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

2. 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

3. 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

4. Normal Arterial Blood Values
pH:
pCO2: 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+] = nmol/L or neq/L

5. Normal Arterial Blood Values
pH:
pCO2: mmHg
HCO3: 22 – 26 mmol/L
pO2, O2 saturation, base excess/deficit
Chemistry panel:
Sodium: mmol/L Potassium: mmol/L
Chloride: 96 – 109 mmol/L Total CO2: 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+] = nmol/L or neq/L

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

7. Maintenance of blood pH
pH = 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

8. 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.

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

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

11. 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

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

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

14. 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

15. Acid–Base Nomogram

16. Anion Gap AG = Na+ - (Cl- + HCO3) Normal: 10 - 14
e.g. AG = ( ) = 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+]: mEq/L; [K+]: mEq/L; [Cl-]: mEq/L; [total CO2] :24-30 mEq/L
If AG > 20 high AG metabolic acidosis is present regardless of the pH or HCO3.

17. 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.

18. 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)

19. 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

20. 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

21. 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

22. 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

23. 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

24. 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

25. 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)

26. 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

27. 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)

28. 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).

29. 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

30. 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

31. 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

32. 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.

33. Thank you for your attention!
Have a nice day!