pulmonary phys Flashcards
relationship between lung volume and resistance of extraalveolar and alveolar arteries
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
alveolar gas equation (find PAO2)
PAO2= PIO2 - (PACO2/R)
normal PIO2 = 150
normal R = .8
PaCO2 = PACO2
if need to calculate PIO2: PIO2 = FIO2 x (PB-PH2O)
PAO2 difference
used to find V/Q inequality, diffusion limitation, or shunt pathways
normal: 5-10 mmHg
PAO2- PaO2
define shunt
deoxygenated blood entering the left ventricle
how to determine if anatomical shunt
administer 100% O2, if PaO2 improves then not due to anatomical shunt
AVR
alveolar ventilation rate
AVR=(tidal volume-anatomical dead space) x ventilation frequency
norm: 4.2 L/min
how can PACO2 be affected
inversely proportional to AVR
directly proportional to VCO2 (metabolic production rate of CO2)
norm: 40 mmHg
calculating physiologic dead space
Bohr equation
dead space/tidal volume = (PaCO2 - PECO2)/PaCO2
J receptors
juxtacapillary receptors
respond to vascular congestion and by physical presence of the emboli and inflammatory mediator release
conditions of metabolic acidosis
low pH
primary problem: low H3O-
compensation: lower PaCO2 by hyperventilating
conditions of metabolic alkalosis
high pH
primary problem: high HCO3-
compensation: increase PaCO2 by hypoventilating
conditions of respiratory acidosis
low pH
primary problem: high PaCO2
compensation: increase HCO3- in the kidney
conditions of respiratory alkalosis
high pH
primary problem: low PaCO2
compensation: decrease HCO3- in kidney
how to determine chronic respiratory acidosis/alkalosis
chronic: 4 mEq/L increase or decrease in plasma HCO3 for each 10 mmHg increase or decrease in PCO2
henderson hasselbalch equation for acid-base distrubances
pH= pKa + log 10 (HCO3-/.03X PaCO2)
what two factors reduce compliance in healthy lung
lung elastic recoil and surface tension of fluid lining alveoli
lateral traction
alveoli stretch eachother and counteract recoil
if lateral traction is loss atelectasis can occur
O2 capacity
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)
O2 content
amount of O2 actually in blood
percent of O2 saturation x Hb concentration x 1.34 plus dissolved O2
dissolved O2 calculation
.003 x PO2
what is the Bohr effect in regards to Hb and O2 binding
Hb affinity for O2 is inversely related to both acidity and CO2 concentration, as both increase, it loses affinity for O2
Ficks law of diffusion equation
(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
calculating diffusion capacity for CO
DLCO = VCO/PACO
bc no CO in the capilaries
normal DLCO and levels that indicate a diffusion impariment
norm: 21-30
diffusion impairment: 1/3 or less (i.e. 7)
PTM
transmural pressure
pressure difference across an airway wall at any point in the tracheo-bronchial tree
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
calculating transmural pressure
Alveolar pressure - intrapleural pressure = transmural pressure
incresing/decreasing transpulmonary pressure has what effect on lung expansion
increasing transpulmonary pressure: lung expansion
decreasing transpulmonary pressure: lung collapse
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
Fick’s principle
measures cardiac output
Q = VO2/ (CaO2-CvO2)
where: VO2 = rate of O2 uptake, (CaO2-CvO2) = content difference in arteries vs vein
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
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
how is system pressure measured
pressure gauge in upper airways with mouth closed (closed system) and respiratory muscles relaxed
how is chest wall pressure measured
its calculated
system pressure = lung recoil + chest wall pressure
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
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
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
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
PEF
peak expiratory flow
MIF
maximum inspiratory flow
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)
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
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
restrictive diseases
cannot get air in
obstructive diseases
cannot get air out
what do peripheral vs central chemoreceptors detect
central: CO2
Peripheral: CO2, O2, and pH
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
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
pulmonary stretch receptors
slowly adapting receptors
lie in smooth muscle of conducting airways
respond to airway stretch, sense lung volume
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
C fiber endings
pulmonary C fibers
located near alveoli
respond to to mechanical stress
juxtapulmoary capillary receptors
J receptors
located in airways
respond to inflammation or vascular conjestion
proprioreceptors
joint, tendon, and muscle spindle receptors
located in chest wall increases motor excitation when movement
