Ch. Eleven: Respiratory System Flashcards

1
Q

External Respiration

A

4 steps:
1. Ventilation: movement of air into and out of lungs
2. O2 and CO2 exchange between air in alveoli and blood within the pulmonary capillaries
3 & 4. blood transports O2 and CO2 exchanged between tissues and blood by diffusion across systemic capillaries

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2
Q

Internal Respiration

A
  • cellular respiration: metabolic processes within mitochondria
  • respiratory quotient (RQ): ratio of CO2 produced to O2 consumes; varies depending on foodstuff consumed
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3
Q

Nonresp. Functions of Resp. System

A
  • route for water loss and heat elimination
  • enhances venous return
  • helps maintain normal acid-base balance
  • enables speech, singing, ect
  • defends against inhaled foreign matte; cilia, mucous, macrophages
  • removes, modifies, activates, or inactivates various materials passing through the pulmonary circulation
  • nose serves as the organ of smell
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4
Q

Lungs

A
  • occupy most of the thoracic cavity
  • 2 lungs divided into several lobes, each supplied by one of the bronchi
  • highly branched airways, the alveoli, the pulmonary blood vessels, and large quantities of elastic connective tissue
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5
Q

Respiratory Airways

A
  • tubes that carry air between the atmosphere and the air sacs
  • nasal passages
  • pharynx- trachea
  • larynx
  • right and left bronchi
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6
Q

Bronchoiles

A
  • no cartilage to hold them open
  • walls contain smooth muscle innervated by ANS
  • sensitive to certain hormones and local chemicals
  • alveoli are clustered at ends of terminal bronchioles
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7
Q

Conducting Zone

A
  • trachea and larger bronchi
  • fairly rigid, nonmuscular tubes
  • rings of cartilage prevent collapse
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8
Q

Respiratory Zone

A
  • bronchioles
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9
Q

Alveoli

A
  • thin-walled inflatable sacs; gas exchange and large surface area
  • walls consist of a single layer of cells: TYPE 1
  • pulmonary capillaries encircle each alveolus
  • TYPE 2 alveolar ells secrete surfactant
  • alveolar macrophages guard lumen
  • pores of Kohn permit airflow between adjacent alveoli (collateral ventilation)
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10
Q

Chest Wall

A
  • outer chest wall (thorax)
  • formed by 12 pairs of ribs
  • rib cage protects the lungs and heart
  • contains the muscles involved in generating the pressure that cause airflow
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11
Q

Main Inspiratory Muscles

A
  • diaphragm: dome-shaped sheet of skeletal muscle separates thoracic cavity from abdominal cavity, innervated by phrenic nerve
  • external intercostal muscles: innervated by intercostal nerve
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12
Q

Lungs

A
  • pleural sac (serosal membrane): double-walled, closed sac
  • pleural cavity
  • intrapleural fluid: secreted by surfaces of the pleura, lubricated pleural surfaces
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13
Q

Resp. Mechanics

A
  • interrelationships among pressures inside and outside the lungs are important in ventilation
  • 4 different pressure considerations important in ventilation:
    1. atmospheric pressure
    2. (intra)Alveloar pressure
    3. (Intra)pleural pressure
    4. Transpulmonary pressure: inside pressure-outside pressure
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14
Q

Pressures Important in Ventilation

A
  • resp. pressure are always relative to atmospheric pressure!
  • measured in mmHg, cmH2O, atmopsheres (atm)
  • sea level= 760mmHg or 1 atm or 1034 cmH2O
  • higher altitudes = less pressure
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15
Q

Transumral Pressure Gradient

A
  • lungs are highly distensible and have elastic recoil
  • thoracic wall is more rigid, but recoils outward
  • transmural pressure: inside pressure-outside pressure
  • keep lung and chest wall together
  • pleural sac always has subatmospheric pressure
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16
Q

Source of the Lungs Elastic Recoil

A
  • how readily the lungs rebound after having been stretched
  • responsible for lungs returning to their preinspiratory volume when inspiratory muscles relax at end of inspiration
  • depends on 2 factors:
    1. highly elastic connective tissue in the lungs; “stretchability”
    2. alveolar surface tension:
  • thin liquid film lines each alveolus, reduces tendency of alveoli to recoil, helps maintain lung stability (newborn resp. distress syndrom)
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17
Q

Alveolar Surface Tension

A
  • water lines alveoli creates surface tension
  • resists alveoli expansion- less compliant
  • tends to shrink alveoli- recoil
  • lungs would collapse if only water lined alveoli
  • smaller the alveoli, greater the surface tension= collapse
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18
Q

Pulmonary Surfactant

A
  • pulmonary surfactant reduces surface tension
  • reduces cohesive force between water molecules
  • deep breathing increases secretion by stretching type 2 cells
  • complex mixture of phosolipids and proteins secreted by type 2 alveolar cells
  • disperses between the water molecules in the fluid lining the alveoli and lowers alveolar surface tension
  • 2 important benefits:
    1. reduces work of the lungs
    2. reduces recoil pressure of smaller alveoli more than larger alveoli
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19
Q

Lack of Pulmonary Surfactant

A
  • huge problem for babies, especially those born prematurely
  • infant resp. distress syndrome (IRDS) or resp. distress syndrome of the newborn (RNSD)
  • too little surfactant allows the alveoli to collapse and then they have to re-inflate every time (huge energy drain)
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20
Q

Pulmonary Surfactant (in uetero)

A
  • normally surfactant is not made until the last two months in utero
  • give mother steroid to help stimulate production
  • but in most emergency births this is not possible so the baby is put on a ventilator
  • artificial surfactant can help
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21
Q

Alveolar Interdependence

A
  • contributes to alveolar stability
  • alveoli connected to each other by connective tissue
  • if an alveolus starts to collapse, neighbouring alveoli resist by recoiling
  • exert expanding force on the collapsing alveolus
  • “tug of war” between neighbouring alveoli
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22
Q

Pneumothorax

A
  • demonstrates the elastic recoil of the lungs
  • thoracic wall springs outward
  • importance of pleural pressure to keep lungs inflated
  • abnormal condition of air entering the pleural space:
  • both pleural and alveolar pressure no equal atm, so pressure gradient no longer exists across lung wall or chest wall
  • with no opposing neg. pleural pressure to keep inflated, lung collapses to its unstretched size
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23
Q

Boyle’s Law

A
  • pressure exerted by a gas varies inversely with the volume of gas
  • P1V1= P2V2
  • during respiration the volume of lungs is made to change
  • drive air flow into or out of the lungs
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24
Q

Changes in Alveolar Pressure

A
  • produce flow of air into and out of lungs

- if alveolar pressure is less than atmospheric pressure= air enters the lungs

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25
Q

How are changes in lung dimensions brought about?

A
  • by altering lung volume:
    pressure changes in the lungs and air flow is generate
  • respiratory muscle activity change volume of thoracic cavity
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26
Q

Inspiratory Muscles

A
  • diaphragm:
    major inspiratory muscles; 75% of thoracic volume change at rest
  • external intercostal muscle
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27
Q

Onset of Inspiration

A
  • expansion during inspiration decreases the intra-pleural pressure
  • lungs are drawn into this area of lower pressure
  • lungs expand
  • this increase in volume lowers the intra-alveolar pressure to a level below atmospheric pressure (Boyle’s Law)
  • air enters the lungs
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28
Q

Onset of Expiration

A
  • relaxation of diaphragm and muscles of chest wall, plus the elastic recoil of the alveoli, decrease the size of the chest cavity
  • inter-pleural pressure increases and lungs are compressed
  • intra-alveolar pressure increases as air molecules are in smaller volume
  • forced expiration can occur by contraction of expiratory muscles: abdominal wall muscles and internal intercostal muscles
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29
Q

Air Flow and Airway Resistance

A
  • air flow dependent on pressure differences and airway resistance
    *remember blood flow regulation!
    F= P/R
  • flow is proportional to the pressure difference between two points and inversely proportional to the resistance
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30
Q

ANS Influence on Resistance

A
  • primary determinant of resistance to airflow is radius of conducting airway
  • ANS controls contraction of smooth muscle in walls of bronchioles
  • both branches of ANS act on airway smooth muscle:
    1. SNS causes bronchodilation: NE and Epinephrine (more important)
    2. ONS causes bronchoconstriction: ACh
  • other neural inputs
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31
Q

Factors Affecrting Airway Resistance

A

bronchoconstriction: allergy-induced spasm and histamine; physical blockage of airways; neural control and local chemical control (decrease CO2)
bronchodilation: neural control, hormonal control and local chemical control (increase in CO2)

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32
Q

Under Healthy Conditions…

A
  • airway resistance is much less than in cardiovascular system under healthy conditions
  • but in disease states the narrow airways: flow can be severely restricted OR work harder to breathe
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33
Q

Chronic Pulmonary Disease

A
  • abnormally increases airway resistance
  • expiration is more difficult than inspiration
  • diseases affecting airway resistance:
  • chronic bronchitis, emphysema, and asthma
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34
Q

Asthma

A
  • due to:
    1. thickening of airway walls brought by inflammation and histamine induced edema
    2. plugging of airways by excessive secretion of very thick mucous
    3. hyper-responsiveness, constriction of smaller airways resulting in spasm of smooth muscle in their walls (allergens and irritants)
35
Q

COPD (chronic Obstructive Pulmonary Disease)

A
  • 80% of cases caused by cigarette smoke
  • other chemicals- asbestos or coal dust
  • smooth muscle contraction IS NOT the cause of obstruction
  • slowly damages airways
36
Q

Chronic Bronchitis

A
  • long-term inflammatory condition of smaller airways
  • prolonged exposure to smoke, allergens, ect.
  • narrowed by edematous thickening of airway linings and thick mucous
  • cannot remove mucous by couching
  • bacterial infections occur because of mucous accumulation
37
Q

Emphysema (COPD)

A
  1. breakdown of alveolar walls
  2. collapse of smaller airways
    - arises from: excessive release of destructive enzymes such as trypsin from macrophages as a defense mechanism
38
Q

Lung Volumes

A
  • max volume of lungs: male= 5.7L and women= 4.2L
  • at rest, lungs contain about 2.2L after expiration- still half-full
  • air remains in alveoli to continue gas exchange
  • about 500mL/breath
  • spirometer consists of an air-filled drum floating in a water-filled chamber
  • measures the volume of air breathed in and out
  • spirogram is a graph that records inspiration and expiration
39
Q

Spirogram

A
  • lung volumes and capacities
  • capacities are the sum of 2 or more lung volumes
  • cannot measure the total lung volume with a spirometer as cannot empty lungs
40
Q

Lung Volumes and Capacities can be determined by:

A

Tidal Volume: volume of air entering or leaving lungs during a single breath (500mL)

Inspiratory reserve volume: extra volume of air that can be max inspired over and above the typical resting tidal volume (3000mL)

Expiratory reserve volume: extra volume of air that can be actively expired by maximal contraction beyond the normal volume of air after a resting tidal volume (1000mL)

Residual volume: min volume of air remaining in the lungs even after a maximal expiration (1700mL)

Function residual capacity: volume of air in lungs at end of normal passive expiration (2200mL)

Vital Capacity: max volume of air that can be moved out during a single breath following a max inspiration (4500mL)

Total lung Capacity: max volume of air that the lungs can hold (5700mL)

41
Q

2 general categories of respiratory dysfunction give abnormal spirometry resultes

A
  1. Obstructive Lung Disease:

- increased airway resistance: FEV1

42
Q

Respiratory Dysfunction

A
  • additional conditions affecting respiratory function:
    1. diseases affecting diffusion of O2 and CO2 across pulmonary membranes
    2. reduced ventilation due to mechanical failure
    3. failure of adequate pulmonary blood flow
    4. ventilation/perfusion abnormalities involving a poor matching of air and blood so that efficient gas exchange does not occur
43
Q

Pulmonary Ventilation

A
  • pulmonary ventilation= minute ventilation
  • volume of air breathed in and out in one minute

pulmonary ventilation= tidal volume x respiratory rate
(6000) = (500) x (12)

44
Q

Alveolar Ventilation

A
  • more important than pulmonary ventilation
  • volume of air exchanged between the atmosphere and the alveoli per minute
  • less than pulmonary ventilation due to anatomic dead space
  • volume of air in conducting airways that is useless for exchange
  • averages about 150mL in adults

alveolar ventilation = (TV-dead space) x respiratory rate

45
Q

Alveolar Ventilation (local controls)

A
  • act on smooth muscle of airways and arterioles to match airflow to blood flow
  • accumulation of carbon dioxide in alveoli decreases airway resistance leading to increased airflow
  • increase in alveolar oxygen concentration brings about pulmonary vasodilation, which increases blood flow to match larger airflow
46
Q

Work of Breathing

A
  • normally requires 3% of total energy expenditure for quiet breathing
  • work of breathing is increased in the following situations:
    1. when pulmonary compliance is decreased (fibrosis)
    2. when airway resistance is increased (COPD)
    3. when elastic recoil is decreased (emphysema)
    4. when there is a need for increased ventilation
47
Q

Gas Exchange

A
  • simple diffusion of O2 and CO2 down partial pressure gradients
  • pulmonary capillaries
  • systemic tissue capillaries
  • until partial pressures are equilibrated
48
Q

Partial Pressures

A
  • partial pressure exerted by each gas in a mixture equals the total pressure times the fractional composition of this gas in the mixture
49
Q

Additional Factors that affect the rate of gas transfer

A
  • as surface area increases, the rate increases (eg. exercise- blood flow and stretch of alveoli)
  • increase in thickness of barrier separating air and blood decreases rate of gas transfer
  • rate of gas exchange is directly proportional to the diffusion coefficient for a gas
50
Q

Alveolar Gas VS Dry Air

A
  • addition of water vapour in airways= 47mmHg

- dilutes all gases by 47 mmHg: PO2= 150mmHg

51
Q

Alveolar Gases

A
  • alveolar air is mixed with large volume of old air remaining in lungs + dead space at end of expiration
  • FRC= 2.2L
  • humidification + small turnover = 100 mmHg
  • less then 15% of the air in the alveoli is fresh air
52
Q

Partial Pressure Gradients of Oxygen and Carbon Dioxide

A

in lungs:

  • O2 diffuses from alveoli to pulmonary capillaries
  • CO2 diffuses from pulmonary capillaries to alveoli
  • blood leaves high in O2, low in CO2

in tissues:

  • O2 diffuses from capillaries to tissue cells
  • CO2 diffuses from tissue cells to capillaries
  • blood leaves low in )2, high in CO2
53
Q

O2 Gas Transfer

A
  • blood spend about .75 sec in a capillary
  • .25 sec required for equilibration, enough time for gas equilibration
  • .4 sec blood transit time during exercise
  • in decreased states )2 equilibration is more impaired than CO2 due to larger CO2 diffusion coefficient
  • at rest diffusion may be sufficient but during exercise transit time may be too quick
54
Q

Effect of SA and Membrane Thickness on Gas Exchange

A
  • inadequate gas exchange can occur when the thickness of the barrier separating the air and blood is pathologically increased
  • as thickness increases, the rate of gas transfer decreases:
  • emphysema, pulmonary oedema, pulmonary fibrosis, pneumonia
55
Q

Local Control of Air/Blood Flow

A
  • lung tissues match airflow to blood supply in region
  • bronchiole SM: respond to CO2
  • effects of CO2 on bronchiolar smooth muscle: dilation/constriction of airway and increased/decreased airflow
    (ia alveolar Pc02 falls, bronchoconstricition to that region diverting ventilation to other lung regions with higher Pc02)
  • pulmonary arteriole SM: respond to O2
  • effects of )2 on pulmonary arteriolar smooth muscle: vasoconstriction.dilation of blood vessels and reducing/increasing blood flow
    (if pressure falls- causes vasoconstricition to that region diverting blood to other better ventilated regions)
56
Q

Local Control on Smooth Muscle of Airways/Arterioles

A
  • accumulation of CO2 in alveoli: relaxes bronchiole SM and decreased airway resistance leading to increased airflow
  • increase in alveolar O2 concentration: pulmonary blood vessel dilate and increases blood flow to match larger airflow
57
Q

Arterial Blood Gases

A
  • normal values: 100mmHg

- body consumes about 250mL per minute under normal conditions

58
Q

Gas Transport

A
  • most O2 in the blood is transported bound to hemoglobin
    Hb+02=HbO2
    (reduced or deoxyhemoglobin) (oxyhemoglobin)
  • carries 98.5% of O2
59
Q

Gas Transport in Lungs and Tissues

A

Lungs:

  • hemoglobin + O2 converted to oxyhemoglobin
  • small percentage of O2 dissolves in the plasma

Tissues:

  • oxyhemoglobin is converted hemoglobin + O2
  • oxygen leaves the systemic capillaries and enters tissue cells
60
Q

PO2 and Haemoglobin Saturation

A
  • each molecule can carry up to 4 O2 molecules
  • PO of blood most important factor in determining % Hb saturation
  • when blood PO increases (pulmonary capillaries) the reaction is driven toward that right, increasing the formation of HbO2
  • when blood PO decreases as in systemic capillaries, the reaction is driven to the left
61
Q

O2 Hemoglobin Dissociation Curve (partial Pressure)

A
  • partial pressure of oxygen is main factor determining the % of hemoglobin saturation
  • %Hb saturation is high where the partial pressure of O2 is high (lungs)
  • % Hb saturation is low where the partial pressure of oxygen is low (tissue cells)
  • at the tissue cells oxygen tends to dissociate from hemoglobin, the opposite of saturation
62
Q

O2 Hemoglobin Dissociation Curve

A
  • not a linear relationship
  • plateau phase: good margin of safety
  • where the partial pressure of oxygen is high (lungs)
  • steep phase: at the systemic capillaries, where hemoglobin unloads oxygen to the tissue cells
63
Q

Other Influences on the O2-Hb Curve

A

CO2:
- shifts to the right, less oxygen binds to Hb
- increases in systemic capillaries as CO2 diffuses down its gradient from the cells to blood
Acid:
- shifts cure to the right, from carbonic acid
Temperature:
- shifts to the right enhancing release of O2
2,3-Biphosphoglycerate:
- factor inside RBCs; shifts to the right in both lungs and systemic (can decrease ability to load oxygen in lung)

64
Q

Bohr Effect

A
  • CO2 producing H+ and other sources of H+
  • pH change surrounding Hb molecules in RBC
  • decreased pH leads to more O2 releases from Hb at a given PO2 level
  • shift Hb saturation curve to right
65
Q

Haldane Effect

A
  • increase in PCO2 leads to less O2 bound to Hb
66
Q

Carbon Dioxide Transport

A
  • travels in 3 ways:
    1. physically bound: 5-10%
    2. bound to haemoglobin: 5-10%
    3. as bicarbonate: 80-90%
67
Q

CO2 transport (Bicarbonate)

A
  • CO2 combines with water to form carbonic acid
  • enzyme carbonic anhydrase facilitates this in erythrocyte
  • carbonic acid dissociates into hydrogen ions an the bicarbonate ion
68
Q

CO2 Transport (summary)

A
  • about 10% of CO2 is bound to hemoglobin in the blood

- about 10% of the transported CO2 is dissolved in the plasma

69
Q

CO2 Transport (CL- Shift)

A
  • exchange of Cl- in for HCO3- out
  • bicarbonate-chloride carrier that facilitates diffusion of ions in opposite directions across membrane: HCO3 but not H+ diffuses down
  • Chloride ions go in to restore electrical neutrality
70
Q

Hypoxia

A
  • condition of having insufficient O2 at the cell level
  • categories:
    1. hypoxic hypoxia: low arterial PO2
  • respiratory malfunction
  • low environmental O2 (high altitude, suffocation)
    2. Anemic hypoxia: reduced O2-carrying capacity of the blood despite normal PO2 levels
  • reduced RBC or Hb
  • CO poisoning
    3. Circulatory hypoxia: delivery of O2 to tissues is insufficient
  • local (vascular spasm)
  • congestive heart failure
  • circulatory shocl
    4. Histotoxic hypoxia: cells cannot use O2 despite normal O2 delivery
  • cyanide poisoning (blocks electron transport chain in mitochondria)
71
Q

Hyperoxia

A
  • condition of having above-normal arterial Po2
  • can only occur when breathing supplemental O2 (cannot occur when at sea level)
  • modest effect on O2-carrying capacity of the blood in non-disease states
  • in pulmonary diseases with reduced arterial PO2 can improve O2 gradient from alveoli to blood
  • can be dangerous: in brain and retinal damage possibly leading to blindness
72
Q

Hypercapnia

A
  • condition of having excess CO2 in arterial blood
  • caused by hypoventilation or lung disease
  • respiratory acidosis (remember the chemical reaction involving CO2)
73
Q

Hypocania

A
  • below normal arterial PCO2 levels
  • respiratory alkalosis
  • brought about by hyperventilation which can be trigger by: anxiety, fever, or aspirin poisoning
74
Q

Control of Respiration

A
  • respiratory centers in the brain stem establish a rhythmic breathing pattern (no automicity in muscle)
  • medullary respiratory centre
    1. dorsal respiratory group (DRG): mostly inspiratory neurons
    2. ventral respiratory group (VRG): inspiratory and expiratory neurons (when increased ventilation is required
75
Q

Pre-Botxinger Complex

A
  • widely believed to generate respiratory rhythm
76
Q

Influenced from Higher Cortex

A
  1. Pneumotaxic centre
    - sends impulses to DRG that help :switch off” inspiratory neurons- “fine tuning”
    - dominated over apneustic centre
  2. Apneustic centre
    - prevents inspiratory neurons from being switched off
    - provides extra boost to inspiratory drive
77
Q

Influence of Chemical Factors on Respiration

A

decreased PO2: activated only when arterial PO2

78
Q

Peripheral Chemoreceptors

A
  • carotid bodies
  • aortic bodies
  • are not sensitive: afferent nerves stimulated
79
Q

Effect of Arterial PCO2 on Ventilation

A
  • peripheral - H+ detection

- normally less important compared to central PCO2

80
Q

Effect of Arterial pH on Ventilation

A
  • peripheral - H+ detection
  • important when H+ from other, non-respiratory sources
  • a rise in arterial H+ concentration reflexly stimulates ventilation by means of the carotid chemoreceptors
81
Q

Effect of PCO2 on Ventilation

A
  • most important regulator of ventilation
  • increase in PCO2 stimulates respiratory centre to increase ventilation
  • decrease in PCO2 reduces respiratory drive
  • central chemoreceptors: near respiratory centre
  • 70% of increased ventilation which decreases arterial PCO2
82
Q

Arterial PCO2 on Ventilation

A
  • pH of arterial blood can change due to situations that change PCO2
  • ventilation changes via peripheral chemoreceptors
  • respiratory change
  1. Respiratory acidosis: pH decreases (increased H+)
    - ventilation cannot change (cause of the problem) COPD
  2. Respiratory alkolosis: pH increases (decreased H+)
    - eg. hyperventilation
83
Q

Arterial H+ and Ventilation (other than change in PCO2 factors)

A
  • pH of arterial blood can change due to situations other than change in PCO2
  • ventilation changes via peripheral chemoreceptors
  • metabolic change
  1. Metabolic acidosis: pH decreases (increased H+)
    - response is to increase ventilation
    - lactic acid, diarrhea
  2. Metabolic alkolsis: pH increases
    - response is to decrease ventilation
    eg. vomiting