Pulmonary Funtion Testing

PhD. MD. Luong Linh Ly

Department of Physiology - Pathophysiology – Immunology
Hong Bang International University
STAGE OF RESPIRATION
 RESPIRATORY FUNCTION TEST

• Basic: • In-depth:
Ø Spirometry Ø Examination of small airways
Ø Residual volume Ø Bronchial reactivity test
Ø Total lung capacity Ø Examination of respiratory
Ø Diffusion capacity (DLCO) muscles
Ø Blood Gas Ø Exercise test
Ø Respiratory control...
Ventilatory function test:

• Spirometry.
• Pulmonology.
• Thoracic lung elasticity test.
• Measurement of airway resistance...

The most common is: spirometry

Spirometry
SPIROMETRY AND RELATED TESTS

¡ Learning Objectives

l Determine whether spirometry is

acceptable and reproducible

l Identify airway obstruction using forced

vital capacity (FVC) and forced expiratory
volume (FEV1)

l Differentiate between obstruction and

restriction as causes of reduced vital
capacity
SPIROMETRY AND RELATED TESTS

¡ Learning Objectives

l Distinguish between large and small

airway obstruction by evaluating flow-
volume curves

l Determine whether there is a significant

response to bronchodilators

l Select the appropriate FVC and FEV1 for

reporting from series of spirometry
maneuvers
What is Spirometry?
¡ a simple and safe test
¡ that measures lung volumes
¡ with a graphical display
¡ gives an estimation of lung function
¡ Allows for diagnosis of
airflow obstruction
¡ Permits good follow-up
for asthma and COPD
 Spirometry
in Practice
• A technique used to measure air flow in and out of
the lungs.
• A recording of lung volumes and capacities defined
by the respiratory process. These recordings may be
static (untimed) or dynamic (timed).
• Assesses the integrated mechanical functions of
lungs, chest wall and respiratory muscles.
•The gold standard for diagnosis, assessment and
monitoring of COPD.
• Better than PEFR (which is effort dependent) for
demonstrating airway obstruction in BA.
• The most commonly used PFT.
 Indications
• Measure airflow obstruction to help make a
definitive diagnosis of COPD
• Detect airflow obstruction in smokers who may
have few or no symptoms
• Assess one aspect of response to therapy
• Perform pre-operative assessment
• Distinguish between obstruction and restriction
as causes of breathlessness
• Perform pre-employment screening in certain
professions
Hand-held spirometer
Spirometer in the fifties..
In the lung function lab
Many types are available..

Simplicity

Spirobank
MicroLoop
SpiroPro

SpiroStar

Datospir 70
What do we measure
with a spirometer?
 Adverse Effects

• Light headedness
• Headache
• Fainting: reduced venous return
or vasovagal attack (reflex)
• Transient urinary incontinence
Normal spirogram:
Volume
8
/ time

Man
6
Volume (L)

176 cm
76 kg
FVC
4
FEV1

5 10 15
Time (s)
 Two important parameters

¡ FVC - Forced Vital Capacity. This is

the total amount of air that you blow
out in one breath.
¡ FEV1 - Forced Expiratory Volume in
one Second. This is the amount of air
you can blow out within one second.
With normal lungs and airways you
can normally blow out most of the air
from your lungs within one second.
 Normal

Obstructive

Restrictive
Normal spirogram: Flow/Volume

12 PEF Man
176 cm
8
76 kg

4
Flow (L/s)

-4

-8
Volume (L)
Spirometry and ageing
10
25 yrs 75 yrs
8 175 cm 171 cm
male male
Flow (l/s)

0
0 1 2 3 4 5 6
Vol (l)
Spirometry allows for

¡ Early detection of airflow obstruction

(often late signs and symptoms)
¡ Better diagnosis (helps to distinguish
between asthma and COPD)
¡ Correct follow-up (compare with blood
pressure meter in hypertension patients)
Reversibility Testing
¡ If airflow obstruction is present, the
test person is given a
bronchodilator (inhalation device)
 Reversibility testing

Short acting b2 agonist

 Bronchodilators
Pre Post D
10 FEV1 2.61 3.95 51%
Flow (L/s )

FVC 5.25 6.08 16%

6

PEF 6.49 9.64 49%

2

+ 12-15 % in FEV1
2 4 6 > 200ml improvement is
considered significant
Vol ( L )
Reversibility Testing

¡ Airflow obstruction disappears:

REVERSIBLE OBSTRUCTION (probably
asthma)
¡ Airflow obstruction remains:
IRREVERSIBLE OBSTRUCTION (probably
COPD)
Predicted Values

¡ Laboratory Normal Ranges

l Laboratory tests performed on a large

number of normal population will show
a range of results
Predicted Values

¡ Laboratory Normal Ranges

Predicted Values

¡ Laboratory Normal Ranges

l Most clinical laboratories consider

two standard deviations from the
mean as the normal range since it
includes 95% of the normal
population.
PFT Reports
o When performing PFT’s three values
are reported:

o Actual – what the patient performed

o Predicted – what the patient should

have performed based on Age, Height,
Sex, Weight, and Ethnicity

o % Predicted – a comparison of the

actual value to the predicted value
PFT Reports

¡ Example

Actual Predicted %Predicted

VC 4.0 5.0 80%

SPIROMETRY

¡ Vital Capacity

The vital capacity (VC) is the volume

of gas measured from a slow,
complete expiration after a maximal
inspiration, without a forced effort.
SPIROMETRY

¡ Vital Capacity
SPIROMETRY

¡ Vital Capacity

l Valid VC measurements important

¡ IC and ERV used to calculate

RV and TLC

¡ Example:
l RV = FRC - ERV
l TLC = IC + FRC
SPIROMETRY

¡ VC: Criteria for Acceptability

1. End-expiratory volume varies by less than
100 ml for three preceding breaths

2. Volume plateau observed at maximal

inspiration and expiration
SPIROMETRY

¡ VC: Criteria for Acceptability

3. Three acceptable VC maneuvers should be
obtained; volume within 150 ml.

4. VC should be within 150 ml of FVC value

SPIROMETRY

¡ VC: Selection Criteria

The largest value from at least 3 acceptable
maneuvers should be reported
SPIROMETRY

¡ VC: Significance/Pathophysiology
l Decreased VC
¡ Loss of distensible lung tissue

l Lung CA
l Pulmonary edema
l Pneumonia
l Pulmonary vascular congestion
l Surgical removal of lung tissue
l Tissue loss
l Space-occupying lesions
l Changes in lung tissue
SPIROMETRY

¡ VC: Significance/Pathophysiology
l Decreased VC
¡ Obstructive lung disease
¡ Respiratory depression or
neuromuscular disease
¡ Pleural effusion
¡ Pneumothorax
¡ Hiatal hernia
¡ Enlarged heart
SPIROMETRY

¡ VC: Significance/Pathophysiology
l Decreased VC
¡ Limited movement of diaphragm

l Pregnancy
l Abdominal fluids
l Tumors

¡ Limitation of chest wall movement

l Scleraderma
l Kyphoscoliosis
l Pain
SPIROMETRY

¡ VC: Significance/Pathophysiology
l If the VC is less than 80% of
predicted: FVC can reveal if caused by
obstruction
SPIROMETRY

¡ VC: Significance/Pathophysiology
l If the VC is less than 80% of
predicted: Lung volume testing can
reveal if caused by restriction
SPIROMETRY

¡ Forced Vital Capacity (FVC)

The maximum volume of gas that

can be expired when the patient
exhales as forcefully and rapidly as
possible after maximal inspiration
(sitting or standing)
SPIROMETRY

¡ FVC (should be within 150 ml of VC)

SPIROMETRY
¡ FVC: Criteria for Acceptability
1. Maximal effort; no cough or glottic closure
during the first second; no leaks or obstruction
of the mouthpiece.
2. Good start-of-test; back extrapolated volume
<5% of FVC or 150 ml, whichever is greater
SPIROMETRY

¡ FVC: Criteria for Acceptability

3. Tracing shows 6 seconds of exhalation or an
obvious plateau (<0.025L for ≥1s); no early
termination or cutoff; or subject cannot or
should not continue to exhale
SPIROMETRY

¡ FVC: Criteria for Acceptability

4. Three acceptable spirograms obtained; two
largest FVC values within 150 ml; two largest
FEV1 values within 150 ml
SPIROMETRY

¡ FVC: Selection Criteria

The largest FVC and largest FEV1 (BTPS)
should be reported, even if they do not
come from the same curve
SPIROMETRY

¡ FVC: When to call it quits !!!

If reproducible values cannot be

obtained after eight attempts, testing
may be discontinued
SPIROMETRY

¡ FVC: Significance and Pathophysiology

l FVC equals VC in healthy individuals

l FVC is often lower in patients with

obstructive disease
SPIROMETRY

¡ FVC: Significance and Pathophysiology

l FVC can be reduced by:

¡ Mucus plugging
¡ Bronchiolar narrowing
¡ Chronic or acute asthma
¡ Bronchiectasis
¡ Cystic fibrosis
¡ Trachea or mainstem bronchi obstruction
SPIROMETRY

¡ FVC: Significance and Pathophysiology

l Healthy adults can exhale their FVC

within 4 – 6 seconds

l Patients with severe obstruction (e.g.,

emphysema) may require 20 seconds,
however, exhalation times >15
seconds will rarely change clinical
decisions
SPIROMETRY

¡ FVC: Significance and Pathophysiology

l FVC is also decreased in restrictive

lung disease
¡ Pulmonary fibrosis
l dusts/toxins/drugs/radiation
¡ Congestion of pulmonary blood flow
l pneumonia/pulmonary hypertension/PE
¡ Space occupying lesions
l tumors/pleural effusion
SPIROMETRY

¡ FVC: Significance and Pathophysiology

l FVC is also decreased in restrictive

lung disease
¡ Neuromuscular disorders, e.g,
l myasthenia gravis, Guillain-Barre
¡ Chest deformities, e.g,
l scoliosis/kyphoscoliosis
¡ Obesity or pregnancy
SPIROMETRY

¡ Forced Expiratory Volume (FEV1)

The volume expired over the first
second of an FVC maneuver
SPIROMETRY
¡ Forced Expiratory Volume (FEV1)
l May be reduced in obstructive or
restrictive patterns, or poor patient
effort
SPIROMETRY
¡ Forced Expiratory Volume (FEV1)

l In obstructive disease, FEV1 may be

decreased because of:
¡ Airway narrowing during forced expiration
l emphysema
¡ Mucus secretions
¡ Bronchospasm
¡ Inflammation (asthma/bronchitis)
¡ Large airway obstruction
l tumors/foreign bodies
SPIROMETRY
¡ Forced Expiratory Volume (FEV1)

l The ability to work or function in

daily life is related to the FEV1 and
FVC
¡ Patients with markedly reduced FEV1
values are more likely to die from COPD or
lung cancer
SPIROMETRY
¡ Forced Expiratory Volume (FEV1)

l FEV1 may be reduced in restrictive

lung processes
¡ Fibrosis
¡ Edema
¡ Space-occupying lesions
¡ Neuromuscular diseases
¡ Obesity
¡ Chest wall deformity
SPIROMETRY
¡ Forced Expiratory Volume (FEV1)

l FEV1 is the most widely used

spirometric parameter, particularly
for assessment of airway
obstruction
SPIROMETRY
¡ Forced Expiratory Volume (FEV1)

l FEV1 is used in conjunction with

FVC for:
¡ Simple screening
¡ Response to bronchodilator therapy
¡ Response to bronchoprovocation
¡ Detection of exercise-induced
bronchospasm
SPIROMETRY
¡ Forced Expiratory Volume Ratio (FEVT%)

l FEVT% = FEVT/FVC x 100

¡ Useful in distinguishing between

obstructive and restrictive causes of
reduced FEV1 values
SPIROMETRY
¡ Forced Expiratory Volume Ratio (FEVT%)

l Normal FEVT% Ratios for Health Adults

¡ FEV 0.5% = 50%-60%

¡ FEV 1% = 75%-85%
¡ FEV 2% = 90%-95%
¡ FEV 3% = 95%-98%
¡ FEV 6% = 98%-100%

l Patients with obstructive disease have

reduced FEVT% for each interval
SPIROMETRY
¡ Forced Expiratory Volume Ratio (FEVT%)

l A decrease FEV1/FVC ratio is the

“hallmark” of obstructive disease

¡ FEV1/FVC <75%
SPIROMETRY
¡ Forced Expiratory Volume Ratio (FEVT%)
l Patients with restrictive disease often have
normal or increased FEVT% values

¡ FEV1 and FVC are usually reduced in equal

proportions

l The presence of a restrictive disorder may

by suggested by a reduced FVC and a
normal or increased FEV1/FVC ration
SPIROMETRY
¡ Forced Expiratory Flow 25% - 75%
(maximum mid-expiratory flow)

l FEF 25%-75% is measured from a

segment of the FVC that includes flow
from medium and small airways

¡ Normal values: 4 – 5 L/sec

SPIROMETRY
¡ Forced Expiratory Flow 25% - 75%

In the presence of a borderline

value for FEV1/FVC, a low FEF
25%-75% may help confirm
airway obstruction
SPIROMETRY
¡ Flow – Volume Curve
l AKA: Flow–Volume Loop (FVL)

The maximum expiratory flow-

volume (MEFV) curve shows flow
as the patient exhales from
maximal inspiration (TLC) to
maximal expiration (RV)

l FVC followed by FIVC

SPIROMETRY
FEF 25% or Vmax 75

¡ FVL
l X axis: Volume
FEF 75% or Vmax 25%

l Y axis: Flow

¡ PEF (Peak Expiratory Flow)

¡ PIF (Peak Inspiratory Flow)

.

¡ Vmax 75 or FEF 25%

FVC Remaining or Percentage FVC exhaled
.
¡ Vmax 50 or FEF 50%
.
¡ Vmax 25 or FEF 75%
SPIROMETRY

¡ FVL
l FEVT and FEF% can be read from
the timing marks (ticks) on the FVL
SPIROMETRY

¡ FVL
l Significant decreases in flow or volume
are easily detected from a single graphic
display
SPIROMETRY

¡ FVL: Severe Obstruction

SPIROMETRY

¡ FVL: Bronchodilation
SPIROMETRY
¡ Peak Expiratory Flow (PEF)
l The maximum flow obtained
during a FVC maneuver
¡ Measured from a FVL
¡ In laboratory, must perform a
minimum of 3 PEF maneuvers
¡ Largest 2 of 3 must be within 0.67
L/S (40 L/min)
¡ Primarily measures large airway
function
¡ Many portable devices available
SPIROMETRY

¡ Peak Expiratory Flow (PEF)

l When used to monitor asthmatics
¡ Establish best PEF over a 2-3 week
period

¡ Should be measured twice daily

(morning and evening)

¡ Daily measurements are compared to

personal best
SPIROMETRY
¡ Peak Expiratory Flow (PEF)
l The National Asthma Education Program
suggests a zone system
¡ Green: 80%-100% of personal best
l Routine treatment can be continued; consider
reducing medications

¡ Yellow: 50%-80% of personal best

l Acute exacerbation may be present
l Temporary increase in medication may be
needed
l Maintenance therapy may need increases

¡ Red: Less than 50% of personal best

l Bronchodilators should be taken immediately;
begin oral steroids; clinician should be
notified if PEF fails to return to yellow or
green within 2 – 4 hours
SPIROMETRY
¡ Peak Expiratory Flow (PEF)
l PEF is a recognized means of
monitoring asthma

l Provides serial measurements

of PEF as a guide to treatment

l ATS Recommended Ranges

¡ 60-400 L/min (children)
¡ 100-850 L/min (adults)
SPIROMETRY

¡ Maximum Voluntary Ventilation

(MVV)

The volume of air exhaled in a

specific interval during rapid, forced
breathing
SPIROMETRY

¡ MVV
l Rapid, deep breathing
l VT ~50% of VC
l For 12-15 seconds
SPIROMETRY

¡ MVV
l Tests overall function of
respiratory system

¡ Airway resistance

¡ Respiratory muscles

¡ Compliance of lungs/chest wall

¡ Ventilatory control mechanisms

SPIROMETRY

¡ MVV
l At least 2 acceptable maneuvers should be
performed

l Two largest should be within 10% of each

other

l Volumes extrapolated out to 60 seconds

and corrected to BTPS

l MVV is approximately equal to 35 time the

FEV1
SPIROMETRY

¡ MVV
l Selection Criteria

¡ The highest MVV (L/min, BTPS) and MVV

rate (breaths / min) should be reported
SPIROMETRY

¡ MVV
Decreased in:

l Patients with moderate to severe

obstructive lung disease

l Patients who are weak or have decreased

endurance

l Patients with neurological deficits

SPIROMETRY

¡ MVV
Decreased in:

l Patients with paralysis or nerve damage

l A markedly reduced MVV correlates with

postoperative risk for patients having
abdominal or thoracic surgery
SPIROMETRY

¡ Before/After Bronchodilator

l Spirometry is performed before

and after bronchodilator
administration to determine the
reversibility of airway obstruction
SPIROMETRY

¡ Before/After Bronchodilator

l An FEV1% less than predicted is a

good indication for bronchodilator
study

l In most patients, an FEV1% less

than 70% indicates obstruction
SPIROMETRY

¡ Before/After Bronchodilator

l Any pulmonary function parameter

may be measured before and after
bronchodilator therapy

l FEV1 and specific airway

conductance (SGaw) are usually
evaluated
SPIROMETRY

¡ Before/After Bronchodilator

l Lung volumes should be recorded

before bronchodilator
administration

¡ Lung volumes and DLco may also

respond to bronchodilator therapy
SPIROMETRY

¡ Before/After Bronchodilator
l Routine bronchodilator therapy should be
withheld prior to spirometry
¡ Ruppel 9th edition, pg. 66: Table 2-2

¡ Short-acting β-agonists 4 hours

¡ Short-acting anticholinergic 4 hours
¡ Long-acting β-agonists 12 hours
¡ Long-acting anticholinergic 24 hours
¡ Methylxanthines (theophyllines) 12 hours
¡ Slow release methylxanthines 24 hours
¡ Cromolyn sodium 8-12 hours
¡ Leukotriene modifiers 24 hours
¡ Inhaled steroids Maintain dosage
SPIROMETRY
¡ Before/After Bronchodilator

l Minimum of 10 minutes, up to 15
minutes, between administration
and repeat testing is recommended
(30 minutes for short-acting
anticholinergic agents)

l FEV1, FVC, FEF25%-75%, PEF,

SGaw are commonly made before
and after bronchodilator
administration
SPIROMETRY

¡ Before/After Bronchodilator

l Percentage of change is calculated

%Change = Postdrug – Predrug X 100

Predrug
SPIROMETRY

¡ Before/After Bronchodilator
l FEV1 is the most commonly used
test for quantifying bronchodilator
response

l FEV1% should not be used to judge

bronchodilation response

l SGaw may show a marked increase

after bronchodilator therapy
SPIROMETRY

¡ Before/After Bronchodilator
Significance and Pathophysiology

l Considered significant if:

¡ FEV1 or FVC increase ≥12% and ≥200 ml

¡ SGaw increases 30% - 40%

SPIROMETRY

¡ Before/After Bronchodilator
Significance and Pathophysiology

l Diseases involving the bronchial

(and bronchiolar) smooth muscle
usually improve most from “before”
to “after”
¡ Increase >50% in FEV1 may occur in
patients with asthma
SPIROMETRY

¡ Before/After Bronchodilator
Significance and Pathophysiology

l Patients with chronic obstructive

diseases may show little
improvement in flows
¡ Inadequate drug deposition (poor
inspiratory effort)
¡ Patient may respond to different drug
¡ Paradoxical response <8% or 150 ml not
significant
SPIROMETRY
¡ Maximal Inspiratory Pressure (MIP)

l The lowest pressure developed

during a forceful inspiration against
an occluded airway
¡ Primarily measures inspiratory muscle
strength
SPIROMETRY

¡ MIP
l Usually measured at maximal
expiration (residual volume)

l Can be measured at FRC

l Recorded as a negative number in

cm H20 or mm Hg, e.g. (-60 cm H2O)
SPIROMETRY

¡ MIP
SPIROMETRY

¡ MIP
Significance and Pathophysiology
l Healthy adults > -60 cm H2O
l Decreased in patients with:
¡ Neuromuscular disease

¡ Diseases involving the diaphragm,

intercostal, or accessory muscles

¡ Hyperinflation (emphysema)
SPIROMETRY

¡ MIP
Significance and Pathophysiology
l Sometimes used to measure
response to respiratory muscle
training

l Often used in the assessment of

respiratory muscle function in
patients who need ventilatory
support
SPIROMETRY
¡ Maximal Expiratory Pressure (MEP)

l The highest pressure developed

during a forceful exhalation against
an occluded airway
¡ Dependent upon function of the
abdominal muscles, accessory muscles
of expiration, and elastic recoil of lung
and thorax
SPIROMETRY

¡ MEP
l Usually measured at maximal
inspiration (total lung capacity)

l Can be measured at FRC

l Recorded as a positive number in

cm H20 or mm Hg
SPIROMETRY

¡ MIP and MEP

SPIROMETRY

¡ MEP
Significance and Pathophysiology
l Healthy adults >80 to 100 cm H2O
l Decreased in:
¡ Neuromuscular disorders

¡ High cervical spine fractures

¡ Damage to nerves controlling

abdominal and accessory muscles of
inspiration
SPIROMETRY

¡ MEP
Significance and Pathophysiology
l A low MEP is associated with
inability to cough
¡ May complicate chronic bronchitis, cystic
fibrosis, and other diseases that result in
excessive mucus production
SPIROMETRY

¡ Airway Resistance (Raw)

l The drive pressure required to

create a flow of air through a
subject’s airway

l Recorded in cm H2O/L/sec

l When related to lung volume at the

time of measurement it is known as
specific airway resistance (SRaw)
SPIROMETRY

¡ Raw

l Measured in a
plethysmograph
as the patient
breathes
through a
pneumo-
tachometer
SPIROMETRY

¡ Raw
l Criteria of Acceptability
¡ Mean of three or more acceptable
efforts should be reported;
individual values should be within
10% of mean
SPIROMETRY

¡ Airway Resistance (Raw)

Normal Adult Values

Raw 0.6 – 2.4 cm H2O/L/sec

SRaw 0.190 – 0.667 cm H2O/L/sec/L

SPIROMETRY

¡ Airway Resistance (Raw)

l May be increased in:

¡ Bronchospasm
¡ Inflammation
¡ Mucus secretion
¡ Airway collapse
¡ Lesions obstructing the larger airways
l Tumors, traumatic injuries, foreign bodies
SPIROMETRY

¡ Raw
Significance and Pathology
l Increased in acute asthmatic episodes

l Increased in advanced emphysema because of

airway narrowing and collapse

l Other obstructive disease, e.g., bronchitis may

cause increase in Raw proportionate to the
degree of obstruction in medium and small
airways
SPIROMETRY

¡ Airway Conductance (Gaw)

l A measure of flow that is generated

from the available drive pressure

l Recorded in L/sec/cm H2O

l Gaw is the inverse of Raw

l When related to lung volume at the

time of measurement it is known as
specific airway conductance (SGaw)
SPIROMETRY

¡ Gaw

l Measured in a
plethysmograph
as the patient
breathes
through a
pneumo-
tachometer
SPIROMETRY

¡ Gaw
l Criteria of Acceptability
¡ Mean of three or more acceptable
efforts should be reported;
individual values should be within
10% of mean
SPIROMETRY

¡ Airway Conductance (Gaw)

Normal Adult Values

Gaw 0.42 – 1.67 L/sec/cmH2O

SGaw 0.15 – 0.20 L/sec/cm H2O/L

SPIROMETRY

¡ Airway Conductance (Gaw)

Significance and Pathology

¡ SGaw Values <0.15 – 0.20

L/sec/cm H2O/L are consistent
with airway obstruction
 (ATS 2005)

[Link]
LOWER LIMIT OF NORMAL
(LLN)
 QUICK RESULTS ANALYSIS

RESTRICTED SYNDROME (+):

FVC (VC) < 80% predicted value

MỨC ĐỘ:
60 to below 80%: mild
■

40 to below 60%: average

below 40%: heavy
 QUICK RESULTS ANALYSIS

OBSTRUCTION SYNDROME (+):

FEV1/FVC < 0.7

MỨC ĐỘ (FEV1%):

ATS/ERS 2005
 QUICK RESULTS ANALYSIS
Bronchodilator TEST

FEV! before and

Bronchodilator* Dose
after
Salbutamol 200 - 400 ụg via 15 minutes
large volume
spacer
Ipratropium 160 ụg** via spacer 45 minutes

FEV1 AFTER TEST INCREASED > 12% AND > 200ML

COMPARED WITH PRE-TEST FEV1 VALUE
DLCO/TLCO
DIFFUSION CAPACITY OF LUNGS for CO
( DLCO ) or
TRANSFER FACTOR of LUNGS for CO
( TLCO )
 DLCO TLCO

Diffusion capacity of lungs for CO Transfer factor of lungs for CO

America Europe

Expressed as ml/min/mm of HG Expressed as mmol/min/KPa

 DLCO/TLCO

• Diffusing capacity of the lungs

estimates the ability of lungs to transfer
oxygen from alveolar gas to red cell
• Also provides objective measurement of lung function
• Originally described by Krogh in 1915
• Carbon monoxide is used as a surrogate for O2
• Mesures the partial pressure difference between the inspired and
exhaled CO
The amount of oxygen transferred is largely determined by three
factors :

• SURFACE AREA (A) of the ALVEOLAR-CAPILLARY MEMBRANE, which consists of the

alveolar and capillary walls

• THICKNESS (T) of the membrane

• DRIVING PRESSURE , that is , the difference in oxygen tension between the alveolar
gas and the venous blood (Δ PO2)

A*Δ PO2
Diffusion of Lung =
T
q Why use of CO ?
• Not normally present in alveoli/blood
• Transfer is diffusion limited rather than perfusion limited
• Avidly binds to Hb (210 times of Oxygen)
• As capillary PCO is very low normally , can be assumed to be
negligible and DlCO is calculated by dividing CO uptake (˙VCO) by
alveolar PCO
• Harmless at low concentrations(<0.3%)
• Less affected by other factors
qOxygen :
• Perfusion limited
• Limited by ventilation perfusion mismatch , shunt etc
• Accurate measurement of PO2 during capillary transfer is very difficult
qNO :
• Highly reactive with oxygen so requires special equipment
• Potential cardiovascular side effect
• Under research
 Indications of DLCO

1. Categorize patients with Restrictive disease or Extrathoracic restriction

(obesity,neuromascular disease)
2. Identify early ILD in high risk patients ( H/O chest radiation,chronic Amiodarone etc)
3. To quantify anatomic emphysema
4. Before lung surgery
5. Pulmonary Vascular disease , chemotherapeutic agents
6. Response to treatment
7. Assess severity and progression
8. Disability documentation for legal purpose
Single – Breath Holding method most widely used and standard
Procedure

1. Normal breathing ( upto RV)

2. Take deep breathing and blow out all in the air (upto TLC , panting )
3. Deep inspiration of supplied gas mixture and hold it for 10 s ( contains
Nitrogen , 0.3% CO , inert tracer gas Heliium , oxygen 18-21%)
4. Blow all the air out
5. Compute all
 Contraindications

• Patient unable to perform maneuver, breath hold

• Smoking within 24 hr
• Vigorous exercise before test
• Significant desaturation
Normal value
 Causes of increased DLCO

Supine position Increased perfusion and blood volume of upper

lobes
Exercise Increased pulmonary blood flow
Asthma Pseudo-Increase , more uniform distribution of pulmonary
flow
Obesity Increased pulmonary blood flow

Polycythemia Increased surface area due to increased RBC mass

Intra-Alveolar Haemorrhage In Goodpasture’s syndrome
Left to Right shunt Increased pulmonary blood flow
 Causes of decreased DLCO

§ Reduced surface area- § Increased thickness of membrane

• Anaemia • IPF , Sarcoidosis , Asbestosis ,
Hypersensivity pneumonitis
• Emphysema
• Heart Failure , Pulmonary HTN
• Lung/Lobe resection
• Collagen Vascular Disease-SLE ,
• Bronchial obstruction by tumor Scleroderma
• Multiple emboli • Drug induced fibrosis

§ Other –Elderly, female , Smoking , Pregnancy ,

ventilation perfusion mismatch
 Reduced DLCO
Anaemia Reduced Hb , reduced surface area

Emphysema Alveolar walls and capillaries are destroyed ,

reducing surface area
Emboli By blocking perfusion , reduces surface are

Bronchial obstruction Reduces lung area and volume

Heart failure lengthens the pathway for diffusion due to fluid

Smoker high CO tension in blood educes driving

pressure
Isolated unexplained reduction of DLCO Primary Pulmonary HTN, Emboli , Obliterative
with normal spirometry and lung volume Vasculopathy
•Adjusting DLCO
• For anaemia : adjusted downwards
• For polycythemia : adjusted upwards
• For low lung volumes : adjusted downwards
• For high lung volumes : adjusted upwards
CRITERIA for ACCEPTABILITY

• Inspired volume ⩾90% of the largest VC in the same test

session
• 85% of test gas Inspired volume inhaled in < 4 second
• A stable calculated breath-hold for 10±2 seconds
• Sample collection completed within 4 second of the start of
exhalation
KCO- TRANSFER CO-EFFICIENT for CO
• KCO in healthy young approximately 1.75 mmol/min/kPa/litre, an elderly
adult may be about 1.25
• If the patient has a disease that causes a decrease in lung surface area, or
had a lung removed or unable to expand , then there is a decrease in
transfer factor but there is a normal KCO
• In fibrosing alveolitis or emphysema, where there is damage to the lung
parenchyma there is a reduction in both transfer factor and transfer
coefficient
• KCO increases with age

• Raised/normal KCO but normal/reduced DLCO :

kypho-scoliosis
Pneumonectomy,lobectomy
Neuromascular disaeses
Ankylosing spondylitis
Blood Gas Analysis and it’s
Clinical Interpretation
Outline
1. Common Errors During ABG Sampling
2. Components of ABG
3. Discuss simple steps in analyzing ABGs
4. Calculate the anion gap
5. Calculate the delta gap
6. Differentials for specific acid-base disorders
Delayed Analysis

}Consumptiom of O2 & Production of CO2

continues after blood drawn
ØIcedSample maintains values for 1-2 hours
ØUniced sample quickly becomes invalid within 15-
20 minutes
}PaCO2 ­ 3-10 mmHg/hour
}PaO2 ¯
}pH ¯ d/t lactic acidosis generated by glycolysis
in R.B.C.
Temp Effect On Change of ABG Values

Parameter 37 C (Change 4 C (Change

every 10 min) every 10 min)

¯ pH 0.01 0.001

­ PCO2 1 mm Hg 0.1 mm Hg

¯ PO2 0.1 vol % 0.01 vol %

FEVER OR HYPOTHERMIA

1. Most ABG analyzers report data at N body temp

2. If severe hyper/hypothermia, values of pH &
PCO2 at 37 C can be significantly diff from pt’s
actual values
3. Changes in PO2 values with temp also predictable

q If Pt.’s temp < 37C

Substract 5 mmHg Po2, 2 mmHg Pco2 and Add
0.012 pH per 1C decrease of temperature

Hansen JE, Clinics in Chest Med 10(2), 1989 227-237

AIR BUBBLES
:
1. PO2 ~150 mmHg & PCO2 ~0 mm Hg in air bubble(R.A.)
2. Mixing with sample, lead to ­ PaO2 & ¯ PaCO2

qTo avoid air bubble, sample drawn very slowly and

preferabily in glass syringe

Steady State:

ØSampling should done during steady state after change in

oxygen therepy or ventilator parameter
ØSteady state is achieved usually within 3-10 minutes
Leucocytosis :
Ø ¯ pH and Po2 ; and ­ Pco2
Ø 0.1 ml of O2 consumed/dL of blood in 10
min in pts with N TLC
Ø Marked increase in pts with very high
TLC/plt counts – hence imm chilling/analysis
essential

}EXCESSIVE HEPARIN
ØDilutionaleffect on results ¯ HCO3- & PaCO2
ØOnly .05 ml heperin required for 1 ml blood.

qSo syringe be emptied of heparin after flushing or only dead

space volume is sufficient or dry heperin should be used
q TYPE OF SYRINGE
1. pH & PCO2 values unaffected
2. PO2 values drop more rapidly in plastic syringes (ONLY
if PO2 > 400 mm Hg)
q Differences usually not of clinical significance so plastic
syringes can be and continue to be used
qRisk of alteration of results ­ with:
1.­ size of syringe/needle
2.¯ vol of sample

q HYPERVENTILATION OR BREATH HOLDING

May lead to erroneous lab results

 COMPONENTS OF THE ABG
} pH: Measurement of acidity or alkalinity, based on the
hydrogen (H+). 7.35 – 7.45
} Pao2 :The partial pressure oxygen that is dissolved in arterial
blood. 80-100 mm Hg.
} PCO2: The amount of carbon dioxide dissolved in arterial
blood. 35– 45 mmHg
} HCO3 : The calculated value of the amount of bicarbonate in
the blood. 22 – 26 mmol/L
} SaO2:The arterial oxygen saturation.
>95%
q pH,PaO2 ,PaCO2 , Lactate and electrolytes are measured
Variables
q HCO3 (Measured or calculated)
Contd…
} Buffer Base:
} It is total quantity of buffers in blood including both
volatile(Hco3) and nonvolatile (as Hgb,albumin,Po4)
} Base Excess/Base Deficit:
} Amount of strong acid or base needed to restore
plasma pH to 7.40 at a PaCO2 of 40 mm Hg,at
37*C.
} Calculated from pH, PaCO2 and HCT
} Negative BE also referred to as Base Deficit
} True reflection of non respiratory (metabolic) acid
base status
} Normal value: -2 to +2mEq/L
CENTRAL EQUATION OF ACID-BASE
PHYSIOLOGY

Ø Henderson Hasselbach Equation:

q [H+] in nEq/L = 24 x (PCO2 / [HCO3 -] )

Ø where [ H+] is related to pH by

q [ H+] in nEq/L = 10 (9-pH)

} To maintain a constant pH, PCO2/HCO3- ratio should be

constant
} When one component of the PCO2/[HCO3- ]ratio is altered,
the compensatory response alters the other component in the
same direction to keep the PCO2/[HCO3- ] ratio constant
Compensatory response or regulation of
pH
By 3 mechanisms:
Ø Chemical buffers:
Ø React instantly to compensate for the addition or
subtraction of H+ ions

Ø CO2 elimination:
Ø Controlled by the respiratory system
Ø Change in pH result in change in PCO2 within minutes

Ø HCO3- elimination:
Ø Controlled by the kidneys
Ø Change in pH result in change in HCO3-
Ø It takes hours to days and full compensation occurs in 2-
5 days
Normal Values
Variable Normal Normal
Range(2SD)

pH 7.40 7.35 - 7.45

pCO2 40 35-45

Bicarbonate 24 22-26

Anion gap 12 10-14

Albumin 4 4
Steps for ABG analysis
1. What is the pH? Acidemia or Alkalemia?
2. What is the primary disorder present?
3. Is there appropriate compensation?
4. Is the compensation acute or chronic?
5. Is there an anion gap?
6. If there is a AG check the delta gap?
7. What is the differential for the clinical processes?
Step 1:
} Look at the pH: is the blood acidemic or alkalemic?

} EXAMPLE :
} 65yo M with CKD presenting with nausea, diarrhea and acute
respiratory distress
v ABG :ABG 7.23/17/235 on 50% VM
v BMP Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr 5.1
} ACIDMEIA OR ALKALEMIA ????
EXAMPLE ONE
v ABG 7.23/17/235 on 50% VM
v BMP Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr
5.1
} Answer PH = 7.23 , HCO3 7
} Acidemia
Step 2: What is the primary disorder?

What disorder is pH pCO2 HCO3

present?
Respiratory pH low high high
Acidosis
Metabolic Acidosis pH low low low
Respiratory pH high low low
Alkalosis
Metabolic Alkalosis pH high high high
Contd….
ØMetabolic Conditions are suggested if
¨pH changes in the same direction as pCO2 or pH is
abnormal but pCO2 remains unchanged

ØRespiratory Conditions are suggested if:

¨pH changes in the opp direction as pCO2 or pH is abnormal
but HCO3- remains unchanged
EXAMPLE

v ABG 7.23/17/235 on 50% VM

v BMP Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr 5.

} PH is low , CO2 is Low

} PH and PCO2 are going in same directions then its most likely
primary metabolic
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)
Acute respiratory acidosis delta pH = 0.008 × (PCO2 - 40)
Chronic respiratory acidosis delta pH = 0.003 × (PCO2 - 40)
Acute respiratory alkalosis delta pH = 0.008 × (40 - PCO2)
Chronic respiratory alkalosis delta pH = 0.003 × (40 - PCO2)

From: THE ICU BOOK - 2nd Ed. (1998) [Corrected]

Step 3-4: Is there appropriate
compensation? Is it chronic or acute?
Ø Respiratory Acidosis
} Acute (Uncompensated): for every 10 increase in pCO2 -> HCO3
increases by 1 and there is a decrease of 0.08 in pH
} Chronic (Compensated): for every 10 increase in pCO2 -> HCO3
increases by 4 and there is a decrease of 0.03 in pH
Ø Respiratory Alkalosis
Ø Acute (Uncompensated): for every 10 decrease in pCO2 -> HCO3
decreases by 2 and there is a increase of 0.08 in PH
Ø Chronic (Compensated): for every 10 decrease in pCO2 -> HCO3
decreases by 5 and there is a increase of 0.03 in PH

q Partial Compensated: Change 1 4

in pH will be between 0.03 to
0.08 for every 10 mmHg 10
change in PCO2
2 5
Step 3-4: Is there appropriate
compensation?
Ø Metabolic Acidosis
Ø Winter’s formula: Expected pCO2 = 1.5[HCO3] + 8 ± 2
OR
D pCO2 = 1.2 (D HCO3)
Ø If serum pCO2 > expected pCO2 -> additional respiratory
acidosis and vice versa
Ø Metabolic Alkalosis
} Expected PCO2 = 0.7 × HCO3 + (21 ± 2)
OR
D pCO2 = 0.7 (D HCO3)
} If serum pCO2 < expected pCO2 - additional respiratory
alkalosis and vice versa
EXAMPLE
v ABG 7.23/17/235 on 50% VM
v BMP Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr 5.

} Winter’s formula : 17= 1.5 (7) +8 ±2 = 18.5(16.5 –

20.5)
} So correct compensation so there is only one
disorder Primary metabolic
Step 5: Calculate the anion gap
} AG used to assess acid-base status esp in D/D of
met acidosis
} D AG & D HCO3- used to assess mixed acid-base
disorders

q AG based on principle of electroneutrality:

} Total Serum Cations = Total Serum Anions
} Na + (K + Ca + Mg) = HCO3 + Cl + (PO4 + SO4
+ Protein + Organic Acids)
} Na + UC = HCO3 + Cl + UA
} Na – (HCO3 + Cl) = UA – UC
} Na – (HCO3 + Cl) = AG
} Normal =12 ± 2
Contd…
} AG corrected = AG + 2.5[4 – albumin]
} If there is an anion Gap then calculate the
Delta/delta gap (step 6) to determine
additional hidden nongap metabolic acidosis
or metabolic alkalosis
} If there is no anion gap then start analyzing
for non-anion gap acidosis
EXAMPLE
} Calculate Anion gap
v ABG 7.23/17/235 on 50% VM
v BMP Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr 5/ Albumin 2.

} AG = Na – Cl – HCO3 (normal 12 ± 2)
123 – 97 – 7 = 19
} AG corrected = AG + 2.5[4 – albumin]
= 19 + 2.5 [4 – 2]
= 19 + 5 = 24
Step 6: Calculate Delta Gap
} Delta gap = (actual AG – 12) + HCO3
} Adjusted HCO3 should be 24 (+_ 6) {18-30}
} If delta gap > 30 -> additional metabolic alkalosis
} If delta gap < 18 -> additional non-gap metabolic
acidosis
} If delta gap 18 – 30 -> no additional metabolic
disorders
EXAMPLE : Delta Gap
v ABG 7.23/17/235 on 50% VM
v BMP Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr 5/ Albumin 4.

} Delta gap = (actual AG – 12) + HCO3

} (19-12) +7 = 14
} Delta gap < 18 -> additional non-gap metabolic
acidosis
} So Metabolic acidosis anion and non anion gap
Metobolic acidosis: Anion gap acidosis
EXAMPLE: WHY ANION GAP?
} 65yo M with CKD presenting with nausea, diarrhea and acute
respiratory distress
v ABG :ABG 7.23/17/235 on 50% VM
v BMP Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr 5.1
} So for our patient for anion gap portion its due to BUN
of 119 UREMIA
} But would still check lactic acid
Nongap metabolic acidosis
} For non-gap metabolic acidosis, calculate the urine anion
gap
} URINARY AG
Total Urine Cations = Total Urine Anions
Na + K + (NH4 and other UC) = Cl + UA
(Na + K) + UC = Cl + UA
(Na + K) – Cl = UA – UC
(Na + K) – Cl = AG

qUAG = UNA + UK – UCL

} Distinguish GI from renal causes of loss of HCO3 by estimating
Urinary NH4+ .
} Hence a -ve UAG (av -20 meq/L) seen in GI, while +ve value (av
+23 meq/L) seen in renal problem.

Kaehny WD. Manual of Nephrology 2000; 48-62

EXAMPLE : NON ANION GAP ACIDOSIS
} 65yo M with CKD presenting with nausea, diarrhea and acute
respiratory distress
v ABG :ABG 7.23/17/235 on 50% VM
v BMP Na 123/ Cl 97/ HCO3 14
v AG = 123 – 97-14 = 12
} Most likely due to the diarrhea
Causes of nongap metabolic acidosis - DURHAM

Diarrhea, ileostomy, colostomy, enteric fistulas

Ureteral diversions or pancreatic fistulas

RTA type I or IV, early renal failure

Hyperailmentation, hydrochloric acid administration

Acetazolamide, Addison’s

Miscellaneous – post-hypocapnia, toulene, sevelamer, cholestyramine ingestion

Metabolic alkalosis
} Calculate the urinary chloride to differentiate saline
responsive vs saline resistant
} Must be off diuretics in order to interpret urine chloride

Saline responsive UCL<25 Saline-resistant UCL >25

Vomiting If hypertensive: Cushings, Conn’s, RAS,
renal failure with alkali administartion
NG suction If not hypertensive: severe hypokalemia,
hypomagnesemia, Bartter’s, Gittelman’s,
licorice ingestion
Over-diuresis Exogenous corticosteroid administration
Post-hypercapnia
Respiratory Alkalosis
Causes of Respiratory Alkalosis

Anxiety, pain, fever

Hypoxia, CHF
Lung disease with or without hypoxia – pulmonary embolus, reactive
airway, pneumonia
CNS diseases
Drug use – salicylates, catecholamines, progesterone
Pregnancy
Sepsis, hypotension
Hepatic encephalopathy, liver failure
Mechanical ventilation
Hypothyroidism
High altitude
Case1.
} 7.27/58/60 on 5L, HCO3- 26, anion gap is
12, albumin is 4.0
} 1. pH= Acidemia (pH < 7.4)
} 2.CO2= Acid (CO2>40)
} Opposite direction so Primary disturbance =
Respiratory Acidosis
} 3 &4: Compensation : Acute or chronic? ACUTE
} CO2 has increased by (58-40)=18
} If chronic the pH will decrease 0.05 (0.003 x 18 = 0.054)
à pH would be 7.35
} If acute the pH will decrease 0.14 (0.008 x 18 = 0.144)
àpH would be 7.26.
Contd.
} 5: Anion gap –N/A
} 6: There is an acute respiratory acidosis, is there
a metabolic problem too?
} ΔHCO3- = 1 mEq/L↑/10mmHg↑pCO2
} The pCO2 is up by 18 à so it is expected that the HCO3-
will go up by 1.8. Expected HCO3- is 25.8, compared to
the actual HCO3- of 26, so there is no additional
metabolic disturbance.
} Dx-ACUTE RESPIRATORY ACIDOSIS
Case.2
} 7.54/24/99 on room air, HCO3- 20, anion
gap is 12, albumin is 4.0.
} 1: pH= Alkalemia (pH > 7.4)
} 2.CO2= Base (CO2<40)
} pH & pCO2 change in opposite Direction So
Primary disturbance = Respiratory Alkalosis
} 3 &4: Compensation ? acute or chronic? ACUTE
} ΔCO2 =40-24=16
} If chronic the pH will increase 0.05 (0.003 x 16 = 0.048)
à pH would be 7.45
} If acute the pH will increase 0.13(0.008 x 16 = 0.128)
àpH would be 7.53
Contd…
} 5:Anion gap – N/A
} 6: There is an acute respiratory alkalosis, is there
a metabolic problem too?
} ΔHCO3- = 2 mEq/L↓/10mmHg↓pCO2
} The pCO2 is down by 16 à so it is expected that the
HCO3- will go down by 3.2. Expected HCO3- is 20.8,
compared to the actual HCO3- of 20, so there is no
additional metabolic disturbance.
} Dx-ACUTE RESPIRATORY ALKALOSIS
Case-3
} 7.58/55/80 on room air, HCO3- 46, anion gap is
12, albumin is 4.0. Ucl -20
} 1: pH= Alkalemia(pH > 7.4)
} 2:CO2= Acid (CO2>40)
} Same direction so Primary disturbance = Metabolic
Alkalosis
} 3&4: Compensation:
} ∆ pCO2=0.7 x ∆ HCO3-
} The HCO3- is up by 22.CO2 will increase by 0.7x22 = 15.4.
Expected CO2 is 55.4, compared to the actual CO2 of 55,
therefore there is no additional respiratory disturbance.
contd
} 5: No anion gap is present; and no adjustment
needs to be made for albumin. Metabolic
Alkalosis
} Urinary chloride is 20 meq/l (< 25 meq/l)so
chloride responsive, have to treat with Normal
saline.

Dx-METABOLIC ALKALOSIS
Case-4
} 7.46/20/80 on room air, HCO3- 16, anion
gap = 12, albumin = 4.0
} 1: pH = Alkalemia (pH > 7.4)
} 2:CO2 = Base (CO2<40)
} So Primary disturbance = Respiratory Alkalosis
} 3 &4: Compensation? acute or chronic? Chronic
} ΔCO2 =40-20= 20.
} If chronic the pH will increase 0.06 (0.003 x 20 = 0.06) à
pH would be 7.46.
} If acute the pH will increase 0.16 (0.008 x 20 = 0.16) àpH
would be 7.56.
Contd….
} 5: Anion gap – N/A
} 6: There is a chronic respiratory alkalosis, is there
a metabolic problem also?
} Chronic: ΔHCO3- = 4 mEq/L↓/10mmHg↓pCO2
} The pCO2 is down by 20 à so it is expected that the
HCO3- will go down by 8. Expected HCO3- is 16, therefore
there is no additional metabolic disorder.
} Dx-CHRONIC RESPIRATORY ALKALOSIS
Case-5
} 7.19/35/60 on 7L, HCO3- 9, anion gap = 18,
albumin = 4.0
} 1: pH = Acidemia (pH < 7.4)

} 2:CO2= Base (CO2<40)

} So Primary disturbance: Metabolic Acidosis
} 3&4: Compensation ?
∆ pCO2=1.2 x ∆ HCO3-
} CO2 will decrease by 1.2 (∆HCO3-) à 1.2 (24-9) à18. 40 – 18=
22à Actual CO2 is higher than expected àRespiratory Acidosis

} 5: Anion Gap = 18 (alb normal so no correction necessary)

Contd…..
6: Delta Gap:
} Delta gap = (actual AG – 12) + HCO3
= (18-12) + 9
= 6 + 9 = 15 which is<18 àNon-AG Met Acidosis

} Dx-ANION GAP METABOLIC ACIDOSIS with NON-ANION GAP

METABOLIC ACIDOSIS with RESPIRATORY ACIDOSIS
Case-6
} 7.54/80/65 on 2L, HCO3- 54, anion gap
12,albumin = 4.0 , Ucl 40 meq/l
} 1: pH = Alkalemia (pH > 7.4)
} 2:CO2= Acid (CO2>40)
} So Primary disturbance: Metabolic Alkalosis
} 3&4: Compensation?
∆ pCO2=0.7 x ∆ HCO3-

} CO2 will increase by 0.7 (∆HCO3-) à 0.7 (54-24) à21à40

+ 21 = 61 àActual CO2 is higher than expected
àRespiratory Acidosis
Contd….
} 5:Anion Gap = 12 (alb normal so no correction
necessary)
} Urinary chloride is 40 meq/l (> 25 meq/l)so
chloride resistant. So treatment would be disease
specific and repletion of potassium

} Dx-METABOLIC ALKALOSIS with RESPIRATORY

ACIDOSIS
Case-7
} 7.6/30/83 on room air, HCO3- 28, anion gap = 12, albumin =
4.0
} 1: pH = Alkalemia (pH > 7.4)
} 2:CO2= Base (CO2<40)
} SoPrimary Disturbance: Metabolic Alkalosis
} 3&4: Compensation ?
∆ pCO2=0.7 x ∆ HCO3-
} CO2 will increase by 0.7 (∆HCO3-) à 0.7 (28-24) à2.8à 40 + 2.8 = 42.8à
Actual CO2 is lower than expected àRespiratory Alkalosis

} Anion Gap = 12 (alb normal so no correction necessary)

} See urinary chloride for further Dx.

} Dx-METABOLIC ALKALOSIS with RESPIRATORY ALKALOSIS

Case-8
} A 50 yo male present with sudden onset of SOB with
following ABG 7.25/46/78 on 2L, HCO3- 20, anion gap = 10,
albumin = 4.0
} 1: pH = Acidemia (pH < 7.4)

} 2:CO2= Acid (CO2>40)

} So Primary disturbance: Respiratory Acidosis
} 3 &4: If respiratory disturbance is it acute or chronic?
ACUTE
} ∆ CO2 = 46-40= 6
} If chronic the pH will decrease 0.02 (0.003 x 6 = 0.018) à
pH would be 7.38
} If acute the pH will decrease 0.05 (0.008 x 6 = 0.048)
àpH would be 7.35.
Contd…
} Anion Gap = 10 (alb normal so no correction necessary)
} 6: There is an acute respiratory acidosis, is there a metabolic
problem too?
} ∆ HCO3- = 1 mEq/L↑/10mmHg↑pCO2
¨ The HCO3- will go up 1mEq/L for every 10mmHg the pCO2goes up
above 40
} The pCO2 is up by 6 à so it is expected that the HCO3- will go up by 0.6.
Expected HCO3- is 24.6, compared to the actual HCO3- of 20. Since the
HCO3- is lower than expected àNon-Anion Gap Metabolic Acidosis
(which we suspected).

} Dx-RESPIRATORY ACIDOSIS with NON-ANION GAP

METABOLIC ACIDOSIS
Case-9
} 7.15/22/75 on room air, HCO3- 9, anion gap = 10, albumin =
2.0
} 1: pH = Acidemia (pH < 7.4)

} 2:CO2= Base (CO2<40)

} So Primary disturbance: Metabolic Acidosis
} 3&4:∆ Compensation ?
pCO2=1.2 x ∆ HCO3-
} Expected pCO2 = 1.2 x ∆ HCO3-à 1.2 (24 -9) à 1.2 (15)à
18. The expected pCO2is 22mmHg. The actual pCO2 is
22, which is expected, so there is no concomitant
disorder.
Contd….
} 5: Anion Gap = 10
} AGc = 10 + 2.5(4-2) = 15 à Anion Gap Metabolic
Acidosis
} 6: Delta Gap:
} Delta gap = (actual AG – 12) + HCO3
= (15-12) + 9
= 3+ 9 = 12 which is<18 àNon-AG Met
Acidosis

} Dx-ANION GAP METABOLIC ACIDOSIS with NON-ANION

GAP METABOLIC ACIDOSIS