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Pulmonology > Pulmonary Physiology > Flashcards

Pulmonary Physiology Flashcards

1
Q

Ventilation vs. Respiration

A

V:

  • Mechanics of moving air
  • “Breathing”–inspiration + expiration

R:

  • Mechanics of gas exchange
  • O2 import + CO2 export
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2
Q

Pulmonary System

A

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)
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3
Q

Conducting Pulmonary System

A
  • 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
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4
Q

Respiratory Pulmonary System

A

= 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
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5
Q

Law of Laplace

A

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
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6
Q

Surfactant

A

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

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7
Q

Infant Respiratory Distress Syndrome

A

“Hyaline Membrane Disease”

  • due to an immature surfactant system
  • leads to alveolar collapse (atelectasis)
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8
Q

Atelectasis

A

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)

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9
Q

Resorption Atelectasis

A
  • 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)

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10
Q

Compression Atelectasis

A
  • 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)

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11
Q

Functional Respiration

A

Proper oxygenation of blood & elimination of CO2 requires…

  1. Ventilation of the lung
  2. Perfusion of alveolus proportional to ventilation
  3. Adequate diffusion of gases across the respiratory membrane (interstitial)
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12
Q

Resting Ventilation

A

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)
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13
Q

Forced Ventilation

A

Inspiration
- External intercostals + Accessory muscles

Expiration

  • Abdominals (rectus and transversus abdominus, internal/external obliques)
  • Internal intercostals
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14
Q

Glottis

A

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)
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15
Q

Aspiration

A
  • 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
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16
Q

Dead Space

A

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
17
Q

Dead Space Types

A
  • 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
18
Q

Tidal Volume

A

Volume of air that moves into lungs w/ each breath

  • Nonlinear relationship d/t resistance (ellipse)
19
Q

Inspiratory/Expiratory Reserve

A

I: volume of air inspired w/ maximal effort in excess of tidal volume

E: volume of air expired with maximal effort after passive expiration

20
Q

Residual Lung Volumes

A

volume of air left in the lungs after max expiration

- does not exit d/t surfactant

21
Q

Vital Capacity

A

= 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)
22
Q

Recoil

A

= 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

23
Q

Compliance

A

= 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
24
Q

Diseases of Reduced/Increased Lung Compliance

A

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
25
Q

Emphysema/COPD Lung Compliance & Recoil

A
  • Loss of elasticity in lung
    • less lung recoil = more compliance
  • Wall recoil > lung recoil –> larger lung volumes
    • larger chest and lungs (“Barrel Chested”)
26
Q

Pulmonary Fibrosis Lung Compliance & Recoil

A
  • Normal tissue replaced by fibrotic tissue
    • more lung recoil = less compliance
  • Lung recoil > wall recoil –> smaller lung volumes
    • smaller chest and lungs
27
Q

Intrapleural Pressure

A
  • 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)

28
Q

Functional Residual Capacity

A

= 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
29
Q

Pneumothorax

A

= 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
30
Q

Ventilation Rate

A
  • Driven mainly by CO2 levels, BUT also depends on oxygen level, blood pH, and volitional action
31
Q

Ventilation-Perfusion Relationship

A

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
32
Q

Ventilation Mechanics: Inspiration

A
  • 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
33
Q

Ventilation Mechanics: Expiration

A

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
34
Q

Airway Resistance

A

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
35
Q

Airway Resistance Changes d/t Pulmonary Disease

A
  • 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
36
Q

Obstructive Lung Disease

A
  • 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
37
Q

Restrictive Lung Disease

A
  • 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%

Pulmonology (8 decks)

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