Effects of selected drugs on serum digoxin concentrations in dogs

Effects of selected drugs on serum digoxin concentrations in dogs

Traumatic renal artery occlusion producing hypertension. Ernst D, Windsor WO, Br J Surg 68:19-20, 1981. The authors present two cases of traumatic ren...

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Traumatic renal artery occlusion producing hypertension. Ernst D, Windsor WO, Br J Surg 68:19-20, 1981. The authors present two cases of traumatic renal artery occlusion and discuss a review of the literature on this problem. The majority of cases result from rapid deceleration-type blunt injuries where the renal vascular pedicle tears the intima from the .relatively immobile aorta. Infrequently, a direct blow to the abdomen may create this injury when the renal artery is compressed against the vertebral column. Eighty percent of the cases present with hematuria in association with flank pain; however, the diagnosis is often delayed if there are other, more obvious, injuries present. The condition should be strongly suspected if a non-functioning kidney is found on the IVP and can be confirmed by arteriography or isotopic renography. Less than 50% of cases develop hypertension, which appears to be produced by an increased renin release from the ischemic kidney. The treatment of choice for prolonged injuries with hypertension is nephrectomy, principally to cure the hypertension. However, revascularization may be attempted depending on the nature of the arterial injury and the onset of ischemia. In order to attempt this, early diagnosis is essential. (Editor's n o t e : Even though the yield is low, traumatic microscopic hematuria is often the only clue to this injury other than the context of major blunt trauma. Therefore, an aggressive ordering of IVP is worth pursuing). John Tucker, MD

renal artery occlusion

Effects of selected drugs on serum digoxin concentrations in dogs. Wilkerson RD, Mockridge WB, Massing GK, Am J Cardiol :!.5:1201-1210, 1980. This study was conducted in order to define the effects of several drugs on serum digoxin concentration. The drugs studied were quinidine, quinine, aspirin, ibuprofen, indomethacin, and acetaminophen. The results obtained were as follows. Therapeutic levels of quinidine and quinine were associated with an average increase in digoxin level of twice the original value. Administration of ibuprofen resulted in an average increase in digoxin level of four times that of baseline. Aspirin and indomethacin produced lesser effects. However, aspirin in dosages sufficient to produce salicylate serum levels greater than 15 mg/100 ml resulted in digoxin levels twice baseline. Possible mechanisms for these effects include: 1) enhanced digoxin absorption; 2) decreased excretion; or 3) displacement of digoxin from binding sites. The authors conclude that: 1) quinidine, quinine, and nonsteroidal anti-inflammatory drugs do significantly increase serum digoxin levels; 2) digoxin levels should be monitored carefully in patients receiving these combinations; 3) these interactions may contribute to arrhythmias and/or death; and 4) additional data in human studies are needed. (Editor's n o t e : More and more patients are being seen with problems relating to drug interactions. This response of digoxin to A S A is intriguing.) Me] D. Robinson, MD

ing metabolic acidemia there is a reduction in the oxygen content associated with the proportionate increase in lactic acid concentrations. The use of bicarbonate greatly exacerbates these changes, resulting in drops of the oxygen content from an average of 48.5 torr to 26.7 torr in the bicarbonatetreated animals, while there is no significant change in the animals managed without bicarbonate. The authors believe that correction of metabolic acidosis with bicarbonate results in decreased oxygen transport to the brain and an increase in cerebral anaerobic pathways generating increased lactic acid. (Editor's note: What is needed is a good study of HCO3 therapy in human ketoacidosis. Acidosis is clearly bad for the heart, but rapid reversal is not good for the brain.)

T. Tercior, MD acidosis, treatment

Antiarr~ythmic efficacy, pharmacokinetics, and clinical safety of tocainide in convalescent myocardial infarction patients. Klein MD, Levine PA, Ryan TJ. Chest 77:726-730, (June) 1980. In this single-blind study, tocainide, an oral analog of lidocaine, was administered to 18 hospitalized myocardial infarction patients in order to determine its pharmacokinetics, antiarrhythmic efficacy, a n d clinical safety. Holter monitoring with computer interpretation was utilized continuously for two days preceding, two days during, and two days after tocainide therapy; placebo therapy in the days prior to and after tocainide therapy served as control. Average daily dosage of tocainide was 17.7 mg/kg, divided into dosages given at eight-hour intervals. The half-life was calculated to be 19.1 -+ 6.8 hours, longer than that previously reported. Seven of the 18 patients had a significant reduction in frequency of ventricular premature beats (VPB) as compared to pre-drug and post-drug placebo frequency. Among these drug responders, there was a 70% decrease in VPB frequency when blood tocainide levels exceeded 3.5 ~g/ml. However, non-responders had an average tocainide level Of 5.64 txg/ml and still demonstrated no suppressio n of VPBs. There were no significant changes in the electrocardiogram, blood pressure, degree of clinical congestive heart failure, or angina frequency in any patient. One patient complained of tremulousness, blurred vision, tinnitus and acroparesthesia - - the only side effects in the 18 patients. The authors conclude that tocainide may prove to be a safe and effective drug for treating complex VPBs in some patients following myocardial infarction. ( E d i t o r ' s note: The search for an oral agent to prevent arrhythmia is important. Rustin has found that the inability to suppress arrhythmia in patients who had survived an out-of-hospital cardiac arrest resulted in sudden death in three of six patients N Engl J Med 303:607-713, 1980. To date, oral agents have all had profound side effects as well as poor effectiveness.) Ken Kulig, MD myocardial infarction, tocainide

serum digoxin, effect of drugs

Cerebral hypoxia from bicarbonate infusion in diabetic acidosis. Bureau MA, Begin R, Berthiaume Y, et al, J Pediatr 96:968-973, 1980. Bicarbonate infusion is one of the most controversial aspects of treatment of metabolic acidosis. The altered cardiovascular physiology of acidosis justifie s prompt correction, but it may result in the catastrophic complications (the pathophysiology of which is uncertain) of cerebral edema and respiratory arrest. I n this study, the oxygen tension, lactic acid level, pH, and carbon dioxide tension in the cerebrospinal fluid at the level of the cisterna magna were measured during 20 episodes of ketotic and non-ketotic acidemia in dogs treated with or without bicarbonate infusion. The study revealed that dur-


Ann Emerg Med

Pharmacologic antagonism of beta adrenergic blockade in dogs. II. Hemodynamic effects of simultaneous intravenous infusion of isoproterenol and dopamine during chronic propranolol administration. Spotnitz HM, et al, J Thorac Cardiovasc Surg 79:103108, (Jan) 1980. The current therapeutic trend toward high-dose pr0Pranolol therapy for angina and hypertension will inevitably lead to clinical situations requiring therapy for low cardiac Output in the face of beta adrenergic blockade. Examples include myocardial infarction, sepsis, and trauma in the patient on propranolol. To determine an effective treatment protocol for these situations, the hemodynamic effects of isoproterenol and dopamine were examined in dogs on long-term oral propranolol. Chronic beta blockage was induced in eight dogs by

10:7 (July) 1981