- Email: [email protected]
Induced in edematous patients by mechanical removal of body fluid
Western
Society for Clinical Research
mEq./day and, in certain cases, to less than 1 mEq/L within three days after the infarction despite a sodium intake generally maintained between 2 to 3 gm. daily. Return to higher urinary sodium concentrations occurred in three to fourteen days in most cases. Decreased sodium excretion was greatest in patients with marked hypotension but occurred also in those not exhibiting a shock-like state or failure. Chloride excretion generally paralleled sodium excretion, as did potassium excretion in most potassium cases, an inverse rate of urinary excretion being manifest in only three patients, Changes in PCV and serum sodium concentration were of slight degree and did not correlate. Serum potassium concentrations showed no significant variations. Oliguria accompanied this salt retention in most of the fifteen cases and was severe in six. Four had an initial diuresis. There seemed to be no uniform correlation of glomerular filtration rate as determined by endogenous creatinine clearance with sodium retention. Evaluation of adrenal cortical activity was attempted in thirteen patients, ten of whom had sodium retention. Eight of these showed an initial eosinopenia and four had significantly elevated uric acid-creatinine ratios. Ketosteroid determinations showed no consistent variations. The results suggest that myocardial infarction generally produces a stress phenomenon with an hormonal, probably adrenal cortical, effect on renal tubules resulting in sodium retention. Low SODIUM SYNDROME AND HYPERPOTASSEMIA
INDUCED IN EDEMATOUS PATIENTSBY MECHANICALREMOVAL OF BODY FLUID.Johnj'. Kelly, Jr. and Quentin B. Deming, Department of Medicine, Stanford University School of Medicine, San Francisco, Calif. It would seem reasonable to suppose that the removal of extracellular fluid by mechanical means (that is, by paracentesis or use of SoutheyLeech tubes) would cause little or no disturbance in the electrolyte pattern, as the electrolytes should be drawn off in the concentrations that exist in extracellular fluid. Contrary to these expectations we have seen three patients with anasarca in whom the rapid removal of extracellular fluid by mechanical means was followed by the low sodium syndrome and hyperpotassemia. Diuretics and a reduced sodium intake had been employed in each of these patients. Many factors are probably operative in producing this clinical picture but we believe that
the mechanism of action rests chiefly upon the following chain of events: (1) With the decrease in tissue pressure following the removal of fluid, the venous pressure and/or plasma volume decrease; a shock-like state follows. (2) As edema reaccumulates (in patients whose dietary intake of sodium but not of water is restricted) there is dilution of body sodium; this also may produce a shock-like state. (3) With (1) or (2) or both operative in any one patient, oliguria occurs and there is subsequent retention of potassium. Case reports and supporting clinical observations will be presented.
ASSOCIATION OFRETROGRADE CONDUCTIONWITH THE RECURRENT VARIETY OF PAROXYSMAL VENTRICULARTACHYCARDIA. DavidA.Rytand,* Department of Medicine, Stanford University School of Medicine, San Francisco, Calif. In each of three recently observed patients with retrograde conduction to the auricles during paroxysms of ventricular tachycardia, the paroxysms were repetitive or recurrent rather than isolated. This unusual experience led to a search of the literature and our own files, with the following results: Retrograde conduction (with or without partial V-A block) was present in thirty-nine of seventy-five patients with recurrent paroxysmal ventricular tachycardia. This variety of paroxysmal tachycardia often is found without associated heart disease, as was true in twenty-six instances of the arrhythmia in which retrograde conduction appeared. On the other hand, retrograde conduction is extremely rare in isolated paroxysms of ventricular tachycardia; it was recorded in not more than five of nearly 100 such examples reviewed, and failed to appear in any of the eighteen subjects in whom a paroxysm was provoked by anesthesia, drugs or the intracardiac catheter. (The bidirectional arrhythmia which follows the use of digitalis glycosides was not included in this study, nor was paroxysmal ventricular tachycardia which complicated auricular arrhythmias.) Retrograde conduction was not apparent in any of thirteen patients with the Wolff-Parkinson-white syndrome and alleged ventricular tachycardia. It appears then that the occurrence of retrograde conduction indicates a less ominous prognosis than usual for the outcome of any of ventricular tachycardia. given paroxysm Furthermore, it seems quite likely that the mechanism of production of repetitive paroxysAMERICAN
JOURNAL
OF
MEDICINE
Society for Clinical Research
mEq./day and, in certain cases, to less than 1 mEq/L within three days after the infarction despite a sodium intake generally maintained between 2 to 3 gm. daily. Return to higher urinary sodium concentrations occurred in three to fourteen days in most cases. Decreased sodium excretion was greatest in patients with marked hypotension but occurred also in those not exhibiting a shock-like state or failure. Chloride excretion generally paralleled sodium excretion, as did potassium excretion in most potassium cases, an inverse rate of urinary excretion being manifest in only three patients, Changes in PCV and serum sodium concentration were of slight degree and did not correlate. Serum potassium concentrations showed no significant variations. Oliguria accompanied this salt retention in most of the fifteen cases and was severe in six. Four had an initial diuresis. There seemed to be no uniform correlation of glomerular filtration rate as determined by endogenous creatinine clearance with sodium retention. Evaluation of adrenal cortical activity was attempted in thirteen patients, ten of whom had sodium retention. Eight of these showed an initial eosinopenia and four had significantly elevated uric acid-creatinine ratios. Ketosteroid determinations showed no consistent variations. The results suggest that myocardial infarction generally produces a stress phenomenon with an hormonal, probably adrenal cortical, effect on renal tubules resulting in sodium retention. Low SODIUM SYNDROME AND HYPERPOTASSEMIA
INDUCED IN EDEMATOUS PATIENTSBY MECHANICALREMOVAL OF BODY FLUID.Johnj'. Kelly, Jr. and Quentin B. Deming, Department of Medicine, Stanford University School of Medicine, San Francisco, Calif. It would seem reasonable to suppose that the removal of extracellular fluid by mechanical means (that is, by paracentesis or use of SoutheyLeech tubes) would cause little or no disturbance in the electrolyte pattern, as the electrolytes should be drawn off in the concentrations that exist in extracellular fluid. Contrary to these expectations we have seen three patients with anasarca in whom the rapid removal of extracellular fluid by mechanical means was followed by the low sodium syndrome and hyperpotassemia. Diuretics and a reduced sodium intake had been employed in each of these patients. Many factors are probably operative in producing this clinical picture but we believe that
the mechanism of action rests chiefly upon the following chain of events: (1) With the decrease in tissue pressure following the removal of fluid, the venous pressure and/or plasma volume decrease; a shock-like state follows. (2) As edema reaccumulates (in patients whose dietary intake of sodium but not of water is restricted) there is dilution of body sodium; this also may produce a shock-like state. (3) With (1) or (2) or both operative in any one patient, oliguria occurs and there is subsequent retention of potassium. Case reports and supporting clinical observations will be presented.
ASSOCIATION OFRETROGRADE CONDUCTIONWITH THE RECURRENT VARIETY OF PAROXYSMAL VENTRICULARTACHYCARDIA. DavidA.Rytand,* Department of Medicine, Stanford University School of Medicine, San Francisco, Calif. In each of three recently observed patients with retrograde conduction to the auricles during paroxysms of ventricular tachycardia, the paroxysms were repetitive or recurrent rather than isolated. This unusual experience led to a search of the literature and our own files, with the following results: Retrograde conduction (with or without partial V-A block) was present in thirty-nine of seventy-five patients with recurrent paroxysmal ventricular tachycardia. This variety of paroxysmal tachycardia often is found without associated heart disease, as was true in twenty-six instances of the arrhythmia in which retrograde conduction appeared. On the other hand, retrograde conduction is extremely rare in isolated paroxysms of ventricular tachycardia; it was recorded in not more than five of nearly 100 such examples reviewed, and failed to appear in any of the eighteen subjects in whom a paroxysm was provoked by anesthesia, drugs or the intracardiac catheter. (The bidirectional arrhythmia which follows the use of digitalis glycosides was not included in this study, nor was paroxysmal ventricular tachycardia which complicated auricular arrhythmias.) Retrograde conduction was not apparent in any of thirteen patients with the Wolff-Parkinson-white syndrome and alleged ventricular tachycardia. It appears then that the occurrence of retrograde conduction indicates a less ominous prognosis than usual for the outcome of any of ventricular tachycardia. given paroxysm Furthermore, it seems quite likely that the mechanism of production of repetitive paroxysAMERICAN
JOURNAL
OF
MEDICINE