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59 Cards in this Set

  • Front
  • Back
small air tubes made of smooth muscle (therefore capable of constricting and/or dilating) in the lower respiratory tract, branch from the bronchi, into the alveoli
part of LOWER respiratory tract
short tube extending from the larynx to the two bronchi
upper respiratory tract - houses vocal cords
two small tubes extending from the trachea, one to each lung. rigid, contain CARTILAGE and smooth muscle, capable of altering their diameter.
pulmonary artery
arising from the right ventricle. splits into smaller artieries which supply aveolar capilaries
pulmonary vein
flowing from the pulmonary venules, which leave the aveolar capillary bed, the pulmonary vein carriesl deoygenated blood to be reoxygenated.
sacs which branch out from the ends and sides of the bronchioles
-where the exchange of gas occurs within the lungs, via diffusion
intrapleural space
the thin fluid filled space between teh plurae lining the inside of the thorax, and the outside of the lungs. interpleural fluid in this space allows the lungs to easily slide within the thoracic cavity (reduces friction).
atmospheric pressure
760 mm Hg
pressure pushing against the inside of the lung.
GREATER than interpleural, forces lung expansion.
Intrapleural pressure
Usually 755 mm Hg
air pushin on the outside of the lung from the intrapleural cavity - LESS THAN THE ATMOSPHERIC PRESSURE.
two layers of very thin tissue between lungs and walls of thorax, lining outside of lung and inside of chest cavity. (Contains the intrapleural space.)
right ventricle
drives all of cardiac output through the lungs to reoxygenate the blood.
a compensatory response to a partially blocked airway, bronchodilation occurs to better match ventilation (air intake) to perfusion (blood flow to circulate gases through the body)

Bronchodilation also occurs in response to bronchiodilator drugs used to treat asthmatic effects of bronchioconstriction - they relax the smooth muscle of the bronchioles.
O2 hemoglobin dissociation curve
as partial oxygen is raised, oxygen concentration in the blood continues to rise until about 80 mm Hg of PO2. After this, the hemoglobin is fully saturated and the plasma can't carry much oxygen.
hemoglobin-oxygen dissociation curve: PO2 arterial blood?
hemoglobin-oxygen dissociation curve: PO2 venous blood?
LOWER than alveolar gas: 40 mm Hg - oxygen has been removed. BUT, the PCO2 is HIGHER - facilitates diffusion of CO2 into aveoli and out of the lungs--> expiration.
thin plate shaped muscle on the floor of the thoracic cavity. (what contracts during hiccups.)
ventilation - perfusion matching.
matching of airflow to blood flow to ensure distribution of gasses. facilitates correct gaseous concentration gradients to ensure gaseous exchange within the lungs. is an intrinsic regulatory mechanism.
decreased amount of oxygen in blood. elicits a series of responses... (not good.)
peripheral chemoreceptors
specialized cells able to sense chemicals within arterial blood
- located outside the CNS, on the outside of the carotid artery and the aorta, in the carotid and aortic bodies
-sense the oxygen levels within the blood supply
-send signals to the brainstem via respiratory neurons if the arterial oxygen supply decreases
-cause the brainstem to increase or decrease respiration to control homeostatic gaseous concentrations
respiratory pump
- elastic forces acting on the lungs and thoracic wall
-intrapleural pressures and pressure differences
- allow the pumping of and therefore gaseous exchange within the body
alveolar ventilation
amount of air flowing into the alveoli
anatomical dead space
volume of the conducting airways that hold air during each inspiration but don't function in gas exchange.
pulmonary perfusion
pulmonary blood flow. affects alveolar PO2, as more blood flow means more oxygen carried away, so LOWER alveolar PO2.
pulmonary ventilation
volume of airflow into and out of lungs per minute. helps determine oxygen and CO2 levels in blood.
#breaths/minute x volume of each breath.
ventilatory rate
number of breaths/minute
tidal volume
volume of air moved with each breath.
residual volume
volume of air which remains in the lungs after exhalation (about 2.5L). If we breathe out as MUCH as we can, there is still about 1L remaining.
vital capacity
volume of the biggest breath we can take: about 5 litres:

6L=total lung volume, minus 1L residual = 5 L.
how stretchable lungs and thorax are. HIGH compliance means VERY stretchable. LOW compliance means NOT.

1. Tissue elasticity
2. surface tension
alveolar surface tension
caused by the thin layer of liquid lining alveolus. Pulls inward, opposing lung expansion. When strong, can make breathing difficult.
pulmonary surfactant
- released by the aveolar cells of the aveoli, and is secreted into the liquid which lines the alveoli
- reduces surface tension, increases compliance (stretchiness)
-aids in ease of breathing
respiratory distress syndrome
- premature babies - very low lung compliance.
- cannot obtain enough oxygen- causes brain damage, 70% of deaths of pre-mature babies
- surfactant production begins late in fetal development, so deficient before this time.

RDS now curable with help of ARTIFICIAL SURFACTANTS sprayed as aerosols into the lungs.
pulmonary edema
due to compensatory response - arteries UPSTREAM from alveoli constrict - when this happens throughout the lung, it causes BACK PRESSURE, causing fluid to diffuse out of blood, through vessel walls and into the alveolar capillaries. Sometimes happens to climbers as a result of lack of oxygen. Fluid begins to fill lungs. is bad.
central chemoreceptors
sense H+ concentrations in CSF
portion of brainstem that controls breathing
cerebro-spinal fluid
partial pressure
pressure exerted by a single gas when more than one gas is present.
partial pressure of oxygen
partial pressure of CO2
aortic bodies and carotid bodies
small structures containing nerves which run to the respiratory neurons in the brainstem. These sense decreased arterial PO2 and cause increased respiratory activity in the brain, therefore increasedcontraction of respiratory muscles therefore increased ventilation.
Hydrogen levels
can interfere with nerve function when in large concentrations:
H+ and CO2 are key to allowing gas exchange across the alveoli - they facilitate the exchange by breaking the bonds on the hemoglobin, releasing O2.
Bicarbonate ions. Carry about 88% of C)2 in the blood.

oxygenated hemoglobin. travels to capillaries where increases in CO2 or H+ weaken bond, releasing O2 to the tissues.
carbamino hemoglobin
7% of the blood CO2 is bound to hemoglobin on the CO2 hemoglobin binding sites

result of a facilitated reaction catalyzed by carbonic anhydrase, molecules of carbonic acid (H2CO3) break down, causing CO2 to bind and be carried with hemoglobin.
air in the interpleural space (as a result of injury, stab wound, etc.)
causes collapse of lung as elastic forces across lung are no longer opposed. (i.e. intrapleural pressure equalizes with atmospheric pressure 760 mm Hg. Lung can't stay expanded.) Is bad.
Pressure gradients : BETWEEN BREATHS
LUNG: 760mm Hg

5 mm Hg pressure difference across lung wall (intrapleural-lung) keeps lung expanded
Pressure gradients: EXPIRATION
LUNG: 761 mm Hg

3 mm Hg pressure difference across lung wall (intrapleural-lung) causes lung to contract.

Muscles relax
thoracic wall moves inward
intrapleural pressure rises
pressure gradient across lungs is reduced
pressure in lungs increases by 1mm Hg above atmospheric, causing air to flow out of lungs against the gradient.
pressure gradients: INSPIRATION
LUNG: 759

7 mm Hg pressure difference across lung wall (intrapleural-lung) lung expands.

muscles pull thorax away from lung
creates suction in intrapleural space
REDUCES intrapleural fluid pressure
expansion causes pressure drop in lungs 1mm Hg
air pressure gradient causes air to be sucked into upper respiratory tract and lungs.
CO2 transport from tissues to capillaries. Why is CO2 released from erythrocytes and plasma into alveolar space?
CO2 travels from tissues to aveolar capillaries in the lungs in the opposite direction to that of oxygen. The majority of CO2 travels as bicarbonate ions within the plasma (about 88%), a smaller amount is bound to hemoglobin (about 7%) and lastly, some is dissolved directly into the plasma as ions (5%). Within the lungs, there is a partial pressure of only about PCO2 40mm Hg, whereas the blood entering the lungs containing the CO2 has a P CO2 of about 46mm Hg. This means that there is a P CO2 gradient (partial pressure CO2 differential) of about 6mm Hg. Similar to other gradients, this difference causes CO2 to diffuse from higher to lower pressure, from the blood in its various forms, to the aveolar air.
Parasympathetic nervous system active, what happens to airway resistance? How does this effect airflow rate?
Parasympathetic = normal - rhythmic breathing, little resistance. sympathetic = constriction = increased resistance = increased ventilation - rate and volume.
partial oxygen pressure of venous blood
40 mm Hg
partial oxygen pressure of arterial blood?
same as alveolar: 100 mm Hg
Why is alveolar PO2 LOWER than atmospheric PO2?
1. mixture of old and new air
2. O2 is taken away from alveolar gas by pulmonary perfusion
3. CO2 + water are added to alveoli.
Chemoreceptor - CENTRAL
senses H+ in CSF
nerves --> CNS
chemoreceptor - PERIPHERAL
in aorta and carotid artery
senses O2 in blood
nerves--> CNS
Partial oxygen pressures of tissues (examples)
skeletal muscle 10 mm Hg
Hot skin 98 mm Hg
connective tissue 40 mm Hg

(PO2 coming in 100mm Hg - causes faster diffusion to more "needy" tissues, i.e. skeletal muscle.)
hyperventilation effect on brainstem control.

peripheral and central H+ chemoreceptors work together - regulate pulmonary ventilation. Both arterial and CSF H+ concentrations effected by arterial PCO2, so arterial PCO2 effects both receptors.

Hyperventilating causes normal respiratory rate to be noticeably reduced.
- decreased activity of peripheral and central chemoreceptors
- this is because PCO2 is effected (REDUCED), but not H+ (which would be due to high fat metabolism, aspirin overdose, kidney failure, etc.)
Why is airflow resistance an important determinant of airflow rates in chronic obstructive pulmonary disease? (COPD)
COPD airflow resistance caused by:
initial inflammation, bronchial wall thickening, edema --> all disrupt or stop airflow to large portions of lungs.

This allows emphyma to take over, which determines airflow rates as it destroys inter-alveolar tissues, creating large spaces. Restricts airflow so drastically that insufficient oxygen available for even the most basic functions.

RESISTANCE = 1/RADIUS 4 (small changes in constriction effect resistance GREATLY.)