Chapter 13 - The Respiratory System Flashcards
Respiratory System Function(s) - Respiration
-gas exchange: supply O2 and eliminate CO2
External Respiration
-entire sequence of events in the exchange of O2 and CO2 between external environment and body cells
Steps on External Respiration
- Breathing (ventilation): movement of air in and out of the lungs between atmosphere and alveoli, regulated according to bodily need for O2 uptake or CO2 removal
- O2 diffusion: O2 diffuses from alveoli into the blood within pulmonary capillaries (CO2 moves in the opposite direction)
- Transport: blood transports O2 from the lungs to tissues and CO2 moves in the opposite direction
- Tissue Exchange: O2 and CO2 exchanged between blood and tissues by diffusion across systemic capillaries
Non-respiratory Respiratory System Functions
-water loss
-heat elimination
-enhancing venous return
-maintain acid-base balance
-vocalization
-defence against foreign matter
-removes substances through pulmonary circulation
-smell
-pressure needed during child birth and defecation
-blood reservoir
Lungs
-two lungs
-divided into several lobes, each supplied by a bronchi
-occupy most of the thoracic cavity
-highly branched airways
-alveoli
-pulmonary blood vessels
-elastic connective tissue
Pharynx
-airway/throat
-common passageway for respiratory and digestive systems
Trachea
-windpipe
Larynx
-voice box
Role of Skeletal Muscles in the Airway
-change the diameter of the larynx and pharynx to prevent aspiration of food into the lungs
-vocalization
-resistance to airflow
Bronchioles
-have no cartilage to hold them open
-walls have smooth muscle innervated by ANS
-sensitive to hormones and local chemicals
Alveoli
-air sacs
-clustered at the ends of terminal bronchioles
-have no muscles to inflate or deflate them (this would interfere with diffusion)
-changes in volume result from dimensional changes in the thoracic cavity (diaphragm, intercostal muscles, abdominal muscles)
Airways
-carry air between atmosphere and alveoli
-begin at nasal passage (nose), pharynx, larynx, trachea (also divides into esophagus)
Preventing Food From Entering Airways
-epiglottis
-skeletal muscle, reflex mechanism closes trachea during swallowing
-esophagus stays closed except during swallowing
-this function originates in the brain stem
Vocal Folds
-two bands of elastic tissue
-lie across larynx opening
-vibrate to produce sounds as air passes them
-also prevent food aspiration
Cartilage Rings
-line trachea and larger bronchioles to ensure airways always remain open
Where does the transition from convection to diffusion occur?
-starts at the respiratory bronchioles
Convection
-requires energy
-produced by muscles that generate flow
Convection Zone
-made up of trachea and larger bronchi
-rigid, non-muscular tubes
-cartilage rings prevent collapse
-no gas exchange occurs here
Diffusion
-doesn’t require energy
Diffusion Zone
-bronchioles
-no cartilage to hold them open
-smooth muscle (ANS) control diameter
Type I Alveolar Cells
-alveolar walls
-single layer of flattened cells
Type II Alveolar Cells
-secrete pulmonary surfactant
Alveolar Macrophages
-guard lumen
-start as a monocyte
-use phagocytosis to guard and clean areas
What mechanisms ensure diffusion is rapid and complete?
-walls of alveoli are only one cell thick
-interstitial space between alveoli and capillaries is super thin
-alveolar surface are is very large
Pores of Kohn and Collateral Ventilation
-gaps between adjacent alveoli that permit airflow between adjoining alveoli (collateral ventilation)
-allow fresh air to enter when terminal conducting airway is blocked due to disease
Chest Wall
-formed by 12 pairs of ribs
-sternum (ribs 1-7) protects anteriorly
-thoracic vertebrae protect posteriorly
-ribs protect lungs and heart
Intercostal Muscles
-muscles in the rib cage
-generate pressure that causes airflow
Muscles of Inspiration
-external intercostals (contracting)
-diaphragm (flat)
-sternocleidomastoid
-scalenes
-parasternal intercostals
Diaphragm
-large sheet of skeletal muscle
-major inspiratory muscle
-forms the floor of the thoracic cavity (separates from abdominal cavity)
-penetrated by esophagus and blood vessels
-innervated by phrenic nerves
-responsible for 75% of volume change at rest
-relaxed/exhale = dome shape
-contracted/inhale = flat
Muscles of Expiration
-internal intercostals
-external abdominal oblique
-internal abdominal oblique
-transverse abdominis
-rectus abdominus
External Intercostal Muscles
-innervated by intercostal nerve
-lift the rib cage up and out
-enlarge thoracic cavity
-aid in inspiration
Internal Intercostals
-used during exhalation
Expiratory Muscles During Activity
-most of the muscles are inactive during rest or in healthy individuals
-activated during activity when ventilation demands increase
-also during coughing, sneezing, vomiting
-**generate higher pressures than inspiratory muscles
Pleural Sac (serosal membrane)
-double walled
-closed sac
-separated each lung from thoracic wall
-prevents friction
-secrete fluid
-allows organs to move past each other
Visceral Pleura
-cover the lung and other internal structures
Parietal Pleura
-lines the inside wall of the thorax
Pleural Cavity
-lines the space between the visceral and parietal pleura
-contains fluid
Intrapleural Fluid
-lubricates the surfaces of the two membranes
-secreted by pleural surfaces
Pressure Gradient
-what airflow depends on
-flow = ΔP/R
-used to overcome elastic stiffness of the respiratory system
-for flow to occur, the pressure in the alveoli must be less than the pressure at the mouth (expiration is vice versa)
ΔP
-equal to atmospheric pressure - alveolar pressure
4 Pressure Considerations
- 𝑃ʙ - Barometric (Atmospheric) Pressure
- 𝑃𝙰 - Alveolar Pressure
- 𝑃𝘱𝑙 - Pleural Pressure
- 𝑃𝑡𝘱 - Transpulmonary Pressure (Lung recoil), inside pressure - outside pressure
Pressure Relationships
-respiratory pressures and atmospheric pressures are always relative to each other
Pressure Measurement Units
-mmHg (diffusion)
-cmH₂O (bulk flow)
-atm (atmospheres)
Pressure at Sea Level
-760 mmHg
-1 atm
-1034 cmH₂O
Pressure at High Altitudes
-pressure is less than at sea level
-ie. in the rocky mountains
Atmospheric (Barometric) Pressure
-the pressure exerted by the weight of the air in the atmosphere on objects on Earth’s surface
-diminishes with increasing altitude
Alveolar Pressure
-aka intrapulmonary pressure
-pressure within the alveoli
Pleural Pressure
-aka intrapleural pressure
-the pressure outside the lungs but within the thoracic cavity (pleural space)
Transpulmonary Pressure Difference
-aka transmural pressure difference
-the pressure gradient across a structure
-equal to the inside pressure - outside pressure or the alveolar pressure - pleural pressure
Elastic Recoil of the Lungs
-a property of lungs that keep the lungs and ribcage together
-how readily the lungs rebound after being stretched
-returns lungs to pre-inspiratory volume
-the thoracic wall is more rigid but recoils outward
Elastic Recoil Depends on:
- Elastic Connective Tissue - stretchability
- Alveolar Surface Tension (70%) - the thin liquid film that lines each alveoli
Alveolar Surface Tension
-alveoli are lined by water
-water molecules on the surface are highly attracted to each other vs in the air (water vapour)
-the unequal attraction, polarity, provides surface tension
-the liquid layer resists expansion of the alveolus
-greater the surface tension, the less compliant the lungs
-shrinks alveoli, leads to recoil
Sub-atmospheric Pressure
-a property of the pleural sac
-means the pressure in the lungs is always lower than the atmosphere
Collapse Alveoli
-the smaller the alveoli, the greater the surface tension = collapse
-beacuse… collapsing pressure = 2xSurface Tension/Alveolar Radius
2 Factors that Oppose Alveolar Collapse:
- Pulmonary Surfactant
- Alveolar Interdependence
Pulmonary Surfactant
-mixture of phospholipids and proteins
-reduces surface tension (the cohesive force between water molecules)
-deep breathing increases secretion by stretching Type II Alveolar Cells
-increases compliance, thus reducing the work of the lungs
-reduces recoil pressure of smaller alveoli (means small and large can work together)
Pulmonary Surfactant and Babies
-premature babies have difficulty breathing due to lack of surfactant
-little surfactant allows alveoli to collapse and then have to re-inflate every time (energy drain)
-surfactant not usually made till last 2 months in utero
-solutions: give mother steroids, put baby on ventilator, artificial surfactant
Alveolar Interdependence
-contributes to alveolar stability
-alveoli are connected to each other by connective tissue
-if one starts to collapse, the others recoil to resist stretch
-this exerts an expanding force on the collapsing one
-like “tug of war”
Forces that Keep Alveoli Open
-positive transmural pressure
-pulmonary surfactant
-alveolar interdependence
Forces Promoting Alveolar Collapse
-elasticity of stretched connective tissue
-alveolar surface tension
Pneumothorax
-demonstrates elastic recoil property of lungs and the importance of pleural pressure to keep lungs inflated
-can result from puncture wound
-contact w/ atmosphere = no pressure difference (𝑃𝙰 and 𝑃𝘱𝑙 = 𝑃ʙ)
-no air flow in/out
-air enters pleural space
-thoracic wall springs outward
-results in a collapsed lung to its un-stretched size (elastic recoil!)
Which pressure needs to change to allow air flow?
-alveolar, specifically pleural pressure must change it by activating muscles to change lung volume
-barometric remains constant
Alveolar Pressure Equation
alveolar pressure = lung recoil pressure (aka transpulmonary pressure) + pleural pressure
Activating Inspiratory Muscles _______ Pleural Pressure
decreases
Activating Expiratory Muscles _______ Pleural Pressure
increases
When does alveolar pressure equal atmospheric pressure?
-before inspiration
-this results in no air flow in/out of the lungs
Boyle’s Law
-v=1/p or v1p1=v2p2
-as pleural pressure decreases, thoracic cavity enlarges (increases lung volume), and the alveolar pressure drops due to decompression
-the number of molecules doesn’t change, they are just more/less compressed
-at a constant temperature
If alveolar pressure is less than atmospheric pressure, air ____ the lungs.
enters
If alveolar pressure is greater than atmospheric pressure, air ____ the lungs.
exits
How does lung volume change?
-by contracting muscles
-intercostals
-diaphragm
Relaxing Inspiratory Muscles
-is the onset of expiration
-**not necessary for the expiratory muscles to be activated for expiration
-ability to expand thorax is decreased
-pleural pressure is less negative
-alveolar pressure is positive
Deeper Inspirations
-contract diaphragm and external intercostals more forcefully
-recruiting the inactive accessory inspiratory muscles
-increase volume of thoracic cavity
Before Inspiration
-alveolar and atmospheric pressure are equal
-no flow
Inspiration
-pleural pressure decreases (due to muscle contraction)
-alveolar pressure decreases (due to decompression)
-air flows inward
End of Inspiration
-inspiratory muscle contraction decreases
-lung recoil pressure is equal to pleural pressure
-alveolar pressure equals atm. pressure
-flow stops
Expiration
-no inspiratory muscle contraction
-lung recoil pressure is greater than pleural pressure
-alveolar pressure is positive
-air flows out
Forced (active) Expiration
-seen during exercise
-empties lungs more rapidly
-sometimes more completely
-inspiratory muscles relaxed
-alveolar elastic recoil
-abdominal expiratory muscles used
-internal intercostals
Airway Resistance (R)
-determined by airway radius
-controlled by autonomic nervous system
-smooth muscle in walls
Bronchoconstriction
-parasympathetic activity
-at rest, when ventilatory demands are low
-smooth muscles contract
-resistance increased
-ACh from nerve endings
Bronchodilation
-sympathetic nervous system
-during activity
-smooth muscles relax
-decreased resistance
-norepinephrine from nerve endings
-epinephrine (hormone)
Pathological Bronchoconstriction Factors
-allergic reaction
-histamine
-physical blockage (mucus)
-edema of the walls
-airway collapse
Local Chemical Bronchoconstriction
-decreased CO2 concentration
Local Chemical Bronchodilation
-increased CO2 concentration
Disease States and Breathing
-flow can be restricted
-muscles work harder to breathe
-greater pressure difference needed to keep flow constant
-expiration is more difficult than inspiration = wheezing
Asthma
-usually episodic and triggered by air, dust, temp, etc.
-smooth muscle spasm = constriction
-airway walls thickened from inflammation or histamine induced edema
-increased mucus secretions
-can lead to infection
Chronic Obstructive Pulmonary Disease (COPD)
-chronic - never goes away
-damages airways
-usually results from smoking, asbestos, coal dust
-not due to smooth muscle contraction
-can be chronic bronchitis or emphysema
Chronic Bronchitis (COPD)
-long term
-inflammation of smaller airways
-airway lining is thickened by mucus
-coughing won’t remove mucus and leads to bacterial infections
Emphysema (COPD)
-collapse of smaller airways
-breakdown of alveolar walls, decreasing the volume to surface area ratio making gas exchange less efficient
-trypsin (enzyme) contributes to breakdown (from macrophages in alveoli)
Spirometer
-used to measure lung volume
-air-filled drum floating in a water-filled chamber
Adult Male Max Lung Volume
5.7L
Adult Female Max Lung Volume
4.2L
Lung Volume at Rest
-2.2L
-about half full even after expiration
Why do the lungs not completely empty?
-alveoli continue gas exchange
Lung Capacity
-the sum of two or more lung volumes
Why can’t you measure total lung volume with a spirometer?
-you can’t completely empty the lungs
*Tidal Volume (TV)
-volume of air entering or leaving lungs
-during a single breath
~500mL
Inspiratory Capacity (IRV)
-extra volume of air maximally inspired over the typical resting tidal volume
~3000mL
Inspiratory Capacity (IC)
-maximum volume of air that can be inspired at the end of a normal expiration
-IC=IRV+IV
~3500mL
Expiratory Reserve Volume (ERV)
-extra volume of air that is actively expired by maximal contraction
-beyond normal volume of air
-after resting tidal volume
~1000mL
*Residual Volume (RV)
-minimum volume of air remaining in the lungs
-even after maximal expiration
~1200mL
Functional Residual Capacity (FRC)
-volume of air in the lungs at the end of normal passive expiration
-FRC=ERV+RV
~2200mL
*Vital Capacity (VC)
-maximum volume of air that can be moved out during a single breath
-following maximal inspiration
-VC=IRV+TV+ERV
~4500mL
*Total Lung Capacity (TLC)
-maximum volume of air that the lungs can hold
-TLC=VC+RV
~5700mL
Forced Expiratory Volume (in 1 second) (FEV₁)
-volume of air that can be expired during the first second of inspiration
Obstructive Lung Disease
-respiratory dysfunction that yields abnormal spirometry results
-increased airway resistance
-FEV₁ less than 80%
Restrictive Lung Disease
-respiratory dysfunction that yields abnormal spirometry results
-normal airway resistance
-reduced vital capacity
Impaired Respiratory Movements
-lung tissue abnormalities
-pleura
-chest wall
-neuromuscular machinery
Other Respiratory Dysfunctions
-diffusion of O2 and CO2
-mechanical failure = reduced ventilation
-inadequate pulmonary blood flow
-poor matching of air and blood = inefficient gas exchange
Pulmonary Ventilation
-minute ventilation
-the volume of air breathed in and out in one minute
-pulmonary ventilation (mL/min) = tidal volume (mL/breath) x respiratory rate (breaths/min)
Alveolar Ventilation
-more important than pulmonary ventilation
-the volume of air exchanged between the atmosphere and alveoli per minute
Why is alveolar ventilation less than pulmonary ventilation?
-anatomic dead space
-the volume of air in conducting airways that is useless for exchange
~150mL
Alveolar Ventilation Equation
alveolar ventilation = (tidal volume - dead space) x respiratory rate
Quiet breathing requires __% of total energy
3
Situations Where Work of Breathing is INCREASED
-need for increased ventilation (ie. exercise)
-decreased pulmonary compliance
-airway resistance decreased (ie. COPD)
-elastic recoil is decreased (ie. emphysema)
Gas Exchange
-the simple diffusion of O2 and CO2 down partial pressure gradients (not conc. gradients)
Where does gas exchange occur?
-pulmonary capillaries in the lungs
-systemic tissue capillaries in vital organs and tissues
When does gas exchange pause?
-when partial pressures are equilibrated
How much gases diffuse depends on:
- partial pressure gradient
- resistance to diffusion
Resistance to diffusion depends on:
- surface area of membrane
- membrane thickness (distance)
- diffusibility of the gas (constant so it doesn’t matter)
Partial Pressure
-total pressure x fractional composition of the gas
-ie. 760 mmHg x 0.79 (for N2)
Why is alveolar PO2 100 mmHg and not 160 mmHg?
-due to the addition of water vapour in airways (47 mmHg)
Effect of water vapour in airways (alveolar air)
-dilutes all gases by 47 mmHg
Typical dry air contains ___% N2 and ___% O2
79; 21
Total Atmospheric Pressure at sea level ____mmHg
760
(the sum of the pressures exerted by N2 and O2)
Alveolar O2 = _____ mmHg
100
Partial Pressure Gradients of O2 and CO2: In Lungs
-O₂ diffuses from alveoli to pulmonary capillaries
-CO₂ diffuses from pulmonary capillaries to alveoli
-blood leaves the lungs high in O₂ and low in CO₂
Partial Pressure Gradients of O2 and CO2: In Tissues
-O₂ diffuses from capillaries to tissue cells
-CO₂ diffuses from tissue cells to capillaries
-blood leaves the tissues low in O₂ and high in CO₂
Why doesn’t all blood O₂ get diffused into the tissue capillaries?
-mixed venous oxygen content
-a reserve that is immediately available when oxygen demands increase
Why doesn’t all blood CO₂ get diffused into the alveoli?
-plays a role in acid-base balance
-generates carbonic acid
-stimulates respiration
Why does CO₂ require a smaller pressure gradient to diffuse?
-it is 20x more soluble than oxygen
As membrane thickness _______, gas exchange ______.
increases; decreases
-found in pulmonary edema, fibrosis, and pneumonia
As surface area ______, diffusion ________.
increases; increases
As the partial pressure gradient ______, diffusion ______.
increases, increases
-major factor
Frick’s Law of Diffusion
-the rate of diffusion depends on the surface area and thickness of the membrane
Blood spends ~_.__ seconds in a capillary
-0.75
-0.25 for equilibrium
-enough time for gas equilibration
-0.4 sec blood transit time (exercise)
___% of oxygen is physically dissolved in blood
1.5
___% of oxygen is bound to hemoglobin
98.5
__-__% of CO₂ is physically dissolved in blood
5-10
__-__% of CO₂ is bound to hemoglobin
5-10
__-__% of CO₂ travels as bicarbonate (HCO₃⁻) in blood
80-90
Hemoglobin Equation
-Hb + O₂ ⇆ HbO₂
-deoxyhemoglobin ⇆ oxyhemoglobin
- alveoli to blood→
- ←blood to tissues
Oxygen bound to hemoglobin _____ contribute to the 𝑃𝑜₂ of the blood
does not
Each hemoglobin molecule can carry up to ___ oxygen molecules
4
What is Hb sats?
how much O₂ is attached to Hb
What does Hb saturation depend on?
𝑃𝑜₂
Hb sat ~__% when blood leaves the lungs
98
Hb sat ~__% when blood leaves the tissues
75
% Hb sat is ____ where the partial pressure of O₂ is _____ (lungs)
high; high
% Hb sat is _____ where the partial pressure of O₂ is _____ (tissue cells)
low; low
Oxygen Hb Dissociation Curve
-not a linear relationship
-shows the relationship between blood 𝑃𝑜₂ and % Hb
-sigmoid shaped curve
Plateau Phase
-where the partial pressure of oxygen is high (lungs), only small % Hb sat increase
-shows a good margin of safety
-Hb almost completely saturated
Steep Phase
-at the systemic capillaries
-Hb unloading O₂ into the tissue cells
Bohr Effect
-CO₂ and lactic acid produced H+ (more acidic pH) that changes the Hb shape and reduce its O₂ affinity
-lower Hb %
-more O₂ is released at a given PO₂ level
The Bohr Effect shifts the Hb sat curve to the _____
right
Factors that increase O₂ unloading
-increased CO₂
-increased H+
-increased temperature
Haldane Effect
-increase in PO₂ leads to less CO₂ bound to Hb
-this increases the capacity for Hb to carry CO₂ in it’s deoxygenated state
Temperature on % Hb
-shifts curve to the right
-more O₂ unloading
2,3-biphosphoglycerate (BPG) on % Hb
-a factor inside the RBCs
-produced during RBC metabolism
-reduces Hb O₂ affinity
-shifts curve to the right
3 Ways CO₂ Travels
- dissolved
- Hb bound
- as bicarbonate
Bicarbonate ion (HCO₃⁻)
-CO₂ combines with H₂O to form carbonic acid (H₂CO₃)
-facilitated by carbonic anhydrase in the RBC cytoplasm
-carbonic acid dissociated into H+ ions and HCO₃⁻
-CO₂ + H₂O (carbonic anhydrase→) H₂CO₃ → H+ + HCO₃⁻
CO₂ binds with the ____ part of hemoglobin
globin
O₂ binds with the ____ part of hemoglobin
heme
________ hemoglobin has a greater affinity for CO₂
reduced (deoxyhemoglobin)
Chloride Shift
-in tissues (does the opposite in alveoli)
-the exchange of Cl- (into RBC) for HCO₃⁻ (out of RBC)
-the HCO₃⁻ out makes an electrical gradient for Cl- to flow in
Apnea
-cessation of breathing
Asphyxia
-oxygen starvation of tissues
-accompanied by CO₂ rise
Cyanosis
-blueness of skin resulting from insufficiently oxygenated blood in arteries
Dyspnea
-difficult or laboured breathing
Eupnea
-normal breathing
*Hypercapnia
-excess CO₂ in arterial blood
-caused by hypoventilation or lung disease
-acidosis
Hyperpnea
-increased pulmonary ventilation to match metabolic demands
Hyperventilation
-increased pulmonary ventilation in excess of metabolic requirements
-alkalosis
-anxiety attack, fever, aspirin poisoning
*Hypocapnia
-below normal PCO₂ in arterial blood
-alkalosis
-brought about by hyperventilation
Hypoventilation
-underventilation
-related to metabolic requirements
-acidosis
Hypoxaemia
-below normal PO₂ in arterial blood
*Hypoxia
-insufficient O₂ at the cellular level
*Anaemic Hypoxia
-reduced O₂ carrying capacity of the blood
-despite normal PO₂ levels
-reduced RBC, Hb
-CO poisioning
*Circulatory Hypoxia
-inadequate oxygenated blood delivered to tissues
-heart attack
-circulatory shock
*Histotoxic Hypoxia
-inability of cells to use available O₂
-cyanide poisoning (blocked ETC)
*Hypoxic Hypoxia
-low arterial PO₂
-inadequate Hb sat
-respiratory malfunction
-low environmental O₂ (altitude, suffocation)
*Hyperoxia
-above normal arterial PO₂
-only when breathing supplemental O₂
-can damage brain or eyes
Dorsal Respiratory Group (DRG)
- in the Medullary Respiratory Centre
-mostly inspiratory neurons that penetrate inspiratory muscles
-firing = inspiration
-cease firing = expiration
Ventral Respiratory Group (VRG)
-in the Medullary Respiratory Centre
-inspiratory and expiratory neurons
-mostly inactive during regular breathing
-activate when increased ventilation is required
pre-Bötzinger Complex
-pacemaker like neurons near the VRG
-generate respiratory rhythm
Pneumotaxic Centre
-sends impulses to the DRG to switch off inspiratory neurons
-dominant over apneustic
Apneustic Centre
-prevents inspiratory neurons from being switched off
-extra boost for inspiratory drive
PO₂ - Controlling Ventilation
-peripheral detection (not sensitive)
-Carotid Chemoreceptors: activated in an emergency (PO₂ below 60 mmHg)
-depresses central chemoreceptors when less than 60 mmHg
A ______ in PO₂ will activate chemoreceptors
-decrease
PCO₂ - Controlling ventilation
-central detection
-Carotid receptors: weakly stimulates, sensitizes to hypoxia
-Central receptor: strongly stimulates (~70% of increased ventilation)
The dominant control of ventilation
-an increase in PCO₂ to stimulate the central chemoreceptors
Increased Arterial H+ - Controlling ventilation
-pH; usually from non-respiratory sources
-carotid: important in acid-base balance
-central: does not affect (can’t cross BBB)
Carotid Bodies
-peripheral chemoreceptor
-lies further north up the aorta, in the carotid sinus
Aortic Bodies
-peripheral chemoreceptor
-lies on the aortic arch
An ______ in PCO₂ will stimulate chemoreceptors
increase
Which mechanism is the most important regulator in ventilation?
PCO₂
