Sodium Bicarbonate In Patients Research Articles

Tricarboxylic Cycle Intermediates in Combination with Calcium Phosphate Chelators and Sodium Bicarbonate Increases eGFR in Patients with Stages 3b, 4 and 5 CKD: A Retrospective Observational Study

Introduction: Currently, the conservative management of chronic kidney disease (CKD) involves treating the primary disease and its consequences, as well as improving altered biochemical markers. Evidence suggests that the key management strategy for slowing down the progression of the disease is nephroprotection. Objective: This study aimed to evaluate the effect of the supply of TCA cycle intermediates in combination with calcium carbonate, calcium lactate, and sodium bicarbonate in patients with CKD. Methodology: A retrospective observational study was undertaken in nephrology and internal medicine clinics in Mexico. The study enrolled patients aged over 18 with stages 3b, 4, and 5 chronic kidney disease (CKD) who were not undergoing renal replacement therapy (RRT) and had received treatment based on TCA therapy. Results: The study included a total of 55 patients with CKD. The results showed an increase in eGFR from a baseline average of 16.73 ± 1,374 mL/min to a final average of 19.18 ± 1,516 mL/min and a decrease in creatinine values from a baseline average of 4.26 ± 2.44 mg/dL to a final average of 3.77 ± 2.23 mg/dL. These changes had a statistical significance P?0.05.Conclusions: The observed benefits of TCA in combination with sodium bicarbonate, calcium carbonate, and calcium lactate include: 1) Increased eGFR, 2) Decreased serum creatinine, 3) Decreased serum urea, 4) Decreased serum phosphorus, 5) Increased serum hemoglobin, and 6) Maintenance of albumin levels within normal ranges. Adjuvant therapy with the combination of TCA could be a useful tool as a new therapeutic option in patients with CKD.

Efficacy and safety of tart cherry supplementary citrate mixture on gout patients: a prospective, randomized, controlled study

BackgroundLow urine pH, which may be mediated by metabolic syndrome (MetS), is common in gout. Tart cherries are shown to improve MetS symptoms and possess anti-inflammatory properties. However, the efficacy of tart cherry supplements on urine pH has yet to be studied.ObjectivesThis study aimed to investigate the efficacy and safety of tart cherry supplementary citrate (TaCCi) mixture on urine pH, serum urate (sUA), C-reactive protein (CRP), and gout flares in gout patients initiating urate-lowering therapy (ULT), in comparison to citrate mixture and sodium bicarbonate.MethodsA prospective, randomized (1:1:1), open-label, parallel-controlled trial was conducted among 282 men with gout and fasting urine pH ≤ 6, who were initiating ULT with febuxostat (initially 20 mg daily, escalating to 40 mg daily if serum urate ≥ 360 μmol/L). Participants were randomized to groups taking either sodium bicarbonate, citrate mixture, or TaCCi mixture. All participants were followed every 4 weeks until week 12. Urine pH and sUA were co-primary outcomes, with various biochemical and clinical secondary endpoints.ResultsUrine pH increased to a similar extent in all three groups. SUA levels declined in all three groups as well, with no significant differences observed between the groups. At week 12, the TaCCi mixture group exhibited a greater reduction in the urine albumin/creatinine ratio (UACR) compared to the other two groups (p < 0.05). Participants taking TaCCi mixture or citrate mixture experienced fewer gout flares than those in the sodium bicarbonate group over the study period (p < 0.05). Additionally, the TaCCi mixture group had a lower CRP level at week 12 relative to the other two groups (p < 0.01). Adverse events were similar across all three groups.ConclusionThe TaCCi mixture had similar efficacy and safety on urine alkalization and sUA-lowering as the citrate mixture and sodium bicarbonate in patients with gout. However, the TaCCi mixture resulted in greater improvements in UACR and CRP, which suggests that tart cherry supplements may provide additional benefits for renal protection and reduce inflammation in gout, particularly when starting ULT.Trial registrationThis project was registered in ChiCTR (www.chictr.org.cn), with the registration number: ChiCTR2100050749.

A Review of Bicarbonate Use in Common Clinical Scenarios

BackgroundThe use of sodium bicarbonate to treat metabolic acidosis is intuitive, yet data suggest that not all patients benefit from this therapy. ObjectiveIn this narrative review, we describe the physiology behind commonly encountered nontoxicologic causes of metabolic acidosis, highlight potential harm from the indiscriminate administration of sodium bicarbonate in certain scenarios, and provide evidence-based recommendations to assist emergency physicians in the rational use of sodium bicarbonate. DiscussionSodium bicarbonate can be administered as a hypertonic push, as a resuscitation fluid, or as an infusion. Lactic acidosis and cardiac arrest are two common scenarios where there is limited benefit to routine use of sodium bicarbonate, although certain circumstances, such as patients with concomitant acute kidney injury and lactic acidosis may benefit from sodium bicarbonate. Patients with cardiac arrest secondary to sodium channel blockade or hyperkalemia also benefit from sodium bicarbonate therapy. Recent data suggest that the use of sodium bicarbonate in diabetic ketoacidosis does not confer improved patient outcomes and may cause harm in pediatric patients. Available evidence suggests that alkalinization of urine in rhabdomyolysis does not improve patient-centered outcomes. Finally, patients with a nongap acidosis benefit from sodium bicarbonate supplementation. ConclusionsEmpiric use of sodium bicarbonate in patients with nontoxicologic causes of metabolic acidosis is not warranted and likely does not improve patient-centered outcomes, except in select scenarios. Emergency physicians should reserve use of this medication to conditions with clear benefit to patients.

The Effect of Oral Care With Black Mulberry Extract on Oral Mucositis, Dry Mouth, and Weight Gain in Patients With Cancer.

For patients receiving chemotherapy, various oral care therapies are used to treat oral mucositis, but the use of black mulberry extract as an effective treatment has not been widely studied. . This study examined whether black mulberry extract is an effective treatment for oral mucositis, dry mouth, and weight gain compared to sodium bicarbonate in patients with cancer. . The control group (N = 20) received sodium bicarbonate, and the intervention group (N = 20) received black mulberry extract. Mucositis and weight gain were evaluated on days 1, 7, and 15 after oral care application. . For both groups, mean scores indicated a statistically significant decrease in mucositis and dry mouth at all three time points. Mean scores were significantly lower in the intervention group on days 7 and 15. At all three time points, increases in weight were statistically significant for the intervention group but not for the control group. Increased weight gain in the intervention group was statistically significant when comparing the two groups on days 7 and 15.

The Effects of Oral Sodium Bicarbonate on Renal Function and Cardiovascular Risk in Patients with Chronic Kidney Disease: A Systematic Review and Meta-Analysis.

ObjectiveOral sodium bicarbonate is often used to correct acid-base disturbance in patients with chronic kidney disease (CKD). However, there is little evidence on patient-level benign outcomes to support the practice.MethodsWe conducted a systematic review and meta-analysis to examine the efficacy and safety of oral sodium bicarbonate in CKD patients. A total of 1853 patients with chronic metabolic acidosis or those with low-normal serum bicarbonate (22–24 mEq/L) were performed to compare the efficacy and safety of oral sodium bicarbonate in patients with CKD.ResultsThere was a significant increase in serum bicarbonate level (MD 2.37 mEq/L; 95% CI, 1.03 to 3.72) and slowed the decline in estimated glomerular filtration rate (eGFR) (MD −4.44 mL/min per 1.73 m2, 95% CI, −4.92 to −3.96) compared with the control groups. The sodium bicarbonate lowered T50-time, an indicator of vascular calcification (MD −20.74 min; 95% CI, −49.55 to 8.08); however, there was no significant difference between the two groups. In addition, oral sodium bicarbonate dramatically reduced systolic blood pressure (MD −2.97 mmHg; 95% CI, −5.04 to −0.90) and diastolic blood pressure (MD −1.26 mmHg; 95% CI, −2.33 to −0.19). There were no statistically significant body weight, urine pH and mean mid-arm muscle circumference.ConclusionTreatment of metabolic acidosis with sodium bicarbonate may slow the decline rate of kidney function and potentially significantly improve vascular endothelial function in patients with CKD.Prospero Registration NumberCRD42020207185.

Relationship between mortality and use of sodium bicarbonate at the time of dialysis initiation: a prospective observational study

BackgroundPatients with chronic kidney disease often experience metabolic acidosis. Whether oral sodium bicarbonate can reduce mortality in patients with metabolic acidosis has been debated for years. Hence, this study was conducted to evaluate the utility of sodium bicarbonate in patients who will undergo dialysis therapy. In this study, we investigated the effect of oral sodium bicarbonate therapy on mortality in patients with end-stage kidney disease (ESKD) initiated on dialysis therapy.MethodsWe conducted an observational study of patients when they started dialysis therapy. There were 17 centres participating in the Aichi Cohort Study of Prognosis in Patients Newly Initiated into Dialysis. Data were available on patients’ sex, age, use of sodium bicarbonate, drug history, medical history, vital data, and laboratory data. We investigated whether patients on oral sodium bicarbonate for more than three months before dialysis initiation had a better prognosis than those without sodium bicarbonate therapy. The primary outcome was defined as all-cause mortality.ResultsThe study included 1524 patients with chronic kidney disease who initiated dialysis between October 2011 and September 2013. Among them, 1030 were men and 492 women, with a mean age of 67.5 ± 13.1 years. Of these, 677 used sodium bicarbonate and 845 did not; 13.6% of the patients in the former group and 21.2% of those in the latter group died by March 2015 (p < 0.001). Even after adjusting for various factors, the use of sodium bicarbonate independently reduced mortality (p < 0.001).ConclusionsThe use of oral sodium bicarbonate at the time of dialysis initiation significantly reduced all-cause mortality in patients undergoing dialysis therapy.

Na/K citrate versus sodium bicarbonate in prevention of contrast-induced nephropathy.

Contrast-induced nephropathy (CIN) is one of the important complications of radiographic procedures, especially in patients with chronic kidney disease. It is also one of the common causes of acute kidney injury. The pathogenesis is postulated to be the effect of oxygen- free radicals and hyperosmolar stress on the renal medulla. It is reported that the production of superoxide is most active at acid environment. K/Na citrate is well known as a urine alkalinization medium, and this has been evaluated earlier with standard hydration for reduction of CIN and was stated to be efficient. We aimed to determine the efficacy of Na/K citrate in reducing the frequency of CIN in comparison to sodium bicarbonate in patients after coronary angiography. Two hundred and ten patients with renal dysfunction [estimated glomerular filtration rate (eGFR), 60 mL/min/1.73 m(2) or less] who underwent elective or emergency coronary angiography (CAG) with/without percutaneous coronary intervention (PCI) at our institution were enrolled into the study. The patients were randomized into two groups, Group 1-Taking Na/K citrate and Group 2-Taking sodium bicarbonate. Radiographic contrast agent iohexol was used. Change in creatinine, percent change in creatinine, percent change in eGFR, change in serum potassium, and urine pH were all compared between the two groups. There was no significant difference for prevention of CIN when comparing the Na/K citrate with sodium bicarbonate solution in patients exposed to CAG with or without PCI. Mean absolute change in eGFR after 48 h after administration of contrast between sodium bicarbonate group and Na/K citrate group was -0.60 ± 1.58 versus -0.71 ± 1.38. Serum potassium decreased postprocedure in the sodium bicarbonate group than in the citrate group (3.90 ± 0.33 vs. 4.14 ± 0.39). Both agents are equally effective in reducing the incidence of CIN, but the citrate would possibly be a safer option for patients at risk of hypokalemia.

The Effect of Buffered Lidocaine in Local Anesthesia: A Prospective, Randomized, Double-Blind Study

Open carpal tunnel decompression under local anesthesia is routinely done by many surgeons. However, patients complain of pain during the injection of local anesthesia. This prospective, double-blind, randomized study was to compare the pain visual analog scale (VAS) scores of local anesthesia using lidocaine with and without sodium bicarbonate in patients with bilateral carpal tunnel syndrome. Twenty-five patients underwent bilateral simultaneous carpal tunnel decompression. All had topical anesthetic cream applied on the palm and wrist before the lidocaine block. In a randomized manner, half of the hands were blocked with nonbuffered lidocaine and half were blocked with buffered lidocaine. Pain was evaluated on a VAS score. The mean pain VAS score in the hand with buffered lidocaine was 4.6 ± 1.5 and 6.5 ± 1.5 for the hand with nonbuffered lidocaine. After adjustment for individual threshold of the pain, the mean pain VAS score changed into 4.6 ± 1.3 with buffered lidocaine and 6.6 ± 1.7 without buffered lidocaine. In open carpal tunnel surgery, the use of buffered lidocaine for local anesthesia reduces the anesthetic pain effectively. Therapeutic I.

Effects of Oral Sodium Bicarbonate in Patients with CKD

Metabolic acidosis contributes to muscle breakdown in patients with CKD, but whether its treatment improves functional outcomes is unknown. The choice of dose and tolerability of high doses remain unclear. In CKD patients with mild acidosis, this study evaluated the dose-response relationship of alkali with serum bicarbonate, its side effect profile, and its effect on muscle strength. In this single-blinded pilot study from March of 2009 to August of 2010, 20 adults with estimated GFR 15-45 ml/min per 1.73 m(2) and serum bicarbonate 20-24 mEq/L were treated during successive 2-week periods with placebo followed by escalating oral NaHCO3 doses (0.3, 0.6, and 1.0 mEq/kg per day). At each visit, handgrip strength and time required to complete 5 and 10 repetitions of a sit-to-stand test were measured. Each 0.1 mEq/kg per day increase in dose produced a 0.33 mEq/L (95% confidence interval=0.23-0.43 mEq/L) higher serum bicarbonate. Sit-to-stand time improved after 6 weeks of oral NaHCO3 (23.8±1.4 versus 22.2±1.6 seconds for 10 repetitions, P=0.002), and urinary nitrogen excretion decreased (-0.70 g/g creatinine [95% confidence interval=-1.11 to -0.30] per 0.1 mEq/kg per day higher dose). No statistically significant change was seen in handgrip strength (29.5±9.6 versus 28.4±9.4 kg, P=0.12). Higher NaHCO3 doses were not associated with increased BP or greater edema. NaHCO3 supplementation produces a dose-dependent increase in serum bicarbonate and improves lower extremity muscle strength after a short-term intervention in CKD patients with mild acidosis. Long-term studies are needed to determine if this finding translates into improved functional status.

Urinary Alkalinisation with Oral Sodium Bicarbonate for Patients at Risk of Contrast‐Induced Nephropathy

ABSTRACTBackgroundIntravenous sodium bicarbonate is used to reduce the risk of contrast‐induced nephropathy (CIN). Intravenous sodium bicarbonate is inconvenient and requires inpatient hospital resources, while oral sodium bicarbonate is less costly and easy‐to‐use.AimTo determine whether oral sodium bicarbonate has a similar effect on urinary pH as intravenous sodium bicarbonate in patients at risk of CIN.MethodThis sequential crossover study was conducted in patients from the cardiology and renal units scheduled for a non‐emergency contrast‐enhanced procedure. Participants received intravenous sodium bicarbonate 150 mmol/L at 3 mL/kg/h, 1 hour prior, then 1 mL/kg/h during and for 6 hours after the procedure. Participants returned to the hospital 2 to 3 weeks after their procedure to receive oral sodium bicarbonate capsules (16 times 840 mg, 160 mmol) over 7 hours with 1 L of water. Urinary pH was measured before and after the administration of intravenous and oral sodium bicarbonate.Results9 participants completed the study. Mean urinary pH after oral sodium bicarbonate was 6.6 (SD 0.6) versus 6.9 (SD 0.5) for intravenous sodium bicarbonate. The mean change in urinary pH was 0.9 (SD 0.7) with oral sodium bicarbonate versus 0.8 (SD 0.5) for intravenous sodium bicarbonate. The difference in change in urinary pH was not statistically significant (p = 0.5).ConclusionOral sodium bicarbonate has a similar effect on urinary pH as intravenous sodium bicarbonate in patients at risk of CIN.

Kalp Etkilenmesine Sebep Olan Trisiklik Antidepresan İlaçlar ve Trisiklik Antidepresan Dışı Diğer Antikolinerjik İlaçlar ile Zehirlenmeye Maruz Kalan Hastalarda Sodyum Bikarbonat Tedavisinin Etkinliğinin Karşılaştırılması

Amaç: Antikolinerjik ilaçlarla zehirlenmeler acil servislerde sık görülen ve yaşamı tehdit eden zehirlenmelerdir. Bu ilaçların kalp hızı değişiklikleri, ritim bozuklukları ve ileti gecikmeleri gibi kalp üzerine ciddi yan etkileri vardır. Çalışmamızdaki amaç QTc?0,45 olan trisiklik antidepresan (TSA) ve TSA dışı antikolinerjik ilaçlarla zehirlenmelerde kalp üzerine olan diğer olumsuz etkilerin benzer özellikte olup olmadığının belirlenmesi ve standart NaHCO3 tedavisinin tüm antikolinerjik ilaç zehirlenmelerinde QRS genişlemesi dışında QTc uzamasında da etkinliğinin karşılaştırılmasıdır. Gereç ve Yöntemler: İleriye dönük olarak planlanan vaka kontrol niteliğindeki çalışmamıza 07.06.2005-30.11.2006 tarihleri arasında Çukurova Üniversitesi Tıp Fakültesi acil servise TSA ve TSA dışı diğer antikolinerjik etkili ilaçlarla zehirlenme sebebiyle başvuran ve geliş anında çekilen elektrokardiografide QTc?0,45 saniye olan hastalar dahil edildi. Çalışmaya alınan hastalara acil serviste 2 meq/kg'dan NaHCO3 tedavisi uygulandı. Her iki grupta gruplara ve zamana göre QTc ve QRS mesafelerindeki değişimler, kardiyak biyokimyasal parametreler ve sistolik kan basıncı ile nabız sayısındaki değişimler karşılaştırıldı. Verilen NaHCO3 tedavisine bağlı gelişebilecek komplikasyonlara ait biyokimyasal parametrelere bakıldı. Bulgular: Hastaların demografik, klinik, elektrokardiyografi ve laboratuar bulguları kaydedilerek analizleri yapıldı. TSA ilaçlarla zehirlenmiş 30, antikolinerjik etkili diğer ilaçlarla zehirlenmiş 28 hasta olmak üzere toplam 58 hasta çalışmaya alındı. Hastaların hepsinde QTc uzaması ve taşikardi mevcut iken %64,9'unda (n=37) QRS?0,1 idi. Acil servise başvuru anındaki QTc ve QRS değerleri ile tedavinin 60. dakikasındaki QTc ve QRS değerleri karşılaştırıldığında bu değerlerin her iki grupta da zamanla istatistiksel açıdan anlamlı olarak azaldığı, fakat bu azalmanın gruplar arasında anlamlı bir fark oluşturmadığı görüldü. Her iki grupta da hastaların geliş anından çıkış anına kadar geçen sürelerde sistolik kan basınçlarında ve kardiyak biyokimyasal parametrelerinde anlamlı bir değişim izlenmedi. Hastaların tamamının takip ve tedavileri acil gözlem ünitesinde yapıldı. Her iki gruptaki hastalarda ölüm meydana gelmedi. Sonuç: NaHCO3 tedavisinin her iki grupta fark olmaksızın semptom ve bulguları tamamen iyileştirmesi ve tedaviye bağlı hipertansiyon, metabolik alkaloz, hipernatremi, hipokalemi, hipokalsemi gibi komplikasyonların gelişmemesi elektrokardiyografide QTc uzaması olan tüm antikolinerjik etkili ilaçlarla zehirlenmelerde standart 2 meq/kg NaHCO3 tedavisinin geçerli, etkin ve güvenli bir tedavi olduğunu düşündürmektedir.

Prevention of Contrast-Induced Nephropathy by Bolus Injection of Sodium Bicarbonate in Patients With Chronic Kidney Disease Undergoing Emergent Coronary Procedures

We conducted a prospective study to determine whether a bolus injection of sodium bicarbonate before emergent coronary procedures in patients with chronic kidney disease (CKD) might prevent contrast-induced nephropathy (CIN). We enrolled 59 patients with CKD, defined by a serum creatinine concentration of >1.1 mg/dl or an estimated glomerular filtration rate of <60 ml/min, who were scheduled at admission to undergo an emergent coronary procedure. The patients were randomized to receive a bolus intravenous injection of 154 mEq/L of sodium bicarbonate (n = 30) or sodium chloride (n = 29) at the dose of 0.5 ml/kg, before contrast administration, followed by infusion of 154 mEq/L sodium bicarbonate at 1 ml/kg/hour for 6 hours in both groups. The primary end point was the occurrence of CIN, defined as an increase by > 25% or > 0.5 mg/dl of the serum creatinine level within 2 days after the procedure. In the sodium bicarbonate group, the serum creatinine concentration remained unchanged within 2 days of contrast administration (from 1.32 ± 0.46 to 1.38 ± 0.60 mg/dl, p = 0.33). In contrast, it had increased in the sodium chloride group (1.51 ± 0.59 to 1.91 ± 1.19 mg/dl, p = 0.006). The incidence of CIN was significantly lower in the sodium bicarbonate group than in the sodium chloride group (3.3% vs 27.6%, p = 0.01). In conclusion, rapid alkalization by bolus injection of sodium bicarbonate was effective for the prevention of CIN in patients with CKD undergoing emergent procedures.

A Comparison of Oral and Intravenous Sodium Bicarbonate on Urinary pH in Patients at Risk of Contrast-induced Nephropathy: A Pilot Study

276 This abstract has been withdrawn. 277 AComparison ofOral and Intravenous SodiumBicarbonate on Urinary pH in Patients at Risk of Contrast-induced Nephropathy: A Pilot Study P. To, F. Chahadi ∗, M. Freeman, M. Pan, O. Farouque, P. Mount Austin Health, Australia Aim: Intravenous sodiumbicarbonate infusionhasbeen shown to reduce the risk of contrast-induced nephropathy (CIN). We sought to determine whether oral sodium bicarbonate has a similar effect onurinepH to intravenous sodium bicarbonate in patients at risk of CIN. Methods:Cardiology and renal patients scheduled for a non-urgent contrast enhanced procedure and who were eligible for intravenous bicarbonate administration per Austin health guidelines to prevent CIN were invited to participate. Participants received intravenous bicarbonate (150mmole) at 3mmol/kg/h one hour prior, then 1mmol/kg/h during and after the procedure. Participants returned to the hospital three weeks post procedure for o 8 p a h

The Response of the Vascular Beds to Sodium Bicarbonate in Patients During Normothermic Bypass

Cardiopulmonary bypass (CPB) provides a unique circumstance to study the effects of drugs on the systemic vasculature. Thus, this study was designed to evaluate the effects of sodium bicarbonate on the systemic circulation during CPB in humans. Randomized, double-blind study. Tertiary care university hospital. Patients presenting for coronary artery bypass graft surgery with CPB. In this double-blind study, 22 consecutive adult patients of both sexes undergoing cardiac surgery were randomized into 2 groups. After establishing CPB and cardioplegia, patients in group 1 (n = 11) received saline (0.9%) (1.2 mL/kg), and group 2 received sodium bicarbonate (SB) (7%) (1.2 mL/kg). The blood level in the cardiotomy reservoir, pump flow, and mean arterial pressure were measured for 25 minutes. The SB-treated patients (group 2) showed significantly greater (p < 0.05) decreases in cardiotomy reservoir blood volume (336 +/- 186 mL) than the saline-treated (140 +/- 97 mL) patients. The mean arterial pressure in group 2 patients significantly (p < 0.05) increased (from 49 +/- 11.9 to 65 +/- 5.3 mmHg) more than in the saline group (from 50 +/- 6.8 to 57 +/- 9.2 mmHg) after 20 minutes. The decrease in reservoir volume significantly (p < 0.05) and inversely correlated (r = -0.61) with the acidotic state of the patients before SB. This study found a biphasic response to SB on the systemic circulation during CPB. Early dilation of venous capacitance vessels occurred followed by arteriolar constriction over the 20-minute study interval.

Paradoxical Effect of Bicarbonate on Cytoplasmic pH

The effect of an abrupt rise in bicarbonate concentration on cytoplasmic pH was studied in human platelets suspended in a Tyrode's buffer. Addition of bicarbonate raised extracellular pH but simultaneously caused pronounced cytoplasmic acidification. This effect may be due to combination of bicarbonate with hydrogen ions in extracellular fluid to form carbonic acid, which is converted by carbonic anhydrase to water and carbon dioxide. Bicarbonate ions do not diffuse rapidly across cell membranes, whereas carbon dioxide is highly diffusible and can combine with water in the cytoplasm, forming carbonic acid and reducing the intracellular pH. In accord with this explanation cytoplasmic acidification by bicarbonate was antagonised by acetazolamide (an inhibitor of carbonic anhydrase). Cytoplasmic acidification could contribute to adverse effects of intravenous sodium bicarbonate in patients with severe acidaemia. These findings add weight to the body of opinion that such treatment is both illogical and dangerous.

Paradoxical effect of bicarbonate on cytoplasmic pH

The effect of an abrupt rise in bicarbonate concentration on cytoplasmic pH was studied in human platelets suspended in a Tyrode's buffer. Addition of bicarbonate raised extracellular pH but simultaneously caused pronounced cytoplasmic acidification. This effect may be due to combination of bicarbonate with hydrogen ions in extracellular fluid to form carbonic acid, which is converted by carbonic anhydrase to water and carbon dioxide. Bicarbonate ions do not diffuse rapidly across cell membranes, whereas carbon dioxide is highly diffusible and can combine with water in the cytoplasm, forming carbonic acid and reducing the intracellular pH. In accord with this explanation cytoplasmic acidification by bicarbonate was antagonised by acetazolamide (an inhibitor of carbonic anhydrase). Cytoplasmic acidification could contribute to adverse effects of intravenous sodium bicarbonate in patients with severe acidaemia. These findings add weight to the body of opinion that such treatment is both illogical and dangerous.