Sodium bicarbonate and sodium chloride: effects on blood pressure and electrolyte homeostasis in normal and hypertensive man

To test the hypothesis that NaCl and NaHCO3 have divergent effects on blood pressure, we carried out a randomly allocated, placebo-controlled, crossover trial in 10 mildly hypertensive and 10 normal subjects. They ingested a fixed daily basal diet of 60 mmol sodium and chloride, 60 mmol potassium and 14 mmol calcium. After balance was achieved (4 days), the subjects were randomly assigned to drink 3 liters/day of a NaHCO3-containing mineral water (26.2 mmol/l sodium and 33.03 mmol/l HCO3) or a control solution containing equimolar amounts of cations as the chloride salt for 7 days (total daily sodium 138 mmol). All urine was collected. Blood pressure was determined by an automated device. One month later the opposite regimen was followed. NaCl did not influence blood pressure, whereas NaHCO3 decreased systolic blood pressure (by 5 mmHg) in the hypertensive subjects. Both regimens decreased plasma renin activity in the hypertensive subjects but did not consistently influence plasma aldosterone or catecholamines. However, urinary calcium excretion, which was greater in hypertensives than in normotensives, and greater in white than in black subjects, increased consistently with NaCl but not with NaHCO3. The excretion of urate was not influenced by the regimens; however, urate excretion was consistently greater in whites than in blacks. The data show that NaCl increases calcium excretion whereas NaHCO3 does not, even at modest levels of intake. NaCl and NaHCO3 may therefore differ in their effects on blood pressure.     

Sodium bicarbonate infusion increases discharge frequency of intrapulmonary chemoreceptors only at high CO2

We felt that earlier determinations of independent effects of extracellular pH and PCO2 on intrapulmonary chemoreceptors (IPC) discharge frequency were difficult to analyze because they used perfused lungs, and ventilation-perfusion changes among parabronchi could not be controlled. We decided to repeat these studies in non-perfused lungs. We cannulated both extrapulmonary bronchi of 10 thoracotomized Pekin ducks anesthetized with sodium pentobarbital (25-35 mg/kg) and unidirectionally ventilated each lung. The perfused right lung maintained gas exchange while the non-perfused left lung received 0.6 L/min of CO2 mixed in air. We recorded the discharge frequency of one IPC per duck at various PCO2, re-established circulation, and infused 3.0 mmol/kg of sodium bicarbonate intravenously. After 15 min, discharge frequencies were again measured from the same IPC in the nonperfused lung. The slopes and intercepts of discharge frequencies vs ln PCO2 relationship were depressed in six IPC, increased in two IPC and not significantly affected in two IPC. Arterial pH was increased significantly (0.11 unit) at 38 Torr arterial PCO2. We conclude that acutely increased extracellular sodium bicarbonate affects IPC discharge only by depressing sensitivity of most IPC to PCO2 and does not have an independent effect through pH.     

Sodium bicarbonate therapy in severe diabetic ketoacidosis

Rates of recovery of plasma glucose and bicarbonate levels, arterial pH, and level of consciousness were determined in a retrospective analysis of 95 episodes of severe diabetic ketoacidosis in patients treated with conventional regimens including low-dose insulin, saline, and potassium administration. No significant differences were found between 73 episodes in 52 patients treated with sodium bicarbonate and 22 episodes in 21 patients not undergoing such treatment. In view of these observations, the potential hazards of sodium bicarbonate replacement therapy, and the fact that sodium bicarbonate is still frequently given, the use of intravenous sodium bicarbonate treatment in patients with severe diabetic ketoacidosis requires reevaluation.     

Haemodynamic and metabolic effects in diabetic ketoacidosis in rats of treatment with sodium bicarbonate or a mixture of sodium bicarbonate and sodium carbonate

Summary To examine factors determining the haemodynamic and metabolic responses to treatment of diabetic ketoacidosis with alkali, groups of anaesthetised and ventilated rats with either diabetic ketoacidosis (mean arterial pH 6.86–6.96, mean arterial blood pressure 63–67 mm Hg) or hypovolaemic shock due to blood withdrawal (mean pH_a 7.25–7.27, mean arterial blood pressure 36–41 mmHg) were treated with sodium chloride (saline), sodium bicarbonate or Carbicarb (equimolar bicarbonate plus carbonate). In the diabetic ketoacidosis series, treatment with either alkali resulted in deterioration of mean arterial blood pressure and substantial elevation of blood lactate, despite a significant rise in myocardial intracellular pH determined by ³¹P-magnetic resonance spectroscopy. These effects were accompanied by falling trends in the ratios of myocardial phosphocreatine and ATP to inorganic phosphate. Erythrocyte 2,3-bisphosphoglycerate was virtually absent in animals with diabetic ketoacidosis of this severity and duration. In contrast, in shock due to blood withdrawal, infusion of saline or either alkali was accompanied by a transient elevation of mean arterial blood pressure and no significant change in the already elevated blood lactate; erythrocyte 2,3-bisphosphoglycerate was normal in these animals. The effect of alkalinization in rats with severe diabetic ketoacidosis was consistent with myocardial hypoxia, due to the combination of very low initial erythrocyte 2,3-bisphosphoglycerate, alkali-exacerbated left shift of the haemoglobin-oxygen dissociation curve and artificial ventilation. No evidence was found for any beneficial effect of Carbicarb in either series of animals; Carbicarb and sodium bicarbonate could be deleterious in metabolic acidosis of more than short duration.Abbreviations DKA Diabetic ketoacidosis - 2,3-BPG 2,3-bisphosphoglycerate - pH_a arterial pH - pH_i intracellular pH - P_aCO₂ arterial PCO₂ - Pi inorganic phosphate - PCr phosphocreatine - MRS magnetic resonance spectroscopy - MABP mean arterial blood pressure     

静脉水化联合碱化预防高危患者对比剂诱发肾病的作用

目的探讨静脉水化联合碱化治疗预防高危患者对比剂诱发肾病的临床效果。方法选择行经皮冠状动脉介入诊疗,对比剂肾病发生风险评分系统评分≥11分的患者80例,治疗组40例,给予0.9%氯化钠溶液1mL·kg-1·h-1的静脉注射12h,联合30mL碳酸氢钠快速静脉注射;对照组40例,仅给予0.9%氯化钠溶液1mL·kg-1·h-1静脉注射12h的水化治疗,比较两组治疗后生化检验结果和对比剂诱发肾病发生率。结果治疗组介入治疗后尿pH值及肾小球率过滤比对照组高,血清肌酐浓度比对照组低,差异有统计学意义[7.11±0.72vs.5.46±0.61,P0.05;37.91%±7.48%vs.30.11%±7.54%,P0.05;(1.40±0.19)mg/Lvs.(1.69±0.22)mg/L,P0.05]。治疗组对比剂诱发肾病发生2例,占5%(2/40),对照组发生8例,占20%(8/40),两者比较,差异有统计学意义(P0.05)。结论静脉水化联合碱化治疗可更有效地防止高危患者经皮冠状动脉介入治疗后对比剂诱发肾病的发生。     

Sodium bicarbonate for the treatment of lactic acidosis

Lactic acidosis often challenges the intensivist and is associated with a strikingly high mortality. Treatment involves discerning and correcting its underlying cause, ensuring adequate oxygen delivery to tissues, reducing oxygen demand through sedation and mechanical ventilation, and (most controversially) attempting to alkalinize the blood with IV sodium bicarbonate. Here we review the literature to answer the following questions: Is a low pH bad? Can sodium bicarbonate raise the pH in vivo? Does increasing the blood pH with sodium bicarbonate have any salutary effects? Does sodium bicarbonate have negative side effects? We find that the oft-cited rationale for bicarbonate use, that it might ameliorate the hemodynamic depression of metabolic acidemia, has been disproved convincingly. Further, given the lack of evidence supporting its use, we cannot condone bicarbonate administration for patients with lactic acidosis, regardless of the degree of acidemia.     

Anginal attack following a sodium bicarbonate and hydrocortisone injection

A case of a 73-year-old man with variant angina who developed chest pain and shock following an injection of sodium bicarbonate and hydrocortisone is reported. The electrocardiogram (ECG) during the chest pain attack revealed ST elevation in leads II, III and aVF. It returned to a normal pattern 10 min later. Coronary angiography, performed 2 hours after the anginal attack, showed no significant coronary arterial stenosis. One month later, an injection of ergonovine (16 micrograms) into the right and left coronary arteries induced spasms in segments 4 and 13, with ischemic ECG changes. Possible causes of the anginal attack are a coronary arterial spasm induced by the allergic reaction to hydrocortisone and/or serum alkalosis due to the sodium bicarbonate injection triggered by hyperventilation.     

Sodium bicarbonate infusion test: a new method for evaluating parathyroid function

We have developed a new test for estimating the secretory capacity of parathyroid hormone (PTH) from the parathyroid gland. Sodium bicarbonate solution [8.4% (w/v); 35 ml/m(2) body surface area] was infused for 2 min, and blood samples for the determination of plasma ionized calcium, plasma PTH (intact, midregion, carboxy-terminus) and related parameters were serially obtained. In 8 healthy volunteers, the mean (+/-SE) plasma ionized calcium fell promptly and significantly (from 1.21 +/- 0.01 to 1.11 +/- 0.01 mmol/L) after the sodium bicarbonate infusion. The mean (+/-SE) plasma intact PTH increased promptly and significantly, by more than four fold (42.3 +/- 4.2 to 182.4 +/- 34.7 pg/ml), and then gradually returned to basal levels. In patients with partial hypoparathyroidism who have detectable basal plasma levels of PTH, the absolute increment in PTH levels was much less, and in the plasma obtained from patients with complete hypoparathyroidism, absolutely no response was observed. Plasma obtained from patients diagnosed with primary hyperparathyroidism (parathyroid adenoma or hyperplasia) has high basal PTH levels. The response to the sodium bicarbonate infusion in these patients was markedly blunted (less than a two-fold increase in all cases examined). No significant adverse effects were observed during the procedure. Therefore, the sodium bicarbonate infusion test is a simple and sensitive method to stimulate PTH release, and is clinically useful for evaluating parathyroid gland function.     

Experimental amitriptyline intoxication: treatment of cardiac toxicity with sodium bicarbonate

Overdose with amitriptyline and other tricyclic antidepressants can result in ventricular conduction abnormalities as well as severe ventricular arrhythmias. The arrhythmogenic effects of these compounds may be attributed to their direct local anesthetic actions in blocking sodium channels in cardiac membranes. Thus tricyclic-induced ventricular arrhythmias usually do not respond well to therapy with standard Class I antiarrhythmic drugs that also have the same direct local anesthetic action and may potentiate the adverse effects of tricyclic antidepressants. Cardiac toxicity was produced in dogs by the administration of amitriptyline, both orally and IV. At serum concentrations less than 2,000 ng/mL, sinus tachycardia occurred with widened QRS complexes. At higher concentrations, QRS duration became more markedly prolonged and was followed by ventricular tachyarrhythmias. Occurrence of ventricular tachyarrhythmias was associated with QRS durations of more than 0.11 second. Sodium bicarbonate (18 to 36 mEq) administered IV over either 30 seconds or two minutes rapidly converted ventricular tachycardia to normal sinus rhythm. Conversion was associated with abbreviation of the QRS complex and was accompanied by a rise in both systolic and diastolic pressures. The duration of sodium bicarbonate effect paralleled the duration of the changes in arterial pH and plasma bicarbonate concentrations. In vitro studies in cardiac Purkinje fibers suggested that reversal of amitriptyline-induced cardiac membrane effects by sodium bicarbonate may be attributed not only to alkalinization but also to increased in extracellular sodium concentration, diminishing the local anesthetic action of amitriptyline and resulting in less sodium channel block.(ABSTRACT TRUNCATED AT 250 WORDS)     

Sodium sensitive and sodium retaining hypertension

The differences between sodium sensitive and sodium retaining hypertension were theoretically considered using a water tank model of body fluid volume-blood pressure regulation. If an outlet valve is attached to a tank with a base area corresponding to the reciprocal of total peripheral resistance (TPR) and water is poured into this tank at a rate corresponding to the amount of Na+ intake, then equilibrium should be achieved at a certain water level, volume and output from the outlet, which represent mean arterial pressure (MAP), cardiac output (CO) and urinary Na+ excretion. The height of the outlet from the tank bottom and the size cross-sectional area, of the outlet correspond to the x-intercept and slope of the renal function (pressure-natriuresis) curve, respectively. In both nonsodium sensitive hypertension, due to the shift of the curve toward a higher blood pressure level (elevated height of the outlet) without change in the slope (size of the outlet), and sodium sensitive hypertension, due to the depressed slope of the curve (reduced outlet size), not only MAP (water level) but also CO (water volume) are increased, resulting in sodium retaining hypertension, if TPR (reciprocal of base area) remained unchanged, while CO is relatively unchanged, resulting in nonsodium retaining hypertension, if TPR is elevated. Thus, the MAP and its sensitivity to sodium intake is determined by the renal function curve. Since body fluid volume is determined by both the renal function curve and TPR, however, changes in TPR during the development of hypertension is a major factor in determining whether or not the body fluid volume has to change only a small amount or a large amount. Therefore, the sodium sensitivity of blood pressure and sodium retention must be considered separately.     

Hypertension corrected by discontinuing chronic sodium bicarbonate ingestion: Subsequent transient hypoaldosteronism

A 52 year old man with a long history of marked hypertension, peptic ulcer disease, nephrocalcinosis and intermittent hypercalcemia was referred to be evaluated for primary aldosteronism suspected on the basis of low plasma renin activity, hypokalemia and blood pressure responsive to spironolactone. Aldosterone excretion, however, was extremely low. Alkaluria, high urinary sodium excretion and hypercalciuria were observed. The patient admitted to chronic ingestion of large amounts of baking soda. Upon cessation of alkali abuse, his blood pressure fell dramatically; orthostatic hypotension, concomitant azotemia, hemoconcentration, hyperkalemia and weight loss occurred. Despite dramatic elevation in plasma renin activity, urinary aldosterone excretion remained low during this period. Adrenal glucocorticoid secretion was intact. All abnormalities of sodium, potassium and aldosterone subsequently returned to normal. A 10 day challenge with oral sodium bicarbonate was associated with a rise in blood pressure, but serum calcium remained normal. The patient remains normotensive 15 months after discontinuing alkali abuse.