[03] 20200708 acid base

1. Acid-Base
Core Review
2020.07.08
CCM F. 김하영

2. Principles
 Hydrogen Ion Concentration and pH
• pH= log(1/[H+])= - log[H+]
• pH= 7.40 (power of hydrogen), [H+]= 40(nEq/L)
 Normal range
• pH= 7.36-7.44 / PCO2= 36-44 mmHg / [HCO3
-]= 22-26 mEq/L
 Definition
• Acidemia: pH < 7.35 / Alkalemia: pH > 7.45
• Acidosis: [H+]↑/ Alkalosis: [H+]↓

3.  Henderson-Hasselbach Equation
• [H+]=24x(PCO2/[HCO3
-])
 Primary Acid-Base Disorders
– Respiratory Change of PCO2 [H+] change
 PCO2↑→ respiratory acidosis  HCO3↑
 PCO2↓→ respiratory alkalosis  HCO3↓
– Metabolic Change of HCO3 [H+] change
 HCO3↓→ metabolic acidosis  PCO2↓
 HCO3↑→ metabolic alkalosis  PCO2↑
Principles

4. Principles
 Secondary Acid-Base Disorders
– Response to Metabolic  Pulmonary
excretion CO2(Minute ventilation)
 Metabolic acidosis
: measured PaCO2 > expected PaCO2
 respiratory acidosis compensation
 Metabolic alkalosis
: not vigorous
– Response to Respiratory  Renal
excretion/formation HCO3(hours to days)
 Acute respiratory disorder
: Acute PaCO2 change have small effect on HCO3
 Chronic respiratory disorder
: Renal response to increase in PaCO2 is increase
HCO3 reabsorption in the proximal renal tubules

5.  Extracellular ion homeostasis
The Gaps

6.  Stewart method
• Changes in [H+] concentration or pH occur NOT as a result of how much [H+]
is added or removed BUT as a consequence of water dissociation in response
to change in [SID], PCO2 and weak acid.
• Actually, HCO3
- and H+ ions represent the effects rather than the causes of
acid-base derangements
 Strong ion differences(SID)
• SID= Na + K + Mg + Ca – (CL + lactate)
• SID + [H+] + [OH-] = 0
• SID + [H+] = 0 , SID = - [H+]
• Lactate↑  SID↓  pH ↓
The Gaps

7.  Stage I: Identify the Primary Acid-Base Disorder(PaCO2, pH)
• Rule1: PaCO2 and/or pH, not normal range  acid-base disorder
• Rule2: PaCO2 and pH, both abnormal  directional change
Rule2a: same direction  primary metabolic acid-base disorder
Ex) ABGA : 7.23(↓) - 23mmHg(↓) – 70mmHg – 21
Rule2b: opposite direction  primary respiratory acid-base disorder
Ex) ABGA : 7.23(↓) - 50mmHg(↑) – 70mmHg – 26
• Rule3: PaCO2 or pH, only one abnormal  mixed
Rule3a: PaCO2 abnormal  respiratory
• ↑PaCO2  respiratory acidosis  metabolic alkalosis (opposite disorder)
Ex) 7.4 – 50 – 70 – 28 (respiratory acidosis mixed with metabolic alkalosis)
• ↓PaCO2  respiratory alkalosis  metabolic acidosis
Acid-Base evaluation: Stepwise Approach

8. Rule3b: pH abnormal  metabolic
• ↓pH  metabolic acidosis  respiratory acidosis (same disorder)
Ex) 7.2 – 40 -70 – 18 (metabolic acidosis mixed with respiratory acidosis)
• ↑pH  metabolic alkalosis  respiratory alkalosis
 Stage II: Evaluate the Secondary Responses
• Additional acid-base disorder
• Rule4: primary metabolic disorder
PaCO2 measured > expected  secondary respiratory acidosis
PaCO2 measured < expected  secondary respiratory alkalosis
Ex) 7.32 – 23 -70 -16 / Expected PaCO2 =40-{1.2*(24-current HCO3)}=30.4
 primary metabolic acidosis with a secondary respiratory alkalosis
Acid-Base evaluation: Stepwise Approach

9. • Rule5: primary respiratory disorder  near-normal HCO3  acute
• Rule6: primary respiratory disorder  abnormal HCO3  chronic
Rule6a: chronic respiratory acidosis
• HCO3 measured < expected  incomplete renal response
• HCO3 measured > expected  secondary metabolic alkalosis
Rule6b: chronic respiratory alkalosis
• HCO3 measured > expected  incomplete renal response
• HCO3 measured < expected  secondary metabolic acidosis
Ex) 7.54 - 23 – 70 – 32 / Expected HCO3 =24+{0.4*(40-current PaCO2)}=31
 Stage III: Use The “Gaps” to Evaluate a Metabolic Acidosis
Acid-Base evaluation: Stepwise Approach

10.  The Anion Gap
• Rough estimate of the relative abundance of unmeasured anions
• Accumulation of non-violatile acids vs. primary loss of bicarbonate
 Determinants
• Na+UC=(Cl+HCO3)+UA
• Anion Gap = (Na+) – (Cl-) – (HCO3
-) = 12 mEq/L
Anion Gap

11.  High AG
• Lactic acidosis
• Ketone acidosis(DKA, AKA)
• ARF(loss of H+ secretion)
• Methanol(formic acid), Ethylene glycol(Oxalic acid), Salicylates(Salicylic
acid)
 Normal AG
• Diarrhea, saline infusion, early renal failure(loss of HCO3 resorption)
• HCO3 ↔ Cl
• Hyperchloremic metabolic acidosis
Anion Gap

12.  Albumin adjusted anion gap
- Weak acid, principal unmeasured anion
- Albumin 1g/dL ~ AG 3mEq/L
= [Na+] - [Cl-] - [HCO3
-] + 2.5 (4.2 – serum albumin) / Normal: 12 (8 ~ 16)
 Potassium adjusted anion gap
= [Na+] + [K+] – [Cl-] - [HCO3
-] / normal: 16 (12 ~ 20)
 Base excess
• calculated by a blood gas analyzer
• subtract the sodium chloride effect & albumin effect
• represent unmeasured anions
(lactate, ketones, uremic acids, toxic alcohols, or other toxins)
Other Anion Gap

13. Respiratory acidosis
 Elevated CO2
hypoventilation  decreased minute
ventilation
decreased lung function or mentation
 hypoxemia: headache, ischemic chest
pain, agitation, collapse
 hypercapnia: somnolence/obtundation
with cerebral vasodilation & increased
ICP

14. Respiratory alkalosis
 Hyperventilation
 Salicylate toxicity: classic syndrome of
tinnitus, hyperthermia, confusion
 Pregnant women hyperventilate
throughout gestation and normally have
a PaCO2 between 31 and 35 mm Hg
 The technique of using a paper bag to
cause re-breathing probably works
through the placebo effect rather than
by changes in PaCO2 and carries the
potential danger of inducing hypoxemia

15. Metabolic acidosis
 Anion Gap = (Na+) – (Cl-) – (HCO3
-) = 12 mEq/L
 The Gap-Gap Ratio
• High AG metabolic acidosis → detect another metabolic acid-base disorder
• AG Excess/HCO3 deficit=(AG-12)/(24-HCO3)
 Mixed Metabolic Acidosis
• gap-gap<1: High with normal AG metabolic acidosis or respiratory alkalosis
• gap-gap=1, △HCO3=△AG: High AG metabolic acidosis
Ex) DKA: gap-gap=1 → <1
 Metabolic Acidosis and Alkalosis
• Gap-gap>1: high AG metabolic acidosis + metabolic alkalosis
(common in ICU, nasogastric suction and diuretics)

16. Mixed acid-base disturbance
 Delta gap: △G = (AG-12) – (24-[HCO3
-])
• The difference between the deviation of AG from normal
the deviation of HCO3
- from normal
 High AG metabolic acidosis with
• Delta gap > +6  coexisting metabolic alkalosis
• Delta gap < -6  coexisting normal AG metabolic acidosis

17. High AG Metabolic acidosis
 Lactic acidosis
• condition with failure of cellular respiration
- shock, thiamine deficiency, high output HF,
Wernicke’s encephalopathy
- metformin, antiretroviral agent, epinephrine,
nitroprusside, linezolid
 Ketoacidosis
• condition with impaired glucose
metabolism
• ketosis d/t lipid/protein metabolism
 Toxic alcohol ingestion
• AG Metabolic acidosis with elevated
Osmolar Gap
(2[Na+]+[glucose/18]+[BUN/2.8])
 Renal failure
• Any condition reduces GFR
• unmeasured anions such as sulfate,
phosphate, urate, hippurate

18. Normal AG Metabolic acidosis
 Urine AG: (UNa+) – (UCl-) – (UHCO3-)
• Nagative UAG: Alkali loss
- GI loss
: diarrhea, enterostomy, pancreatic
/biliary diversion, ureterosigmoidostomy
- Renal loss
: proximal RTA(type 2 RTA)
- Hyperchloremia
: large volume N/S infusion
• Positive UAG
: Type 1,4 RTA, early kidney failure

19. Metabolic acidosis treatment
 Chronic metabolic acidosis
• [HCO3] 22-23 mmol/L
• NaHCO3 1~3g/day
 Acute metabolic acidosis
• Identification and treatment of the underlying cause (seizure, ongoing shock)
• NaHCO3 treatment
: < pH 7.2, < pH 7.1 + V/S unstable(in lactic acidosis, ketone acidosis)
- HCO3 deficit = 0.6 x BW x (15 – [HCO3]measured)
- Caution: Paradoxical CNS acidosis, Hypokalemia, Hypocalcemia, Hypernatremia,
Volume overload, Hyperosmolality, Overshoot alkalosis
- Bivon(sodium bicarbonate) 1@ 20mL: Na & HCO3 each 20mmol
: Bivon 7.5@ + 5DW  150mmol/L bicarbonate
- Endpoints of therapy include pH above 7.1 and [NaHCO3] above 10 mEq/L

20. Metabolic alkalosis
 Loss of gastric secretions /
vomiting
• H+ loss  Alkalosis (pH ↑)
• Cl- loss (major factor)
- HCO3
- reabsorption in Kidney
• HCO3
- production
• K+ loss
• Volume loss
 Treatment
• treatment of the underlying cause
• UCl-< 10mEq/L: Salt or N/S hydration
• HypoK correction

21. Reference
 Paul L. Marino, The ICU book, 4th edition, Wolters Kluwer
 Ron Walls, Rosen's Emergency Medicine, 9th edition, Elsevier
 Department of internal medicine, SNUH manual of medicine, 5th edition,
Seoul national university college of medicine
 Richard A. preston, Acid-Base, fluid and electrolytes, 2nd edition, 대한의학