Pulm Physiology 1

Question 1

intrapulmonary vs intrapleural vs transmural pressure

Answer 1

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

Question 2

what pressure change is required for air to move out of the alveoli during expiration?

Answer 2

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)

Question 3

describe the difference in intrapleural pressure in simple vs tension pneumothorax

Answer 3

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

Question 4

how would the graph of lung compliance change in a patient with emphysema? (x axis = transpulmonary pressure, y axis = lung volume)

Answer 4

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)

Question 5

how would the graph of lung compliance change in a patient with pulmonary fibrosis? (x axis = transpulmonary pressure, y axis = lung volume)

Answer 5

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

Question 6

what are the 3 respiratory centers within the medulla and what are their respective functions?

Answer 6

1. dorsal respiratory group (DRG): inspiration
2. ventral respiratory group (VRG): inspiration and expiration
3. Pre-Botzinger complex of the VRG: respiratory rhythm

Question 7

how do the external intercostals and sternocleidomastoid act as accessory muscle in inspiration?

Answer 7

external intercostals: raise and enlarge the rib cage

sternocleidomastoid: elevates the sternum

Question 8

which receptors control PNS and SNS mechanisms, respectively, in the bronchial smooth muscle?

Answer 8

1. vagus (CN X) enables PNS-dependent constriction —> ACh from post-ganglionic fibers binds Type 3 cholinergic-muscarinic receptors
2. circulating epinephrine from adrenal medulla binds beta2 adrenergic receptor activation induces dilation (no SNS fiber innervation)

Question 9

what do albuterol and salmeterol both bind in the lung?

Answer 9

beta2 receptor agonists - cause bronchodilation

used in treatment of asthma and COPD

Question 10

what does Fick’s law demonstrate?

Answer 10

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]

Question 11

what does the DLCO indicate about lung function?

Answer 11

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

Question 12

how would the following cause a decrease in DLCO?
a. edema
b. fibrosis
c. emphysema
d. decreased cardiac output
e. anemia

Answer 12

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

Question 13

what are the normal values for the following:
a. PiO2
b. PaO2
c. PaCO2
d. PvCO2
e. PvO2

Answer 13

a. PiO2 (inspired): 150mmHg
b. PaO2 (arterial): 95-98mmHg
c. PaCO2 (arterial): 40mmHg
d. PvCO2 (venous): 45mmHg
e. PvO2 (venous): 40-45mmHg

Question 14

why is there a large arterial-to-venous difference in the partial pressure of oxygen, but not carbon dioxide?

Answer 14

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-

Question 15

functional residual capacity (FRC) vs residual volume (RV)

Answer 15

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)

Question 16

match with the analogous term and explain:
obstructive and restrictive lung disease

concentric and eccentric hypertrophy of the heart

Answer 16

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

Question 17

what are 5 general causes of hypoxemia?

Answer 17

1. hypoventilation
2. decreased ambient PO2
3. diffusion impairment
4. V/Q mismatch
5. shunt

Question 18

how could markedly increase cardiac output cause a decrease in the A-a gradient?

Answer 18

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

Question 19

in a healthy patient, PaO2 will be diffusion or perfusion limited?

Answer 19

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

Question 20

PaO2 vs SaO2 vs SpO2 vs CaO2

Answer 20

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

Question 21

left vs right shift of oxygen dissociation curve

Answer 21

right = LESS affinity (low pH, high BPG, high temp, etc)

left = MORE affinity (fetal Hb)

Question 22

as PCO2 rises, afferent signals from aortic chemoreceptors via ____ and from carotid chemoreceptors via ______ are sent to the ventilatory regulatory centers in the medulla

Answer 22

aortic - CN X (vagus)

carotid - Hering’s nerve (branch along CN IX, glossopharyngeal)

Question 23

central chemoreceptors respond exclusively to…

Answer 23

elevated PCO2 (do not respond to hypoxemia)

most likely sense increased [H+] in CSF

Question 24

what are the 3 main determinants of mean pulmonary artery pressure?

Answer 24

1. left atrial pressure
2. pulmonary blood flow
3. pulmonary vascular resistance*

*PVR is itself affected by lung volume, alveolar and interpleural pressures, right ventricular output, and gravity

Question 25

explain how the transmural pressure gradients of pulmonary vessels changes to cause increase or decrease of vessel diameter

Answer 25

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)

Question 26

how does the shape/size of alveoli change with inspiration/expiration?

Answer 26

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

Question 27

how does the shape of large pulmonary arteries and veins change with inspiration/ expiration?

Answer 27

inspiration - distend

expiration - compress

Question 28

describe the critical opening pressure of pulmonary capillaries

Answer 28

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)

Question 29

which of the following will DECREASE pulmonary vascular resistance?
a. alveolar hypercapnia
b. histamine
c. norepinephrine
d. bradykinin
e. beta-2 antagonist

Answer 29

d. bradykinin —> deceased PVR (= more blood flow/ perfusion)

Question 30

describe hypoxic vasoconstriction

Answer 30

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)

Question 31

physiological vs anatomic pulmonary shunting

Answer 31

physiological: occurs when there is perfusion to a completely unventilated alveoli

anatomic: blood leaves right heart and enters left heart without traversing pulmonary capillaries

Question 32

in absolute pulmonary shunt, what happens to alveolar partial pressures?

Answer 32

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!!!

Question 33

what does a high V/Q ratio indicate?

Answer 33

some ventilation but no perfusion (as V/Q gets larger/approaches infinity)

such as in alveolar dead space

Question 34

how does V/Q ratio change from lung apex to base?

Answer 34

higher V/Q at apex, decreases on the way down to base

much more perfusion at base of lung (gravity dependent)

Question 35

in which patient population is primary (idiopathic) pulmonary HTN more prevalent (though it is rare)?

Answer 35

younger women - usually progressive, poor prognosis

Question 36

the removal of net fluid accumulation from tissue interstitium is accomplished by…

Answer 36

the lymphatic system (to prevent edema), which returns fluids to blood plasma at subclavian vein

Question 37

briefly describe the physiological response to hypobaric hypoxia (high altitude breathing)

Answer 37

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)