Pulmonary Physiology Flashcards
Ventilation vs. Respiration
V:
- Mechanics of moving air
- “Breathing”–inspiration + expiration
R:
- Mechanics of gas exchange
- O2 import + CO2 export
Pulmonary System
Gas exchange organs (lungs) + a pump that ventilates the lungs (brain, nerves, chest wall, muscles)
- Tidal Volume (Vt): At rest, 500 mL of gas per breath, at a normal 10-15 breaths per min = 5L/min.
- Inhaled O2 into the blood & CO2 from the blood into the alveoli (gas exchange sac)
Conducting Pulmonary System
- no respiration here, only transport of gas
- the first 16 airway divisions (out of 30, left and right)
- high air flow
- nasopharynx, oropharynx, larynx
- trachea
- primary bronchi
- secondary bronchi
- bronchioles, terminal bronchioles
Respiratory Pulmonary System
= the acinus
- respiration occurs here
- the remaining 7 airway divisions
- low air flow
- respiratory bronchioles (specialized bronchiole containing alveoli)
- alveolar ducts -> alveolar sacs -> alveoli
- ~300,000,000 alveoli = surface area of 75 m2
Law of Laplace
Pressure (P) in a distensible hollow sphere (alveolus) = 2x the wall tension (T) divided by the radius (r) of the sphere
- P = 2T/r
Ex. For a given P, when r is small (end of expiration), T is high
- -> thus, at the end of expiration, alveoli would collapse d/t high wall tension
- -> BUT, this doesn’t happen d/t surfactant
Surfactant
Surface tension lowering compound
- Alters the law of Laplace to keep alveoli open during expiration
- Composed of lipoproteins (protein and fat)
- Made by type II pneumocytes’ lamellar bodies
- Prevents pulmonary edema (fluid from capillaries into alveoli)
Tobacco smoke decreases surfactant levels
Infant Respiratory Distress Syndrome
“Hyaline Membrane Disease”
- due to an immature surfactant system
- leads to alveolar collapse (atelectasis)
Atelectasis
Alveolar collapse
= No ventilation –> blood doesn’t get oxygenated –> leads to hypoxia
2 types: Resorption and Compression
*Consider a ventilation-perfusion mismatch condition (blood to alveolus, but not oxygenated)
Resorption Atelectasis
- Obstruction prevents air from reaching distal airspaces
- Trapped air eventually gets absorbed & collapse follows
- Can affect 1 lung, 1 lobe, or 1 segment
MCC = mucus or mucopurulent plug
(i.e., post-op, asthma, bronchiectasis, bronchitis, foreign body aspiration in children)
Compression Atelectasis
- Intrapleural fluid, blood, or air mechanically collapse the adjacent alveoli
MCC = pleural effusion d/t CHF, pneumothorax, elevated diaphragm in bedridden pts or ascites (liver disease)
Functional Respiration
Proper oxygenation of blood & elimination of CO2 requires…
- Ventilation of the lung
- Perfusion of alveolus proportional to ventilation
- Adequate diffusion of gases across the respiratory membrane (interstitial)
Resting Ventilation
Inspiration
- DIAPHRAGM (phrenic nerve, C3/4/5)
- External intercostals
- Accessory muscles (SCM, trapezius, pectoralis minor, scalenes)
Expiration
- Passive, elastic recoil of lungs
- Abdominal muscles (obliques, rectus abdominus)
Forced Ventilation
Inspiration
- External intercostals + Accessory muscles
Expiration
- Abdominals (rectus and transversus abdominus, internal/external obliques)
- Internal intercostals
Glottis
Inspiratory action–laryngeal abductors contract, pulling the vocal cords apart & opening the glottis
- Swallow/Gag Action: laryngeal adductors contract, closing the cords and glottis to prevent passage of fluid, food, and vomitus into the lungs
- Laryngeal muscles run by vagus (CN 10)
Aspiration
- Improper functioning of glottis causing vomitus to pass into the lungs –> aspiration pneumonia or chemical pneumonitis
- Elderly, alcohol intoxication
- Paralysis of the vagus nerve –> inspiratory stridor –> aspiration
Dead Space
Volume of air in the conducting zone, which is not involve with respiration
- Equal to body weight in pounds
- Ex. 150# male = 150 mL dead space –> 350/500 mL inhaled is available for respiration
Dead Space Types
- Anatomic: conducting zone volume only
- Physiologic: volume of air not available for respiration
- Normally, they are the same*, but physiologic DS increases in diseased states
- Ventilatory or alveolar dysfunction disallows ventilated air to interact w/ blood
- Perfusion or capillary dysfunction disallows blood access to ventilated air
Tidal Volume
Volume of air that moves into lungs w/ each breath
- Nonlinear relationship d/t resistance (ellipse)
Inspiratory/Expiratory Reserve
I: volume of air inspired w/ maximal effort in excess of tidal volume
E: volume of air expired with maximal effort after passive expiration
Residual Lung Volumes
volume of air left in the lungs after max expiration
- does not exit d/t surfactant
Vital Capacity
= Forced vital capacity (FVC)–the maximum volume of air that can be expired after maximal inspiratory effort
* VC = Vt + IR + ER * Normal = 5L * Decreased in restrictive lung DZ * Normal or increased in obstructive lung DZ
- Forced expiratory volume (FEV1) is the fraction of the FVC expired in the first second
- Both FVC and FEV1 are very useful pulmonary function tests (PFTs)
Recoil
= The tendency to return to a previous shape
based mainly on elasticity (elastic tissue function)
-chest wall’s natural recoil is to expand
*chest wall always wants to come out
-lung’s natural recoil is to collapse
*lung itself always wants to shrivel up
Compliance
= The feasibility of movement; “stretchability”
-volume change per unit pressure change
The inverse of recoil
- Compliance increases if recoil decreases –> if a structure doesn’t want to return to a previous shape, then it is easy to move
- Compliance decreases if recoil increases –> if a structure really wants to keep its shape, then it isn’t easy to move
Diseases of Reduced/Increased Lung Compliance
Reduced compliance (stiff lung):
- fibrous tissue (PulmFibrosis)
- alveolar fluid (PulmEdema)
- increased pulmonary venous pressure (backup of fluid from L Atrium and L Vent dysfunction)
Increased compliance (floppy lung):
- Emphysema (elastin loss)
- Emphysema + Chronic Bronchitis = COPD
- Usually in smokers
- Emphysema + Chronic Bronchitis = COPD
Emphysema/COPD Lung Compliance & Recoil
- Loss of elasticity in lung
- less lung recoil = more compliance
- Wall recoil > lung recoil –> larger lung volumes
- larger chest and lungs (“Barrel Chested”)
Pulmonary Fibrosis Lung Compliance & Recoil
- Normal tissue replaced by fibrotic tissue
- more lung recoil = less compliance
- Lung recoil > wall recoil –> smaller lung volumes
- smaller chest and lungs
Intrapleural Pressure
- Normally, the intrapleural space allows slippage, but not separation –> “tug-of-war” between chest wall’s desire to expand (recoil) and lung’s desire to contract (recoil)
–> set up the intrapleural pressure (normal = -2 mmHg)
Functional Residual Capacity
= the lung volume that exists at the equilibrium between chest wall recoil and lung recoil
- Normal = 2.5 L
- Increased FRC –> emphysema
- (low recoil = high compliance = high FRC)
- Decreased FRC –> pulmonary fibrosis
Pneumothorax
= hole in lung (visceral pleura; ex. Spontaneous pneumothorax) or chest wall (parietal pleura; ex. knife wound)
- disallows any pressure to set up, so lung collapses, and chest wall expands
- -> destroys the ability of the chest wall to ventilate the lungs
Ventilation Rate
- Driven mainly by CO2 levels, BUT also depends on oxygen level, blood pH, and volitional action
Ventilation-Perfusion Relationship
Ventilation: more at base, less at apex
- When upright, gravity pulls the base closer to the chest wall -> less ability to ventilate the expanded alveoli (apex) & more ability to ventilate closed alveoli (base)
Perfusion (pulmonary capillary blood flow): thus, greater at base, less at apex
- Perfuse the area that is better ventilated
- Normally, this inequality is kept at a minimum, but diseases can result in large mismatches b/t ventilation & perfusion
- ventilation of underperfused lung (pulmonary embolism) -> hypoxemia
- perfusion of an underventilated lung (pulmonary shunt or airway obstruction) -> shunted venous blood passes w/o being oxygenated, then mixes w/ oxygenated blood -> hypoxemia
Ventilation Mechanics: Inspiration
- diaphragm contracts (abdomen pushed down -> vertical dimension of thorax increased)
- external intercostals contract (ribs lifted up and out -> transverse dimension of thorax increased)
- SCMs contract (sternum raises)
- scalenes contract (first 2 ribs lifted up)
- decreased intrapleural pressure “sucks” the lung against the chest wall, expanding the lung
Ventilation Mechanics: Expiration
Mainly passive recoil of lung
Forced expiration:
- abdominals contract -> push diaphragm upward -> vertical dimension of thorax decreased
- forceful abdominals = cough, vomit, defecation
- internal intercostals contract -> pull ribs down and in -> transverse dimension of thorax decreased
Airway Resistance
Air flow through tubes causes turbulence & resistance
- Highest in medium-sized bronchi & lowest in small bronchioles
- At end expiration, recoil (& thus, the “pull” on airways) decreases –> airways get smaller & resistance increases –> airway collapses, trapping air (residual volume)
- Asthma = bronchoconstriction = increased resistance
- Pulmonary fibrosis: Interstitial wall thickening (fibrosis) -> lungs are less compliant & have more recoil = more pull on airway walls = larger airways = less resistance
Airway Resistance Changes d/t Pulmonary Disease
- Bronchoconstriction (i.e., asthma, COPD) increases resistance
- Higher resistance –> smaller airways –> less recoil –> more air trapped in lungs
- Higher recoil (i.e., pulmonary fibrosis), decreases resistance
- Thickened interstitial walls d/t fibrous tissue –> less compliance, more recoil (esp. in expiration) –> more pull on walls –> larger airways –> less resistance
Obstructive Lung Disease
- Airway obstruction increases airway resistance thus, decreasing airflow –> air gets trapped in the lung during expiration (high residual volume)
- Low air flow = Longer time to get air out of lungs –> less out in 1st second (i.e., very small FEV1 and FEV1/FVC% (characteristic of obstructive) - FVC normal or decreased
Restrictive Lung Disease
- Abnormal alveolar connective tissue –> stiff, noncompliant, high recoil lung –> less lung parenchymal expansion –> decrease in all lung volumes
- b/c all lung volumes are decreased, airflow (which is a function of total lung volume) stays normal or is slightly reduced
- -> FEV1 decreases proportionately to the decrease in overall lung volume
- -> FVC decreases
- -> Near normal FEV1/FVC%
