Lecture 32: Gases And Respiration 2 Flashcards Preview

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Flashcards in Lecture 32: Gases And Respiration 2 Deck (18):

What are the 4 primary pressures associated with ventilation?

Atmospheric pressure
Alveolar pressure
Intrapleural pressure
The above two are known together as transpulmonary pressure


Atmospheric pressure

Pressure of the outside air
-assumed constant at 760mm Hg


Intra-alveolar pressure (Palv)

Palv represents the pressure of air within the alveoli
-varies with phases of respiration during bulk air flow
-at rest Palv = Patm = 760 mm Hg
-as Patm doesn't changed Palv must increase/ decrease for air flow to occur
-pressure inside alveoli changes during breathing due to:
1. Changes in the lung volume
2. Airflow into or out of the lungs
As atmospheric pressure is quite constant, alveolar pressure determines air flow into and out of lungs


Intra-pleural pressure (Pip)
Also why is Pip always less than Pav?

Pip represents pressure inside the pleural space
-varies with phases of respiration
Pip= 756 mmHg (-4 mmHg) at rest
-Pip is always negative relative to Patm
-always less than Palv due to opposing forces of chest wall and lungs

-lungs and chest wall are both elastic
-at rest, chest was is comressed and wants to recoil outwards
-in contrast, lungs are semi-inflated and want to recoil inward eg inflated balloon


Pulmonary pressure
Why don't the opposing forces if the lungs and chest wall cause separation of the pleurae?

Surface tension, resulting from the pleural fluid, prevents the parietal and visceral pleura from pulling apart


4. Transpulmonary pressure (Ptp)

Ptp is the difference between Palv and Pip
Palv- Pip 760- 756 = +4mmHg
-represents the pull that keeps the lungs distended
-an increase in Ptp creates a larger dis tending force across the lungs and the lungs expanded
-always positive under normal conditions


What happens if Tip is zero (ie Palv = Pip)?

Lung will collapse due to inherent elastic recoil
Means air flow into your intrapleural space until it is equal with the atm pressure


Describe the changes in pressure gradients, volume changes and muscle movements cause airflow?

Muscle changes volume of thorax --> change in thoracic pressure --> change in lung volume --> change in alveoli pressure --> airflow


List the muscles if pulmonary ventilation and name their action

External intercostal muscles: pulls the ribs up and out when they contract, increasing the size of the thoracic cavity
Diaphragm: pulls down when it contracts, increasing the size of the thoracic cavity
Internal intercostal muscles: pulls ribs inwards when they contract
Abdominal muscles: pull lower ribs inwards when they contract , causing intestines and liver to push up on the diaphragm


Control of ventilation

Voluntary or involuntary
-always an active process involving energy to contract muscles
1. External intercostal muscles
2. Diaphragm

1. Neural input to inspiratory muscles
2. Diaphragm and external intercostal muscles contract
3. Diaphragm moves down, sternum/ ribs move up and out
4. Thorax expands increasing volume
1. Decrease in Pip, leads to increase transpulmonary pressure
2. Lung volume increases (suction pulls lungs outwards)
3. Decrease ub Palv creates pressure gradient (Patm > Palv)
4. Air flows into alveoli down pressure gradient until Palv= Patm


Mechanics of passive expiration and active expiration

Passive expiration:
-doesn't require energy
-involves relaxation if muscles that were contracted in inspiration
-occurs during quiet normal breathing

Active expiration:
-requires energy
-involves contraction of internal intercostal and abdominal muscles.
-produces stronger, faster contraction of the lungs
-important during exercise (fast breathing) and disease

1. Diaphragm and external intercostals relax
2. Thorax, lungs and diaphragm return via elastic recoil
3. Lung volume decreases
1. Alveolar pressure increases above Patm (Palv > Patm)
2. Air flows down pressure gradient until Palv = Patm


Emphysema and expiration

-with destruction of alveolar walls, elastic recoil if the lungs is lost
-lungs are easy to distend but difficult to empty
-patients must actively expire to prevent chronic over-inflation of the lung


Dead space

Only a portion of inspired air reaches the alveoli to participate in gas exchange.
Dead space is the combined volume of non-exchanging airways
3 types of dead space:
1. Anatomical: ie all the passages were gas moves through but isn't involved in exchange
-following expiration, residual stale air remains in conducting zone
-during inspiration, stale air enters respiratory zone first, followed by atmospheric air
-consequently P O2 in alveoli is less than P O2 in atmosphere
2. Alveolar dead space:
-dead space that exists within alveoli
-occurs when ventilated alveoli have no blood supply in adjacent capillaries
-negligible in healthy individuals, increased in lung disease
3. Equipment/ mechanical dead space:
-dead space caused by respiratory equipment
-eg ET tubes, face masks, tubing
-important to chose appropriately sized anaesthetic equipment


Gas exchange in lungs

Primary 'driver' of O2 and Co2 exchange is partial pressure gradient!
-gas diffusion is influenced solely by individual partial pressure gradients
Gas exchange is complete when equilibrium between blood and alveoli is reached


Describe hypoventilation and hyperventilation

-alveolar ventilation is insufficient to meet tissue demands.
-cells continue to produce CO2 and consume O2 yet ventilation is unable to keep up with demand
-blood pCO2 increases above normals levels
-blood pO2 falls below Normal levels

-alveolar ventilation exceeds demands of tissues
-excess CO2 is removed and excess O2 is inspired for bodies requirement
-blood pCO2 falls bellow normals levels
-blood pO2 increases above normal levels


Sensory input to respiratory centres

1. Chemoreceptors
2. Stretch receptors
3. Irritant receptors
4. Proprioceptors



-Chemically sensitive receptor cells
-monitor pO2, pCO2 and H+ (pH) at several sites in the body (brain and major arteries)
-small changes in pCO2 and pH produce major changes in ventilation
-low oxygen has little effect on ventilation until large decrease in pO2 occur.


Why do you experience light headed ness when you hyperventilate?

Decreased Co2 mimics decreased metabolism, causing vasoconstriction of cerebral blood vessels