Respiratory Mechanics and Lung Volumes Flashcards

1
Q

what is each lung surrounded by

A

visceral pleurae

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2
Q

what do the lungs “sit” in

A

water-filled pleural sacs

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3
Q

what surrounds the chest wall (rib cage, sternum, thoracic tissue and intercostal muscles) and diaphragm

A

parietal pleura

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4
Q

parietal and visceral pleura in a healthy person

A

stuck with water lining.

the space between them is called called the pleural cavity and its filled with intrapleural fluid - its not a real space

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5
Q

why is the pleural cavity at lower than atmospheric pressure at rest (relaxed, when not breathing in or out)

A

even with surfactant molecules the avioli still have an inward water surface tension, which pulls the visceral pleura that surrounds them in, making the pleural cavity slightly larger and slightly decreasing its pressure (since it doesn’t have a connection to the atmosphere - closed in system)

don’t need to know this but also elasticity of lungs (tendency to collapse lungs) and chest wall (tendency to expand lungs)
another side note lymphatic vessels drain the fluid in pleural cavity so that it maintains pressure and doesn’t weigh on the lungs

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6
Q

what is the transmural pressure gradient and why is it important

A

negative pressure that holds the visceral and parietal pleura together

forces wanting to recoil or collapse lung are stronger than ones that want to expand it
if pressure is equalised to atmospheric, the lungs would collapse (because lower pressure allows higher pressure alviolar area to expand and oppose collapsing forces)

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7
Q

how does pneumothorax look visually

A

ribs would protrude (pop out) as no force holding them in anymore (pleural cavity becomes a real cavity, so parietal and visceral pleura are no longer connected, no tension)

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8
Q

Q problems in premature babies and intrapleural pressure

A

type II cells don’t produce enough surfactant molecules
greater water tension on alveoli, increased pressure of pleura cavity
lung would shrink more than normal since transpulmonary pressure is increased (ask about this dont really get which one is stronger, aka . is this difference in pressure as strong as the surface tension? doesn’t it account for the ack of surfactant molecules)

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9
Q

what does the lung do in quiet breathing (hint: during exhalation)

A

recoil passively

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10
Q

what is airflow rate equal to

A

pressure gradient / airway resistance (size/diameter of airways, cased by friction molecules experience along airway walls)

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11
Q

why is pressure lost along the airway

A

due to airway resistance and bronchioles above alveoli level also being subject to intrapleural pressure
this lower pressure also keeps these vessels from collapsing
side note large airways surrounded by cartilage rings are outside of the intrapleural space

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12
Q

what happens to intrapleural pressure during forceful exhalation

A

intrapleural pressure is increase up to 786 or positive 26
excepting pressure on the alveoli and upper level bronchioles, causing them to push air out more rapidly
lungs are contracted before they fully expand

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13
Q

what is dynamic small airway closure !!!

A

when the elevated intrapleural pressure during forceful exhalation starts to equal the pressure within small airways on the way to the lungs, closing those airways (as they don’t have cartilage around them) restricting breathing

at end of forced expiration there is always some leftover air in alveoli - residual volume

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14
Q

forceful expiration in asthmatic people

A

pressure within alveoli and small vessels is lost quicker, reaching equilibrium with the high intrapleural pressure sooner, meaning there is more air left in lungs
causes air trapping

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15
Q

what is anatomical dead space (airway dead space) and how is it significant when you breathe out

A

volume of inhaled air that does not take part in the gas exchange, when alveoli are full some air about 150 mL is left in the small bronchioles or airways

first 150 mL you breathe out is the fresh air that was sitting in your airways, only 350 ml of old alveoli air is actually expelled, 150 of old remain is dead space

those 150 ml of old air is than inhaled

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16
Q

what increases first during exercise and why

A

tidal volume (volume of air)
when its increased the alveolar ventilation increases proportionally
whereas if respiratory rate (rate of air) was increased alveolar ventilation would be increased by a smaller amount as more effort is required to shift air to and from the anatomical deadspace

17
Q

what is pulmonary ventilation (ml/min)

A

amount shifted in and out of respiratory system

= tidal volume (ml/breath) X respiratory rate (breath/min)

18
Q

What is alveolar ventilation equal to

A

(tidal volume - dead-space volume) X respiratory rate

= ml/min

19
Q

what is an example of a physiological dead space

A

V/Q>1, aka ventilation is greater than perfusion

due to pulmonary capillary being constricted, the avioli becomes a dead space

20
Q

what is ventilation and what is perfusion

A

V - flow of air into and out of alveoli
Q - flow of blood to alveolar capillaries
(in many cases ratio should equal 1)

o2 would be higher co2 lower as no gas exchange has occurred. this higher o2 directly affects the capillary bed by relaxing (dilating it) allowing more blood flow

reversely low co2 contracts smooth muscles of bronchioles decreasing airflow

21
Q

what is a physiological shunt

A

V/Q < 1
normally perfused capillary bed but alveolus is constricted
capillary bed allows blood to flow from the right side of the heart to the left or arterial side without taking part in gas exchange
capillary bed is the physiological shunt
this time oxygen levels at capillary bed are low co2 high, low 02 constricts capillary reducing blood flow to the shunt.
high co2 relaxes bronchioles allowing more ventilations
like in physiological dead space the associated actions act to reduce the miss match between V and Q
present in asthmatics

also remember anatomical shunt in heart allowing veinous blood to flow into arterial directly without any gas exchange

22
Q

what happens in asthmatic people in regard to physiological shunts

A

local control mechanisms don’t work anymore as too many alveoli are cut off from ventilation
blood flow in capillary beds that cover unventilated alveoli, Po2 40 and Pco2 45 9hardly any gas exchange occurring)

this mixed with blood coming from ventilated areas and the resulting mixed blood has Po2 and Pco2 below normal

low po2 causes the patient to hyperventilate