Unit 4: Respiratory System Flashcards
O2 path
environment -> lungs -> blood -> body tissue
CO2 path
body tissue -> blood -> lungs -> environment
general function of respiratory system
obtain O2 for use by body cells and eliminate CO2 body cell production
two separate but related respiratory system processes
- internal respiration
- expiration respiration
internal respiration
- cellular respiration within the mitochondria for aerobic energy
- oxidative phosphorylation
- an exchange of gases between the cells of the body and the blood
external respiration
exchange of oxygen and carbon dioxide between atmosphere and body tissues
O2% in air
21
nitrogen % in air
79
external respiration steps
ventilation definiton
gas exchange between the atmosphere and alveoli in the lungs
does the brain control the atria and ventricles contracting simultaneously
no, no neural input
ways to lower resting heart rate
exercise
average heart rate
70
average breaths per minute
12
average heart size
6L
secondary functions of respiratory system
- short term regulation of pH (acid-base balance)
- enable speech, singing, and other vocalizations
- defend against pathogens in airways
- removes, modifies, activates or inactivates materials passing through pulmonary circulation
- eliminate heat and water
- assist venous return
- nose is the smell organ
why do we humidify the air we breathe
to help gas exchange
upper airway anatomy and labeled
- nasal cavity (nose)
- oral cavity
- pharynx
does the pharynx allow passage of food/drink or air
both
conducting zone anatomy and labeled
- larynx
- glottis
- trachea
- cartilage rings
- left lung
- right lung
- primary bronchi
- secondary bronchi
- tertiary bronchi
- terminal bronchioles
- diaphragm
- terminal bronchiole
respiratory zone anatomy and labeled
- terminal bronchiole
- respiratory bronchioles
- alveolar sac
- alveoli
alveoli
- site of gas exchange
- high capillary net
- pores of kohn
trachea structure
- 2.5 cm diameter
- 10 cm long
- c-shaped cartilage bands for structural rigidity
primary bronchi structure
- right and left
- rings of cartilage
secondary bronchi structure
- 3 right side (to 2 lobes of right lung)
- 2 left side (to 2 lobes of left lung)
tertiary bronchi structure
- 20-23 orders of branching
- up to 8 million tubules
bronchioles structure
- less than 1 mm diameter
- no cartilage, risk of collapse
how bronchioles minimize risk of collapse
walls of elastic fiber and smooth muscle
air passageway volume and function
- 150 mL volume
- dead space
functions of the conducting zone
- air passageway
- increase air temperature to body temperature
- humidify air
epithelium of the conducting zone
- process: mucus escalator
- goblet cells
- ciliated cells
goblet cells of the conducting zone
- secret mucus
- trap foreign particles
ciliated cells of the conducting zone
propel the mucus up the glottis to be swallowed or expelled
what is paralyzed in the conducting zone in smokers and how do they compensate
- ciliated cells
- cough to expel mucus
function of the respiratory zone
exchange gases between air and blood by diffusion
epithelium of the respiratory zone
- epithelial cells of alveoli
- endothelial cells of capillary
pores of kohn function
permit airflow between adjacent alveoli (collateral ventilation)
3 alveoli cell types
- type 1 alveolar cells
- type 2 alveolar cells
- alveolar marchophages
type 1 alveolar cells
- walls of alveoli
- single layer epithelial cells
type 2 alveolar cells
- secrete surfactant
- reduce surface tension in alveolar walls
- helps prevent alveolar collapse
alveolar macrophages
removes foreign particles
respiratory membrane diffusion barrier width and composition
- 0.2 microns thick
- alveoli (type 1 cells and basement membrane)
- capillaries (endothelial cells and basement membrane)
hypoxemia
- low O2 carrying capacity
- inefficient gas exchange
pleural sac composition
- visceral pleura
- parietal pleura
- intrapleural space
three pressures important in ventilation
- atmospheric (barometric) pressure
- intra-alveolar (intrapulmonary) pressure
- intrapleural pressure (intrathoracic pressure)
atmospheric pressure
- 760 mmHg at sea level
- decreases as altitude increases
- normally other lung pressure given relative to atmospheric (set Patm = 0 mmHg)
intra-alveolar pressure
- pressure of air in alveoli
- varies with respiration phases (negative or less than atmospheric during inspiration; positive or more than atmospheric during expiration)
- difference between Palv and Patm drives ventilation
intrapleural pressure
- pressure inside pleural sac
- varies with respiration phases (at rest, 756 or -4 mmHg
- always less than Palv
- always negative under normal conditions at rest
- negative pressure due to elasticity in lungs and chest wall (lungs recoil inward, chest wall recoils outward, opposing pulls on intrapleural space, surface tension of intrapleural fluid hold wall and lungs together - H2O molecules are polar, attract to each other -, sub-atmospheric P due to vacuum in the pleural cavity)
functional residual capacity (FRC)
volume of air in lungs between breaths
what does pneumothorax cause
collapsed lung
traumatic vs spontaneous pneumothorax
- traumatic: physical trauma to the chest (ex: puncture wound in chest wall)
- spontaneous: sudden onset of a collapsed lung without any apparent cause (ex: hole in lung)
mechanics of breathing
- atmospheric pressure is constant
- changes in alveolar pressure create gradients
- Boyle’s law
- alveolar pressure can change by volume change
air flow equation
R = resistance to air flow (resistance related to radius of airways and mucus)
boyle’s law
pressure is inversely related to volume in an airtight container
factors determining intra-alveolar pressure
- quantity of air in alveoli
- volume of alveoli
intra-alveolar pressure during inspiration
- lungs expand, alveolar volume increases
- Palv decreases
- pressure gradient: air into lungs
- quantity of air in alveoli rises
- Palv increases
intra-alveolar pressure during expiration
- lungs recoil, alveolar volume decreases
- Palv increases
- pressure gradient: air out of lungs
- quantity of air decreases
- Palv decreases
respiratory muscle activity during inspiration
principle muscles of inspiration
- external intercostals (elevate ribs)
- interchondral part of internal intercostals (also elevate ribs)
- diaphragm (domes descend, increase chest dimension and elevate lower ribs)
accessory muscles of inspiration
- sternocleidomastoid (elevates sternum)
- scalenus anterior middle and posterior (elevate and fix upper ribs)
muscles of expiration during quiet breathing
passive recoil of lungs
muscle of expiration during active breathing
- internal intercostals (except interchondral parts)
- adbominal muscles (depress lower ribs, compress abdominal contents)
- rectus abdominis
- external oblique
- internal oblique
- transversus abdominis
respiratory muscle activity during expiration
flow-volume loop
a plot of inspiratory and expiratory flow (on the Y-axis) against volume (on the X-axis) during the performance of maximally forced inspiratory and expiratory maneuvers
factors affecting pulmonary ventilation
- lung compliance
- airway resistance
lung compliance
- ease with ehich lungs can be stretched
- less compliant lungs = more work required to produce a given degree of inflation
- affected by elasticity and surface tension of lungs and alveoli
airway resistance
- affected by passive forces, contractile activity of smooth muscle and mucus secretion
- increased in pathologies
quiet breathing requires what % of total energy expenditure
3
lungs normally operate at …
half full
work of breathing is increased in which situations
- pulmonary compliance decrease
- airway resistance increase
- elastic recoil decrease
- increased ventilation needed
spirometer
measures the amount of air you can breathe out in one second and the total volume of air you can exhale in one forced breath
(pulmonary) minute ventilation definition
total volume of air entering and leaving respiratory system each minute
minute ventilation equation
V(T) x RR
normal minute ventilation
500 mL x 12 breaths/min = 6000 mL/min
alveolar ventilation
- volume of air exchanged between the atmosphere and alveoli per minute
- less than pulmonary ventilation due to anatomical dead space
- more important than pulmonary ventilation
anatomical dead space
- volume of air in conducting airways that is useless for gas exchange
- 150 mL in adults
why does hyperventilation not allow for oxygen to come in
old air is not fully pushed out, pushed down during inspiration, no new O2 able to enter
high volume = ______ resistance
low
perfusion definition
blood flow
does gravity affect perfusion or ventilation more
perfusion
two main classifications of respiratory diseases
- obstructive
- restrictive
obstructive respiratory diseases
- airway narrowing
- increased airway resistance
- reduced flow during expiration
restrictive respiratory diseases
- reduced compliance
- scar tissue formation
- fibrosis
obstructive respiratory disease examples
- emphysema
- chronic bronchitis
- asthma
restrictive respiratory disease example
pulmonary fibrosis
fibrosis
thickening or scarring of tissue
other conditions that impair diffusion of O2 and CO2
- neuromuscular disorders (affect inspiratory muscle contraction)
- inadequate perfusion (gas exchange)
- ventilation:perfusion imbalances
forced expired volume (FEV)
- measures how much air a person can exhale during a forced breath
- over 80% is normal, under 80% is a sign of disorder
what is used to diagnose obstructive respiratory diseases
forced expired volume tests
forced vital capacity
the total amount of air exhaled during the FEV test
asthma clinical symptoms
- airway hyper-reactivity
- reversible airway narrowing
- mucous thickening
- smooth muscle constriction by spasms in small airways
- most common childhood respiratory disease
- severe narrowing is lethal
asthma causes
- allergens, pollens, animal fur, dust
- smoking, smog, airborne pollutants
- changes in air temp, humidity, pressure
- exercise
- emotional stress, anxiety
asthma treatment
- bronchodilators
- anti-inflammatory
- O2
bronchitis clinical symptoms
- airway wall inflammation
- excessive mucous production
- airway narrowing and coughing (but cough cannot get rid of mucous)
- reversible
bronchitis causes
- bacterial and viral infections
- smoking
- airborne pollutants
- chronic irritation
emphysema clinical symptoms
- irreversible
- destruction of alveolar walls (small airway collapse)
- enlargement of air sacs
- increased lung compliance via destruction of elastic fibers, excessive release of trypsin enzyme (trypsin can break alveolar walls), and reduced elastic lung recoil (trapped air)
emphysema causes
- smoking induced inflammation
- cilia destruction, tar accumulation
- airborne contamination
- genetic lack of anti-trypsin production
pulmonary fibrosis
- diffuse interstitial lung disease
- results from over 130 disorders
pulmonary fibrosis clinical symptoms
- reduced elasticity
- reduced compliance of lung and chest wall
- increased work to breathe
- slim patients (breathing requires effort)
pulmonary fibrosis causes
- no known cause in 2/3 of cases
- asbestos fiber breathing (also causes lung cancer)
- inflammation
- scar tissue formation
total pressure
the sum of all partial pressures
partial pressures of a gas depend on
- fractional concentration of the gas
- total pressure of gas mixture
composition of air
- 79% nitrogen
- 21% oxygen
- trace amounts carbon dioxide, helium, argon, etc.
- water depends on humidity
ficks’ law (rate of diffusion)
- Vgas = rate of diffusion
- A = surface area (increases during exercises, more pulmonary capillaries open, alveoli expand for deep breaths)
- T = thickness (normally constant, increases in pathological conditions)
- (triangle)P = pressure difference
- D = diffusion constant
- S = gas solubility
- MW = molecular weight
CO2 diffusion rate is ? than O2
2x bigger
do O2 and CO2 equilibrate at similar rate
yes
at rest blood spends ? sec in the capillary
0.75
normal O2 and CO2 equilibrium within how much time in capillary transit
1/3 (0.25 sec)
O2 and CO2 diffusion process affected by
- exercise (risk of exercise induced arterial hypoxemia in highly trained athletes)
- thickening of blood-gas barrier
pulmonary oedema
- fluid accumulation in alveoli and/or interstitial space
- impairs diffusion (higher distance from alveoli to blood)
- leakage in unprotected capillaries
- increases breathing work (decreased
- in arterial blood: lower PO2 and higher PCO2
causes of pulmonary oedema
- increased capillary pressure (via left heart failure)
- reduced atmospheric pressure at altitude
pulmonary oedema treatment
administering oxygen and diuretics
2 forms of oxygen transport
- 1.5% dissolved in plasma
- 98.5% bound to hemoglobin
hemoglobin (Hb)
- found only in red blood cells
- tetrameric globular protein with 4 hem groups
- cooperative reversible binding of up to 4 O2 molecules, 4 CO2 molecules (normally 2 at most in venous blood)
- transports 98.5% of O2 in blood
- function: greater oxygen carrying capacity
changes in affinity of hemoglobin for oxygen
- describes changing affinity of Hb for O2
- right shifted = decreased oxygen affinity (wants to give oxygen away)
- left shifted = increased oxygen affinity (reluctance to release oxygen)
3 forms of CO2 transport
- 10% dissolved
- 30% bound to Hg
- 60% bicarbonate (HCO3-) mostly in plasma
hypoxia definition
insufficient cellular O2
types of hypoxia
- hypoxic hypoxia
- anemic hypoxia
- circulatory hypoxia
- histotoxic hypoxia
hypoxic hypoxia
- low PaO2 (hypoxemia) -> reduced Hb saturation
- inadequate gas exchange
- low PB
- cyanosis (skin bluish tint) = <70% Hb saturation
anemic hypoxia
- reduced total blood O2 content with normal PaO2
- reduced circulating rbcs; reduced rbc Hb content
- CO poisoning (no cyanosis - HbCO is pink, pale skin)
circulatory hypoxia
- reduced supply of oxygenated blood with normal O2 content and PaO2
- vessel blockage, congestive heart failure
histotoxic hypoxia
- O2 delivery to tissue normal but cells unable to use it
= cyanide poisoning (cyanide blocks essential enzymes for cellular respiration)
hyperoxia
above normal arterial O2 (O2 toxicity)
effect of hyperoxia on a healthy person
no big effect
effect of hyperoxia with other diseases with reduced PaO2
- can improve gradient but can be dangerous as high O2 can damage brain (cause blindness)
- when O2 is the main driver of ventilation: high O2 can increase the risk of decreased peripheral chemoreceptor sensitivity
types of abnormal PaCO2
- hypercapnia
- hypocapnia
hypercapnia
- excess PaCO2
- via hypoventilation
- occurs with most lung diseases
- occurs in conjunction with reduced PaO2
hypocapnia
- below normal PaCO2
- via hyperventilation
- occurs with anxiety and fear
- no impact of PaO2 (except at low PB where low PaO2 stimulates hyperventilation)
hyperpnea
increased breathing/ventilation to match metabolic demand (exercise)
basic respiratory control centers in the brain stem
peripheral chemoreceptors location
- carotid bodies (near baroreceptors in carotid sinus)
- aortic bodies (aortic arch)
peripheral chemoreceptors function
- respond to reduced PaO2 (<60 mmHg)
- respond to increased PaCO2 and hydrogen (provide 20% respiratory drive)
- aortic bodies rarely respond to reduced total arterial O2 content (anemia, carbon monoxide poisoning)
central chemoreceptors location
the medulla
central chemoreceptors function
detect changes in pH
effects of arterial O2 on ventilation
- not much of a change until PO2 </= 60 mmHg
- response due to activation of peripheral chemoreceptors only
effects of arterial CO2 on ventilation
- large effects of PCO2 on ventilation
- effects mediated through both central and peripheral chemoreceptors but CO2 must be converted to H+ first
hypoventilation negative feedback
hyperventilation negative feedback
increasing altitude __________ respiration
increases
cause of hyperventilation as an adaptation to altitude
reduced PaO2 acting on carotid body peripheral chemoreceptors
adaptation to altitude (hyperventilation)
- CO2 clearance increases
- blood pH increases
- respiratory alkalosis reduces ventilation
- to prevent alkalosis: kidneys excrete bicarbonate ions, more acid remains in the blood, alkalosis reversed, pH normal in 2-3 days
- ventilation increases again
polycythemia
- body’s reaction to high altitude
- RBC and Hb content increase in order to increase O2
- hypoxemia stimulates EPO from kidney after 3 hours (stimulates reticulocytes reticulocyte maturation and release)
- despite reduced PaO2 and Hb saturation
- total O2 content may be normal or elevated
- elevated blood viscosity (increased cardiac work)
other adaptations to altitude
- right shifted O2-Hb dissociation curve moderate altitude (better unloading at tissue level, caused by increase in 2,3-DPG)
- left shifted O2-Hb dissociation curve high altitude (better loading at pulmonary capillaries, caused by respiratory alkalosis)
- improved diffusion capacity (expanded surface area via greater lung volume on inflation, angiogenesis or increased tissue capillarisation)
- endothelial cells release up to 10 times more nitric oxide
- reduced skeletal muscle fiber size with increased oxidative capacity and mitochondria numbers
acute mountain sickness symptoms
- headaches, loss of appetite, insomnia, nausea, vomiting, dyspnea
- 6 hours to 48 hours after arrival to altitude (most severe days 2 and 3)
- worse at night (respiratory drive reduced)
- 15% higher in women
- physical condition has no effect
- higher altitude = more severe
high altitude pulmonary/cerebral oedema
- linked to pulmonary vasoconstriction (hypoxia), high protein oedema fluid from damaged capillaries
- fluid accumulation leads to persistent cough, shortness of breath, cyanosis of lips and fingernails and loss of consciousness
- could lead to high altitude cerebral oedema (fluid accumulation in cranial cavity)
- treatment: descending to lower altitude and supplemental oxygen
altitude training strategies to maximize sea-level performance
live high and train high
- benefit: increase rbcs
- problem: difficult to train at same volume/intensity as at sea level
live high and train low
- most effective
- problem: logistics and finances
- new modalities (hypoxic sleeping devices/houses)
live low and train high
- weak effect
intermittent hypoxia at rest
- wear effect
respiration at depth
- total pressure increases
- gas partial pressures increase
- problems: gas cavities (lung and middle ear) compress with descent and over-expand with ascent, behavior of gases
nitrogen narcosis
- at sea level: N2 is poorly soluble, low N2 dissolved
- at depth: increased nitrogen partial pressures leads to increases nitrogen solubility; high nitrogen dissolved in blood and fatty substances (influences ion regulation and neurons); increased depth = increased nitrogen dissolved
- increased nitrogen solubility leads to reduced neuron excitability leads to nitrogen narcosis
nitrogen narcosis at 50 m (150 ft)
euphoria and drowsiness
nitrogen narcosis at 50-90 m (150 - 300 ft)
- fatigue and weakness
- loss of coordination
- clumsiness
nitrogen narcosis at 100-120 m (350-400 ft)
lose consciousness
nitrogen narcosis prevention
- use nitrogen free gas
- helium substitute
- 100% O2 not appropriate (O2 toxicity)
decompression sickness in diving
- during rapid ascent and decreased pressure
- N2 less soluble, N2 comes out of solution (bubble formation = champagne cork effect)
effects depend on size and location of bubbles
- gas embolus in circulation (tissue iscaemia) may be critical in brain, coronary, or pulmonary circulations, avascular necrosis common in head of femur
- bubble formation in the myelin sheath (compromise nerve conduction in dizziness or paralysis)
- bubble/gas expansion (the bends in muscle and joints, ear: vestibular disturbances and deafness, lung: tissue rupture with increased bubble dispersal and multiple emboli)
decompression sickness prevention
- slow ascent (depends on depth, time, N2 wash in and wash out times, tissue types)
- N2 gas replacement (half solubility of N2)
- exhale during ascent
decompression sickness treatment
recompression
