Pulm Physiology 1 Flashcards
intrapulmonary vs intrapleural vs transmural pressure
intrapulmonary = pressure within alveoli, positive or negative
intrapleural = pressure between visceral/parietal pleura, always negative
transmural (transpulmonary): pressure that actually inflates the lung, difference between intrapulmonary/intrapleural pressure, always positive (it’s a magnitude)
transmural pressure is the same value as intrapleural pressure, but positive rather than negative
what pressure change is required for air to move out of the alveoli during expiration?
chest wall collapse —> increased intrapleural pressure (less negative, or positive with forced expiration) —> alveoli recoil, increasing intrapulmonary (alveolar) pressure
once alveolar pressure supersedes atmospheric pressure, air moves outward (down pressure gradient)
describe the difference in intrapleural pressure in simple vs tension pneumothorax
simple pneumothorax: intrapleural space is in open communication with atmospheric pressure, allowing it to equilibrate with atmospheric pressure (but can’t get greater than that) - mediastinal shift will occur with inspiration, revert with expiration
tension pneumothorax: intrapleural pressure increases due to 1 way valve with atmospheric pressure, allowing it to exceed atmospheric pressure as more and more air gets trapped following inspiration - mediastinal shift will occur and remain during inspiration/expiration
how would the graph of lung compliance change in a patient with emphysema? (x axis = transpulmonary pressure, y axis = lung volume)
emphysema - steep compliance curve relative to normal, aka a large change in volume occurs with relatively small change in pressure
this increases the work of breathing (more difficult to expel air due to loss of elastic recoil)
how would the graph of lung compliance change in a patient with pulmonary fibrosis? (x axis = transpulmonary pressure, y axis = lung volume)
fibrosis and other restrictive pulmonary diseases will have a flat compliance curve relative to normal - indicates much greater change in pressure required to move a given volume
increases the work of breathing because the lungs are resistant to inflation
what are the 3 respiratory centers within the medulla and what are their respective functions?
- dorsal respiratory group (DRG): inspiration
- ventral respiratory group (VRG): inspiration and expiration
- Pre-Botzinger complex of the VRG: respiratory rhythm
how do the external intercostals and sternocleidomastoid act as accessory muscle in inspiration?
external intercostals: raise and enlarge the rib cage
sternocleidomastoid: elevates the sternum
which receptors control PNS and SNS mechanisms, respectively, in the bronchial smooth muscle?
- vagus (CN X) enables PNS-dependent constriction —> ACh from post-ganglionic fibers binds Type 3 cholinergic-muscarinic receptors
- circulating epinephrine from adrenal medulla binds beta2 adrenergic receptor activation induces dilation (no SNS fiber innervation)
what do albuterol and salmeterol both bind in the lung?
beta2 receptor agonists - cause bronchodilation
used in treatment of asthma and COPD
what does Fick’s law demonstrate?
amount of gas which diffuses across the blood-gas and blood-tissue barriers is proportional to the area of the tissue layer, the diffusion constant, and the differences in partial pressure
inversely proportional to the thickness
[diffusion constant is proportional to gas solubility, inversely proportional to square root of molecular weight]
what does the DLCO indicate about lung function?
DLCO = diffusion capacity of [the lungs for] carbon monoxide
determined clinically, indicates diffusing capacity of the lungs
exercise in a healthy person should increase DLCO, but DLCO would be decreased with thickened barrier (edema, fibrosis), decreased surface area (emphysema, low CO), reduced uptake by erythrocytes (anemia), and V/Q mismatch
how would the following cause a decrease in DLCO?
a. edema
b. fibrosis
c. emphysema
d. decreased cardiac output
e. anemia
DLCO indicates diffusing capacity of lungs
a. edema and b. fibrosis: thickened diffusion barrier
c. emphysema: decreased surface area
d. decreased cardiac output: less perfusion to lungs decreases surface area for diffusion
e. anemia: reduced uptake by erythrocytes
what are the normal values for the following:
a. PiO2
b. PaO2
c. PaCO2
d. PvCO2
e. PvO2
a. PiO2 (inspired): 150mmHg
b. PaO2 (arterial): 95-98mmHg
c. PaCO2 (arterial): 40mmHg
d. PvCO2 (venous): 45mmHg
e. PvO2 (venous): 40-45mmHg
why is there a large arterial-to-venous difference in the partial pressure of oxygen, but not carbon dioxide?
PaO2 = 95-98mmHg
PvO2 = 40-45mmHg
arterial O2 is uptake by cells
PaCO2 = 40mmHg
PvCO2 = 45mmHg
lots of CO2 is produced, but mostly in the form of HCO3-
functional residual capacity (FRC) vs residual volume (RV)
FRC = volume of gas remaining in lungs after tidal (normal) expiration
RV = volume of gas remaining in lungs after maximal inspiration (cannot get rid of this air with force)
match with the analogous term and explain:
obstructive and restrictive lung disease
concentric and eccentric hypertrophy of the heart
obstructive lung disease is like eccentric hypertrophy of the heart - it’s too stretched out and can’t expel the volume efficiently… loss of elastic recoil, air has a hard time getting OUT —> TLC may be increased, but FEV1/FVC is decreased
restrictive lung disease is like concentric hypertrophy of the heart - it’s too stiff and can’t get volume in… loss of compliance, air has a hard time getting IN —> TLC is decreased, but FEV1/FVC may be increased
what are 5 general causes of hypoxemia?
- hypoventilation
- decreased ambient PO2
- diffusion impairment
- V/Q mismatch
- shunt
how could markedly increase cardiac output cause a decrease in the A-a gradient?
A-a gradient = alveolar to arterial O2 difference
with very high CO, the alveolar capillary transit time is too short to allow unloading of alveolar O2 to blood
in a healthy patient, PaO2 will be diffusion or perfusion limited?
normal physiology: perfusion limited - oxygen in blood depends on rate at which blood transits alveolar capillaries
pathophysiology: diffusion limited, because of abnormalities in alveolar membrane, pulmonary edema, low atmospheric PO2 (altitude), etc
PaO2 vs SaO2 vs SpO2 vs CaO2
PaO2 = oxygen dissolved
SaO2 = oxygen bound to hemoglobin (oxygen saturation as measured by arterial blood draw)
SpO2 = oxygen saturation (pulse ox)
CaO2 = total blood O2
left vs right shift of oxygen dissociation curve
right = LESS affinity (low pH, high BPG, high temp, etc)
left = MORE affinity (fetal Hb)
as PCO2 rises, afferent signals from aortic chemoreceptors via ____ and from carotid chemoreceptors via ______ are sent to the ventilatory regulatory centers in the medulla
aortic - CN X (vagus)
carotid - Hering’s nerve (branch along CN IX, glossopharyngeal)
central chemoreceptors respond exclusively to…
elevated PCO2 (do not respond to hypoxemia)
most likely sense increased [H+] in CSF
what are the 3 main determinants of mean pulmonary artery pressure?
- left atrial pressure
- pulmonary blood flow
- pulmonary vascular resistance*
*PVR is itself affected by lung volume, alveolar and interpleural pressures, right ventricular output, and gravity
explain how the transmural pressure gradients of pulmonary vessels changes to cause increase or decrease of vessel diameter
transmural pressure gradient: difference between inside and outside pressures of a vessel
large pressure gradient - pulmonary vessel diameter increases
low pressure gradient - pulmonary vessel diameter decreases (negative transmural pressure causes compression/collapse of a vessel)
how does the shape/size of alveoli change with inspiration/expiration?
inspiration - alveoli expand and elongate (reduction in diameter of alveoli capillaries —> increased resistance to blood flow, more time for diffusion)
expiration - alveoli shrink, less resistance to blood flow in capillaries
how does the shape of large pulmonary arteries and veins change with inspiration/ expiration?
inspiration - distend
expiration - compress
describe the critical opening pressure of pulmonary capillaries
at resting cardiac output, pulmonary capillaries surrounding less-ventilated alveoli are constricted and relatively non-perused (don’t want to waste air)
with increased metabolic demand, increased flow (due to CO) causes opening of these capillaries (at their critical opening pressure) - elevations in ventilation are matched with elevations in perfusion
(mostly at apex/top, since gravity pulls blood down to base of lungs lower portions will be better perfused at rest)
which of the following will DECREASE pulmonary vascular resistance?
a. alveolar hypercapnia
b. histamine
c. norepinephrine
d. bradykinin
e. beta-2 antagonist
d. bradykinin —> deceased PVR (= more blood flow/ perfusion)
describe hypoxic vasoconstriction
phenomenon by which lungs divert blood flow to well ventilated regions of lungs, and away from poorly ventilated regions (don’t want to waste air!)
can result from alveolar hypoxia, atelectasis, local response by vasoactive mediators (histamine, catecholamines, some prostaglandins)
physiological vs anatomic pulmonary shunting
physiological: occurs when there is perfusion to a completely unventilated alveoli
anatomic: blood leaves right heart and enters left heart without traversing pulmonary capillaries
in absolute pulmonary shunt, what happens to alveolar partial pressures?
absolute shunt (aka capillary shunting): perfused but non-ventilated alveoli (no blood oxygenation occurs in these regions, V/Q = 0)
alveolar partial pressures equilibrate with that of mixed venous blood: PAO2 = 40mmHg, PACO2 = 45mmHg
will not respond to supplemental oxygen!!!
what does a high V/Q ratio indicate?
some ventilation but no perfusion (as V/Q gets larger/approaches infinity)
such as in alveolar dead space
how does V/Q ratio change from lung apex to base?
higher V/Q at apex, decreases on the way down to base
much more perfusion at base of lung (gravity dependent)
in which patient population is primary (idiopathic) pulmonary HTN more prevalent (though it is rare)?
younger women - usually progressive, poor prognosis
the removal of net fluid accumulation from tissue interstitium is accomplished by…
the lymphatic system (to prevent edema), which returns fluids to blood plasma at subclavian vein
briefly describe the physiological response to hypobaric hypoxia (high altitude breathing)
fall in PaO2 triggers hypoxia inducing factor (transcription factor)
within minutes, peripheral hypoxic drive raises tidal volume and respiratory rate —> lowered PaCO2 induces respiratory alkalosis, and hypocapnia in turn dampens central ventilatory drive
minutes - elevated CO and HR, but SV not altered
hours/days - plasma volume decreases and renal compensation drives HCO3- excretion, turning central ventilatory drive up again (increased PAO2)
