Surgical Procedures/Acid Base Disorder
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Acid Base Disorder
editIn 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
edit- Acidosis is a process that causes the accumulation of acid.
- Alkalosis is a process that causes the accumulation of alkali.
Respiratory Acidosis-Alkalosis
editDisorders that initially alter arterial PCO2 (arterial CO2 concentration) are termed respiratory acidosis-alkalosis.
Metabolic Acidosis-Alkalosis
editDisorders initially affecting HCO3– (serum electrolytes) concentration are termed metabolic acidosis-alkalosis.
Metabolic Alkalosis
editCauses
edit- 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).
- The most common causes in the surgical practice include:
- 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:
editMeasurement 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:
editGoal 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.
- Acetazolamide (5 mg/kg/day IV or PO) can be used.
- 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
editThe 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:
editCan be estimated by the following equation: NH4Cl (mmol) = 0.2 × wt (kg) × [103 – serum Cl– (mmol/liter)]
Metabolic Acidosis
edit(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
editMetabolic Acidosis is caused if:
- Accumulation of nonvolatile acids.
- Reduction of renal acid excretion.
- Loss of alkali.
Mnemonics
editMUD 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:
edit- 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.
- From G.I.T:
Clinical Feature
edit- 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)
editAnion 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:
editIncreased anion gap Metabolic Acidosis:
edit- Increased acid production:
- Ketoacidosis
- Diabetic
- Alcoholic
- Starvation
- Lactic acidosis
- Toxic ingestion:
- Salicylates.
- Ethylene glycol.
- Methanol.
- Ketoacidosis
- Renal failure.
Normal anion gap (hyperchloremic) Metabolic Acidosis:
edit- 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:
edit- 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–
edit- 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.
- Risks of bicarbonate therapy:
Serial arterial blood gases and serum electrolytes should be obtained to assess the response to HCO3– therapy.
Rate of HCO3– replacement:
edit- 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.