Acid-Base Analysis Pediatric Critical Care Medicine Emory University Children’s Healthcare of Atlanta

Sources of acids H 2 O + dissolved CO 2 H 2 CO 3 Volatile acids Non-volatile acids Inorganic acid Organic acid Lactic acid Keto acid H + + HCO 3 -

Henderson-Hasselbalch pH = pK a + log [A - ] [HA] and pH = pK a + log [HCO 3 - ] = log [HCO 3 - ] s x PCO x PCO 2 H + + HCO 3 - H 2 CO 3 CO 2 + H 2 O Anion Gap [Na + ] = [CL - + HCO 3 - ] ~ 10-15

Acid-Base States Acidosis: pH<7.35 –Metabolic: increased acid or decreased in bicarb –Respiratory: increased PCO 2 Alkalosis: pH>7.45 –Metabolic: increased bicarb or loss of H + –Respiratory: decreased PCO 2

Compensation Acute: –Minutes –Respiratory: PCO 2 regulation Chronic –Hours to days –Renal: via regulation of bicarb excretion

Acidosis: Respiratory Decrease PCO 2 excretion via hypoventilation –Respiratory etiology –CNS pathology –Intoxication pH decreases 0.08 unit/10 mmHg increase in PaCO 2 Bicarb and base excess are normal

Acidosis: Metabolic Change in pH by increased in acid or decrease in bicarb Anion Gap Acidosis: MUD PILES M ethanol P araldehyde U remia I ron, isoniazid (INH) D iabetic ketoacidosis L actic acid E thanol, ethylene glycol S alicylates Non-Anion Gap Acidosis: USEDCARP U retorostomy C arbonic anhydrase inhibitors (acetazolamide) S mall bowel fistula A drenal insufficiency E xtra Chloride R TA D iarrhea P ancreatic fistula

Alkalosis: Respiratory Decrease in PCO 2 by hyperventilation Compensate by increase renal excretion of HCO 3 -

Alkalosis: Metabolic Increase in H + loss or increase in HCO 3 - PaCO 2 increase by 0.5-1/1 mEq/L of increase in HCO 3 -

Nomenclature

Partial Pressure

Atmosphere pCO 2 pO 2 alv extravascular fluid cells Capillary 4597 ~47 <39 <54~5 >55<1 systemic circulation

Cells ECF Endothelium RBC CO2 Dissolved CO2 = pCO2 5% 30% 65% CO 2 + Hb = HbCO 2 CO2 + H2O = HCO3 + H + CarboxyHgb Utilizes carbonic anhydrase CO 2 Transport

Excretion of CO 2 Metabolic rate determines how much CO 2 enters blood Lung function determines how much CO 2 excreted –minute ventilation –alveolar perfusion –blood CO 2 content

Hgb dissociation curve % Sat pO

Dissociation curve % Sat pO 2 Shifts

Alveolar oxygen equation Inspired oxygen = 760 x.21 = 160 torr Ideal alveolar oxygen = PAO 2 = [PB - PH 2 O] x FiO 2 - [PaCO 2 /RQ] = [ ] x [40/0.8] = [713] x [50] = 100 torr or 100 mmHg If perfect equilibrium, then alveolar oxygen equals arterial oxygen. ~5% shunt in normal lungs

Normal Oxygen Levels

Predicting ‘respiratory part’ of pH Determine difference between PaCO 2 and 40 torr, then move decimal place left 2, ie: IF PCO 2 76: = 36 x 1/2 = = 7.22 IF PCO 2 = 18: = = 7.62

Predicting metabolic component Determine ‘predicted’ pH Determine difference between predicted and actual pH 2/3 of that value is the base excess/deficit

Deficit examples If pH = 7.04, PCO 2 = 76 Predicted pH = = x 2/3 = 12 deficit If pH = 7.47, PCO 2 = 18 Predicted pH = = x 2/3 = 10 excess

Hypoxemia - etiology Decreased PAO 2 (alveolar oxygen) –Hypoventilation –Breathing FiO 2 <0.21 –Unde rventilated alveoli (low V/Q) Zero V/Q (true shunt) Decreased mixed venous oxygen content –Increased metabolic rate –Decreased cardiac output –Decreased arterial oxygen content

Blood gases PaCO 2 : pH relationship –For every 20 torr increase in PaCO 2, pH decreases by 0.10 –For every 10 torr decrease in PaCO 2, pH increases by 0.10 PaCO 2 : plasma bicarbonate relationship –PaCO 2 increase of 10 torr results in bicarbonate increasing by 1 mmol/L –Acute PaCO 2 decrease of 10 torr will decrease bicarb by 2 mmol/L

24 Sources of blood acids INFORMATION

25 Sources of blood acids INFORMATION