This document discusses acid-base homeostasis and disorders. It begins by outlining the physiology of acid-base balance, noting the roles of the respiratory, renal, and buffering systems in maintaining homeostasis. It then covers the four primary acid-base disorders: respiratory acidosis, metabolic acidosis, metabolic alkalosis, and respiratory alkalosis. The document provides frameworks for evaluating acid-base status using an arterial blood gas and for interpreting compensatory responses. Sample cases are presented and analyzed to demonstrate applying these evaluation frameworks in clinical scenarios.

1. Practical Acid Base
Hugo Carmona, MD
Division of Pulmonary, Critical Care and Sleep Medicine
University of Washington

2. Learning Objectives
• To discuss the physiology of acid-base homeostasis
• To explain the pathogenesis, risk factors, and clinical
manifestations of acid-base imbalances
• To build a framework for solving acid-base problems based on
history and lab data
There are many acid base disorders. This talk will not cover the underlying diseases
themselves in any great detail. We will instead build a framework for approaching
the problems.

3. Main principles of Acid-Base Homeostasis
• Cellular metabolism creates volatile and nonvolatile acids
• Volatile acid (Carbonic acid) is excreted by the lungs
• Nonvolatile acid (metabolic) is excreted by the kidneys: lactic acids
• Acids must be excreted to maintain homeostasis
• Buffers are the primary mechanism for maintaining pH balance
• Compensations in each system cause abnormalities in order to
maintain pH balance

4. Why does it matter to maintain homeostasis?
• Proper cell function, metabolism, protein function, salts,
• Cardiac, and brain activities

5. 3 Main Systems for Dealing with Acid/Base
Imbalance
• Buffers – immediate control
• Respiratory system – “delayed”
• Not as fast as buffer
• Renal system – delayed
• Can take days to compensate
Buffer
Renal
Respiratory

6. Commit these to memory!

7. 4 major primary disorders
• Respiratory acidosis
• Metabolic acidosis
• Metabolic alkalosis
• The above 3 co-exists
• Respiratory alkalosis
• You can not have resp alkalosis with resp acidosis

8. Introduction to buffering system
• Each buffer is a weak acid and a base
• Donates H+ when too alkalotic
• Receives H+ when too acidic
• Primary buffer – carbonic acid-bicarbonate (extracellular)
• Bicarbonate HCO3
- is weak alkalotic, CO2 is the acid
• Bicarbonate made in RBC (Carbonic Anhydrase), gastric parietal cells and
kidney
• Other buffers: Phosphate (intracellular, renal tubules), hemoglobin (RBC),
protein (intracellular, blood)

9. pH
• 20:1 ratio
bicarbonate:
carbonic acid
Acidemia pH < 7.35
Acidosis:
Respiratory CO2 > 45
Metabolic HCO3 <22
Alkalemia pH > 7.45
Alkalosis:
Respiratory CO2 < 35
Metabolic HCO3 >26

10. Respiratory System
• Respiratory system: eliminates volatile acid (H2CO3)
• Eliminate carbonic acid via CO2
• System adjusts ventilation (rate, depth = minute ventilation) to amount of
carbonic acid remaining
• Thus, if PaCO2 building up, carbonic acid is building up
Lungs

12. Renal System
• All other acids are nonvolatile = metabolic acids: lactic, keto,
phosphorus,
• Kidneys can excrete all metabolic acids (and cannot excrete volatile
acids)
• During normal excretion
• 1. distal tube secretes H+ -> acidify urine.
• 2. Phosphate and ammonia buffer to prevent over acidification
• Lots of acid? -> Lots of ammonia production
• 3. HCO3- (bicarbonate ion) reabsorbed to allow more blood buffering

15. pH
• 20:1 ratio
bicarbonate:
carbonic acid
Acidemia pH < 7.35
Acidosis:
Respiratory CO2 > 45
Metabolic HCO3 <22
Alkalemia pH > 7.45
Alkalosis:
Respiratory CO2 < 35
Metabolic HCO3 >26

16. Three Methods for Evaluating Acid Base
Disorders
• Base excess – using algorithms and charts (nomograms) to determine
amount of acid or base required to restore pH
• Often lab will calculate this for you
• Doesn’t identify co-existing metabolic disorders
• Physiochemical – Using PaCO2, SID, total nonvolatile weak acids
• Physiologic – Using HCO3 and anion gap
• Identifies four major disorders

17. Physiologic Method of Evaluating Acid Base
Disorder
• Henderson-Hasselbach Equation
• Isohydric principle = Acid is a H+ donor and base is a H+ acceptor
• Requires serum lab values and blood gas analysis
• Use this balance as a principle

18. How do you evaluate your patient’s acid base
status?
• Build a framework
• General appearance
• VS/RR
• Hx gathering
• CMP
• UA
• ABG
• pH
• Hco3-
• Co2
• Resp
• Kidney?
• GI?

19. Analyzing Acid-Base Status: A framework
• ABG: pH/PaCO2/PaO2/HCO3- (SEQUENCE!)
• Examine the pH and comparing it to the normal range
• Identify the primary process that led to the change in pH
• Calculate the serum anion gap
• Identify the compensatory process (if one is present)
• Identify if any other disorders are present or there is a mixed acid-
base process. (delta delta)
From A Luks. “A Primer on ABG Analysis”

21. From A Luks. “A Primer on ABG Analysis”

22. Some cases
• 7.26/58/60/25
• Respiratory acidosis; uncompensated
• 7.55/30/60/24
• Respiratory alkalosis; uncompensated
• 7.14/27/100/14
• Metabolic Acidosis, compensated
• 7.52/35/100/38
• Metabolic Alkalosis, trying compensated
From A Luks. “A Primer on ABG Analysis”

23. Reading an ABG
• pH/PaCO2/PaO2/HCO3-
• Examine the pH and comparing it to the normal range
• Identify the primary process that led to the change in pH
• Calculate the serum anion gap
• Identify the compensatory process (if one is present)
• Identify if any other disorders are present or there is a mixed acid-
base process. (delta delta)
From A Luks. “A Primer on ABG Analysis”

24. Serum Anion Gap
The serum AG
attempts to
capture
“unmeasured”
metabolic acids:
other acids that
was not
measured
Ajkdblog.org

25. Serum Anion Gap
• Anion gap = [Na+] – ([Cl-] + [HCO3])
• Adjust for serum albumin
• For every 1 pt drop in albumin, anion gap is likely about 3 pts larger
• In other words, a normal serum anion gap = serum albumin * 2.5
• Normal anion gap is usually about 10 +/- 2
Na
K
Cl
HCO3
BUN
Cr
Gluc

26. Calculate the anion gap
• AG: 140 – (100+28) = 12
• Normal AG = 5
• AG: 130 – (110+16) = 4
• Normal AG = 10
140
3.5
100
28
20
2.5
110
Albumin 2
130
3.5
110
16
20
1
110
Albumin 4

27. DDx of Anion-Gap Metabolic Acidosis (AGMA)
MUDPILES
• Methanol
• Uremia
• DKA
• Phenformin,paraldehyde
• INH
• Lactic acid
• Ethanole, ethylene glycol
• Salicylates
GOLDMARK
• Glycols (ethylene, propylene)
• Oxoproline
• L-Lactate
• D Lactate
• Methanol
• Aspirin
• Renal failure (uremia)
• Ketoacidosis

28. DDx of Non- Anion Gap Metabolic Acidosis
(NAGMA)
• Normal saline
• GI loss of bicarbonate – diarrhea, fistulas
• Renal Tubular Acidosis (RTA)
• Renal insufficiency / injury
• Ureteroileostomy

29. Generally AGMA
Generally NAGMA

30. Reading an ABG
• pH/PaCO2/PaO2/HCO3-
• Examine the pH and comparing it to the normal range
• Identify the primary process that led to the change in pH
• Calculate the serum anion gap
• Identify the compensatory process (if one is present)
• Identify if any other disorders are present or there is a mixed acid-
base process. (delta delta and serum osm gap)
From A Luks. “A Primer on ABG Analysis”

31. Break then Cases!
• What is/are the acid/base process(es) present? What is primary
process? If any, what are the compensatory processes?
• What is the differential diagnosis for this kind of disease?

32. Case 1
• 18 yo presents with abdominal pain, nausea, and confusion.
• Siblings were sick with a “stomach bug” for a few days beforehand
• Hasn’t been able to take any medication or eat due to nausea
132
5.5
80
14
45
1.5
425 ABG: 7.18/26/90/15
Albumin 4
Anion gap: 132 – (80+14) = 38

33. DDx of Anion-Gap Metabolic Acidosis (AGMA)
MUDPILES
• Methanol
• Uremia
• DKA
• Phenformin,paraldehyde
• INH
• Lactic acid
• Ethanole, ethylene glycol
• Salicylates
GOLDMARK
• Glycols (ethylene, propylene)
• Oxoproline
• L-Lactate
• D Lactate
• Methanol
• Aspirin
• Renal failure (uremia)
• Ketoacidosis

34. Metabolic Acidosis
• Increase in metabolic acid production or loss of base
• Signs and symptoms: headache, abdominal pain, CNS depression

36. Compensation?
Buffer Lungs
Compensatory loss

37. Case -1 Revisited. Is compensation
appropriate?
• Winter’s Formula: is the resp compensation in metabolic appropriate?
• PCO2=1.5 X[HCO3-]+8+/-2
• Even if the CO2 is low, the pt still has respiratory acidosis because the value is
over than what is expected

39. From A Luks. “A Primer on ABG Analysis”

40. Treatment entirely depends on cause

41. Case 2
• 70yo is found in their acute care room obtunded, with pinpoint pupils
and cyanosis
• They are POD1 s/p cholecystectomy
• They have no other medical problems
140
3.5
109
24
20
2
110 ABG: 7.15/90/53/24
Albumin 3
Anion gap: 140 – (109+24) = 7
Normal anion gap = 7.5

42. DDx of Respiratory Acidosis
PaCO2
Production
Elimination

43. Respiratory Acidosis
• Excessive carbonic acid
• S/sx include tachycardia, headache, neurologic abnormalities
(somnolence, blurred vision)

44. Respiratory Acidosis Compensation
• “Metabolic” compensation: Renal excretion of metabolic acids
• Requires days
• Loss of metabolic acids means more HCO3- around, restores pH
balance

45. Respiratory Acidosis Compensation

46. Case 3
• 19 yo presents presents with severe depression. They are admitted
for “medical clearance”
• In the morning, they have a rapid response for tachypnea with RR in
the 30s after the phlebotomist came in to take bloodwork
• They deny taking any medications
140
4
110
22
15
0.6
100
ABG: 7.49/26/110/23
Albumin 4
Anion gap: 140-(110+22)=8

47. DDx of Respiratory Alkalosis

48. Respiratory Alkalosis
• Deficit of carbonic acid
• S/sx: paresthesias, tetany, fainting (cerebral vasoconstriction)

49. Respiratory Alkalosis Compensation
• Decreased renal excretion of metabolic acids

50. Case 4
• That same patient is readmitted with a suspected suicide attempt.
• They were found outside, delirious, and tachpneic
• They have evidence of emesis on them
142
3.6
85
28
30
1
120
ABG: 7.46/55/105/28
Albumin 4
Anion gap: 142-(85+28) = 29

51. DDx of Metabolic Alkalosis

52. Metabolic Alkalosis
• Excessive base or loss of metabolic acid
• Stomach is a large reservoir of gastric acid
• S/sx: muscle weakness, hypokalemia, hypovolemia, parasthesia,
seizure

53. Metabolic Alkalosis Compensation
• Respiratory compensation – hypoventilation
• Usually incomplete compensation due to hypoxemic drive

54. Chronic Compensation for Metabolic Alkalosis

55. Mixed acid-base disorders
Metabolic Alkalosis
Metabolic Acidosis
Respiratory Acidosis
Respiratory Alkalosis

56. Questions?
Feedback is appreciated:
hcarmona@uw.edu