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NBS1 > Respiratory Physilogy > Flashcards

Respiratory Physilogy Flashcards

1
Q

Pulmonary ventilation

A

Convective air move to due to pressure gradients created by respiratory muscle activity
Inspiration–pressure in the intrathoraci airways are less than atmospheric
Expiration–pressure gradient is reversed and higher pressure within the lungs causes air to flow out

Brings the O2 atmospheric air to gas exchange regions (respiration) and alveolar space

Shorten the diffusion distance by ventilating the lungs

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2
Q

Respiration

A

Diffusion of O2 into pulmonary capillaries for uptake by the blood plasma and RBCs
O2 moves down partial pressure gradient
CO2 moves down its gradient from capillary to alveolar airspace

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3
Q

Pressure gradients for ventilation vs respiration

A

For ventilation, gases move down airway pressure gradients

For respiration, gases move through regions by partial pressure gradients

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4
Q

Path of diffusion of O2 and CO2 in the lungs

A

O2 diffuses from alveolar spaces to pulmonary capillaries

CO2 from pulmonary vasculature into acinar space (terminal respiratory unit) then pulmonary ventilation into air

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5
Q

Hypercapnia and Hypoxemia

A

Hypercapnia–Excess partial pressure of CO2 in the respired air or arterial blood

Hypoxemia–low oxygen availability that can only be sensed on the arterial side of the blood. Results in anaerobic respiration and lactic acid buildup

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6
Q

2 major results from inadequate ventilation

A

Compromises O2 uptake by the lungs and delivery to the tissue (anaerobic metabolism—>non-volitile acid production (lactic acid)—>acidosis)

Compromises CO2 removal–>buildup of volatile acid–>acidosis

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7
Q

Phonation

A

Respiratory muscles contracting to create air movement over the vocal cords within the larynx for vocal communication

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8
Q

Lymphatic function of the respiratory system

A

Largest in body, always taking in air, pathological bacterial,

First line of defense-mucosa lining the airways
Lymphocytes migrate there
Drain into subclavian veins

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9
Q

Changes of air via heat and water exchange

A

47 mmHG of H2O at 37 degrees Celsius to protect the alveoli

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10
Q

What causes humidification and warming of the inspired ear

A

Mucous membranes of the nose, turbinates, and pharynx due to their large surface area and rich blood supply

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11
Q

Mucociliary elevators

A

Small particulates are trapped in bronchial secretions (100 ml/day) which are moved upward toward the pharynx and mouth for removal

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12
Q

Pulmonary artery contents

A

Out put of the right ventricle (all CO) through the pulmonary artery (contains a minute of all venous blood from all regions of the body) through pulmonary capillary network

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13
Q

Filtration of blood in pulmonary circulation

A

Ideal for trapping circulating blood clots
Conversion of ATI to ATII
Degredation of Bradykinin
Prostoglandin E series, F2 alpha, completely removed from circulation with one pass
Protoglandin A series adn I2 are unaffected
Circulating epinephrine I not affected,
Norepinephrine is affected

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14
Q

V dot

A

Gas volume/unit time

V dot O2–O2 consumption per minute

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15
Q

F

A

Fractional concentration in dry gas phase

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16
Q

D

A

Diffusing capacity

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17
Q

Va

A

Volume of alveolar gas

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18
Q

STPD and BTPS

A

Standard temperature and pressure (0 degrees Celsius, 760 mmHg)
BOdy temperature and pressure saturated with water vapor

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19
Q

Vt

A

Tidal volume

Either in or out of lungs–not a summation

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20
Q

Pc bar O2

A

Mean capillary O2 partial pressure

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21
Q

SvO2

A

Saturation of HB with O2 in mixed venous blood

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22
Q

Arrangement of airways, pulmonary arteries, and pulmonary veins

A

Airways are associated with deoxygenated pulmonary arteries, mixed venous blood

Pulmonary veins–oxygenated

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23
Q

What generates the motive force to move air from mouth to gas exchange areas

A

Sub atmospheric pressure within the thorax

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24
Q

Describe the branching pattern of airways

A

23 generations of irregular dichotomous branching tubes to maximize alveolar surface area for smallest volume
Subsequent branching is narrower in diameter and shorter in length

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25
Q

Conducting airway of bronchi

A

Branches 1-10 with cartilaginous support–not engaged with gas exchange, the lobar bronchus

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26
Q

Change of cartilage and muscle through bronchi branching

A

Down the length of the branching airways, cartilage cilia, and mucous secreting cells decline

Smooth muscles increase, allowing to dilate or constrict through neural and reflex stimulation

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27
Q

Changes in airway diameter are _____ of lung volume

A

Independent, if caused by neural and reflex stimulation

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28
Q

When does cartilage rings disappear from bronchi

A

When they enter the parenchyma—surrounded by alveolar tissue

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29
Q

Bronchioles (Branching)

A

Non cartilaginous conducting from 11-16th generation of branching
Respiratory bronchioles–17-19
Airway dependent on lung volume

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30
Q

Difference between lung volume dependence on airway diameter for bronchi and bronchioles

A

Bronchi–independent changes to airway diameter

Bronchioles–dependent on air volume

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31
Q

What divisions of the airway are dependent on systemic blood supply

A

1-16… Depend on bronchial circulation

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32
Q

Pulmonary artery and airways

A

Associated as they branch and they receive the venous drainage of the alveoli

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33
Q

First bronchioles to be part of gas exchange area

A

17, smooth muscles isolated areas and elastic fibers

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34
Q

Acinus

A

Terminal respiratory unit (17th-23rd)
Functional unit of the lung
Involved in gas exchange
Distal to terminal bronchiole, specifically, the respiratory bronchiole, alveolar duct, alveolar sac, and alveolus (23rd branch)
Squamous epithelium
Metabolic requirements are met by diffusion for O2
Metabolic for amino acids, glucose, etc–pulmonary capillary blood supply`

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35
Q

Acinus support

A

No ciliated epithelium

Relies on surrounding lung tissue (lung parenchyma) via tethering

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36
Q

Parasympathetics to bronchioles

Sympathetic so to bronchioles

A

Constriction to increase velocity of air movement– want to get debris to bigger airway–think coughing

Dilutions of airways to decrease resistance to airflow

All occurs via smooth muscle in airway walls

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37
Q

Local hypocapnia vs local hypercapnia

A

Local bronchiole radio construction, directing ventilation away from alveolar regions with poor perfusion

Hypercapnia or hypoxia causes bronchiolar dilation–airflow to alveolar regions with better perfusion

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38
Q

Causes of constriction of bronchi

A 
Parasympathetics 
Alpha adrenergic antagonists
Local irritants
Chemoreceptors activation
Increased air velocity
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39
Q

Dilation of broncholes

A

Sympathetic innervation
Beta 2 adrenergic ago it’s
Inhibition of phosphodiesterase (not breaking down CAMP, less Ca2+, relaxation)
Decreased airway resistance

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40
Q

Gas content of perfused vs non-perfused atmospheric air

A

Perfused–you will have high CO2, low O2

Non-perfused–high O2, low CO2

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41
Q

Alveoli

A

Small, polyhedral shaped sacs
Walls-type 1
Elastic and I elastic fibers and capillaries within alveolar walls
Thin barrier to diffusion
Largest biological membrane in the human body

Type II can differentiate to become type I

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42
Q

Macrophages

A

Only thing that can attack Bacteria at level of alveolus because alveoli do not have cilia

Migration to lymphatic system
Clean up phospholipase surfactant that is broken down

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43
Q

Pores of Kohn

A

Openings between alveoli to allow macrophage and Type II cells to move from one to the other
Gas exchange

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44
Q

Blood-Gas interface

A

Capillary surface area is nearly equal to alveolar surface area

Thin layer 0.2-0.5 microns thick

Epithelium, interstitial space, capillary endothelium, plasma, and erythrocytes membranes

RBC spends less than a second in alveolar capillary network
Most lung mass is blood in lung

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45
Q

Pulmonary circulation

A 
Pulmonary artery (deoxy)
Pulmonary capillaries (oxy)
Pulmonary veins (oxy blood mixed with deoxygenated blood from bronchial veins)
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46
Q

Right to left blood shunt

A

Blood flow drainage into the pulmonary veins from visceral pleura and airways
5% cardiac output
Pulmonary veins have less oxygen in them when they get to the heart than when they started right after the pulmonary capillaries due to venous to arterial right to left shunt

Pleural effusion (abnormal)

The vein (deoxy) from bronchial artery capillary system goes into the pulmonary being from pulmonary capillary

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47
Q

Bronchial circulation

A

Provide conducting airways with nutrients and oxygen

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48
Q

Pulmonary circulation resistance, pressure, compliance

A

Low resistance, low pressure, compliant system (15mmHg MAP)
Reduces work of right heart

Helps prevent flooding of alveoli
Decreases diffusion efficiency by increasing distance

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49
Q

Lung parenchyma–alveoli

A

I elastic fibrous network in the most peripheral airways, strong backbone

Elastic fibers–hold open non-cartilaginous supported bronchioles and alveolar ducts–tethering effect

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50
Q

Tethering effect

A

Elastic fibers holding open the non-cartilaginous supported bronchioles and alveolar ducts… Air diameter in the lung periphery is dependent upon lung volume

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51
Q

Composition of atmospheric Air

A
  1. 93% O2
  2. 04% CO2
  3. 03% N2
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52
Q

Partial pressure

A

Barometric pressure times fractional concentration of each gas
So, at the high altitude, total barometric pressure is less and the partial pressure are less

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53
Q

Partial pressure of PO2 at seas level

A

PB times FiO2 (Pressure barometric times fraction of O2 that is the whole) or 159 mmHg

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54
Q

Dalton’s Law

A

Each individual gas acts as if it occupies the total volume of the mixture and the pressure it exerts is proportional to its concentration
Dependent on the fraction that the gas of a particular species is in the gas mixture and the total pressure exerted by mixture

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55
Q

Reduction of PO2 by warming and humid flying

A

Go from 0.2093x 760 to 0.2093 times 713 to make up for the addition of water diluting the other inspired gases
The total pressure exerted by other inspired gases is now lower, lowering all of their partial pressures

Decreases from dry ambient air–160 to tracheal(inspired) at 150

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56
Q

Alveolar air PO2 and CO2

A

1) water vapor added as diluent
2) metabolism and gas exchange continue through both inspiration and expiration
3) volume of air inspired in a tidal breath is small compared to the volume of gas left in the lung at end-expiration

This is why pO2 decreases to 100 and CO2 increases to 40.

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57
Q

Difference between alveolar air and arterial blood

A

Normal inequalities of gas exchange and normal right to left shunting of blood
Bronchial and coronary circulation dump deoxygenated blood into oxygenated blood pathways present in right to left shunts (from pleura and airways)
Gravity on us, maldistribution of alveolar ventilation and pulmonary capillary perfusion within lungs

CO2 is essentially the same due to the large diffusivity of CO2 and the small a-v to CO2 gradient

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58
Q

Differences between PO2 and PCO2 between systemic arterial and mixed venous blood

A

Metabolism
Consumes the O2 to generate ATP and sustain life.
90% of CO2 is produced by metabolism in the venous side of systemic circulation,but this is transported as bicarbonate, not CO2, so that’s only a few mmHg higher

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59
Q

Numbers for changes of PO2 and PCO2 from ambient air, inspired air, alveolar air, arterial blood, and resting venous mixed blood

A

PO2- 160,150,100,90,40

PCO2–.3,.3,40,40,46

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60
Q

Resting Mixed venous blood

A

From 90 to 40 mmHg –5ommHG to tissue

From 40-46 mmHg–6 ml from tissue..due to bicarbonate

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61
Q

Two components of Gas exchange

A 
Ventilation (moving air into an out of alveolar regions) 
External respiration (gas diffusion across the alveolar-capillary membranes)
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62
Q

How do you measure VA (alveolar ventilation

A

VA=(TWV-DSV) X RR

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63
Q

Minute ventilation (VE)

A

Volume of gas entering the lungs per minute.

VT-RR

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64
Q

Oxygen delivery by cardiac output

A

Oxygen Delivery = CO (L/min) X Oxygen content of the blood (mL of O2)

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65
Q

LaPlace’s law

A

Pressure necessary to keep a sphere open is directly proportional to the surface tension and inversely proportional to the radius of the sphere

Pressure–negative pressure generated by the contraction of the diaphragm

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66
Q

IRV

A

Additional air that can be forcibly inhaled after the inspiration of normal tidal volume

67
Q

ERV

A

The maximum volume of air expired from the resting end-expiratory position (FRC)

68
Q

RV

A

The volume of air remaining in the lungs after maximum respiration

69
Q

Inspiratory capacity

A

IRV plus TV

70
Q

Vital capacity

A

The maximum volume of air expired from the point of maximum inspiration

71
Q

Inspiratory vital capacity

A

Maximum volume of air inspired from the point of maximum expiration

72
Q

FRC

A

Sum of RV (the plume of air remaining in the lungs after maximum expiration) and ERV (the volume of air expired from FRC)

73
Q

TLC

A

The sum of all volume compartments or the volume of air in the lungs after maximum inspiration

74
Q

What lung capacity and volumes increase with age? Decrease?

A

Decrease? ERV and VC

Increase? FRV and RV

75
Q

TLC=?

A

IRV+ERV+TV+RV

76
Q

FRC=?

A

ERV plus RV

77
Q

Muscle movements during inspiration

A

Diaphragm contracts, increasing longitudinal area of chest wall, expands until lower ribs elevated=limit of abdominal wall compliance

External intercostals fix anterior posterior area of thorax (oriented obliquely downward and anteriorly), raising ribs

Scalene–elevation of first 2 ribs, enlarging upper rib cage
SCM–anterior posterior thorax and increase thoracic volume

78
Q

Passive description of expiration

A

Recoil of elastic and I elastic structures of the lungs and surface forces
Elastic and inelastic fibers of lung parenchyma—lung volume back to FRC

Expansion of lungs alters attractive forces between fluid molecules, reduce alveolar volume.

79
Q

Muscles of expiratoin

A

Internal intercostals–obliquely downward and posteriorly, ribs downward and inward, decreasing anterior-posterior dominions
Abdominal muscles–pull down ribs and inward, compression of abdominal cavity, diaphragm upward into thoracic cavity, decreasing longitudinal distance

80
Q

Pathological decrease in lung recoil

A

Emphysema
Rl decreases, less opposition to Rcw–less Ppl (less negative, closer to atmosphere), chest wall move to a larger thoracic volume (unopposed)

New equilibrium is at a larger thoracic volume and a less negative intraplueral pressure

81
Q

Pathological increase in lung recoil

A

Pulmonary fibrosis

More Rl to oppose normal Rcw, more resistance, more negative Ppl, smaller volume in chest

82
Q

Inspiration and recoil

A

Increasing thoracic volume via muscle contraction leads to lung expansion through coupling with chest wall, Ppl more negative since elastic recoil of the lungs increases with lung expansion

Increase in thoracic volume results in a Decrease in pressure within the thorax–.>alveolar pressure, air moves down gradient

83
Q

Ppl and elastic recoil with lung expansion

A

Ppl more negative since elastic recoil of lung increase with lung expansion

84
Q

Ppl, elastic recoil, lung volume on expiratoin

A

Lung volume back to normal (FRC), decrease in thoracic and lung volume results in an increase of alveolar pressure, air from lungs into atmosphere
Relaxed breathing–Ppl still remains negative

Active expiration–Ppl can be positive with respect to atmosphere, compression of lung due to elastic and surface forces and chest wall movement.

85
Q

Alveolar pressure is zero?

A

End-inspiration and end-expiration

86
Q

Alveolar pressure on inspiration and expiration

A

Inspiration– negative

Positive–expiration

87
Q

Cl measurement, normal value

A

Distensibility of the lung (how easy or difficult to expand the lungs)
Volume of change produced by a unit of transpulmonary pressure change
200 ml/cm H20

88
Q

What what volume is the lung most compliant?

A

FRC

89
Q

Airway structure/geometric arrangement/inelastic/elastic at FRC

A

At FRC, collagen/fibrin and elastin are stretched to twice their resting length due to their geometry

Account for less than half of elasticity

90
Q

Hysteresis

A

More difficult to open previously closed airways on inflation from low volume (high surface tension) and likewise, airways that are open at high volumes (low surface tension) tend to stay open as pressure is reduced.

They are influenced by the history of the previous volume.
Due to the surface forces acting at the air-fluid interface

91
Q

Hysteresis is due to:

A

Surface forces within the lungs
Non-perfect elasticity of the lungs
Inertia of the lungs

92
Q

Addition of saline (hysteresis curve)

A

Elimination of surface forces…which means that surface forces act to make the lung stiffer or harder to inflate

93
Q

Surfactant in small alveoli vs large alveoli

A

Small alveoli, surfactant is packed to keep surface tension low and prevent collapse
Large alveoli, unpacking of surfactant so the surface tension is proportional to alveolar size.

Small surface tension is small alveoli, increase surface tension is larger alveoli

94
Q

A-a gradient is normal in situations of hypoxia:

A

Hypo ventilation

High altitude.. Low Fi inspired O2

95
Q

Hyperventilation effect on CO2

A

Decreases lower than normal (

96
Q

What causes airway obstruction in asthma? What produces relaxation (drug)?

A

Constricted bronchioles

Relaxation beta 2 adrenergic

97
Q

Volume of lungs during inspiration

A

FRC+TV

98
Q

ERV equation

A

ERV=VC-(TV+IRV)

99
Q

Intrapleural pressure and transpulmonary pressure at base vs apex

A

Intraplueral pressure is more negative and transpulmonary pressure is more positive at the top of the thorax because the lung is pulling away from the surrounding thoracic cage

100
Q

Pressure gradients for the 3 lung zones

A

Zone 1 PA>Pa>Pv (no perfusion)
Zone 2 Pa>PA>PV
Zone 3 Pa>PV>PA (high perfusion)

101
Q

Highest resistance airways

A

Medium sized bronchi

Early changes in resistance in alveoli are often unnoticed

102
Q

When Patm=PA, what is happening with airflow and where are the lungs at (Capacity)?

A

When Patm=PA there’s no airflow. No pressure gradient.

Lungs are in functional residual capacity

103
Q

Compliance of lung+chest wall vs lung OR chest wall

A

Compliance of lung or chest wall alone is greater than that of the combined system (slopes of curve steeper than individual slopes

104
Q

V/Q at base vs apex and PCO2 vs PO2 in capillaries

A

V/Q is higher in apex than at the base because the differences in ventilation aren’t as great as for perfusion, so more ventilation at apex
More ventilation at apex means higher PO2 in capillaries, lower PCO2 in capillaries
Base–less PO2, higher PCO2

105
Q

Stimulation of peripheral chemoreceptors

A

Carotid and aortic bodies, hypoexemia=hyperventilation

106
Q

Stimulation of central (medullary) chemoreceptors

A

CO2 or H+

107
Q

ventilation rate and O2 consumption during exercise

A

Ventilation rate increases ot match the increased O2 consumption and increased CO2 production
No change in mean PO2 or PCO2
Venous PCO2 increases
No increase in PCO2 of arteries because we have an increased ventilation to combat

108
Q

What occurs in the blood during transport of CO2 from tissues

A
  • -H2O joins CO2 to form H+ and bicarbonate
  • -H+ is buffered by deoxy heme
  • -acidification of RBCs
  • -bicarbonate out, Cl in.
  • -bicarbonate is carried into the lungs via plasma***
  • -CO2 binds directly to Hb, carbaminoHb
109
Q

Causes of decreased O2 in the blood

A
  • -decreased Hb concentration (anemia)
  • -decreased O2 binding capacity of Hb (CO poisoning)
  • -decreases arterial PO2 (Hypoxemia)
110
Q

Only form of hypoxia associated with an increased A-a gradient

A

Right to left shunt
Lack of O2 equilibration between alveolar gas and systemic arterial blood
Right heart output is not oxygenated in lungs and is thereby dilutes the PO2 of normal oxygenated blood.

111
Q

Hypoxia with a normal A-a gradient

A

High altitude, hypoventilation. Both alveolar and arterial PO2 are decreased

112
Q

Decreased PaCO2 and breathing

A

Result of Hyperventilation which increases pH, inhibition of breathing.

113
Q

Hyperventilation

A

Respiratory alkalosis

114
Q

FEV1, FEV1/FVC, and FEF25-75 for fibrosis and emphysema

A

FEV1– lower for both
FEV1/FVC–lower for emphysema, normal or increased for pulmonary fibrosis
FEF25-75–decreased in emphysema, increased or near normal in fibrosis

115
Q

Emphysema and Fibrosis comparisons for capacity and volumes

A

E- decrease Recoil, increase compliance, increase RV, increase FRC, increase TLC
F–increase recoil, decrease compliance, decrease RV, FRC, TLC

116
Q

Location of central chemosensitive regions

A

Ventral lateral medulla
Ventilators response to hypercapnia (increase PaCO2)
Minute to minute control of ventilation
Unaltered after denervatio now peripheral chemoreceptors

117
Q

Law of Laplace

A

P=2T/r pressure inside the alveolus
Without surfactant, this law states that the pressure inside small alveoli would be greater than that in large alveoli.
So small alveoli would empty into large alveoli and collapse

118
Q

Two forces that prevent alveolar flooding

A

Negative intrapleural pressure and surfactant

119
Q

Compliant work vs resistive work

A

Compliant–surface forces and elastic and inelastic forces

Resistive–flow-resistive and inertialyes forces of lung and chest wall

120
Q

Resistance to airflow in the respiratory system

A

R= 8nl/pi r^4

If airway is reduced by 1/2, the resistance increases 16 fold. If driving pressure doesn’t increase, airflow will be reduced by 16-fold

R=driving pressure/flow ratE

121
Q

Total airway resistance in inspiration vs expiration

A

Higher during expiration because during inspiration, tethering occurs
Airway resistance decreases, diameter increases on inspiration

122
Q

Major structures for airway resistance

A

Mouth/nasal cavity (20%)

Medium sized bronchi

123
Q

Effort and lung volumes/airflow rate

A

During expiration after lung volume is less than FRC heading toward RV, effort only compresses the airways more, increasing resistance to airflow. This is the effort-independent region.

Everywhere else, size of loop depends on effort

124
Q

Airflow rates for emphysema vs fibrosis

A

Emphysema– diminished peak expired airflow rates despite high lung volumes because of reduced lung recoil

Fibrosis–increased lung recoil but diminished peak expired airflow rates because of low lung volume

125
Q

Increasing effort at mid-low lung volumes

A

Increases intrapleural pressure, pressure gradient from alveolus to mouth increases–airflow

126
Q

Alveolar ventilation vs minute ventilation

A

Alveolar is always less than minute ventilation

The degree depends on the dead space fraction of the tidal volume and frequency of breathing

Increasing VT is a better increaser
If you increase dead space without increasing minute ventilation, you have a decreased alveolar ventilation

127
Q

Physiological dead space

A

Sum of anatomical dead space and volume of gas in non functioning alveoli

Ventilated but not perfused

Anatomical DS + 25% of Vt at rest

128
Q

Perfused but not ventilated

A

Right to left shunt

129
Q

Mixed expired CO2 and dead space

A

As you increase dead space, you decreases the amount of mixed expired CO2

130
Q

Hyperventilation and hypoventilation on O2 and CO2

A

hyper–Increases alveolar O2 while decreasing alveolar CO2

131
Q

Ventilation of basal vs apical alveoli based on gravity

A

Basal will be more ventilated than apical due to less transpulmonary pressure
Base is more compliant, so a lot of ventilation for a small pressure (less transpulmonary pressure allows this)

More transpulmonary pressure, larger alveoli==less compliant

132
Q

FRC, alveoli, compliance, transpulmonary pressure, apex

A

Greater transpulmonary pressure, greater dinstending pressure, alveoli are larger. Slide up the pressure-volume curve, region is less compliant and less ventilated

133
Q

Increase pulmonary vascular pressure

A

Decrease pulmonary vascular resistance due to recruitment of the capillaries opened by pressure increase and increase in individual capillary diameter

134
Q

Global hypoxia

A

Global vasoconstriction, pulmonary hypertension, increase workload on the right ventricle, pulmonary edema

135
Q

Alveolar blood vessels vs extra-alveolar blood vessels during inspiration

A

Alveolar–compressed during inspiration

Extra-alveolar–tethered open by lung parenchyma`

136
Q

Perfusion and ventilation at apex and base compared to each other

A

Perfusion is greater than ventilation at the base
Ventilation is greater than perfusion at the apex

Think 3 lung regions that are based on perfusion (not ventilation)

Basal alveoli will be better ventilated than apex

137
Q

PRG vs DRG

A

PRG is fine tuning, upper pons

DRG inspiratory to phrenic motor neurons and VRG (external and accessory respiratory muscles

138
Q

PRG

A
  • -bilateral upper pons
  • -fine tuning respiratory rate, switching from inspiration to expiration
  • -NPM and K-F
  • -modulates medullary centers responses to other stimuli
139
Q

Apneustic Area

A

Inspiratory gasps

Not part of PRG, but does have effect on inspiration

140
Q

Cut between PRG and apnuestic area

A

Increases Vt and decreases respiratory rate

Vagus nerve

141
Q

DRG

A

Ventral lateral NTS
Inspiratory neurons to phrenic motoneurons
Afferents from 9th and 10th cranial nerves
Integrate visceral sensory information to determine respiratory motor response or drive
To I neurons of the VRG

142
Q

Interneurons from DRG to VRG

A

Elicit increased activity in non-phrenic inspiratory muscles

143
Q

VRG

A

Inspiratory and expiratory neurons
Expiratory–internal intercostals and abdominal

Inspiratory–external intercostals, accessory, and phrenic

Inhibitory expiratory neurons prevent inspiratory discharge during expiration

144
Q

Mechanism for carotid chemoreceptors

A

Hypoxia, hypercapnia, and acidosis inhibit K+ channels, depolarizing cells, increasing glom us Ca, inducing transmitter release, and stimulating afferent fiber

145
Q

What stimulates peripheral chemoreceptors

A 
Decreased Ocygen (hypoxia or Hypoxemia)
Hypercapnea
Acidosis

Increase firing rate to increase ventilation

Accute response to hypoxia, metabolic acidosis or alkalosis,

146
Q

Location of CCR

A

Ventrolateral medulla

147
Q

CCR detect?

A

Changes in CO2 and H+

Hypercapnia

Minute to minute control of ventilation

H+ in intersitial fluid–hypoxia (anaerobic metabolism)

148
Q

Moderate brain Hypoxemia vs severe brain Hypoxemia

A

Moderate–switch to anaerobic metabolism, lactic acid and H+ formation, stimulation of breathing

Severe–depressed breathing.

149
Q

Affects of arterial hypercapnia and arterial blood pH on CSF

A

Not a lot of buffer proteins (only buffer is bicarbonate), arterial hypercapnia leads to a greater change in CSF pH than arterial blood pH because H+ cannot diffuse through the membrane like CO2 which becomes hydrated

150
Q

How does CSF restore pH

A

Active transport of bicarbonate from blood to CSF

Low CO2, bicarbonate goes from CSF to blood

151
Q

Pulmonary stretch receptors

A

Mechanoreceptors
Stimulated by distension of the lungs
Activation causes inhibition of inspiratory activity to prevent hyperventilation
Hering-Breuer inflation reflex
To PSR increased Vt,decreased breathing rate

152
Q

RARs

A

Irritant receptors
Between airway epithelial cells, vagus nerve
Noxious gases, dust, smoke, cold air, and rapid volume changes
Hyperventilation, bronchostriction, coughing

153
Q

C-fibers

A

Alveolar-capillary interstitial space, bronchi
Non-myelinated vagus
Distension or congestion
Bronchoconstriction, rapid, shallow breathing, and increased mucous secretion into airways (turbulant airflow)

154
Q

Hypoxic Hypoxemia

A

Less than normal PO2 in inspired air, decreased O2 in plasma, stimulation of breathing

155
Q

Anemic Hypoxemia

A

Carotid bodies uneffected, normal PO2
CO poisoning
If severe enough, anaerobic metabolism, metabolic acidosis, increased ventilation

156
Q

Stagnant hypoxia

A

Low blood flow, anaerobic metabolism, CB stimulated due to metabolic acidosis increasing firing rate, increasing ventilation

157
Q

Histotoxic hypoxia

A

Low ATP production, blocking ETC of ATP (CN)
Anaerobic metabolism, acidosis, stimulation of breathing,

CBs respond as if there’s not O2

158
Q

Ventilation PO2 and PCO2

A

You must decrease PO2 by 50% to produce a doubling in ventilation

Increase PCO2, you increase ventilation at a much higher PO2 than you would with a normal PCO2(40)

You only have to increase PCO2 by 5mmHg (10%) to get a doubling of ventilation

159
Q

At any PCO2, what is the relationship between CO2 and ventilation if pH is changed

A

If the pH is decreased, ventilation will increase. Addind acidosis increases ventilation, but does not change the sensitivity of CO2.

Changing arterial pH does change ventilators threshold. If you are acidotic, you begin to breath at a lower CO2 than under normal conditions

160
Q

Ventilatory sensitivity to CO2 in response to CO2 and O2

A

Change CO2, sensitivity doesn’t change
Change O2, sensitivity is altered (increasing PO2 decreases the carotid bodies sensitivity to elevated CO2)

Threshold is unchanged by CO2 but changed by PO2

161
Q

High Altitude

A

Reduced PaO2, normal A-a, normal PaCO2 unless O2 drops below 60mmHG

162
Q

Alveolar hypoventilation

A

Reduced PAO2 and PaO2
Normal A-a
Increased PaCO2

163
Q

Diffusion impairment

A

Normal PaO2 but increased diffusion barrier leads to reduced PaO2
Widened A-a
Nml (CO2 isn’t diffusion limited)or reduced PaCO2 (reduced if the hypoxia stimulates breathing)

Causes- thickening of alveolar-capillary gas barrier, decreased in ST, and pulmonary capillary transit time (ncreased flow)

164
Q

Right to left shunt

A 
Perfused but not ventilated
Bronchial and coronary circulation
Dependent on shunt fraction of cardiac output, mixed venous O2 content, and O2-Hb dissociation curve 
Increased PaCO2
Widened A-a
Normal PA, abnormal PaO2

NBS1 (9 decks)

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