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Final FRCA SOE > Respiratory physiology > Flashcards

Respiratory physiology Flashcards

1
Q

Factors affecting gas exchange

A

Dead space = proportion of tidal volume not involved in gas exchange
Diffusing capacity = volume of gas transferred over membrane per unit time
shunt = proportion of blood entering left heart without being oxygenated

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2
Q

Dead space

A

Anatomical = upper airways and conducting zone of respiratory tract. AMV = (TV - dead space) x RR
Alveolar = proportion of alveolar minute ventilation not taking part in gas exchange due to entering under-refused alveoli

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3
Q

Ficks law of diffusion

A

diffusion of substance affecting by
- concentration different
- diffusion coefficient
- surface area
- thickness (inversely)

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4
Q

O2 diffusion alveoli –> circulation at rest

A

250ml.min

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5
Q

Shunt

A

Extrapulmonary
- Thesbian veins (physiological)
- ASD / VSD
Pulmonary
- Bronchial arteries (physiological)
- Atelctasis / consolidation

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6
Q

V/Q

A

Alveoli ventilated but not perfused have V/Q infinity
Perfused not ventilated have V/Q 0
Normal AMV = 4000ml
Normal CO = 5000ml
Normal V/Q = 0.8

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7
Q

Alveolar gas equation

A

Partial pressure of alveolar PO2 can’t be measured. Calculated from alveolar gas equation
PA02 = PIO2 - (PaCO2/R)
PIO2 = FiO2 x (PATM - PH20)
PH20 = SVP H20 6.3kPA
PATM = 101.3kPa
Assume PaCO2 = PACO2 and R = 0.8

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8
Q

Arterial Oxygen content

A

O2 bound to Hb + dissolved
Hb x 1.39 x (SaO2 / 100) + PO2 x 0.003
20ml/100ml

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9
Q

DO2

A

CaO2 x CO
CaO2 normal value = 20ml/dL
CO = 5L/min
Normal DO2 1000ml/min

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10
Q

VO2

A

Oxygen consumption per minute
CO x (CaO2 - VaO2) / 100
5 x (20 - 15) = 250ml/min

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11
Q

Oxyhaemoglobin dissociation curve

A

2a 2b subunits each bind 1 molecule O2, each molecule enhances affinity
P50 = PO2 at which 50% binding sites occupied (3.5kPA)
Sigmoid shape has physiological advantages
- flat upper portion means if PO2 drops, loading of O2 unaffected
- as red cells takes up O2, large partial pressure difference between alveoli and blood continues when most of O2 has been transferred
- steep part of curve means tissues can withdraw large amount of O2 for small drop in capillary O2

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12
Q

Bohr Effect

A

Describes different affinity for O2 at different pH
At higher pH (lungs) - Hb has greater affinity for O2 (left shift, lower p50) facilitating uptake
At lower pH (tissues) - Hb has lower affinity for O2 (right shift, higher p50) facilitating delivery

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13
Q

Shift of oxyhaemoglobin dissociation curve

A

LEFT shift (increased affinity)
- Higher pH
- Less 2,3-DPG
RIGHT shift (reduced affinity)
- Lower pH
- Higher temperature
- More 2,3-DPG

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14
Q

2,3-DPG

A

Produced by side reaction of glycolysis
Present in RBCs
Binds to beta subunits of Hb
Reduces affinity for O2
Increases O2 delivery
Increased in anaemic states, low O2 tension

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15
Q

Hypoxia

A

Inadequate PO2 to maintain aerobic metabolism in cells
1. Hypoxic hypoxia
- Hypoxic atmosphere (altitude), hypoventilation, V/Q mismatch, diffusion issue
2. Anaemic hypoxia
- Reduced RBC e.g. bleeding, reduced Hb e..g iron deficiency, reduced O2 binding e.g. haemoglobinopathy
3. Stagnant hypoxia
- Hb and PO2 normal but inadequate delivery e.g. shock states
4. Histiotoxic hypoxia
- cells can’t use oxygen e.g. cyanide poisoning

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16
Q

Respiration

A

Process of producing energy from oxidation of complex organic molecules using O2 and releasing CO2
Phase 1 - production of 2 carbon molecules. 2 ATP
Glucose –> 2 pyruvate –> 2 AcetylCoA
FFA –> AcetylCoA
AA –> pyruvate / AcetylCoA
Phase 2 - Kreb cycle 2 ATP 6NADH2+ 2FADH2
AcetylCoA + oxaloacetate –> citrate
Phase 3 - Electron transport chain. Reduced electrons re-oxidised releasing electrons and energy, passed down the chain and accepted by O2
NADH2+ –> 3 ATP. FADH2 –> 2 ATP
Aerobic = all 3 phases. Glucose –> 38 ATP
Anaerobic = phase 1 only. Glucose –> 2 ATP and lactate

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17
Q

Cellular hypoxia effects

A
  • aerobic –> anaerobic metabolism
  • fall in pH –> inhibition of chemical reactions
  • fall in ATP –> insufficient energy for functions e.g. ion transport
  • loss of cell function —> loss of tissue function
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18
Q

Compensation for hypoxia

A

Early
1. Local - changes in Hb:O2 affinity (right shift), vasodilation
2. Ventilatory - peripheral chemoreceptors –> increased minute ventilation
3. CVS - chemoreceptors respond to low O2 –> vasoconstriction, tachycardia to increase perfusion
Late
- increase RBCs via EPO

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19
Q

Special circulations and hypoxia

A

Brain - auto regulation, very dependent on oxidative phosphorylation of glucose. PO2 below 6.7kPA –> exponential rise in CBF
Coronary - high O2 extraction (75%)
Pulmonary - HPVC - divert blood away from less oxygenated lung

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20
Q

CO2

A

PACO2 approximates to PaCO2
ETCO2 lower than PaCO2 as mixed with lung units that aren’t perfused
CO2 output 200ml.min
AMV 4000ml.min
Alveolar CO2 = 5%

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21
Q

PACO2 affected by change in production / elimination

A

Decreased
- Respiratory hypcapnia (pain, anxiety, hypoxia)
- compensatory (met. acidosis)
Four course of hypercapnia
1. Increased inspired CO2 (rebreathing)
2. Hypoventilation e.g. CNS, T2RF
3. Increased production - sepsis, MH
4. Compensatory for met. alkalosis

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22
Q

Physiological effects of hypercapnia

A

Neuro - Low GCS, confusion, flap
- Inc CBF and ICP (vasodilation)
- Narcosis > 12kPa
Resp - tachypnoea
- Inc AMV mediated by central chemoreceptors
- Pulm vasoconstriction (inc PVR)
- right shift Hb:O2 dissociation
CVS - Tachycardia, HTN
- Direct - reduced myocardial contractility, arterial vasodilation, arrhythmia
- Indirect - inc catecholamine - Inc HR and SV, vasoconstriction
Metabolic
- Inc K+ leakage from cells

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23
Q

Volumes and capacities

A

4 volumes
- Tidal volume 6-8ml/kg
- Inspiratory reserve volume
- Expiratory reserve volume
- Residual volume 20ml/kg
3 Capacities
- Vital capacity (TV + Exp reserve + Ins reserve)
- Functional residual capacity (Exp reserve + residual)
- Total lung capacity (TV + Exp reserve + Ins reserve + RV)

Residual volume (+ FRC + TLC) can’t be measured by spirometry

24
Q

FRC

A

2500ml
Point where elastic recoil of lungs = elastic recoil of chest wall
Functions
- O2 resevoir
- Prevention of airway collapse (at FRC lung is splinted open)
- Optimal compliance - FRC on steep part of compliance curve, if reduced and on flat part of compliance curve then increased WOB
- Optimal pulmonary vascular resistance (lung not squashed or overinflated)
Increased FRC
- Male, tall, emphysema (inc. compliance), upright, prone positions
Decreased FRC
- short, female, decreased compliance (e.g. ARDS), increased abdominal pressure e.g. pregnancy, obesity, ascites

25
Q

Airway collapse / closing capacity

A

Gravity
- apical lung stretched
- basal lung compressed
Compression at bases causes airways to collapse
Lung volume at which this occurs is closing capacity

Airway closure occurs when lung volume equals closing capacity (closing volume + residual volume)
CC < FRC in healthy. If FRC reduced or CC increased (smoking, age) airway collapse may occur

26
Q

Dead space

A

Volume of inspired air not involved in gas exchange
Physiological = anatomical (conducting airways) + alveolar (poorly perfused alveoli)

27
Q

Measuring anatomical dead space

A

Fowlers method
normal air, then vital capacity of 100% O2
measure exhaled N2
Initially on exhalation just O2
Midpoint of steep slope of N2 = anatomical deadspace
Then flatter slope of alveolar gas
Then steep inflection after closing capacity

28
Q

Measuring physiological dead space

A

Bohr Equation
VD / VT = (PaCo2 - PECO2) / PaCO2

29
Q

V/Q relationships

A

Lower, dependent lung better ventilated than upper
At bases intrapleural pressure less negative therefore lung relatively compressed with lower resting lung volume - on steep part of compliance curve
Apex shallower portion of compliance curve

30
Q

West Zones

A

Zone 1
- PA > Pa > Pv
- Shouldn’t occur in health
- Reduced arterial pressure or IPPV. Lead to dead space
Zone 2
- Pa > PA > Pv
- perfusion determined by difference between PA and Pa
Zone 3
- Pa > Pv > PA
- Perfusion determined by arteriovenous pressure gradient

When supine, posterior blood flow greater than anterior

31
Q

Shunt equation

A

Qt x CaO2 = (Qs x CVO2) + (Qt - Qs) x CCO2
Qt/Qs = CCO2 - CaO2 / CCO2 - CVO2

32
Q

Ventilation / perfusion ratios apex –> base

A

Both ventilation and perfusion increase towards the base
Perfusion increases more than ventilation
V/Q at apex therefore > 1
V/Q at base therefore < 1

33
Q

Increased A-a gradient

A

Abnormally low V/Q ratios
- ventilation reduced relative to perfusion
- reduced PAO2
- Overcome by increasing FiO2
Abnormally high V/Q ratios
- Perfusion reduced relative to ventilation
- dead space ventilation e.g. PE

34
Q

Work of breathing. Respiratory muscles have to overcome..

A
  1. Lung elastic forces
  2. Chest wall elastic forces
  3. Lung tissue restrictive forces
  4. Chest wall restrictive forces
  5. Airway resistive forces
35
Q

Normal compliance

A

200ml/cmH20
volume change per unit pressure
Hysteresis
- volume in expiration at any given pressure is greater
- base of lung on steeper part of compliance curve. at lower lung volumes may encroach on shallower part.

36
Q

Surface tension

A

Arises when forces between adjacent liquid molecules greater than between liquid and gas. Liquid surface becomes as small as possible. Greater in smaller alveoli as P = 4T/r (LaPlace) meaning small alveoli empty in to large alveoli
Prevented by surfactant
- Type 2 pneumocytes
- Dipalmitayl phosphatidylcholine

37
Q

Flow charceteristics

A

Laminar / transitional / turbulent
Laminar flow - viscosity of gas has impact rather than density
Turbulent - density rather than viscosity
Re = density x velocity x diameter / viscosity

38
Q

Diffusion of different gases

A

Carbon Monoxide rapidly binds to Hb therefore doesn’t exert partial pressure. Transfer is diffusion limited
N20 doesn’t bind to Hb and therefore exerts partial pressure - transfer is perfusion limited
O2 in between

39
Q

DLCO

A

Volume of CO transferred in ml/min/mmHg alveolar partial pressure. Normal is 25
Ficks law VGas ~ A/T x D (P1 - P2)
A, T can’t be measured. D2 = diffusing capacity of lung. P1 = alveoli P2 = blood (negligible)
Therefore D2 = VCO / PACO
Single inspiration of CO mixture and rate of disappearance from alveolar gas during 10 second breath hold

40
Q

Pulmonary vascular resistance

A

Low pressure low resistance system
25 / 8 PA pressure mean 15mmHg
At higher lung volume, vessels splinted open - lower resistance
At highest lung volumes - stretching reduces calibre and increases resistance
Inverse bell shape

41
Q

Metabolic functions of lung

A
  • ACE AngI –> AngII
  • Bradykinin inactivated
  • Serotonin removal
  • Arachidonic acid metabolites metabolised
42
Q

Four causes of hypoxaemia

A
  1. Hypoventilation - overcome by increasing FiO2. Alveolar ventilation halved, PCO2 doubled. Fall in PO2 and rise in PCO2 via alveolar gas equation
  2. Diffusion limitation
  3. Shunt - not overcome by inc FiO2 (shunted blood bypasses ventilated lung units)
  4. Ventilation-perfusion inequality - regional differences top to bottom. PO2 changes from base to apex more so than PCO2
    - High V/Q areas have high o2 (apex) but base has more blood supply. Adds relatively little O2
    - Higher CO2 compensated for by increasing RR (more so than low PO2)
43
Q

CO2 transport

A
  1. Dissolved (20x more soluble than O2, 10%)
  2. Bicarbonate. CO2 + H2O <–> H2CO3 <–> HCo3- + H+ reaction faster in RBCs due to CA. H+ remains in RBC (HCO3- replaced by Cl-) and binds to reduced Hb (more so than oxygenated). Haldane effect.
  3. Carbamino compounds
44
Q

Control of breathing

A

Central controller = pons, medulla
Sensors = chemoreceptors, lungs
Effectors = respiratory muscles
Central controller
- Medullary respiratory centre - intrinsic rhythm, inspiratory action potentials
- Apneustic centre
- Pneumotaxic centre - switch off inspiration and regulate volume and rate
Cortex can overide

45
Q

Sensors in breathing control

A
  1. Central chemoreceptors - ventral surface of medulla. H+ (CO2) stimulates breathing. CSF, blood flow, local metabolism. BBB permeable to CO2 - liberates H+ in CSF. CSF minimal buffering, therefore CO2 causes greater change in pH. Prolonged CO2 exposure - HCO3- increase in CSF
  2. Peripheral chemoreceptors - carotid bodies (bifurcation of carotid) and aortic bodies. Rich capillary supply. Respond to low O2, low pH, high CO2. Fast response to arterial hypoxaemia, 20% of response to PCO2
  3. Lung receptors
    - pulmonary stretch receptors
    - Irritant receptors
    - J receptors
46
Q

Response to PCO2 / PO2

A

If CO2 normal, PO2 reduced to 6.6 before increase in ventilation
Higher CO2 increase in ventilation for any given PO2
Chronically (altitude) large increase in ventilation - res alkalosis
Severe lung disease pH CO2 buffered and blood pH buffered by renal HCO3-. Arterial hypoxaemia more important

47
Q

Severe exercise

A

Resting O2 consumption inc from 250 –> 3000ml.min
CO2 production 200 —> 3000ml/min
O2 consumption increases linearly until becomes constant above certain work rate (VO2max)
Ventilation increases linearly with work, but at high VO2 increases further (Anaerobic threshold) as lactate production ventilatory stimulus.
Increase in cardiac output from SV and HR but less so than ventilation

48
Q

Altitude

A

Barometric pressure reduces exponentially
PIO2 reduces as result - at 5800m 70mmHg of O2, 130mmHg at sea level
Acclimitisation
- Hyperventilation - hypoxic stimulus to peripheral chemoreceptors. Low PCO2 but CSF pH normalises in 24hrs releasing break on hyperventilation
- Polycythaemia - EPO
- Right shift OxyHb dissociation curve due to 2,3-DPG
- Hypoxic pulmonary vasoconstriction - increase right heart strain

49
Q

Apnoeic oxygenation

A

VO2 = 250ml/min
In apnoeic patient - 250ml O2 will move from alveoli to blood stream
20ml/min CO2 move from blood to alveoli
Net pressure in alveoli becomes sub-atmospheric
draws gas from upper airway by mass flow. If this is reservoir of 100% O2 then 240ml O2 will be drawn down to alveoli, only 10ml less than requirement
Oxygenation can be maintained for 100mins in healthy, but significant hypercapnia will arise.

50
Q

Desaturation during apnoeic oxygenation influenced by

A
  1. FRC
  2. Preoxygenation
  3. Maintenance of patent airway
  4. Hb level
  5. VO2
51
Q

Hypoxic pulmonary vasoconstriction modified by

A

Enhanced by
- Hypercapnoea
- Acidosis
Reduced by
- Alkalosis
- Hypocapnia
- volatile
- vasodilators

52
Q

Physiological effects of smoking

A

Resp
- Increased sputum production
- impaired mucociliary elevator function
- thickening of airway wall
- inflammation and bronchoconstriction of airways
- destruction of alveolar surface
- increased carbon monoxide and reduced oxygen carrying capacity, left shift oxyHb curve
- accelerated atherosclerosis
CVS
- nicotine - sympathetic stimulation with tachycardia, increased SVR
- increased Myocardial O2 demand
- Polycythaemia
CNS
- relaxation
-addiction
GI
- nausea
- ulcers
Surgical
- impaired wound healing
Pharm
- Induction of CYP450 (reduced theophylline)

53
Q

Pre-op smoking cessation

A

Carbon monoxide half life 4hrs
Nicotine half life 30 mins
12-24 hrs - CO and nicotine levels normal
2-3 days - some ciliary improvement
2 weeks - sputum volume decreases to normal
weeks - reduction in cough, wheeze
months - years - reduction in lung cancer, COPD, IHD, CVA
Post-op respiratory morbidity - reduction needs 6-8weeks cessation

Vaping - heat solvent, nicotine, flavouring. likely less harmful. Nicotine therefore same CVS SE, longterm safety unknown.

54
Q

Dynamic spirometry

A

Forced - full inspiration to full expiration hard and fast
- FEV1 and FVC
Obs
- FEV1/FVC < 0.7
Restrictive
- FEV1/FVC > 0.7
- FEV1 and FVC < 80% predicted

55
Q

flow-volume loop

A

inspiratory and expiratory flow volume curve
diagnose location of obstruction
- fixed upper airway - reduced in and out (flattened)
- variable extra thoracic e.g. VC. inspiratory restricted as pulls cords together, expiratory unchanged therefore flattened inspiratory
- variable intrathoracic e.g. tumour - inspiration pulls airways apart but collapse on expiration. exp flattened insp normal

Final FRCA SOE (11 decks)

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