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Pulmonary > The Respiratory System > Flashcards

The Respiratory System Flashcards

1
Q

The respiratory system consists of

A

lungs

chest wall

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2
Q

Chest wall consists of

A 
Rib cage
Thoracic spine
All structures attached to them:
-respiratory muscles (including diaphragm)
-other sk. muscles and fat
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3
Q

Function of resp. system

A

Maintain a normal partial pressure of oxygen (PaO2) and carbon dioxide (PaCO2) in the arterial blood

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4
Q

Maintaining normal partial pressures depends on 3 interrelated processes:

A
  • ventilation
  • matching of ventilation and perfusion
  • Gas diffusion
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5
Q

Ventilation regulates what. Ventilation is regulated by?

A

Regulates PaCO2

Is regulated by neurons in the medulla (receive input from cerebral cortex and peripheral receptors)

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6
Q

Ventilation-perfusion relationships are important because:

A
  • The V/Q ratio of each alveolus determines the PO2 and PCO2 of the alveolar gas
  • The PaO2 falls and the PaCO2 rises as the range or distribution of V/Q ratios increases
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7
Q

Rate of gas diffusion varies directly with? inversely with?

A

Directly with:

  • the contact area btw alveolar gas and capillary blood
  • the partial pressure gradient

Inversely with:
-diffusion distance

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8
Q

Lung inflation stimulates what receptors?

A 
Non-chemical stretch receptors (lungs and airways)
Muscle spindles (chest wall musculature)
Tendon organs (chest wall musculature)
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9
Q

Regulatory cortex, complex, groups.

A

Cerebral motor cortex
-input to brainstem motor neurons, for adjustments in breathing

Pre-Botzinger complex (brainstem)
-where the rhythm generator exists

Dorsal Respiratory Group (pons and medulla)
-Activate inspiratory neurons

Ventral Respiratory Group (pons and medulla)
-Activate primarily expiratory neurons, some inspiratory neurons

Output from these neurons govern phrenic and intercostal motor neurons, and those of the pharyngeal and laryngeal muscles

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10
Q

Stimuli that evoke a response from the respiratory control system

A

Hypoxemia
Hypercapnia
pH

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11
Q

Chemoreceptors sense?

A

Oxygen tension (PaO2)
Carbon Dioxide tension (PaCO2)
pH

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12
Q

Peripheral Chemoreceptors- consist of, location, cell types, sends info where/how?

A

Consists of: carotid bodies
Location: bifurcation of the common carotid artery and aortic bodies

Cells:
Type I (glomus) cells- act as sensors and contain/release catecholamines from cytoplasmic vesicles
Type II (sheath) cells- encircle glomus cells in a supporting structural role

Send information related to blood gas tensions and pH to CNS via:

  • carotid sinus nerve
  • glossopharyngeal nerve
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13
Q

Central Chemoreceptors- location, primarily sensitive to, directly stimulated by? Result of stim?

A

Location: throughout lower brainstem (area classically descriibed as ventrolateral medulla)

Primarily sensitive to: CO2 tension (PCO2)

Once CO2 diffuses across the BBB, it is rapidly hydrated and dissociates to form H+ and HCO3-
It is the H+ ions that act as the stimulus to the central chemosensitive cells

Augments ventilatory drive and increases alveolar ventilation

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14
Q

Ventilatory response quicker to peripheral or central chemoreceptors?

A

Quicker response to peripheral chemoreceptors.

Bc greater blood flow to the carotid bodies

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15
Q

Non-chemical control of breathing- main groups of receptors and their innervation.

A

Slowly and rapidly adapting receptors: innervated by myelinated vagal fibers

J (juxtacapillary) receptors - innervated by unmyelinated vagal C fibers

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16
Q

Slowly adapting receptors

Hering-Breuer Inflation Reflex

A

Increase firing rate immediately in response to stimuli
Firing rate decreases despite continued stimulus.
Located among airway smooth muscle cells
Some are stretch receptors
-Participate in Hering-breuer Inflation Reflex:
Sustained inflation of lung inhibits further inspiratory activity and results in a period of apnea

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17
Q

Rapidly Adapting Receptors- response, stimulated by, results of stim

A

Decrease firing rate in response to stimulus
Located among airway epithelial cells
Stimulated not only by lung inflation but also by exogenous factors: particulate matter, edogenous agents- histamine and prostaglandins

Result: cough, hyperpnea, bronchocontriction

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18
Q

Juxtacapillary Receptors -location, innervatated by ___ which are stim by…? Result of stim?

A

Located in the pulmonary interstitial space in close proximity to the pulmonary and bronchial circulations

Innervated by unmyelinated vagal C-fibers
C-fibers are stimulated by:
-pulmonary congestion
-other pathologic processes within the pulmonary interstitium
-Bronchoconstriction
-lung inflation
-exogenous and endogenous agents such as capsaicin, histamine, bradykinin, serotonin and prostaglandins

Result: Apnea followed by rapid shallow breathing and bradycardia and hypotension (pulmonary chemoreflex)

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19
Q

Ondine’s curse

A

Loss of the ability for automatic control of respiration while maintaining voluntary control

Children sufferring from Ondine’s curse need continuous ventilatory support
By adulthood, usually required only during sleep.

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20
Q

Heart-Lung Transplantation. Changes in innervation, relfex?

A

Vagal innervation of both heart and lungs are lost

Loss of vagal efferent input to heart- increase in resting heart rate
Loss of vagal afferent input from lungs- no signifcant change to rate/depth of breathing

No longer cough response to stim of smaller airways
Trachea remains innervated and can still elicit normal cough response

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21
Q

Repiratory pattern of a cough

A

A deep inspiration followed by a forced expiration against a closed glottis that builds up large pressures until the glottis is suddenly opened and the air escapes

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22
Q

Respiratory pattern of a sneeze

A

Series of superimposed inspirations in the presence of an open glottis that is followed by a rapid expiration of air at several hundred miles per hour.

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23
Q

Respiratory pattern of a hiccup

A

Spasmodic contraction of the inspiratory muscles timed exactly with sudden closure of the glottis.
No apparent useful purpose

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24
Q

Respiratory pattern of a yawn

A

Deep inspiration followed by a slow expiration over a 5-6 sec period.
Possibly stretches the lung to open up under-ventilated and collapsed portions

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25
Q

Breathing during normal sleep. During non-REM sleep, during REM sleep.

A

Normal sleep: reduction in tidal volume
Non-REM sleep:
-reduction in PaO2 and oxyhemoglobin saturation
-increase in PaCO2
-diminished ventilatory response to hypercapnia and hypoxemia

REM sleep:
-further reduction in ventilatory response to hypercapnea and hypoxemia
-blood gasses variable since sleep stage is non-homogeneous condition (phasic REM and tonic REM)
-Irregularity in breathing due to loss of accessory muscles such as intercostals
(ventilation becomes solely dependent on the diaphragm)

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26
Q

Sleep associated breathing problems

A

Obstructive sleep apnea:

  • reduced tone of the upper airway respiratory muscles
  • periods of airway collapse during sleep

Cheyne-Stokes respiration:
-waxing and waning periods of hyperventilation and apnea
-most commonly seen in people acending to high altitude or in patients with severe heart failure
Possible pathogenesis factors:
1. pulmonary congestion
2. delay in circulation time btw lungs and central chemoreceptors due to cardiac insufficiency in heart failure patients
3. Alterations in the threshold for PaCO2 to stimulate breathing, potentially accounting for the increased susceptibility to develop this breathing pattern during sleep

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27
Q

Respiratory control in obese individuals

A

Severe obesity leads to mechanical loads on the resp. system which may result in underventilation of parts of the lung

Adipose tissue produces endocrine and signaling factors that may help determine whether resp. control mechanisms are able to compensate for the mechanical loads imposed by severe obesity

Ex: Leptin- regulator of satiety/metabolism. Acts on neuronal groups in hypothalamus. Can also alter central respiratory control mechanisms

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28
Q

Transpulmonary pressure equation

A

Alveolar pressure minus pleural pressure

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29
Q

Equation for the pressure gradient across the chest wall

A

Pleural pressure minus body surface (atmospheric) pressure

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30
Q

Alveolar pressure is equal to?

A

Pressure measured at the airway opening proximal to site of airway occlusion

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31
Q

How is pleural pressure approximated?

A

By measuring the pressure within the lower 2/3 of the esophagus using a balloon catheter

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32
Q

Equation for elastic recoil pressure of the entire respiratory system. It is equal to?

A

Transpulmonary pressure plus pressure gradient across chest wall. It is equal to the pressure recorded at the airway opening.

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33
Q

Measured lung volumes are determined primarily by what factors?

A
  • Elastic recoil of the lungs and chest wall

- Strength of the respiratory muscles

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34
Q

Functional residual capacity (FRC)

A

Volume remaining in the lungs at the end of a passive expiration

  • Point at which the inward recoil of the lungs is exactly balanced by the outward recoil of the chest wall
  • Since Prs = 0, no respiratory muscle activity is required to maintain this volume, and FRC represents the resting or equilibrium position of the respiratory system.
35
Q

Total lung capacity (TLC)

A

Volume present in the lungs after maximal inspiration
-when the combined elastic recoil of the lungs and chest wall is balanced by the maximum pressure that can be generated by the inspiratory muscles

36
Q

Residual volume (RV)

A

Volume of gas remaining in the lungs after a maximal expiration
-determined by balance between the elastic recoil of the chest wall and maximal expiratory effort

37
Q

Vital Capactiy (VC)

A

Volume of gas that can be exhaled after a maximal inspiration
-Difference between total lung capacity and residual volume

38
Q

Equation for Compliance

A

C = deltaV/deltaP

39
Q

Compliance varies directly or inversely with elastic recoil?

A

Compliance varies INVERSELY with elastic recoil

40
Q

The slope of the volume-pressure curve is equal to?

A

Compliance

41
Q

Equation for alveolar pressure

A 
P = 2T/r
(T= surface tension)
(r = alveolar radius)
42
Q

Tissue forces result from?

A

Deformation of elastic elements in the lung parenchyma and chest wall

43
Q

Surface forces are unique to? Produced by?

A

Unique to lung parenchyma

Produced by layer of surfactant that coats the alveolar epithelium

44
Q

Surface tension is generated by? Tends to…

A

Generated by surfactant
Tends to reduce alveolar size
Tends to increase pressure required to maintain a given lung volume

45
Q

Surface tension of surfactant is unique because?

A

Is it not constant.
Varies directly with the size of the air-liquid interface.
Increases as alveolar volume increases

46
Q

Viscous forces. Percentage accounted for by..

A

35% of viscous forces during ventilation accounted for by upper airway (mouth, pharynx, larynx)

47
Q

Equation for Resistance. It quantifies what force?

A

Quantifies viscous forces.
R = deltaP/V
R = 8nL/pi r^4

48
Q

Define Tidal Volume

A

Volume of gas inhaled (or exhaled) during a breath

Resting adult: 500mL

49
Q

Define Residual Volume. It is determined by?

A

Amount of gas remaining in the lungs after maximal expiration.
Determined by:
-inward pressure generated by the expiratory muscles
-outward elastic recoil of the respiratory system
Normal adult: 1.5:

50
Q

Define Expiratory reserve volume

A

Volume of gas that can be forced from the lungs starting at the end of a normal tidal expiration

51
Q

Define Inspiratory Reserve Volume

A

Volume of gas that can be inhaled during a maximal inspiration starting at the end of a normal tidal inspiration.

52
Q

Functional Residual Capacity

A

Volume remaining in the lungs at the end of a passive expiration
-Represents equilibrium position of the respiratory system
Point at which inward elastic recoil of the lungs is balanced by outward elastic recoil of the chest wall

53
Q

Total lung capacity. Define. Determined by?

A

Volume in the lungs at the end of a maximal inspiration
Determined by:
-max force generated by inspiratory muscles
-inward elastic recoil of the lungs and chest wall

54
Q

Vital Capacity

A

Volume of gas that can be exhaled during a maximal effort beginning at the end of a maximal inspiration.
= IRV + ERV + Vt
= TLC- RV

55
Q

Inspiratory capacity

A

Amount of gas that enters the lungs during a maximal inspiration beginning at the end of a normal tidal expiration.
= IRV + Vt

56
Q

Equation for pressure exerted by a gas

A 
Pgas = Ptotal x Fgas
Ptotal = total pressure of all gases in mixture
F = fractional concentration
57
Q

What is the partial pressure of water vapor (PH2O) at body temp?

A

about 47mmHg

58
Q

Equation for gas partial pressure in the airways

A

PIgas = (Pb - PH2O) x Fgas

59
Q

Alveolar air equation

A

Used to calculate the average alveolar PO2
assuming “ideal” conditions (no mismatching of ventilation and perfusion)
PAO2= (PB-PH2O) FiO2 - (PACO2/R)
R = VCO2/VO2

60
Q

Pa-aO2 or A-a gradient

A

The difference between the calculated alveolar and measured arterial PO2.
Normally 8-12 mmHg

61
Q

Anatomic dead space

A

Nose, mouth, pharynx, larynx, and conducting airways
Does not participate in gas exchange
Estimated as: 1mL per pound of ideal body weight

62
Q

Alveolar dead space

A

Alveoli that either receive no blood flow or are under-perfused relative to the amount of ventilation they receive

63
Q

Physiologic dead space

A

Sum of the anatomic and alveolar dead space

64
Q

Dead Space Volume

A

Amount of gas entering the physiologic dead space

65
Q

Alveolar volume. Define. Equation.

A

The volume of gas that actually reaches the alveoli and participates in gas exchange during a tidal breath
VA = Vt - Vd
(tidal volume - dead space volume)

66
Q

Minute Ventilation

A

Total volume of gas that enters or leaves the lungs each minute
VE= VT X RR

67
Q

Vessels of pulmonary circulation vs. systemic circulation. Histiological differences. Which lead to what differences.

A

Pulmonary arteries have thinner walls and larger lumens.
Less vascular smooth muscle.
No muscular vessels analogous to systemic arterioles.
1. Pulmonary vascular resistance is normally much less than that of systemic circulation
2. Vascular resistance is fairly evenly distributed btw the arteries, capillaries, and veins
3. Pulmonary arteries are much more distensible and compressible

68
Q

Factor that affects resistance in alveolar vs. extra-alveolar vessles

A 
Alveolar vessels (primarily pulmonary capillaries) resistance increases when alveolar volume increases
Extra-alveolar vessel resistance increases when pleural pressure increases.
69
Q

Active vs. Passive factors that affect Pulmonary Vascular Resistance

A

Active:
Neural factors, Humoral factors
Passive:
Lung volume, Cardiac Output, Gravity

70
Q

How does cardiac output affect Pulmnonary Vascular Resistance?

A

Increases in CO must be balanced by a fall in PVR
Decrease in PVR is mediated not by alterations in vascular tone but rather due to two passive processes:
1. pressure rises transiently and opens or recruits capillaries and other small vessels that had been closed due to insufficient intra-vascular pressure
2. The increase in pressure causes distention of the pulmonary vasculature

These lead to decrease in PVR and minimize any flow-induced increase in pulmonary vascular pressure

71
Q

How does gravity affect PVR?

A

Intra-vascular pressure increases in the dependent (bottom) portions of the lungs.
In an upright subject, press. gradient causes:
-vascular distention toward lung bases
-narrowing near the apices

72
Q

Descibe the zones of the lung

A

Zone 1: PA>Pa>Pv, no blood flow, apex
Zone 2: Pa>PA>Pv, flow driven by Pa-PA, mid-lung
Zone 3: Pa>Pv>PA, flow driven by Pa-Pv, base

73
Q
  1. Higher alveolar pressures and low intra-vascular pressures will increase which zone(s)?
  2. Lower alveolar pressures and higher intra-vascular pressures will increase which zone(s)
A
  1. Zone 1 and Zone 2

2. Zone 3

74
Q

Gravity-induced change is greater in perfusion or ventilation?

A

Perfusion

75
Q

How does cardiac output affect Pulmnonary Vascular Resistance?

A

Increases in CO must be balanced by a fall in PVR
Decrease in PVR is mediated not by alterations in vascular tone but rather due to two passive processes:
1. pressure rises transiently and opens or recruits capillaries and other small vessels that had been closed due to insufficient intra-vascular pressure
2. The increase in pressure causes distention of the pulmonary vasculature

These lead to decrease in PVR and minimize any flow-induced increase in pulmonary vascular pressure

76
Q

High V/Q regions cause…

A

Increase alveolar and physiologic dead space

77
Q

Bohr Equation. What does it tell us?

A

Ratio of dead space volume to tidal volume
VD/VT = (PaCO2 - PECO2) / PaCO2

Tells us that the difference btw arterial and exhaled PCO2 increases with the proportion of dead space in a tidal breath.

78
Q
  1. Higher alveolar pressures and low intra-vascular pressures will increase which zone(s)?
  2. Lower alveolar pressures and higher intra-vascular pressures will increase which zone(s)
A
  1. Zone 1 and Zone 2

2. Zone 3

79
Q

Gravity-induced change is greater in perfusion or ventilation?

A

Perfusion

80
Q

Low V/Q regions and shunts cause…

A

Decrease in PaO2

Increaein PA-aO2 and PaCO2

81
Q

High V/Q regions cause…

A

Increase alveolar and physiologic dead space

82
Q

Bohr Equation. What does it tell us?

A

Ratio of dead space volume to tidal volume
VD/VT = (PaCO2 - PECO2) / PaCO2

Tells us that the difference btw arterial and exhaled PCO2 increases with the proportion of dead space in a tidal breath.

83
Q

What happens to PeCO2 and physiological dead space with pulmonary embolism?

A

PeCO2 decreases.

Physiological dead space increases.

Pulmonary (6 decks)

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