Ventilation Flashcards by Mady Pitcathley

What are the primary functions of the respiratory system?

To obtain O₂ from external environment for metabolism in body cells.
To eliminate CO₂ from cells and remove to the external environment.

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What are the 3 phases of respiration?

External
- Ventilation (breathing)
Internal
- Pulmonary gas exchange
- Gas transport
- Systemic gas exchange
Cellular
- Metabolism

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Describe phase 1 of respiration (external).

Ventilation (breathing)
- Air is moved into / out of the lungs to facilitate gas exchange between the atmosphere and alveoli (air sacs) in lungs.
  - Rate is regulated according to necessity to remove waste CO₂ and metabolic demand for O₂.

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Describe phase 2 of respiration (internal).

Pulmonary gas exchange
- Diffusion of O₂ / CO₂ between alveoli and blood, via pulmonary capillaries.
Gas transport
- O₂ / CO₂ transported in blood between lungs and tissues.
  - Facilitated by the circulatory system.
Systemic gas exchange
- Diffusion of O₂ / CO₂ between blood and tissues via systemic (tissue) capillaries.
  - Facilitated by the circulatory system

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Describe phase 3 of respiration (cellular).

Cellular metabolism
- Intracellular metabolic processes carried out in mitochondria.
  - O₂ and nutrients are converted to ATP, H₂O and CO₂.

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Label all the components of the respiratory system.

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Describe the structure of the lung.

2 lungs, each supplied by one bronchus.
Lungs divided into lobes.
Lung tissue comprises highly branched airways, alveoli, pulmonary vessels and elastic connective tissue.

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Describe the conducting and non-conducting zones of the respiratory tree.

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Describe the structure of alveoli?

Sites of gas exchange between air and blood.
150-300 million per lung.
250-300µm diameter.
Thin-walled (single cell thickness) - huge surface area.
Surrounded by pulmonary capillaries, separated by a very small gap (0.2-0.5µm).
Thickness very small, surface area very large (50-100m²) so excellent diffusion.
Walls not muscular - inflation / deflation occurs by altering thoracic capacity.

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Describe the structure of alveolar membranes.

Composed of:

Type 1 cells
- Simple, flat epithelial cells where gas exchange occurs.
Type 2 cells
- Septal cells
- Specialised surfactant secreting cells
- Free surface has microvilli
Alveolar dust cells
- Wandering macrophages removing debris - defence
Pores of Kohn
- Permit collateral airflow between alveoli
- Number varies - more in well ventilated areas (not well understood)

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Describe alveolar gas exchange using Fick’s Law.

Q (net rate of diffusion is dependent on Fick’s Law.
Where:
- ΔC = concentration gradient
- A - surface area of membrane
- ΔX = thickness of membrane
- D = diffusion coefficient, where D = P/√MW
- P = permeability of membrane
- MW = molecular weight of diffusing substance
All of these are constant, except concentration gradient.

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Describe lung compliance.

Compliance = ease with which the lungs are stretched.
- A lung with ‘normal’ compliance can be stretched easily with a small transmural pressure gradient.
- Poorly compliant lung = ‘stiff lung’ - not very stretchy.
  - Emphysema - destruction of elastic tissue.

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What factors do elastic recoil and compliance depend upon?

Alveolar surface tension created by the thin film of liquid lining each alveolus.
Surface tension pulls alveolus inwards because water molecules are involved in H- bonding strongly attracted to each other.
Mesh of elastin fibres (connective tissue) also has a role in recoil and compliance.

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Describe alveolar surface tension and how it is controlled.

Surface tension induced by H-bonding and strongly elastic fibres is very strong.
Unchecked, these forces would collapse alveoli completely, making inspiration very difficult.
- Think of a balloon - you stretch it before you blow it up. The work of the alveoli would be too much to start from completely deflated and unstretched every time.
Surface tension is decreased by pulmonary surfactant.
- (Secreted by type 2 alveolar cells)
- So, decreased work is required to inflate the lungs.
  - Decreased tendency to recoil.
  - Prevents collapse.

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Describe LaPlace’s Law.

Where

P = inward directed collapsing pressure.
T = surface tension.
r = radius of alveoli.
I.e. The smaller the alveolus, the smaller the radius, the greater the tendency to collapse.

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What would happen if two alveoli of unequal size were connected by an airway?

REMEMBER P = {2T / r}
Left ‘unchecked’ the smaller one will tend to collapse and the air will be expelled into the larger one.
This doesn’t happen in health. Why?

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What are the components which overcome collapse forces?

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Surfactant - reduces surface tension more in smaller alveoli.
Surrounding alveoli - if one alveolus starts to collapse, the surrounding alveoli, joined by connective tissue, resist the collapse due to their own elasticity.
This is interdependence.

Describe the role of surfactant in the new-born.

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Prematue babies (under 7 months) are not able to produce surfactant so cannot overcome alveolar surface tension.
Lings tend to collapse after exhalation.
Lots of effort is required to inflate the lungs - they are not compliant and baby has underdeveloped muscles.
May die due to exhaustion / lack of O₂.
It is thought that surfactant production has a role in triggering labour.

Which three pressures are critical in ventilation?

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Atmospheric pressure - the pressure exerted by the weight of the gas in the atmosphere on objects on the earth surface - 760mmHg at sea level.
Intra-alveolar pressure - the pressure within the alveoli - 760mmHg when equilibrated with atmospheric pressure.
Intrapleural pressure - the pressure within the pleural sac; the pressure exerted outside the lungs within the thoracic cavity, usually less than atmospheric pressure at 756mmHg.

What is the transmural pressure gradient across the lung wall?

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Transmural pressure gradient across the lung wall = intra-alveolar pressure minus intrapleural pressure.

What is the transmural pressure gradient across the thoracic wall?

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Transmural pressure gradient across the thoracic wall = atmospheric pressure minus intrapleural pressure.

What are the major muscles of inspiration?

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Major muscles of inspiration contract every inspiration; relaxation of these muscles causes passive expiration.
Diaphragm
External intercostals

What are the accessory muscles of inspiration?

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Accessory muscles of inspiration contract only during forceful inspiration.
Sternocleidomastoid
Scalenus

What are the muscles of active expiration?

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Muscles of active expiration contract only during forced expiration.
Internal intercostals.
Abdominal muscles.

Describe the action of the muscles of inspiration.

* Contraction of external intercostal muscles causes elevation of the ribs, which increases the lateral dimension of the thoracic cavity. * Elevation of the ribs causes the sternum to move upward and outward, which increases anterior-posterior dimension of the thoracic cavity. * Lowering of the diaphragm on contraction increases vertical dimension of the thoracic cavity.

Describe Boyle's Law.

* At constant temperature the volume (V) of a given mass of gas is inversely proportional to the pressure (P). * **The higher the pressure, the smaller the volume.**

Describe inspiration.

* Inspiration is an **active** process brought about by **contraction of inspiratory muscles.** * The chest wall and lungs are stretched. * The increase in the size of the lungs make the intra-alveolar pressure to fall. * This is because air molecules become contained in a larger volume (Boyle's Law). * The air then enters the lungs down its pressure gradient until the intra-alveolar pressure becomes equal to the atmospheric pressure.

Describe expiration.

* Normal expiration is a passive process brought about by relaxation of inspiratory muscles. * The chest wall and stretched lungs recoil to their preinspiratory size because of their elastic properties. * The recoil makes the intra-alveolar pressure rise. * This is because air molecules become contained in a smaller volume (Boyle's Law). * Air leaves the lungs down the pressure gradient until intra-alveolar pressure equals atmospheric pressure.

Describe the changes in intra-alveolar and intra-pleural pressures during the respiratory cycle.

What is a pneumothorax?

Air in the plural space.

What is the effect of a pneumothorax on the transmural pressure gradient?

Pneumothorax abolishes the transmural pressure gradient. $

Describe a spirogram produced by a 'normal' healthy individual and list the expected volumes.

* TV = tidal volume (500ml) * IRV = inspiratory reserve volume (3,000ml) * IC = inspiratory capacity (3,500ml) * ERV = expiratory reserve volume (1,000ml) * RV = residual volume (1,200ml) * FRC = functional residual capacity (2,200ml) * VC = vital capacity (4,500ml) * TLC = total lung capacity (5,700ml)

Describe the spirogram produced by a patient with obstructive lung disease.

* Normal total lung capacity. * High functional residual capacity. * High residual volume.

Describe the spirogram produced by a patient with restrictive lung disease.

* Low vital capacity. * Low total lung capacity. * In restricetive lung disease the lungs have a reduced volume.

What is dead space?

* There are 2 kinds - anatomical and physiological. In disease states physiological dead space increases greatly. It is a measure of the amount of lung tissue which is not actively involved in gas exchange. * Not all inspired gas gets to the site of gas exchange (alveoli). Part remains in the conducting airways (e.g. the trachea) where there is no gas exchange. * This is called the anatomical dead space (AKA airway dead space). * Average healthy young adult - the volume of the conducting airways is approximately 150ml. * For every 500ml we breathe in, only 350ml reaches the site of gas exchange. * In 'normal' breathing, the breaths we take dilute the old air in the lungs with fresh air.

Describe the state of dead space after inspiration, before expiration.

Describe the state of dead space during expiration.

Describe the state of dead space during inspiration.

What is physiological dead space?

* The volume of the lungs which do not eliminate CO₂. * In healthy individuals the volume of anatomical dead space will be very nearly the same as the physiological dead space. * The volume of physiological dead space is likely to be much higher in subjects with lung disease.

How do you calculate the pulmonary (minute) ventilation?

* Air breathed in / out in 1 minute. * Pulmonary ventilation (PV) = air breathed in / out in 1 minute. * PV = Tidal volume (TV) x Respiratory rate (RF)

How do you calculate alveolar ventilation (AV)?

* Alveolar ventilation (AV) is the volume of air exchanged between atmosphere and alveoli per minute. * AV = (TV - Dead Space (DS)) x RF

How is air and blood flow to individual alveoli controlled?

* Both air flow (ventilation) and blood flow (perfusion) can be controlled. * Individual airways supplying individual alveoli can be adjusted in response to change in local conditions, allowing efficient exchange of CO₂ and O₂. * For most efficient ventilation; ventilation and perfusion are matched.

Ventilation Flashcards

(42 cards)