Respiratory Physiology Flashcards

1
Q

functions of the respiratory system

A

1: oxygenation of blood
2: removal of carbon dioxide
3: control of acid-base balance
4: production of vocalization

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2
Q

respiration

A

=process of delivering O2 to cells and removing by-product of metabolism (CO2)

includes gas exchange in the lungs, circulation of gases through blood stream and transfer of gases at cellular level.

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3
Q

respiratory system

A

Pulmonary ventilation
-inflow/outflow of air in the lung space

External pulmonary ventilation:
-exchange of gases between lungs and blood

Internal tissue respiration:
-exchange of gases between blood and tissues

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4
Q

upper respiratory system

A

Nose/mouth
-filters, humidifies, warms/cools

Pharynx

  • vocal cords
  • conduit to larynx and trachea

*mouth breathers are at a disadvantage- don’t get nose benefits

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5
Q

lower respiratory system

A

LARYNX:

  • epiglottis
  • cricoid: complete cartilage ring- provides attachments for muscles, ligs. involved in opening and closing airway and speech production

TRACHEA

BRONCHI

LOBES

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6
Q

anatomy acinus

A

-alveolar walls contain 2 types of cells

Type I and II

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7
Q

Type I alveolar cells

A

squamous cells where gas exchange occurs

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8
Q

Type II alveolar cells

A

produce surfactant that lowers surface tension and helps keep alveoli open and helps them to expand more easily

  • surface tension between water and air makes alveoli collapse. to counteract, type II cells produce surfactant to keep it open.
  • big breaths produce more surfactant
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9
Q

muscle components of respiration

A

1: inspiration
2: expiration
3: accessory

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10
Q

inspiration muscles

A

1: diaphragm
2: external intercostals
3: interchondral intercostals

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11
Q

expiration muscles

A

1: abdominals
2: internal intercostals (except interchondral portion)

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12
Q

accessory respiration muscles

A

1: scalenes
2: sternocliedomastoid
3: serratus anterior & pecs

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13
Q

diaphragm

A
  • dome shaped musculofibrous septum
  • separates the thoracic and abdominal cavity
  • convex upper surface forming thoracic floor
  • concave under surface forming abdominal roof
  • innervated by phrenic nerve (C3-C5)

-optimal length-tension ratio with max tension at FRC (normal resting lung volume)

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14
Q

inspiration

A

Intercostal muscles and diaphragm contract to expand the chest with inhalation:

  • diaphragm flattens and moves downward
  • intercostals move ribs upward and outward

Increased size of chest decreases intrapulmonary pressure so air from outside (atmospheric pressure) is not at higher pressure gradient and rushes inward.

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15
Q

exhalation in quiet breathing

A
  • passive process
  • inspiratory muscles relax to their resting position
  • results from recoil of lungs and chest wall
  • size of chest decreases
  • intrapulmonary pressure increases and air flows out of lungs
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16
Q

exhalation during exertion, forced expiration and coughing

A
  • active contraction of the expiratory muscles (plus closure of the glottis during coughing)
  • marked rise in intrathoracic pressure so that expiration occurs more rapidly and completely
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17
Q

pressure

A

intrapulmonary pressure
intrapleural pressure
transpulmonary pressure

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18
Q

intrapulmonary pressure

A
  • pressure in the alveoli
  • rises and falls with expiration/inspiration
  • will equalize to atmospheric pressure (760 mmHg)
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19
Q

intrapleural pressure

A
  • pressure in pleural cavity between parietal and visceral pleura
  • 0.4 mmHg from the intrapulmonary pressure
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20
Q

transpulmonary pressure

A

difference between intrapulmonary and intrapleural pressures

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21
Q

lung compliance

A

Relates to elasticity of tissues (measured by pressure-volume curve)

chest wall compliance + lung compliance can change lung volumes

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22
Q

decreased lung compliance

A

lungs stiffer and more difficult to expand

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23
Q

increased lung compliance

A

lungs easier to distend

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24
Q

neurologic control of breathing

A
  • largely automatic; however, can be voluntarily controlled.
  • chemoreceptors near aorta and carotid arteries are sensitive to increase in CO2, acid concentration & decrease in PaO2. when receptors sense acidity or high CO2, they stimulate brain to increase the speed and depth of breathing.
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25
Q

2 mechanisms of neurologic breathing control

A

1: medulla- controls rate and depth of respiration
2: pons- moderates rhythm of inspiration/expiration

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26
Q

lung volumes

A

tidal volume
inspiratory reserve volume
expiratory reserve volume
residual volume

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27
Q

tidal volume (TV)

A

=volume of gas inspired or expired during each respiratory cycle- reflects depth of breathing

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28
Q

inspiratory reserve volume (IRV)

A

max amount of gas inspired from peak inspiratory tidal volume

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29
Q

expiratory reserve volume (ERV)

A

max amount of air expired after a normal expiration

30
Q

residual volume

A

gas remaining in lungs after max expiration

31
Q

total lung capacity (TLC)

A

max amount of air contained in lungs after a max inspiratory effort
TLC= TV + IRV + ERV +RV
sum of all 4 volumes

32
Q

vital capacity (VC)

A

max amount of air that can be expired after a max inspiratory effort
VC= TV + IRV + ERV

33
Q

inspiratory capacity (IC)

A

max amount of air that can be inspired after a normal expiration
IC= TV + IRV

34
Q

functional residual capacity (FRC)

A

volume of air remaining in the lungs after a normal tidal volume expiration
FRC= ERV + RV

35
Q

lung capacities

A

total lung capacity
vital capacity
inspiratory capacity
functional residual capacity

36
Q

breathing

A
take a breath, air goes into nose (warmed, filtered, humidified)
nasal passages
pharynx
larynx
trachea
R & L main stem bronchus
lobar bronchi
segmental bronchi
bronchioles
alveolar ducts
alveoli where gas exchange takes place
37
Q

dead space

A

=a portion of each breath does not participate in gas exchange

anatomic
alveolar
physiological

38
Q

anatomical dead space

A

normally ~150 mL

conducting airways- pharynx, larynx and airways

39
Q

alveolar dead space

A

ventilated, not perfused (pulmonary emboli)

40
Q

physiological dead space

A

no gas exchange (disease process, emphysema)

example: in emphysema elastic tissue of lungs is destroyed and the inward pull of the lungs is less than normal (increased compliance); therefore the chest wall is pulled out and the FRC is increased
- chest wall compliance and pressure volume relationships are due to the elastic tissue properties of the ribs and diaphragm. any pathology that changes elastic properties will impact breathing- kyphoscoliosis, skeletal muscle disorders, abdominal disorders

41
Q

gas exchange

A

-takes place in the respiratory units or acini

42
Q

acini

A

=portion of the lung distal to the terminal bronchiole comprising respiratory bronchioles. alveolar ducts, alveolar sac and alveoli

43
Q

gas exchange in alveoli

A

-several hundred million alveoli which provide a surface area about the size of a tennis court for gas exchange

gas exchange occurs by process of diffusion

affected by:

  • partial pressure gradients
  • gas solubility
  • structural characteristics of respiratory membrane
  • functional aspects (ventilation/perfusion)

Inspired air (saturated with water vapor)

  • PO2 160 mmHg
  • PCO2 0.3 mmHg

Blood entering alveolar capillaries

  • PO2 40 mmHg
  • PCO2 45 mmHg

Gas diffuses across alveolar membrane in direction of least pressure

  • O2 goes toward blood and is bound to Hb
  • CO2 diffuses toward alveolus & mixes w/ air
44
Q

partial pressure of gases

A

All gases in air exert a partial pressure independent of other gases. Dry air

  • 21% O2
  • 0.04% CO2
  • 78.06% nitrogen
  • 1% other gases (argon and helium)

atmospheric pressure is 760 mmHg.
amount of pressure due to O2= 760 x 0.21 = 160 mmHg

45
Q

gas exchange in tissues

A

Blood leaving alveoli:

  • PO2 104 mmHg
  • PCO2 40 mmHg
  • returns to LA via pulmonary veins
  • pumped by LV to all tissues of the body
  • O2 dissociates from arterial hemoglobin
  • diffuses across capillary membrane into muscle cells
  • mitochondria use O2 to create ATP used for energy

Metabolic waste from muscle contraction is eliminated following the same transport pathway, but in reverse :

  • CO2 diffuses from muscle cells into capillaries
  • transported back to the heart (RA) through venous system
  • RV pumps blood to lungs where CO2 diffuses from capillaries into alveoli and is exhaled

Expired air:

  • PO2 120 mmHg
  • PCO2 27 mmHg
46
Q

transport of gases in blood

A

CO2 is more soluble than O2 and dissolves in blood

dissolved CO2 forms a bicarbonate (base) and small amount of carbonic acid:

  • CO2 combines with H2O and forms H2CO3 (carbonic acid). lungs regulate this volatile acid by manipulating CO2 levels
  • H2CO3= H2O + H (bicarbonate and H+). The kidneys regulate the pH level by excreting more or less H+

This interaction manages the acid/base balance

47
Q

gas exchange in a nut shell

A

O2 status is affected by acid-base status. when blood is too acidic, less O2 is bound to hemoglobin; raising pH increases binding allowing more total O2 to be carried in the blood

CO2 transported through blood by conversion to H2CO3 (carbonic acid) which breaks down into H+ and HCO3

H+ ion binds to hemoglobin and serves as vehicle for transporting CO2 to lungs

hemoglobin and bicarbonate act as buffer for acid produced by metabolism and transport this acid to lungs for elimination

48
Q

ventilation/perfusion ratios

A

V/Q is the ratio of alveolar ventilation to pulmonary blood flow (Q). matching ventilation to perfusion is critical for ideal gas exchange.

49
Q

normal value for V/Q

A

=0.8

this means that alveolar ventilation (L/min) is 80% of the value for pulmonary blood flow (L/min)

if V/Q is 0.8, then PaO2 will be 100 mmHg and PaCO2 will be 40 mmHg.

50
Q

oxyhemoglobin dissociation curve

A

shift to the left (acute alkalosis, hypocapnia, increased body temp)

shift to the right: hyperthermia, hypercarbia acidosis

51
Q

ventilation/perfusion matching

A

=degree of correspondence between ventilated and perfused areas of the lungs

52
Q

optimal V/Q ratio=

A

=0.8

4 parts ventilation to 5 parts perfusion to maintain normal gas exchange

53
Q

oxygen-hemoglobin (O2-Hb) binding

A

=percent of O2 saturated in arterial blood

normal SaO2=95% or more

54
Q

perfusion in the lungs

A

lung apices are perfused, but at a low rate
-typically in lung apices, arterial pressure is just high enough to prevent closure of the pulmonary capillaries

BF within the lung is uneven due to effect of gravity

  • supine: BF is nearly uniform bc gravitational effect is the same all over
  • standing: BF is lowest at apex of the lung and highest at the base

pressures in the pulmonary vessels is much lower than in the systemic vasculature

55
Q

PA

A

=alveolar pressure

56
Q

Pa

A

=arterial pressure

57
Q

Pv

A

venous pressure

58
Q

blood flow distribution in the lung

A

3 zones (1 at the apex, 3 at base)

lowest BF= PA>Pa>Pv
medium BF= Pa>PA>Pv
highest BF= Pa>Pv>PA

59
Q

middle lobe perfusion

A

zone 2

  • gravitational effect on hydrostatic pressure is such that arterial pressure is higher than alveolar
  • alveolar pressure is still higher than venous pressure
  • BF here is due to the difference between arterial and alveolar pressure
60
Q

lower lobe perfusion

A

zone 3

  • gravity has increased arterial and venous pressure and both are now higher than alveolar pressure
  • BF here is drive by the difference between arterial and venous pressure
  • greatest number of capillaries are open and blood flow is highest
61
Q

shunting of blood

A

Sometimes a portion of cardiac output is re-routed or shunted (heart defect)

Right to Left shunt can occur if wall between RV and LV is defective.

L to R shunt is more common and usually does not cause hypoxemia. (patient ductus arteriosus, or traumatic injury)

r to L shunt (tetrology of fallet; V septal defect , increased pulm pressure) or transposition of the great vessels

L to R patent ductus arteriosus

62
Q

V/Q distribution in the lung

A

zone 1:

  • lowest BF
  • lower alveolar ventilation
  • highest V/Q
  • highest PaO2
  • lower PaCO2

zone 3:

  • highest BF
  • higher alveolar ventilation
  • lowest V/Q
  • lowest PaO2
  • higher PaCO2
63
Q

defense of lungs

A

several lines of defense against inhaled organisms and particles:

  • nasal mucosa
  • nasal hair/cilia
  • type II pneumocytes
  • alveolar macrophages
  • B lymphocytes
  • polymorphonuclear leukocytes
  • mast cells
64
Q

nasal mucosa

A
  • Goblet cells and bronchial seromucous glands produce mucous which contains immonglobulin A
  • protects underlying tissue and traps organisms
  • mucous production increases with inflammation (asthma and bronchitis)
65
Q

nasal hair/cilia

A
  • hair-like structures which remove debris

- impaired by nicotine, inflammation, infection, anesthesia

66
Q

type II pneuomocytes

A

produce surfactant which protects tissue and repairs damage to alveolar epithelium

67
Q

alveolar macrophages

A
  • kill bacteria

- activity impeded by nicotine, air pollution, alcohol, corticosteroid therapy & radiation

68
Q

B lymphocytes

A

produce gamma globulin for production of antibodies to fight infections

69
Q

polymorphonuclear leukocytes

A

engulf and kill blood born gram negative organisms

70
Q

mast cells

A
  • release inflammatory mediators to alter permeability of epithelial and vascular permeability
  • those who smoke and those with asthma have more mast cells
71
Q

chest and respiration with aging

A
  • decreased elastic recoil of lung tissue
  • decreased chest wall compliance (stiff chest)
  • diaphragm position lower and less mechanically efficient- decreasing force generating ability
  • decreased lung volumes and expiratory flow rates
  • airway resistance increases so expiratory time is prolonged
  • diffusing capacity decreases as a result of reductions in the alveolar surface area-reduces efficiency of gas exchange
  • peripheral and central chemoreceptors become less sensitive to increasing levels of CO2 and hypoxia
72
Q

observation of the chest

A

barrel chest
kyphosis
pectus excavatum
pectus carinatum