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

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

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

Maintenance of blood pH

pH = 6.1 + log [HCO3]

(pCO2)(0.0301)

Maintenance of blood pH

pH = 6.1 + log [HCO3]

(pCO2)(0.0301)

pH α [HCO3]

pCO2

pH α [HCO3]

pH 1/α pCO2

Regulation of pCO2

CO2 production ≈ pCO2 elimination

glucose metabolism ventilatory forces

neural drive bellows apparatus

airways

Regulation of plasma HCO3-

• Via kidneys:1. Reabsorption of filtered HCO3

2. Formation of titratable acid

3. 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

PCO2 =

12-14 mm Hg

Metabolic Alkalosis

PCO2 =

0.6 mm Hg for each 1 mEq/L [HCO3

-]

PCO2 =

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

[HCO3-] =

12-15 mEq/L

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

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

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

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-

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

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

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.

Interpretation of Acid - Base Disorders

• Calculate the Anion GapRULE: 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.

Thank you for your attention!

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