimuli produce either a return cycle at 100% to 110% of tachycardia cycle length or a return cycle that decreases as stimuli become more premature. A: Schemas of the three types of curves we have observed (flat, increasing, and mixed). B, C: A theoretical mechanism of what is occurring in the reentrant circuit is shown at coupling intervals of X and X-50. The reentrant circuit is depicted as having a separate entrance and exit in each pattern. Each tachycardia impulse is followed by a period of absolute refractoriness (thick dark area), which is then followed by a period of relative refractoriness (stippled area) of a variable duration. A: On the left, a flat curve results when the stimulated impulse reaches the tachycardia circuit and finds a fully excitable gap between the head and tail of the tachycardia impulse. This curve results when the initial impulse producing resetting enters the tachycardia circuit when the excitable gap is partially refractory. The curve continues to increase at a coupling interval of X-50 because the tissue is still in a relatively refractory state. A mixed curve results when extrastimuli delivered at long coupling intervals find the reentrant circuit fully excitable and reset it, as in the typical flat curve shown on the left. However, at a coupling interval of X-50 the impulse finds the excitable gap partially refractory, and an increasing component of the curve results. Changes in circuit length or wavelength might result in changes in the characteristics of the excitable gap; (4) different effects of intervening tissue (anisotropy, curvature, impedance mismatch) on conduction of the stimulated wavefront into the circuit. This phenomenon suggests that the barriers (lines of block) and, consequently, the size of the circuit are at least partially functionally determined and can be markedly influenced by nonuniform anisotropy and/or that the stimulated wavefronts P. It is highly likely that all tissue in the reentrant circuit is not the same and that conduction velocity, excitability, and refractoriness vary at different sites along the reentrant pathway. The variable directions of the incoming wavefronts, due to the different sites of stimulation, will necessarily be associated with different 29 51 52 311 conduction velocities dependent on the arrangement of fibers that the wavefront encounters. Corrected coupling intervals of extrastimuli are shown on the X axis and the return cycles on the Y axis. Note that the slopes of the increasing component of the resetting curves from both sites is similar. The variable contribution of functional and anatomic barriers in human ventricular tachycardia. In these cases, the use of multiple extrastimuli, more commonly overdrive pacing, can demonstrate resetting. The use of overdrive pacing at decreasing cycle lengths with the addition of an incremental number of extrastimuli to each train of pacing at each cycle length can allow one to recognize (a) how many extrastimuli are required before the tachycardia is first reset and (b) the phenomenon of continuous resetting (entrainment).

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