Acid Base

• • • • • Quick way to check the type of RTA: First look at Sr. K: if hyperkalemia it’s RTA type IV, and urine pH is low (<5.3). If not, then look at urine pH: if more towards high (basic)>5.3 it’s RTA type I; if it is variable, it is RTA type II. It is elevated during the initial bicarbonaturia when filtered bicarbonate exceeds the threshold for reabsorption, and low when the filtered load is below this threshold.

        • The presence of alcohol (methanol, ethanol, ethylene glycol) can be determined by laboratory assays. Clinical suspicion for toxic alcohol ingestion is corroborated by an increased osmolal gap.

        • Osmolal gap

        • If a normal anion gap is present, the GI HCO3- losses can be differentiated from RTAs via the urine anion gap.

        • UAG

• • • • Nonrenal HCO3- loss in diarrhea, pancreatic fistula, biliary, urinary diversion, ileostomy.

      • Cholestyramine, or ingestion of Ca and Mg chloride

      • Rapid infusion of NS

      • Spironolactone, TMP, ACE-I, pentamidine, NSAIDs, cyclosporine, acetazolamide (CI inhibitors),beta blockers

• • Use Winter's formula. PaCO2 = 1.5 x HCO3- + 8 +/- 2, i.e., the PaCO2 is expected to decrease 1.25 mmHg for each mmol/L decrease in HCO3-.

• When the primary process is Metabolic acidosis, calculate the anion gap (AG)?

AG = Na+ - (Cl- + HCO3-). Normal value = 12 mmol/L +/- 4.

Correct for hypoalbuminemia.

Normal anion gap (AG) = serum albumin x 3. High AG >10-12. mEq/L.

Correct for alkalosis: A pH >7.5 causes a high anion gap just by uncovering negative sites on albumin.

1. Calculate the delta AG = Pt.'s AG - Normal AG (12)

2. Corrected HCO3- = Pt.'s HCO3- + delta AG

If corrected bicarbonate = normal serum bicarbonate there is simple metabolic acidosis.

If corrected bicarbonate is < normal bicarbonate, then there is concomitant nonanion gap metabolic acidosis. An additional process has caused GI or renal loss of bicarbonate.

If corrected bicarbonate > normal bicarbonate, then there is concomitant metabolic alkalosis.

ANOTHER EASY WAY OF ASSESSING THE DELTA AG:

• • If the ∆AG = ∆HCO3, this is a simple AG metabolic acidosis.

  • If the ∆AG > ∆HCO3. It means that the HCO3 did not decrease as much as expected. It mean this is AG metabolic acidosis and metabolic alkalosis.

  • If the ∆AG < ∆HCO3. It means that the HCO3 decreased more than expected. It means this is AG metabolic acidosis and nongap metabolic acidosis.

• Tx for metabolic acidosis:

  • • Correct underlying cause.

    • Severe acidosis (pH <7.2), may need to be treated with parenteral bicarbonate.

      • Correct bicarbonate only to 15 mEq/L, and correct no more than half the deficit in 12 hours to avoid overshoot alkalosis.

      • 1 ampoule of 8.4% NaHCO3 = 50 mEq NaHCO3 = 1000 mEq Na/L

      • Give in D5W.

      • To give HCO3- in acute setting:

        • HCO3^- deficit in mEq= 0.5 x lean body wt in Kg (24 - HCO3 measured). Keep the desired HCO3 15 mEq/L.

      • 0.5 x body wt in kg (15 - bicarb measured)

        • Give 1/2 the dose slowly x 12 hours, only.

        • D5W + Sodium bicarbonate is generally the fluid of choice in Pts who are oliguric, hyperkalemic, and acidotic.

      • Hypernatremia, hypokalemia, hypocalcemia, and fluid overload may result in pulmonary edema, which can be dangerous in the setting of CHF or renal failure.

      • Serum electrolytes should be followed closely.

      • NaHCO3 tablet, 650 mg PO provides only 7 mEq of HCO3-, while one ampule of NaHCO3, IV contains 50 mEq.

METABOLIC ALKALOSIS. ▲pH, ▲ HCO3, and a compensatory ▲ in PaCO2. Development of persistence metabolic alkalosis requires both generation (an inciting cause) and maintenance ( a persistence impairment of the corrective renal response).

Primary increase in plasma HCO3- may be due to either HCO3- gain from alkali administration or, more commonly, excessive H+ loss. The latter results from the loss of H+ rich fluids, including upper GI secretions. Contraction alkalosis refers to the contraction of volume around a fixed content of bicarbonate.

Maintenance of metabolic alkalosis requires a concomitant impairment in renal HCO3- excretion, since the kidney normally has a large capacity to excrete HCO3-. This occurs as a result of a decreased GFR from impairment in renal HCO3- excretion or enhanced tubular HCO3- reabsorption from chloride depletion, volume contraction, and hypokalemia. Hypokalemia contributes to alkalosis by increasing tubular H+ secretion and Cl- wasting. A decrease in filtered chloride is sensed by the macula densa and as a result of tubuloglomerular feedback, reduces filtered HCO3 and stimulates aldosterone release. It also limits adaptive distal HCO3 secretion. Metabolic alkalosis is often described as being chloride responsive or chloride unresponsive.

• • Etiology: measuring the urinary chloride is the preferred method for assessing the renal response to circulating volume in patients with metabolic alkalosis. The cause of metabolic alkalosis can be divided into those associated with a decreased extracellular volume, or the posthypercapneic state (low urine chloride level), and those associated with normal or increased extracellular volume or recent diuretic use (normal or high urine chloride level)

    • Chloride responsive: urine chloride <20 mEq/L

      • Vomiting or prolonged NGT drainage

      • Pyloric stenosis

      • Villous adenoma

      • Cystic fibrosis

    • Laxative abuse

    • Diuretic use in the past

    • Post-hypercapnic states

    • Non-absorbable anions (PCN)

    • Antacids

    • Contraction alkalosis

  • Chloride unresponsive: urine chloride >20 mEq/L

    • Increased ECV

    • Severe Mg and K deficiency

    • Hypoparathyroidism

    • Increased mineralocorticoids (Cushing's synd, and primary alosteronism, renal artery stenosis, hypereninemic hyperaldosteronism), exogenous steroids

    • Current and recent diuretic use

    • Refeeding alkalosis

    • Licorice, chewing tobacco

    • Bartter's synd, Liddle's syndrome. Inherited defect in the thick ascending limb of loop of Henle w/ clinical features: Hypokalemia, metabolic alkalosis, and normal to low blood pressure.

• pH 7.50, PaCO2 of 48, HCO3 of 36. Pt. is alkalemic, the elevated HCO3 is the primary abnormality and the patient has a metabolic alkalosis with respiratory compensation.

• Respiratory compensation is hypoventilation, which will raise PaCO2 and pH. The respiratory compensation is limited by hypoxic drive. Usually, when PaCO2 rises to the high 40s or low 50s, hypoxic drive is stimulated to maintain a PaO2 >60 mm Hg.

• For every 1 mEq/L ▲ HCO3, the PaCO2 ▲ by 0.7 mm Hg, OR

  • Pa_CO2 = [HCO₃ ^-] + 15

    • Compare the calculated PaCO2 to actual measured PaCO2 on ABG.

    • If actual PaCO2 < PaCO2 calculated, then respiratory alkalosis coexists with metabolic alkalosis.

    • If actual PaCO2 > PaCO2 calculated, then respiratory acidosis coexists with metabolic alkalosis.

    • If actual PaCO2 = PaCO2, then only metabolic alkalosis exists.

  • Tx:

    • Mild metabolic alkalosis requires no treatment.

    • Correct the underlying cause

    • Chloride responsive metabolic alkalosis:

      • Hydration with isotonic NS

      • Hypokalemia and hypomagnesemia should be corrected.

    • Chloride unresponsive causes do not improve with administration of NaCl; in fact, it may be hazardous.

      • K+ sparing diuretics like amiloride or spironolactone for some form of hyperaldosteronism. Replete K+ deficit.

      • Alkalosis from excessive alkali administration will quickly resolve once the HCO3- load is withdrawn, assuming normal renal function.

      • Hypokalemia will perpetuate some degree of alkalosis regardless of other interventions. Potassium must, therefore, be repleted in all cases of metabolic alkalosis.

      • Acetazolamide may be useful if the alkalosis persists despite the above interventions, or if saline administration is limited by a patient's volume overload. This therapy promotes bicrabonaturia, although renal K+ loss is enhanced as well. Acetazolamide, 250 mg PO q6h x 4, or with a single dose of 500 mg.

      • Severe alkalemia (pH >7.7) with ECF volume excess and/or renal failure can be treated with isotonic (150 mEq/L) HCl administered via a central vein. The amount of HCl required can be calculated as: (0.5 x lean wt. in kg) x (HCO3-) - 24. Correction should occur over 8 - 24 hours.

RESPIRATORY ACIDOSIS. pH of 7.25, PaCO2 of 60, HCO3 of 26. This person is acidemic with an increased PaCO2 and a normal HCO3: a respiratory acidosis with no evidence of metabolic compensation.

Hypoventilation from any cause ▲ the PaCO2, and ▼ the serum pH. There is a compensatory ▲ in bicarbonate.

• • Etiology:

    • Lung: COPD, ILD, FBAO, PTx, pneumonia PE

    • Neuro: myasthenia gravis, muscular dystrophy, GB-syndrome, muscular dystrophy, increased ICP.

    • Botulism, tetanus, organophosphate poisoning

    • Narcotic overdose, general anesthesia, sleep apnea.

  • For Acute Resp Acidosis:

  • For every 10 mmHg increase in PaCO2 above normal (i.e., 40 mm Hg), pH decreases by 0.08 and HCO3- rises 1 mEq/L.

  • For Chronic Respiratory acidosis: pH of 7.34, PaCO2 of 60, HCO3 of 31. In this person both the PaCO2 and HCO3 are elevated, two abnormalities with opposite effects on pH. Which one is the primary abnormality and which is compensatory? Because the pH is lower than 7.40, the primary d/o is a respiratory acidosis. The elevated HCO3 indicates the metabolic compensation has occurred and that the acidosis is chronic.

    • In severe COPD, the presence of hypercapnia leads to a compensatory increase in serum bicarbonate. Significant hypercapnia may be present with and arterial pH close to normal; but will never be completely corrected.

  • Differentiating acute from chronic respiratory acidosis has important clinical implications. Acute respiratory acidosis is a medical emergency that may require emergent intubation and mechanical ventilation, whereas chronic respiratory acidosis is often clinically stable condition. Attention to the pH and HCO3 values will differentiate acute from chronic.

  • For every 10 mmHg increase in PaCO2 above normal, pH decreases by 0.03 and HCO3- rises by 4 mEq/L.

  • Tx:

    • Treat the underlying cause.

    • Mechanical hyperventilation

    • Renal compensation takes several days to develop fully.

ACUTE RESPIRATORY ALKALOSIS: Consider a patient with pH of 7.50, PaCO2: 29, HCO3 of 22. Because the patient is alkalemic, the low PaCO2 is a primary disturbance and a respiratory alkalosis is present. The lack of normal compensation-that is, the normal HCO3 indicates that the d/o is acute.

▲ in arterial pH, and hyperventilation resulting in ▼PaCO2 and compensatory ▼ in serum bicarbonate.

• • Etiology:

    • anxiety, pain, hyperventilation, shock, sepsis

    • CVA, tumors, fever, PE

    • Pregnancy, liver disease, hyperthyroidism, salicylates, pulmonary disease, catecholamine, progesterone, mechanical ventilation.

• For every 10 mmHg decrease in PaCO2 below normal, pH rises 0.08 and HCO3- lowers by 2 mEq/L.

CHRONIC RESPIRATORY ALKALOSIS: For every 10 mm Hg ▼ in PaCO2, the HCO3 ▼ by 4 mEq/L.

• Tx:

  • • Treat the underlying cause

    • Psychogenic hyperventilation may be treated by rebreathing from a paper bag.

Use of modified Henderson Hasselbach's to verify correct ABG values.

H+ = 24 x PaCO2 divided by HCO3-

Then, find the pH using the following formula:

H+ = (7.80 – pH)100

Venous blood gases can be used to estimate ABGs:

Venous bicarbonate + 2 = arterial bicarbonate

Venous PaCO2 - 6 = arterial PCO2

Venous pH + 0.04 = arterial pH

Maintenance of pH is essential for normal cellular functions. Three general mechansims exist to keep it within a narrow window:

• • Chemical buffering is mediated by HCO3- in the ECF and by protein and phosphate buffers in the ICF.

  • Alveolar ventilation minimizes variations in the pH by altering the pCO2.

  • Renal H+ handling allows the kidney to adapt to changes in acid-base status via HCO3- reabsorption and excretion of titratable acid (e.g., H2PO4) and NH4+

Acid base disorders are manifestations of underlying clinical d/o. Establishing a specific diagnosis is clinically important because treatment is best aimed at correcting the underlying cause of the acid-base abnormality rather than correcting the abnormality per se.

Summary.