PowerPoint presentation on Acid Base Balance including ABG analysis by Dr.Tinku Joseph

1. ACID BASE BALANCE
DR TINKU JOSEPH
DM Resident
Department of Pulmonary Medicine
AIMS, Kochin
Email ID-: tinkujoseph2010@gmail.com
Life is a struggle, not against sin, not against Money Power . . but against hydrogen ions.
--H.L. Mencken

2. OVERVIEW OF DISCUSSION
 Basics of acid-base
balance.
 Role of Renal/Respiratory
system in acid-base
homeostasis.
 Step-wise approach in
diagnosis of acid-base
disorders.
 Some practical examples

3. Acid Base Balance
 The body produces acids daily
 15,000 mmol CO2
 50-100 mEq Nonvolatile acids
 The primary source is from metabolism of sulfur containing
amino acids (cystine, methionine) and resultant formation
of sulfuric acid.
 Other sources are non metabolized organic acids,
phosphoric acid, lactic acid, citric acid.
 The lungs and kidneys attempt to maintain balance

4. Respiratory Regulation
• 10-12 mol/day CO2 is accumulated
and is transported to the lungs as
Hb-generated HCO3 and Hb-bound
carbamino compounds where it is
freely excreted.
H2 O + CO2 ↔H2 CO3 ↔H+ + HCO3
-
• Accumulation/loss of Co2 changes
pH within minutes

5. Respiratory Regulation
 Balance affected by neurorespiratory control of
ventilation.
 During Acidosis, chemoreceptors sense ↓pH and
trigger ventilation decreasing pCO2.
 Response to alkalosis is biphasic. Initial
hyperventilation to remove excess pCO2 followed
by suppression to increase pCO2 to return pH to
normal

6. Renal Regulation
 Kidneys are the ultimate defense against the
addition of non-volatile acid/alkali
 Kidneys play a role in the maintenance of this HCO3¯
by:
– Conservation of filtered HCO3 ¯
– Regeneration of HCO3 ¯
 Kidneys balance nonvolatile acid generation
during metabolism by excreting acid.

7. Renal Regulation
• Renal Excretion of acid –
combining hydrogen
ions with either urinary
buffers to form titrable
acid. eg: Phosphate,
urate, ammonia

8. Acid Base Status
• Assessment of status via
bicarbonate-carbon dioxide
buffer system in blood.
– CO2 + H2O <--> H2CO3 <-->
HCO3
- + H+
– Henderson-Hasselbach
equation
– PH = 6.10 + log ([HCO3] /
[0.03 x PCO2])

9. DEFINITIONS AND TERMINOLOGY
3 Component Terminology
 Acidosis/Alkalosis
 Respiratory/Metabolic
 Compensated/Uncompensated

10. Basic terminology
• pH – signifies free hydrogen ion concentration. pH is
inversely related to H+ ion concentration.
• Acid – a substance that can donate H+ ion, i.e. lowers pH.
• Base –a substance that can accept H+ ion, i.e. raises pH.
• Anion – an ion with negative charge.
• Cation – an ion with positive charge.
• Acidemia – blood pH< 7.35 with increased H+ concentration.
• Alkalemia – blood pH>7.45 with decreased H+
concentration.
• Acidosis – Abnormal process or disease which reduces pH
due to increase in acid or decrease in alkali.
• Alkalosis – Abnormal process or disease which increases pH
due to decrease in acid or increase in alkali.

11. Assessment of acid base balance
ABG-: pH, PaO2, PaCO2, SaO2, HCO3. Complete and objective overview of respiratory
physiology

12. The pulse-oxymeter or saturation
meter
 Non invasive measurement
 Finger probes and ear probes
 Percutaneous measurements

13. Pulse Oximeter Sensor
 Two LEDs emit red and infrared
wavelengths of light through skin
 Hb absorbs red wavelengths
HbO2 absorbs infrared wavelengths
 Photodetector on other side picks up
intensity of transmitted light
 SpO2 is calculated by analyzing received
light
 Utilizes cardiac pulse to distinguish arterial
blood from other mediums

14. Pulse Oximetry Board
 Low power
 Data outputs: SpO2 and pulse
rate
 Eight second average (or
 instantaneous)
 Serial communication

15. Pulse Oximetry
FALSE HIGH RESULTS
• Carbon monoxide
intoxication (heavy smoker)
• Strong lights
• UV lights (anti bacterial)
• Infra red light (neonatal
ICU)
FALSE LOW RESULTS
• Vascular disease
(extremities)
• Movements of the fingers
• Nail polish
• High bilirubinemia
• Detector obstructions
• Wrong placement of the
probe
• Blood pressure
fluctuations

16. Why Order an ABG?
 Aids in establishing a
diagnosis
 Helps guide treatment plan
 Aids in ventilator
management
 Improvement in acid/base
management allows for
optimal function of
medications
 Acid/base status may alter
electrolyte levels critical to
patient status/care.
 Pre operative fitness.

17. Logistics
• Where to place -- the options
– Radial
– Femoral
– Brachial
– Dorsalis Pedis
– Axillary
• When to order an arterial line --
– Need for continuous BP monitoring
– Need for multiple ABGs

18. Technical Errors
• TYPE OF SYRINGE - Glass vs. plastic syringe:
 pH & PCO2 values unaffected
 PO2 values drop more rapidly in plastic syringes (ONLY if
PO2 > 400 mm Hg)
 Other adv of glass syringes:
Min friction of barrel with syringe wall
Usually no need to ‘pull back’ barrel – less
chance of air bubbles entering syringe
Small air bubbles adhere to sides of plastic
syringes – difficult to expel
Though glass syringes preferred, differences usually not
of clinical significance  plastic syringes can be and
continue to be used

19. Technical Errors
•Excessive Heparin
Dilutional effect on results  HCO3
- & PaCO2
Syringe be emptied of heparin after flushing
Risk of alteration of results  with:
1) size of syringe/needle
2) vol of sample
25% lower values if 1ml sample taken in 10
ml syringe (0.25 ml heparin in needle)
Syringes must be > 50% full with blood
sample

20. Technical Errors
Hyperventilation or Breathholding
 May lead to erroneous lab results
Air bubbles
 PO2 150 mmHg & PCO2 0 mm Hg in air bubble.
 Mixing with sample lead to  PaO2 &  PaCO2
 Mixing/Agitation  diffusion  more erroneous results
 Discard sample if excessive air bubbles
 Seal with cork/cap after taking sample
Fever or Hypothermia
 Most ABG analyzers report data at N body temp
 If severe hyper/hypothermia, values of pH & PCO2 at 37 C
can be significantly diff from pt’s actual values
 Changes in PO2 values with temp predictable

21. Technical Errors
 Values other than pH & PCO2 do not change with
temp
 Hansen JE, Clinics in Chest Med 10(2), 1989 227-237
 Some analysers calculate values at both 37C and pt’s
temp automatically if entered
 Pt’s temp should be mentioned while sending
sample & lab should mention whether values being
given in report at 37 C/pts actual temp

22. Technical Errors
 WBC COUNT
0.1 ml of O2 consumed/dL of blood in 10 min in pts
with N TLC
Marked increase in pts with very high TLC/plt
counts – hence chilling/analysis essential

23. Venous Sample
 Only the person who has drawn the sample can tell if
he has drawn a pulsating blood’ OR blood under
high pressure
 PaO2 < 40
 Partly mixed sample- Difficult to recognize
ARTERIAL VENOUS
pH 7.38-7.42 7.36-7.39
PaO2 80-100 38-42
PaCO2 36-44 44-48
HCO3 22-26 20-24
SaO2 95-100 75
CENTRAL VENOUS
7.37-7.40
50-54
45-49
22-26
78

24. Acid Base Disorders
The primary disorders:
• Respiratory Acidosis
– Acute
– Chronic
• Respiratory Alkalosis
– Acute
– Chronic
• Metabolic Acidosis
• Metabolic Alkalosis

25. Acid Base Disorders
Acidosis/Alkalosis:
Any process that tends to
increase/decrease pH
• Metabolic: Primarily affects
Bicarbonate
• Respiratory: Primarily affects
PaCO2
Acidemia/Alkalemia:
Net effect of all primary and
compensatory changes on
arterial blood pH.

26. Normal ABG values
pH 7.35 - 7.45
PaCO2 35 - 45 mm Hg
PaO2 70 - 100 mm Hg
SaO2 93 - 98%
HCO3
¯ 22 - 26 mEq/L
Base excess -2.0 to 2.0
mEq/L
----- XXXX Diagnostics ------
Blood Gas Report
248 05:36 Jul 22 2000
Pt ID 2570 / 00
Measured 37.0
o
C
pH 7.463
pCO2 44.4 mm Hg
pO2 113.2 mm Hg
Corrected 38.6
o
C
pH 7.439
pCO2 47.6 mm Hg
pO2 123.5 mm Hg
Calculated Data
TPCO2 49
HCO3 act 31.1 mmol / L
HCO3 std 30.5 mmol / L
BE 6.6 mmol / L
O2 CT 14.7 mL / dl
O2 Sat 98.3 %
ct CO2 32.4 mmol / L
pO2 (A - a) 32.2 mm Hg
pO2 (a / A) 0.79
Entered Data
Temp 38.6 oC
ct Hb 10.5 g/dl
FiO2 30.0 %
Measured values should be considered
And
Corrected values should be discarded

27. The
Habits of
Highly
Successful
Blood Gas
ABG Interpretation Analysts

28. Step 1
Look at the pH
Is the patient acidemic pH < 7.35
or alkalemic pH > 7.45

29. • Step 2
• Is it a metabolic or respiratory disturbance ?
• Acidemia: With HCO3 < 20 mmol/L = metabolic
• With PCO2 >45 mm hg = respiratory
• Alkalemia:With HCO3 >28 mmol/L = metabolic
• With PCO2 <35 mm Hg = respiratory

30. Step 3
If there is a primary respiratory disturbance, is
it acute?
Expect D pH = 0.08 x D PCO2 / 10
• Step 4
• For a respiratory disorder is renal compensation OK?
• Respiratory acidosis: <24 hrs: D [HCO3] = 1/10 D PCO2
• >24 hrs: D [HCO3] = 3/10 D PCO2
• Respiratory alkalosis:1- 2 hrs: D [HCO3] = 2/10 D PCO2
• >2 days: D [HCO3] = 6/10 D PCO2

31. Primary disorder Primary defect Compensatory
response
Respiratory acidosis ↑ PCO2 ↑ HCO3
Respiratory Alkalosis ↓ PCO2 ↓ HCO3

32. • Step 5
• If the disturbance is metabolic is the respiratory
compensation appropriate?
• For metabolic acidosis:
Expect PCO2 = (1.5 x [HCO3]) + 8 + 2
• (Winter’s equation)
• For metabolic alkalosis:
• Expect PCO2 = (0.7 x [HCO3]) + 21 + 1.5
• If not:
• actual PCO2 > expected : hidden respiratory acidosis
• actual PCO2 < expected : hidden respiratory alkalosis

33. Primary disorder Primary defect Compensatory response
Metabolic Acidosis ↓ HCO3 ↓ PCO2
Metabolic alkalosis ↑ HCO3 ↑ PCO2

34. During compensation HCO3¯ & PaCO2
move in the same direction

35. Respiratory
compensation
is always FAST …12-24
hrs
Metabolic compensation
• is always SLOW...5 -7
days

36. • Step 6
• If there is metabolic acidosis, is there an anion gap?
• Na - (Cl-+ HCO3
-) = Anion Gap usually <12
• Normal AG -: (loss of HC03, increase in chloride) – Diarrhoea,
RTA, carbonic anhydrase inhibitor use.
• High AG-: If >12, Anion Gap Acidosis : Methanol
• (Decreased excretion of acids) Uremia
• Diabetic Ketoacidosis
• Paraldehyde
• Infection (lactic acid)
• Ethylene Glycol
• Salicylate

37. • Step 7
• Does the anion gap explain the change in bicarbonate?
• (to rule out co-existence of 2 acid-base disorders)
• D anion gap (Anion gap -12) Delta Gap
• Delta Gap + [HCO3] = 22-26 mmols/l
• If Delta anion gap is greater(>26); consider additional
metabolic alkalosis
• If D anion gap is less(<22); consider additional nonanion gap
metabolic acidosis

38. RESPIRATORY ALKALOSIS

39. 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

40. • 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

41. Manifestations of Resp Alkalosis
• NEUROMUSCULAR: Related to cerebral A
vasoconstriction &  Cerebral BF
1. Lightheadedness
2. Confusion
3. Decreased intellectual function
4. Syncope
5. Seizures
6. Paraesthesias (circumoral, extremities)
7. Muscle twitching, cramps, tetany
8. Hyperreflexia
9. Strokes in pts with sickle cell disease

42. • CARDIOVASCULAR: Related to coronary
vasoconstriction
1. Tachycardia
2. Angina
3. ECG changes (ST depression)
4. Ventricular arrythmias
• GASTROINTESTINAL: Nausea & Vomitting (cerebral
hypoxia)
• BIOCHEMICAL ABNORMALITIES:
3-
 CO2 PO4
Cl-  Ca2+

44. Homeostatic Response to Resp Alkalosis
 In ac resp alkalosis, imm response to fall in CO2 (&
H2CO3)  release of H+ by blood and tissue buffers 
react with HCO3-  fall in HCO3- (usually not less
than 18) and fall in pH
 Cellular uptake of HCO3- in exchange for Cl-
 Steady state in 15 min - persists for 6 hrs
 After 6 hrs kidneys increase excretion of HCO3-
(usually not less than 12-14)
 Steady state reached in 11/2 to 3 days.
 Timing of onset of hypocapnia usually not known
except for pts on MV. Hence progression to subac and
ch resp alkalosis indistinct in clinical practice

45. 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.

46. RESPIRATORY ACIDOSIS

47. 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

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

49. 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

50. Causes of Chronic Respiratory Acidosis
• 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

51. Manifestations of Resp Acidosis
• NEUROMUSCULAR: Related to cerebral A
vasodilatation &  Cerebral BF
1. Anxiety
2. Asterixis
3. Lethargy, Stupor, Coma
4. Delirium
5. Seizures
6. Headache
7. Papilledema
8. Focal Paresis
9. Tremors, myoclonus

52. Manifestations of Resp Acidosis
• CARDIOVASCULAR: Related to coronary
vasodilation
1. Tachycardia
2. Ventricular arrythmias (related to hypoxemia
and not hypercapnia per se)
• BIOCHEMICAL ABNORMALITIES:
 CO2
 Cl-
 PO4
3-

54. Homeostatic Response
to Respiratory Acidosis
 Imm response to rise in CO2 (& H2CO3)  blood
and tissue buffers take up H+ ions, H2CO3
dissociates and HCO3- increases with rise in pH.
 Steady state reached in 10 min & lasts for 8
hours.
 PCO2 of CSF changes rapidly to match PaCO2.
 Hypercapnia that persists > few hours induces an
increase in CSF HCO3- that reaches max by 24 hr
and partly restores the CSF pH.
 After 8 hrs, kidneys generate HCO3-
 Steady state reached in 3-5 d

55. Treatment of Respiratory Acidosis
• Ensure adequate oxygenation -
care to avoid inadequate
oxygenation while preventing
worsening of hypercapnia due
to supression of hypoxemic
resp drive
• Correct underlying disorder if
possible

56. Treatment of Respiratory Acidosis
 Alkali (HCO3) therapy rarely in ac and never in
ch resp acidosis  only if acidemia directly
inhibiting cardiac functions
 Problems with alkali therapy:
1)Decreased alv ventilation by decrease in pH
mediated ventilatory drive
2)Enhanced carbon dioxide production from
bicarbonate decomposition

57. METABOLIC ACIDOSIS

58. Metabolic Acidosis
• pH, HCO3
• 12-24 hours for complete activation of
respiratory compensation
• PCO2 by 1.2mmHg for every 1 mEq/L HCO3
• The degree of compensation is assessed via
the Winter’s Formula
PCO2 = 1.5(HCO3) +8  2

59. Causes
• Metabolic Anion Gap
Acidosis
– M - Methanol
– U - Uremia
– D - DKA
– P - Paraldehyde
– L - Lactic Acidosis
– E - Ehylene Glycol
– S - Salicylate
Non Gap Metabolic
Acidosis
Hyperalimentation
Acetazolamide
RTA (Calculate
urine anion gap)
Diarrhea
Pancreatic Fistula

61. Treatment of Met Acidosis
• When to treat?
•Severe acidemia  Effect on Cardiac function most
imp factor for pt survival since rarely lethal in absence
of cardiac dysfunction.
•Contractile force of LV  as pH  from 7.4 to 7.2
•However when pH < 7.2, profound reduction in
cardiac function occurs and LV pressure falls by
15-30%
•Most recommendations favour use of base when pH <
7.15-7.2 or HCO3 < 8-10 meq/L.

62. How to treat?
Rx Undelying Cause
HCO3- Therapy
• Aim to bring up pH to 7.2 & HCO3- 
10 meq/L
• Qty of HCO3 admn calculated:
0.5 x LBW (kg) x HCO3 Deficity
(meq/L)

63. Why not to treat?
 Considered cornerstone of therapy of severe
acidemia for >100 yrs
 Based on assumption that HCO3- admn would
normalize ECF & ICF pH and reverse deleterious
effects of acidemia on organ function
 However later studies contradicted above
observations and showed little or no benefit from
rapid and complete/over correction of acidemia
with HCO3.

64. Adverse Effects of HCO3- Therapy
  CO2 production from HCO3 decomposition 
Hypercarbia (V>A) esp when pul ventilation
impaired
 Myocardial Hypercarbia  Myocardial acidosis
Impaired myocardial contractility &  C.O.
  Cor A perfusion pressure 
Myocardial Ischemia esp in pts with HF
 Hypernatremia & Hyperosmolarity  Vol
expansion  Fluid overload esp in pts with HF
 Intracellular (paradoxical) acidosis esp in liver &
CNS ( CSF CO2)

65. • gut lactate production,  hepatic lactate extraction
and thus  S. lactate
CORRECTION OF ACIDEMIA WITH OTHER BUFFERS:
•Carbicarb
- not been studied extensively in humans
- used in Rx of met acidosis after cardiac arrest
and during surgery
- data on efficacy limited

66. • THAM (Trometamol/Tris-(OH)-CH3-NH2-CH3) -
biologically inert amino alcohol of low toxicity.
• Capacity to buffer CO2 & acids in vivo as well as in
vitro
• More effective buffer in physiological range of blood
pH
• Initial loading dose of THAM acetate (0.3 ml/L sol)
calculated:
BW (kg) x Base Deficit (meq/L)
Max daily dose ~15 mmol/kg
• Use in severe acidemia (pH < 7.2):

67. METABOLIC ALKALOSIS

68. Metabolic Alkalosis
 Met alkalosis common (upto 50% of all disorders)
• pH, HCO3
• PCO2 by 0.7 for every 1mEq/L  in HCO3
 Severe met alkalosis assoc with significant mortality
1)Arterial Blood pH of 7.55  Mortality rate of 45%
2)Arterial Blood pH of 7.65  Mortality rate of 80%
(Anderson et al. South Med J 80: 729–733, 1987)
 Metabolic alkalosis has been classified by the
response to therapy or underlying pathophysiology

69. Pathophysiological Classification of Causes of
Metabolic Alkalosis
1) H+ loss:
GIT Chloride Losing Diarrhoeal Diseases
Removal of Gastric Secretions
(Vomitting, NG suction)
Renal Diuretics (Loop/Thiazide)
Mineralocorticoid excess
Hypercalcemia
High dose i/v penicillin
Black RM. Intensive Care Medicine 2003; 852-864

70. 2) HCO3- Retention:
Massive Blood Transfusion
Ingestion (Milk-Alkali Syndrome)
Admn of large amounts of HCO3-
3) H+ movement into cells
Hypokalemia
Black RM. Intensive Care Medicine 2003; 852-864

71. Clinical features
Adrogue et al, NEJM 1998; 338(2): 107-111

72. Treatment of Metabolic Alkalosis
 Rx underlying cause resp for vol/Cl- depletion
 While replacing Cl- deficit, selection of
accompanying cation (Na/K/H) dependent
on:Assessment of ECF vol status
 Presence & degree of associated K depletion,
 Pts with vol depletion usually require replacement of
both NaCl & KCl.

73. Dialysis
• In presence of renal failure or severe fluid overload
state in CHF, dialysis +/- UF may be reqd to exchange
HCO3 for Cl & correct metabolic alkalosis.
Adjunct Therapy
• PPI can be admn to  gastric acid production in cases
of Cl-depletion met alkalosis resulting from loss of
gastric H+/Cl- (e.g. pernicious vomiting, req for
continual removal of gastric secretions.

74. MILK-ALKALI SYNDROME & OTHER
HYPERCALCEMIC STATES
• Cessation of alkali ingestion & Ca sources (often milk
and calcium carbonate)
• Treatment of underlying cause of hypercalcemia
• Cl- and Vol repletion for commonly associated
vomiting

75. • ----- XXXX Diagnostics ------
• Blood Gas Report
• Measured 37.0
o
C
• pH 7.523
• pCO2 30.1 mm Hg
• pO2 105.3 mm Hg
• Calculated Data
• HCO3 act 22
mmol / L
• O2 Sat 98.3 %
• pO2 (A - a) 8 mm Hg D
• pO2 (a / A) 0.93
• Entered Data
• FiO2 21.0 %
Case 1
30 year old female with
sudden onset of dyspnea.
No Cough or Chest Pain
Vitals normal but RR 26,
anxious.

76. • ----- XXXX Diagnostics ------
• Blood Gas Report
• Measured 37.0
o
C
• pH 7.301
• pCO2 76.2 mm Hg
• pO2 45.5 mm Hg
• Calculated Data
• HCO3 act 35.1 mmol / L
• O2 Sat 78%
• pO2 (A - a) 9.5 mm Hg D
• pO2 (a / A) 0.83
• Entered Data
• FiO2 21 %
Case 2
60 year old male
smoker
with progressive
respiratory
distress
and somnolence.

77. • ----- XXXX Diagnostics ------
• Blood Gas Report
o
• Measured 37.0
C
• pH 7.23
• pCO2 23 mm Hg
• pO2 110.5 mm Hg
• Calculated Data
• HCO3 act 14 mmol / L
• O2 Sat %
• pO2 (A - a) mm Hg D
• pO2 (a / A)
• Entered Data
• FiO2 21.0%
Case 3
28 year old
diabetic with
respiratory distress
fatigue and
loss of appetite.

80.  8) I shall practice gentle
mechanical ventilation and not
to try bring ABG to perfect
normal.
 9) I shall treat the patient, not
the ABG report.
 10) I shall always correlate ABG
report clinically.

81. References
 ICU Book, The, 3rd Edition - Paul L. Marino
 Diagnosing Acid-Base Disorders : JAPI •
VOL. 54 • SEPTEMBER 2006
 Harrison‘s PRINCIPLES OF INTERNAL
MEDICINE Eighteenth Edition
 Washington Manual of Critical Care - 2nd
Ed
 Selected Websites – Listed in next slide

82. References
• Selected Acid-Base Web Sites
http://www.acid-base.com/
http://www.qldanaesthesia.com/AcidBaseBook/
http://www.virtual-anaesthesia-textbook.com
/vat/acidbase.html#acidbase
http://ajrccm.atsjournals.org/cgi/content/full/162/6/2246
http://www.osa.suite.dk/OsaTextbook.htm
http://www.postgradmed.com/issues/2000/03_00/fall.htm
http://lungpowerpoints.com
http://uptodate.com