Surgical Procedures/Acid Base Disorder

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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

1. 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).
2. 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:

1. Removing and identifying underlying causes, Discontinuing exogenous alkali, repairing Cl–, K+, and volume deficits.
2. Correction of volume deficits (can be used 0.9% NaCl) and hypokalemia.
3. H2-receptor antagonists or other acid-suppressing medications can be used after vomiting or nasogastric suctioning.
4. 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.
5. 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.
6. HCl more rapidly corrects metabolic alkalosis.
7. 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

1. Usually in severe cases Kussmaul's respiration can be present.
2. 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:

1. Increased AG metabolic acidosis.
2. Normal AG metabolic acidosis.

Causes according to Anion Gap:

Increased anion gap Metabolic Acidosis:

1. Increased acid production:
   1. Ketoacidosis
      1. Diabetic
      2. Alcoholic
      3. Starvation
   2. Lactic acidosis
   3. Toxic ingestion:
      1. Salicylates.
      2. Ethylene glycol.
      3. Methanol.
2. Renal failure.

Normal anion gap (hyperchloremic) Metabolic Acidosis:

1. Renal tubular dysfunction
   1. Renal tubular acidosis.
   2. Hypoaldosteronism.
   3. Potassium-sparing diuretics.
2. Loss of alkali.
   1. Diarrhea.
   2. Ureterosigmoidostomy.
   3. Carbonic anhydrase inhibitors.
3. 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.

1. Infusion of NaHCO3, stopped when H+ is normal.
2. Monitoring H+ and HCO3-
3. 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.