Acid-Base Equilibrium in Patients With Chronic Renal Failure in Whom Life is Sustained by Periodic Hemodialyses

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IN the absence of normal renal function, acid-base equilibrium depends on the buffering capacity of the blood, the intracellular shift of hydrogen ions, and respiratory compensation. Pulmonary complications, to which the uremic patient is prone, render the respiratory compensatory mechanism a precarious one. Thus impairment of gaseous diffusion through the walls of the pulmonary alveoli may occur as a result of congestion secondary to heart failure, infection, or repeated pulmonary emboli.

That hemodialysis can correct the acidosis of uremia was reported by one of us (W.J.K.) in 19441 and in 1947,2 and reconfirmed by Weller, Swan, and Merrill3 in 1953. However, the seriousness of the deviations that cause comparatively slight clinical symptoms in patients with chronic uremia has not been generally appreciated. Some of our patients with severe renal failure in whom life was sustained by periodic hemodialyses had pH values so low that they would have been considered incompatible with life only a few years ago. Surprisingly, these patients were living at home, had no obvious signs of discomfort, and returned to the hospital only for treatment with the artificial kidney. Periodic hemodialyses can maintain patients without excretory renal function in reasonably good clinical condition for months or years. Permanently indwelling arteriovenous shunt cannulas of the type described by Hegstrom and co-workers4 facilitate access to the blood vessels.

Schwartz and Relman5 have recently indicated that the traditional measurements of pH, pCO2, and plasma bicarbonate concentration continue to be the most reliable biochemical guides in the analysis of acid-base disturbances.



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