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2. HDS Pulmonary > Pulmonary Physiology Review > Flashcards

Pulmonary Physiology Review Flashcards

1
Q

Ventilation

Definition

A

How gases get into the alveoli.

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2
Q

Diffusion

Definition

A

How gases move across the alveolar walls into the blood or vice versa.

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3
Q

Perfusion

Definition

A

How blood vessels remove gas from the lungs.

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4
Q

Pulmonary Functions

A
  1. Gas exchange
  2. Metabolize certain compounds
  3. Filter small clots out of the blood
  4. Reservoir of blood
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5
Q

Conducting Zones

A
  • first 16 generations including:
    • trachea
    • bronchi
    • bronchioles
    • terminal bronchioles
  • do not contain alveoli = no gas exchange
    • makes up the anatomical dead space (~150ml)
  • serves to warm and humdify incoming air
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6
Q

Transitional & Respiratory Zones

A
  • after the 16th generation including:
    • respiratory bronchioles
    • alveolar ducts
    • alveolar sacs
  • alveoli start to appear ⇒ gas exchange
  • increased cross-sectional area ⇒ decreased resistance ⇒ increased flow ⇒ decreased velocity
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7
Q

Alveolar Structure

A
  • Blood-gas barrier consists of:
    • alveolar epithelia
    • capillary epithelia
    • associated basement membranes
  • Contains:
    • Type I Pneumocytes
      • Thin and flat
      • comprise ~ 90% of alveolar surface area
    • Type II Pneumocytes
      • smaller cells
      • filled with lamellar inclusions
        • contain pulmonary surfactant
      • can transform into Type I pneumocytes if needed
    • Macrophages present
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8
Q

Pulmonary Vasculature

A

Lungs receive blood from two different sources:

  1. Pulmonary circulation
    • brings O2-poor venous blood via pulmonary arteries to blood-gas interface in alveoli
    • O2/CO2 exchange occurs
    • oxygenated blood travels via pulmonary veins to left-sided heart
    • receives entire cardiac output (~5 L/min at rest)
    • low pressure (~15 mmHg)
  2. Bronchial Circulation
    • part of systemic circulation
    • supplies conducting airways
    • comes from aorta and bronchial capillaries
    • drain into:
      • bronchial veins
      • anatomoses with pulmonary capillaries into veins of pulmonary system = physiological shunt
        • Allows small amount of deoxygenated blood to enter systemic circulation
        • Decreases pulmonary vein spO2 by 1-2%
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9
Q

Pleural Pressure

( Ppl )

A

Pressure in the pleural fluid between the lung and the chest wall.

Subatmospheric at rest, approximately -5 cm H2O.

Due to inward elastic recoil of the lungs and outward recoil of the chest wall.

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10
Q

Airway Pressure

( Paw )

A

Pressure within the airway.

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11
Q

Alveolar Pressure

( PA )

A

Pressure inside the alveoli.

At rest with no airflow = 0 cm H2O.

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12
Q

Transpulmonary Pressure

( PL )

A

Difference between the alveolar pressure and pleural pressure.

PL = PA - PPl

~ -5 cm H2O at rest

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13
Q

Transairway Pressure

( Pta )

A

Pressure difference across the airways.

Pta = Paw - Ppl

Responsible for keeping the airways open during forced expiration.

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14
Q

Tidal Volume

(VT)

A

The amount of air that enters and leaves the lung during quiet breathing.

~ 500 ml

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15
Q

Total Lung Capacity

(TLC)

A

Total air capacity of the lungs.

~ 6 L

TLC = VC + RV

= IRV + VT + ERV + RV

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16
Q

Functional Residual Capacity

(FRC)

A

The amount of air remaining in the lungs after a tidal exhalation.

Cannot be determined by spirometry.

FRC = RV + ERV

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17
Q

Inspiratory Reserve Volume

(IRV)

A

The additional air brought in beyond the tital volume by deep inspiration.

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18
Q

Inspiratory Capacity

(IC)

A

The amount of air which can be brought in after a tidal expiration.

Sum of the tidal volume and IRV.

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19
Q

Expiratory Reserve Volume

(ERV)

A

The additional air beyond a tidal expiration which can be moved out due to deep exhalation.

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20
Q

Residual Volume

(RV)

A

The air that remains in the lung after a deep exhalation.

Cannot be determined by spirometry.

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21
Q

Vital Capacity

(VC)

A

The maximal amount of air that can be exhaled after a deep inspiration.

VC = ERV + VT + IRV

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22
Q

Spirometry

A

Measurement of the volume and speed of airflow under conditions of quiet breathing, maximal inspiration, and maximal expiration.

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23
Q

Helium Dilution Technique

A

Used to measure the residual volume and thus determine the FRC and TLC.

Helium insoluble in the blood so entire volume remains in the lungs.

C1 + V1 = C2 x (V1 + V2)

V2 = V1 x [(C1 - C2)/C2]

  1. Subject breaths in air containing known concentration of helium (C1).
  2. Amount of helium in the system before equilibrium mest be the same as after equilibrium with the lungs.
  3. If inspiration of He starts and ends at the end of a tidal breath, V2 = FRC
  4. If inspiration starts and ends with forced expiration, V2 = RV.
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24
Q

Rates of Airflow

Spirometry

A

Forced vital capacity (FVC) = air expired as rapidly as possible after a maximal inspiration ⇒ ~ 5 L in healthy adult male

FEV1 = volume of forced air expiration in 1 second

FEV1 / FVC = ratio of air expired over 1 second over the total ⇒ normal ~ 80%

Usually lung diseases involve mixed restrictive and obstructive patterns.

Ex. asthma.

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25
Q

Obstructive Lung Disease

A

Allows air to enter the lungs but makes expiration difficult.

Ex. emphysema, bronchitis, and bronchiectasis.

Both FEV1 and FVC are reduced.

FEV1 reduced to a greater extent.

FEV1 / FVC ratio decreased.

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26
Q

Restrictive Lung Disease

A

Makes inspiration difficult but does not affect expiration.

Ex. fibrosis, bronchitis, and respiratory distress syndrome (due to surfactant deficit or lung injury).

FEV1 and FVC reduced to more or less the same extent.

FEV1 / FVC ratio is normal or sometimes increased.

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27
Q

Inspiration

A

Active Process

  1. During tidal breath, diaphragm contracts, controlled by the phrenic nerve
  2. Abdomen pushed downward and forward
  3. Ribs lifted and moved out
  4. During forced inspiration/exercise, additional muscles such as the external intercostal muscle recruited
  5. All serve to increase transverse diameter of the thorax
  6. Ppl and PA​ becomes more negative drawing air in.
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28
Q

Expiration

A

Passive process during quiet breathing.

Active process during forced expiration.

  1. Diaphragm relaxes.
  2. Chest wall and lung return to equilibrium positions.
  3. Ppl becomes less negative and PA become positive. Air is moved out.
  4. During forced expiration/exercise, additional muscles such as abdominal muscles and internal intercostal muscles contract.
  5. Ppl becomes positive (only time). Air forced out at greater rate.
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29
Q

Pulmonary

Pressure-Volume Curves

A

As Ppl becomes more negative and PA falls below atmospheric pressure, the lungs will expand.

Volume measured with spirometry as a function of pressure.

Slope of the curve represents compliance.

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30
Q

Hysteresis

A

Pulmonary pressure-volume curves during inflation and deflation are different.

Mostly due to differences in compliance.

Lung volume at any given pressure during deflation is larger than during inflation.

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31
Q

Lung Compliance

A

C = ΔV / ΔP

  • In the normal range of expanding pressures (-5 to -10 cm H2O):
    • Lung very compliant
    • P-V curve steep
  • As expanding pressures get higher:
    • Lung becomes stiffer due to elastic recoil
    • Seen as flattening of the P-V curve at higher expanding pressures
  • During deflation, lungs start at a lower compliance state:
    • Deflation curve starts out flat
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32
Q

Factors Affecting

Lung Compliance

A
  1. Surface tension decreases compliance
  2. Fibrosis decreases compliance
    • seen in restrictive disorders
  3. Alveolar edema decreases compliance
    • excess fluid accumulation in the lungs
  4. Increased pulmonary venous return reduces compliance
    • excess blood accumulation in the lungs
    • seen in heart failure
  5. Loss of elastic tissue increases compliance
    • seen with emphysema or aged lungs
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33
Q

Pulmonary Disease

PV-Loop & Compliance Changes

A

Restrictive diseases decrease lung compliance.

Results in narrowing of the PV-loop.

Obstructive diseases increase lung compliance.

Results in widening of the PV-loop.

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34
Q

Total Pulmonary Compliance

A

Chest wall elastic recoil pulls outward.

Greater at low lung volumes.

Tendency for the lung to expand indicated as negative transmural pressure.

Alveoli elastic recoil pulls inward.

Greater at high lung volumes.

Tendency for the lung to collapse indicated as positive transmural pressure.

Combined pulmonary compliance is the sum of the two.

At FRC, lung elastic recoil = chest elastric recoil so transmural pressure ⇒ 0.

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35
Q

Pulmonary Disease

Combined Compliance Changes

A

Chest wall compliance remains constant.

Pulmonary diseases affects compliance of the lung.

Alters equilibrium point of the lung and chest wall.

Obstructive disorders increase compliance & equilibrium point (i.e. FRC).

Restrictive disorders decrease compliance & equilibrium point (i.e. FRC).

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36
Q

Surface Tension

A

Thin liquid film coats each alveolus affecting the P-V relationship.

Molecules of liquid more attracted to each other than to gas accounting for surface tension.

Saline-filled lung more compliant than air-filled lung = no hysteresis.

Foam from pulmonary edema with tiny air bubbles extremely stable = low surface tension.

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37
Q

LaPlace’s Law

A

Pressure (P) required to keep an alveolus of radius (r) open affected by surface tension (T).

P = 2T / r

If surface tension constant, pressure in smaller alveolus greater than in larger one.

Pressure gradient drives air from smaller to larger alveolus causing collapse of the smaller alveolus ⇒ atelectasis.

Common at lower lung volumes.

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38
Q

Surfactant

A

Lipid/protein mixture secreted by Type II pneumocytes.

Mostly dipalmitoyl phosphatidylcholine (DPPC).

Alters the surface tension with changes in diameter.

  • Surfactant density increases with lung deflation ⇒ reduces surface tension ⇒ decreases pressure
  • Lowers surface tension to a greater extent in smaller alveoli
  • Prevents atalectasis

Increases lung compliance.

  • As lung inflates, surfactant / area decreases
  • Compliance will decrease as lung inflates
  • Partially accounts for flattening of the inflation curve at high volumes

Helps prevent pulmonary edema.

  • Surface tension promotes fluid movement from capillaries to alveolar spaces.
  • Surfactant decreases surface tension preventing movement of fluid into alveoli.
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39
Q

Infant Respiratory Distress Syndrome

(IRDS)

A
  • Surfactant production starts ~ 34 weeks gestation
  • Insufficiency seen with premies
  • Difficulty in inflating lungs due to high surface tension
  • Treat with CPAP and exogenous surfactant until neonate able to synthesize enough
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40
Q

Regional Compliance

Upright Lung

A

Compliance is greater at the base of the upright lung than the apex.

  • Gravity causes weight of the lung to pull down on the alveoli.
  • Ppl more negative at apex compared to base.
    • Alveoli at the apex more inflated at rest.
  • Apex rests at higher point on compliance curve than base.
    • Alveoli at the base inflate more easily
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41
Q

Respiratory Cycle

A
  1. Before inspiration:
    • Ppl negative due to elastic recoil of lung
    • PA = 0
    • No airflow
  2. Inspiration:
    • Ppl more negative due to diaphragm contraction
    • PA becomes negative
      • Alveoli mechanically tethered to chest wall
    • Pressure difference draws air in
    • Alveoli expand ⇒ PA increases ⇒ stops becoming more negative ⇒ still subatmospheric so airflow continues
  3. End of Inspiration / Beginning of Expiration:
    • Ppl more negative
    • PA = 0
    • No airflow
  4. Expiration:
    • Breathing muscles relax
    • Alveolar elastic recoil high
    • Ppl becomes less negative
    • PA starts to become positive
    • Air flows out of alevoli
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42
Q

Airflow

&

Airway Resistance

A

Airway diameter main determinant of airflow.

Main site of resistance in the intermediate-sized airways.

Governed by Poiseuille’s Law and Ohm’s Law:

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43
Q

Airway Resistance

Factors

A
  1. Lung Volume
    • Higher volume ⇒ airway opened ⇒ greater diameter ⇒ decreased resistance
  2. Bronchial Smooth Muscle
    • ANS ⇒ vagus nerve ⇒ Ach ⇒ β2-adrenergic receptors ⇒ bronchodilation ⇒ decreased resistance
      • Albuterol = β2-adrenergic agonist
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44
Q

Dynamic Compression

of

Airways

A

Flow rate is independent of effort towards low lung volumes.

  • During forced expiration, flow rate declines as more air expired.
  • Occurs whether expiration starts with maximal effort or slowly and accelerates
  • Due to airway compression by increased Ppl
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45
Q

Forced Expiration

A
  1. Pre-inspiration (A)
    • Pleural pressure (Ppl) = -5 cm H2O
    • Alveolar pressure (PA) = 0
    • Transairway pressure (PL) = +5 cm H2O
  2. Beginning of Inspiration (B)
    • Diaphragmatic contraction causes both Ppl and PA to become -2 cm H2O more negative
    • Airflow causes 1 cm H2O pressure drop in airway
    • PL = +6 cm H2O
  3. End of Inspiration (C)
    • PA = O
    • PPL = -8 cm H2O
    • PL = +8 cm H2O
  4. Forced Expiration (D)
    • Both Ppl and PA increase by +38 cm H2O
    • Outward airflow causes a pressure drop along the airway
    • PL drops along the airway until Ppl = PA
    • When PL = 0 ⇒ equal pressure point
    • Negative PL beyond this point ⇒ tendancy to close airway
      • EPP in healthy person occurs at a point high enough where cartilage present and prevents closure
    • As expiration continues, EPP moves deeper into lung
46
Q

EPP Changes

Obstructive Lung Disease

A
  • Emphysema causes loss of alveoli and elastic recoil
  • Lowers PA further during forced expiration
  • Pushes EPP lower in the lung
  • Causes airway to collapse closer to alveoli where cartilage not present
  • Results in difficulty with expiration ⇒ hyperinflated lungs ⇒ barrel chest
  • Breathing through pursed lips inc. resistance at the mouth causing a pressure drop
    • Moves EPP back up to conducting zone
47
Q

Flow-Volume Loops

A

Airway resistance stable during quiet breathing.

Forced expiration causes compression of airways resulting in greater airway resistance.

Flow-volume loops generated by:

  1. Inhale to TLC
  2. Forced expiration to RV as quickly and forcefully as possible
  3. Forcibly inhale back to TLC

Upper part of the loop is the flow-volume curve.

Can be used to detect various types of airways diseases.

48
Q

Pulmonary Disease

Flow-Volume Curves

A
  • Restrictive Disorders
    • Lung fills to lower volume.
    • Maximum flow rate decreased.
    • Total volume exhaled reduced.
  • Obstructive Disorders
    • Lung fills to a greater volume.
    • Maximum flow rate decreased.
    • Total volume exhaled reduced.
49
Q

Dalton’s Law

A

PIgas = FIgas x PB

PIgas = partial pressure of the inspired gas

FIgas = fraction of that gas in total mixture

PB​ = barometric pressure (760 mmHg @ sea level)

The total pressure of a gas mixture is equal to the sum of the partial pressure of each gas.

Each gas exerts a partial pressure that is proportional to its concentration and independent of the other gases.

50
Q

Alveolar Humidified Air

A

Conducting zones warm and humidify air so it contains water vapor when it reaches the alveoli.

Partial pressure water vapor at 37° is 47 mmHg.

Taken into account via modied Dalton’s Law:

PIgas = FIgas x (PB - PH2O)

51
Q

Partial Pressures

of

Respiratory Gases

52
Q

Minute Ventilation

(V̇E)

A

The amount of air that enters per minute.

(mls/min)

V̇E = Bf x VT

Bf = breathing frequency (breaths/min)

VT = tidal volume

53
Q

Dead Spaces

A
  • Anatomic dead space
    • Volume of air which remains in the conducting zone and is unavailable for gas exchange.
    • Normal ~ 150 mls
  • Alveolar dead space
    • Volume of functional dead space which is unable to participate in gas exchage due to pathological process
    • Ex. poor perfusion
  • Physiological dead space (VD)
    • Anatomical dead space + alveolar dead space
    • Normally, VD = anatomic dead space
54
Q

Bohr Equation

A

Physiological dead space determined using partial pressure of CO2 in alveolar gas (PACO2) and expired gas (PECO2).

Assumptions:

No CO2 in inspired gas.

All of the CO2 in expired gas comes from the alveoli.

Because PCO2 in alveolar gas virtually identical to arterial PCO2​ in healthy individuals, values from standard blood gas measurements used.

55
Q

Alveolar Ventilation Rate

(V̇A)

A

V̇A = B<em>f</em> x (VT - VD)

The amount of gas that actually makes it to the alveoli and is available for gas exchange.

56
Q

Alveolar Ventilation Alterations

A
  • Two main ways of altering alveolar ventilation:
    1. Breathing frequency (B<em>f </em>)
    2. Volume inspired
  • Dead space constant under normal conditions.
  • Alveolar ventilation is best increased by increased tidal volume.
  • Hyper-respiration essentially moving air in and out of conducting zones without inspiring fresh air into lungs.
57
Q

Alveolar Ventilation Estimation

A

Alveolar ventilation rate can be estimated without knowing the dead space volume.

58
Q

Alveolar Ventilation

&

PCO2

A

If rate of CO2 production is constant:

Alveolar ventilation rate is inversely proportional to alveolar (and arterial) PCO2.

  • Decreased B<em>f</em> results in hypercapnea.
  • Hyperventilation is a physiological response to hypercapnia.
  • If CO2 production increases, alveolar ventilation will increase to paintain a constant PaCO2.
59
Q

Alveolar Gas Equation

A

Relationship between PAO2, PACO2, and the rate of CO2 generation and O2 consumption.

Estimates alveolar O2 levels using easily obtained parameters.

  • PIO2 = O2 partial pressure in moist inspired air
  • R = respiratory quotient
    • amount of CO2 relative to O2 consumed in one breath
    • R = 0.8 for typical diet with carbs and fats
  • F = correction factor
    • ~ 2 mmHg
    • often ignored
  • Arterial CO2 used as surrogate for alveolar CO2
60
Q

Regional Ventilation

Upright Lung

A

Ventilation is the highest at the base of the lung and lowest at the apex.

  • Gravity causes a more negative pleural pressure at the apex compared to base.
  • Top is already partially inflated and can inflate less upon inspiration.
  • Bottom somewhat compressed and can expand more upon inspiration.
  • Determined using radioactive 133Xe
61
Q

Typical Lung

Volumes and Flows

62
Q

Pulmonary & Cardiovascular

Typical Partial Pressures

63
Q

Pulmonary Hemodynamics

Basics

A
  • Low resistance, low pressure system
    • Pulmonary vascular resistance (PVR) ~ 1/10th of systemic circulation
  • Pulmonary arteries less elastin and smooth muscle
  • Pulmonary arterioles thin-walled and less smooth muscle
    • Less ability to constrict compared to systemic arterioles
  • Pulmonary capillary beds form mesh-like network
    • Blood flows as a sheet over alveoli
64
Q

PVR

Effects of Cardiac Output

A

Inc. CO ⇒ Inc. pulmonary arterial pressure ⇒ Dec. PVR ⇒ Inc. blood flow.

Due to two mechanisms:

  1. Recruitment of capillaries
    • Some capillaries partially or fully closed at rest
      • Particularly at the top due to low perfusion pressure
    • As CO increases, vessels “inflate” to decrease PVR
      • Added in parallel
  2. Distention of capillaries
    • Increases diameter of the vessels lowering PVR

Recruitment precedes distension.

65
Q

PVR

Effects of Lung Volume

A

Extra-alveolar vessels affected by pleural pressure.

Alveolar vessels affected by alveolar pressure.

  • High lung volumes:
    • Pleural pressure most negative
      • Extra-alveolar vessel resistance at minimum
    • Alveolar volume/pressure is highest
      • Alveolar vessel resistance at maximum
  • Low lung volumes:
    • Pleural pressure less negative
      • Extra-alveolar vessel resistance at maximum
    • Alveolar volume/pressure is lowest
      • Alveolar vessel resistance at minimum

​

Total resistance of the circulation is the combination of both types of vessels.

Lowest resistance at FRC.

66
Q

PVR

Effects of Oxygen

A

PVR increased by alveolar hypoxia or hypoxemia.

Hypoxia induces vasoconstriction of small pulmonary arteries.

Two types of alveolar hypoxia can occur:

  1. Regional hypoxia:
    • vasoconstriction localized to a region
    • useful in shifting blood away from poorly-ventilated alveoli
    • does not usually cause increased PVR due to parallel pulmonary capillaries
  2. Generalized hypoxia:
    • vasoconstriction throughout lungs
    • increased PVR
    • occurs in low oxygen environments
    • can lead to pulmonary edema
      • can result in right-sided hypertrophy and heart failure
67
Q

Pulmonary Fluid Exchange

A

Forces regulating pulmonary capillary fluid flow:

  1. Starling forces:
    • Capillary hydrostatic pressure ⇒ fluid out
    • Capillary oncotic pressure ⇒ fluid in
    • Interstitial hydrostatic pressure ⇒ fluid out ⇒ ~ 0
    • Interstitial oncotic pressure ⇒ fluid in
  2. Surface tension
    • Pulls inward lowering interstitial hydrostatic pressure (Pi)
    • Help to draw fluid into interstitial space
  3. Alveolar pressure
    • Compresses interstitial space increasing interstitial hydrostatic pressure
    • Helps prevent fluid from leaving capillary

Normally, net movement of fluid is from the alveoli to the interstitial space.

Removed by the lymphatic system.

68
Q

Causes of Pulmonary Edema

A
  1. Increased capillary hydrostatic pressure
    • Due to increased pumonary venous pressure
      • Heart failure
      • Mitral valve stenosis
  2. Increased capillary permeability
    • pulmonary vascular injury
    • inflammation
    • neurogenic shock
  3. Increased surface tension
    • Loss of surfactant
      • Adult respiratory distress syndrome
69
Q

Regional Blood Flow

Upright Lung

A

Pulmonary blood flow greatest at the base.

Due to relationship between pulmonary artery pressure, alveolar pressure, and pulmonary vein pressure caused by gravity.

Creates 3 functional zones of the lung:

  • Zone 1: PA > Pa > Pv
    • Alveolar pressure greater than arterial pressure
    • Collapses blood vessels
    • Allows no blood flow
    • Absent under normal condition
    • Can occur with:
      • positive pressure ventilation
      • low pulmonary blood flow (ex. hemorrhage)
  • Zone 2: Pa > PA > Pv
    • Arterial pressure greater than alveolar pressure
    • Blood flow determined by difference between Pa and PA
    • Occurs in the middle of the lungs
    • As we move further down into the lung:
      • Pa increases while PA stays fairly constant
      • Pressure difference increases ⇒ inc. pulmonary blood flow through recruitment
      • Continuous increase in pressure difference as one moves down the lungs ⇒ waterfall effect
  • Zone 3: Pa > Pv > PA
    • Venous pressure greater than alveolar pressure
    • Blood flow dictated by difference between Pa and Pv
    • Inc. in pulmonary blood flow due to distention
70
Q

Other Functions of the Lung

A
  1. Reservoir of blood
  2. Filter out small thrombi
  3. Secretion of mucous as a protective system
  4. Metabolic functions
    • Activation of Ang I → Ang II
    • Inactivation of many vasoactive substances
71
Q

V/Q Relationships

A
  • Normal conditions (A)
    • Alveolar gas content between between venous and atmospheric
      • O2 entering
      • CO2 leaving
  • Airflow blocked / Perfusion normal (B)
    • No ventilation (V=0)
    • V/Q ratio = 0
    • Blood equilibrates with gases in alveoli
    • Alveolar gas similar to venous blood gas values
      • Low O2
      • High CO2
  • Airflow normal / No perfusion (C)
    • Q = 0
    • V/Q ratio = ∞
    • Alveolar gas similar to atmospheric air
      • High O2
      • No CO2

​

As V/Q ratio increases, PAO2 increases and PACO2 decreases.

72
Q

V/Q Ratios

Regional Variations

A

Both ventilation and perfusion greatest at the base.

Perfusion varies to a greater extent.

V/Q ratio will vary along the height of the lung with greatest value at the apex.

Between 0.5 and 2.5.

73
Q

Alveolar Gas Composition

Regional Variations

A

Alveolar gas composition varies along the height of the lung.

Highest PAO2 and lowest PACO2 at the apex.

Due to regional V/Q variations.

74
Q

V/Q Variations

Effects on Oxygenation

A

Lung is not as efficient at oxygenating arterial blood due to uneven V/Q ratios.

Apex with higher PAO2 (~ 132 mmHg) but lower perfusion.

Base with lower PAO2 (~89 mmHg) but greater perfusion.

Majority of the blood leaves from the base.

Arterial blood has values closer to that of the base than the apex.

75
Q

V/Q Mismatch

A

Normal (Left)

  • Ventilation and perfusion more or less matched
  • Majority of ventilation and blood flow goes to regions with V/Q ratio ~ 1

COPD

  • Much of the ventilation and blood flow associated with normal V/Q ratios ~ 1
  • Significant blood flow associated with areas with V/Q << 1
    • Ineffective movement of O2 into and CO2 out of the blood
      • Alveolar & arterial PO2 low ⇒ hypoxia
      • Alveolar & arterial PCO2 high ⇒ hypercapnea
    • Depresses overall PaO2 returning to systemic circulation
  • Compensate by increasing ventilation to other regions
    • Results in V/Q ratios greater than normal
    • Due to insuffient blood flow, regions may be ineffective at eliminating CO2
    • Increased ventilation to compensate for hypercapnea
      • Not as effective for oxygen due to dissociation curves
    • Results in normal PaCO2 but arterial hypoxia
76
Q

Alveolar-arterial (A-a) Oxygen Gradient

A

The difference between alveolar and arterial oxygen concentrations

Normal A-a gradient ~ 5-15 mmHg.

PAO2 = ~ 100 mmHg and PaO2 = ~ 85-95 mmHg

  • In a healthy person due to:
    1. Regional V/Q variations
    2. Mixing of venous blood with arterial blood due to anatomical shunts (~1-2% of total blood)
      • Bronchial circulation drains into pulmonary vein
      • Coronary venous blood drains directly into left ventricle via Thebesian veins
  • A-a gradient determined using:
    • Measurements of arterial blood gasses (PaO2 and PaCO2)
    • Alveolar gas equation to determine PAO2
77
Q

Hypoxemia

A

Defined as PaO2 < 85 mmHg.

A-a gradient and response to O2 therapy can distinguish among the 4 types of respiratory causes.

  • Respiratory causes
    • regional hypoventilation
    • generalized hypoventilation
    • larger than normal anatomic shunt
    • diffusion block across blood-gas barrier
  • Non-respiratory causes
    • reduced O2 content of inspired air
78
Q

Fick’s Law

A

Describes the diffusion of gases across the blood gas barrier:

  • A = area for diffusion
  • T = thickness of diffusion path (~0.3 µm in blood-gas barrier)
  • D = diffusion coefficient
    • proportional to solubility
    • inversely proportional to sq. rt of MW
  • (P1 - P2) = partial pressure gradient of gas
79
Q

Factors Affecting Diffusion Rates

A
  1. Emphysema
    • Destruction of alveoli
    • Decreased SA for gas exchange
  2. Pulmonary edema
    • Inceases thickness of path gas must traverse
  3. High altitudes
    • Decreases barometric pressure
    • Reduced PIO2
  4. Cardiac output
    • Changes transit time of RBC through pulmonary circulation
    • Unlikely to change CO so much that equilibrium does not occur
80
Q

Nitrous oxide

(N2O)

A

Perfusion-limited gas

  • Diffuses across blood-gas barrier
  • No affinity for hemoglobin
  • Partial pressure rises in blood rapidly
  • Equilibrates between blood and alveoli quickly
    • No additional diffusion occurs d/t no gradient
    • Only way to increase amount absorbed is to increase blood flow
81
Q

Carbon Monoxide

(CO)

A

Diffusion-Limited Gas

  • Diffuses through alveolar-capillary membrane
  • Strong affinity for hemoglobin
    • Essentially all of it rapidly binds to Hb
    • PaCO ~ 0
  • Partial pressure gradient never becomes 0
    • Driving force present throughout entire RBC transit time
  • Diffusion-limited gas but not limited by blood flow
82
Q

Oxygen

(O2)

A

Perfusion-limited

  • Diffuses across blood-gas barrier
  • Affinity for hemoglobin
  • Equilibrates in blood in ~ 0.25 sec
    • RBC transit time ~ 0.75 sec
  • Normally perfusion-limited
  • Some diseases can cause thickening of interface effecting kinetics of O2 uptake
    • Measure diffusing capacity
83
Q

Diffusing Capacity

A

Rate of gas transfer relative to a partial pressure gradient.

Diffusing capacity (DL) = AD/T

Fick’s Law becomes:

V̇ = DL x (P1 - P2)

84
Q

Diffusing Capacity of Carbon Monoxide

(DLCO)

A

DLCO = V̇CO / PACO

  • Measures rate of CO disappearance in alveolar gas.
  • CO diffusion-limited so partial pressure gradient is PACO.
  • Provides information about the integrity of the alveolar-capillary surface for gas exchange.
  • Pulmonary fibrosis
    • Increases thickness of alveolar wall
    • Decreases in DLCO
  • Decreased hematocrit
    • Fewer RBC arriving at the lungs
    • Decreases DLCO
85
Q

Oxygen Transport

A

O2 transported in the blood in two forms:

Dissolved in blood (2%)

Bound to hemoglobin (98%)

86
Q

Henry’s Law

A

Amount of oxygen dissolved in the blood:

[O2] = 0.003 x P<strong>O2</strong>

0.003 ⇒ solubility constant for O2 in the blood at 37°

(ml O2/dL-mmHg)

Concentration of O2 (ml O2/dL blood)

87
Q

O2 Saturation

A
  • % saturation of Hb with O2 (SaO2)
    • ratio of oxygen content to capacity
  • Oxygen content ([HbO2])
    • the actual amount of O2 bound to hemoglobin
    • most important guage for oxygenation
    • normal ~ 20 ml / 100 ml
  • Oxygen-carrying capacity ([HbO2]max)
    • maximal capacity for Hb to carry O2 in the blood
    • assuming normal Hb concentration is ~ 20.1 ml O2/dL blood

The amount of oxygen bound to Hb depends on both O2​ partial pressure and amount of Hb present.

Aortic blood SaO2 ~ 98%

Mixed venous blood SaO2 ~ 75%

88
Q

Oxyhemoglobin Dissociation Curve

A

S-shaped curve provides key physiological advantages:

  • Plateau region ⇒ loading region
    • O2 loaded onto Hb in pulmonary circulation
    • Allows saturation of Hb in the high partial pressure areas of the lung
    • Increasing PO2 above 100 mmHg does not increase amount of O2 bound to Hb
    • PO2 down to ~60 mmHg before there is significant drop in Hb saturation
    • Safety net ensuring Hb saturation over wide range of PaO2
  • Steep region ⇒ unloading region
    • Large changes in oxygen saturation with small changes in PO2
    • Allows Hb to release large amounts of O2 to tissues with small changes in PO2​
  • P50 = PaO2 where Hb is 50% saturated
89
Q

Hemoglobin Oxygen Affinity

Effectors

A

Physiologically relavent effectors:

Decreases Hb oxygen affinity

Shifts dissociation curve to the right

Greatest effect on the unloading or steep phase.

Facilitates release of O2.

Assessed via P50 → normal ~ 28 mmHg.

  • Increased levels of CO2
  • Increased temperature
  • Increased 2,3-BPG
  • Decreased pH
  • Decreased PO2 due to tissue consumption

*Effects of CO2 and pH termed Bohr effect.

90
Q

Effects of Hb Content

A

Anemia

  • Decreased Hb content
  • Reduced O2 content
  • Normal PaO2
    • Depends only on solubility of gas in plasma
  • Normal SaO2
    • oxygen content and max O2 capacity reduced to similar degrees

Polycythemia

  • Increased Hb content
  • Increased O2 content
  • Unchanged SaO2 and PaO2
91
Q

Effects of Carbon Monoxide

A

Reduces O2 content without affecting SaO2 or PaO2.

  • CO has much stronger affinity for Hb than O2
  • See reduction in O2 content if 33% of sites bound with CO
  • Shifts dissociation curve slightly left
  • Makes it harder to unload any O2 bound to Hb
92
Q

CO2 Transport

A

CO2 transported in the blood in 3 forms:

1. Dissolved in plasma (~10%)

Governed by Henry’s Law:

[CO2] = 0.67 x PCO2

2. Bicarbonate (HCO3 ~ 60%)

CO2 + H20 ↔︎ H2CO3 ↔︎ H+ + HCO3-

Catalyzed by carbonic anhydrase in RBCs.

H+ cannot exit & binds to Hb unloading O2 ⇒ Bohr effect.

HCO3- exchanged for Cl- by Cl/HCO3- exchanger ⇒ Chloride shift.

3. Carbamino Proteins (~30%)

CO2 + Hb-NH2 ↔︎ Hb-NHCOOH

CO2 reacts with terminal amine groups on Hb producing carbaminohemoglobin.

Hb can bind more CO2 than it can bind O2 to heme.

93
Q

CO2-Hb Dissociation Curve

A

More or less linear over normal arterial CO2 range.

(35-50 mmHg)

Higher [O2] shifts curve downward ⇒ Haldane effect.

Load more CO2 at the tissues (low PO2)

Unload CO2 at the lungs (high PO2)

94
Q

Blood O2 and CO2

A
  • Arterial content of CO2 much greater than O2.
  • Slope and linearity of CO2 curve:
    • allows lungs to remove large amounts of CO2 over extended range as PCO2 increases
95
Q

Respiratory Acid-Base Regulation

A

Role of pulmonary system in the regulation of pH.

  • HCO3- is the major physiological buffer
  • Ability of cells to maintain stable pH affected by:
    • alveolar ventilation rate
    • PaCO2​
  • Decreased alveolar ventilation ⇒ increased PaCO2​
    • Increased [H+]plasma via carbonic anhydrase
  • Increased alveolar ventilation ⇒ decreased PaCO2​
96
Q

Blood pH

A
  • Buffers
    • HCO3- is the major physiological buffer
    • Proteins and phosphates act as non-bicarbonate buffers
  • Calculate blood pH using the Henderson-Hasselbach equation
  • Since CO2 obeys Henry’s Law, equation can be modified as below.
    • Use solubility constant of 0.03 due to conversion from mmHg to molar
  • Normal plasma [CO2] = 40 mmHg and [HCO3-] = 24 mM
  • Normal plasma pH = 7.4
97
Q

Davenport Diagram

A

Relationships between pH, PCO2, and HCO3-.

We exist at the intersection of:

Buffer line (BAC)

CO2 isopleths ⇒ represents constant PCO2

98
Q

Acid-Base Disturbances

A

Respiratory Disturbances

When PCO2 altered by respiratory mechanisms, the change in [HCO3-] will alter pH by traveling along the buffer line.

Compensation via renal regulation of:

HCO3- levels

H+ production/excretion

Moves up or down to a new buffer line.

  • Respiratory Acidosis (A ⇒ B)
    • Decreased alveolar ventilation → increased PCO2
    • Kidney increases plasma [HCO3-] (B ⇒ D)
  • Respiratory Alkalosis (A ⇒ C)
    • Increased alveolar ventilation → decreased PCO2
    • Kidney reduces plasma [HCO3-] (C ⇒ F)

Metabolic Disturbances

Underlying cause due to alteration in plasma [HCO3-].

Alter PCO2 via respiratory compensation.

Moves to a new CO2 isopleth.

99
Q

Respiratory Control

Overview

A

Automatic process with a certain degree of voluntary control.

Alter breathing rate and alveolar ventilation in response to blood chemistry.

Functions through feedback loops:

  • Central and peripheral sensors
    • Chemoreceptors - detect blood gases
    • Proprioceptors - detect position
    • Mechanoreceptors - detect stress and irritants
  • Feed into the respiratory center - central controller
  • Controls muscles of respiration - effectors
100
Q

Medullary Respiratory Center

A

Breathing mainly regulated by two centers with some degree of cross-communication and synchrony:

Dorsal Respiratory Group (DRG) ⇒ inspiratory center

  • Cell membrane potential with an intrinsic oscillatory activity
    • Increases in magnitude until threshold cross and action potential generated
  • AP → Phrenic nerve → Diaphragm and inspiratory muscles → initiate inspiration

Ventral Respiratory Group (VRG) ⇒ expiratory center

  • Quiescent during quiet breathing
    • Tidal exhalation is a passive process
  • Role in forced expiration
  • Cells turn off inspiration to start expiration
  • Activate expiratory muscles to increase depth of expiration

Output modulated by inputs from peripheral sources

Breathing rate proportional to PCO2 and inversely proportional to PO2.

101
Q

Pontine Respiratory Group

A

Involved in fine-tuning the medullary centers:

Apneustic Center

  • In lower pons
  • Excitatory effect on the inspiratory center

Pneumotaxic Center

  • In upper pons
  • Switch off inspiration
102
Q

Cerebral Cortex

A

Alters the pulmonary system through conscious effort.

Allows for fine control of breathing movements.

Voluntary control eventually overidden by the central control systems in response to blood gas concentrations.

103
Q

Central Chemoreceptors

A

Sensitive to PCO2 only through changes in pH.

60-80% of PaCO2 effect on ventilation rate due to central chemoreceptors.

  1. When PCO2 rises, CO2 diffuses across BBB into CSF and brain extracellular fluid (BECF)
    • BBB impermeable to HCO3- and H+
  2. H+ generated through formation of bicarbonate
  3. H+ activates central chemoreceptors in medulla
  4. Alters breathing rate via unknown mechanism
  • CSF and BECF with lower non-bicarb buffering capacity than plasma due to lower protein content
    • For given PCO2 rise, change in [H+] greater in CSF than plasma
    • With prolonged respiratory acidosis, HCO3- levels increase
    • Blunts or eliminates the response to increases in PCO2
104
Q

Peripheral Chemoreceptors

A

Sensitive to PCO2, PO2, and pH.

Located in carotid (more important) and aortic bodies.

20-40% of PaCO2 effect on ventilation rate due to peripheral receptors.

  • Only carotid receptors respond to fall in arterial pH
    • Both respiratory and metabolic causes
    • H+ transported into cells where they stimulate the cell
  • Do not resond to changes in PO2 unti < ~ 80 mmHg (hypoxia)
    • Tracks arterial blood O2 saturation
    • Mechanism likely involves inhibition of K+ channels leading to depolarization
    • Leads to neurotransmitter release to excite sensory afferents to CNS
  • O2 and CO2 chemoreceptors interact
    • Ex. drop in pH or PO2 increases sensitivity of receptors to changes in PCO2
105
Q

Central and Peripheral Chemoreceptors

Combined Responses

A

Central and peripheral chemoreceptors vie for respiratory center control.

Central receptors predominate until PaO2 below 60 mmHg.

Response to mild hypoxia over-ridden in favor of stable CO2 concentration.

  • Increased PCO2
    • Peripheral receptors act almost immediately
      • Leads to rapid increase in ventilation rate
    • Central receptors slower to respond
      • Eventually predominate to drive up ventilation rate
      • System resets to new higher PCO2 with increased [HCO3-] in CSF
  • Decreased PO2
    • Peripheral receptors not activated until very low PO2
    • Changers in PO2 between 60-100 mmHg have little effect
  • Interactions between PO2 and PCO2
    • At given PAO2, increases in PACO2 increase ventilation rate due to central and peripheral receptors.
    • Hypoxia increases sensitivity of the response to PACO2
      • Seen as changing slopes of curve in left panel
    • At given PACO2, decreasing PO2 increases ventilation due to peripheral receptors
    • Hypercapnea increases sensitivity of the response to hypoxia
      • Seen as curves becoming steeper in the higher PAO2 region of right panel
106
Q

Cheyne-Stokes Breathing

A

Cyclic breathing pattern (~30-100 secs):

  1. Periods of apnea
  2. Series of breaths of progressively increasing respiratory effort towards a maximum
  3. Waning back to apnea

Seen mostly in heart failure or at high altitudes.

Low perfusion rates diminishes brainstem’s ability to monitor effects of changing ventilation rates on gas composition in real time.

  • Time delay between central increase in ventilation rate and observation of changes in blood gas.
  • Overshoot in response reduces PaCO2 below desired levels causing suppressed ventilation.
  • Same delay occurs with response to hypocapnia causing periods of apnea.
107
Q

Pulmonary Receptors

Overview

A

Afferent fibers located within vagus nerve.

Three main groups of pulmonary receptors:

  1. Pulmonary Stretch Receptors
  2. Irritant Receptors
  3. Juxtapulmonary Capillary Receptors (J-receptors)
108
Q

Pulmonary Stretch Receptors

A

Slowly Adapting Pulmonary Stretch Receptors

Hering-Breuer Reflex

  • Located within airway smooth muscle
  • Discharge in reponse to distention of the lung
  • Activation triggers excitation of the inspiratory OFF switch
  • Prolongs expiration
  • Reflex inactive in humans unless tidal volume > 1 L
    • Role in humans unclear
109
Q

Irritant Receptors

A

Rapidly Adapting Receptors

  • Located in epithelium of larger conducting airways
  • Stimulated by:
    • noxious gases
    • cigarette smoke
    • inhaled dust
    • cold air
  • Impulses travel up vagus nerve
  • Stimulation results in:
    • bronchoconstriction
    • mucous secretion
    • coughing
  • Relatively inactive during normal breathing
  • Can be stimulated by lung inflation
    • Responses wanes after a short period
  • Implicated in bronchoconstriction triggered by histamine release with asthma attacks
110
Q

Juxtapulmonary Capillary Receptors

(J-receptors)

A
  • Unmyelinated C fibers located within alveoli
  • Similar characteristics and responses to irritant receptors
    • Rapidly adapting
  • Impulses travel via vagus nerve
  • Can trigger:
    • rapid shallow breathing
    • bronchoconstriction
    • mucous secretion
111
Q

Chest Wall Proprioceptors

A
  • Joint, tendon, and muscle spindle receptors
  • Located in chest wall
  • Sense wall movement and effort associated with breathing
  • Stimulation allows for increased movement of chest wall when movement impeded
112
Q

Limb Proprioceptors

A
  • Proprioceptors located in limb joints
  • May trigger increased inhalation and exhalation during exercise

2. HDS Pulmonary (28 decks)

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