This document provides an overview of acid-base disorders and interpreting arterial blood gases (ABGs). It begins with a brief preview of the approach to ABGs, which involves checking pH, pCO2, selecting a compensation formula, determining appropriate compensation, and checking the anion gap and delta-delta ratios if needed. Expected changes in primary acid-base disorders are shown in a table. The document then discusses respiratory alkalosis and acidosis in more detail, including causes and expected physiological changes and compensation. Treatment approaches for respiratory alkalosis and acidosis are also summarized.

1. ABG series
ANAS SAHLE , MD
DAMASCUSE HOSPITAL

2. Acid-Base Disorders and the
ABG 6

3. BREIF PREVIEW

4. Summary of the Approach to
ABGs
1. Check the pH
2. Check the pCO2
3. Select the appropriate compensation formula
4. Determine if compensation is appropriate
5. Check the anion gap
AG=NA – (HCO3 + CL):12 4
6. If the anion gap is elevated, check the delta-delta
G:G Ratio =Δ AG (12-AG) Δ HCO3 (24-HCO3)
7. If a metabolic acidosis is present, check urine pH
8. Generate a differential diagnosis

5. EXPECTED CHANGES IN
ACID-BASE DISORDERS
Primary Disorder Expected Changes
Metabolic acidosis PCO2 = 1.5 × HCO3 + (8 ± 2)
Metabolic alkalosis PCO2 = 0.7 × HCO3 + (21 ± 2)
PCO2= 0.9 * HCO3 +16
Acute respiratory acidosis delta pH = 0.008 × (PCO2 - 40)
ΔHCO3 = 0.1 × (PCO2-40)
Chronic respiratory acidosis delta pH = 0.003 × (PCO2 - 40)
ΔHCO3 = 0.35 × (PCO2-40)
Acute respiratory alkalosis delta pH = 0.008 × (40 - PCO2)
ΔHCO3 = 0.2 × (40 – PCO2 )
Chronic respiratory alkalosis delta pH = 0.003 × (40 - PCO2)
ΔHCO3 2nd × (40 – PCO2)
From: THE ICU BOOK - = 0.4 Ed. (1998) [Corrected]

6. PH
PH>7,43 PH:7,37-7,43 PH<7,37
MIXED VS
ALKALOSIS NORMAL ACIDOSIS
PCO2>40 PCO2<40 PCO2<40 PCO2>40
M.AL R.AL M.AC R.AC

7. PCO2<36, RES.ALK+
HCO3<21 M.AC
PCO2>44, RES.AC +
PH(7,37-7,43)
HCO3>27 M.ALK
PCO2(nor),
M.AC +M.ALK
HCO3(nor)
AG

8. Respiratory system includes:
1. CNS (medulla)
2. Peripheral nervous system (phrenic nerve)
3. Respiratory muscles
4. Chest wall
5. Lung
6. Upper airway
7. Bronchial tree
8. Alveoli
9. Pulmonary vasculature

9. Potential causes of Respiratory Failure

10. RESPIRATORY
ACIDOSIS / ALKALOSIS
CO2 + H2O H2CO3 H+ + HCO3-
Respiratory Acidosis
Respiratory Alkalosis
10

11. RESPIRATORY ALKALOSIS

12. RESPIRATORY ALKALOSIS
Normal 20:1 ratio is increased
pH of blood is above 7.4
H2CO3 HCO3-
= 7.4
=
0.5
1 : 20
12

13. RESPIRATORY ALKALOSIS
Cause is Hyperventilation
Leads to eliminating excessive
amounts of CO2
Increased loss of CO2 from the lungs
at a rate faster than it is produced
Decrease in H+
CO2 CO2
CO2 CO2 CO2 CO2 CO2
CO2 CO2 CO2
CO2 CO2
13

14. HYPERVENTILATION
Hyper = “Over”
Elimination of CO2
H +
pH 14

15. RESPIRATORY ALKALOSIS
Can be the result of:
1) Anxiety, emotional
disturbances
2) Respiratory center
lesions
3) Fever
4) Salicylate poisoning
(overdose)
5) Assisted respiration
6) High altitude (low PO2)
15

16. RESPIRATORY ALKALOSIS
Anxiety is an emotional disturbance
The most common cause of
hyperventilation, and thus respiratory
alkalosis, is anxiety
Respiratory center lesions
Damage to brain centers responsible
for monitoring breathing rates
Tumors
Strokes
16

17. RESPIRATORY ALKALOSIS
Fever
Rapid shallow
breathing blows off
too much CO2
17

18. RESPIRATORY ALKALOSIS
Salicylate poisoning
(Aspirin overdose)
Ventilation is
stimulated without
regard to the status of
O2, CO2 or H+ in the
body fluids
18

19. RESPIRATORY ALKALOSIS
Assisted Respiration
Administration of CO2 in the exhaled
air of the care - giver
Your insurance won’t
cover a ventilator any
longer, so Bob here will be
giving you mouth to mouth
for the next several days
19

20. RESPIRATORY ALKALOSIS
High Altitude
Low concentrations of O2 in the arterial
blood reflexly stimulates ventilation in an
attempt to obtain more O2
Too much CO2 is “blown off” in the
process
20

21. Causes of Respiratory Alkalosis
CENTRAL RESPIRATORY STIMULATION
(Direct Stimulation of Resp Center):
Structural Causes Non Structural Causes
• Head trauma Pain
• Brain tumor Anxiety
• CVA Fever
• Voluntary
PERIPHERAL RESPIRATORY STIMULATION
(Hypoxemia  Reflex Stimulation of Resp Center via Peripheral Chemoreceptors)
• Pul V/Q imbalance
• Pul Diffusion Defects Hypotension
• Pul Shunts High Altitude

22. INTRATHORACIC STRUCTURAL CAUSES:
1. Reduced movement of chest wall & diaphragm
2. Reduced compliance of lungs
3. Irritative lesions of conducting airways
MIXED/UNKNOWN MECHANISMS:
1. Drugs – Salicylates Nicotine
Progesterone Thyroid hormone
Catecholamines
Xanthines (Aminophylline & related compounds)
2. Cirrhosis
3. Gram –ve Sepsis
4. Pregnancy
5. Heat exposure
6. Mechanical Ventilation

23. RESPIRATORY ALKALOSIS
Kidneys compensate by:
Retaining hydrogen ions
Increasing bicarbonate excretion
HCO3-
HCO3-
H +
H+
HCO3 -
HCO3-
H +
H+ H+
HCO3-
HCO - H
+
3
H+ HCO3-
HCO3- H+
HCO3-
H +
HCO3- H
+
H+
26

24. RESPIRATORY ALKALOSIS
Decreased CO2 in the lungs will
eventually slow the rate of breathing
Will permit a normal amount of
CO2 to be retained in the lung
27

25. RESPIRATORY ALKALOSIS
metabolic balance before onset of -
alkalosis
pH = 7.4-
respiratory alkalosis-
pH = 7.7-
- hyperactive breathing “ blows off ” CO2
- body’s compensation
- kidneys conserve H+ ions and eliminate
HCO3- in alkaline urine
- therapy required to restore metabolic
balance
- HCO3- ions replaced by Cl- ions
28

26. RESPIRATORY ALKALOSIS
H2CO3 : Carbonic Acid
HCO3- : Bicarbonate Ion
H2CO3 HCO3-
(Na+) HCO3-
(K+) HCO3-
1 : 20 (Mg++) HCO3-
(Ca++) HCO3-
metabolic balance before onset of alkalosis-
pH = 7.4-
29

27. RESPIRATORY ALKALOSIS
CO2
CO2 + H2O
0.5 : 20
respiratory alkalosis-
pH = 7.7-
hyperactive breathing “ blows off ” CO2-
30

28. RESPIRATORY ALKALOSIS
HCO3-
0.5 : 15
Alkaline Urine
BODY’S COMPENSATION
- kidneys conserve H+ ions and eliminate HCO3- in
alkaline urine31

29. RESPIRATORY ALKALOSIS
H2CO3 HCO3- Cl-
Chloride
containing
0.5 : 10 solution
- therapy required to restore metabolic balance
- HCO3- ions replaced by Cl- ions 32

30. RESPIRATORY ALKALOSIS
Usually the only treatment needed is to
slow down the rate of breathing
Breathing into a paper bag or holding
the breath as long as possible may help
raise the blood CO2 content as the
person breathes carbon dioxide
back in after breathing it out
33

31. Treatment of Respiratory Alkalosis
 Resp alkalosis by itself not a cause of resp
failure unless work of increased breathing
not sustained by resp muscles
 Rx underlying cause
 Usually extent of alkalemia produced not
dangerous.
 Admn of O2 if hypoxaemia
 If pH>7.55 pt may be sedated/anesthetised/
paralysed and/or put on MV.

32. RESPIRATORY ACIDOSIS
39

33. RESPIRATORY ACIDOSIS
Caused by hyperkapnia due to
hypoventilation
Characterized by a pH decrease
and an increase in CO2
pH
CO2 CO
CO2 CO2
CO CO2
2 CO2
COCO2
2 CO2 CO2
pH CO2
CO2
40

34. HYPOVENTILATION
Hypo = “Under”
Elimination of CO2
H +
pH 41

35. RESPIRATORY ACIDOSIS
The speed and depth of breathing control the
amount of CO2 in the blood
Normally when CO2 builds up, the pH of the
blood falls and the blood becomes acidic
High levels of CO2 in the blood stimulate the
parts of the brain that regulate breathing,
which in turn stimulate faster and deeper
breathing
44

36. RESPIRATORY ACIDOSIS
Respiratory acidosis
develops when the
lungs don't expel CO2
adequately
This can happen in
diseases that severely
affect the lungs, such
as emphysema, chronic
bronchitis, severe
pneumonia, pulmonary
edema, and asthma
45

37. RESPIRATORY ACIDOSIS
Respiratory acidosis can also develop when
diseases of the nerves or muscles of the chest
impair the mechanics of breathing
In addition, a person can develop respiratory
acidosis if overly sedated from narcotics and
strong sleeping medications that slow
respiration
46

38. RESPIRATORY ACIDOSIS
The treatment of respiratory acidosis
aims to improve the function of the lungs
Drugs to improve breathing may help
people who have lung diseases such as
asthma and emphysema
47

39. RESPIRATORY ACIDOSIS
Decreased CO2 removal
can be the result of:
1) Obstruction of air
passages
2) Decreased respiration
(depression of
respiratory centers)
3) Decreased gas
exchange between
pulmonary capillaries
and air spacs of lungs
4) Collapse of lung
48

40. RESPIRATORY ACIDOSIS
1) Obstruction of air passages
Vomit, anaphylaxis, tracheal cancer
49

41. RESPIRATORY ACIDOSIS
2) Decreased Respiration
Shallow, slow breathing
Depression of the respiratory centers in the
brain which control breathing rates
Drug overdose
50

42. RESPIRATORY ACIDOSIS
3) Decreased
gas exchange
between
pulmonary
capillaries and
air sacs of lungs
Emphysema
Bronchitis
Pulmonary
edema
51

43. RESPIRATORY ACIDOSIS
4) Collapse of lung
Compression injury, open thoracic
wound
Left lung
collapsed
52

44. Causes of
Acute Respiratory Acidosis
EXCRETORY COMPONENT PROBLEMS:
1. Perfusion:
Massive PTE
Cardiac Arrest
2. Ventilation:
Severe pul edema
Severe pneumonia
ARDS
Airway obstruction
3. Restriction of lung/thorax:
Flail chest
Pneumothorax
Hemothorax

45. 4. Muscular defects:
Severe hypokalemia
Myasthenic crisis
5. Failure of Mechanical Ventilator
CONTROL COMPONENT PROBLEMS:
1. CNS: CSA
Drugs (Anesthetics, Sedatives)
Trauma
Stroke
2. Spinal Cord & Peripheral Nerves:
Cervical Cord injury LGBS
Neurotoxins (Botulism, Tetanus, OPC)
Drugs causing Sk. m.paralysis (SCh, Curare,
Pancuronium & allied drugs, aminoglycosides)

46. Causes of
Chronic Respiratory Acidosis
EXCRETORY COMPONENT PROBLEMS:
1. Ventilation:
COPD
Advanced ILD
 Restriction of thorax/chest wall:
Kyphoscoliosis, Arthritis
Fibrothorax
Hydrothorax
Muscular dystrophy
Polymyositis

47. CONTROL COMPONENT PROBLEMS:
1. CNS: Obesity Hypoventilation Syndrome
Tumours
Brainstem infarcts
Myxedema
Ch sedative abuse
Bulbar Poliomyelitis
2. Spinal Cord & Peripheral Nerves:
Poliomyelitis
Multiple Sclerosis
ALS
Diaphragmatic paralysis

48. RESPIRATORY ACIDOSIS
metabolic balance before onset of -
acidosis
pH = 7.4-
respiratory acidosis-
pH = 7.1-
breathing is suppressed holding CO2 in -
body
body’s compensation-
kidneys conserve HCO3- ions to restore -
the normal 40:2 ratio
kidneys eliminate H+ ion in acidic urine-
- therapy required to restore metabolic
balance
- lactate solution used in therapy is
40
converted to bicarbonate ions in the liver
59

49. RESPIRATORY ACIDOSIS
H2CO3 : Carbonic Acid
HCO3- : Bicarbonate Ion
H2CO3 HCO3-
(Na+) HCO3-
(K+) HCO3-
1 : 20 (Mg++) HCO3-
(Ca++) HCO3-
- metabolic balance before onset of acidosis
- pH = 7.4
60

50. RESPIRATORY ACIDOSIS
CO2 CO2
CO2
CO2
2 : 20
breathing is suppressed holding CO2 in body-
pH = 7.1-
61

51. RESPIRATORY ACIDOSIS
H2CO3
HCO3-
HCO3-
+
H+
2 : 30
acidic urine
BODY’S COMPENSATION
kidneys conserve HCO3- ions to restore the -
normal 40:2 ratio (20:1)
kidneys eliminate H+ ion in acidic urine-
62

52. RESPIRATORY ACIDOSIS
Lactate
H2CO3 HCO3- LIVER
Lactate
HCO3-
2 : 40
- therapy required to restore metabolic balance
- lactate solution used in therapy is converted to
bicarbonate ions in the liver 63

53. TREATMENT OF
RESPIRATORY ACIDOSIS
 The goal is to increase the exhalation of
CO2. The treatments are :
– Based on the underlying causes
– By providing ventilation therapy
– Intravenous administration of HCO3-
– Reversal of sedation or neuromuscular
relaxants
– Intubation and artificial ventilation (in severe
cases)

54. CASE -1
 A 28 year old woman was admitted electively to a
HDU (high dependency unit) following a caesarian
section.
 A diagnosis of 'fatty liver of pregnancy' had been
made preoperatively.
 She was commenced on a continuous morphine
infusion at 5 mg/hr and received oxygen by mask.
 This was continued overnight and she was noted to
be quite drowsy the next day. ABG
 Arterial blood gases were PH 7,16
PCO2 61,9
PO2 115
HCO3 21,2

55. • ACIDOSIS
PH<7,37
• RESPIRATORY
PCO2>40
• ∆HCO3=0,1(62- 40)=2,2(+24)
• 26,2 ≠21
ACUTE.R.AC • concomitant M.AC
COMP
AG=? • ???
Normal AG (12 4)

56. CASE-2
A 69 year old patient had a cardiac arrest
soon after return to the ward following an
operation.
Resuscitation was commenced and
included intubation and ventilation.
Femoral arterial blood gases were
collected about five minutes after the
arrest.

57. LAB :
Anion gap 24,
Lactate 12 mmol/l.
ABG
PH 6,85
PCO2 82
PO2 214
HCO3 14

58. PH<7,37 • ACIDOSIS
PCO2>40 • RESPIRATORY
• ∆HCO3=0,1(82- 40)=4,2 (+24)
ACUTE.R.AC • 28,2 ≠14
• concomitant M.AC
COMP
AG=24 • High AG M.AC
Normal AG (12 4)
• NO other metabolic disorders
GAP:gap=1,2

59. Discussion
Cardiac arrest with low cardiac output and tissue
hypo-perfusion causing a:
– severe lactic acidosis.
Ventilation is depressed causing a:
– respiratory acidosis.
Inadequate ventilation in this pre-arrest phase may
have been related to several factors, in particular :
– inadequate reversal of neuromuscular paralysis,
– airway obstruction in a supine sedated patient or
– acute pulmonary oedema.

60. CASE-3
A 70 year old man was admitted with severe
congestive cardiac failure.
He has been unwell for about a week and
has been vomiting for the previous 5 days.
He was on no medication.
He was hyperventilating and was very
distressed.
Admission biochemistry is listed below.
He was on high concentration oxygen by
mask.

61. LAB:
BIOCHEMISTRY ABG
NA 127 PH 7,58
K 5,2 PCO2 21
CL 79 PO2 154
HCO3 20 HCO3 19
UREA 50,5 mmoll
CREAT 0,38 mmoll
GLUCO 9,5 mmoll
AG 33
Creat = 5 mgdl (0,075) Urea =141,4 (0,357)
cNA=128 Glucose =171 (*18)
Corrected Sodium = Measured sodium + 0.016 * (Serum glucose - 100)

62. PH>7,43 • ALKALOSIS
PCO2<40 • RESPIRATORY
• ∆HCO3=0,4(40 -21)=24 – 7,6
C,R .ALK • 16,4 ≠19
• concomitant M.ALK
COMP
AG=28 • HIGH AG M.AC
Normal AG (12 4)
GAP:gap • concomitant M.ALK
(=4 >2)

63. Discussion
The history suggests the following
possibilities:
Respiratory alkalosis in response to the dyspnoea
associate with the congestive heart failure
A lactic acidosis is possible if cardiac output is low
and tissue perfusion is poor
Vomiting suggests metabolic alkalosis
The renal failure could be associated with
a high anion gap acidosis

64. Discussion
This patient has a triple acid-base
disorder:
Acute metabolic acidosis probably due to renal
failure (?prerenal failure) and possibly to lactic
acidosis (hypoperfusion due heart failure and
hypovolaemia)
Metabolic alkalosis due to severe vomiting
Respiratory alkalosis due to dyspnoea from
congestive heart failure.
The pO2 is elevated due to administration
of a high inspired oxygen concentration

65. NEXT LECTURE
1. Approche to hypoxiemic patient
2. Cases