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Primary FRCA > Physiology 12 > Flashcards

Physiology 12 Flashcards

1
Q

Outline the function of the peripheral chemoreceptors

A

Carotid bodies: respond to PaO2, PaCO2 and [H+]

Aortic bodies: respond to PaO2 and PaCO2. Less influential than carotid bodies

Peripheral chemoreceptors are the main receptors that stimulate ventilatory response to low PaO2

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2
Q

Outline the anatomy and structure of the carotid body

A

Cluster of chemoreceptor cells adjacent to carotid bifurcation

Consists of 2 types of glomus cells

  • Type 1 (chief cells) - Chemoreceptors rich in dopamine. Synapse with the sinus nerve (CN IX)
  • Type 2 (sheath cells) - Resemble glial cells, act as ‘supporting cells’
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3
Q

What is the blood flow to the carotid bodies?

How does this compare to cerebral blood flow?

Why is this important?

A

2000ml/min/100g

More than cerebral (50ml/min/100g)

This means that a-v O2 difference is very low and carotid bodies can derive all their O2 from dissolved O2 and respond primarily to changes in O2 tension rather than total O2 content

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4
Q

How does a carotid body chemoreceptor respond to changes in PaO2?

A

Type 1 glomus cells have a graded reduction in intracellular ATP in response to changes in PaO2, causing increased nerve activity. Response is most marked to PaO2 <7.89 kPa

Response is augmented by acidosis and hypercapnia.

Response is rapid, with a time constant of a few seconds

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5
Q

Outline the response of the carotid body to changes in PaCO2

A

Response is dependent on carbonic anhydrase and likely responds to both PaCO2 and [H+] through intracellular [H+]

Efferent nerve activity is much increased by raised intracellular [H+] in conjunction with hypoxia

Less than 20% of the response to CO2 is peripheral, but it is more rapid and may be the only response to short-lived PaCO2 changes.

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6
Q

How do the carotid bodies respond to hypotension?

A

SBP <60mmHg causes ‘stagnant hypoxia’ leading to increased ventilation

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7
Q

Outline the chemoreceptor function of the aortic bodies

A
  • Blood supply lower than carotid bodies therefore greater a-v difference and less sensitivity to changes in PaO2 and PaCO2.
  • Aortic bodies (unlike carotid bodies) respond to total O2 content and are thus sensitive to anaemia and CO poisoning etc
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8
Q

Outline the role of the pulmonary stretch receptors

A
  • Between SM cells in large airways
  • Are slowly-adapting receptors (SARs)
  • Respond to distension of lungs
  • Send afferents via CN X
  • Stimulation causes termination of inspiration via Hering-Breuer reflex
  • Strong stimulation causes activation of expiratory neurones
  • Thought to be relevant at normal TV in infants but possibly only at increased TVs for adults (?via Hering-Breuer)
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9
Q

Outline the role of the pulmonary irritant receptors

A
  • Rapidly adapting receptors (RARs)
  • Between epithelial cells of large airways
  • Respond to mechanical and chemical irritation
  • Have a role in coughing, sneezing and bronchoconstriction
  • Efferents travel via myelinated fibres in CN X
  • Also found in nose and upper airways; implicated in laryngospasm
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10
Q

Outline the role of the pulmonary juxtacapillary (J) receptors

A
  • Located in alveolar cell walls close to capillaries
  • Respond to chemical stimuli and oedema
  • Can cause reflex rapid, shallow breathing
  • Efferents travel via unmyelinated fibres in CN X
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11
Q

What is a normal ventilatory response to increasing PaCO2 at a normal PO2?

How does hypoxia change this?

A

15-20 L/min increase in MV per kPa rise in PaCO2

Hypoxia increases this response (via integrated peripheral/central chemoreceptor mechanism)

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12
Q

How does the ventilatory response to metabolic acidosis differ to respiratory acidosis?

A
  • Increased [H+] stimulates carotid chemoreceptors, increasing MV
  • Resulting fall in PaCO2 reduces central ventilatory drive and thus blunts ventilatory response to metabolic acidosis
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13
Q

How does hypocapnia affect ventilatory response to hypoxia?

A

Reduced response to hypoxia (threshold reduced to <5 kPa)

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14
Q

Outline what is known about the ventilatory response to exercise

A

Extreme exercise may increase MV to >120L/min. Cause of increase largely unknown.

PaCO2 does not increase and falls during extreme exercise
PaO2 increases
Some increase in [lactate] and [H+] but only heavy exercise

Possible mechanisms for increased MV:

  • Lactic acidosis
  • PaCO2 oscillations
  • Muscle afferents
  • Catecholamines
  • CO2 load
  • Enhanced PO2 response
  • Learned response
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15
Q

Define respiratory failure

A

Inability to maintain appropriate arterial gas tensions

T1RF / T2RF

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16
Q

Define ventilatory failure

A

Pathological reduction in alveolar ventilation below level required to maintain normal alveolar gas tensions

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17
Q

For a normal person at rest how much CO2 is produced per day?

A

288L

200mL/min

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18
Q

What are the possible causes of ventilatory failure?

A

Neurological / Muscular / Thoracic / Airway

Neurological:

  • Central (drugs, severe PCO2/PO2 derangement, lesions)
  • UMN (tumours, strokes, demyelination)
  • Anterior horn cells (polio)
  • LMN (GBS, MND, phrenic nerve injury)

Muscular:

  • NMJ (toxins, autoimmunity)
  • Respiratory muscles (inflammatory disease, dystrophies, atrophy, mechanical splinting)

Thoracic:

  • Altered elasticity (fibrosis, contusions, plaques, kyphoscoliosis, burns, external pressure)
  • Structural integrity (Trauma - flail chest, tension PTX)

Airway:

  • Obstructive lung disease
  • Upper airway obstruction (many causes)
  • Increased dead space (emphysema, PE)
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19
Q

What is the normal quantity of CO2 in the body?

What effect does this have in the context of increased VCO2?

A

Around 120L

This acts effectively as a buffer to increased CO2 production, thus levels change slowly in response to increased VCO2

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20
Q

What is the normal quantity of O2 in the body?

A

Around 1.5L

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21
Q

What is the rate of PaCO2 rise during apnoea?

A

0.4-0.8 kPa/min

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22
Q

In acute alveolar hypoventilation (on room air), which gas tension gives the best warning?

A

Reduction in PO2 can be a useful first sign, as PaCO2 may not have had time to rise

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23
Q

How is distribution of alveolar ventilation affected by rate of inspiration during IPPV?

A

Fast inspiration: Distributed to areas with short time constants

Slow inspiration: Distributed according to regional compliances

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24
Q

What are the different ways of controlling the length of the respiratory cycle during IPPV?

A

Time cycling
Volume cycling
Pressure cycling

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25
Q

What is the most common I:E ratio?

A

1:2

26
Q

What is the consensus view on acceptable minimum inspiratory time?

A

1 second

27
Q

Explain the concept of inverse I:E ratio

A

Increases mean lung volume and airway pressure, conferring similar benefits to PEEP.

Used in ARDS typically but requires NM blockade and sedation.

However, risk of barotrauma is increased and thus inverse I:E ratio is contraindicated in obstructive airway disease

28
Q

What is the preferred ratio for inverse I:E ventilation?

A

2:1 but can be higher

29
Q

Summarise the systemic effects of IPPV

A

Respiratory / CV / Renal / Other

Resp:

  • Reversed intrapleural pressure profile
  • Reduced FRC and lung compliance
  • Atelectasis

CV:

  • Increased intrathoracic pressure leading to ^PVR and reduced CO
  • Raised CVP, reduced drainage from head and neck
  • Reduced LV compliance ad filling

Renal:

  • Reduced renal arterial and reduced renal venous pressures
  • Reduced GFR and RAAS activation

Other:

  • Ileus with prolonged IPPV
  • RIsks associated with intubation
  • Barotrauma/volutrauma
  • Undetected disconnection
  • Raised ICP
30
Q

Summarise CNS oxygen toxicity

A

Seizures may occur at partial pressures of O2 exceeding 2atm and reliably at 3atm.

This is due to depression in GABA activity and production of free radicals

31
Q

Outline the pulmonary effects of oxygen toxicity

A

Directly related to PO2

100% O2:

For 12-24h - tracheobronchial irritation and discomfort. No permanent damage up to 48h

After 24-36h - Reduced compliance, VC and diffusion capacity. Increase in dead space and shunt. Reduced mucus clearance. Immune infiltration. Decrease in surfactant.

Up to 50% O2 thought to be safe for any period

Incidence of fibrosis increased with bleomycin

32
Q

Summarise the changes in respiratory epithelial cell morphology along the respiratory tree

A

Pseudostratified ciliated columnar cells: Nose, pharynx and trachea. Closely packed.

Ciliated columnar cells: Bronchi (>1mm diameter)

Cuboidal epithelial cells: Bronchioles (0.3-1mm diameter). Flatten gradually to merge with alveolar epithelial cells

33
Q

How does temperature and humidification vary through the respiratory cycle?

A

Inspiration: Airway epithelium cools as evaporation and humidification occurs

Expiration: Water condenses on airway epithelium and warming occurs

34
Q

What features of the upper airways increase efficiency of air warming and humidification (W+H)?

A

Nose breathing increases distance over which W+H can take place.

Nasal turbinates increase surface area and induce turbulent flow, bringing air into closer contact with respiratory epithelium

35
Q

How does air warming and humidification throughout the respiratory tree vary during rest/exercise?

A

At rest, inspiratory air is fully humidified and at body temp in the trachea

During exercise, mouth breathing and increased RR mean that heat and moisture exchange are not complete until air reaches the bronchioles

36
Q

Summarise the important features and functions of airway lining fluid

A

Present throughout the respiratory tract, produced by epithelial and goblet cells

Larger airways completely lined, smaller airways have mucus ‘islands’. Distal to small bronchioles there is no mucus layer.

Two layers:

  • Mucus/gel layer, secreted by goblet cells in response to irritation/infection. Contains viscoelastic proteins (mucins) which trap particles. Retains large amounts of water.
  • Periciliary/sol layer, secreted by ciliated epithelial cells by active secretion of Na+ and Cl- followed by water through osmosis. Little protein content.
37
Q

Why is control of the periciliary layer of airway fluid important? How is this achieved?

A

Correct depth ensures cilia can beat efficiently

Achieved through:

  • Active control of ion channels on apical surface of epithelium
  • Passive movement of water between mucus and periciliary layers
38
Q

How effective is the mucus layer in ensuring correct depth of periciliary layer during dehydration?

A

Mucus layer can continue to donate fluid to the periciliary layer, maintaining correct depth up until depth of mucus layer is reduced by 70%

39
Q

How many litres of air does an average person breathe per day?

A

10,000 L

40
Q

Describe the function of the airway cilia (or mucociliary escalator)

A

Cilia ensure continuous movement of airway lining fluid cephalad.

Each cilium beats 12-14 times per second

Each beat has two phases:

  1. Recovery Stroke (75% of time) - slow movement away from resting position (sideways) with tip through periciliary layer to prepare for next phase.
  2. Effective stroke (25% of time) - Tip grips underside of mucus layer and propels along before pulling out to resting position

Cilia co-ordinate strokes to produce waves of activity, likely through physical stimulation of adjacent cilia during recovery stroke.

41
Q

What is the tracheal mucus velocity generated by ciliary activity?

A

4 mm/min on avg.

42
Q

What factors govern deposition of inhaled particles in the respiratory tract?

A
  • Particle size

- Breathing pattern during inhalation

43
Q

Explain the mechanisms of deposition of inhaled particles

A

Three mechanisms:

  1. Inertial impaction - momentum of particle causes it to impact wall of airway.
    - Large particles (>10um) deposited in larger airways, smaller (3-10um) in smaller airways
    - Affected by particle velocity, thus faster inspiratory flow rates -> more distal deposition
  2. Sedimentation - Slow gas velocity allows small (1-3um) particles to fall out of suspension
    - Occurs in smaller airways and alveoli
    - These particles may be deposited or exhaled. Deposition is favoured by breathholding following inhalation
  3. Diffusion - caused by Brownian motion of particles <1um in diameter
    - Should be inhaled and exhaled with minimal deposition
44
Q

What is the importance of PM10?

A

PM10 refers to particulate matter of <10um diameter.

This includes diesel fumes. These particles are a major cause of airway disease in the urban population

45
Q

What is the importance of PM2.5?

A

Fine particulate air pollution of <2.5um diameter penetrates into alveoli and can cause inflammatory changes both in the lung and systemically

46
Q

What are the particle sizes produced by a MDI? Why is this important?

A

1-35 um

This large range accounts for some side effects caused by deposition phenomena. Eg. large particles deposited in pharynx, smallest absorbed across alveoli into systemic circulation

47
Q

What is the effect of microgravity on effect of inhaled particles?

A

Lack of weight makes inertial impaction and sedimentation less effective, thus large particles may reach the alveoli and may have consequences in the long term

48
Q

How are particles deposited in the alveoli removed?

A

Alveolar macrophages

Variable persistence and stimulatory potential of particulate matter within alveolar macrohages

49
Q

What mechanisms exist to deal with pathogens that are not expectorated following deposition?

A

Chemical inactivation / Protease-Antiprotease / Humoral immunity

Chemical inactivation:

  • Lysozyme destroys G+ve bacterial cell walls
  • β defensins induce bacterial cell wall damage and act as chemokines
  • Surfactant protein A acts as a chemokine in response to bacteria

Protease/antiprotease system:

  • Elastase and metalloproteinases released in response to pathogens/irritants and act as antimicrobials
  • Also damage lung tissue and thus mostly confined to mucus layer. Inactivated by anti-protease enzymes (eg. α1-antitrypsin) in lung tissue

Humoral immunity:

  • IgA seen in upper airway and larger airways, reduces epithelial binding of pathogens
  • IgG in smaller, distal airways
50
Q

What are the additional functions of the pulmonary circulation aside from those relating to gas exchange? Explain

A

Filtration / Metabolism

Filtration:
-Prevents particulate matter or air in venous circulation passing to systemic circulation

Metabolism:

  • Large surface area of blood/endothelial interface (126 m^2) due to capillary network and invaginations/projections of endothelium
  • Despite metabolic activity, endothelial cells are mitochondria- and SER-poor.
51
Q

Which important molecules are activated by the pulmonary capillary endothelium?

A
  • Peptide: Angiotensin I
  • Arachidonic acid
  • Steroid: Cortisone
52
Q

Which important molecules are inactivated by the pulmonary capillary endothelium?

A
  • Amines: 5-HT, noradrenaline
  • Peptides: Bradykinin, endothelins
  • Eicosanoids: PGD2, PGE2, PGF2α, Leukotrienes
  • Purine derivatives: Adenosine, ATP, ADP, AMP
  • Steroids: Progesterone, beclometasone
  • Basic drugs: Fentanyl, Lidocaine, Propranolol
53
Q

Where are the metabolically active enzymes on pulmonary endothelial cells found?

A

Membrane-bound / Cytoplasmic

Membrane-bound:

  • ACE
  • deactivators of bradykinin and adenosine compounds

Cytoplasmic:
-metabolism of eicosanoids, prostaglandins, 5-HT and other amines

54
Q

Outline the metabolism of amines/catecholamines in the pulmonary circulation

A

MAO and COMT abundant in endothelial cytoplasm

Specifically remove 33% of noradrenaline and 98% of 5-HT due to selective uptake on apical membrane.

Adrenaline, dopamine and histamine are unaffected

55
Q

Outline the role of the pulmonary circulation in drug metabolism

A

Basic (with pKa >8) and lipohilic drugs are bound by pulmonary circulation - acts as first pass filter for IV administration.

These bound drugs may then be released slowly or quickly if displaced by another compound. Plasma levels may rise rapidly if binding capacity becomes saturated.

Acidic drugs preferentially bind to plasma proteins

56
Q

Outline the role of ACE in the lung

How do ACEIs work?

A

-Zinc-containing carboxypeptidase with two active sites within grooves which bind substrate allowing zinc moiety to cleave.

  • Coverts AT1 to AT2 (cleaving phenylalanine-histidine bond)
  • Also cleaves and inactivates bradykinin (phenylalanine-arginine bond)

ACEIs cover binding site in grooves of ACE molecule

57
Q

Outline the role of the lung in metabolism of eicosanoids

A
  • Major site of eicosanoid synthesis, metabolism, uptake and release.
  • Synthesised in endothelium, smooth muscle, mast cells, epithelial and vascular muscle cells
  • Activation of PLA2 occurs through variety of noxious/immune stimuli
  • COX1 constitutively expressed at low levels
  • COX2 induced by inflammation
  • Role of isoforms in lung unclear - in some patients with asthma, COX1 inhibition causes bronchospasm but COX2 inhibition does not
58
Q

Summarise the effects of eicosanoids in the lung

A

Bronchoconstrictors:
-PGD2/F2α/G2/H2 + thromboxane

Bronchodilators:
-PGE1/2

Pulm vasodilators:
-PGE1 + PGI2

Pulm vasoconstrictors:
-PGF2α + PGH2

59
Q

Which eicosanoids are NOT metabolised by the lungs?

A

PGA2 and PGI2

60
Q

How are the airways involved in drug metabolism?

A

Airway tissue contains mixed function oxidase and CyP450 enzymes which can metabolise drugs eg. inhaled steroids

61
Q

Does the lung have an endocrine function?

A

Not formally

Some (usually pathological) molecules exert a systemic effect eg. histamine, eicosanoids, endothelin.

NO is rapidly taken up by Hb and thus unlikely to exert a notable distant effect

Primary FRCA (34 decks)

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