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Physiology > Respiration and Breathing > Flashcards

Respiration and Breathing Flashcards

1
Q

State Laplace’s and Fick’s laws:

A

LaPlace’s:
Pressure = 4(surface tension)/r

In alveoli divide by two as only one surface is a liquid-gas interface

Fick’s law:
dQ/dt = (Δp x A x d)/t

Diffusion rate = (Δpartial pressure x diffusion coefficient x area)/thickness.

d ∝ sqrt(molecular weight)

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2
Q

What is Henry’s law and what does it describe?

A

Describes concentration of gas in blood:
Concentration = partial pressure x solubility

[Blood O2] = (1.39 x [Hb] x % saturation) + (0.003 x PO2)

Don’t forget the dissolved O2!!

Partial pressure = (atmospheric pressure - 47) x (%gas/100) in mmHg from DRY percentage

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3
Q

What is functional residual capacity and how is it created?

A

FRC: the point at which elastic recoil forces inwards equals the outward forces from the chest wall.

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4
Q

What is a collapsed lung?

A
  • A breaking of the air-tight seal of the interpleural space
  • Meaning negative pressure not maintained.
  • Therefore force inwards due to elastic recoil overcomes force outward = collapse inwards
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5
Q

What is compliance of the lung? What does it depend on?

A

ΔP/ΔV (gradient) = the pressure required to cause a given volume change.

Human lung shows marked hysteresis (lung volume at given pressure is larger on deflation

  • Rigidity
  • Shape of thoracic cage
  • Expanding muscle strength
  • Elastic properties (e.g. surface tension)
  • Lung size
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6
Q

What is specific compliance?

A
  • Compliance divided by functional residual capacity
  • Adjusts for lung size
  • Roughly constant throughout animal kingdom
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7
Q

What is regional compliance of the lung?

A
  • Lung is more compliant at the base (maybe due to more surfactant)
  • Pressure also higher in base due to gravity meaning larger volume expansion at base (for same mean pressure)
  • Leads to base accepting a disproportionately large fraction of tidal volume
  • During expiration opposite effect seen (base constricted more)
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8
Q

How can regional compliance/tidal volume distribution be shown?

A
  • (133)Xe gas inhaled with oxygen and the radiation distribution measured
  • Graph drawn to show data (unit volume against distance up lung gives +ve proportional relationship during inspiration)
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9
Q

Define trans total pressure; transmural pressure; trans chest wall pressure and transpulmonary pressure.

A

Trans chest wall pressure = pressure inside lung – atmospheric pressure

Transmural pressure = pressure inside - pressure outside

Trans chest wall pressure = pleural space pressure – atmospheric pressure

Transpulmonary pressure = pressure inside lung - pleural space pressure

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10
Q

What are the effects of abnormally high and low lung compliance?

A

Compliance effects FRC

Abnormally high compliance (distensible lung):
- Elastic properties reduced (recoil force less)
- Exhaling becomes energy expensive as FRC now at much larger volume
- E.g. emphysema

Abnormally low compliance (stiff lung):
- More work required to increase -ve pressure high enough to expand lung
- Occurs during scarring/fibrosis e.g. after irritant exposure (silica/carbon particles, smoking)

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11
Q

What factors affect lung compliance? Give examples.

A

Shape and rigidity of thoracic cavity:
- Extreme obesity can deform thorax, reducing compliance
- Fat deposits/deformation may narrow airways (increased resistance)
- Increased force required to expand thoracic cavity due to surrounding tissue (not compliance but added factor)

Surface tension:
- Generated by air-liquid interface (LaPlace law)
- Hugely affected by surfactant: shown by IRDS

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12
Q

What do the Von Neergaard experiments show?

A
  • Replaced air with saline solution to inflate lung
  • Recorded pressure required to reach certain volume
  • Pressure was much lower using saline and showed very little hysteresis
  • Showed that surface tension accounts for large proportion of lung stiffness.
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13
Q

How does pulmonary surfactant work?

A
  • Surfactant molecules are highly organised due to their strong polarity (DPPC molecules)
  • Forms a layer on inner surface stopping water from depositing and thereby reducing surface tension of lung
  • Its ability to dynamically change in thickness during inhalation/expiration could explain hysteresis of lung compliance.
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14
Q

How is pulmonary surfactant produced?

A
  • Secreted by type II alveolar cells from precursors: glucose/choline/palmitate
  • High turnover rate due to continued removal of surfactant on inner alveolar surface
  • Forms highly organised (due to polarity) DPPC
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15
Q

What are the roles of surfactant?

A
  • Keeps lung dry (stops high surface tension of a water layer)
  • Reduces water being drawn out from capillaries
  • Reduces overall surface tension of lung, hence also compliance and therefore, work required to breath
  • Allows alveoli of different sizes to coexist: normally there is increased pressure in smaller alveoli (forces air out causing collapse), surfactant opposes this by reducing surface tension inversely to increased pressure, allowing expansion
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16
Q

Give evidence for surfactants’ role:

A
  • IRDS: premature babies babies (alveolar type II cells not yet formed) who have limited surfactant struggle to breath due to increased surface tension
  • Thoracic surgery patients who do not breath deeply for a period of time, leading to poor surfactant distribution and atelectasis also struggle.
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17
Q

How might the structure of surfactant explain hysteresis of lung compliance?

A
  • Magnitude of surfactant effect is dependent on the surface area and thickness of layer
  • Due to structure, thickness can change between inhalation and exhalation
  • Surfactant can expand (unlike most liquids) during inhalation = relatively thinner until molecules forced out of layer
  • On expansion, molecules are fitted in again (harder) so lung relatively MORE compliant on exhalation
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18
Q

What is a langmuir trough and what does it show?

A
  • Set up: very stable tray containing test liquid with a high sensitivity force transducer, the force required to move the transducer perpendicular to the surface is the St.
  • Area of the surface can be changed to simulate lung volume changes
  • Surfactant is special as it reduces surface tension dependent on surface area
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19
Q

What factors affect resistance to airflow in the lungs?

A

Think Poiseuille’s’ law: (8ηl/πr^4)

Radius of airways:
- Increased on inhalation as small airways are suspended in parenchyma which connects them to surrounding tissues.
- Contraction state of smooth muscles under parasympathetic control (ACh causes constriction and mucus secretion; adrenaline causes dilatation and mucus inhibition)
- PCO2 induces dilatation

Viscosity of gas increases resistance to movement.

Mucus secretion also increases resistance.

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20
Q

What is the equal pressure point?

A
  • Must always be a pressure gradient towards to mouth during expiration
  • Therefore pressure inside airways decreases along length
  • At some point the pressure inside = inward pressure from pleural contraction
  • Transmural pressure = 0
    This is EPP.
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21
Q

What are the consequences of the EPP in the lungs?

A

Limits flow rate of expiration due to potential airway collapse:
- Intrathoracic pressure increases during expiration (to create pressure gradient)
- Alveolar recoil and added pressure from contraction of pleural space increases pressure inside airways
- The steeper the pressure gradient, the lower EPP.
- Gradient must be shallow enough to make sure EPP occurs in supported airways (with cartilage rings)

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22
Q

What factors control where EPP occurs?

A
  • Lung compliance (since added to recoil) - shown by low EPP in emphysema
  • Strength of thoracic muscle contraction
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23
Q

Why does CO2 equilibrium never limit gas exchange?

A
  • CO2 is 23 times more soluble than O2 in plasma (e.g. coefficient for CO2 is 0.7; for O2 is 0.03)
  • This outweighs effect of molecule size (changes with sqrt(Mr)
  • Therefore CO2 equilibrium always reached first.
24
Q

How does the lung continue to reach equilibrium on decreased transit time of blood (e.g. increased HR in exercise)?

A
  • At rest, lung has diffusion reserve = spare transit distance where equilibrium already reached
  • Gives roughly 0.3 seconds of spare time
  • Lung can increase capacity (more alveoli open) by increasing breathing depth (vital; rather than tidal capacity)
25
Q

What is the difference between oxygen partial pressure and oxygen content in blood?

A
  • O2 PP: only affected by dissolved O2
  • Oxygen content is dissolved AND bound to haemoglobin
26
Q

Describe the structure of haemoglobin:

A
  • 2α and 2β peptide chains
  • Shows polymorphism (Adult = A; fetal = F; sickle cell = S)
  • Reversibly binds 4 oxygen molecules (oxygenation) in porphyrin ring
  • Sequential binding affects affinity of next binding sites (positive cooperativity)
27
Q

Name some factors which alter haemoglobin affinity:

A

Bohr effect: decreased pH shifts curve right (decreases affinity)

Haldane effect: higher CO2 concentration shifts curve right (weak acid) and forms more carbonamino compounds (think equilibrium)

2,3 DPG: shifts curve right (F Hb is less sensitive to this)

28
Q

What is one problem caused by leaving blood for a long time before transfusion?

A

2,3 DPG degrades over time, meaning blood may have an overly high affinity.
- Reduces unloading at tissue bed

29
Q

Describe 5 blood gas disorders:

A

Hypoxic hypoxia: low arterial pO2, with low Hb saturation
Anaemic hypoxia: reduced O2 carrying capacity (e.g. low RBC count)
Circulatory hypoxia: Poor delivery of oxygenated blood to tissues (haemorrhage)
Histotoxic hypoxia: normal O2 delivery but cells unable to use O2 (e.g. cyanide poisoning)
Hyper/hypocapnia: describes CO2 partial pressure due to hypo/hyper ventilation

30
Q

Why is carbon monoxide so deadly (and a fabulous poisonous gas)?

A
  • CO has 240 times the affinity for Hb as O2
  • Hence shifts curve left: increases affinity (but O2 beat out by CO) and prevents unloading of any O2 at tissues
  • Hence 0.1% contaminated air can kill
  • Tasteless, odourless, colourless, no hypoxic signs (blood still bright red)

Also impairs feedback mechanisms as arterial pO2 can be normal

31
Q

How is CO2 transported in blood?

A
  • 5-10% dissolved
  • 90% as bicarbonate (acts as buffer)
  • 5% as carbonamino compounds (replaces one H on amide group)
32
Q

Describe the two buffer equilibria in blood for CO2:

A

Bicarbonate buffer:
CO2 + H2O <–carbonic anhydrase–> H2CO3 <—–>HCO3- + H+
- Made faster by carbonic anhydrase in RBCs

Carbonamino compounds:
R-NH2 + CO2 <—–> R-NHCOOH <—–> R-NHCOO- + H+
- Proteins can reversibly bind CO2 to amine groups.
- On Hb: CO2 binds to imidazole groups on histidine residues of α/β chains

33
Q

Detail three effects interacting in RBCs to control CO2 concentration:

A

Bohr effect: right shift to oxygen dissociation curve due to lower pH (better unloading at tissues)

Haldane effect: higher PO2 decreases Hb affinity for CO2 (allows better loading of O2 at lungs)

Hamburger’s phenomenon: allows right shift to bicarbonate equilibrium (more HCO3-) to be formed in RBC without net loss of anions. Allows CO2 to be drawn in.

34
Q

Explain Hamburger’s phenomenon:

A
  • Cl- exchanged for HCO3- by BAND3 transporters
  • Allows more HCO3- to be produced from shift of bicarbonate equilibrium
  • Draws more CO2 into RBCs when pCO2 high
35
Q

Give adaptations of the pulmonary circulation:

A

Low resistance:
- Many parallel vessels (redundancy)
- High compliance (= capillary distension) meaning it is not limiting during increased flow

Important to prevent high pressure which leads to oedema.

36
Q

How can pulmonary arterial pressure be measured?

A

Using a Swan-Ganz catheter

37
Q

Which factors influence pulmonary resistance?

A

Increased CO:
- Recruitment
- Capillary distension = high compliance

Lung volume:
- Extra-alveolar vessels are opened by -ve pleural pressure so open (even when internal alveolar pressure constricts)
- At FRC resistance is lowest

Hypoxia:
- Causes vasoconstriction (effective locally to divert blood to better area but problematic over whole lung e.g. at altitude).

38
Q

What is Starling’s equation and what does it describe?

A

fluid flux = k[(Pcapillary – Pinterstitial) - σ[(πpleural - πinterstial)]

= Hydrostatic – colloid pressure

Describes fluid exchange between capillaries and interstital spaces.

39
Q

Using principles from Starling’s equation - how might pulmonary oedema be caused (give specific examples)?

A
  • Increased capillary pressure: E.g. general hypoxia (altitude, emphysema); left heart failure.
  • Decreased capillary colloid osmotic pressure: E.g. starvation resulting in plasma protein loss.
  • Increased interstitial pressure: E.g. increased surface tension (causing increased -ve pressure) from IRDS.

May also be due to:
- Blocked lymphatic drainage
- Increased capillary wall permeability

40
Q

What are the mechanisms of fresh and salt water drowning?

A

Fresh water: lysis of RBCs; and cardiac fibrillation following increased Na+/K+ due to cell bursting.

Salt water: water drawn out of pulmonary capillaries into interstitium = death by asphyxiation

41
Q

What effect does gravity have on blood distribution in the lungs and why?

A
  • 22mmHg difference between bottom and top
  • Therefore most collapsed capillaries are in the top of the lung
  • Middle pressure higher due to heart proximity not gravity
42
Q

Name some functions of the pulmonary circulation other than perfusion:

A
  • Bronchial circulation provides warmth and humidity
  • Serves as blood reservoir (10% of blood volume evenly distributed)
  • Filtration
  • Metabolism of vasoactive hormones
43
Q

How does the pulmonary circulatory system filter blood?

A
  • Emboli/fat/clots: traps small blockages in capillaries protecting downstream organs (able to due to high redundancy)
44
Q

Give examples of the role of pulmonary circulation in metabolising hormones:

A
  • Angiotensin I: locally converted to angiotensin II by ACE on endothelial cells
  • Inactivation of hormones: E.g. SHT, NA, bradykinin, prostaglandins to reduce oedema due to damage from inflammation.
  • Adrenaline/HA/ADH unaffected by passage through
45
Q

What is the ventilation-perfusion mismatch?

A
  • Ventilation and perfusion increase down lung
  • Perfusion increased more due to greater effect from gravity
  • Therefore down lung ventilation/perfusion ratio changes from 3 –> 0.7
46
Q

How does the body oppose a change to average ventilation/perfusion ratio (Va/Q)?

A
  • Low VA/Q ratio requires an increase in overall ventilation: regional vasoconstriction induced by localised hypoxia (shunts blood away)
  • High VA/Q ratio suggests ventilation is wasted (local PCO2 will fall): Increase in pH and localised airway resistance (shifting ventilation to other alveoli)
47
Q

What is venous admixture? Why does it occur?

A

= Mixing of oxygenated and deoxygenated blood

Wasted air:
- Air in dead space does not oxygenate blood; blood

Wasted flow (any blood not fully oxygenated):
- Physiological shunting: blood bypasses alveoli (e.g. septum hole in heart, venous drainage of bronchial circulation). Approx 1-2% of CO.
- Alveolar shunting: blood contacts alveoli but does not become fully oxygenated (e.g. oedema, pneumonia, atelectasis)

48
Q

What is the alveolar gas equation?

A

Alveolar gas equation: PAO2 = PIO2 – PACO2[FIO2 + (1 - FIO2)/R]

  • PIO2 is the partial pressure of inspired oxygen
  • FIO2 is the fractional concentration of oxygen
  • R is the respiratory exchange ratio
49
Q

Why does altitude cause problems for breathing?

A
  • Reduced barometric pressure means much harder to draw air into lungs (transpleural pressure reduced) and speed of inhalation reduced.
  • Main consequence is reduced pO2 (>4 fold drop at everest summit)
  • Augmented by 5-fold ventilation increase to compensate
  • Equilibrium may still not be achieved (all of diffusion reserve used) as diffusion gradient also shallower
  • Oedema may result from generalised vasoconstriction causing high pressure
50
Q

What are the consequences of hyperventilation?

A

pH against pO2 battle:
- Decreasing pCO2 alkalises CSF opposing signals from peripheral chemoreceptors to increase pO2
- Sustained hypoxia overcomes pH signals allowing hyperventilation
- [HCO3-] must be reduced in CSF (kidney compensation)
- Over time chemoreceptors may become more active

51
Q

Give examples of adaptations to high altitude:

A

Polycythaemia (increased RBCs):
- Haemoglobin saturation lower so more need.
- Stimulated by increased endogenous erythropoietin
- In Peruvian Andes overcompensation seen!
- Not always true (Sherpa populations can show lower RBC to increase flow rate)

2,3 DPG increase:
- Causes right shift to oxygen dissociation curve
- Aids unloading at tissues

52
Q

How does SCUBA kit help?

A

Self-contained underwater Breathing Apparatus:

  • Increased pressure in tank to match surrounding hydrostatic pressure
  • Maintains trans total pressure so pressure gradient can be created (otherwise force needed is too large)
53
Q

What are ‘the bends’?

A
  • Sustained high surrounding pressure forces low solubility gases into solution
  • particularly N2 into fat
  • During sudden decompression (e.g. ascent from underwater chamber) bubbles of gas escape, causing pain and potentially death (emboli in brain)
54
Q

How is the risk of ‘the bends’ reduced?

A
  • He-O2 mixture used to breath rather than nitrogen (diffuses more quickly out and does not have narcotic effects of N2 under high pressure)
  • Slow ascent to equilibrate; treatment = hyperbaric chamber
55
Q

Why does exercise increase O2 requirement?

A
  • Muscle recruitment: more muscles to serve
  • Muscle requirement increases
  • Oxygen debt when anaerobic threshold reached (to metabolise lactate and restock PCr

Ventilation normally not limiting

56
Q

What are the two main muscle types and how do their oxygen requirements differ?

A

Type I (‘red’): slow twitch so mainly aerobic
Type II (‘white’): fast twitch so mainly glycolytic

Physiology (8 decks)

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