VIVA: Physiology - Respiratory Flashcards

1
Q

What are the initial physiological responses to high altitude?

A

3/5 to pass:
- Hyperventilation: decreases CO2 > O2
- Alkalosis: limited by movement of bicarbonate from CNS (1-2 days) and renal excretion of HCO3-
- Increased 2,3-DPG: R shift O2-Hb dissociation curve (early), then L shift at higher altitudes due to alkalosis
- Alveolar hypoxia induces pulmonary vasoconstriction, then pulmonary HTN
- Decreased work of breathing

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2
Q

What are the longer-term physiological effects of altitude exposure?

A

3 to pass:
- Polycythaemia
- Increased viscosity of blood
- Increased O2 carriage
- Pulmonary HTN resulting in RVH
- More capillaries
- Increased oxidative enzymes
- Increased mitochondria

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3
Q

Describe factors affecting airway resistance

A

In laminar flow, resistance is proportional to the length * of the tube and viscosity *, and inversely proportion to fourth power of the radius * of the tube (as per Poiseuille’s Law *: R = 8 x L x viscosity / n x radius^4)
- Turbulent flow is most likely to occur at high Reynold’s numbers: that is, when inertial forces dominate over viscous forces (Reynold’s number = density x diameter x velocity / viscosity)
- Resistance is highest in medium-sized bronchi and low in very small airways
- Airway resistance decreases as lung volume rises because the airways are then pulled open by radial traction
- Bronchial smooth muscle is controlled by the autonomic nervous system: stimulation of B-adrenergic receptors causes bronchodilation, reduced alveolar pCO2 causes increased resistance

*needed to pass

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4
Q

Define dynamic compression of airways and its effects on flow

A
  • Intrapleural pressure > alveolar pressure causes airway compression
  • Dynamic compression of airways limits airflow during forced expiration
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5
Q

How is carbon dioxide transported in the blood?

A

Percentages for arterial blood:
1. Dissolved (5-10%):
- CO2 20x more soluble than O2, therefore dissolved CO2 plays a significant role in its carriage
- 10% of gas evolved into the lung from blood is in dissolved form
2. Bicarbonate (90%) *:
- Formed by sequence CO2 + H20 <-> H2CO3 <-> H+ + HCO3- (first step aided by carbonic anhydrase)
3. Carbamino compounds (5%):
- Combination of CO2 with terminal amine groups in blood proteins
- Most important is globin in haemoglobin: reduced Hb binds more CO2 as carbaminohaemoglobin than HbO2

*needed to pass + 1 other

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6
Q

What is the chloride shift?

A

Hamburger effect:
- Ionic dissociation of carbonic acid results in HCO3- and H+ formation within the red cell
- HCO3- diffuses out but H+ cannot as the cell membrane is relatively impermeable to cations
- To maintain electrical neutrality, Cl- ions move into the cell from the plasma
- Cl- levels thus lower in systemic venous blood than systemic arterial blood

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7
Q

Describe how respiration compensates for acid-base changes

A
  • CO2 + H2O <-> H2CO3 <-> H+ + HCO3-
  • Rapid responder
  • Respiratory centre responds to H+, mainly at peripheral chemoreceptors but also transferred to CSF by CO2
  • Metabolic acidosis triggers increased ventilation, decreasing CO2 -> decreased H+ and HCO3- (base deficit)
  • Metabolic alkalosis triggers decreased ventilation, increasing CO2 -> increased H+, increased HCO3- (base excess)
  • In reality there is often no compensation
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8
Q

What clinical conditions might cause metabolic acidosis? Metabolic alkalosis?

A

Metabolic acidosis: DKA (due to lactic acid)
Metabolic alkalosis: vomiting (due to loss of acid)

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9
Q

Describe the factors that determine the airway resistance in the lung

A

Decreases with:
- Stimulation of B-adrenergic receptors causing bronchodilation

Increases with:
- Parasympathetic nerve stimulation causing bronchoconstriction
- Histamine
- Reduction in lung volume
- Decreased pCO2
- Increased density and viscosity of gas

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10
Q

With regard to lung compliance, give examples of diseases that reduce compliance

A

3 to pass:
- Pulmonary fibrosis
- Pulmonary oedema
- Pulmonary haemorrhage
- Atelectasis
- Loss of surfactants (e.g. respiratory distress syndrome)

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11
Q

What factors cause turbulent flow in airways?

A

Expressed by Reynold’s number:
- Reynold’s number = fluid density * x diameter * x velocity of flow * / viscosity *
- Laminar flow only occurs in small airways, transitional in most areas, turbulent in trachea (especially with rapid breathing)

*3/4 needed to pass

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12
Q

What factors affect the radius of the airway?

A
  • Bronchial smooth muscle (under control of sympathetic and parasympathetic activity)
  • Lung volume
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13
Q

Describe the symptoms of acute mountain sickness

A
  • Headache
  • Fatigue
  • Dizzy
  • Palpitations
  • Nausea
  • Loss of appetite
  • Insomnia
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14
Q

What is the alveolar gas equation?

A

Useful formula to measure the relationship between the fall in pO2 and the rise in pCO2 that occurs in hypoventilation (a useful measure of the V/Q inequality)

PAO2 = FiO2 x (Patmos - PH2O) - (PaCO2 / RQ) + F

Where:
- PAO2 is the alveolar oxygen partial pressure
- PiO2 is the partial pressure of inspired oxygen (fraction of inspired oxygen 21% multiplied by difference between atmospheric pressure 760mmHg and water vapour pressure 47mmHg in the alveolus, usually comes to ~149mmHg)
- PaCO2 is the arterial CO2 partial pressure
- RQ is the respiratory quotient (CO2 production:O2 consumption, typically 0.8)
- F is a small correction factor for inert gases (typically 2mmHg and can be ignored)

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15
Q

How do you calculate the alveolar-arterial gradient?

A

Difference between PAO2 (alveolar oxygen partial pressure) and PaO2 (arterial oxygen partial pressure)

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16
Q

What is the physiological significance of the A-a gradient?

A

V/Q mismatch (e.g. shunting or dead space)

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17
Q

What is the role of central chemoreceptors in control of ventilation?

A
  • Located near ventral surface of medulla
  • Rise in blood CO2 increases CO2 in CSF *
  • CSF has poor buffering capacity so pH changes rapidly
  • Liberated H+ ions stimulate chemoreceptors (increasing pH has reverse effect) *
  • Efferents stimulate medullary respiratory centre to increase ventilation and return CO2 to normal *
  • Chronic CO2 elevation gives normal CSF pH and insensitivity

*needed to pass

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18
Q

What is the role of peripheral chemoreceptors?

A

3/5 to pass:
- Located in carotid and aortic bodies that have high blood flow
- Respond mostly to decrease in O2 below 100mmHg
- Impulses transmitted to respiratory centre to increase ventilation
- Responsible for all of the ventilatory response to hypoxaemia
- Also responsible for small but rapid response to rise in CO2 and decrease in pH (carotid bodies)

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19
Q

What is the role of red blood cells in CO2 transport?

A

1/3 to pass:
1. Carbonic anhydrase:
- Only found significantly in red cells
- Role in major buffer for CO2 and H+
2. Haldane effect:
- Hb (particularly deoxy) is also a major H+ buffer allowing increased/faster H+/HCO3- dissociation
- Cl- shift is mediated by Band 3 Cl- transporter in RBC membrane, and allows 70% HCO3- diffusion into plasma, maintaining ionic neutrality
3. Hb protein:
- Major carbamino protein (better when deoxyHb as more negative charge)

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20
Q

What is the Haldane effect?

A
  • H+ + HbO2 <-> H+-Hb + O2
  • DeoxyHb binds more H+ than oxyHb and forms carbamino compounds more readily
  • Binding of O2 to Hb reduces its affinity for CO2
  • Enhances removal of CO2 * from O2-consuming tissues (e.g. muscles) into the blood
  • Promotes dissociation of CO2 from Hb in the presence of O2 * (e.g. the lungs) which is vital for alveolar gas exchange

*needed to pass

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21
Q

Draw and explain the carbon dioxide dissociation curve

A
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22
Q

What is pulmonary compliance?

A
  • Compliance = volume change / pressure change *
  • Maximal in mid-inspiration
  • Lower at extremes
  • Approximately 200ml/cm H2O

*needed to pass

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23
Q

What factors decrease or increase pulmonary compliance?

A

Decreased (3 examples):
- Alveolar oedema
- Pulmonary fibrosis
- Pulmonary venous hypertension
- Unventilated lung

Increased (1 example):
- Age
- Emphysema

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24
Q

What are the physiological effects of surfactant of the lung?

A

2/4 to pass:
- Increased lung compliance
- Reduced work of breathing
- Improved stability of alveoli
- Keeps alveoli dry

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25
Q

What are the main determinants of compliance of the thorax?

A
  • Surface tension of the alveoli (2/3)
  • Elastin/collagen fibres (1/3)
  • Alveolar surface tension depends on alveolar pressure, alveolar radius, surfactant (Law of Laplace: P = 2 x T/R)
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26
Q

How does compliance vary throughout the upright lung?

A

Higher at the base than the apex, because apex is already more distended (hence better ability to ventilate base compared with apex)

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27
Q

Draw the pressure-volume curve of a normal lung

A
  • Sigmoid curve of intrapleural pressure vs volume, does not reach 0% lung volume
  • Shows lung volume is higher during deflation than inflation for any given pressure (hysteresis)
  • Shows that lung contains residual air, without any expanding pressure (due to airway closure)
  • Shows that compliance decreases at higher lung volumes (lung becomes stiffer due to reaching limits of elasticity)
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28
Q

Which areas of the brain control respiration?

A

2 to pass:
- Medulla: medullary respiratory centre (in particular the Pre-Botzinger Complex) generates intrinsic rhythm
- Pons (apneustic centre and pneumotaxic centre): may modulate activity of medulla
- Cerebral cortex: voluntary control
- Limbic system and hypothalamus: change respiration in response to emotions

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29
Q

Explain the central response to rising carbon dioxide

A

pCO2 is tightly controlled and is the most important stimulus to ventilation *:
1. Main response is mediated by central chemoreceptors in medulla:
- CO2 diffuses freely across the BBB then liberates H+ in the CSF
- Central chemoreceptors stimulate respiration in response to increasing H+ in the CSF
2. Peripheral chemoreceptors (in carotid bodies and aortic bodies) also increase ventilation in response to rising pCO2:
- The response is smaller in magnitude but faster compared to central chemoreceptors

The response is magnified if pO2 is low, and is reduced by sleep, age, sedative drugs and chronic CO2 retention

*1 chemoreceptor response with explanation to be at standard

30
Q

Which other sensors are involved in control of respiration?

A

3 to pass:
- Pulmonary stretch receptors in airway smooth muscle
- Irritant receptors between airway epithelial cells (also in nose and upper airway)
- J receptors in alveolar walls
- Bronchial C receptors
- Joint and muscle receptors
- Gamma system in muscle spindles
- Arterial baroreceptors
- Pain and temperature afferents

31
Q

How does hypoventilation affect respiration?

A
  • BBB is permeable to CO2 and relatively impermeable to HCO3-
  • Increased blood pCO2 -> increased CSF pCO2 -> increased H+ in CSF -> stimulation of ventilation
  • Increased H+ in CSF stimulates ventilation
  • Decreased H+ in CSF inhibits ventilation, causing cerebral vasodilation -> enhanced diffusion of pCO2 into CSF
  • CSF pH 7.32: less buffering than blood, CSF pH changes more for given pCO2
  • Prolonged pH changes compensated by HCO3- transport across BBB (chronic CO2 retention has near-normal CSF H+)
32
Q

What is the anatomical dead space?

A
  • The anatomical dead space refers to the airway volume with ventilation and no blood flow *
  • The conducting airways (to division 16) take no part in gas exchange *
  • Volume = approx 150ml

*needed to pass

33
Q

How does anatomical dead space differ from physiological dead space?

A
  • Anatomical dead space is determined by morphology of the airways and lung
  • Physiological dead space is the volume of the airways and lung that does not eliminate CO2
  • The two dead spaces of volume are almost the same in normal subjects *, but the physiological dead space in increased in many lung diseases * due to inequality of blood flow and ventilation in the lung (V/Q mismatch)

*needed to pass

34
Q

How are the anatomical and physiological dead spaces measured?

A

Anatomic dead space:
- Fowler’s method

Physiological dead space:
- Bohr’s method calculates fraction of tidal volume by measurement of mixed expired CO2 and arterial CO2
- Vd = VT x (PaCO2 - PECO2) / PaCO2

35
Q

What are the effects of exercise on the respiratory system?

A
  1. Gas exchange:
    - Increased respiratory uptake and consumption of O2 (VO2) and production and excretion of CO2 (VCO2): increases by 10-20x
    - Increased lung diffusing capacity due to increased diffusing capacity of the membrane and the pulmonary blood volume
    - Decreased ventilation-perfusion inequality
  2. Ventilation:
    - Increased RR and MV
    - Increased TV
    - Decreased FRC
  3. Pulmonary blood flow:
    - Distension and recruitment of pulmonary vessels increases total cross-sectional area of the pulmonary vasculature
    - Increased total pulmonary blood volume
    - Increased CO and pulmonary blood flow
    - Increased pulmonary vascular pressures
    - Decreased pulmonary vascular resistance
  4. Other respiratory effects:
    - Increased respiratory exchange ratio (R) from 0.8 to 1.0 due to carbohydrate metabolism, and may exceed 1.0 due to anaerobic glycolysis
    - The Hb-O2 dissociation curve shifts to the right in the tissues and back to the left in the lungs
    - Additional capillaries open in peripheral tissues
36
Q

What changes occur in blood gases during exercise?

A
  • ABG are little affected by moderate exercise but at high workloads pH falls due to lactic acidosis, PaCO2 often falls to compensate for the acidosis and PaO2 rises
  • Arteriovenous pH, PaO2 and PaCO2 differences increase
37
Q

What are the factors which keep fluid out of the alveoli?

A

Starling’s Law (theoretical concept, exact values of pressures unknown; net pressure probably slightly outward):
1. Hydrostatic pressure (of column of blood):
- In the capillaries (positive thus outwards) = Pc
- In the interstitium (probably negative and thus also outwards) = Pi
2. Colloid osmotic pressure (of proteins in blood):
- In the capillaries (inwards) = πc
- In the interstitium (outwards) = πi

Lymphatic drainage

Alveolar epithelial cells

38
Q

Explain Fick’s law of diffusion

A
  • Gases diffuse across a surface by passive diffusion
  • Fick’s law says that the rate of diffusion is directly proportional to the area of the diffusion membrane, the pressure gradient across the membrane and the diffusion constant
  • It is inversely proportional to the thickness of the membrane
39
Q

What is the difference between a diffusion-limited and perfusion-limited gas?

A

Perfusion-limited gas:
- One where the partial pressure on both sides of the membrane equilibrates rapidly such that no further diffusion into the blood can occur from the alveoli unless the blood perfusion rate increases
- In the graph, there is no gap between the alveolar partial pressure of the gas at the time blood leaves the pulmonary capillary
- E.g. O2

Diffusion-limited gas:
- One where the partial pressure of the gas does not achieve equilibrium in the time that blood spends in the pulmonary capillaries
- In the graph, there is a gap between the partial pressure of the gas at the end of the pulmonary capillary perfusion time
- E.g. CO2

40
Q

What factors influence the rate of oxygen transfer from the alveolus into the pulmonary capillary?

A
  • Passive diffusion
  • Determined by Fick’s law of diffusion: Vgas ∝ D x (P1-P2) x A / T
  • Affected by surface area (A), membrane thickness (T), difference in partial pressures gas between alveolus (P1) and capillary (P2), and diffusion constant (D)
  • D ∝ gas solubility / √molecular weight gas
41
Q

How is diffusion capacity measured?

A
  • Carbon monoxide is used for measurement because its uptake is diffusion-limited (not dependent on amount of blood available, only diffusion properties of blood-gas barrier)
  • Single breath test method can also be used
42
Q

Give some clinical examples of when the rate of transfer of oxygen from the alveolus into the pulmonary capillary may be affected

A
  • Exercise
  • Alveolar hypoxia
  • Thickening of blood-gas barrier
43
Q

What are the causes of hypoxaemia in general?

A
  1. Hypoventilation:
    - E.g. drugs (morphine, barbiturates), chest wall damage, respiratory muscle paralysis
  2. Diffusion limitation:
    - Impaired diffusion process of oxygen across the pulmonary capillary (e.g. exercise, thickened blood-gas barrier state, low O2 mixture inhaled)
  3. Shunt:
    - Refers to blood entering the arterial system without going through ventilated areas of the lung
    - E.g. abnormal vascular connection (AV fistula, CCHD defect in R or L sides of heart)
  4. Ventilation-perfusion inequality:
    - Most common
    - V/Q ratio determines gas exchange for any respiratory unit
    - Regional variance exists
    - Hypoxaemia caused by V/Q mismatch cannot be eliminated with increased ventilation
    - E.g. pulmonary embolism
44
Q

Describe the different types of tissue hypoxia

A
  1. Hypoxaemia (hypoxic hypoxia): arterial PO2 reduced
  2. Anaemic hypoxia: arterial PO2 normal but Hb reduced
  3. Ischaemic/stagnant hypoxia: blood flow and O2 delivery decreased
  4. Histotoxic hypoxia: because of toxin, cells cannot utilise O2
45
Q

Describe the respiratory mechanisms leading to hypoxaemia and give examples

A

2 to pass:
1. Reduced ventilation (asthma)
2. V/Q mismatch (PE)
3. Shunt (CHD)
4. Diffusion limitation (APO, LVF, pulmonary fibrosis)

46
Q

Describe the clinical effects of acute hypoxia

A

2 to pass:
- Disorientation
- Confusion
- Headache
- Loss of consciousness
- Tachycardia
- HTN, hypotension
- AMI
- Arrest
- Diaphoresis
- Tachypnoea

47
Q

Draw a diagram that demonstrates the components of total lung volume

A

3/6 correctly labelled to pass:
- TLC, VC, FRC, TV, RV, ERV

48
Q

What are the typical lung volumes?

A

2/4 to pass:
- TLC: 7000ml
- VC: 4500-5000ml
- RV: 1200ml
- FRC: 2400ml
- TV: 500ml

49
Q

Which lung volumes can be measured in the ED? How are other lung volumes measured?

A

In ED (1/2 to pass):
- Spirometer for FEV1 and FVC
- TV on ventilator

Other volumes:
- Helium dilution or body plethysmography for TLC, FRC and RV

50
Q

Draw and describe the oxygen haemoglobin dossciation curve

A

Correct shape and labels with 2 points of saturation to pass

51
Q

What are the implications of the shape of the O2 dissociation curve?

A

UPPER:
- Flat upper part means if pO2 in alveolar gas falls (e.g. ARDS in acute pancreatitis), loading of O2 is little affected

LOWER:
- Steep lower part means peripheral tissue can draw large amount of O2 for only small drop in capillary pO2

52
Q

What factors shift the O2 dissociation curve?

A

3 factors to pass:
Right:
- Increased temperature, pCO2, H+ (decreased pH), 2,3-DPG

Left:
- Decreased temperature, pCO2, H+ (increased pH), 2,3-DPG

53
Q

How is oxygen carried in the blood?

A
  1. Dissolved *:
    - Amount dissolved proportional to partial pressure (Henry’s law)
    - 0.3ml O2 / 100ml blood at PO2 100mmHg
  2. Combined with Hb (majority) *:
    - 20.8ml O2 / 100ml blood (at Hb level of 15g/dL)
54
Q

In an alveolus, what factors affect oxygenation?

A
  • Ventilation *
  • Perfusion *
  • Diffusion across the blood-gas barrier *
  • Alveolar-pulmonary capillary pO2 gradient

*3 to pass

55
Q

Describe the oxygen uptake along a pulmonary capillary

A
  • Alveolar pulmonary capillary O2 gradient * (alveolar pO2 = 100mmHg, pulmonary capillary pO2 = 40mmHg)
  • Blood gas barrier thickness 0.3microns
  • RBC transit time = 0.75secs *
  • Under normal circumstances, O2 uptake is perfusion-limited (complete in 0.25secs) and alveolar end-capillary O2 difference is minimal *
  • Rate of rise of end-capillary pO2 is steep (see O2-Hb dissociation curve)

*3/4 needed to pass

56
Q

How does hypoxia affect oxygenation?

A

Alveolar pulmonary capillary O2 gradient is decreased *, O2 diffusion is decreased *, and rate of rise of pO2 for given O2 concentration in blood is less

*needed to pass

57
Q

How is lung compliance affected in emphysema?

A
  • Compliance is increased because of loss of lung elasticity * / destruction of lung connective tissue and elastin (easy to inflate but reduced capacity to recoil)
  • Patients have to force their expiration to expel air from lungs
  • Resultant increase in FRC
58
Q

Describe the normal distribution of pulmonary blood flow

A

Influenced by gravity with three main zones:
1. Zone 1 (apex): PA>Pa>Pv, least blood flow
2. Zone 2 (middle): Pa>PA>Pv
3. Zone 3 (base): Pa>Pv>PA, most blood flow

59
Q

How is the distribution of pulmonary blood flow actively controlled?

A

Hypoxic pulmonary vasoconstriction:
- Alveolar hypoxia constricts pulmonary arteries and directs blood away from poorly ventilated diseased lung areas
- Mechanism involves NO, endothelin 1, TXA2, low pH, and autonomic nervous system

60
Q

Explain how cardiogenic pulmonary oedema occurs

A

Due to Starling’s Law:
- Differences in capillary and interstitial hydrostatic and colloid osmotic pressures
- Significant increases in net outward pressure of Starling equation results in interstitial oedema especially at perivascular and peribronchial spaces
- Further increases of outward pressure results in fluid entering alveolar spaces

61
Q

What two mechanisms allow pulmonary vascular resistance to fall? What other influences are there on pulmonary vascular resistance?

A
  1. Recruitment of normally closed (non-perfused) pulmonary capillaries
  2. Distension at higher vascular pressures, from near-flat to circular cross-section capillaries

Other influences:
1. Lung volume:
- When low, pulmonary vascular resistance is increased due to smooth muscle and elastic tissue contraction
- When high, again rises due to capillary stretching and reduction in calibre
2. Hypoxia:
- Increases pulmonary vascular resistance from pulmonary vasoconstriction
3. Drugs:
- Increased by serotonin, histamine, NA (contracts vessel smooth muscle)
- Decreased by ACh and isoprenaline

62
Q

Describe the normal relationship between ventilation and perfusion in an upright lung

A

Pulmonary circulation is affected by gravity:
1. Apex:
- Less blood flow
- Larger alveoli
- Slightly less ventilation
- Ventilation > perfusion *
- High V/Q ratio *
2. Middle:
- Ventilation = perfusion
- V/Q = 1
3. Base:
- More blood flow
- Smaller alveoli
- More ventilation
- Perfusion > ventilation *
- Low V/Q ratio *

*needed to pass

63
Q

What conditions can increase V/Q mismatch?

A
  • PE * (high V/Q ratio)
  • Pulmonary oedema
  • Pneumonia
  • Emphysema (low V/Q ratio)

*needed to pass + 1

64
Q

Which tests can be done in clinical practice to demonstrate a V/Q mismatch?

A

A-a gradient (also V/Q scan, CTPA)

65
Q

Explain the reasons for the normal alveolar-arterial O2 difference

A

Due to physiological shunt and physiological V/Q mismatch
- A-a gradient = measure of the difference between alveolar and arterial concentration of O2
- Normally 5-10mmHg
- Even though alveolar pO2 at apex 40mmHg above base, most of blood flow (Q) comes from base where alveolar pO2 is low -> decrease in arterial pO2
- Shunt: bronchial blood and coronary blood
- Also non-linear shape of O2 dissociation curve means that addition of small amount of shunted blood with low O2 concentration greatly decreases pO2 of arterial blood and units with high pO2 have little effect on O2 concentration because curve is flat at high O2 concentration

66
Q

What does ventilation-perfusion ratio mean?

A

The concentration of oxygen (pO2) in any respiratory unit is determined by the ratio of the amount of air getting to the alveolus (ventilation) and blood flow through the pulmonary capillary
V/Q ratio is 0.8 (4.2L gas flow / 5.5L blood flow)

67
Q

What are the causes of hypoxaemia in a patient breathing room air?

A

3/4 to pass:
1. Hypoventilation
2. Diffusion limitation
3. Shunt
4. Ventilation/perfusion inequality

68
Q

What is the effect of ventilation-perfusion inequality on arterial pO2 and arterial pCO2?

A

Much greater influence on pO2 than CO2 *:
- O2 dissociation curve non-linear *: areas with high V/Q ratio add relatively little O2 with increased ventilation, whereas areas with low V/Q ratio have lower pO2 (close to mixed venous) - overall pO2 is reduced
- CO2 dissociation curve is linear in the working range *: chemoreceptor stimulation increases ventilation and CO2 output especially in lung areas with high V/Q ratios, minimal change to pCO2 (remains normal)

*needed to pass + concept

69
Q

What factors determine work of breathing?

A
  1. Elastic forces of lungs and chest wall
  2. Viscous resistance of the airways and tissues
70
Q

What variables affect elastic workload?

A

Larger tidal volumes increase elastic workload *

Elastic workload is increased by reduced compliance * due to:
- Lung volume: a person with only one lung has halved compliance
- Slightly lesser during inflation than during deflation
- Increased tissue mass (fibrosis, pulmonary congestion, chest wall restriction)
- Loss of surfactant

*needed to pass

71
Q

What variables affect viscous resistance?

A

2 to pass:
- Higher respiratory rates increasing flow rates
- Decreased airway radius due to lower lung volumes, bronchoconstriction
- Increased air density (e.g. scuba diving)
- Increased air viscosity