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Biomedical subjects

A D Sharma

Publications and source records attributed to A D Sharma.

104 records · Page 6Linked to original sources

Use of electrical pacemakers in the treatment of ventricular tachycardia and ventricular fibrillation.

Significant advances have been made in the therapy of ventricular arrhythmias. Many new antiarrhythmic drugs have expanded the medical armamentarium to treat ventricular tachycardia and ventricular fibrillation, and the use of intracardiac electrophysiologic studies has aided in predicting long-term drug efficacy. Major advances have also been made in the surgical treatment of arrhythmias. However, there remain a number of patients in whom ventricular arrhythmias remain a major therapeutic problem and, in some of these, electrical devices may aid in treatment. Overdrive pacing may prevent certain cases of ventricular arrhythmias, and antitachycardia devices may be useful in terminating paroxysmal ventricular tachycardia. In certain circumstances, internal cardioversion or defibrillation may be an alternative. At present, antitachycardia pacing and internal countershock must be considered as forms of therapy to be used when medical and surgical therapy are impractical or have failed. Careful selection is necessary to delineate patients in whom these forms of therapy may be indicated.

Cardiac Catheterization↗

Pathophysiology and management of atrial and ventricular arrhythmias in the critically ill.

The general principles that apply to treatment of arrhythmias in the critically ill include, first, an immediate correction of arrhythmias that result in hemodynamic deterioration. This more frequently necessitates DC cardioversion, pacing, or intravenous therapy than is seen in an otherwise healthy patient. Second, having resuscitated the patient and treated the arrhythmia, the physician should be acutely aware of any precipitating factors, which should then be corrected in order to prevent recurrence of the arrhythmia. Third, the physician should also be aware of the potential proarrhythmic effects of his or her antiarrhythmic drug therapy and be prepared to withdraw therapy when it appears that the arrhythmia has worsened following drug treatment. In the future, new technologic developments, including improved defibrillation systems, intracardiac catheters for defibrillation, and automatic arrhythmia detectors using intravascular catheters, may aid in the diagnosis and treatment of recurrent arrhythmias in the critically ill.

Arrhythmias, Cardiac↗

Diagnostic assessment of recurrent syncope.

The definitive diagnosis of a cardiac arrhythmia as the basis for syncope is made by electrocardiographic monitoring during a syncopal episode. In the absence of this evidence, abnormalities demonstrated by an electrophysiologic study may suggest the etiology of syncope. Cardiac electrophysiologic testing in patients with recurrent syncope should probably be limited to patients with underlying cardiac disease. These patients are at a higher risk for sudden death and have a high incidence of electrophysiologic abnormalities. In particular, ventricular tachycardia may be evoked and specific therapy for this abnormality is associated with remission of syncope. In contrast, electrophysiologic studies in patients with no underlying cardiac disease have a very low yield of abnormal findings in the order of 10-20%, and should be performed only when there are reasons to suspect the presence of arrhythmias. Furthermore, in patients with no underlying cardiovascular disease there is a high spontaneous remission rate of syncope and the late incidence of sudden death is low, and related to the presence of other systemic illnesses. At present, the significance of nonsustained ventricular tachycardia or ventricular fibrillation induced during cardiac electrophysiologic studies in patients with no documented arrhythmias is unknown, and further prospective studies are necessary to define appropriate therapy for these patients. Further investigation is also required to clarify the spontaneous remission rate of syncope, as this information is of vital importance in assessing the success of any therapeutic modality.

Arrhythmias, Cardiac↗

Concealed conduction in accessory atrioventricular pathways: an important determinant of the expression of arrhythmias in patients with Wolff-Parkinson-White syndrome.

Concealed conduction into accessory atrioventricular pathways has been postulated to explain variability of R-R intervals during atrial fibrillation in patients with Wolff-Parkinson-White syndrome. We examined the occurrence of concealed conduction into atrioventricular pathways using extrastimulus techniques in 26 consecutive patients undergoing electrophysiologic studies for the Wolff-Parkinson-White syndrome. Anterograde pathway concealment was demonstrated (10 patients) by introducing a second atrial extrastimulus (A3) after block in the accessory pathway occurred following the first extrastimulus (A2). The apparent effective refractory period (ERP) of the atrioventricular pathway with A3 (after A2 blocked in the pathway), or ERPB, was always greater than the ERP of the atrioventricular pathway (505 +/- 100 vs 323 +/- 105 msec, mean +/- SD; p less than .001), a finding explained by concealment into the pathway by the blocked A2. A measure of the apparent prolongation of refractoriness due to anterograde concealment (delta ERPB), defined as the difference between ERP and ERPB at a given cycle length, was derived. The average R-R interval in atrial fibrillation correlated better with delta ERPB (r = .8, p less than .01) than with the ERP (r = .6, p = NS), supporting the influence of anterograde atrioventricular pathway concealment in modulating the ventricular response during atrial fibrillation. By similar techniques, concealed retrograde conduction in the atrioventricular pathway could be demonstrated in 16 of 26 patients. In two of these patients "bystander" atrioventricular pathway conduction during orthodromic reciprocating tachycardia that did not involve the atrioventricular pathway did not occur, even though the ERP of the pathway should have permitted it, a finding readily explained by repetitive retrograde concealment into the atrioventricular pathway during tachycardia. Concealed conduction can be demonstrated in most patients with Wolff-Parkinson-White syndrome and is an important factor in the clinical expression of their arrhythmias.

Adolescent↗

Alpha adrenergic-mediated accumulation of calcium in reperfused myocardium.

Reperfusion of ischemic myocardium is associated with increases in total myocardial calcium (Ca+2), which may influence the ultimate extent of ischemic damage as well as the development of arrhythmias. Since reperfusion is also associated with enhanced alpha-adrenergic responsivity, this study was performed to determine the potential interactions between alpha-adrenergic receptors and myocardial calcium during reperfusion. Cats were subjected to 35 min of left anterior descending coronary artery occlusion and 10 min of reperfusion. Total myocardial calcium was measured by atomic absorption spectrometry. Intracellular calcium was calculated from measurements of extracellular space [( 3H]inulin). In control animals with reperfusion, total calcium increased from 0.32 +/- 0.03 to 0.65 +/- 0.05 mmol/100 g dry tissue (P less than 0.0001), while intracellular calcium increased from 0.15 +/- 0.03 to 0.40 +/- 0.05 mmol/100 g dry tissue (P less than 0.001). Pretreatment with the alpha-adrenergic blocking agents phentolamine or prazosin prevented the increase in total and intracellular calcium. Phentolamine and the aqueous soluble alpha 1-adrenergic antagonist BE-2254 administered as late as 2 min before reperfusion similarly attenuated the increase in tissue calcium. Although administration of BE-2254 2 min before reperfusion failed to block the reperfusion-induced increase in extracellular space, the increase in calculated intracellular calcium was prevented. beta-Adrenergic blockade with propranolol partially attenuated but did not prevent an increase in total tissue calcium. Labetalol, a combined alpha- and beta-adrenergic blocking agent completely blocked the increase in tissue calcium during reperfusion. Additional experiments performed after 70 min of ischemia with reperfusion demonstrated a 49% attenuation of the increase in tissue calcium with alpha-adrenergic blockade. Electron microscopy with pyroantimonate and x-ray microprobe analysis demonstrated a large increase in calcium precipitate in mitochondria after reperfusion in untreated animals. Though alpha-adrenergic blockade prevented the calcium deposition in mitochondria, other criteria of ischemia persisted. Thus, alpha-adrenergic blockade specifically prevents the increase in intracellular calcium during reperfusion in reversibly injured tissue, independent of alterations in extracellular space and tissue water.

Adrenergic alpha-Antagonists↗

Effect of adrenergic stimulation and blockade on ventricular defibrillation in the rat.

Ventricular fibrillation was electrically induced in 60 rats and the effects of adrenergic stimulation ad blockade on the time taken to spontaneous reversion to sinus rhythm were determined. Alpha adrenergic stimulation by norepinephrine and phenylephrine infusion shortened ventricular fibrillation from 3.21 +/- 0.42 (+/- S.E.M.) to 1.48 +/- 0.17 sec (P less than .001) and from 5.13 +/- 0.77 to 2.18 +/- 0.27 sec (P less than .001), respectively. Nonselective beta adrenergic stimulation with isoproterenol prolonged the time to defibrillation from 1.65 +/- 0.20 to 7.01 +/- 0.95 sec (P less than .001), whereas beta-2 adrenergic stimulation with salbutamol produced no change. Alpha adrenergic stimulation antagonized the effect of a concomitant isoproterenol infusion (P less than .05). Alpha adrenergic blockade with phenoxybenzamine prolonged ventricular fibrillation (P less than .001) whereas beta blockade with propranolol or metoprolol shortened the duration of fibrillation. It was concluded that these effects were due to direct stimulation and blockade of cardiac adrenergic receptors. These actions were associated with changes in ventricular refractoriness. Cardiac alpha adrenergic stimulation prolonged the ventricular effective refractory period and promoted spontaneous defibrillation. Beta adrenergic stimulation shortened the ventricular effective refractory period and prolonged the time to defibrillation.

Albuterol↗

Reflex mechanisms responsible for early spontaneous termination of paroxysmal supraventricular tachycardia.

The incidence and possible mechanism of early spontaneous termination of paroxysmal supraventricular tachycardia was studied in 20 consecutive patients. Episodes of induced tachycardia that terminated spontaneously within the 1st minute after initiation were included. Tachycardias ending spontaneously were associated with a reproducible course of hypotension at the onset followed by blood pressure recovery above control levels and termination. Spontaneous termination of tachycardias occurred within the A-V node 18 to 45 seconds (mean +/- standard error of the mean 27.9 +/- 5.3) after their onset. In the supine position (0 degrees) 9 (45 percent) of 20 patients showed spontaneous termination in 36 (16 percent) of 219 episodes of tachycardia. In the head-dependent position (-20 degrees) only 1 (8 percent) of 13 patients manifested spontaneous termination in 2 (4 percent) of 54 episodes. In the head up position (+60 degrees) only 1 (6 percent) of 18 patients exhibited termination in 2 (2 percent) of 102 episodes. After partial cholinergic blockade with intravenous hyoscine butylbromide, 20 mg, or atropine, 0.6 mg, none of five patients showed spontaneous termination in 25 episodes. After beta adrenergic blockade with 10 mg of propranolol intravenously, none of 16 patients showed spontaneous termination in 87 episodes of tachycardia. We conclude that the initial hypotension during tachycardia evokes a sympathetic response that increases blood pressure and this increase in turn causes a rise in vagal tone that breaks the tachycardia.

Adrenergic beta-Antagonists↗

Continuous on-line beat-to-beat analysis of AV conduction time.

A simple analog circuit is described which is capable of measuring on a beat-to-beat basis P-R, R-P, P-P, and R-R intervals during sinus rhythm and paroxysmal supraventricular tachycardia. In addition the circuit will emit a pulse when the consecutively alternating P and R wave sequence is interrupted thereby signalling a trigger problem or a change in rhythm. The operation of the device requires proper P and R wave sensing and provides outputs which are linear over a range of rates which are applicable to the human heart.

Atrioventricular Node↗

Vagal techniques for termination of paroxysmal supraventricular tachycardia.

Maneuvers that reflexly increase vagal tone were deployed to terminate the tachycardia in 68 consecutive patients with paroxysmal supraventricular tachycardia. The order and success rate of the protocol was as follows: 57 episodes were terminated with carotid sinus pressure alone or after pretreatment with edrophonium, 5 were terminated with the Valsalva maneuvers and 6 were terminated with phenylephrine. Potency testing showed that phenylephrine evoked the greatest increase in vagal tone. All cases demonstrated slowing of tachycardia ranging from 40 to 220 ms +/- standard error of the mean (mean 79.0 +/- 3.8 ms) followed by abrupt termination. Pauses after termination ranged from 900 to 3,300 ms (mean 1,683.8 +/- 66.6) with 54 patients showing pauses of 2,000 ms or less. Termination was highly reproducible showing an overall success of 148 (92 percent) of 160 trials among 22 selected cases. The extent of increased vagal tone needed to terminate paroxysmal supraventricular tachycardia was raised by augmented sympathetic tone (infusion of isoproterenol) and decreased by reduced sympathetic tone (pretreatment with propranolol). Thus, paroxysmal supraventricular tachycardia can be rapidly, safety and consistently terminated by maneuvers that reflexly increase vagal tone.

Adolescent↗

Valsalva termination of ventricular tachycardia.

Nine patients with recurrent ventricular tachycardia (VT) that could be repeatedly terminated by a Valsalva maneuver are described. In two, the tachycardia would cease for only a few seconds and then resume, whereas in seven, the tachycardia could be permanently and reproducibly terminated with a Valsalva maneuver. In all patients the tachycardia ended during the strain phase of the Valsalva maneuver, when blood pressure and radiographic measurement indicated that cardiac dimensions had been reduced dramatically. The speed with which the Valsalva maneuver terminated VT incresed in direct proportion to the strain pressure. Maneuvers such as standing or nitroglycerin, which independently reduce cardiac dimensions, enhanced the potency of the Valsalva maneuvers. Pretreatment with atropine or propranolol in four patients did not alter the response of VT to the Valsalva maneuver. Thus, it appears that a strong Valsalva maneuver can terminate some forms of VT, most likely related to an abrupt reduction in cardiac dimensions.

Adolescent↗

Allergic contact dermatitis in patients with atopic dermatitis: A clinical study.

BACKGROUND: Atopic dermatitis (AD) is a chronically relapsing dermatitis with no known cure. Due to the chronic nature of the condition, frequent and long term topical therapy is used. This may lead to sensitization, resulting in allergic contact dermatitis (ACD). AIMS: The aim of the study was to observe the frequency of ACD in atopic patients in this part of the country using Indian standard battery. METHODS: A total number of 30 cases of AD were taken for the study. Diagnosis of AD cases was based on the criteria of Hannifin and Rajka (1980). All the selected cases of AD had mild to moderate grade of severity. All these cases were treated and patch tested during the remission period. The duration of the study was 12 months. RESULTS: Out of the 30 AD cases, 7 cases showed positive ACD with patch test allergens. CONCLUSION: This study shows that ACD is not uncommon amongst atopic individuals.

Adolescent↗