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R D Gupta

Publications and source records attributed to R D Gupta.

6 recordsLinked to original sources

Electrocardiographic changes in tetanus: a serial study.

Serial electrocardiograms (ECGs) were recorded in 20 consecutive male patients admitted to the Infectious Diseases Hospital, Calcutta with generalised tetanus. Age of patients varied from 5 to 40 years (mean age 20.4 years). Ten patients died. ECGs were recorded daily for the first week after admission and later every 2nd or 3rd day. Altogether, 167 ECGs were analysed. Sinus tachycardia was present in 17 (85%) patients, prolonged QT interval in 12 (60%) patients, non-specific ST-T abnormalities in 12 (60%) patients and P wave changes in 10 (50%) patients. Other abnormalities recorded, included short PR interval, supraventricular tachycardia, intraventricular conduction delay, sinus bradycardia, 1 degree A-V block, abnormal axis deviation, right ventricular hypertrophy and sino-atrial Wenckebach phenomenon, although all of the findings cannot clearly be attributed to tetanus. Spatial QRS-T angle was calculated in 18 of these patients to determine any possible change in this parameter of prognostic significance. Two out of 9 who survived had abnormally wide (greater than or equal to 55 degrees) spatial QRS-T angle on admission; the angle narrowed with recovery. In the non-survivor group, 4 patients had abnormally wide QRS-T angles on admission; further widening was noted in patients on whom follow-up tracings were available. The difference in spatial QRS-T angle between the survivor and the non-survivor groups was statistically significant (p less than 0.05). Spatial QRS-T angle changes have not been reported in tetanus before. Although non-specific, serial study in individual cases would be useful in assessing prognosis.

Adolescent

Familial occurrence of sinus bradycardia, short PR interval, intraventricular conduction defects, recurrent supraventricular tachycardia, and cardiomegaly.

Four members of a family presenting with sinus bradycardia, a short P-R interval, intraventricular conduction defects, recurrent supraventricular tachycardia (SVT), syncope, and cardiomegaly had His bundle studies and were found to have markedly shortened A-H intervals (30 to 55 msec.) with normal H-V times (35 to 50 msec.). Right atrial pacing at rates as high as 170 to 215 per minute failed to increase the A-H or H-V intervals significantly. The data are compatible with the presence of an A-V nodal bypass tract (James bundle) or even complete absence of an A-V node. Ventricular pacing and spontaneous ventricular premature beats resulted in a short ventriculoatrial conduction time (110 msec.) suggesting that if A-V nodal bypass tracts exist, they are utilized in an antegrade and retrograde fashion. None of the features of WPW syndrome was present. The mechanism of syncope in the mother and daughter was intermittent third-degree heart block. Both went on to develop permanent complete heart block despite electrophysiologic studies demonstrating 1:1 A-V conduction at extremely rapid atrial pacing rates and both required implantation of permanent pacemakers. The mechanism of syncope in the two brothers was possibly marked sinus bradycardia, but transient complete heart block has not been ruled out. Permanent pacemaker therapy was recommended for both. The nature of the cardiomegaly, which was mild in three patients, is not known. Although not well documented, several maternal relatives have had enlarged hearts, SVT, complete heart block, and syncope.

Adolescent

Tissue digoxin concentrations at digoxin intoxication in normal, acutely hypokalemic, and acutely hyperglycemic dogs.

Thirty intact dogs were studied to determine digoxin concentration in various tissues after ventricular tachycardia had been induced by digoxin infusion. A control group was infused solely with digoxin. A second group was made acutely hypokalemic by glucose-insulin infusion before the digoxin infusion. A third group was infused with glucose and digoxin to determine the effect of increased blood glucose levels and osmalarity on the induction of ventricular tachycardia. Results were: (1) The amount of digoxin infused to produce ventricular tachycardia did not differ getween the normal and hypokalemic groups. (2) The concentration of digoxin in various parts of the heart, other muscle tissue, renal cortex, and liver did not differ between the normal and acutely hypokalemic dogs although the amount excreted in bile and urine was reduced in hypokalemia. (3) Acute hypokalemia did not sensitize the myocardium to the arrhythmogenic effects of digoxin. (4) Ventricular tachcardia occurred at a similar plasma digoxin level in normal and acutely hypokalemic dogs. (5) In dogs with a lowered plasma potassium level, junctional tachycardia occurred whereas it did not occur in normal dogs or those with only a high blood glucose level. (6) Ventricular tachycardia occurred in the hyperglycemic dogs at a plasma digoxin level of 170 ng/ml, which was significantly greater than in the other experiments (7) Acute hyperglycemia reduced the mean rate of myocaridal uptake of digoxin into atria and right and left ventricular tissue; and the concentration of digoxin in atria, left ventricle, and interventricular septum was lower at the time of ventricular tachycardia than occurred in normal dogs. (8) Lowering the plasma potassium level in the presence of acute hyperglycemia, which occurred with the glucose-insulin infusion, did increase the myocardial uptake of digoxin. Similar effects of hyperglycemia were noted on mean hepatic uptake and excretion of digoxin and also the renal uptake of the glycoside.

Animals

Echocardiography.

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Echocardiography