Pulmonary Ventilation Flashcards

1
Q

What are the muscles of inspiration? How do we breathe in?

A

external intercostals and diaphragm
- life the alveoli in ribs and decrease pressure by increasing volume
- air moves from high to low pressure

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2
Q

What are the accessory inspiratory muscles? What are they used for?

A

used when taking the deepest breath possible

scalene muscles - neck
pectoralis minor - scapula
serrates anterior
sternocleidomastoid muscle

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3
Q

What are the muscles of passive expiration? Active expiration?

A

no muscles for passive expiration - only relaxation of inspiration muscles

active - when blowing a balloon
- internal intercostals: pulls rubs down
- abdominal muscles - rectus abdominus, internal/external oblique, transverse: compresses abdomen and forces diaphragm higher

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4
Q

Describe what happens during inspiration

A
  1. external intercostal muscles contract - raise diaphragm
  2. Thoracic V increases, intrathoracic P decreaes
  3. Surface tension btw parietal and visceral pleura expand lungs to air in increased intrapulmonary V
  4. air flows into lungs until intrapulmonary P and atm P are equal
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5
Q

What happens when the external intercostal and the diaphragm contract? What about the internal intercostals? What nerves control these muscles?

A

external intercostals - v pattern that lifts ribs when it contracts
- increases diameter of ribs
- innervated by intercostal nerve

diaphragm - when contract, it increases the diameter of fibs from top to bottom
- innervated by phrenic nerve

forced exhalation - internal intercostals
- inverted V pattern that pulls ribs down
- innervated by intercostal nerve

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6
Q

What is Boyle’s law?

A

PV = NRT
- P and V have inverse relationship at constant T

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7
Q

At different elevations, what changes: gas percentiles or amount of gas particles?

A

gas percentiles remain the same at different elevations

relative amount of particles decreases as elevation increases

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8
Q

Describe the relationship between alveolar, atmospheric and pleural pressure

A

atmospheric - air around the body, dependent on elevation, around 760 mmHg

alveolar - fluctuates with changes in thoracic P
- 759-761 mmHg

pleural - closed space in a healthy individual, can rise and fall but always less than alveolar
- creates a negative space that helps keep the lungs inflated/expanded
- 754-756 mmHg

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9
Q

Describe the relationships between alveolar, atmospheric and pleural pressure during inspiration, exhalation ad holding breath.

A

Inspiration: Atm P > Alveolar P > Pleural P
Exhalation: Alveolar P > ATM P > Pleural P
Holding breath: Alveolar P = ATM P = no air movement

Pleural P will never be more than P atm or P alveolar as longs as its in tact

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10
Q

What is transmural pressure?

A

the difference between intrapulmonary (alveolar) and intrapleural pressures

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11
Q

What are the forces that act to collapse the lung?

A

Decreased pulmonary volume - increases alveolar pressure
inherent elasticity - allows lungs to recoil
surface tension of areolar fluid - alveoli tend to collapse

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12
Q

What are the forces that act to expand the lungs?

A

increased pulmonary volume - decreases alveolar pressure
surface tension of pleural fluid - lung surfaces tend to adhere to parietal pleura

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13
Q

What happens during a pneumothorax? Which side is more severe than the other?

A

puncture in pleural cavity forces air into pleural cavity
- with each breath in and out, air from the ATM and alveoli move into the pleura to equalize pressure
- with more air in the pleural space, it becomes increasingly hard for the lung to expand

tension pneumothorax - can push R lung towards L side of body
- compresses L lung, shifts trachea and heart towards L

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14
Q

What is atelectasis?

A

collapse of the lung
can be caused by a pneumothorax

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15
Q

What are the factors the influence pulmonary ventilation?

A

airway resistance, lung compliance, elasticity and surface tension

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16
Q

What are the factors that influence airway resistance in pulmonary ventilation?

A

inverse relationship with diameter of bronchioles
- primary control over resistance to airflow

length of airway
- difficult for normal person to change length of airway

viscosity of air
- humidity and pollutants increase viscosity

17
Q

What are the ways the the parasympathetic and sympathetic nervous systems affects bronchiole diameter?

A

Parasympathetic innervation - vagus nerve - constrict
- ACh binds to muscarinic 2 receptors that constrict airway
- can be triggered by airborne irritants, cold air, PS stimulation, histamine

Sympatethic - dilates bronchioles
- epinephrine binds to B2 receptors to increase airflow

18
Q

Describe lung compliance. How is it measured?

A

ease of expansion measured by change in lung volume that occurs with specific change in alveolar pressure
- more lungs expand, greater the compliance

high compliance - less elastic recoil
low compliance - high elastic recoil

19
Q

What are the factors that lung compliance are dependent on? What reduces compliance?

A

dependent on - elasticity of lung tissue and thoracic wall

reduced by:
- reduction of natural lung resilience - disease, age
- blockage of bronchi/bronchioles - asthma, tumors
- impairment of thoracic cage flexibility
- increase surface tension of alveoli

20
Q

Describe what happens to lung compliance with emphysema and fibrosis?

A

emphysema - high compliance due to alveolar walls being destroyed
- decreased elasticity, difficult to breath out, increased lung volume

pulmonary fibrosis - increased CT in alveolar walls
- difficult to expand, decreased compliance
- increased distance from O2 from capillaries an alveoli
- decrease in gas exchange

21
Q

Describe what airway elasticity is and how it is related to surface tension

A

ability of lung to recoil during expiration
- alveoli walls have elastic fibers

surface tension helps collapse lungs
- H2O molecules on sides of alveoli helps with collapse
- helps alveoli resist stretching and recoils

Surfactant: lipoprotein nonpolar secretion that coats alveoli to help reduce H bonding and surface tension
- produced by alveolar Type II cells - highest # in alveoli

22
Q

What is infant respiratory distress syndrome and what causes it?

A

increased surface tension in the alveoli
- requires more pressure to open

smaller alveoli require more pressure to open
- surfactant is thicker in small alveoli

insufficient production of surfactant in newborns leads to IRDS

23
Q

Describe what happens to small alveoli during inhalation and exhalation

A

inhalation - as alveoli gets larger, surface tension increases due to dilution of surfactant

exhalation - alveoli decreases in size, surface tension decreases as the ratio of surfactant to alveolar surface is high

24
Q

How doe surfactant affect lung compliance?

A

increases lung compliance as surfaces forces are reduces

surfactant promotes alveolar stability
- prevents smaller alveoli from collapsing at low volumes

promotes dry alveoli
- collapsed alveoli tend to draw fluid into them from pulmonary capillaries

25
Q

Describe the following respiratory volumes: tidal V, inspiratory reserve V, expiratory reserve V, residual V
What is vital capacity?

A

tidal: amount of air moving in/out of lungs with each breath
- 500 mL

inspiratory reserve: difference btw max total inspiratory V minus max normal
- inspired forcibly beyond tidal volume
- 2100-3200 mL

expiratory reserve: difference between max total expiratory minus max normal
- use of accessory muscles to forcibly expire air after tidal expiration
- 1000-1200 mL

residual: amount of air still in lungs after breathing out as much as possible
- 1200 mL

vital capacity: TV + IRV + ERV = ~ 4800 mL
- total volume you can breath in and out

26
Q

Describe the forced expiratory volume test and what it measures.

A

take deepest breath possible and blood out as fast as you can
- measures vital capacity - FVC - forced vital capacity
- FEV1 - how much total vital capacity you can expire in 1 second

normal ~ 80% of to total VC
obstructive airway disease: <80% of total VC

27
Q

Describe what the minute ventilation tests

A

AKA pulmonary ventilation
total amount of gas that flows in/out of the respiratory tract in 1 minute
- increases with exercise

pulmonary ventilation = RR x tidal volume
average = 12 x 500 = 6000 mL/min

28
Q

What is the difference between obstructive pulmonary disorders and restrictive pulmonary disorders?

A

obstructive - decreased FEV1
- blockage of air flow - narrowed airway or dilated alveoli
- increased air resistance due to: increased residual volume, functional residual capacity or total lung capacity
- emphysema, chronic bronchitis

restrictive - decreased FVC
- loss of alveolar space/volume - part of alveoli blocked
- decreased lung volume: decreased residual volume, functional residual capacity, or total lung capacity
- pneumonia, pulmonary fibrosis or edema

29
Q

What is the alveolar ventilation rate? What is anatomical dead space?
What is total dead space?

A

respiration rate X (tidal volume - anatomical dead space)
anatomical dead space - air conducting conduits that do not contribute to gas exchange
- 150 mL

total dead space - anatomical dead space + any nonfunctional (due to pathology) exchange in volume