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76 Cards in this Set

  • Front
  • Back
Pulmonary function test (PFT)
measures parameters of lung function and describe what extent physiological function is compromised by lung disease
PFT measures 2 mechanical properties
1. restrictive lung disease
2. obstructive lung diseae

PFT most sensitive and objective indices of presense of lung involvement and of changes in lung disease
Restrictive lung disease
Dec compliance--> Stiff lungs--> Difficult to inflate --> inc work of breathing

Defined by dec (small) lung volume (Dec TLC)
Examples of restrictive lung disease
pneumonia
pulmonary edema
pulmonary fibrosis
iterstitial peneumonitis
muscular dystrophy
scoliosis
Lung volumes reduce due to...
intrinisic pulmonary disease
extrinsic chest wall restriction
neuromuscular disorders
Obstructive Lung Disease
Airway obstruction
1. Inc resistance --> 2. Airway obstruction --> 3. Narrow airways--> 4. Dec max expiratory flow --> 5. Inc work of breathing

Defined by dec maximal expiratory flow rates and increased airway resistance

When airways narrow--> inability to exhale rapidly
Obstructive lung disease due to...
bronchospasms
airway inflammation
extrinsic compression of the airway
Examples of airway obstruction
asthma
COPD
cystic fibrosis
Normal Values of PFT
Diff lung sizes, PFT compared against expected normal values based on gender, age, height of pt

Normal range is 80-120% predicted
Functional Residual Capacity (FRC)
- most stable lung volume, V we live at bc determined by physiological mechanisms (not voluntary)

- volume at end of normal expiration

Equilibrium between outward chest wall recoil and inward lung recoil
- Chest wall recoil springs outward INC lung volume
- Elastic recoil collapses the lungs DEC lung volume
Total Lung Capacity (TLC)
- total volume of air in the lungs after max inhalation
- measures lung size
Decrease in TLC
is definition of restrictive lung disease

TLC dec by
1. dec lung compliance
2. ventalatory muscle weakness
3. extrinsic compression by chest wall
Vital Capacity (VC)
Amt of air exhaled from a maximal inhalation (TLC) to a maximal exhalation

Usuable lung volume

Volume exhaled form TLC to RV
Decrease in VC
1. Dec lung compliance
2. Dec ventilatory muscle strenght
3. Extrinsic compression from chest wall abnormalities
4. Hyperinflation (Inc RV)
Residual Volume (RV)
Volume of air left in the lung after complete exhalation

Prevents R-L shunt after exhalation and permits gas exchange to occur throughout resiratory cycle
Inability to exhale further (reduce RV) is due to..
1. Airway closure
2. Inability of expiratory muscles to compress the outward chest wall recoil
Increase in RV (hyperinflation)
seen in airway obstruction
Measurements of FRC
1. Nitrogen washout
2. Helium dilution
3. Body plethysmography
Airway obstruction characterized by
reduction in maximal expiratory airflow
How to measure expiratory airflow

Spirogram
During forced exhalation from TLC, volume is plotted against time

FEV1- volume exhaled in the first second

FEV 25-75%- mean flow rate in the middle half of the exhaled VC is the exhalation, reflects middle and small airways more than the FEV1
Maximal expiratory Flow Volume Curve (MEFV) Curve
measures maximal expiratory flow that can be achieved at specific lung volume

Flow is plotted against lung volume from TLC to RV
What does MEFV curve tell you
tells you which airways are most obstructed: large, middle, or small
What does normal MEFV look like

Obstructive lung disease?
Rises to peak expiratory flow rate (PEFR) near TLC and decrease in a nearly linear fashion to zero at RV

Obstructive lung disease produces a scooped configuration curve
What does MEFV look like in..

Small airway obstruction

Large airway obstruction
Small airway obstruction would cause a concave appearance near RV

Large airway obstruction cause the MEFV to be truncated near TLC
Bronchodilator response

When a patient shows airway obstruction, PFT are repeted after inhalation
If expiratory flow rates improve by >= 15% this suggest that the airway obstruction is acutely reversible.

Due to bronchospasm from asthma
Hyperinflation
Airway obstruction causes airway closure, traps air in lungs during exhalation

Inc lung volume (at end of normal exhalation )--> hyperinflation

Measured as inc RV
Airway obstruction
most common pulmonary function abnormality in children/adults

1. asthma
2. chronic obstructive pulmonary diseases
(chronic bronchitis and emphysema)
3. cystic firbosis
Work of breathing
= Pressure x Volume
Pressure to inflate the lungs (P TP)
sum of elastic pressure (Pel to voercome volume) + resistance pressure (Pres, to overcome airflow)

PTP= V/CL +(flow X R)

CL- compliance
PFT

Restrictive Lung diseases
- Decreased lung volumes TLC
- Decreased compliance
PFT

Obstructive Lung Diseases
- narrow and/or obstructed airways
- decrease maxmal expiratory flow rates
- increased resistance
Compliance is dec --> lungs are stiff-->
Pel is larger component of PTP.

More effort req to inc lung volume when lungs are stiff
Resistance is inc--> airway obstruction dec airflow
Pres is larger component of PTP

More effort req to inc flow thorugh narrow airways
Breathing patter
always ones that minimizes work of breathing
Restrictive disease breathing pattern
rapid shallow breathing patter,

do not have to inflate stiff lungs and minimize Pel
Airway obstruction breathing pattern
slow deep breathing matterns-

do not have to generate high airflowa nd minimize Pres
Time constants
Distribution of ventilation is affected by time takes to fill up a region of lung which depends on compliance and resistance

time constant = compliance * resistance
Compliance
Volume/pressure
Resistance
Pressure/flow
Which lung regions will fill first and empty first?

First in; First out
Lung regions with Dec resistance fill rapidly due to inc flow

Lung regions with dec compliance fill rapidly de to dec volume

Lung regions with dec time constant are best ventilated
Alveolar volume for lung regions of

1. Dec resistance

2. Inc compliance
1. bc dec resistance fill rapidly they have inc alveolar volume

2. bc inc compliance has potential to inc volume but takes more time to fill--> they actually have dec alveolar volume bc inspiratory time is too short
Ptp Pleural gradient
gradient in intrapleural pressure from base (~-2cm H2O) to the apex (~-10cm H2O) of the lung

Gradient due to gravity

Elastic recoil greater at apex than base
Effects of gradient
Alveoli large at FRC in apex

Alveoli small at FRC in base
Alveoli large--> tidal volume is smaller

Alveoli small--> tidal volme larger

Ventilation is greater at the base of the lung than at the apex
Two roles of elastic recoil
1. Dec lung volume and causes exhalation to be passive

2. Supports the patency of intra-pulmonary structures when lung volume is fixed
Ppl gradient
- More negative at apex and less negative at the base
- due to gravity
This pressure gradient affects distribution of ventilation
- Alveoli are larger in apex than the base
- There is geater ventilation at the base than at the apex
Gravity affects distribution of ventilation in normal lungs by alterations in
Ppl, Pel, Cl and Raw

Abnormal Cl and Raw also affect the distribution of ventilation

Lung disease pathologic changes in Cl and Raw have a greater effect on distribution than gravity
Distribution of perfusion
-the pulmonary vascular bed is a high compliance, low resistance circuit

- blood flow to the lung regions depend on wheater a blood vessel is open or not

- the patency of pulmonary blood vessels depends primarily on intravascular pressure vs extravascular pressure
Distribution of perfusion
- the gradient in Qp from apex to base of the lung is due to gravity
- there is less Qp gradient in the supine position or when gravity is minimized (outerspace)
- inc in Pa like excercies will eliminate Zone 1 and make the distribution of perfusion more uniform
Zone 1
Alveolar pressure > both pulmonary artery and pulmonary venous pressures.

Capillaries are compressed, and there is no flow.
Zone 2
Arterial pressure > alveolar pressure
alveolar pressure > venous pressure

Flow is difference between arterial and alveolar pressures, and it increases as one descends in vertical height.
Zone 3
Both arterial and venous pressures > alveolar pressure.

Flow is the difference between arterial and venous pressures, and it increases slightly as one descends.
Distribution of V/Q
Ventilation and perfusion are greater in the base than in the apex.

the gradient in perfusion is much steeper than that of ventilation--> V/Q is greater at the apex than at the base.
Pulmonary Circulation Function
1. bring unoxygenated blood to the alveoli
2. serve as a reservoir
3. serve as a filter
4. metabolize (detoxify) some substances as they pass through the lungs.
Pulmonary vascular resistance (PVR)
is extremely low

~10% of systemic vascular resistance

Low PVR even when therse an increase in cardiac output (as during exercise) by:
1. highly distensible pulmonary capillaries
2. by recruitment of capillaries, which were closed at lower cardiac outputs
Extra-alveolar vessels
pulmonary arteries and veins

Subjected primarily to intrapleural pressures

At inc lung volume, dec Ppl distends these vessels, dec PVR.

At dec lung volume, inc Ppl compresses these vessels, inc PVR.
Intra-alveolar vessels
-Pulmonary capillaries

-subjected primarily to alveolar pressures

-At inc lung volume, the stretch on alveolar tissues compresses capillaries, inc PVR

-At dec lung volume, alveolar pressure decreases, distending pulmonary capillaries, and dec PVR.
Pulmonary vascular resistance (PVR)
Intra-alveolar and extra-alveolar vessels are in series--> resistances are additive.

At inc lung volume, PVR is inc in intra-alveolar vessels and dec in extra-alveolar vessels.

At dec lung volume, PVR is inc in extra-alveolar vessels and dec in intra-alveolar vessels. Therefore, PVR is lowest at FRC, the volume at which lungs exist most of the time.
What affects PVR
PAO2 is the most important regulator of pulmonary vascular tone.

Hypoxia causes local pulmonary vasoconstriction --> protective reflex--> directs blood flow away from hypoxic regions of lung.

This preserves V/Q matching.

Acidosis and Inc PAco2 exacerbate the effect of hypoxia on PVR.
Fluid exchange in pulmonary capillary
alveolar-capillary membrane is porous

fluid needs to stay in cap not in alveolus
What forces keep fluid in capillary

Moving fluid into the Capillary

Moving fluid into the Alveolus
Into the Cap:
- Inc colloid osmotic pressure
- Inc alveolar P

Into the Alveolus
-Inc capilarry hydrostatic P
- Inc Alveolar surface tension
What happens in heart failure
Large increases in capillary hydrostatic pressure push fluid into the alveoli--> pulmonary edema

Lesser increases in capillary hydrostatic pressure -> push fluid into interstitial space dec compliance
Pulmonary Lymphatics
clears fluid from interstitial space

drain through the hilum to the thoracic duct into the superior vena cava
Heart failure and pulmonary edema

Left heart failure
blood backs up from the L ventricle to the lungs

Inc cap pressure--> pulmonary edema
Heart failure and pulmonary edema

Right heart failure
blood backs up from the R ventricle into systemic veins

Dec throacic duct flow

Dec pulmonary fluid clearance--> pulmonary edema
Host defense mechanisms

Larger particles (>10u)
move in a straight line, do not follow airways

impact upper airway and do not reach lungs
Host defense mechanisms

Middle size particles (2-10u)
carried in turbulent flow in large airways

Sediment out in turbulent eddies

5-10u Deposit in trachea and are removed by cough

2-5u deposit in bronchi removed by mucocilary activity
Host defense mechanisms

Small sized particles (<2u)
carried in airflow to respiratory bronchioles and alveoli

deposited by diffusion

removed by alveolar macrophages

very small ones are exhaled back out
Cough
clears the airways of secretions

Large airways mechanisms is high airflow velocity (85% of speed of sound)

Cough is primary mechanism for removing secretions when cilia are damaged from inflammation
Cough receptors
located in upper airway, nasopharyns, oropharyns, large airways and esophagus

NOT located in small airways or alveoli
Deposition of B2 particles in lung
deposition of inhaled paricles in large airway is greater for larger particles

bronchodilator effect (Inc FEV1) is greater for larger inhaled particles

Deposition in the periphery is greater for small inhaled particles

Deposition is greater for all particles with slower inspiratory flow rates
Ineffective cough result from
-Abnormalities or alterations in the cough reflex
-unresponsive to repeated stimulation
-receptor not present in alveoli or lung parenchyma
-suppressed by CNS depressant medications
-neuromuscular diseases or abdominal wall muscle weakness
-laryngeal abnormalities preventing glottic closure
Mucocillary clearance
Mucous layer traps inhaled materials and propels them toward large airways by cilia

cilia beat 600-900 times per minutes (10-15Hz)
D 0.25um and L 5-8um

Cilia beat in serous layer below mucous blanket
Cilia
have microscopic hooks, attach to underside of mucous blanket to propel it
Mucocillary action damanged
1. Cilia can be abnormal (genetic mutation of contractile structure of cilia--> primary cilary dyskinesia)

2. Substances can affect cilary activity

3. Mucous can be too thick--> bc of chronic infection, difficult to remove

4. Cystic fibrosis

5. # of substances can affect viscosity of mucous

6. Respiratory viral infections can inactivate mucocilary clearance
Cystic fibrosis
where fluid layer under mucous blanket is dehydrated--> inability to propel mucous
mucous in large areas
then removed by cough

Absence of mucociliary activity--> moves mucous in the airway is gravity