Metabolic and hemodynamic consequences of sodium bicarbonate administration in patients with heart disease.
OBJECTIVE
The use of sodium bicarbonate (NaHCO3) in cardiopulmonary arrest has been questioned, but the effects of NaHCO3 in patients with heart disease are not known. We therefore prospectively evaluated the effects of NaHCO3 in patients with congestive heart failure.


METHODS
Ten patients received NaHCO3 and control infusions of equimolar sodium chloride (NaCl). Measurements were made of blood gases, 2,3-diphosphoglyceric acid (2,3-DPG), glucose, lactate, cardiac hemodynamics, and oxygen consumption.


RESULTS
The arterial oxygen tension (pO2) fell an average of 10 mm Hg after NaHCO3 administration in patients with congestive heart failure, whereas it rose with NaCl (p less than 0.005). Myocardial oxygen consumption decreased by 17% (p less than 0.002) without an accompanying change in oxygen demand. Systemic oxygen consumption fell by 21%. Red blood cell 2,3-DPG levels were elevated at baseline, but did not change with NaHCO3 administration. The oxygen pressure at 50% hemoglobin saturation (P50) was correspondingly elevated at baseline in these patients and decreased significantly with NaHCO3 (Bohr effect) (p less than 0.003). The arterial and mixed venous carbon dioxide tensions increased with NaHCO3 but decreased with NaCl administration (p less than 0.05). Blood glucose concentrations fell by 1.7 mmol/L with NaHCO3 (p less than 0.003) and blood lactate concentrations increased uniformly (p less than 0.001). Three patients developed net myocardial lactate generation during NaHCO3 administration; two of these three developed symptoms of angina. Coronary blood flow did not change with NaHCO3 but increased with NaCl (p less than 0.04). Two patients developed transient pump failure.


CONCLUSIONS
These data demonstrate that NaHCO3 impairs arterial oxygenation and reduces systemic and myocardial oxygen consumption. The decrease in oxygen utilization is associated with anaerobic metabolism, enhanced glycolysis, and elevation of the blood lactate level, and may lead to transient myocardial ischemia in some patients. Thus, the use of NaHCO3 in such patients warrants re-evaluation.
Bersin
R M
RM
Cardiology Division, University of California Medical Center, San Francisco.
Chatterjee
K
K
Arieff
A I
AI
D000368:Aged; D000369:Aged, 80 and over; D001158:Arteries / Q000502:physiology; D001639:Bicarbonates / Q000009:adverse effects*; D001784:Blood Gas Analysis; D001786:Blood Glucose / Q000378:metabolism; D003326:Coronary Circulation / Q000187:drug effects; D003327:Coronary Disease / Q000209:etiology; D004573:Electrolytes / Q000097:blood; D005260:Female; D006333:Heart Failure / Q000378:metabolism / Q000503:physiopathology*; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D007773:Lactates / Q000097:blood; D008297:Male; D008875:Middle Aged; D010101:Oxygen Consumption / Q000187:drug effects*; D012965:Sodium Chloride / Q000494:pharmacology
D001639:Bicarbonates; D001786:Blood Glucose; D004573:Electrolytes; D007773:Lactates; D012965:Sodium Chloride