碳酸氫鈉
**碳酸氫鈉**是一種全身性及尿液鹼化劑，廣泛應用於獸醫急診與重症監護，以及特定疾病的慢性管理。 - **急診酸鹼管理**：主要用於校正嚴重的代謝性酸中毒，特別是當潛在原因無法迅速逆轉且血液 pH 值降至危險水平時。 - **電解質危機**：作為危及生命的**高血鉀症**（促使鉀離子進入細胞內）及**高血鈣症**的輔助治療。 - **尿液鹼化**：口服給藥以提高尿液 pH 值，用於管理或預防特定尿結石（如尿酸鹽、胱氨酸結石）。 > **臨床要點**：在心肺復甦（CPR）和糖尿病酮酸血症（DKA）中常規使用碳酸氫鈉的做法已不被推薦。在 DKA 中，它可能惡化細胞內低血鉀並引起矛盾性中樞神經系統酸中毒；在 CPR 中，若病患未獲得充分通氣，可能導致高碳酸血症。
作用機制: Sodium bicarbonate acts as an exogenous source of bicarbonate anion (**$HCO_3^-$**), which is the primary extracellular buffer in the body. - **Buffering Acidosis**: $HCO_3^-$ combines with free hydrogen ions ($H^+$) to form carbonic acid ($H_2CO_3$), which then dissociates into water ($H_2O$) and carbon dioxide ($CO_2$). - **Pathway**: **$HCO_3^-$ + $H^+$ → $H_2CO_3$ → $H_2O$ + $CO_2$** (The $CO_2$ must be exhaled via the lungs, highlighting the need for adequate ventilation). - **Hyperkalemia Management**: By increasing blood pH, it stimulates the $Na^+/H^+$ exchanger and subsequently the $Na^+/K^+$-ATPase pump, driving **potassium into cells** and rapidly lowering serum potassium levels. - **Urinary Alkalinization**: Bicarbonate is excreted in the urine, raising the pH. This increases the solubility of weak acids (like uric acid and cystine) and decreases the solubility of weak bases.
各物種劑量
- Acidosis (Ruminants) · 2-5 mEq/kg IV for a 4-8 hour period · IV · Once · Over 4-8 hours
- Acidosis (Ruminants) · 2-5 mEq/kg IV for a 4-8 hour period · IV · Once · Over 4-8 hours
- Severe metabolic acidosis · mEq of bicarbonate required = 0.5 x body weight in kg x (desired total CO2 mEq/L minus measured total CO2 mEq/L). Give 1/2 of the calculated dose slowly over 3-4 hours IV. · IV · Once · Over 3-4 hours · Recheck blood gases and assess clinical status. Avoid over-alkalinization.
- Metabolic acidosis secondary to uremia · 0.3 x body weight (kilograms) x the base deficit. Administration of one third of this dose slowly IV and the rest placed in the intravenous fluids. OR 1-2 mEq/kg of bicarbonate can be given as a slow IV bolus if blood gas is not possible. · IV · Once · Over several hours · Avoid rapid IV boluses. Recheck blood gas after 2-4 hours.
- Adjunctive therapy of diabetic ketoacidosis · Dose (in mEq) = body weight in kgs. x 0.4 x (12 - patient's bicarbonate) x 0.5. Give above dose over 6 hours in IV fluids. · IV · Once · Over 6 hours · Only if plasma bicarbonate is <=11 mEq/L. Recheck and repeat if still <=11 mEq/L. Use is controversial.
- Adjunctive treatment of hypercalcemic crisis · mEq of bicarbonate required = 0.3 x body weight in kg x (desired plasma bicarbonate mEq/L - measured plasma bicarbonate mEq/L); or 1 mEq/kg IV every 10-15 minutes; maximum total dose: 4 mEq/L · IV · q10-15m · Until effect or max dose
- Adjunctive therapy for hyperkalemic crises · 2-3 mEq/kg IV over 30 minutes (if decreased tissue perfusion/renal failure and no DKA) OR 1-2 mEq/kg IV slowly · IV · Once · Over 30 minutes or slowly · Must be used judiciously.
給藥途徑
禁忌症
- Metabolic or respiratory alkalosis
- Excessive chloride loss secondary to vomiting or GI suction
- Patients at risk for development of diuretic-induced hypochloremic alkalosis
- Hypocalcemia (alkalosis may induce tetany)
- Hypoventilating patients
- Hypercapnoeic patients
- Animals unable to effectively expel carbon dioxide
不良反應
- Metabolic alkalosis
- Hypokalemia
- Hypocalcemia
- 'Overshoot' alkalosis
- Hypernatremia
- Volume overload
- Congestive heart failure
- Shifts in the oxygen dissociation curve (decreased tissue oxygenation)
- Paradoxical CNS acidosis leading to respiratory arrest
- Hypercapnia (if not well ventilated during CPR)
- Predisposition to ventricular fibrillation
- Hypernatraemia
- Congestive heart failure (due to sodium load)
- Decreased tissue oxygenation (shift in oxygen dissociation curve)
- Paradoxical CNS acidosis
- Respiratory arrest
藥物相互作用
- Anticholinergic agents · Concomitant oral sodium bicarbonate may reduce absorption; administer separately
- Azole antifungals (ketoconazole, itraconazole) · Concomitant oral sodium bicarbonate may reduce absorption; administer separately
- Ciprofloxacin, Enrofloxacin · Solubility is decreased in an alkaline environment; monitor for signs of crystalluria
- Corticosteroids · Patients receiving high dosages of sodium bicarbonate and ACTH or glucocorticoids may develop hypernatremia
- Diuretics (e.g., thiazides, furosemide) · Concurrent use in patients receiving potassium-wasting diuretics may cause hypochloremic alkalosis
- Ephedrine · When urine is alkalinized, excretion may be decreased
- Histamine2 blocking agents (e.g., cimetidine, ranitidine) · Concomitant oral sodium bicarbonate may reduce absorption; administer separately
- Iron products · Concomitant oral sodium bicarbonate may reduce absorption; administer separately
- Oral medications (general) · Can increase or reduce absorption rate/extent; avoid giving other drugs within 12 hours of oral sodium bicarbonate
- Quinidine · When urine is alkalinized, excretion may be decreased
- Salicylates · When urine is alkalinized, excretion of weakly acidic drugs may be increased
監測
- Acid/base status (venous or arterial blood gases)
- Serum electrolytes (especially potassium, calcium, and sodium)
- Urine pH (if being used to alkalinize urine)
- Blood gas analysis (pH, pCO2, HCO3-)
- Serum electrolytes (Na+, K+, Ca2+)
- Respiratory rate and effort
- Clinical signs of fluid overload or congestive heart failure
過量
Overdose or overly rapid administration can cause **severe alkalosis**, leading to irritability, muscle twitching, or **tetany** (due to a sudden drop in ionized calcium). - **Mild Overdose**: May only require discontinuing the bicarbonate therapy or using a rebreathing mask. - **Severe Alkalosis**: May require intravenous calcium therapy to treat tetany. - **Electrolyte Correction**: Sodium chloride or potassium chloride may be necessary if hypokalemia or hypochloremia is present. > Always thoroughly check dosages and frequently monitor electrolyte and acid/base status during administration.
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