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However order lady era 100 mg amex, as depicted in the panel on the right lady era 100mg low cost, during pacing at a shorter cycle length lady era 100 mg on line, 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. Entrainment of ventricular tachycardia: explanation for surface electrocardiographic phenomena by analysis of electrograms recorded within the tachycardia circuit. This obviously requires a constant stimulus to local presystolic electrocardiogram conduction time in the orthodromic direction (e. The Xs represent the conduction time from the stimulus to the left ventricular electrogram in the presence of a change in the initial component of this electrogram. Note that there is no significant change in conduction time over a range of cycle lengths when the morphology of the electrogram is preserved. Although there is dramatic change in conduction time from the stimulus to the left ventricular electrogram at the site of origin when there is a change in the morphology of this electrogram, once the electrogram has changed in morphology, the conduction time remains stable over a wide range of paced cycle lengths. Entrainment of ventricular tachycardia: explanation for surface electrocardiographic phenomena by analysis of electrograms recorded within the tachycardia circuit. To reiterate, when an increase in orthodromic conduction is observed during overdrive pacing resetting of the reentrant circuit is taking place. It is only when a stable state of orthodromic conduction follows an incremental number of paced complexes that entrainment is said to be present. Examples of atrial pacing entraining tachycardias are shown in Figures 11-181 and 11-182. This ultimately results in total supraventricular capture with appropriate A-H and H-V intervals. Following termination of pacing, the tachycardia resumes with a prolonged return cycle. Thus, I believe that slow conduction in the orthodromic direction is likely due to the nonuniform anisotropic characteristics and abnormalities of gap junctions of the circuit. Although depolarized fibers using partially inactivated sodium channels are associated with slow conduction, such fibers also demonstrate decremental properties. As noted earlier in the chapter, the response of the arrhythmogenic substrate to pharmacologic agents is most consistent with normally polarized 54 myocardial fibers. It is also theoretically possible that the prolonged conduction time reflects a longer pathway of activation in the orthodromic direction and is unrelated to conduction velocity per se. Interval-dependent conduction delays may be seen in ventricular muscle and the His–Purkinje system, both of which are not considered to have “decremental” properties. Overdrive acceleration has been observed during rapid pacing, but in this instance, a more rapid rhythm ensues on cessation of rapid pacing without acceleration or deceleration during that tachycardia. In this instance, it is as if the rapid pacing decreases the size of the reentrant circuit or produces double wave reentry. It is also consonant with the functional nature of 320 barriers as demonstrated by different resetting curves from different sites of stimulation. They include tachycardia cycle length, refractoriness at the stimulation site, conduction time from the stimulation site to the site of origin of the tachycardia, and in the case of reentrant arrhythmias, the duration of the excitable gap. The hemodynamic tolerance of the tachycardia also determines whether pacing modalities or direct current cardioversion is used to terminate the rhythm. Other factors such as the presence of antiarrhythmic agents can influence the ability to terminate the tachycardia both favorably and unfavorably (see subsequent paragraphs). Although certain generalizations can be made, much of the subsequent discussion relates to personal experience with the tachycardias studied in our laboratory. The tachycardia cycle length seems to be the main determinant of whether the tachycardia can be terminated by 322 323 324 325 some form of programmed stimulation or pacing or will require cardioversion. Regardless of the mode of stimulation used, termination is usually abrupt, which distinguishes it from termination of triggered activity. The tachycardia cycle length has the most marked influence on the mode of termination. In a consecutive series of patients, we found that rapid ventricular pacing was the most efficacious way of 322 terminating the tachycardia (Table 11-14). Although we did not compare the use of single, double, or triple extrastimuli and/or rapid pacing in each patient, the success of termination was directly related to the number of 1 122 194 195 322 323 324 325 extrastimuli used. In fact, 80% of tachycardias terminated by single extrastimuli had cycle lengths of >400 msec (Fig. Nonetheless, occasionally, tachycardias with cycle lengths between 300 and 350 msec can be terminated by single extrastimuli (Fig. Occasionally two extrastimuli are required to terminate tachycardias that are not too rapid P. Rapid pacing is the most effective form of termination, regardless of tachycardia cycle length (Fig. In fact, all tachycardias that are terminable by single or double extrastimuli can be terminated by rapid pacing. Failure of rapid pacing to terminate an arrhythmia that has previously been shown to be terminated by single or double extrastimuli suggests that the tachycardia was terminated then reinitiated before discontinuation of pacing. Thus, care must be taken to begin ventricular pacing at long cycle lengths and continue for a variable number of complexes before cessation of pacing. This probably occurs by creating “double wave reentry,” in which two wavelengths can fit in the same circuit previously used by 51 351 a single wavelength. We have arbitrarily defined acceleration of a tachycardia as a sustained shortening of the tachycardia cycle length by >30 msec following cessation of pacing. In our experience, this 322 323 324 325 occurs in approximately 25% of tachycardias. Acceleration is rare, using single or double 322 323 324 325 extrastimuli (<5%) but approaches 35% during rapid pacing. In one-half of these patients, the accelerated tachycardia may be terminated by even faster pacing. Thus, approximately 50% of patients with tachycardias having cycle lengths <300 msec will require cardioversion either due to rapid hemodynamic collapse without any attempts at termination by pacing or as a result of acceleration of the tachycardia (approximately evenly divided). The first extrastimulus delivered at 290 msec fails to influence the tachycardia but changes the path of ventricular activation and shortens local ventricular refractoriness so that a second extrastimulus delivered at 230 msec penetrates the reentrant circuit and terminates the tachycardia. The mechanisms of the different forms of acceleration probably differ, but documentation would require detailed study with multisite mapping of the reentrant circuit. When the morphology of the accelerated tachycardia is identical to that of the original tachycardia, one must assume that the exit from the tachycardia circuit is the same. First, it is possible that pacing could somehow increase conduction velocity in the circuit. In this circumstance the proposed mechanism of acceleration could not be operative.
Electrophysiologic effects of atropine on atrioventricular conduction studied by His bundle electrogram order lady era toronto. Electrophysiologic effects of procaineamide in patients with intraventricular conduction delay discount lady era 100 mg with mastercard. Intermittent atrioventricular block: procainamide administration as a provocative test order genuine lady era line. Chapter 6 Miscellaneous Phenomena Related to Atrioventricular Conduction Concealed conduction, the gap phenomenon, and supernormality are physiologic events that may be considered to be variants of the normal response. These phenomena are responsible for many unusual or unexpected responses of atrioventricular (A-V) conduction. This chapter addresses these separate but interrelated phenomena of cardiac conduction. Concealed Conduction The definition of concealed conduction has been irrevocably altered by the availability of intracardiac electrophysiologic studies. The concept of concealed conduction, an explanation for the effects of incomplete penetration of an impulse into a portion of the A-V conduction system, was introduced (and then expanded on) by 1 2 3 Langendorf , and by Katz and Pick. Because intracardiac recordings can directly document the presence of these impulses during the electrophysiologic study, they are no longer truly concealed. Although the A-V node is the structure with which concealed conduction has been most often associated, this phenomenon can occur in any portion of the A-V conduction system. The impulse producing concealment may originate anywhere in the heart – in the sinus node, an ectopic atrial 7 site, the A-V junction, the fascicles, or the ventricles. The most common site manifesting the effects of concealed conduction is the A-V node. The effects of retrograde concealment in the A-V node under different circumstances are shown in Figures 6-1 through 6-4. The effect of His bundle, fascicular, or ventricular extrasystoles on subsequent A- V nodal conduction is inversely related to the coupling interval of the premature depolarization. Slow pathway can be maintained by retrograde invasion into the fast pathway (see Chapter 8). Retrograde concealment at multiple levels of the A-V conduction system may also occur (Fig. The levels of concealment depend on the relative timing of antegrade and retrograde impulses. The most frequent clinical circumstances in which concealed conduction is operative are: (a) atrial fibrillation during which the irregular ventricular response is due to the varying depth of penetration of the numerous 8 wavefronts bombarding the A-V node ; (b) prolongation of the P-R(A-H) interval or production of A-V nodal block by a premature depolarization of any origin; (c) reset of a junctional (His bundle) pacemaker by atrial or subjunctional premature depolarizations; and (d) perpetuation of aberrant conduction during tachyarrhythmias. In the latter circumstance, retrograde penetration of the blocked bundle branch subsequent to transeptal 12 13 conduction perpetuates aberration. His bundle depolarizations are frequently not recognized because they must conduct antegrade and/or retrograde to have any P. Incomplete penetration (concealment) of His bundle depolarizations in either direction, producing unexpected abnormalities of antegrade or retrograde conduction, may present a particularly 9 10 difficult diagnostic problem. The first beat is a conducted sinus beat, with an A-H = 100 msec, H-V = 80 msec, and a right bundle branch block configuration. Note that there is no manifest conduction above the atrioventricular (A-V) junction (i. Note, however, in the next sinus beat that the A-H interval is prolonged to 135 msec, indicating that the retrograde wavefront from the preceding beat partially penetrated (concealed) in the A-V node, rendering it relatively refractory to the next sinus impulse. A, atrial deflection; H, His bundle deflection; Hr, retrograde His deflection; V, ventricular deflection. A-V dissociation is present, and there is no retrograde activation of the atria by the His bundle escape rhythm. The A-V nodal block in the first beat and the A-V nodal delay in the third beat are due to concealed retrograde conduction of the His bundle beats into the A-V node. Thus, despite antegrade intra-His block, the distal His bundle escape rhythm can conduct retrogradely and affect antegrade conduction (i. The right panel represents ventricular tachycardia without manifest retrograde conduction. Block of the first and third sinus impulses in the atrioventricular (A-V) node results from retrograde concealed conduction of the ventricular beats into the A-V node, rendering it refractory. This results in concealed conduction so that the subsequent sinus complex is a block in the A-V node. The rhythm is sinus, with ventricular pacing at a cycle length of 1200 msec (S, arrow). Following the second stimulated complex, the sinus impulse blocks in the A-V node, indicating concealed conduction to that structure. Following the third stimulated complex, the sinus impulse blocks below the His bundle, indicating concealment into the His–Purkinje system, rendering it totally refractory to the antegrade impulse. Although interference with normal antegrade conduction or with a subsidiary pacemaker by a concealed premature depolarization may be easy to conceptualize, unexplained facilitation of conduction requires further explanation. Simultaneous shortening of refractoriness and providing more time to recover excitability is the most common mechanism. These and other mechanisms of facilitation explain some instances of pseudo-supernormal conduction. During atrial pacing at a cycle length of 440 msec, 2:1 block below the His bundle occurs. Gap Phenomenon 16 The term gap in A-V conduction was originally used by Moe et al. The gap phenomenon was attributed to functional differences of conduction and/or refractoriness in two or more regions of the conducting system. With earlier impulses, proximal delay is encountered, which allows the distal site of early block to recover excitability and resume conduction. A: Atrial pacing at a cycle length of 310 msec produces right bundle branch block aberration. B: Pacing at a longer cycle length of 350 msec produces left bundle branch block aberration. A and B: At the longer basic cycle length (S1-S1) of 700 msec and an S1-S2 of 400 msec, (A) the S2-H2 is 210 msec with standard stimulation (method I). All measurements are in milliseconds; pertinent deflections and intervals are labeled. Atrioventricular nodal conduction and refractoriness after intranodal collision from antegrade and retrograde impulses. The major significance of the gap phenomenon is its contribution to the understanding of conduction and refractoriness of the A-V conducting system. In particular, the resumption of conduction at shorter coupling intervals has frequently been interpreted as a form of “supernormal” conduction.
Treatment revolves round therapy for primary infection and cholecystectomy in some cases buy cheap lady era online. Liver is remarkably vulnerable to insult from certain drugs because of its vital role in drug metabolism order 100mg lady era with amex. Administration Approach to Evaluation of two hepatotoxic drugs increases the chances of liver Evaluation of hepatomegaly should include a good history damage purchase lady era 100 mg online. Direct (dose-dependent) hepatotoxicity: It results from agents that are directly hepatotoxic and disrupt History and Physical Examination the hepatic cells, cause microsomal and mitochondrial Enquiry should focus on history of jaundice, pruritus, injury and damage the canalicular apparatus. Examples anorexia, blood transfusions, injections/pricks, familial/ of agents in this category are paracetamol, chlorprom- sibling involvement, etc. In the former, allergic kinship in hepatomegaly and splenomegaly may be as a symptoms like rash, fever, eosinophilia and granuloma result of: 602 Box 30. Investigations Liver function tests, imaging studies and liver biopsy Portal hypertension: Noncirrhotic portal hypertension depending on the merit of the clinical scenario. It revolves around supportive and symptomatic care Infections/immunological: Malaria, (especially chron- together with the attention to the etiological condition. Liver abscess(es) may be pyogenic, amebic or rarely, Hematological malignancies: Leukemias (especially because of other causes (infected echinococcal cyst, chronic myeloid leukemia*), lymphomas (especially Candida infection in immunocompromised subjects or splenic lymphoma*), histiocytosis, myelin (prolifera- neonates). Etiology Chronic hemolytic anemia: Talassemia*, sickle-cell It is usually polymicrobial, the most common pathogen anemia. Examination may reveal, Defnition jaundice (in biliary tract obstruction), tender hepatomegaly or right upper abdominal mass. As already described in Chapter 2 Diagnosis (Pediatric History-taking and Physical Examina- It is confrmed by imaging (Fig. It consists of: Etiology Appropriate chemotherapy—a combination of peni- cillinase resistant penicillin (cloxacillin) plus an ami- Box 30. Diagnostic Approach Percutaneous needle aspiration, catheter drainage and open surgical drainage. Clinical Work-up Good history and physical examination are of paramount Prognosis importance. Most patients present with increasing Following prompt diagnosis and appropriate treatment, abdominal distention (Fig 30. In minimal ascites (at least 200 mL of fuid), Complications one needs to elicit puddle sign (Lawson sign). Prominent Tese include pleuropulmonary involvement, peritonitis, collaterals in fanks and over back point to inferior vena subphrenic abscess, abscess-duodenum, fstula, hemobilia, cava obstruction. Note the dilated veins spreading peripherally z With portal hypertension: Extrahepatic (splenic vein thrombosis, from umbilicus in a child with massive ascites secondary to cirrhosis. Sup- portive treatment consists of sodium and fuid restriction, diuretics (potassium sparing aldosterone antagonists like spironolactone, loop like frusemide and combination of Table 30. Polymicrobial infection Intestinal perforation Similar histopathology is seen in a newly-identifed High concentration of urea Uroascitis disorder,hepatic copper overload syndrome, in American and creatinine in ascitic fuid children. Tis form of cirrhosis has a genetic disturbance High ascitic bilirubin Biliary tree/upper intestinal perforation in copper metabolism as in Wilson disease. However, Milk-like ascitic fuid due Tuberculous abdomen onset is early and the afected children die before the age to high Concentration of of 6 years or so. Stage I is characterized by enlarged frm liver with Colloidal replacement with dextran or albumin sharp leafy border. Indian childhood cirrhosis, once dubbed as a frustrating Indian childhood cirrhosis is a disease peculiar to the situation for which no specifc treatment was available, Indian infants and children, usually 6 months–4 years of may respond to D-penicillamine when therapy is initiated age. Te syndrome has been reported in twins, siblings and ofspring’s of frst-cousin marriages. Te most note- worthy observation is that a strong epidemiologic connec- tion of Reye syndrome with prior administration of aspirin Fig. The child presented in children sufering from viral illnesses like infuenza B or with defnite jaundice, hepatosplenomegaly, ascites, edema, anemia chickenpox stands established. Just like the drug (aspirin), toxins (afatoxin), viral infections (varicella, infuenza) and some inborn errors of Table 30. In nutshell, Reye Source of high dietary copper Action plan to lower it syndrome appears to be a stereotyped reversible reaction in Brass and copper vessels for Use of aluminum and steel for mitochondria arising from an interaction of viral, toxic and transportation, storage and tin-coating on brass host-genetic factors. Hypoglycemia, hyperammonemia and increased levels of fatty acids— Food cooked and stored in brass Encourage use of aluminium and copper utensils and steel acting singly or in combination may be important contributory factors. It has been suggested that inhibition Introduction of animal milk Promotion of breastfeeding of fatty acid oxidation in the endothelial cerebral edema before 2–3 months of age underlies the development of cerebral edema. Defective Copper content of drinking water Demineralize water oxidative phosphorylation within the cells may interfere under 0. Foods rich in copper content Avoid them or minimize their (liver, nuts, chocolates) consumptions Pathology Te pathologic features of the disease are well defned. Etiological role of copper has received considerable Identical changes are found in the kidney minus support from the fact that avoidance of brass and copper glomeruli, blood vessels and interstitial tissue. Markedly reduced activity of all mitochondrial enzymes in frst 26 days of disease (White Liver Disease, Encephalopathy with Fatty may be demonstrated. Degeneration of the Viscera) Reye syndrome, earlier reported by Khan from India in 1956 Clinical Features under the semantic Jamshedpur fever, was frst described Clinical spectrum ranges from relatively mild to rapidly from Australia by Reye and coworkers in 1963. Metabolic acidosis and respiratory alkalosis may z Grade 5: Deep coma, deep tendon refexes lost, respiratory arrest, coexist in the same patient. Treatment z Survivors show greater incidence of neurological Specifc Measures sequelae. Manifestations in children and adolescents: Since the etiology is at best speculative, treatment is simply z The syndrome manifests 3–4 days after the onset empirical. Double volume exchange transfusion and peritoneal z Hypoglycemia, hepatomegaly and hepatic dys- dialysis may prove of value in correcting metabolic function are the other prominent manifestations. In view of hepatic failure, a diet low in proteins with Complications sufcient carbohydrates for calories (energy) reduces Pneumonitis exogenous protein catabolism. Neomycin by nasogas- Respiratory failure tric tube and enema—as used in hepatic coma—is also Cerebral problems a useful measure. Cardiac arrhythmias L-carnitine, if used at an early stage, may be of value Diabetes insipidus. Hemorrhagic shock with encephalopathy Prognosis Toxins: Hypoglycin A, valproate Drug ingestion, e. Factors that indicate poor prognosis early Blood ammonia is elevated in most cases. Complications Stage 2–4: Encephalopathy Tese include septicemia, vascular thrombosis, biliary z Age under 1 year complications, poor graft function, chronic rejection, renal z Rapid progression of symptoms to stage 4 encephalopathy z Ammonia over 6 times the normal failure, hypertension, intestinal perforation and hematem- z Creatine phosphokinase over 10 times the normal esis (Fig. Neurological sequelae it is a usual practice to give triple immunosuppression such as mental retardation, epilepsy, hydrocephalus, behavioral with prednisolone, azathioprine and cyclosporine post- problems, spasticity and hemiplegia may occur in others. In case of rejection, pulse prednisolone therapy have also been recorded though only infrequently. First successful liver transplant done at z End-stage liver failure: Apollo Hospital, New Delhi, has completed its 14 years.