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FRCEM Primary > Physiology - Respiratory > Flashcards

Physiology - Respiratory Flashcards

1
Q

Definition of tidal volume

A

Normal inspiration and expiration. 0.5L

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2
Q

Definition of vital capacity

A

Full inspiration and full expiration 4.8L (IRV+Vt+ERV)

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3
Q

Definition of residual volume

A

Volume remaining after maximal expiration 1.2L

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4
Q

Definition of functional residual capacity

A

Volume remaining after normal expiration 2.4L (ERV+RV)

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5
Q

Definition of anatomical dead space

A

Airways to the terminal bronchioles

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6
Q

Definition of alveolar dead space

A

Alveoli incapable of gas exchange

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7
Q

Which cells carry out mucociliary clearance?

A

Ciliated columnar epithelial cells

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8
Q

How does mucus contribute to pathogen clearance?

A

Proteases break down trapped pathogens. Alpha 1 antitrypsin from alveoli inhibits proteases to protect lung tissue

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9
Q

Implication of increased mucus viscosity?

A

Traps pathogens but cannot be moved

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10
Q

Role of type 1 pneumocyte?

A

Gas exchange

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11
Q

Role of type 2 pneumocyte?

A

Produces surfactant

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12
Q

What is compliance?

A

The relationship between lung volume and pressure and is a combination of static and dynamic factors

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13
Q

Static compliance factors

A 
Distensibility changes with 
Age
Sex
Stiffness
Size
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14
Q

What is dynamic compliance?

A

The airway resistance which is the measure of pressure and volume in the oesophagus at the end of inspiration and expiration.

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15
Q

What is surfactant?

A

A tension reducing phospholipid mixture made by type 2 pneumocytes

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16
Q

What law describes lung compliance?

A

Laplace’s Law

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17
Q

Clinical consequences of reduced surfactant?

A

Neonates with no surfactant have increased pressure causing poor compliance leading to atelectasis and IRDS. Small alveoli collapse under the increased pressure.

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18
Q

Parasympathetic effect on airway smooth muscle

A

Constriction and increased mucus secretion using Ach signalling

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19
Q

Sympathetic effect on airway smooth muscle

A

Dilatation and decreased mucus using adrenaline B2 receptors.

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20
Q

Physiological basis on the clinical airway effects of asthma

A

Asthma features bronchoconstiction so it is treated with a B2 agonist to stimulate the sympathetic input and ipratropium which is an Ach antagonist to block the parasympathetic input

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21
Q

What does PEFR measure and what factors does it depend on?

A

Measures resistance. Depends on lung volume. Chart is based on sex, age and height

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22
Q

What does FEV1/FVC measure? What is normal and what is an obstructive and restrictive picture?

A

A composite measure of function. Normal is 0.8.

Obstructive is reduced, restrictive is the same.

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23
Q

What do the curves look like in obstructive and restrictive V over time graphs?

A

Obstructive reaches the same or slightly lower FVC at a slower, more steady rate. Reduced FEV1
Restrictive reaches a much lower FVC with a normal FEV1.

24
Q

What is partial pressure?

A

The contribution to barometric pressure exerted by a gas

25
Q

Partial pressure of oxygen and nitrogen in ambient room air

A

O - 159

N - 593

26
Q

What is Henry’s Law

A

The amount of dissolved gas in a liquid is proportional to its partial pressure above the liquid

27
Q

Oxygen partial pressures in
Inspired air
Alveolar air
Expired air

A

Inspired - 159
Alveolar - 104
Expired - 116

28
Q

Carbon dioxide partial pressures in
Inspired air
Alveolar air
Expired air

A

Inspired - 0.3
Alveolar - 40
Expired - 32

29
Q

In alveolar diffusion, what does gas flow depend on?

A

Surface area, permeability and partial pressure differences

30
Q

Limitations of gas transfer

A

CO2 diffuses and O2 perfuses. The barrier is more permeable to CO2>O2, but the diffusion gradient is better for O2>CO2

31
Q

What is the transfer factor and how does it change using CO as an example

A

Transfer factor is an indicator of the rate of gas transfer. It is affected by decreased ventilation and decreased surface area, but it increases with increased blood flow.

32
Q

How is oxygen transported in circulation?

A

Mostly bound to haemoglobin which is a co-operative binder. A small amount dissolves.

33
Q

What is the relation between blood oxygen content and PO2?

A

A curvilinear oxygen dissociation curve.
A small drop in alveolar PO2 hardly affects Hb.
Tissues get a lot of O2 for a small PO2 drop in the capillaries.

34
Q

What shifts the oxygen dissociation curve to the right (increased O2 dissociation)?

A
  • Increased temperature (working muscle)
  • Increased 2,3 DPG (Chronic hypoxia)
  • Drop in pH
  • Increase PCO2
35
Q

What shifts the oxygen dissociation curve to the left (decreased O2 dissociation)?

A
  • Rise in pH

- Decrease PCO2

36
Q

Effect of foetal Hb on the dissociation curve and why

A
  • Foetal Hb is left shifted - saturated with less pO2. It has a higher affinity for O2 to take from maternal Hb.
37
Q

Effect of anaemia on the dissociation curve

A

Downward shift - there is less O2 carrying capacity.

38
Q

How is CO2 transported in plasma?

A

60% bicarbonate
30% Hb
10% dissolved

39
Q

How is CO2 transported by Hb?

A

Binds the amine group making carbaminohaemoglobin

40
Q

CO2 - Carbonic acid - Bicarb equation

A

CO2 + H2O H2CO3 H+ + HCO3-

41
Q

What is the chloride shift?

A

In red blood cells carbonic anhydrase catalyses the hydration of CO2 to carbonic acid which then spontaneously dissociates to form Bicarbonate ions which are exported and exchanged for Cl-. Cl concentration is therefore lower in venous circulation than arterial. The reverse happens in pulmonary capillaries where PO2 is high and PCO2 is low. H+ concentration increases as CO2 is displaced and Cl- is exchanged out so bicarb can come in and be driven back to CO2 for expiration.

42
Q

How does Hb buffer?

A

The Haldane effect - in low O2 states (respiring tissue), Hb can bind more H+ and CO2. Oxygenation displaces the CO2

43
Q

Respiratory centre groups

A

Dorsal and ventral in the medulla and pontine in the pons

44
Q

Pontine respiratory centre control

A

2 areas - pneumotaxic centre and apneustic centre.
Pneumotaxic controls rate and pattern. It limits inspiration by limiting the burst of action potentials in the phrenic nerve which decreases tidal volume and respiratory rate.
Apneustic centre promotes inhalation by signalling to the dorsal group to delay the switch off of the inspiration. Controls the intensity of breathing. Inhibited by the pulmonary stretch receptors to prevent over inflation and pneumotaxic centre.

45
Q

Dorsal receptor group control

A

Initiates inspiration through input from the pontine respiratory group, the phrenic nerve, the glossopharyngeal nerve and integrates peripheral chemoreceptors, baroreceptors and stretch receptors. It modifies rate of respiration.

46
Q

Ventral respiratory group control

A

Acts on inspiration and expiration for forceful breathing.

47
Q

Voluntary control of breathing

A

Cortical structures in the brain act on respiratory muscles via pyramidal tracts.

48
Q

Explain how central chemoreceptors control respiration. Where are they and what is the influence of pH.

A

Central chemoreceptors are located in the medulla. CO2 becomes H+ + HCO3- in CSF and H+ is detected. High PCO2 causes cerebral vasodilation increasing diffusion of CO2 into CSF. High H+ (low pH) increases alveolar ventilation, low H+ (high pH) decreases ventilation.

49
Q

Where are peripheral chemoreceptors, what do they detect and what outcome do they have?

A

Arch of the aorta (Aortic bodies) and bifurcation of common carotid artery (Carotid bodies).
Detect pCO2, pO2 and H+. They stimulate glossopharyngeal nerve (IX) and vagus nerve (X) to act on medullary centre. Hypoxaemia increases ventilation.

50
Q

Where are stretch receptors, what innervates them and what do they do?

A

Vagally- innervated bronchial wall receptors. They inhibit inspiration to stop tidal volume becoming greater than inspiratory capacity. They inhibit cardiac vagal motor neurones causing a sinus arrhythmia. When exposed to noxious substances they cause bronchoconstriction and cough.

51
Q

Where are J receptors, what innervates them, what do they detect and what do they cause?

A

Juxtacapillary receptors are in alveolar walls next to capillaries. They are innervated by the vagus nerve. They detect capillary engorgement and interstitial fluid in alveolar walls. They cause you to feel SOB and increase the respiratory rate with odema, emboli or inflammation.

52
Q

V/Q ration in the apex

A

High

53
Q

V/Q ration in the base

A

Low

54
Q

What is an area with no ventilation called and what is the V/Q ratio? What happens physiologically.

A

A shunt. V/Q ratio is 0. Blood is redirected to an area of better ventilation because of hypoxic vasoconstriction. It has a low blood PO2 and PCO2

55
Q

What is an area of no perfusion called and what is the V/Q ratio?

A

Dead space. V/Q ratio is infinity.

56
Q

When does increasing inspired FiO2 not help?

A

When there is a shunt. In a R->L intracardiac shunt venous and arterial blood is mixed. Low ventilation areas of the lung have their perfusion limited so increasing FiO2 doesn’t help.

57
Q

What has the biggest effect on V/Q relationship

A

Altering gravity by changing patient position alters V/Q relationship most.

FRCEM Primary (32 decks)

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