Respiratory Flashcards
area of lung w/ largest physiologic dead space
apex
IC =
IRV + TV
FRC =
RV + ERV
VC =
IRV + TV + ERV
TLC =
IRV + TV + ERV + RV
Vd (physiologic dead space) =
Vt x [(PaCO2 - PECO2)]/PaCO2
Vt = tidal vol PECO2 = expired air CO2 PaCO2 = arterial CO2
=anatomic dead space + functional dead space (ex. in apex of lung)
equilibration of O2 in NORMAL individual @ rest is what-limited?
perfusion-limited
what causes equilibration to become diffusion-limited?
emphysema, pulmonary fibrosis, increased exercise
what does it mean to be diffusion-limited?
gas doesn’t equilibrate by the time blood reaches end of capillary
what does it mean to be perfusion-limited?
diffusion only increased IF blood flow increases
equilibration normally occurs along first 1/3 of capillary
primary TB likes to be where?
lower lung fields
2ndary TB likes to be where?
upper lobes
A-a gradient =
PAO2 - PaO2
should be 10-15mmHg
increased in right to left shunt, diffusion limitation, V/Q mismatch
PAO2 = alveolar PO2 PaO2 = arterial PO2
PAO2 equation
= 150 - (PaCO2)/0.8
or
= PIO2 - (PaCO2)/R
PIO2 = PO2 in inspired air
causes of hypoxemia w/ normal A-a gradient?
high altitude
hypoventilation
causes of hypoxemia w/ increased A-a gradient?
V/Q mismatch (pneumonia, COPD, pulm embolism)
R–>L shunt (EIsenmenger synd)
pulmonary fibrosis (diffusion limited)
minute ventilation =
TV x breaths/min
ALL air!
alveolar ventilation =
(TV - dead space) x breaths/min
ONLY AIR participating in gas exchange
diffusion of gas (Vgas) =
A/T x Dk (P1 - P2)
A = area (decreased in emphysema)
T = thickness (increased in pulmonary fibrosis)
Dk (P1 - P2) = diff in partial pressure
in diffusion limited states what’s the main physiologic change
increased partial pressure difference b/w alveolar air + pulm capillary blood
cause of primary pulm HTN
BMPR2 inactivating mut (inhib vasc SM prolif normally)
TGF-beta!!!
causes of 2ndary pulm HTN
COPD
mitral stenosis
recurrent thromboemboli (decreases cross-sectional area of pulm bed)
autoimmune disease
L –> R shunt
sleep apnea
living @ high altitudes (hypoxic vasoconstriction)
PVR =
[P(pulm artery) - P(pulm wedge pressure)]/cardiac output
pulm wedge pressure is the same as what?
LA pressure
Resistance (R) =
(change in P)/Q
Q = flow
as viscosity increases, R –>
increases
as vessel length increases, R –>
increases
as vessel RADIUS increases, R –>
decreases (prop to the 4th power)
O2 content of blood =
(O2 binding capacity x %sat) + dissolved O2
1g of Hb can normally bind how much O2
1.34mL O2
as Hb falls, what changes happen in blood O2
O2 content decreases
O2 sat and arterial pO2 DON’T change!!
PAO2 =
150 - PaCO2/0.8
if PaO2/FiO2 =
300-500 (normal)
<200 (severe hypoxia)
increased A-a gradient usually seen in what state
hypoxemia
O2 changes in anemia
decreased TOTAL O2 content
no change in PaO2, O2 sat
O2 changes in COPD
decreased PaO2
physio shunt –> decreased O2 extraction ratio
decreased blood O2 content
O2 changes in exercise
decreased venous PO2 (bc increased demand)
right shift of curve
PaO2 doesn’t change
as V/Q –> 0, what happens?
airway obstruction, aka SHUNT!
100% O2 doesn’t improve condition bc air can’t REACH alveoli
as V/Q –> infinity, what happens?
blood flow obstruction aka PHYSIOLOGIC DEAD SPACE
100% O2 DOES improve if <100% dead space bc blood rerouted to other areas of lung w/ better O2 content
physio @ zone 1 (apex) of lung
PA > Pa > Pv physiologic dead space V/Q > 1 pulmonary capillaries collapsed decreased perfusion
physio @ zone 2 of lung
Pa > PA > Pv
pulsatile blood flow (increases as BP increases)
physio @ zone 3 (base) of lung
Pa > Pv > PA
decreased ventilation
V/Q < 1
SHUNTING
ventilation and perfusion are BOTH greatest @
base of lung than at apex
majority of CO2 transported in blood as
bicarb
cabaminohemoglobin (aka CO2 bound to Hb) is bound to Hb at what position?
@ N-terminus of GLOBIN not heme
Haldane effect?
lungs –> oxyg of Hb promotes dissociation of H+ from Hb –> leads to CO2 formation –> CO2 released from RBC
Bohr effect?
periph tissue –> increased H+ from tissue (from increased pCO2) –> shifts curve right –> unloads O2 (due to histidine side chains found on alpha + beta Hb subunits)
RBC exports bicarb out cell by exchanging for
plasma Cl-
body response to high altitude
decreased PAO2 –> decreased PO2
increased ventilation –> decreased PCO2
increased erythropoietin –> increased Hct, Hb
increased 2,3-BPG (unload more O2)
increased mitochondria
increased renal excretion of bicarb (to comp for resp alkalosis)
chronic hypoxic vasoconstriction –> RVH
body response to exercise
increased O2 consumpt + increased CO2 prod
increased ventilation rate
V/Q ratio uniform throughout lung (bc capillaries dilated in apices to lessen O2 wasting)
increased pulm BF bc of increased cardiac output
decreased pH (2ndary to lactic acidosis)
increased venous CO2, decreased venous O2, decreased venous pH; NO change in PaO2, PaCO2
Homan’s sign?
dorsiflexion –> calf pain
for DVT!
triad for fat embolus
hypoxemia
neuro abnorm
petechial rash
(TCP - from platelets coating fat microglobules)
amniotic fluid emboli can cause?
DIC
2 histo findings in asthma
Curshmann spirals (shed epith forming mucus plugs) Charcot-Leyden crystals (from breakdown of eosinophils in sputum)
anthracosis
coal mines
black lung, but asympt
no increased risk of lung cancer
UPPER lobes
silicosis
foundries, sandblasting
macrophages –> release fibrogenic factors –> fibrosis
silica can disrupt phagolysosome –> impair macrophages –> increased risk of TB
increased risk of bronchogenic carcinoma
UPPER lobes
“eggshell” calcifications in hilar LN
all pneumoconioses increase risk of?
cor pulmonale
Caplan’s synd (pneumoconiosis w/ rheumatoid arthritis - present w/ intrapulm nodule)
asbestosis
shipbuilding, roofing, plumbing
calcified parietal pleural plaques (not precancerous)
increased of bronchogenic carcinoma (1), mesothelioma (2)
LOWER lobes
asbestos bodies - golden-brown rods (“dumbbell shaped”) [aka ferruginous bodies - bc contain Fe]
Berylliosis
aerospace manufacturing
non-caseating granulomas (from CMI)
increased risk of lung cancer
RF for neonatal RDS
maternal diabetes, pre-maturity
therapeutic supplemental O2 in neonatal RDS can lead to?
retinopathy
bronchopulmonary dysplasia
due to ROS!!
low compliance is when
stiff lung and means extra work is required to bring in a normal volume of air (ex. pulm fibrosis)
high compliance is when
due to the poor elastic recoil –> no problem inflating the lungs but have extreme difficulty exhaling air
**extra work is required to get air out of the lungs.
Compliance also increases with increasing age
2 lung cancers not ass w/ smoking
BRonchial carcinoid
BRonchoalveolar carcinoma
tumors located peripherally
adenocarcinoma
large cell carcinoma
tumors located centrally
small cell
squamous cell
bronchoalveolar subtype carcinoma from what cells?
Clara cells
adenocarcinoma ass w/ what mutation
activating k-ras
squamous cell carcinoma of lung arises from?
hilar mass from bronchus
mesothelioma features?
hemorrhagic pleural effusions + pleural thickening
can arise in tunica vaginalis (sac around testes) as well
psammoma bodies
SVC synd signs
facial plethora
JVD
edema of UE
pneumonia caused by exacerbation of COPD =
H.influenza
granulomatous rxn w/ eosinophils
hypersensitivity pneumonitis
chlyothorax findings
milky fluid
increased TG content (from chylomicrons)
one cause of spontaneous pneumothorax
rupture of apical blebs (ass w/ paraseptal [distal acinar] emphysema)
straddle embolus occludes what
bifurcation of pulm arteries
EKG changes/lab changes seen in PE
wide S in lead I
large Q, inverted T in lead III
“SIQ3T3”
elevated D-dimer
when in pulmonary vascular resistance lowest?
@ FRC
