Respiratory Pathophysiology Review Flashcards
1
Q
purpose of pulmonary system (5)
A
supply O2 from atmosphere to the blood while removing CO2 help maintain acid base balance allow for phonation provide for pulmonary defense provide oxygen for metabolism
2
Q
Partial Pressure of Nitrogen O2 CO2 H2O Other gases
A
Nitrogen: 597.4 O2: 158.8 CO2: .3 H2O: 3mmHg Other gases: .5mmHg
3
Q
Anaerobic Metabolism cascade
A
pyruvate ferments to lactic acid and produces 2 ATP
4
Q
Aerobic Metabolism Cascade
A
AcetylCOA in mitochondria creates byproducts of CO2 and 2 more ATP then oxidative phosphoylation creates 34 ATP. Aerobic metabolism uses glycolysis (krebs cycle) as well as oxidative phosphorylation
5
Q
where does glycolysis take place
A
cytoplasm
6
Q
which 2 electron carriers are pertinent for ATP formation
A
NAD and FAD
7
Q
what are the byproducts of aerobic metabolism
A
CO2 H2O and heat
8
Q
Nose
A
used for filtration, smell, humidification of incoming air
9
Q
9 cartilages in larynx
A
aretynoid, corniculate, cuneiform
epiglottis, thyroid, cricoid
10
Q
what does RLN innervate (motor)
A
all but the cricothyroid musle
11
Q
SLN internal
A
sensory innervation to vocal cords and above
12
Q
RLN sensory
A
innervation (sensory) below vocal cords
13
Q
abduction of the vocal cords
A
posterior cricoaretynoid
“please come apart”
14
Q
adduction of the vocal cords
A
lateral cricoaretynoid
“lets close airway”
15
Q
tension of the vocal cords
A
cricothyroid
“cords tense”
16
Q
relaxation of vocal cords
A
thyroarytenoid
“they relax”
17
Q
angle of R and L bronchus
A
R: 25 degrees or more vertical
L: 45 degrees
18
Q
TLC of R lung and lobes
TLC of L lung and lobes
A
R lung 55% TLC and 3 lobes
L lung 45% TLC AND 2 LOBES
19
Q
Both lungs have how many bronchopulmonary segments and how many generations?
A
10 bronchopulmonary segments
20-25 generations (bifurcations)
20
Q
diaphragm innervation
A
C3,4,5
C3,4,5, keep diaphragm alive:
21
Q
External and internal intercostals role during respiration
A
external intercostals help with forced inhalation
internal intercostals help with forced expiration
22
Q
lungs made up of 3 types of pneumocytes
A
1: structural
2: surfactant producing
3: macrophages (monocyte moved into tissue bed, only part of conducting airways, help with ciliary buildup)
23
Q
humans have how many alveoli by age 9? how many meters squared is this?
A
300 million
60-80 meters squared
24
Q
distance from front incisors to carina
A
26 cm
(incisors to larynx 13cm)
(larynx to carina 13cm)
25
2 zones of lungs
conducting zone
| respiratory zone
26
```
conducting zone
gas exchange
where it starts to where it ends
type of cells here (3)
blood supply (name 3 arteries)
diameter
```
no gas exchange here.
starts at nose, ends at terminal bronchioles
goblet cells, secretory cells, microcilia
blood supply from thyroid, bronchial, internal thoracic arteries from left heart/systemic circulation
terminal bronchioles measure 1mm diameter and lose cartilaginous plates
27
```
respiratory zone
gas exchange
where it starts to where it ends
type of cells
blood supply
diameter
```
gas exchange here based on diffusion
consists of bronchioles (where it starts), alveolar ducts, alveolar sacs, alveoli
initially have cuboidal cells but transition to squamous epithelium
blood supply from pulmonary circulation
respiratory bronchioles have .5mm diameter and smaller.
28
anatomic dead space and 3 ways its estimated
made up of conducting zone. estimated by
150ml in 70kg 6' man
1/3 TV
1ml/lb or 2ml/kg IBW
29
Mechanics of Breathing: Inspiration
nerve impulse sent to phrenic nerves and travels to diaphragm
diaphragm contracts and increases superior-inferior dimension of chest
external intercostal muscles help to lift sternum and elevate rubs. increases A-P diameter
loss of intercostal muscles usually has little effect on ventilation
30
Mechanics of Breathing: Expiration
increase in intrathoracic pressure pushes air out
primarily passive process
elastic forces in lung, chest wall, and abdomen help compress the lungs
internal intercostals can help in forceful exhalation
31
Mechanics of Breathing: Accessory Muscles for inspiration and expiration
inspiratory: sternocleidomastoid, scalene lift
expiratory: rectus, internal/external obliques, transversus abdominus
32
you see (+) intrathoracic pressure only during
exhalation or autopeep
33
trans pulmonary pressure
difference between intrapleural and intra alveolar pressures and it determines size of lungs. a higher transpulmlonary pressure corresponds to a larger lung
34
what actually sends signal to DRG
medulla
35
neuronal control of lungs via
medulla and pons in brainstem. pons modifies medulla output but signal comes from medulla
36
Medullary control: DRG
stimulates inspiration, pacer for breathing via external intercostals and diaphragm.
37
Medullary control: VRG
stimulates inspiration/expiration. helps with forced inspiration/expiration via accessory muscles and internal intercostals.
38
Pons: Pneumotaxic Center
decreases TV for fine control of TV. located high in pons
39
Pons: apneustic center and 2 factors that limit it
increases TV for long and deep breathing (ex neuro patient doing kussmaul)
located lower in PONS
output limited via baroreflex input from lung, input from pneumotaxic center
40
central chemoreceptors
respond to H+ ion levels (also pH)
41
peripheral chemoreceptors
respond to CO2 (also pH and hypoxemia)
42
normal stimulus to breathe is
hypercapnea
43
cranial nerve X
carries aortic arch and lung stretch signals to DRG
44
cranial nerve IX
carries carotid body signals to DRG
45
parasympathetic control of airway
```
from vagus (and dominant over SNS)
causes mucus secretion, increased vascular permeability, vasodilation, bronchospasm
bronchoconstriction is greatest in upper airways
activation of M3 receptors mediates bronchoconstriction
```
46
sympathetic control of airway
has very little input on tissues in lung
inhibit mediator release from mast cells
increase mucociliary clearance via reducing viscosity and helping to expel faster
activation of B2 exogenously = bronchodilation
47
TV equation for men and women
based on IBW
men: 50kg + 2.3 * (ht(in)-60)
women: 45.5kg + 2.3* (height(in)-60)
48
residual volume
cannot be measured with spirometry. whats left in lung after forced exhalation
49
4 capacities of lung
inspiratory capacity
vital capacity (everything you can control)
FRC (where all O2 comes from when not ventilating)
TLC
50
inspiratory capacity (IC)
IRV+Vt
| 3L + 500ml = 3.5L
51
Vital Capacity (VC)
IRV+Vt+ERV
52
Functional Residual Capacity (FRC)
RV+ERV
| 1.2L + 1.1 L = 2.3L
53
Total Lung Capacity (TLC)
IRV+Vt+ERV+RV
54
FRC definition and positions that effect it
```
represents point where elastic recoil force of the lung is in equilibrium with elastic recoil of chest wall. respresents oxygen reserve
effected by:
upright and prone position, increases
supine position, decreases
muscle relaxation, decreases
```
55
normal tidal breathing brings in _____ml of fresh air into respiratory zone
350mL (21% is O2).
| this is in addition to the 2 liters in FRC
56
each exhalation is approximately _____ of gas containing ______ CO2
350mL
| 5-6%
57
how many mL of O2 diffuse from alveoli to blood versus how much CO2 diffuses from blood to alveoli?
250mL O2 versus
200mL CO2
this is why RQ is .8 (200/250)
58
types of thoraces(?) (7)
```
pneumothorax (air)
tension pneumo (air under pressure)
hemothorax (blood)
peffusion (excess serous fluid)
empyema or pyothorax (pus)
fibrothorax (organized blood clot)
chlyothorax (lymph)
```
59
compliance equation
change in volume over change in pressure
60
static compliance
compliance of lung and chest wall with no air movement. ex) Pplat
airway resistance doesnt play a role in this calculation
61
reasons for decreased static compliance
fibrosis, obesity, edema, vascular engorgement, ARDS, external compression, atelectasis
62
(static compliance) Cst=
TV/(Pplat-PEEP)
| normal value 60-100mL/cmH2O
63
reasons for reduced dynamic compliance
bronchospasm, tube kinking, mucous plugs, increased RR, anything that increases airway resistance
64
dynamic compliance
compliance of lung and chest wall during a breath
65
dynamic compliance calculation
=TV/(Ppeak-PEEP)
| normal 50-100mL/cmH2O
66
elastic recoil of lung and part that plays largest role
elastic forces are greatest in collapsed and hyper inflated alveoli. this means they require a greater change in pressure to achieve a set increase in volume
surfactant plays largest role in reducing surface tension. helps prevent atelectasis and small airway collapse
67
greatest airway resistance is where?
medium size bronchi
68
reynolds number and significance
```
predicts when flow will be laminar or turbulent
Re=pvd/n
P: density of fluid/gas
V: velocity of fluid/gas
D: diameter of vessel (biggest impact)
N: viscosity of fluid
```
69
laminar, turbulent, transitional flow numbers
<2000 laminar
>4000 turbulent (big airways)
2000-4000 transitional flow
70
Poiseulles Law and significance
```
resistance to flow
R=8nL/R^4
R=resistance
N=viscosity
L=length
R=radius
```
71
Zone 1
alveolar>arterial>venous pressure
| VQ>1, worst
72
Zone 2
arterial>alveolar>venous pressure
| VQ=1
73
Zone 3
arterial>venous>alveolar
VQ: .8
alveoli have greatest compliance and perfusion, zone where PA cath tip should be placed
74
Zone 4
arterial>interstitial>venous>alveolar
VQ<1
pedema/fluid buildup
75
as far as zones and art v venous
arterial should always be >venous
76
closing volume
volume above residual volume where small airways close
77
closing capacity
absolute volume of gas in lung when small airways close (CV+RV)
increased by supine position, pregnancy, obesity, COPD, CHF, aging
78
if CV>FRC,
airway closure occurs during tidal breathing causing poorly ventilated or unventilated alveoli and intrapulmonary shunting
79
HGB consist of
4 protein subunits, 2 alpha and 2 beta
4 heme subunits
iron-porphyrin compound
80
each gram of HGB binds how much O2
1.34 mL
81
left shift of OxyHGB dissociation curve "left loves"
```
increased affinity of HGB for O2, higher saturation for given PO2
decreased temp
decreased CO2
increased pH
decreased 2,3 diphosphoglycerate
```
82
right shift of OxyHGB dissociation curve "right release"
decreased affinity of HGB for O2, O2 is given up to tissue more easily
increased temp
increased CO2
decreased pH
increased 2,3 diphosphoglycerate (increased metabolism)
83
haldane effect
oxygenation of blood displaces CO2 from HGB
this occurs at alveolocapillary membrane of lungs
release CO2 to bind O2
shift curves up and left with PO2 decreases, down and right with PO2 increases)
84
bohr effect
tissue R shift release O2 in the presence of increased CO2. HGB's affinity for O2 is inversely related to CO2 levels
acidic environments cause rightward shift
this is the environment at the tissue level
85
Oxyhemoglobin P50
26-28mmHg
| PaO2 at which 50% of HGB is saturated
86
HGB affinity at SaO2 of:
50%
70%
90%
27mmHg at 50%
40mmHg at 70%
60mmHg at 90%
87
DLCO
why we use it
results and what they mean
how its performed
tests the lungs diffusing capacity for carbon monoxide
normal is >75% up to 140%
mild: 60% to lower limit of normal
moderate: 40-60%
severe: <40%
indicated in evaluation of parenchymal and non parenchymal lung disease in conjunction with spirometry. patient is asked to take large breath. hold breath for 10 seconds then exhale fully. measured amount of CO is used to calculate DLCO
88
CO2 is transported in blood in 3 ways
physical solution 5-10% dissolved in blood
chemically combined with amino acids of blood proteins 5-10% bound to HGB
bicarb ions 80-90% (most CO2 in this form)
89
carbonic anhydrase and CO2
carbonic anhydrase assists rapid inter conversion of carbon dioxide and water into carbonic acid, protons and bicarbonate ions
CO2 + H2O -->carbonic anhydrase -->HCO3- + H+
90
hamburger shift
HCO2 leaves RBCs and chloride enters to maintain electrical neutrality. this is also called a chloride shift
91
hypoxic hypoxia
generally an issue within the lungs
| decrease of FiO2 (
92
hypoxic hypoxia clinical examples
```
high altitudes
O2 equipment error
drug OD
COPD
PFibrosis
PE
atelectasis
congenital heart disease
```
93
circulatory hypoxia and examples
reduced CO, supplemental oxygen will have minimal effect. lungs may be OK but test of body may be POO.
examples: severe HF, dehydration, sepsis, SIRS
94
hemic hypoxia and examples
reduced HGB content/function
examples: anemia, carboxyhgbemia, methemoglobinemia.
supplemental O2 will have minimal effect, will increase PaO2 but not O2 carrying capacity
95
methemoglobinemia reasons
iron in ferric (Fe3) versus normal ferrous (Fe2) state. caused by nitrate poisoning (NTG, nitroprusside) or prilocaine. treat with supplemental O2 methylene blue 1-2mg/kg IV over 5 minutes
96
demand/histotoxic hypoxia and clinical examples
increased O2 consumption or inability to utilize O2
examples: fever, seizures, cyanide toxicity
supplemental O2 will help
97
HPV and MOA, why it happens and what its affected by (4 things)
reflex contraction of pulmonary vasculature in response to low regional partial pressure of O2. intended to match regional perfusion to ventilation in lungs. diverts blood away from hypoxic areas of lungs to areas with better ventilation and oxygenation to correct VQ mismatch.
affected by PAO2 levels, pH, PCO2, temperature
MOA: alterations in leukotriene and prostaglandin synthesis, inhibition of NO production in endothelium. down regulation of these decreases vasodilation.
98
HPV effect of CO2/acidosis on pulmonary vasculature
increased PCO2 = vasoconstriction (acidosis)
| decreased PCO2=vasodilation
99
HPV is reduced or eliminated by
elevated FiO2
| volatile agents above 1 mac down regulate HPV
100
causes of dead space (increased V/Q)
```
pembolism
hypovolemia
cardiac arrest
shock
anything that causes decrease in pBF
```
101
causes of shunts (decreased V/Q)
```
mucus plugging
ETT in R or L mainstem
atelectasis
PNA
pedema
anything that causes alveoli to collapse or fill
```
102
anatomical dead space definition
air that is present in airway that never reaches alveoli and therefore never participates in gas exchange
103
alveolar dead space definition
air found within alveoli that are unable to function, such as those affected by disease or abnormal BF
104
physiologic dead space =
anatomical dead space + alveolar dead space. (represents all of air in respiratory system that is not being used for gas exchange)
105
Deadspace Bohrs equation
=VT[(PaCO2-PeCO2)/PaCO2]
PaCO2-PeCO2 gradient usually 2-5. increases with VQ mismatch
"PaCOPeCOPaCO"
106
venous admixture definition
result of mixing of non oxygenated blood with oxygenated blood distal to alveoli ex from L atrium.
- shows communication between bronchial and pulmonary circulation
- thebesian veins,
- low VQ areas
107
mixed venous definition
oxygen tension (PVO2) represents overall balance between O2 consumption (VO2) and O2 delivery (DO2)
108
factors that lower PVO2
decrease CO
increase O2 consumption
decreased HGB concentration
109
absolute shunt
supplemental O2 won't do shit hunni.
VQ=0
hypoxia unresponsive to supplemental O2
110
shunt like alveoli
low VQ, have low PO2 and high PaCO2. think venous blood, will stay the same
111
deadspace like alveoli
high VQ, have high PO2 and low PCO2
| think atmospheric air, will stay same
112
URI sx (10)
```
elevated WBC's
mucopurulent nasal secretions
inflamed and reddened mucosa
positive chest finding (congestion, rales)
temp above 37 c
tonsilitis
viral ulcer in oropharynx
fatigue
laryngitis
sore throat
```
113
allergies sx (histamine mediated) (8)
```
sneezing
ash or boggy mucosa
itchy/runny nose
conjunctivitis
wheezing
hives
possible swollen lips, tongue, eyes or face
dry, red, cracked skin
```
114
ficks law of diffusion equation
Vgas=D*A*deltaP/T
Vgas: rate of gas diffusion across permeable membrane
D: diffusion coefficient of that particular gas for that membrane
A: surface area of membrane
delta P: difference in partial pressure of gas across membrane
T: thickness of membrane
115
alveolar gas equation, alveolar oxygen tension (PAO2)
```
=(PB-PH2O) * FiO2-(PaCO2/.8)
=(760-47) * .21-(40/.8)
=100
(PH2O is 47mmHg at 37c)
(this calculate how much PAO2 is yielded for an FiO2)
```
116
Alveolar Arterial O2 Tension Gradient P(A-a)O2
=PAO2-PaO2
normal value 5-15
increases with age, obesity, supine position, heavy exercise (because decreases I time)
117
PaO2=
102-(age/3)
118
Arterial/Alveolar Oxygen Tension (A/a) Ratio
=PAO2/PaO2
good indicator of overall gas exchange
normal >75%
119
Arterial Oxygen Content CaO2
```
=(HGB * 1.34 * SaO2) + (PaO2 * .003)
=O2 bound to HGB + O2 dissolved in blood
=(15*1.34*1)+(100*.003)
=20.1+.3
=20.4
```
120
CaO2-CvO2
CaO2 20mL O2/100mL blood
CvO2 15mL O2/100mL blood
(CaO2-CvO2) = about 5mL of/100mL blood used
121
DO2 (oxygen delivery)
DO2=QT * CaO2
QT=CO
5L/min * 200mL/min=1000mL min of O2 delivery at baseline so we have excess/ reserve
122
Fick Equation of Oxygen consumption VO2
=Qt* (CaO2-CvO2)
| 5L/min*(200mL-150mL)=250mL/min
123
CO2/Alveolar Ventilation. PaCO2=
VCO2/VA
=(VCO2-total CO2 production)/VA-alveolar ventilation)
shows that PaCO2 levels are inversely proportional to alveolar ventilation
ex) if CO2 is .5 double alveolar ventilation not minute ventilation (?)
124
PF Ratio
```
PaO2/FiO2
=100/.21
=476
normal PaO2 80-100
normal PF Ratio 400-500
lower than 400=issue
<300 mild ARDS
<200 moderate ARDS
<100 severe ARDS, taking 100% O2 to yield normal PaO2
(PF ratio can be used clinically in place of PAO2/PaO2 ratio)
```
