CORRESPONDENCE

SODIUM BICARBONATE ADMINISTRATION IN PATIENTS WITH HEART DISEASE To the Editor: Bersin et al (Am J Med 1989; 87: 7-14) observed that administra- tion of sodium bicarbonate to pa- tients with congestive heart fail- ure caused a decrease in arterial oxygen tension, impeded periph- eral and myocardial oxygen up- take, and perhaps induced cardi- ac ischemia and transient wors- ening of cardiac output. The authors speculated that sodium bicarbonate therapy increased carbon dioxide generation, with consequent intracellular acidosis causing the adverse effects. This hypothesis is unproven, however, as the mean carbon dioxide ten- sion (pCO2) following alkali ad- ministration increased by less than 4 mm Hg in either arterial or mixed venous samples. The rise in arterial pH, from 7.44 to 7.51, was more impressive. The true lesson at hand may be that even mild metabolic alkalosis poses a threat to individuals with ad- vanced heart disease.

The relative risks and benefits of bicarbonate therapy for meta- bolic acidosis remain subjects of controversy and debate. It is by no means self-evident that the aforementioned results are rele- vant to patients with advanced acidemia, and it seems wholly un- warranted to extrapolate the findings from this study “as a strong argument against the rou- tine use of sodium bicarbonate in cardiac arrest,” as espoused in the editorial that accompanied the article (Am J Med 1989; 87: 5-6). Although other studies sup- port such caution, the data at hand do not apply.

DAVID A. GOODKIN, M.D. Conejo Nephrology and Medical

Group, Inc. Thousand Oaks, California

Submitted February 21, 1990, and accepted June 14, 1990

The Reply:

Although Dr. Goodkin states that we attributed the adverse effects of sodium bicarbonate therapy in patients with heart failure to car- bon dioxide generation, this is an inference by Dr. Goodkin not stated by us in the article. We hy- pothesized that carbon dioxide generation increases with sodium bicarbonate therapy, as is well known, but that carbon dioxide levels changed little in this study as a result of adequate ventila- tion. Moreover, we speculated that pCOs is the regulator of cor- onary blood flow rather than [H+], as the pH change was great- er than the change in pCOs and coronary blood flow remained relatively constant. Nowhere do we state that the adverse effects of sodium bicarbonate therapy are attributable to carbon diox- ide generation in the patients studied. To the contrary, we state very clearly in the conclusions that the adverse effects appear to be related to alterations of tissue oxygen extraction and that the mechanisms by which tissue oxy- gen extraction are modified are complex and are related not only to changes in oxygen-hemoglobin binding, but also to changes in ar- terial vascular tone.

On the other hand, we agree with Dr. Goodkin that extrapola- tions of our data to patients with cardiopulmonary arrest are haz- ardous and are not necessarily valid. We indicated in the conclu- sions that other patients critical- ly dependent on tissue oxygen transport to meet oxygen de- mands, such as children with con- genital heart disease and adults with acute myocardial infarction or cardiac arrest, are likely to manifest similar responses to so- dium bicarbonate administra- tion, but this is by no means prov- en. Thus, I would agree with Dr. Goodkin that the data at hand cannot be directly applied to pa- tients with cardiopulmonary ar- rest, and that the statement made by Ayus and Krothapalli in

the accompanying editorial is perhaps too strong. However, when taken in the aggregate with other studies performed in pa- tients with cardiopulmonary ar- rest per se, the argument against the use of sodium bicarbonate in cardiopulmonary arrest appears valid.

ROBERT M. BERSIN, M.D. The Sanger Clinic, P.A.

Charlotte, North Carolina

A CPT CODE FOR “CARING” To the Editor: I read with great enjoyment Dr. Glick’s (Am J Med 1990; 88: 449- 451) editorial, and I completely agree with his prescription for the infusion of “intensive caring, rather than intensive care” into the role model of the clinician- teacher. I was fortunate to have several mentors throughout my medical school and residency training who taught by example that caring for the patient is a crucial aspect of patient care. I am not afraid to admit to my “so- phisticated friends” that I have examined my “post-Freudian” motivation and can honestly state that I get a great degree of “self-fulfillment” through exer- cising my “desire to serve.” I even committed the grievous sin of ad- mitting this fact to my Division Chairman (horrors!) one after- noon. Perhaps the psychoana- lysts would call it a sublimation, but all I know is that taking care of patients is fun. Even the more difficult patients (“GOMERs”) I encounter hold lessons for me; sometimes in human nature, of- ten in humility.

Unfortunately, like Dr. Glick, I also live in an era of “runaway medical costs” and of dramatic intervention of third-party pay- ers and federal health adminis- trators into the very core of the medicine I practice. Cost-cutting is made in the name of efficiency,

October 1990 The American Journal of Medicine Volume 89 549