pulmonary phys Flashcards

(53 cards)

1
Q

relationship between lung volume and resistance of extraalveolar and alveolar arteries

A

extraalveolar arteries are exposed to pleural pressure
alveolar arteries are exposed to alveolar pressure
at RV: extraalveolar resistance is at its highest and alveolar resistance is at its lowest
at TLC: vice versa
total pulmonary resistance is lowest at FRC

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2
Q

alveolar gas equation (find PAO2)

A

PAO2= PIO2 - (PACO2/R)
normal PIO2 = 150
normal R = .8
PaCO2 = PACO2

if need to calculate PIO2: PIO2 = FIO2 x (PB-PH2O)

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3
Q

PAO2 difference

A

used to find V/Q inequality, diffusion limitation, or shunt pathways
normal: 5-10 mmHg
PAO2- PaO2

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4
Q

define shunt

A

deoxygenated blood entering the left ventricle

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5
Q

how to determine if anatomical shunt

A

administer 100% O2, if PaO2 improves then not due to anatomical shunt

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6
Q

AVR

A

alveolar ventilation rate
AVR=(tidal volume-anatomical dead space) x ventilation frequency
norm: 4.2 L/min

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7
Q

how can PACO2 be affected

A

inversely proportional to AVR
directly proportional to VCO2 (metabolic production rate of CO2)
norm: 40 mmHg

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8
Q

calculating physiologic dead space

A

Bohr equation

dead space/tidal volume = (PaCO2 - PECO2)/PaCO2

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9
Q

J receptors

A

juxtacapillary receptors

respond to vascular congestion and by physical presence of the emboli and inflammatory mediator release

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10
Q

conditions of metabolic acidosis

A

low pH
primary problem: low H3O-
compensation: lower PaCO2 by hyperventilating

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11
Q

conditions of metabolic alkalosis

A

high pH
primary problem: high HCO3-
compensation: increase PaCO2 by hypoventilating

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12
Q

conditions of respiratory acidosis

A

low pH
primary problem: high PaCO2
compensation: increase HCO3- in the kidney

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13
Q

conditions of respiratory alkalosis

A

high pH
primary problem: low PaCO2
compensation: decrease HCO3- in kidney

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14
Q

how to determine chronic respiratory acidosis/alkalosis

A

chronic: 4 mEq/L increase or decrease in plasma HCO3 for each 10 mmHg increase or decrease in PCO2

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15
Q

henderson hasselbalch equation for acid-base distrubances

A

pH= pKa + log 10 (HCO3-/.03X PaCO2)

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16
Q

what two factors reduce compliance in healthy lung

A

lung elastic recoil and surface tension of fluid lining alveoli

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17
Q

lateral traction

A

alveoli stretch eachother and counteract recoil

if lateral traction is loss atelectasis can occur

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18
Q

O2 capacity

A

amount of O2 in the blood when Hb is 100% saturated
Hb concentration x 1.34 plus dissolved O2
(norm Hb concentration is 13.5)

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19
Q

O2 content

A

amount of O2 actually in blood

percent of O2 saturation x Hb concentration x 1.34 plus dissolved O2

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20
Q

dissolved O2 calculation

A

.003 x PO2

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21
Q

what is the Bohr effect in regards to Hb and O2 binding

A

Hb affinity for O2 is inversely related to both acidity and CO2 concentration, as both increase, it loses affinity for O2

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22
Q

Ficks law of diffusion equation

A

(A x D)/T= diffusion capacity
where A= area, D= diffusion constant, T= thickness

or

Vgas/(P1xoP2x)=Dlx
where Vgas= rate of gas exchange, and pressure differences across membrane

23
Q

calculating diffusion capacity for CO

A

DLCO = VCO/PACO

bc no CO in the capilaries

24
Q

normal DLCO and levels that indicate a diffusion impariment

A

norm: 21-30

diffusion impairment: 1/3 or less (i.e. 7)

25
PTM
transmural pressure | pressure difference across an airway wall at any point in the tracheo-bronchial tree
26
functional residual capacity
end of quite expiration all respiratory muscles are relaxed tendency of lungs to colapse is balanced by the tendency of chest wall to expand
27
calculating transmural pressure
Alveolar pressure - intrapleural pressure = transmural pressure
28
incresing/decreasing transpulmonary pressure has what effect on lung expansion
increasing transpulmonary pressure: lung expansion | decreasing transpulmonary pressure: lung collapse
29
transpulmonary pressure at FRC
no airmovement so PALV is 0 PTP = PALV - PIP so: PTP= -PIP you can messure Pip with esophageal balloon (-5 cmH20) Pip= -5 cmH2O so PTP = -(-5) = +5 cm H2O since chest wall and lung recoil are equal and oppostie, chest wall is 2.5 and lung recoil is 2.5
30
Fick's principle
measures cardiac output Q = VO2/ (CaO2-CvO2) where: VO2 = rate of O2 uptake, (CaO2-CvO2) = content difference in arteries vs vein
31
regarding lung and chest wall pressures, are negative/positive pressures expanding or collapsing
negative lung or chest wall pressure is expanding (lung never negative) positive lung and chest wall pressure is collapsing
32
how is lung recoil pressure measured
intrapleural pressure is measured with an esophageal balloon and in an open system Palv will be 0 so can calculate using PTP=-Pip and PTP will be used for the lung recoil here
33
how is system pressure measured
pressure gauge in upper airways with mouth closed (closed system) and respiratory muscles relaxed
34
how is chest wall pressure measured
its calculated | system pressure = lung recoil + chest wall pressure
35
condition 1
open system --> PALV = 0 holding volume constant with muscles --> cancels affects of chest wall with esophageal balloon, able to measure PTP which will be -Pip only since Palv = 0
36
condition 2
alveoli/airways closed system--> air cannot escape lungs and causes a resistant pressure negating lung recoil relaxing all muscles: allows chest wall to pull/push measure the system with pressure gauge Pip= CW only
37
effects of obstructive vs restrictive on FEV1/FVC
FVC (forced vital capactiy) FEV1 (forced expired volume in first second) FEV1/FVC decreases in obstructive and either stays the same or increases in restrictive
38
why is rate of air flow only effort dependent at high volumes
at low lung volumes, reduced mecahnical thethering cannot oppose tendency toward airway collapse so any effort put into exhaling will be negated
39
PEF
peak expiratory flow
40
MIF
maximum inspiratory flow
41
what are the two points on the x axis of a flow volume loop
TLC (total lung capacity, usually on left side of graph, the larger volume) and RV (residual volume, usually on right side of graph, the smaller volume)
42
EPP
equal pressure point when pressure is less than intraplural pressure therefore collapsible in healthy individuals this is at the noncollapsible portions of the airways but in patients with COPD this is in the collapsible portions causing collapse and therefore cannot get air out
43
what are the mechanisms of obstruction in a COPD patient
decreased airway pressure due to increased lung compliance cannot prevent dynamic compression of lower compressible airways decreased mechanical tethering between lung tissue which usually tends to keep alveoli and compressible airways stretched open bronchial narrowing due to bronchitis
44
restrictive diseases
cannot get air in
45
obstructive diseases
cannot get air out
46
what do peripheral vs central chemoreceptors detect
central: CO2 Peripheral: CO2, O2, and pH
47
inspiratory control centers and expiratory control centers
inspiratory: dorsal respiratory group and intermediate portion of ventral respiratory group expiratory: rostral and caudal portions of ventral respiratory group
48
how do central chemoreceptors respond to CO2 levels
once acrossed the blood-brain barrier, CO2 is converted into H+ and bicarb, the central chemoreceptors detect the H+ ions and sends signal to medullary respiratory center resulting in pumlonary ventilation
49
pulmonary stretch receptors
slowly adapting receptors lie in smooth muscle of conducting airways respond to airway stretch, sense lung volume
50
irritant receptors
rapidly adapting receptor lie beneath surface of larger conducting airways stimulated by histamine, serotonin, prostaglandins liberated during allergy and inflammation stimulation causes cough, gasping, and prolonged inspiration time
51
C fiber endings
pulmonary C fibers located near alveoli respond to to mechanical stress
52
juxtapulmoary capillary receptors
J receptors located in airways respond to inflammation or vascular conjestion
53
proprioreceptors
joint, tendon, and muscle spindle receptors | located in chest wall increases motor excitation when movement