Surgical Procedures/Acid Base Disorder

Information http://en.wikibooks.org/wiki/Wikibooks:Medical_disclaimer Acid Base Disorder In general : H+ = 24 × PCO2/HCO3– (Usually in clinical practice, H+ concentration is expressed as pH.) Normal pH = 7.35–7.45. Acidemia = pH < 7.35. Alkalemia = pH > 7.45. PaCO2 (Arterial CO2 concentration normal = 35–45 mm Hg). HCO3– (Serum electrolytes normal = 22–31 mmol/liter). Acidosis-Alkalosis Acidosis is a process that causes the accumulation of acid. Alkalosis is a process that causes the accumulation of alkali. Respiratory Acidosis-Alkalosis Disorders that initially alter arterial PCO2 (arterial CO2 concentration) are termed respiratory acidosis-alkalosis. Metabolic Acidosis-Alkalosis Disorders initially affecting HCO3– (serum electrolytes) concentration are termed metabolic acidosis-alkalosis. Metabolic Alkalosis Causes Chloride-responsive. The most common causes in the surgical practice include: Diuretic therapy (e.g., contraction alkalosis). Acid loss through GI secretions (e.g., nasogastric suctioning, vomiting). Exogenous administration of HCO3– or HCO3– precursors (e.g., citrate in blood). Chloride-unresponsive metabolic alkalosis is comparatively less common and includes: Hyperaldosteronism Marked hypokalemia Renal failure Renal tubular Cl– wasting (Bartter’s syndrome) Oedematous states. Diagnosis: Measurement of urinary chloride concentration. Suggestive causes of the metabolic alkalosis if Urine Cl– concentration is <15 mmol/liter: vomiting. nasogastric suctioning. postdiuretic administration. posthypercapnia. Sughgestive causes of the metabolic alkalosis if Urine Cl– concentration is > 20 mmol/liter: Mineralocorticoid excess. Alkali loading. Concurrent diuretic administration Presence of severe hypokalemia. Treatment principles in metabolic alkalosis: Goal of Treatments can be: Removing and identifying underlying causes, Discontinuing exogenous alkali, repairing Cl–, K+, and volume deficits. Correction of volume deficits (can be used 0.9% NaCl) and hypokalemia. H2-receptor antagonists or other acid-suppressing medications can be used after vomiting or nasogastric suctioning. If Edemea: Acetazolamide (5 mg/kg/day IV or PO) can be used. Eases fluid mobilization while decreasing renal HCO3– reabsorption. Tolerance to this diuretic may develop after 2–3 days. Ammonium chloride (NH4Cl) can be used in severe alkalemia (HCO3– >40 mmol/liter; rate not exceeding 5 ml/minute). Approximately one-half of the calculated volume of NH4Cl is usually administered and the acid-base status and Cl– concentration is usually rechecked to determine the need of further treatment. Hepatic failure is contraindication for NH4Cl. HCl more rapidly corrects metabolic alkalosis. Dialysis: Can be considered in the volume-overloaded situation with renal failure and intractable metabolic alkalosis. Estimation of the amount of H+ requirement The amount of H+ to administer may be estimated by the following equation: H+(mmol) = 0.5 × wt (kg) × [103 – serum Cl– (mmol/liter)] Estimation of the amount of NH4Cl requirement: Can be estimated by the following equation: NH4Cl (mmol) = 0.2 × wt (kg) × [103 – serum Cl– (mmol/liter)] Metabolic Acidosis (Low pH with low CO2 content) Reduction in plasma Bicarbonate and a consequence rise in H+. PaCO2 is reduced secondarily by Hyperventilation, which mitigates the rise in H+. Causes Metabolic Acidosis is caused if: Accumulation of nonvolatile acids. Reduction of renal acid excretion. Loss of alkali. Mnemonics MUD PILES 1. Methyl Alcohol. 2. Uremia. 3. Diabetic Ketoacidosis 4. Para-Aldehyde poisoning. 5. Ischemia. 6. Lactic acidosis. 7. Ethylene Glycol Alcohol ingestion. 8. Salicylic Poisoning. Other commonest causes are: Addition of excessive acids to plasma. Ketoacidosis, Lacticacidosis. Methanol, ethylene glycol and salicylic poisoning. Failure to excrete acid: Chronic Renal Failure. Acute Renal Failure etc Loss of Bicarbonate (base): From G.I.T: Diarrhea. Fistulae. In Urine: Proximal renal tubular acidosis. Carbonic anhydrase inhibitors. Clinical Feature Usually in severe cases Kussmaul's respiration can be present. When H+ >70 mmol/L; then, Cardiac-Out-Put falls. Blood pressure decreases. Frequnet confusion. Drowsiness. Diagnostic Classsification (Anion Gap) Anion gap (AG: normal, 3–11 mmol/liter) AG (mmol/liter) = Na+ (mmol/liter) – [Cl– (mmol/liter) + HCO3– (mmol/liter)] It is useful diagnostically to classify metabolic acidosis into: Increased AG metabolic acidosis. Normal AG metabolic acidosis. Causes according to Anion Gap: Increased anion gap Metabolic Acidosis: Increased acid production: Ketoacidosis Diabetic Alcoholic Starvation Lactic acidosis Toxic ingestion: Salicylates. Ethylene glycol. Methanol. Renal failure. Normal anion gap (hyperchloremic) Metabolic Acidosis: Renal tubular dysfunction Renal tubular acidosis. Hypoaldosteronism. Potassium-sparing diuretics. Loss of alkali. Diarrhea. Ureterosigmoidostomy. Carbonic anhydrase inhibitors. Administration of HCl (ammonium chloride, cationic amino acids). Management/Treatment of metabolic acidosis: Directed primarily towards the underlying cause of the acid-base disturbance. Bicarbonate therapy is considered when there is moderate to severe metabolic acidosis, depending on the etiology. Infusion of NaHCO3, stopped when H+ is normal. Monitoring H+ and HCO3- Treatment of underlying causes. The HCO3– deficit (mmol/liter) can be estimated by the following equation: HCO3– deficit (mmol/liter) = Body weight (kg) × 0.4 × [desired HCO3– (mmol/liter) – measured HCO3– (mmol/liter)] (This equation serves only as a rough estimate .) The goal of HCO3– To raise the arterial blood pH to 7.00 or the HDRO3– concentration to 10 mmol/liter. Risks of bicarbonate therapy: Hypernatremia. Hypercapnia. Cerebrospinal fluid acidosis. Overshoot alkalosis. Serial arterial blood gases and serum electrolytes should be obtained to assess the response to HCO3– therapy. Rate of HCO3– replacement: In nonurgent situations: Continuous intravenous infusion over 4–8 hours (50-ml ampule of 8.4% NaHCO3 solution provides 50 mmol of HCO3–) can be added to 1 liter of D5W or 0.45% NaCl. In urgent situation: Deficit can be administered as a bolus over several minutes.