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BMS242 - CVS and Respiration > Respiration > Flashcards

Respiration Flashcards

1
Q

Define compliance

A

A measure of the lungs ability to stretch and expand

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2
Q

How does the value of airway resistance differ in healthy subjects compared with those with COPD?

A

Normal - 0.5 - 2.0

COPD - 5.0 (small airways = 70%)

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3
Q

Define airway resistance

A

The opposition of flow caused by forces of friction

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4
Q

Define laminar flow

A

Particles passing any point have the same speed and direction

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5
Q

Which airways have laminar flow

A

Trachea and bronchi

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6
Q

Define turbulent flow

A

The average velocity passes a critical value causing vortices to develop, increasing the resistance to flow

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7
Q

Which airways have turbulent flow

A

Bronchioles

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8
Q

What does a Reynolds number of less than 1000 indicate

A

Laminar flow

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9
Q

What does a Reynolds number of more than 1500 indicate

A

Turbulent flow

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10
Q

What is Reynolds equation?

A

Re=2dvp/n (d = diameter, v = velocity, p = density of gas, n = viscosity)

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11
Q

What are the factors that effect airway resistance?

A

Nervous factors, chemical factors, humoral factors and mechanical factors

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12
Q

How do nervous factors effect airway resistance?

A

Contribute to bronchial tone. In the parasympathetic NS the vagus nerve releases ACh which binds to M3 receptors. In the sympathetic NS NE is a weak agonist to B2 adrenergic receptors that leads to dilation and decreased glandular secretions via cAMP.

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13
Q

Which drug blocks the bronchoconstriction caused by the binding of ACh to M3 receptors?

A

Atropine

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14
Q

What are the chemical factors that effect airway resistance?

A

Endogenous (histamine, adrenaline, leukatrines, PACO2) and exogenous (B2 agonists and muscarinics)

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15
Q

What are the humoral factors that effect airway resistance?

A

Epinephrine - released from the medulla and more potent than NE
Leukotrienes LTC4 and LTD4 are more potent than epinephrine

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16
Q

How do Ptm, Ptp, Pip and Pa change during inspiration?

A

All values of Ptm increase but these begin to decrease down the airways, Pa decreases and also decreases down the airways, Pip decreases

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17
Q

How do Ptm, Ptp, Pip and Pa change during expiration?

A

Ptm decreases but these values increase down the airways. Pa increases and increases down the airways. Pip increases.

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18
Q

Describe what happens to the airways in Emphysema

A

There is a loss of elastic tissue and the alveolar walls break down, the tethering between adjoining air spaces is reduced. This leads to the airways becoming flimsy therefore they are less likely to resist collapse during expiration and the compression of the airways becomes exaggerated.

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19
Q

How do patients overcome Emphysema?

A

Slow exhalation and exhaling through pursed lips

20
Q

Define ventilation

A

The volume of air moved out of the lung per unit time

21
Q

What is the anatomical dead space?

A

The first portion of air that enters the respiratory zone and is referred to as stale air. It is approx. 0.15 litres

22
Q

Which area of the lungs is ventilation at its highest?

A

The base

23
Q

Describe the process of capillary recruitment

A
  1. Some capillaries are open and conduct blood, however some are open and not conducting or collapsed and not conducting
  2. Perfusion pressure increases. During recruitment, the previously collapsed capillaries are now open but still not conducting. The previously open but not conducting airways now conduct blood. Distension widens vessels that were already open and conducting blood.
  3. Perfusion pressure further increases. Later in recruitment previously collapsed vessels conduct blood. All vessels dilate and hence resistance falls.
24
Q

What are extra-alveolar blood vessels?

A

Blood vessels that don’t surround alveolar air spaces

25
Q

When is pulmonary resistance at its lowest?

A

When lungs are at functional residual capacity

26
Q

Where is the reference point for pulmonary ventilation circulation pressures?

A

Outside the heart at the level of the left atrium

27
Q

How do Ppa and Ppv change above and below the atrium?

A

They fall by about 1cm H20 for every 1cm above the left atrium and increase by 1cm H20 for every 1cm below the left atrium

28
Q

What happens to the ventilation/perfusion ratio when the alveoli aren’t ventilated?

A

It becomes 0, therefore the gas composition will become that of venous blood (40mmHg O2 and 46mmHg CO2)

29
Q

What happens to the ventilation/perfusion ratio when the alveoli aren’t perfused?

A

It tends to infinity. The gas composition becomes the same as that of inspired, humidified air (149 mmHg O2 and 0 mmHg CO2)

30
Q

What are the values of the V/Q ratio at the apex, base and overall?

A

Apex - 3.3
Base - 0.6
Overall -0.84

31
Q

What is the ventilation/perfusion mismatch?

A

Alveolar dead space ventilation - local reduction in perfusion (e.g. from pulmonary embolism). V/Q becomes infinite. This is compensated by blood being redirected, bronchioles are constricted and a reduction in surfactant production.
Shunt - local reduction in ventilation (e.g. from tumour or foreign body). Composition becomes same as mixed venous blood as gas can’t be removed from an area.

32
Q

How do Gs, Gq and Gi coupled receptors control airway smooth muscle?

A

Gq leads to bronchoconstriction through M3, H1 and Bk receptors.
Gs leads to airway relaxation througb B2 and VIP receptors. Activated Bk leads to hyperpolarisation and inactivation of Ca2+ channels.
Gi inhibits adenylate cyclase and counteracts the stimulatory effect of the Gs pathway. It inhibits the Bk pathway and is stimulated through M2 receptors.

33
Q

How is the parasympathetic NS responsible for the control of bronchial smooth muscle?

A

ACh from the vagus nerve acts on muscarinic receptors that lead to constriction. Muscle contraction controlled by stimulation of M3 receptors. Negative feedback of M2 on post-ganglionic nerve.

34
Q

Describe how M3 receptors lead to muscle contraction

A

ACh binds to M3 in the membrane. This stimulates the G protein which causes the dissociation of Gq-alpha from the beta and gamma subunits.
Gq-alpha activates PLC which activates IP3.
PLC also activates DAG which can activate PKC or lead to calcium influx.
IP3 leads to calcium release from stores and calcium binds to CaM.
Activated CaM phosphorylates MLCK which leads to cross bridge formation.

35
Q

What are some ways in which muscle contraction can be stopped?

A

PKA decreases MLCK activity
Activation of K+ channels decreases Ca2+ influx
MLCP dephosphorylates MLC which leads to muscle relaxation

36
Q

Asthma is associated with increased activity of which branch of the nervous system?

A

The parasympathetic nervous system

37
Q

Which muscarinic receptors are affected in asthma?

A

M2

38
Q

Describe the mechanism of asthma

A

Activated eosinophils release major basic protein
MBP inhibits M2 receptors
Too much ACh is released and leads to airway constriction
Asthma activates the Gs pathway (???)

39
Q

How is asthma treated?

A

B2 adrenergic agonists (salbutamol and salmeterol)
Anti-cholinergics (tiotropium - acts via m1 and m3 receptors and blocks the effects of endogenous ACh)
Glucocorticoids (beclometasone - anti-inflammatory effect)

40
Q

What is the control centre for respiration?

A

The medulla - ventral and dorsal

41
Q

What are the ventral and dorsal areas of the medullary respiratory centre responsible for?

A

Ventral - forced inspiration and expiration

Dorsal - quiet inspiration but no link to expiration

42
Q

What is the Pre-Botzinger Complex?

A

A neural network in the brainstem that is responsible for generating and modulating respiratory rhythm

43
Q

What matches the Pre-Botzinger complex output?

A

The hypoglossal nerve

44
Q

What are the different pattern outputs from the Pre-Botzinger complex?

A

Eupneic (normal/fast and low), sigh (slow and large amplitude rhythm) and gasp (faster rise, shorter bursts and lower frequency)

45
Q

How do these different patterns occur?

A

By pacemaker and non-pacemaker neurons. Pacemaker cells demonstrate the the spiking and bursting activity. Sodium leak currents give the gradual depolarisation. Persistent Na channel eventually becomes inactivated.

46
Q

Discuss the importance of the NALCN

A

It contributes to the depolarisation phase. Mutants can’t maintain a normal pattern and have an increased aponeas. There is also a loss of slow depolarisation and they are kept hyperpolarised.

BMS242 - CVS and Respiration (5 decks)

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