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
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
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
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
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
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
7
Q
Conducting Zone
A
- trachea and larger bronchi
- fairly rigid, nonmuscular tubes
- rings of cartilage prevent collapse
8
Q
Respiratory Zone
A
- bronchioles
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)
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
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
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
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
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
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
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)
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
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
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)
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
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
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
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
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
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
26
Q
Inspiratory Muscles
A
- diaphragm:
major inspiratory muscles; 75% of thoracic volume change at rest - external intercostal muscle
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
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
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
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
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)
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
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
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
- breakdown of alveolar walls
- 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
- 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
- Pneumotaxic centre
- sends impulses to DRG that help :switch off” inspiratory neurons- “fine tuning”
- dominated over apneustic centre - 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
- Respiratory acidosis: pH decreases (increased H+)
- ventilation cannot change (cause of the problem) COPD - 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
- Metabolic acidosis: pH decreases (increased H+)
- response is to increase ventilation
- lactic acid, diarrhea - Metabolic alkolsis: pH increases
- response is to decrease ventilation
eg. vomiting
