Respiratory System Flashcards
Respiration definition
gas movement & gas metabolism
Internal respiration definition
intra- cellular metabolic processes (in mitochondria) that use O2 & produce CO2
– “cellular respiration”
External respiration definition
events involved in exchange of O2 & CO2 between cells & external environment
4 steps of external respiration
1- Ventilation (breathing)
2- Respiratory exchange (at lungs or gills)
3- Circulation
4- Cellular exchange (between blood & cells)
What is gas exchange governed by?
partial pressure (Molecules diffuse down concentration gradients But gases diffuse down partial pressure gradients)
Partial pressure (PP or P)
pressure exerted by a particular gas within a mixture of gases
measured in mm Hg
Total atmospheric pressure
sum of partial pressures that each gas in atmosphere contributes
Pressure exerted on objects by atmospheric air can push a column of mercury (Hg) up some amount of mm = total atmospheric pressure
Atmospheric air contains N2 (~79%), O2 (~21%), plus small amounts of CO2, H2O vapor, other gases, & pollutants
Calculating partial pressures
Total atmospheric pressure at sea level = 760 mm Hg
21% of that = O2 so PO2 = 160 mm Hg
At elevation, total atmospheric pressure drops = partial pressure of all gases drops = less drive for O2 diffusion into tissues
strategies for increasing gas exchange:
Diffusion is slow except over short distances
- To maximize gas exchange, epithelial lining of respiratory surface (e.g. lungs) must be very thinAlso want as much surface area as possible for as much diffusion as possible to take place
- To increase surface area, respiratory surfaces in vertebrates have specialized folds: invaginations (in-pockets) & evaginations (out-pockets)
Steeper partial pressure gradient = faster diffusion - Respiratory pigments (e.g. hemoglobin in erythrocytes) bind O2, which means it is no longer freely dissolved & no longer contributing to partial pressure inside the body
Maintains low PO2 inside body, keeping gradient steep & allowing for greater diffusion, plus prevents any backwards diffusion
Respiratory anatomy
In vertebrates, water respirers have gills while air respirers have lungs
Each is adapted to specialized needs
Less O2 in water
Potential for desiccation in air
Gills
have many evaginations & very thin epithelial cells to increase gas exchange
1 other adaptation: countercurrent blood flow
Blood flows counter to water across gills – causes PP gradient all along gills rather than reaching equilibrium & O2 diffusion stopping
lungs
Dry air can cause desiccation (& death) of sensitive epithelial cells in the lungs
Lungs must stay moist & lubricated for protection & easy movement during inhalation & exhalation
Mucus-secreting cells produce an aqueous mucus lubricant: “pulmonary surfactant”
Ciliated cells are lined with tiny hairs that help distribute the mucus
Mammals have a very high metabolic rate affect on lungs
had to significantly increase lung surface area
Accomplished this with numerous small alveoli covered by incredibly dense capillaries
Alveoli = small sacs in grape-like clusters where gas exchange in lungs takes place
~300 million in a human!
Anatomy of mammalian lungs
Nasal passages pharynx (throat) trachea right & left bronchi bronchioles alveoli
The trachea & larger bronchi must be open most or all of the time, so are rigid structures with cartilaginous rings to prevent compression
Smaller bronchioles do not have cartilage – instead have smooth muscle with autonomic innervation & sensitivity to hormones
thus can have altered contraction to regulate amount of air flow
Alveoli
have no cartilage or smooth muscle to help them inflate & deflate
Instead rely on on muscles in the thoracic (chest) cavity: diaphragm, external intercostal, abdominal wall, & internal intercostal muscles
these change the volume of the thoracic cavity, causing a corresponding change in lung volume
Mammalian lungs
take up most of the thoracic cavity
Each lung is enclosed within the double- walled pleural sac
inside of sac is filled with fluid allowing the layers to slide past each other during respiratory movement
The inside of the pleural sac (where the lungs are) = pleural cavity
Inspiration (inhalation)
breath in
When relaxed, the diaphragm muscle is in a dome shape, protruding into thoracic cavity
Upon contraction, diaphragm moves downward, thereby enlarging area in thoracic cavity & causing inward air flow
Contraction of the external intercostal muscles also enlarges the thoracic cavity by expanding ribs & sternum outward, allowing inward air flow
Passive expiration (exhalation) = breath out
As inspiratory muscles relax back into thoracic cavity & lungs exhibit elastic recoil, air is passively pushed out of lungs, with gases diffusing down their PP gradients
While expiration occurs passively during quiet breathing, it is possible to actively push air out too
moves air out more completely & rapidly, especially useful for quick breathing during exercise
when contracted, abdominal wall muscles push the diaphragm even further into the thoracic cavity
Internal intercostal muscles
have opposite effect of external intercostal muscles, causing ribs to flatten
Airways normally offer very little resistance
Allows adequate air flow even when pressure gradients are very small (1 or 2 mm Hg)
Various respiratory diseases can narrow airways, increasing resistance & thus decreasing airflow
e.g. COPD = chronic obstructive pulmonary disease, a group of lung diseases including chronic emphysema, bronchitis, & asthma
Lung volumes can be measured by:
a spirometer
fits over mouth & measures volume of air breathed in & out generates a spirogram
this shows the various volumes & capacities of the lungs
Total lung capacity (TLC)
the maximum amount of air lungs can hold
~5.7L in humans, though affected by build, age, lung health, & disease
However, not all of TLC can be exchanged
residual volume(RV)
air that cannot be expelled
Tidal volume (TV)
amount of air moving into or out of the lungs during any one breathing cycle
At rest, human TV = ~2.2L at end of expiration to ~2.7L at end of inspiration
Functional residual capacity (FRC)
volume of air left in lungs after passive expiration – during quiet breathing, lungs are not close to max expiration or inspiration
inspiratory reserve volume (IRV)
After normal inspiration it is possible to breathe in additional air
expiratory reserve volume (ERV)
After normal expiration it is possible to exhale additional air from the lungs
vital capacity (VC):
3 values (TV, IRV, & ERV) added represent it
amount of air we can control through inhalation & exhalation
usually ~3-5L in vol.
Pulmonary ventilation
the volume of air breathed in & out in 1 minute
PV= TV x Respiratory Rate
Increasing TV or rate increases pulm. ventilation
However: more advantageous to increase TV rather than rate because of anatomic dead space – the area where air is not available for gas exchange at alveoli (can’t get past conducting airways like bronchi)
Thus a better measure of gas exchange = alveolar ventilation, where dead space is accounted for
Obstructive lung disease
any problem that doesn’t allow air to move smoothly from alveoli out through trachea (or vice versa) when breathing
e.g. COPD, & smoking cigarettes also permanently damages alveoli, leading to lung obstruction
Spirometry data can be helpful in diagnosing obstructive & restrictive lung diseases
Restrictive lung disease
normal airflow but decreased lung volumes
e.g. due to pulmonary fibrosis, asbestos poisoning, respiratory distress syndrome, & pneumonia
obesity can also cause decreased lung volumes because of increased pressure on the chest wall
forced expired volume in one second (FEV1)
FEV1 = the volume expired in the first second of maximal expiration after a full inspiration – is a measure of how quickly the lungs can be emptied
In healthy adults the FEV1/FVC ratio = ~80%
Decreased by obstructive lung disease, damage, or naturally with age (~70% or less)
Oxygen is dissolved in blood:
as free gas, though very little because O2 is poorly soluble in warm fluids (only 1-5%)
bound to respiratory pigments in erythrocytes, like hemoglobin
The vast majority of O2 in blood is carried in circulation by:
hemoglobin
ensures enough O2 gets to tissues
also remember: bound O2 doesn’t contribute to PP, so helps keep PP gradient steep
hemoglobin (Hb)
Main respiratory pigment in vertebrates Hemoglobin contains iron (Fe) molecules & forms a loose, easily reversible combo between Fe & O2
Hb unbound = deoxyhemoglobin, or “reduced”
HbO2 = oxyhemoglobin
So why does Hb combine with O2 in the lungs but release O2 at the tissues?
1st: Hb & O2 binding increases when the PP of O2 is high &decreases when low
2nd: HbO2 tends to dissociate under several conditions that occur at tissues (but not lungs) & are especially increased at tissues working hard
Increased PCO2
Increased acidity (e.g. lactic acid)
Increased temp
Increased free phosphates inside erythrocytes (affects lungs too – produced during RBC metabolism)
So how is CO2 transported in the blood?
1- As freely dissolved gas
CO2 more soluble than O2, but still only ~5-10% of CO2 in blood is dissolved
2- Bound to hemoglobin
~25% of CO2 in blood is carried bound to Hb (HbCO2)
only in mammals – fish have altered Hb which can’t bind CO2
3- As bicarbonate (HCO3-)
CO2 is converted into HCO3
HCO3- is the most important means of CO2 transport because
HCO3- is more soluble in the blood than CO2 – thus easier to transport than free gas
HCO3- cannot diffuse through membranes on its own – thus more controllable than free gas
HCO3- / Cl- antiport carrier passively facilitates diffusion across erythrocyte membrane
Allows plasma to “soak up” CO2, preventing buildup in RBCs
exchange with Cl- (“chloride shift”) prevents change in electrical gradient across membrane
Back at lungs, transport moves in opposite direction
Causes restoration of Cl- gradients
HCO3- reaction takes place in reverse to allow release of CO2 from blood to lungs as free gas
We’ve now seen that Hb can bind to O2, CO2, & H+ - so how does it choose which one & where?
Remember: high PO2 at lungs encourages binding (HbO2), & conditions at tissues (low O2, high CO2, high acidity, etc.) encourage dissociation
As HbO2 unbinds, the affinity of Hb for CO2 & H+ increases called the “Haldene effect”
Results in HbH+ & HbCO2
Dissociate at lungs & cycle starts again
Carbon monoxide (CO)
can also bind to Hb
CO2, O2, & H+ all readily dissociate from Hb
CO binds to Hb preferentially (more than O2) & does NOT readily dissociate
not enough O2 to tissues, CO poisoning
Hypoxia
insufficient O2
Hypercapnia
excess CO2 in blood
caused by excess CO2 in environment or hypoventilation
Hypercapnia–> elevated carbonic acid production–> excess H+ –> respiratory acidosis
Hypocapnia
low CO2 in blood
caused by hyperventilation
Hypocapnia –> drop in carbonic acid production–> less H+ than usual –> respiratory alkalosis
Why are changes in CO2 dangerous?
Changes in blood CO2 affect acid-base balance
CO2 + H2O H2CO3 H+ + HCO3-
Remember the importance of homeostasis, including of pH: low (acidic) or high (basic) pH = denaturation of proteins & irreversible cell damage
bronchodilation
Sympathetic stimulation
during exercise or other times when O2 needs increase
bronchoconstriction
Parasympathetic stimulation
when quiet & relaxed
Like arterioles, the smooth muscle on bronchioles is sensitive to local CO2 levels
High CO2 levels act directly on the smooth muscle, causing relaxation / dilation, while low CO2 levels cause contraction / constriction
Like blood flow, air flow is detected by peripheral chemoreceptors in the aorta & carotid artery
Chemoreceptors detect low O2, high CO2, & high H+
send info to respiratory center of the brain (in medulla)
However, these are only weakly stimulated – main regulators of ventilation are central chemoreceptors
Central chemoreceptors (in the brain) detect CO2 (weakly) & H+ (strongly), sending signals to the respiratory center to adjust ventilation
H+ cannot cross BBB on its own, but is produced in the brain when the bicarbonate reaction takes place
