Week 6 Flashcards
1
Q
Pulmonary physical exam and middle lobe
A
right middle lobe can only be examined on anterior side of ches
2
Q
Trachea deviation
A
indicates enlargement of space in left lung area pushing mediastinum to right or collapse of lobe on right (lung cancer)
3
Q
Increased resonance
A
more hollow sounding: pneumothorax or advanced empysema
4
Q
Dullness to percussion
A
more dense area (fluid, tissue)
5
Q
auscultation of lungs bell or diaphragm?
A
only use diaphgragm because of high pitch sounds
6
Q
Bronchial breath sounds
A
normal sounds over trachea
7
Q
vesicular breath sounds
A
normal sounds over lung fields (opening and closing of alveoli)
8
Q
crackles (rales)
A
fluid in alveoli
9
Q
wheezing
A
narrow airways (COPD, asthma)-hhg pitched continuous sound during expiration (sometimes inspiration)
10
Q
vocal resonance
A
increased or decreased (increased if consolidation)
11
Q
whispered pectoriloquy
A
increased in pneumonia and consolidation
12
Q
egophony
A
increased in pneumonia and consolidation
13
Q
when assessing a CXR
A
ABCDE: air, bones, cardiac, diaphragm, effusion
14
Q
Pneumothorax (air in pleural space)
A
increased volume of involved side (taking up extra space)
percussion: more air so hyper resonance (hollow)
Auscultation: decreased breath sounds, decreased vocal resonance
heart may be pushed over on CXR
15
Q
Pleural effusion (fluid in pleural space)
A
inspection: decreased expansion
Percussion: dullness
Auscultation: absent breath sounds (fluid in way), decreased vocal resonance
16
Q
Pneumonia
A
Inspection: splinting (not taking deep breaths due to pain)
Percussion: dullness
auscultation: crackles, bronchial breath sounds, increased vocal resonance, ego phony, whispered pectorliquy
17
Q
Emphysema
A
loss of normal alveoli (impaired airflow), air can get in but not out of alveoli so air trap
barrel chested appearance
18
Q
COPD
A
Inspection: AP diameter increased, accessory muscle use
Percussion: increased resonance all throughout, decreased diaphragm movement
Auscultation: decreased breath sounds and heart sounds, wheezes, prolonged expiration
CXR: flatter diaphragm and larger lungs
19
Q
CHF
A
crackles/rales usually in dependent lung fields
wheezing
20
Q
Respiratory system functions
A
provide oxygen and eliminate O2
Regulates blood’s hydrogen ion concentration (pH)
form speech sounds
defend against microbes
influence arterial concentrations of chemical messengers by adding/removing
trap and dissolve blood clots arising from systemic veins (legs)
21
Q
Produced and Added by lung cells
A
bradykinin, histamine, serotonin, heparin, prostaglandin E2, F2alpha, endoperoxidases
22
Q
Metabolized, cleared by lung cells
A
prostaglandins E1, E2, F2alpha, NE
23
Q
Conducting zone
A
trachea through terminal bronchioles
24
Q
Respiratory zone
A
Respiratory bronchioles through alveolar sacs
25
Cartilaginous rings
Trachea and bronchi for maximal air flow
26
Air filtration
mechanical/chemical stimulation of airway receptors can cause bronchoconstriction
stimulation of nose receptors: sneeze
stimulation trachea receptors: cough
mucuciliary escalator
27
Inspiratory muscles: Diaphragm
Diaphragm: contraction leads to inspiration (downward movement, increasing thoracic cavity size)
relaxation leads to expiration (abdominal pressure forces muscle to resting position to decrease cavity size)
28
Inspiratory muscles: paradoxical movement
if hemiparalyzed, diaphragm that is paralyzed moves up with inspiration due to negative inter thoracic pressure pulling upwards
29
Inspiratory muscles: external intercostal muscles
connect adjacent ribs, slope down and forward
| during contraction, pulled upward and forward to increase thoracic cavity
30
Inspiratory muscles: Accessory muscles
scalene and sternocleidomastoid which elevate first two ribs and sternum (exercise to assist inspiration)
31
Expiratory muscles: abodominal wall muscles
during contraction, increase intra abdominal pressure to force diaphragm upward
32
Expiratory muscles: internal intercostal muscles
pull ribs down and inward (decrease intrathoracic cavity size)
33
Innervation of respiration
C345 phrenic nerve for diaphragm
| External and internal intercostal nerves
34
Pressure volume breathing
Muscle contraction-->intrathoracic volume increases-->intrathoracic pressure decreases--> air enters alveoli (boil's law)
35
Factors of lung mechanics
```
Elastic recoil
surface tension
alveolar interdepencence
intrapleural pressure
lung compliance
```
36
Elastic recoil
tendency of structure to return to its natural state
```
CW outward (increase volume)
lung: alveoli inward (decrease volume)
```
37
Pulmonary parenchyma
gas exchanging part of the lung-composed of elastin and collage fibers
38
Functional residual capacity
chest wall elastance=lung elastance and Palveolar=Patm=0
seen at end expiration
39
Surface tension
elastic tendency of fluid surface to acquire least SA possible (liquid cohesive forces)
40
LaPlace's law
P=2T/r T=surface tension and r= radius
so if surface extension were constant in 2 differently sized alveoli: pressure in smaller alveoli would be much greater than large and this would cause air to move to larger alveoli and promote lung collapse
41
Surfactant and surface tension
PL secreted by Type II alveolar epithelial cells (85% lipid and 15% protein)-detergent and reduces surface tension at air fluid interface-keeps lungs open
reduces elastic recoil of lung
reduces hydrostatic pressure in tissue outside the capillary (preventing pulmonary edema)
42
Alveolar interdependence
structural support of individual alveolus by surrounding alveoli via elastic tissue network
43
Intrapleural Pressure
pleura: normal pressure created by elastic recoil is -3-5 cmH20
44
Intrapleural and alveolar pressure during inspiration
intrapleural pressure -8 cmH20
| alveolar pressure -1 cmH20
45
transpulmonary pressure
pressure difference across whole lung (keeps lung open) Ptp=Palv-Pip
it it equals 0 lungs will collapse
46
Lung compliance
ease with which lung is distended for a given force C=V/P
| at low lung volumes, highly compliant
47
hysteresis
slopes of lung compliance different in expiration and inspiration. surfactant may have decreased effects of decreasing surface tension on inspiration (takes higher P to get to same TLC)
48
Total compliance
1/total= 1/lung compliance +1/CW compliance
49
Measurements of Oxygen
Hb-O2 oxyhemoglobin: % saturation
dissolved arterial oxygen: PaO2
arterial O2 saturation: SaO2 % saturation
peripheral O2 saturation (most common)
50
absorption spectra of oxygen
Deoxyhemoglobin: absorbs red (600-750 nm)
oxyhemoglobin: absorbs infrared (850-1000 nm)
51
Pulse ox confounding factors
```
anemia, vasoconstriction, low bP
increased venous pulsation
external lights ources
dyes and pigments (methylene blue, nail polish)
dyshemoglobinemias (carboxyhbg, methb)
```
52
Hemoglobin spectra
oxyhemoglobin and carboxyhemoglobin absorbed at same spectra-gives spuriously elevated SpO2
methhb absorbs same as reduced hbg=high concentrations of meting low SpO2 but patient asymptomatic
53
Oxygen delivery
DO2=COxCaO2 (oxygen content) volume of oxygen delivered to systemic vascular bed permit minute
oxygen content: 1.36 x Hbg x SaO2/100 +0.003 PaO2 (dissolved O2 in plasma)
54
Hypoxia
PaO2 less than 60 mmHg (or less than 80)
55
Aa gradient not affected
alveolar hypoventilation
| decreased O2 tension
56
Aa gradient affected
VQ mismatch
shunt
diffusion impairment
57
Aa gradient normal range
Age in years/4 +4
58
VQ mismatch
most common: mismatch between ventilation and perfusion
| will partially correct with supplemental O2
59
Shunt
extreme version of VQ mismatch
adequate blood flow, poor ventilation
ex: intracardiac spatial defects VSD, ASD, PFO
ex: intrapulmonary: arteriovascular malformations ,ARDS
Does NOT correct with oxygen
60
Diffusion impairment
increased thickness of alveolar capillary membrane
decreased are for diffusion (less SA emphysema)
decreased blood transit time (exercise)
HYPOXIA ONLY WITH EXERTION
61
Alveolar hypoventilation
PAO2=PiO2 - (1.25xPaCO2) so if you retain more CO2 you will decrease oxygen. ex: advanced COPD, neuromuscular disease, drug overdose
Aa gradient normal because PAO2 decreases s the PaCO2 increases
Improves with oxygen
62
Decreased oxygen tension
altitude decreased barometric pressure
63
Acute mountain sickness (high altitude illness
headache, fatigue, lightheaded, anorexia, nausea
via vasogenic brain edema from disruption of blood brain barrier induced by hypoxemia at high elevation
typically above 2000m
not protected by youth/fitness but obesity and heavy exertion increase risk
Tx: supplemental oxygen, acetazolamide, descent
64
High altitude cerebral edema
ataxia, decline in mental function/consciousness
| elevation above 3000-3500 m
65
High altitude pulmonary edema
occurs 2-4 days after ascent above 2500m, most common cause of death at high altitude, high risk of recurrence
66
Periodic breathing of altitude
mirrors Cheyne Stokes
67
Hemoglobin T state
open state- binds O2 with low affinity
68
Hemoglobin R state
closed state- binds O2 with high affinity
69
hemoglobin vs myoglobin
myoglobin can only bind one oxygen molecule
release O2 at very low PO2 (storage protein in muscles)
hemoglobin: sigmoidal curve: multiple oxygens can bind
Release O2 in tissues at 20-30 torr (low pressures)
binding is cooperative
70
O2 affects hemoglobin
O2 binds iron and pulls it up in the plane of the heme which tugs on the histidine-leads to alterations and local changes in structure of hemoglobin subunit the destabilize contacts formed in t state --allows hemoglobin to form R state
71
Factors affecting gas transport by hemoglobin
2,3 BPG, H+, CO2, CO, fetal hemoglobin
72
2-3 BPG and hemoglobin
stabilizes the T state--highly negatively charged small molecule-binds central pocket in T state to stabilize and promote O2 release
shift saturation curve to the right--promotes O2 release so you can release O2 at higher PO2
73
23BPG and fetal hemoglobin
gamma chain in fetal hemoglobin is less positively charged than beta chain so this means HbF has lower affinity for negatively charge 23BPG. Has a higher O2 affinity (good for fetal rbc transfer)
shifts curve left compared to maternal oxyhemoglobin--lower PO2 results in higher saturation
74
H+ bohr effect
binding of H+ favors T state- H+ protonates the histidine side chain promoting oxygen dissociation from hemoglobin
shifts curve right-able to release at higher PO2
75
CO2 Haldane effect
favors T state
1. preferentially binds T state-weakens oxygen binding
2. CO2+H2O-->H2CO3-->H +HCO3- so CO2 leads to increase in H+ which decrease pH contributing to Bohr effect
76
CO effects on hemoglobin
binds hbg 200 times stronger than O2 and dissociates slowly--can be fatal
77
Conducting airways
Nasal cavity, pharynx (shared passage), larynx, and trachea
78
Respiratory Epithelium
lines most of the conducting airways
pseudostratified columnar ciliated epithelium with goblet cells
lamina propria and submucosa contain numerous seromucous glands-water mucous to cilia
79
Respiratory epithelium cell types
```
Ciliated
Goblet
Granule
Brush
Basal
```
80
Respiratory epithelium changes throughout airways
```
From columnar to cuboidal
height of epithelium decreases
goblet/glands decrease
cartilage decrease
relative amounts of smooth muscle and elastic fibers INCREASE
```
81
Larynx function and landmarks
maintain airway (cartilage) and close off airway (muscles)
close: swallow, cough, speech (vocal folds on lateral walls)
landmarks: epiglottis and vocal folds
82
Vocal folds
not lined by respiratory epithelium--instead stratified squamous epithelium (resist high friction)
83
True and false vocal folds
True: stratified squamous epithelium, overlie vocal ligaments (inferior to false)
False or vestibular: respiratory epithelium, overlie vestibular ligaments, contain glands (lubricate vocal vibrations), not involved in sound production)
84
Three regions of Larynx
1. Vestibule: opening of larynx to vestibular folds
2. Ventricle: between the vestibular and vocal folds
3. infraglottic cavity: vocal folds to trachea
85
Laryngeal cartilages
1. Epiglottis (elastic)
2. thyroid (hyaline, shield, doesn't cover posterior)
3. cricoid (hyalin, only complete ring of cartilage)
4. arytenoid (hyaline, sits on cricoid, attach vocal ligaments)
86
Laryngeal muscles
skeletal muscles (attach to arytenoids) close off airway and regulate vocal ligaments
87
Larynx innervation
recurrent laryngeal (vagus nerve cranial nerve X)
88
Vocal sounds
Tenser/shorter vocal cord: fast vibration and high pitch
| Losser/longer vocal fold: slower vibration and lower pitch
89
Trachea
branches t4/5 for carina at sternal angle, superior to heart
| forms the right and left primary main bronchi
90
Histology of trachea
16-20 C shaped hyaline cartilages-patent airway
smooth muscle on posterior side to allow esophageal expansion
lined with respiratory epithelium
91
Histology of tracheas
Respiratory epithelium
seromucous glands
hyaline cartilage
same pattern through bronchi with smooth muscle around cartilage
92
Lingula
tongue shaped projection in super lobe of left lung above the oblique fissure.
93
Hilus of lung
only place where structures enter/exit
1. bronchi
2. blood vessels (pulmonary A/V, bronchia A/V)
3. lymphatics
4. nerves
RALS
94
pulmonary arteries and veins
Arteries follow bronchia tree (segmental)
| veins travel between bronchopulmonary segments (intersegmental)
95
Right lung superior lobe segments
Apical, Anterior, Posterior
96
Right lung middle lobe segments
lateral, medial
97
Right lung inferior lobe segments
Superior, Anterior basal, medial basal, lateral basal, posterior basal
98
Left lung superior lobe segments
apicoposterior, anterior, superior lingular, inferior lingular
99
Left lung inferior lobe segments
superior, anterior basal, medial basal, lateral basal, posterior basal
100
Bronchi vs bronchiole histology
Bronchi: CARTILAGE, conducting system only
Bronchiole: NO cartilage, smooth muscle more prominent, conducting and respiratory system
101
Bronchioles and respiratory bronchiole histology
Conducting: respiratory epithelium, smooth muscle, elastic fibers, no cartilage
Respiratory: directly lead to alveoli, smooth muscle, elastic fibers, no cartilage
102
Alveolar cell types
Type I pneumocytes; flat make diffusion barrier with capillary endothelial cells
Type II pneumocystis (5%) surfactant
Macropage dust cells
103
Gas exchange membrane
surfactant layer-->Type I pneumocyte epithelium-->shared basement membrane-->endothelial cell of capillary
104
Parts of the parietal pleura
1. costal pleura : adjacent to ribs
2. diaphragmatic pleura: adjacent to diaphragm
3. mediastinal pleura: adjacent to pericardial sac
105
Pleural recesses
1. Costomediastinal recess: between heart percardium and ribs
2. costodiaphragmatic recess: between ribs and diaphragm
become larger during expiration--can get fluid for infection/bleeding
106
Diaphragm
```
dome shaped central tendon (pulls down during contraction)
moves 4-6 cm with each breath
vena cava (T8), esophageal hiatus T10, aortic hiatus T12, are the three foramen
```
107
Vagus nerve Cranial nerve X
originates in brainstem
superior laryngeal and recurrent laryngeal nerves innervate larynx. (right loops around subclavian and left loops around aortic arch)
108
Intrapleural and alveolar pressure
Intrapleural: during inspiration, decrease from -5 to -8 creates gradient for breathing
Alveolar: at mid inspiration -1, end of inspiration/expiratoin 0, and mid expiration +1
109
Situations where Intrapleural pressure is increased
Forced exhalation (dynamic compression)
stiff chest wall (decreased CW compliance, lose outward elastic recoil)
fluid or air in pleural space (pleural effusion or pneumothorax)
110
Pneumothorax symptoms and exam
chest pain, dyspnea, asymptomatic
decreased breath sounds, decreased chest excursion, hyperresonnant to percussion, decreased/absent tactile fremitus
111
Pneumothorax causes:
Primary: no known lung disease (rupture of apical sub pleural blebs shear force, tall young smokers)
Secondary: underlying lung disease
Iatrogenic
traumatic: GSW, broken rib
112
penetrative pneumothraox
puncture chest wall, air into intrapleural space which increases the intrapleural pressure (Alveolar pressure still 0. Tp is O or negative.
don't die right away
113
Non penetrative pneumothorax (tension)
trapped air in pleural space that can't get out
| hemodynamic instability-elevated intrapleural pressure impairs venous return to heart-die
114
Pneumothorax management
small and asymptomatic: observe (maybe oxygen)
symptomatic moderate to large: chest tube
tension: needle decompression 2nd intercostal space in mid clavicular line
115
Vital capacity
Inspiratory reserve volume, tidal volume and expiratory reserve volume
116
alveolar gas equation
PAO2= [(Pb-PH2O)xFiO2] -(PaCO2/RQ)
no CO2 in inspired air
inert uses in equilibrium(nitrogen)
alveolar and arterial CO2 are in equilibrium
ignore change in volume between inspired and expired air
117
Simplified alveolar gas equation
PAO2=(760-47)x.21 - (40/.8) =99
118
PACO2
PACO2= CO2 production/alveolar ventilation
119
minute ventilation effects on PACO2 and PAO2
hyperventilation: decrease PACO2 and increase PAO2 (indirectly via PCO2)
hypoventilation: increase PACO2 (direct) and decrease PAO2 (indirect)
120
diffusion factors
area of membrane, difference in partial pressure of gases, diffusion constant (membrane properties and gas properties ie. MW, solubility)
inversely proportional to membrane thickness
121
Blood-gas (capillary/alveolar) interface
oxygen in alveoli-->epithelium-->interstitial space and basement membrane-->endothelium-->plasma (PaO2)-->erythrocyte membrane-->RBC cytoplasm-->Hemoglobin (SO2)
122
limitations of oxygen diffusion
transit time of blood in pulmonary capillary
1. disease states thickening membrane
2. low inspired PO2 (decrease pressure gradient takes longer for equilibrium to occur)
3. exercise (decreased time)
123
CO2 diffusion across alveolar membrane
CO2 diffuses 20x more rapidly (higher solubility), small difference in partial pressure
124
CO2 transport in blood
1. dissolved (5-10%)
2. bicarbonate (in RBC via carbonic anhydrase) 60-90%
3. carbaminohemoglobin (HHb-CO2) Haldane 5-30%
125
Conditions affecting gas diffusion due to less surface area
ventilation perfusion matching
| decrease in lung parenchyma
126
conditions affecting gas diffusion due to alveolar interstitum wall thickening
edema, inflammation, fibrosis, sarcoidosis, hypersensitivity pneumonitis, radiation, busulfan, collage disorders
127
conditions affecting gas diffusion due to smaller differences in partial pressure
altitude, gases added to inspired air (helium, nitrogen, anesthetics)
128
conditions affecting gas diffusion due to changes in perfusion
fast pulmonary capillary transit times (exercise)
129
conditions in oxygen reaction with Hbg
altered by other gases binding with Hb (CO)
abnormal hemoglobin structure (methHbg)
oxygen reaction with hemoglobin is not linear
changes in the oxygen dissociation curve
130
normal PaO2
at sea level: PaO2=104-(.27xage)
131
in healthy person, small Aa gradient is normal
50% due to VQ mismatch
| 50% due to true shunt (thebesian and bronchial circulations)
132
hypoxemia and Aa gradient
Normal aA gradient-you would have to start with low alveolar PO2
increased Aa gradient-alveolar PO2 is normal but arterial Po2 is low
133
Aa gradient alternatives
P:F ration: PaO2/FIO2
| oxygenation index: mean airway pressure x FIO2 x 100/PaO2
134
minute ventilation
volume of air leaving lung each minute
Ve=fB x VT (RR x tidal volume)
Ve=Vd+VA (dead space ventilation + alveolar ventilation)
alveolar ventilation is volume of air leaving alveoli each minute that has participated in gas exchange
135
Tidal volume has 2 components
Vt=Vd+VA
136
measuring alveolar ventilation
VA=VCO2/FACO2
| carbon dioxide production/exhaled alveolar CO2
137
Measuring anatomic dead space (Fowler's method)
inhale 100% oxygen, start at expiration there is no nitrogen because you just inhaled oxygen. point where nitrogen and oxygen are mixed (area under curve) is the anatomic dead space.
138
Physiologic dead space
anatomic dead space+alveolar dead space (air going in and out but no blood going by it)-no CO2 excretion.
139
Bohr Equation for estimating physiologic dead space using dead space fraction Vd/Vt
Vd/Vt=PaCO2-PECO2/PaCO2
PECO2-mixed expiration CO2 (use end tidal CO2)
normal 0.2-0.3
140
Alveolar PCO2 determined by
VCO2=CO2 production=O2 consumption x RQ
CO2 eliminated through ventilation of alveoli
VA=VE (1-Vd/Vt)
assume no CO2 inspired, inert gases equilibrium
141
Calculating Alveolar PACO2
PACO2= VCO2/VE(1-Vd/Vt)
increased PACO2: increased Co2 production, decreased minute ventilation, increased dead space fraction
142
How to increase alveolar ventilation
increasing total minute ventilation (increasing tidal volume, increasing respiratory rate), decreasing dead space ventilation
143
alveolar dead space
where alveoli is normal and ventilated, but not perfused (not participating in gas exchange)
144
lower lung
ventilates and perfuses better
145
diffusion limited CO2
very soluble gas, moves from alveoli to RBC with no increase in partial pressure so it is only limited by diffusion properites
146
perfusion limited NO
not soluble, as it moves into RBC, partial pressure quickly equals the alveolar pressure and there is no additional movement, depends on blood flow
147
Both diffusion and perfusion limited O2
oxygen is soluble, but not fully, still a rise in partial pressure in rBC. Resting conditions: perfusion dependent, abnormal: diffusion depednet
148
what happens when alveolar pressure>capillary pressure
capillary collapse (transmural pressure is difference between inside and outside of capillaries)
149
Uneven distribution of blood flow (lower more) due to pressures (IN abnormal circumstances)
Zone 1: PA>Pa>Pv (collapse capillaries)
Zone 2: Pa>PA>Pv (blood flow determine by arterial/alveolar pressure differences)
Zone 3: Pa>Pv>PA (blood flow determined by arterial-venous differences)
150
Concentration of gas in lung/cap
depends on both ventilation and perfusion
151
Normal V/Q ratio
1
152
dead space
area ventilated but not perfused
153
VQ ratios and alveolar gas
Shunt: VQ=0
Normal: 1
Dead space infinity
154
VQ ratios at different lung levels
VQ ratio HIGHEST at top of lung. Both ventilation and perfusion increase toward bottom, perfusion at a faster rate so it make the VQ ratio smaller at lower lung levels
155
high VQ can not compensate for low VQ units
high VQ means not perfusion so you have a low contribution to oxygen content
156
Causes of uneven ventilation
regional changes in elasticity, regional obstruction, regional check valves, regional disturbances in expansion
157
Causes of uneven perfusion
embolization, occlusion, compression, fibrosis, loss of capillary surface area
158
VQ mismatch and CO2/O2
as you increase PaCO2, the concentration of CO2 increases in linear fashion.
as you increase PaO2, relationship of concentration is less linear.
159
examples of shunt
lobar pneumonia and ARDS
160
examples of VQ mismatch with high VQ ratio
COPD: increased VQ ratio, increased physiologic dead space, wasted ventilation, high frequency low tidal volume breathing.
Pulmonary embolism
Compression of pulmonary capillaries due to high alveolar pressure
shock (pulmonary vascular hypotension)
161
examples of VQ mismatch with low VQ ratio
```
asthma
chronic bronchitis
acute pulmonary edema
airway obstruction (aspiration)
cystic fibrosis
```
162
airway resistance in small vs large airways
in smaller airways, flow is more laminate, larger-more turbulent
163
resistance is inversely proportional to
the radius of a tube (smaller radius=larger resistance)
164
airway resistance is inversely proportional to
lung volume (higher lung volume, lower resistance)
165
How does lung volume affect airway resistance
as inspiring, create large negative intrapleural pressure which increase transpulmonary pressure-airway distension, dilating the airways drops the resistance
dynamic compression-forced expiration makes the intrapleural pressure positive, decreasing transpulmonary pressure (can overcome the alveolar elastic recoil and traction on bronchiolar wall-collapse airway)
166
alveolar dead space due to poor blood flow
decreased cardiac output due to CHF and obstruction to blood flow due to PE
167
Measure anatomic dead space
Fowler's method or 1 mL/lb of ideal body weight
168
Measure physiologic deadspace via estimation through
Bohr equation
169
dead space fraction
Vd/Vt normal 1:3 or .30
170
dead space fraction during exercise
anatomic dead space increases during inspiration due to distending airways
however, Vd/Vt decreases during inspiration due to increase in Vt (during exercise)
alveolar dead space decreases (Due to increased CO)
physiologic dead space decreases
171
dead space fraction in exercise with cardiopulmonary disease states
elevated Vd/Vt ratio
CHF: lower CO (inadequate blood flow ares increase Vd)
COPD, ILD, PH: already have issues with ventilation and can't increase Vt enough
172
cardiopulmonary exercise test
use to evaluate unexplained dyspnea, exercise intolerance, pt with cardio or pulmonary disease, disability, pre op
173
what are PFTs
spirometry, lung volumes, and diffusion capacity
174
FEV1, FVC, FEV1/FVC ratio
FVC: forced vital capacity
FEV1: forced expiratory volume at 1 second
ratio of the two normal above 70%
175
spirometry in obstructive
reduced FEV1 and FEV1/FVC ratio
176
spirometry in restrictive
FVC is surrogate for TLC. TLC is reduced in restrictive lung disease. the ratio is relatively normal
177
peak expiratory flow loops effort
effort dependent at high lung volumes
effort independent at low lung volumes due to dynamic compression from increase Pip and less alveolar elastic recoil leading to less traction on airways
178
Flow volume curve obstructive
FEV1 reduced relative to FVC due to increased airway resistance
reduced peak flow, curvilinear effort independent phase (scoop), vital capacity possibly reduced from hyperinflation
179
Flow volume curve restrictive
steep descent in effort independent phase, vital capacity reduced (due to disease specific factor limiting TLC)
180
Variable extrathoracic obstruction
during inspiration, airway pressure is less than atmospheric pressure (creating obstruction by collapsing airway?) giving truncation of inspiratory limb
expiration is normal: airway pressure exceeds atm pressure
ex: paradoxical movement of vocal cords
181
Variable intrathoracic obstruction
inspiration is normal: airway pressure is larger than pleural pressure
expiration: pleural pressure exceeds airway pressure decreasing airflow and flattening of the expiratory loop,
ex: tumor in trachea
182
fixed airway obstruction
truncation of both limbs (exp and insp)
| ex: tracheal stenosis
183
Inspiratory reserve volume vs inspiratory capacity
IRV: amount of air breathed in on top of TV
IC: IRV and TV
184
Expiratory reserve volume and FRC
ERV: amount that can be breathed out on top of tidal volume
FRC: ERV and RV
185
Measuring lung volumes: body plethysmography
breathing in increase the pressure in the chamber and they can calculate the volume
186
Measuring lung volumes: helium dilution or nitrogen washout
```
measures FRC (breathing in helium)
Nitrogen washout-fowler's method
```
187
Measure diffusion capacity
CO (b/c purely diffusion limited) DLCO
188
Determinants of DLCO
alveolar cap SA and pulmonary cap volume (reduced in emphysema)
alveolar cap thickness (increased in Pulm fibrosis)
lung volume/SA (reduced in obesity)
Hbg concentration ( reduced in anemia)
carboxyhemoglobin concentration (elevated in smokers)
distribution of VQ in lung
189
Bronchial smooth muscle innervation in airways
smooth muscle from trachea to alveoli, controlled by cholinergic parasympathetic and adrenergic sympathetic
190
Bronchial smooth muscle and cholinergics
stimulation leads to contraction and increased glandular mucus secretion (AcH stimulates muscarinics)
191
Bronchial smooth muscle and adrenergics
stimulation leads to relaxation and inhibition of glandular secretion (beta 2 receptors)
192
Bronchodilators
B2 agonists: albuterol, anti cholinergic: ipratropium, NO, increased PCO2 and increased O2 in small airways
193
Bronchoconstrictors
Ach, alpha agonists, inhaled irritants, histamine, leukotrienes, serotonin, endothelia, decreased PCO2 in small airways
194
Obstructive lung disease
asthma, COPD, CF
195
Wheezing
continuous adventitial lung sounds, high pitched whistling
| due to fluttering of airway walls/fluid
196
stridor
high pitched monophonic sound over anterior neck from oscillation of narrowed airway
inspiratory stridor: occurs in extrathoracic region (supraglottic and glottic/subglottic)
expiratory stridor: occurs in intrathoracic region
197
Cough
duration (acute, subacute, chronic >8wk) chronic most likely inflammation.
198
Resistance in lung airways
higher resistance in larger airways (even though large radius) because surface area is low. Higher surface area in small airways-less resistance because flow is dissipated.
199
Mechanisms of lower airway obstruction
```
mucous (asthma)
airway wall thickening/bronchoconstriction (asthma)
decreased tethering (emphysema)
```
200
Where is the obstruction
trachea/bronchomalacia: degradation of cartilage-floppy airways
chronic bronchitis or bronchiectasis-irreversible mucus hypersecretin
asthma: smooth muscle hypertrophy/bronchoconstriction, mucus hypersecrtion, REVERSIBLE
emphysema: destruction of elastin fibers, decreased tethering, floppy airways IRREVERSIBLE
201
Asthma summary
episodic triad: wheeze, cough, dyspnea
reversible airway obstruction, hyperactivity mucus (more goblet)
cellular inflammation eosinophilic
repetitive airway injury-->basement membrane thickening
multiple phenotypes (gene by environment)
202
Hygiene hypothesis
Type I: exposed to infections, microbes, animals-develop tolerance-healthy
Type II: few infections, sterile environment--have an allergic reaction to same allergen
203
Asthma potential protective factors
Contact with animals
high exposure to endotoxin (activates innate immune response)
early exposure to bacterial products
204
Respiratory infections in asthma
healthy infant exposed to respiratory infections that cause wheezing may resolve or develop asthma (if proper genetic background)
can exacerbate symptoms, lung function
can make asthma more severe if its persistant
205
Asthma is characterized by
airway obstruction (reversible)
hyper responsiveness (twitchiness)
inflammation
mucuous production
206
Asthma and PFTs
low FEV1/FVC, typically corrected by bronchodilator
207
Asthma and lung volumes
Mild: no changes
Acute or severe: increased RV (hard to exhale)
most severe: FRC and TLC usually normal, but may lose elasticity in sever (increased TLC)
208
airway hyperresponsiveness in asthma
increased bronchoconstriction (most severe in asthma) from methacholine, cold air, exercise
209
methacholine challenge
normal person nothing happens
| asthma-casdues smooth muscle constriction and loss of FEV1
210
airway inflammation in asthma
leukocyte infiltration-->cell activation-->damages airway epithelium-->exposes the basement membrane-->leads to increased mucus-->this happens repetitively it will cause airway remodeling
211
`mast cells in asthma
have IgE which bind specific allegergen to activate mast cell-->produce mediators like histamin/leukotriene, cytokines (recruit eosinophils), growth factors, for angiogenesis or scarring, metalloproteinases-balance profibrotic/antifibrotics
212
Eosinophils in asthma
cause airway hyper responsiveness, inflammation via cytokines, airway remodeling via growth factors, bronchial obstruction via leukotrienes, epithelial injury
213
Histamine in asthma
made by mast cells and basophils, leads to bronchoconstriciton, vasodilation, edema, itching
214
Eicosanoids in asthma
derived from phospholipase A2 activity (prostaglandins, thromboxanes, leukotrienes,) contribute to bronchoconstriction
215
asthma inflammatory cascade
stimulus
cell activation/mediator release (recruit T cells which produce cytokines which recruit eosinophils, mast cels)
inflammation
smooth muscle hypertrophy, bronchial hyperresponsiveness
216
Airway remodeling in asthma
more inflammation = subepithelial fibrosis, increased smooth muscle mass, new vessel formation and mucus gland hyperplasia
217
Causes of airway narrowing
contraction of smooth muscle, cellular debris/mucus, edema of airway wall, airway remodeling (hypertrophy of smooth muscle, subepithelia fibrosis)
218
Asthma Dx
episodic cough, wheezing, dyspnea with triggers
FH
during severe attacks: wheezing, tachypnea, accessory muscle use
219
asthma triggers
```
allergen exposure
viral infections
exercise
occupational exposure
medications
circadian variation
```
220
Confirming asthma Dx
low FEV1/FVC, increased airway resistance, reversible with beta agonists, hyper responsive with methacholine
increased eosinohils, IgE sensitivity (not necessary diagnostic)
221
Tx asthma
controll inflammatory stimuli by environment control
control inflammation and hyper responsiveness with anti-inflammatory (corticosteroids and leukotriene modifiers)
control symptoms with bronchodilators (beta 2 agonists, muscarinic antagonists
222
COPD characterized by
respiratory symptoms (cough, exertion dyspnea), airflow obstruction (reduced FEV1/FVC) and is IRREVERSIBLE
223
COPD chronic bronchitis
smoker's cough (cough/sputum for 3 mo)
disease of airways (bronchi/bronchioles)
srutctureal changes in airways (neutrophilic inflammation, metaplasia of epithelium, expanded mucus glands)
mucus hypersecretion
224
COPD chronic bronchitis histology
dramatic expansion of submucosal glands
225
COPD chronic bronchitis mechanisms
intralumenal blockage (secretions) or edema/inflammation/hypertrophy
226
COPD emphysema
```
destructive process of elastic fibers in lung parenchyma
destroy alveolar walls and associated capillaries
enlarged airspaces (losing surface area and diffusion capacity)
```
227
Collapsible bronchioles in emphysema
Losing elastic fibers that tether airway open-can collapse if put force on. reduced radial traction (airways aren't staying open on exhalation)
228
COPD pathogenesis
SMOKING
229
Respiratory Bronchiolitis
earlier abnormality of COPD in smokers
| inflammation, goblet cell metaplasia, smooth muscle hypertrophy, fibrosis/narrowing in bronchioles
230
Emphysema pathogenesis
smoke induced inflammation drives alveolar destruction, respiratory infections aid this process, neutrophilic inflammation, chemokine trigger imbalance of proteases (steroid resistant)
231
Emphysema: protease/antiprotease imablance
antiprotenase deficiency or protease excess--> leads to free protease (found in neutrophils) which destroy connective tissues (elastin)
232
COPD and PFTs
```
invariable low FEV1/FVC and low FEV1 (FVC may be normal or reduced in advanced)
normal or elevated TLC hyperinflation
normal or elevated FRC
normal or elevated RV
reduced DLCO
```
233
emphysema and lung compliance
increased
234
diaphragm in COPD
flattened and shortened muscle fiber length (less stretch-generate less tension so it's harder to breathe when hyper inflated) leads to weakness
235
COPD exacerbations
increased symptoms, 50% due to bacterial/viral infection, Tx: antibiotics and systemic steroids
236
COPD and PA hypertension
result of alveolar hypoxia and resultant vasoconstriction, compensatory RV hypertrophy and RV failure (cor pulmonate) Tx: O2 supplementation
peripheral edema
237
Diagnosing COPD
chronic symptoms, exclude asthma (see if reversible), spirometry FEV1/FVC
238
COPD symptoms
persistent/progressive dyspnea, chronic productive cough (sputum discoloration), wheezing, lower extremity edema (cor) orthopnea, hemoptysis
239
COPD physical exam
may be normal
barrel chest
hyper resonant percussion and low diaphragm
diminished breath sounds
prolonged expiratory phase
rhonchi (rattling), wheeze
lower extremity edema, cyanosis, cachexia
240
COPD radiograph
hyper lucency-decreased peripheral vascular lung markings
hyperinflation (low, flat diaphragm, increase in retrosternal air space, narrow cardiac silhouette)
enlarged pulmonary arteries
241
Pink puffer type a
```
emphysematous phenotype
extertional dyspnea
little sputum
infrequent exacerbations
hyper inflated, use of accessory muscles
pursed lip breathing
normal oxygenation
thin
```
242
Blue bloater type b
```
bronchitic phenotype
cough and sputum
frequent exacerbations
less dyspnea
chronic hypoxemia
pulmonary HTN
corpulmonale right sided heart failure
normal habits or obese
```
243
Tx:
SMOKING CESSATION
immunizations
bronchodilator with anticholinergics and beta agonists
suppress inflammation with corticosteroids (not effective)
treat hypoxia
manage exacerbations
pulmonary rehab
244
COPD measures for oxygen therapy
PaO2<55 mmHg, sat <88%
| or <60 mmHg end organ dysfunction
245
Long term oxygen therapy in COPD
survival benefit
