IM-PULMONOLOGY

Clinical Interpretation of Arterial Blood Gas and Oxygenation

(Dr. Pio T. Esguerra II, MD, FPCP, FPCCP, DIH)
Date: August 6, 2015
FEU-NRMF Institute of Medicine
-----------------------------------------------------------------------------------------------------------------------------------------------------------
Arterial Blood Gases and Oxygenation
Ventilatory Lung Disturbances

Spirometry – used to assess lung function and

other lung defects.

Three volumes and capacities not measured by lung

spirometry:

Residual volume
Functional residual capacity
Total lung capacity (TLC)

Obstructive Lung Defect – there is a narrowing in Fig. 1. Ventilatory Organs (Thoracic Pump)

the airways The problem in the thoracic pump is that there is

 Ex: Bronchial asthma, COPD, Emphysema, hypoventilation. The pathognomonic sign seen in
Bronchiectasis, Chronic Bronchitis hypoventilation is hypercapnia (↑ levels in
 need to use the FEV1/FVC PCO2)
 sometimes there is a need to use post-
bronchodilator spirometry for assessment. In a patient’s ABG w/ ↑ CO2, label it right away as
 1 spirometry → nebulize px with β2-agonist hypoventilation w/ or w/o hypoxemia. Hypoxemia
or in combination w/ short-acting anti- will always follow hypoventilation or hypercapnia.
cholinergic → spirometry after 15 mins
o Done to check if there is reversibility Gas Exchange Organs
in obstruction of the airway
o Reversibility means you are dealing The gas exchange organs
w/ Bronchial asthma rather than are the airways, alveoli,
COPD and its corresponding
blood vessels (alveolo-
Restrictive Lung Defect – there is a problem in the capillary membrane)
lung parenchyma, chest wall or pleura (which where exchange of CO2
restricts the expansion of the lung parenchyma) → and O2 occur. The O2 is
↓TLC being taken by the
 Ex: Interstitial lung dse, problems in the unoxygenated blood via
bony thorax (Kyphoscoliosis), pleural the pulmonary artey and
thickening, fibrothorax the CO2 will be taken by
 screening: Forced vital capacity (FVC) the air so that the CO2 will be blown off.
 confirmatory: TLC
Clinical Manifestation of Respiratory Dse
 dyspnea
 cough
 chest pain
 hemoptysis

FAITH ANGELI J. LADIA (3A) 1


Laboratory Tests:
 Sputum analysis
 Culture & sensitivity
 ABG
 Sputum cytology
Oxygen-Hemoglobin Dissociation Curve
 proportion of hemoglobin in its saturated
form on the vertical axis against the
prevailing oxygen tension on the
horizontal axis.
 important tool for understanding how our
blood carries and releases oxygen.
 relates oxygen saturation (sO2) and partial
pressure of oxygen in the blood (pO2)
 determined by what is called "Hemoglobin
affinity for oxygen" (acquires and releases
oxygen molecules into the fluid).
 A hyperbolic curve showing the affinity of O 2
to Hgb: 1 Hgb molecule = 4 O2 molecules
 O2 that binds to Hgb is the one that is free
and depending upon Hgb levels
o ↓ Hgb – no matter how good
saturation is, O2 content of the body
is still low
 Ex: Normal Hgb for Females is 12-14g/dL. If
px’s Hgb is 9g/dL, even if there is 100% O 2
sat, only the 9g/dL will be fully saturated. O 2
content still not enough for px.
 Be careful of px with CO poisoning or
methemoglobin bc this also saturates Hgb at
a much faster rate than O2 and it will reflect
in pulse oximetry as a fully saturated Hgb
but these are not O2, these are CO2 → death
FACTORS THAT SHIFT THE CURVE
TO THE LEFT TO THE RIGHT
Alkalemia Acidemia
↓ CO2 ↑ CO2
Hypothermia Hyperthermia
↓ 2,3-BPG ↑ 2,3-BPG
Table 1. Factors that shift the O2 curve
 Shift to Left: O2 has high affinity to Hgb – no
release of O2
o Haldane effect: - describes how O2
concentrations determine Hgb’s
affinity for CO2
o This happens in the lungs so that O2
from the air will be taken by
unoxygenated blood via the
pulmonary arteries.
 Shift to Right: O2 has low affinity to Hgb – O2
release
o Bohr effect: describes how CO2 and
H+ affect Hgb’s affinity for O2
o Happens in tissues because they
need O2
Note: these effects are not exclusive to the lungs
and tissues bc the lung is still a tissue! It needs O2.
The bronchial artery corresponds to the Bohr effect
so that the lungs can get nutrients and O2 from the
blood.
In another perspective, the lungs have high affinity
to O2 bc Hgb in the lungs is unsaturated. Presence
of a very high tension of O2 affects the release of
CO2 in the lungs. Presence of high CO2 will bring
about increase in O2 affinity to Hgb and this will in
turn release CO2 so you can blow it off in the
atmosphere (gas exchange). The opposite
happening in the tissues.
 Presence of high tension of one gas
affects the affinity to hemoglobin of
another gas.
ABG SPECIMEN AND MATERIALS
 Specimen:
o Arterial blood
o “arterialized” capillary blood – for
neonates
 Materials:
o cotton balls (wet), rubber stopper
o syringe
FAITH ANGELI J. LADIA (3A) 2
 o heparin ( 0.5ml of 1000-U/ml per
5ml blood) The normal pH needed by our bodies for
o ice for transport homeostasis is maintained by the interaction of the
base (bicarbonate – controlled by kidneys) and the
Factors affecting levels of Arterial Blood Gases acid (CO2 – controlled by the lungs) so that all
physiologic acts can be carried out.
 Exposure to ambient atmosphere (or air
bubble) – results in over-oxygenated blood → uncompensated metabolic
 Temperature (gas pressures & pH) acidosis
 Excess heparin (lower pCO2 by 12-25%)
 Transport on ice - Stable for 30 minutes
→ uncompensated respiratory
Reference Values: MEMORIZE! acidosis
Blood Gases and Electrolytes
Arterial Venous → uncompensated metabolic
pH: 7.35-7.45 mmHg Na: 135-148 mEq/L alkalosis
pCO2: 35-45 K: 3.5-5.3
pO2: 80-100 Cl: 98-106 → uncompensated respiratory
O2 sat: 95% of pO2 Anion gap: 12-18
HCO3: 22-26 Serum osmolality: 285- alkalosis
310 mOsm/kg H2O
Table 2. Internationally accepted values for ABG measurement → partly compensated respiratory
Anion gap: ONLY assessed for metabolic acidosis acidosis

Note: when taking ABG… → compensated respiratory acidosis

 Measure ABG at 37C → combined respiratory &

 For each degree (°C) increase in temp.
metabolic alkalosis
 pO2 falls by 7%
 pCO2 rise by 3%
→ combined respiratory &
*ABG taken from px who is febrile or in a room that metabolic acidosis
is very hot reveals relative hypoxemia and
hypercapnia bc of the effect of temp to the gases –  compensation – change in the amount
can lead to wrong assessment and healing pointing to the same direction
intervention  ex: Partly compensated respiratory acidosis
- ↓pH d/t ↑PCO2. HCO3 compensates by ↑
SUMMARY ALGORITHM FOR ACID-BASE to bring pH back to normal
INTERPRETATION: Check Appendix A  change in HCO3 and CO2 pointing to
opposite direction – COMBINED
If pH w/in normal range – NORMAL or FULLY
COMPENSATED acid-base balance
All 3 values abn – PARTIAL COMPENSATION ABNORMALITY COMPENSATION

2 abn values: pH Abnomal, 1 normal - RESPIRATORY ↑CO2 ↑ HCO3

ACIDOSIS
UNCOMPENSATED ALKALOSIS
↓CO2 ↓ HCO3

METABOLIC ↓ HCO3 ↓ CO2

HENDERSON-HASSELBACH EQ’N ACIDOSIS ↑ HCO3 ↑ CO2
ALKALOSIS

FAITH ANGELI J. LADIA (3A) 3

 INTERPRETATION: OXYGEN STATUS (ABG
Case 1: 26, F, complaining of dyspnea and chest TAKEN, PATIENT RECEIVING O2
pain, RR = 30/min SUPPLEMENTATION)

pH 7.49 ↑  Adequate oxygenation: 80-100

pCO2 30 ↓  Inadequate oxygenation: <80
pO2 98 N  More than adequate oxygenation: >100
HCO3 24 N
O2 sat 99% N Case 2: 66, COPD patient, 5 days progressive
dyspnea, in respiratory distress. RR = 35. ABG at
Uncompensated respiratory alkalosis RA.

OXYGENATION pH 7.32 ↓
pCO2 77 ↑
AT ROOM AIR pO2 55 Moderate
Patients < 60 y/o 80 – 100 mmHg hypoxemia
Patients > 60 70 – 100 mmHg; HCO3 32 ↑
adjustment from 60 – O2 sat 88% N
100 mmHg (lecturer)
Partly compensated respiratory acidosis w/
Expected pO2 = 80 – ( moderate hypoxemia
yrs above 60)
Ex. 70 year-old male Case 3: 50, diabetic female, 3 days progressive
Expected pO2 = 80 – 10 alteration in sensorium. T = 39°C, RR = 24, rapid
= 70 and deep. ABG at 6LPM.
(ppt)
pH 7.2 ↓
OXYGENATION STATUS pCO2 32 ↓
pO2 78 Inadequate
Patients < 60 pO2 RESULT oxygenation
y/o <80 Hypoxemic HCO3 14 ↓
80 – 100 Normal
O2 sat 90% N
>100 More than
adequate
Partly compensated metabolic acidosis
Patients > 60 pO2 RESULT
with inadequate oxygenation
< expected Hypoxemic
expected Normal
Fraction of Inspired Oxygen (FiO2)
> expected More than
adequate 21% = 0 LPM (baseline, don’t start adding 4 yet)
24% = 1 (start here)
INTERPRETATION: OXYGENATION STATUS 28% = 2
(ABG TAKEN AT ROOM TEMP) 32% = 3
36% = 4
 Normal 40% = 5
 Hypoxemia 44% = 6LPM
o Mild: 60-79
o Moderate: 40-59 *100% FiO2 can be given when a patient is
o Severe: <40 intubated and hooked to a mechanical ventilator.

FAITH ANGELI J. LADIA (3A) 4

Degree of compensation: Detection of CAUSES OF HYPOXEMIA
underlying acid-base abnormality
Not thoroughly discussed  HYPOVENTILATION
Hallmark: hypercapnia
Metabolic Acidosis  DECREASED FiO2
Determine anion gap Especially in persons in high altitude
Anion gap: Na- (Cl+HCO3) areas where FiO2 ↓21%
Expected pCO2: 1.5 X actual HCO3 + 8 (+/-2)  V/Q MISMATCH
Example: pH=7.2 HCO3=19.3  SHUNT
Expected pCO2= 1.5 X 19.3 + 8  DIFFUSION ABNORMALITIES – if your
= 36.5 (+/-2) (range=34.5 - 38.5) alveolo-capillary membrane is thick.

Metabolic Alkalosis DIAGNOSTIC APPROACH TO PATIENT W/

Expected pCO2= 0.75 X actual HCO3 + 20 HYPOXEMIA: See Appendix B
(+/-5)
Example: pH= 7.47 HCO3=38 Used in the diagnosis of patients in an ABG where
Expected pCO2= 0.75 X 38 + 20 there is ↓pCO2 to get the mechanism of hypoxemia.
= 48 (range 43.5-53.5)
Hypoventilation – brought about by mechanisms
Respiratory Acidosis or pathologies that decrease the drive to breathe.
Expected compensation Ex. Px w/ neuromuscular dse s/a Guillian-
Acute: HCO3 rises 1mEq/L for each Barre syndrome, botulinum toxin, sedatives,
10mmHg rise in pCO2 neuroparalytics
Chronic: HCO3 rises 3.5 mEq/L for each
10mmHg rise in pCO2 Shunt – d/t shunting of unoxygenated blood to a
blood vessel that is already oxygenated. Hypoxemia
Respiratory Alkalosis is seen.
Expected compensation
Acute: HCO3 falls 2mEq/L for each 10mmHg Most common mechanism of hypoxemia in clinical
fall in pCO2 practice: V/Q mismatch
Chronic: HCO3 falls 5mEq/L for each
10mmHg fall in pCO2 Both shunting and V/Q mismatch are hypoxemic
conditions. To differentiate, give high flow O2. If
corrected, it is V/Q mismatch.
Acid-base Compensation Limit
disturbance (mmHg) ABG INTERPRETATION
Metabolic acidosis pC02= 1.5 X HCO3 + 8 (+/-2) 10

Metabolic Each meq ↑ in HCO3  0.5- 55  Check pH : Normal or Abnormal?

alkalosis 1.0 mmHg ↑ in pCO2  If abnormal, is it acidemia or alkalemia?
Respiratory  Check for PaCO2, is it respiratory or
acidosis: metabolic?
Acute HCO3 ↑ by 3-4 meq/L 30
HCO3 ↑ by 0.4 meq/L
 Check for compensation (same direction)
Chronic 40
Respiratory  Check for combined acid-base abnormality
alkalosis: (opposite direction)
Acute HCO3 ↓ by 2-4 meq/L 18
Chronic HCO3 ↓ by 0.5 meq/L 12-15
 Check for oxygenation (room air;
supplementation)
*Summary: Underlying acid-base abnormalities
Metabolic acidosis is the exact opposite of
respiratory alkalosis. Same goes with metabolic
alkalosis, the exact opposite is respiratory acidosis.

FAITH ANGELI J. LADIA (3A) 5

DIFFICULT TO INTERPRET ABG  Non-anion gap
o Diarrhea
Please take note: o Renal tubular acidosis (RTA)
 pH, PaO2 & pCO2 are directly measured.
 HCO3- derived or computed parameter  Increased Anion gap
(prone to mistake). o Lactate (sepsis, ischemia)
o Aspirin,Methanol
Example: o Uremia, DKA
 pH- 7.43 pH- 7.41 o INH
 pCO2- 40 pCO2- 34
 pO2- 80 pO2- 90 Respiratory Acidosis
 HCO3- 29 HCO3- 23  Hypoventilation
 COPD
1. Normal Acid Base balance with normal  Pickwickian syndrome
oxygenation (NORMAL ABG)  Obesity
 Suffocation
*pH and pCO2 normal = normal ABG no matter  Opiate overdose
what the value of HCO3 is (shortcut)  Sleep apnea

2. Compensated Respiratory Alkalosis with

normal oxygenation
Sources: ppt and recordings
*how to know which parameter compensated:
7.4 – mean normal pH
7.41 – relatively alkalotic so look at which
parameter renders alkalosis. (bicarbonate)

ACID-BASE DISTURBANCES

Metabolic Alkalosis
 Exogenous steroids
 GI loss (vomitting, etc.)
 Renal loss (Conn syndrome, Cushing)
 Decreased chloride intake
 Diuretics
 Bicarbonate administration
 Contraction alkalosis

Respiratory Alkalosis
 Hyperventilation of any cause
 Anemia
 Pulmonary embolism
 Sarcoid
 Anxiety
 Pain

Metabolic Acidosis
 Anion gap=(Na+K)-(HCO3+Cl)
o NV= 8-14

FAITH ANGELI J. LADIA (3A) 6

 SUMMARY ALGORITHM FOR ACID-BASE INTERPRETATION

pH

< 7.35 7.35 – 7.45 > 7.45

ACIDOSIS NORMAL ALKALOSIS

or
COMPENSATED
Uncompensated Uncompensated
Metabolic Acidosis 35 - 45 PaCO2 PaCO2 35 - 45 Metabolic Alkalosis
pH
< 35 > 45
Partly Compensated < 7.4 > 7.4 Partly Compensated
Metabolic Acidosis Metabolic Alkalosis
> 45 < 35
Normal or Normal or
Compensated Compensated
Respiratory Acidosis Alkalosis Respiratory

Compensated PaCO2 Compensated

22 - 26 HCO3 HCO3 22 - 26
Metabolic Respiratory
Acidosis < 35 Alkalosis
> 26 < 22 > 26 < 22
Uncompensated Compensated Compensated Uncompensated
Respiratory Acidosis > 45 Respiratory Alkalosis
Respiratory Metabolic
Acidosis Alkalosis
Partly Compensated Combined 35 - 45 Combined Partly Compensated
Respiratory Acidosis Respiratory Respiratory Respiratory Alkalosis
and Metabolic and Metabolic
Acidosis Normal Acid-Base Alkalosis

Appendix A: Algorithm for ABG Interpretation

Appendix B: Different mechanisms of hypoxemia

FAITH ANGELI J. LADIA (3A) 7