Approach to Acid-Base Disorders Antonio Renato B. Herradura, M.D. F.P.C.P, F.P.C.C.P UERMMMC

Importance of Acid-Base Disorders Among the most common clinical problems encountered in hospitalized patients, especially ICU patients Lead to significant physiologic effects Proper management may be life-saving Pneumonia >>>>respiratory alkalosis; Diarrhea >>>>metabolic acidosis; persistent vomiting >>>>metabolic alkalosis Met acidosis >>>> predisposes to cardiac arrhythmias, pulmonary congestion; bone calcium loss (chronic) Respiratory acidosis >>>> transient increase ICP, headache, hypertension Resp alkalosis >>>> decreased ionized calcium >>>>sx of hypocalcemia

Acid – Base Disorders Principles of A-B homeostasis and disturbances Recognition of A-B disorders Specific disorders: common etiologies, pathogenesis, clinical features, general principles of management Interpretation of ABG and electrolyte results

Normal Arterial Blood Values pH: 7.35 - 7.45 pCO2: 35 - 45 mmHg HCO3: 22 – 26 mmol/L pO2, O2 saturation, base excess/deficit HCO3 is not measured but just calculated from H-H equation. A chemistry panel shows the [total CO2], [Cl-], [K+] and [Na+], [glucose], [BUN] and [creatinine]. Normal [H+] = 35-45 nmol/L or neq/L

Normal Arterial Blood Values pH: 7.35 - 7.45 pCO2: 35 - 45 mmHg HCO3: 22 – 26 mmol/L pO2, O2 saturation, base excess/deficit Chemistry panel: Sodium: 135 - 145 mmol/L Potassium: 3.5 - 5 mmol/L Chloride: 96 – 109 mmol/L Total CO2: 23 -30 mmol/L Glucose, BUN, Creatinine HCO3 is not measured but just calculated from H-H equation. A chemistry panel shows the [total CO2], [Cl-], [K+] and [Na+], [glucose], [BUN] and [creatinine]. Normal [H+] = 35-45 nmol/L or neq/L

Maintenance of blood pH pH = 6.1 + log [HCO3] (pCO2)(0.0301) Equation describes the relationship between blood pH, pCO2 and HCO3.

Maintenance of blood pH pH = 6.1 + log [HCO3] (pCO2)(0.0301) pH α [HCO3] pCO2 pH 1/α pCO2 (pCO2)(0.301) = [CO2] in mmoles/liter; May use the H-H equation to determine if the results are accurate

CO2 production ≈ pCO2 elimination Regulation of pCO2 CO2 production ≈ pCO2 elimination glucose metabolism ventilatory forces neural drive bellows apparatus airways The respiratory-neural drive system is the chief determinant of pCO2.

Regulation of plasma HCO3- Via kidneys: Reabsorption of filtered HCO3 Formation of titratable acid Excretion of NH4+ in urine

Maintenance of blood pH Maintenance of the ratio of HCO3 to pCO2 via compensatory responses by the kidneys and lungs

Maintenance of blood pH Maintenance of the ratio of HCO3 to pCO2 via compensatory responses by the kidneys and lungs Chemical buffering: includes HCO3, phosphates, proteins, hemoglobin, bone carbamates

Compensation for Acid – Base Disorders Primary metabolic Compensatory disturbance respiratory response HCO3 pH (met. acidosis) pCO2 HCO3 pH (met. alkalosis) pCO2

Compensation for Acid – Base Disorders Primary respiratory Compensatory disturbance metabolic response pCO2 pH (resp. alkalosis) HCO3 pCO2 pH (resp. acidosis) HCO3

Prediction of Compensatory Responses on Simple Acid - Base Disorders Primary Acid-Base Disorder Expected Range of Compensation Limits of Compensation Metabolic Acidosis PCO2 = 1.5[HCO3-] + 8 12-14 mm Hg Metabolic Alkalosis  PCO2 = 0.6 mm Hg for each 1 mEq/L  [HCO3-] 55 mm Hg Respiratory Acidosis  [HCO3-] = 1(acute) – 4 (chronic) mEq/L for each 10 mm Hg  PCO2 [HCO3-] = 45 mEq/L Respiratory Alkalosis  [HCO3-] = 2 (acute) -5 (chronic) mEq/L for each 10 mm Hg  PCO2 12-15 mEq/L Important rule: compensation is not complete. Compensation does not result in over correction of pH. Harrison: Resp Alk HCO3 increases by 4/10 pCO2

Acid–Base Nomogram

Anion Gap AG = Na+ - (Cl- + HCO3) Normal: 10 - 14 e.g. AG = 140 - (105 + 24) = 140 – 129 = 11 Represents those unmeasured anions in the plasma Increase in AG is due to increased in the amount of unmeasured anions, and less commonly due to a decrease in unmeasured cations Normal values: [Na+]: 135-145 mEq/L; [K+]: 3.5-5.0 mEq/L; [Cl-]: 96-109 mEq/L; [total CO2] :24-30 mEq/L If AG > 20 high AG metabolic acidosis is present regardless of the pH or HCO3.

Determinants of AG Unmeasured Anions Unmeasured Cations Albumin (15mEq/L) Calcium (5 mEq/L) Organic Acids (5 mEq/L) Potassium (4.5 mEq/L) Phosphate (2 mEq/L) Magnesium (1.5 mEq/L) Sulfate (1 mEq/L) ---------------------------- --------------------------- Total UA (23 mEq/L) Total UC (11 mEq/L) AG = UA – UC = 12 mEq/L AG represents those unmeasured anions in the plasma If albumin is decreased by 50%, AG = 4-5 mEq/L Increase in AG is due to increased in the amount of unmeasured anions, and less commonly due to a decrease in unmeasured cations If AG > 20 high AG metabolic acidosis is present regardless of the pH or HCO3.

Metabolic Acidosis PATHOGENESIS May be due to: Increased endogenous acid production (e.g. lactate and ketones) Loss of bicarbonate (e.g. diarrhea) Decreased excretion of endogenous acids (e.g. renal failure)

Common Causes of Metabolic Acidosis HIGH ANION GAP NORMAL ANION GAP Lactic Acidosis Diarrhea Ketoacidosis Isotonic saline infusion ESRD Early renal insufficiency Methanol ingestion RTA Ethylene glycol ingestion Acetazoleamide Salicylate toxicity Ureteroenterostomy NAG acidosis = hyperchloremic acidosis

Metabolic Acidosis CLINICAL EFFECTS Kussmaul breathing, dyspnea Headache, nausea, vomiting, confusion, stupor, coma Decreased myocardial contractility and response to catecholamine; peripheral vasodilatation with central venoconstriction predisposing to pulmonary edema; arrhythmias

Metabolic Acidosis MANAGEMENT Identify and treat underlying cause. Give alkali therapy (oral or i.v.) to patients with normal AG acidosis, mixed hyperchloremic and AG acidosis, and AG acidosis due to nonmetabolizable anion in the face of renal failure. Give modest quantities of i.v. alkali in patients with pure AG acidosis due to metabolizable organic acid anion Goal: increase pH to 7.15 or [HCO3] to 10 mEq/L

Metabolic Alkalosis PATHOGENESIS Due to net gain of HCO3 or loss of volatile acid (usually HCl by vomiting) 2 stages: GENERATIVE STAGE: loss of acid MAINTENANCE STAGE: failure of kidneys to compensation by excreting HCO3, because of volume contraction, low GFR, or depleted K+ or Cl- Addition of alkali is unusual

Metabolic Alkalosis CLINICAL EFFECTS increases the affinity of hemoglobin for oxygen ----- decrease tissue unloading Decreases ventilation Decreases ionized calcium ----- neuromuscular hyperirritability Supraventricular and ventricular arrhythmias

Metabolic Alkalosis MANAGEMENT Identify and correct the underlying stimulus for HCO3 generation Remove the factors that sustain HCO3 reabsorption (e.g. ECF contraction or hypoK+) Acetazoleamide Dilute 0.1N HCl or NH4Cl Hemodialysis

ETIOLOGY and PATHOGENESIS Respiratory Acidosis ETIOLOGY and PATHOGENESIS may be due to severe pulmonary disease (e.g. advanced COPD), respiratory muscle fatigue, or abnormalities in ventilatory control (e.g. stroke)

Respiratory Acidosis CLINICAL EFFECTS depends on severity and acuteness may be dyspneic or tachypneic Systemic vasodilation especially cerebral vasodilation ----- increased ICP ----- pseudotumor cerebri Myoclonic jerks, asterixis, tremors, restlessness, coma

Respiratory Acidosis MANAGEMENT Depends on severity and rate of onset May be life-threatening Measures to reverse underlying cause Restoration of adequate alveolar ventilation Avoid rapid correction of hypercapnea May need tracheal intubation and mechanical ventilation. Rapid correction of pCO2 may cause the same complications noted with acute respiratory alkalosis (e.g. cardiac arrhythmias, reduced cerebral perfusion, seizures)

Respiratory Alkalosis ETIOLOGY and PATHOGENESIS Develops when a sufficiently strong ventilatory stimulus causes CO2 output in the lungs to exceed its metabolic production in the tissues May be due to stimulation of CNS (e.g. pain, anxiety), peripheral chemoreceptors (e.g. hypoxemia 2o to pneumonia), chest receptors (e.g. PTE).

Respiratory Alkalosis CLINICAL EFFECTS Panic, weakness, and sense of impending doom Paresthesias about the hands and feet Trousseau’s and Chvostek’s signs Possible tetany, seizures

Respiratory Alkalosis MANAGEMENT Directed toward alleviation of underlying disorder Change in dead space, tidal volume and respiratory frequency, if on MV Re-breathing from paper bag during symptomatic attacks of hyperventilation syndrome

Interpretation of Acid - Base Disorders Determine if sample is arterial or venous. Compare HCO3 on ABG and electrolyte panel to verify accuracy Determine if pH or pCO2 are normal or abnormal. If any of above are abnormal determine primary A-B disturbance Compute for expected compensation to determine presence of mixed disorders. The HCO3 value on the ABG result should fall within 2 mmol/L of the measured [HCO3] or total CO2 on the electrolyte panel. The [total CO2] is the sum of the measured [CO2] + [HCO3-]. Thus the [HCO3-] from the blood gas and the [total CO2] from the electrolyte panel usually are within 2 mEq/L. Otherwise the measurements are in error or were taken at different times. If pH and pO2 are normal, check AG: if normal then normal A-B

Interpretation of Acid - Base Disorders Calculate the Anion Gap RULE: If AG > 20 high AG metabolic acidosis is present regardless of the pH or HCO3. Compare the change in AG (ΔAG) with change in HCO3 (ΔHCO3). RULE: If change (i.e. increase) in AG is < change( i.e. drop) in HCO3, there is combined high AG met acidosis and normal AG (hyperchloremic) acidosis. RULE: If ΔAG is > ΔHCO3, there is combined high AG metabolic acidosis and metabolic alkalosis. If AG > 20 high AG metabolic acidosis is present regardless of the pH or HCO3. ΔAG = patient’s AG – 10 (normal AG) ΔHCO3 = 24 (Normal HCO3) minus patient’s HCO3 If change (i.e. increase) in AG is < change( i.e. drop) in HCO3, there is combined high AG met acidosis and normal AG (hyperchloremic) acidosis. If ΔAG is > ΔHCO3, there is combined high AG metabolic acidosis and metabolic alkalosis.

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