Respiratory Medicine 1

Respiratory Function test

Inspiration Chest wall moves outside Diaphragm goes down Intrathoracic pressure
becomes negative Elastic parenchyma becomes bigger Airway is attached to elastic
parenchyma and it gives radial traction to airways Atmospheric air comes into the
lungs

Expiratory phase Air has to come out Two factors Airway squeezed by elastic
parenchyma recoil inwards This is maximum during early phase of expiration(
initial 1st second)
Second factor is Resistance by airways( minimum during 1st second) I unit
diameter decrease increases the resistance by four times Therefore resistance is the
main and the most important factor

Obstructive Disease Chronic Bronchitis: main problem in diameter of airway

Emphysema: elastic recoil issue, less drop in first second
Obstructive graph is right and above the normal Restrictive is left and below the
normal

Spirometry graph Air that is exhaled out FVC: 4.5 liter assumed
L shaped, normal value L shaped, less value than normal, restrictive Almost
straight line, obstructive
Normal value

FVC: 80-120% of predicted

FEV1: 70-80% of observed FVC
FEV1/ FVC: >70%
Analysis Look at the ratio of FEV1/FVC first

scleroderma can present as pulmonary HT and ILD( restrictive) as well

FEF 25-75%: forced expiratory flow rate during 25-75% of FVC Aka peak mid
expiratory flow rate Denotes air flow from small airways
Sensitive marker for small airways disease Bronchial asthma Bronchiolitis (RSV)
PEFR: peak expiratory flow rate Indicates maximum velocity achieved Clinically
not very important Used in monitoring response to treatment in Asthma
One liners

Most sensitive marker of COPD : FEV1/FVC

Most sensitive marker of Asthma: FEF 25-75%
Prognostic marker of COPD: FEV1 decrease
Prognostic marker of Asthma: FEV1 decrease
2. Lung volume studies
Measurement of Air parameters inside lungs Therefore more important in
restrictive diseases
Helium dilution method Pt. Inhales and exhale helium( inert and not absorbed)
Initial conc. noted Final conc. of helium noted Helium will be diluted Therefore
the difference is the lung volume But if the lung has bullae/ slow communicating
cavity This will overestimate the lung capacity Therefore not done of these
conditions present
Whole body plethysmography Useful in bullae/ slow communicating cavity
Pt sits in a chamber During inspiratory phase, lung pressure decrease Chamber
pressure increases in turn Expiratory phase, lung pressure increase, and chamber
pressure

decreases Boyle's law Pressure is inversely related to volume

Total lung capacity(TLC): air inside lung after maximum inspiration
Residual volume(RV): air inside lungs after maximum excretion
Vital Capacity: TLC- RV
FVC is not VC

3. DLCO Diffusion lung capacity for Carbon Monoxide Rapidly diffusible gas
Diluted CO inhaled Hold the breath for 8-10 seconds( time for one pulmonary
circulation cycle) CO gets absorbed Now pt. Exhales and we measure the exhaled
CO
Therefore DLCO= iCO- eCO Normal is 80-120% of predicted
Low Pulmonary vascular disease( spirometry was normal) Interstitial lung disease
Emphysema( decreased capillary density over alveoli as alveoli merges due to
septa destruction)

Severe anemia
High DLCO
Pulmonary vascular congestion/ dilation Polycythemia Good pasture Syndrome
(alveolar hemorrhage) , is an ILD
4. Alveolar arterial gradient
PAO2- PaO2= 0-15 mm Hg Alveolar minus arterial

gravity plays important part Apical part gets less pressure of blood
PAO2-PaO2= increased
Indicates Ventilation Perfusion disorder Therefore there is some sort of intrinsic
pulmonary disease
Pt comes with decreased PaO2( hypoxemia) If high altitude The gradient will be
normal Will be increased in intrinsic disease
Scenario Normal FiO2 at sea level is 21%(0.21) Rep rate is 15/ min Tidal volume=
500 ml Dead space= 150 ml Therefore the transferable air is 350 ml In 1 min,
oxygen in alveoli will be 0.21*350*15= 1100 1100 ml oxygen is available for
transfer
Therefore the conditions which can decrees the available air FiO2 decreased ( high
altitude) Respiratory rate decreased( central hypo ventilation syndromes) Dead
space increased Decrease the Tidal volume

Therefore in these conditions, hypoxemia( decreased PaO2) will be there but the
gradient will be normal
But in ventilation perfusion disorders, gradient will increase
V:Q disorders( gradient increases)
A. Ventilation normal, perfusion decreased Pulmonary vascular disease
Emphysema ILD All these have decreased DLCO as well
B. Ventilation decreased, perfusion normal Alveolar filling present Pulmonary
edema( fluid) ARDS( exudates) Pneumonia( consolidation)
All these fall under physiological shunting


ARDS
Mechanism: exudative filling of alveoli due to cytokines, which are increased
either due to infective or non infective pathologies
Causes
Pulmonary causes Pneumonia is the most common cause Inhalation of toxic
fumes/gas Aspiration of gastric contents Lung contusions Near drowning Never the
cause COPD Asthma
Systemic causes Most common is sepsis overall Acute pancreatitis multiple
fractures Fat embolism Massive blood transfusion
Pathology
Stage 1= initiation/ exudation stage Main cells affected: type 1 alveolar cells(
pneumocytes)

Thus Most common abnormality is decreased PaO2 This will lead to

Hyperventilation Leading to PaCO2 decrease CO2 is easily diffusible in fluid
while oxygen is not diffusible Therefore CO2 is washed out from diseased alveoli
also
Stage 2: maintenance Main damage is to Type 2 Alveolar cells Surfactant
decreases, lung compliance decreases, leading to stiff lungs
Type 2 convert to type 1 cells Therefore, maximum damage is to type 1 cells
Stage 3: resolution/ fibrosis
If fibrosis, leads to interstitial lung disease
Criteria for ARDS( 2012 Berlin criteria) C/F 1. Onset within one week of primary
injury

2. PaO2/FiO2 200-300= mild ARDS ( previously ALI) 100-200= moderate <100=

severe
3. No evidence of increased left atrial pressure( clinical or ECHO) ( old= PCWP
<18 mm Hg= non cardiogenic pulmonary edema)
4. Bilateral infiltrates ( either on CXR or CT)
Management
Mainstay is Mechanical Ventilation
1. normal alveoli has to be protected from barotrauma Therefore TV has to be kept
low It decreases mortality Low= 6 ml/ kg body wt ( normal= 10 ml/ kg body wt)
2. Prone position ventilation It increases functional units of lower lobe
3. PEEP( positive end expiratory pressure)

The tube has multiple lumen One provides oxygen The other keeps the alveoli
open at the end of expiration to increase oxygen transfer
4. FiO2 less than 60% To prevent free oxygen damage This also improves
PaO2/FiO2
Diuretics Help in shifting of the fluid out of the alveoli into the vessels( not
diuresis) But avoid hypotension
Nitric oxide Causes vasodilation Which in turn increases the oxygen diffusion
Steroids Anti inflammatory effect Limited benefits