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Respiratory Flashcards

1
Q

Fick’s Law of diffusion

A

Amount of gas that moves across a sheet of tissue is proportional to the area of the sheet and concentration gradient but inversely promotional to its thickness

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2
Q

Anatomical dead space volume

A

Conducting airways
~150mL

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3
Q

Airway anatomy

A

23 generations
Divided into conducting zone (0-16, 150mLs) and respiratory zone (17-23, FRC 2.5-3L)
Volume of alveolar region ~2.5-3L
Gas moves by bulk flow down a pressure gradient in the conducting zone
Fas movement in the alveolar region is chiefly by diffusion

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4
Q

Lung volumes

A

Vt - volume inspired/ expired during normal quiet breathing
-> ~500mL
- 6-8mL/kg

Inspiratory reserve volume - volume of additional air that can be inspired over tidal volume
-> 2500mL

Expiratory reserve volume - volume of additional air that can be expired following normal tidal expiration
-> 1500mL

Residual volume - volume that remains in the lung at maximal expiration
-> 1500mL (20mL/kg)
-> Governed by the balance between the max force generated by expiratory muscles and the elastic forces opposing reduction of lung volume
-> In older subjects or disease, closure of small airways may prevent further expiration increasing RV

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5
Q

Lung Capacities

A

FRC = RV + ERV
-> Lung volume at end tidal expiration, i.e resting lung volume at equilibrium of lung and chest wall elastic recoil
-> 3000mL (40ml/kg or 30ml/kg supine)

VC = ERV + VT + IRV
-> Volume of maximal inspiration and expiration
-> 4500mL

Inspiratory capacity
-> = VT + IRV
-> 3000mL

TLC
-> Occurs at maximal inspiration - note expiratory muscles also contract strongly at max inspiration
= RV + ERV + VT + IRV
= 6000mL (80ml/kg)

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6
Q

FRC - importance of and factors affecting FRC

A

Importance
- O2 buffer
- Prevention of alveolar collapse
- Optimal lung compliance

Factors affecting FRC
Overall - body size, sex, age, ethnicity
Reduces - position (falls when supine), raised IAP, anaesthesia, lung disease (restrictive)
Increases - PEEP, emphysema, asthma/ obstructive airway disease

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7
Q

Lung volume measurement

A

All lung volumes except RV can be measured by spirometry. Any capacities including RV cannot be directly measure by spirometry - TLC and FRC.

FRC can be calculated by
- Gas dilution
-> At end of normal expiration, known conc of He breathed in
-> C1V1 = C2 x (V1 + V2)
-> V2 = FRC
-> Measure only communicating gas/ ventilated lung volume

  • Body plethysmography
    -> Boyle’s Law, PV = K (constant) at constant temp
    -> Large airtight box, end of expiration, mouthpiece shutter closes - inhale against closed mouthpiece and thus gas in lung expands, volume within plethysmograph decreases proportionally
    -> P1V1 = P2(V1-∆V); [∆V = change in volume of box (or lung)]
    -> P3V2 = P4(V2 + ∆V); [V2 = FRC]
    -> Measures titan volume of gas in the lung incl any trapped gas
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8
Q

Alveolar ventilation

A

Amount of fresh inspired air available for gas exchange
= (VT - anatomical dead space) x RR
V’A = V’E - V’D

Alveolar ventilation (V’A) = (V’CO2/PCO2) x k

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9
Q

Dead space

A

Volume of inspired air playing no role in gas exchange - conducting airways or non-perfused alveoli such as in PE

Anatomical Dead space
- Volume of upper airways and first 14-16 generations of bronchial tree which form conducting airways
- Approx 150mL, 2ml/kg (roughly 1/3 of Vt)

Alveolar dead space
- Total volume of ventilated alveoli that are unable to take part in gas exchange due to insufficient perfusion
- West zone 1

Physiological dead space
- Total dead space in the lung -> sum of anatomical and alveolar

In normal subject - anatomical and physiological dead space are nearly the same

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10
Q

Anatomical dead space measurement

A

Fowlers method
- Subject breaths through a valve box, and the sampling tube of a rapid N2 analyser continuously samples gas at the lip
- Following single VC breath of 100% O2, anatomical deadspace fill with 100% O2 and N2 conc in alveoli has been diluted.
- The first part of exhaled gas comes from the anatomical dead space, with zero N2 content
- This is followed by a rapid rise in N2 conc - transition between anatomical dead space gas and mixed alveolar gas
- Follow by a pleateau, represents mixed alveolar gas
- Dead space found by plotting N2 conc against expired volume and drawing a vertical line such that area A = area B. VD is the volume expired up to the vertical line.
- This method measure the volume of the conducting airways down to the midpoint of the transition from dead space to alveolar gas

~2ml/kg

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11
Q

Physiological dead space measurement

A

Bohr’s method
- All expired CO2 comes from the alveolar gas and none from the dead space
- Blood gas to be taken at the sam time as capnography is measured
-> VT. FECO2 = VA. FACO2
-> VT. FECO2 = (VT - VD). FACO2
Bohr’s equation -> VD/VT = (PACO2 - PECO2)/ PACO2
PACO2 ~ PaCO2 in healthy
Enghoff modification -> VD/VT = (PaCO2 - PECO2)/ PaCO2

  • Measure volume of lung that does not eliminate CO2 - physiological dead space
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12
Q

Alveolar Gas Equation

A

PAO2 = [(PB - PH2O)xFiO2] - [PaCO2/0.8)
= PIO2 - (PACO2/R) + F

PAO2 = alveolar partial pressure O2
PB = barometric pressure
PH2O = saturate vapour pressure of water at 37oC
PaCO2 = arterial partial pressure CO2
R = respiratory quotient = 0.8

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13
Q

Rate of diffusion

A

Proportional to SA, concentration gradient and solubility; inversely proportional to thickness and √MW

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14
Q

Diffusion limitation

A

Amount of gas transferred from alveolus to capillary blood, per unit time, is limited by the diffusion properties of the blood-gas barrier, and not by the amount of blood flow.

Partial pressures in blood and alveolus DO NOT reach equilibrium.

E.g CO, and O2 in abnormal conditions, e.g when diffusion properties of lung are impaired

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15
Q

Perfusion limitation

A

Amount of gas transferred from alveolus to capillary blood, per unit time, is limited by the amount of blood flow, and not by the diffusion properties of the blood-gas barrier.

Partial pressures in blood and alveolus reach equilibrium.

E.g N2O, and O2 in normal conditions

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16
Q

DLCO

A

DL = V’CO/PACO
- CO used to measure as it is diffusion limited

Single breath method
- Single VC breath of 0.3% CO held for 10s and then exhaled
- Inspired and expired PCO are measured via infrared gas analyser
- difference is the amount of CO now bound to Hb
- Alveolar CO is not constant in breath hold but allowances made
- He is also added to measure lung volume by dilution
- Adjustments made for Hb as this effects DLCO

Normal DLCO = 25ml/min.mmHg - can increase 2-3x with exercise

Decreased in
- thickened alveolar capillary membrane (ILD)
- reduced SA (emphysema, PE, lobectomy)

Increased in
- exercise (recruitment and distension)
- alveolar haemorrhage (Hb present with lung binds CO)
- asthma (potentially due to increased apical flow)
- obesity (potentially due to incr CO)

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17
Q

Reaction rates with Hb

A

O2 reaction with Hb is fast (0.2s), but can become limiting

Uptake of O2 (or CO) occurs in 2 stages
1. Diffusion of O2 through the blood-gas barrier (incl plasma and red cell interior)
2. Reaction of O2 with Hb

Two elements resisting diffusion of O2
1. Resistance of the blood gas barrier which is equal to the inverse of DL, i.e 1/DM where M is membrane
2. Rate of reaction with Hb (diffusion capacity of the blood)
⍬ describes the rate of reaction of O2 with Hb in mL/min. ⍬ multiplied by volume of capillary blood Vc gives the effective diffusing capacity of O2 with Hb, the inverse gives the resistance

Total diffusion resistance 1/DL = (1/DM) + (1/⍬.Vc)

DLCO is affected by volume of alveoli, distribution of diffusion properties, and capillary blood

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18
Q

Reaction rates with Hb

A

O2 reaction with Hb is fast (0.2s), but can become limiting

Uptake of O2 (or CO) occurs in 2 stages
1. Diffusion of O2 through the blood-gas barrier (incl plasma and red cell interior)
2. Reaction of O2 with Hb

Two elements resisting diffusion of O2
1. Resistance of the blood gas barrier which is equal to the inverse of DL, i.e 1/DM where M is membrane
2. Rate of reaction with Hb (diffusion capacity of the blood)
⍬ describes the rate of reaction of O2 with Hb in mL/min. ⍬ multiplied by volume of capillary blood Vc gives the effective diffusing capacity of O2 with Hb, the inverse gives the resistance

Total diffusion resistance 1/DL = (1/DM) + (1/⍬.Vc)

DLCO is affected by volume of alveoli, distribution of diffusion properties, and capillary blood

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19
Q

PulmVR decreases with exercise?

A

As arterial or venous pressure increases, pulmonary vascular resistance decreases via two mechanisms
- Recruitment and distension of capillaries

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20
Q

Starling’s equation

A

Net fluid out = K[(Pc-Pi) - σ(πc-πi)]

K = filtration coefficient (constant)
Pc = hydrostatic pressure in capillaries
Pi = hydrostatic pressure in ISF
σ = reflection coefficient
πc = colloid osmotic pressure of proteins in blood
πi = colloid osmotic pressure of proteins in ISF

Net pressure is outward

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21
Q

4 causes of hypoxaemia

A
  • Hypoventilation
  • Diffusion limitation
  • Shunt
  • V/Q inequality
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22
Q

Shunt + shunt equation

A

Venous blood entering the arterial system that doesn’t pass through the ventilated areas of the lung
- Passes from R to L heart without participating in gas exchange
- Deoxygenated venous blood passes directly into arterial system reducing PaO2

Shunt equation
- Used to calculate the proportion of the CO that is shunted from the venous to the arterial system (actually calculated venous admixture)
- Qs/Qt = (CcO2 - CaO2) / (CcO2 - CvO2)
Qs/Qt = shunt fraction (shunt flow divided by total cardiac output)
CcO2 = pulmonary end-capillary O2 content, same as alveolar O2 content
CaO2 = arterial O2 content
CvO2 = mixed venous O2 content

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23
Q

2 causes of hypercapnia

A

Hypoventilation
V/Q inequality

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24
Q

Fast and slow alveoli

A

Fast alveoli
- Low resistance and/or low compliance
- Fast to fill/ empty completely (shorter time constant)
- High V/Q ratio
- Apical alveoli

Slow alveoli
- High resistance and/ or high compliance
- Slow to fill/ empty completely
- Low V/Q ratio
- Basal alveoli

25
Q

O2 dissociation curve points and causes for R) and L) shift

A

PO2 100 SO2 97.5, PO2 40 SO2 75, PO2 27, SO2 50
Sigmoid shape of curve due to cooperative binding

R) shift - incr unloading/ decr affinity of O2
- Think exercising muscle
- Incr pH, incr CO2, incr temp, incr 2,3 DPG

L) shift - decr unloading/ incr affinity
- Opposite of above
- COHb, MetHb, HbF

26
Q

Bohr Effect

A

Metabolically active tissues produce CO2, heat, H+ ions thus shifting curve to right and offloading O2 where it is most needed - 25% of O2 uptake by tissues may be due to Bohr effect

27
Q

CO2 carriage in blood

A

3 forms
- Dissolved (10%)
- As bicarbonate (60%)
- Combination with proteins as carbamino compounds (30%); enhanced by deoxygenation of the blood (Haldane effect)

28
Q

Henry’s Law

A

Gas law - amount of dissolved gas in a liquid is directly proportional to its partial pressure above the liquid, at a constant temperature

29
Q

Haldane Effect

A

Deoxygenation of the blood increases its ability to carry CO2

30
Q

Components of compliance

A

Compliance = change in volume per unit change in transmural pressure

Components
- Surface tension
- Elastic recoil of lung parenchyma
- Airway resistance - dynamic only
- Tissue resistance/ frictional or viscous forces - dynamic only

31
Q

Dynamic and static compliance

A

Dynamic compliance
- Volume change divided by the initial change in transmural pressure gradient during normal quiet breathing
- Includes non-elastic resistance force - airway and viscoelastic resistance
(hence always lower than static)

Static compliance
- Volume change divided by the steady state change in transmural pressure gradient
- Non-elastic resistance excluded

Dynamic compliance is always less than static compliance, due to
- Time dependent behaviours of the lung
- Airway resistance (resistive work)

32
Q

Hysteresis

A
  • Is the dependence of the state of a system on its history
  • Lung volume at any given pressure is large in deflation than inflation, i.e more pressure than expected in inflation
  • Caused by airway resistance and time dependence
  • Elastic hysteresis and is present in most deforming elastic bodies
  • Dynamic hysteresis - due to resistance forces acting against change in lung volume
  • Static hysteresis - due to viscous resistance of pulmonary surfactant
33
Q

Surface tension

A

Force (in dynes) acting across an imaginary line 1cm long in the surface of the liquid

33
Q

LaPlace’s Law

A

P = 4T/r

P = pressure
T = surface tension
r = radius
When only one surface is involved in a liquid-lined spherical alveolus, numerator is 2 rather than 4

34
Q

Role of surfactant

A

Phospholipid containing DPPC
Produced by type II alveolar epithelial cells

  • Reduces surface tension, increasing compliance of lung
  • Increases stability of alveoli
  • Help keep alveoli dry (reduces hydrostatic pressure in the tissues, preventing transudation of fluid)

Absence = reduced lung compliance, atelectasis, tendency to pulmonary oedema

35
Q

Poiseuille Equation

A

For laminar flow:
V = Pπr^4/8nl
P = K.V (V = flow)

R = 8nl/πr^4

R = resistance
n = viscosity
l = length
r = radius

36
Q

Reynolds number

A

Whether flow will be laminar or turbulent

Re = 2rvd/n

r = radius
v = average velocity
d = density
n = viscosity

Re >4000 = turbulent, P = KV^2
Re <2000 = laminar
Re 2000-4000 = transitional

37
Q

Airway resistance + factors affecting

A
  • Highest in medium bronchioles. Small airways contribute little resistance due to large number of them.
  • Decreases as lung volume rises because airways pulled open
  • Breathing a dense gas, as when diving, increases resistance (heliox used to mitigate this)

R = 8nl/πr4

Determinants - lung volume, density and viscosity, bronchoconstriction

38
Q

Dynamic compression of airways

A
  • Flow-related airway resistance
  • At high lung volumes, exp flow rate incr with effort, but at low volume, flow rate is fixed - flow is effort independent

Pressure limiting flow downstream of the collapse (equal pressure point) becomes the intrapleural pressure.
Equal pressure point is the point that intrathoracic P = intraluminal P

Exaggerated in lung disease where elastic recoil is impaired and resistance increased, i.e COPD

39
Q

FEV1

A

Volume in 1 second of maximal expiration, normally 80% of FVC

Restrictive disease
- FEV1 and FVC reduced, FEV1/FVC % normal/ increased

Obstructive disease
- FEV1 reduced more than FVC, FEV1/FVC% reduced

40
Q

Work of breathing

A

Work (J) = pressure x volume
(the are under the pressure-volume curve)

Inspiration - work to overcome elastic and non elastic/ viscous/ resistive forces (35%)
- resistance to airflow/ airway main factor
- flow type, Reynolds number and Poiseuille (radius)

Expiration + triangle - work to overcome elastic work, stored as potential energy (65%)
- surface tension most important

RR optimised to minimised WOB
- restrictive - high RR small Vt
- obstructive - low RR bigger Vt

41
Q

Time constant

A
  • Mathematical concept used to describe the time course of an exponential process
  • Time required to reach completion if initial rate of change maintained in first order system

1 time constant is the time taken to achieve 63% of maximal inflation or deflation of lung unit, 2 = 86%, 3 = 95%

t = 1/k = t1/2 x 0.693 = compliance x resistance

Time constant of normal alveolus = 0.2s

42
Q

Closing capacity

A

The volume at which the small/ dependent airways begin to close - occurs as the lung volume is reduced towards RV.

Closing volume = closing capacity - RV

CC = FRC at 44yrs in supine
= FRC at 65yrs in upright

  • Measured using Fowler’s method (single breath N2 washout)

Factors altering closing capacity
- Expiratory airflow
- Expiratory effort
- Small airway disease
- Increased pulmonary blood volume
- Decreased pulmonary surfactant
- Parenchymal lung disease
- Age

43
Q

Central chemoreceptors

A
  • Located near the ventral surface of the medulla
  • Sensitive to PCO2 of blood
  • Responds to change in pH of the ECF/CSF when CO2 diffuses out of cerebral capillaries
44
Q

Peripheral chemoreceptors

A
  • Located in the carotid bodies (via CN IX) and aortic bodies (via CNX)
  • Respond to decreased arterial PO2, and increased PCO2 and H+. Very little response until pO2 <100mmHg
  • Rapidly responding
  • Contain 2 types of glomus cells
    => Type I - large content of dopamine and nerve endings
    => Type II - sustentacular cells (supportive function)
45
Q

Lung receptors

A
  • Pulmonary stretch receptors (slowly adapting)
    => Hering-Breuer inflation reflex - increased expiration in response to stimulation/ distension and slowing of respiratory frequency
  • Irritant receptors (rapidly adapting)
  • J (juxtacapillary) receptors
  • Bronchial C fibres
  • Nose and upper airway receptors
  • Joint and muscle receptors
  • Gamma system
  • Arterial baroreceptors
  • Pain and temp receptors
46
Q

Venous admixture

A
  • Degree of mixed venous blood with pulmonary end capillary blood that would be required to produce the observed difference between the arterial and the pulmonary end capillary pO2
  • Components
    => Low V/Q matching
    Physiological - normal V/Q scatter from gravity
    Pathological - Lung disease (e.g COPD), vasodilators impairing HPV
    => Shunt
    Physiological- thebesian veins, bronchial veins
    Pathological - heart (PFO), lung (AVM)
47
Q

Oxygen content of blood

A

CaO2 = (1.34 x [Hb] x Sao2) + (0.003 x PaO2)

CaO2 (ml/100ml O2) - typically 20ml/100ml O2
Hb (g/dL)
1.34 = constant for Hb (max amount of Hb-bound O2 per unit volume of blood), sometimes quoted as 1.39
SaO2 = oxygen saturation in number
0.03 = solubility constant in ml/L/mmHg of dissolved O2 in blood

48
Q

Oxygen delivery

A

O2 flux equation
DO2 = Q x CaO2 x 10
= CO x 1.34 x [Hb] x SaO2 + 0.003 x PaCO2

10 = conversion factor as Q (L/min), and CaO2 ml O2/100mL
Q = CO, typically 5L/min at rest
Typical DO2 at rest is 1000ml/min

Factors governing DO2
- CO or regional blood flow
- Arterial SaO2
- Hb conc

49
Q

Oxygen consumption

A

Global O2 consumption is the volume of O2 consumed by the body per minute (VO2)

Reverse Fick principle
VO2 = Q x (CaO2 - CvO2) x 10

VO2 essentially reflected as the difference in O2 content between arterial and mixed venous blood (as measured by a pulmonary artery catheter)

Baseline O2 consumption ~250ml/min at rest (1MET = 3.5 ml/kg/min)

50
Q

Hypoxia

A

PaO2 < 60mmHg

Responses
- incr alveolar ventilation
- HPV (improved V/Q matching)
- incr SNS output -> incr CO

Anaesthesia
- suppression of all responses
- dose dependent effects

51
Q

Pulmonary Vascular Resistance

A

Factors affecting:
- Pulmonary blood flow - recruitment and distension
- HPV
- Lung volume - U-shaped, PVR lowest at FRC
- Metabolic and endocrine factors - e.g CoO2, lactate, H+, pH -> vasoconstriction
- ANS - a1 - vasoconstriction, B2 vasodilation
- Blood viscosity - incr with incr viscosity
- Drugs

52
Q

Time Constant

A

= Time required to reach completion if initial rate of change were maintained in a first order system

= Time constant (τ) is the time required for inflation up to 63% of the final volume, or deflation by 63%
= Resistance x Compliance

3x time constants = completion

53
Q

Static lung compliance

A

Intrinsic elasticity
- Decr -> decr inward recoil -> decr LC
- Elderly/ smoking = incr LC
- Fibrosis/ oedema = decr LC

Surfactant
- LaPlace’s Law T = Pxr/2
- Reduces surface tension at air water interact, incr compliance, decr collapse

Actual lung size
- Male > female
- Taller > shorter

Relative lung columes
- High volumes - surfactant spreads out -> incr surface tension -> decr LC
- Low volumes - small radius -> incr surface tension, collapse -> decr LC (pregnancy and obesity)
- Max LC at FRC

Gravity
- Apex - incr traction, larger alveoli, more -ve IPP -> decr LC
- Base - smaller alveoli, less -ve IPP -> incr LC

Posture
- Supine - decr LC
- Prone - incr LC

Pulm blood volume
- Congestion = decr LC (HF, supine)

54
Q

Airway Resistance

A

Gas properties affecting flow
- Gas density (incr density -> incr turbulence -> incr R)
- Gas viscosity (incr viscosity -> laminar flow -> decr R)

Airway diameter
- Lung volume (decr R with higher V)
- Physiological variation
- Pathological
=> Mechanical obstruction or compression, extrinsic (tumour), dynamic compression, artificial airways
=> Decr internal crossection - oedema, mucosal or SM hypertrophy, encrusted secretions
=> Decr SM tone - bronchodilators, SNS agonists
=> Incr SM tone - bronchospasm, irritants, PSNS agonists

Airway length
- Lung volume (incr V stretches and elongate bronchi)
- Artificial airway (incr length - ETT, decr - trache)

Flow rate
- RR (incr RR -> incr flow rate)
- Insp + exp work (e.g voluntary forced exp)
- Insp flow pattern generated by mechanical ventilation

Affect resp resistance as whole
- Resistance from deformation of tissues (tissue resistance from lung parenchyma and CW)
- Inertance of air and thoracic tissues (important at high RR)
- Compression of intrathoracic gas (important with high resp pressures)

55
Q

Respiratory quotient

A

Volume of carbon dioxide released over the volume of oxygen absorbed during respiration. Amount of CO2 depends on the energy substrate

CHO, lactate, glucose = 1
Protein = 0.8
Fat = 0.6

56
Q

Hypoxia

A
  • Oxygen delivery to the tissues that is inadequate to meet its metabolic demands
  • Tissue pO2 levels that are inadequate to support oxidative phosphorylation

Classification
- Hypoxic hypoxia (anoxic)
Hypoxia due to hypoxaemia
Low piO2
Hypoventilation
Diffusion limitation
Shunt
V/Q mismatch
Diffusion hypoxia

  • Anaemic hypoxia
    Anaemia causing reduced O2 carrying capacity
    Anaemia
    CO poisoning
  • Circulatory hypoxia (stagnant)
    Shock with failure to deliver oxygen to the tissues
    Hypovoalemic
    Cardiogenic
    Obstructive
    Distributive
    Septic
    Neurogenic
  • Histotoxic hypoxia (cytotoxic)
    Inability of the tissues to utilise O2, even if it is present at adequate concentrations
    Cyanide toxicity
57
Q

Non-resp functions of lung

A

AFIRM TITS

  • Acid base
  • Filtration
  • Immune
  • Reservoir
  • Metabolism
  • Thermoregulation
  • Inhalation
  • Taking up drugs
  • Surfactant synthesis
58
Q
A

Definitions (14 decks)

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