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N932 Pathophysiology > Respiratory Pathophysiology Review > Flashcards

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
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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
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3
Q

Anaerobic Metabolism cascade

A

pyruvate ferments to lactic acid and produces 2 ATP

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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

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5
Q

where does glycolysis take place

A

cytoplasm

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6
Q

which 2 electron carriers are pertinent for ATP formation

A

NAD and FAD

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7
Q

what are the byproducts of aerobic metabolism

A

CO2 H2O and heat

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8
Q

Nose

A

used for filtration, smell, humidification of incoming air

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9
Q

9 cartilages in larynx

A

aretynoid, corniculate, cuneiform

epiglottis, thyroid, cricoid

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10
Q

what does RLN innervate (motor)

A

all but the cricothyroid musle

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11
Q

SLN internal

A

sensory innervation to vocal cords and above

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12
Q

RLN sensory

A

innervation (sensory) below vocal cords

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13
Q

abduction of the vocal cords

A

posterior cricoaretynoid

“please come apart”

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14
Q

adduction of the vocal cords

A

lateral cricoaretynoid

“lets close airway”

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15
Q

tension of the vocal cords

A

cricothyroid

“cords tense”

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16
Q

relaxation of vocal cords

A

thyroarytenoid

“they relax”

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17
Q

angle of R and L bronchus

A

R: 25 degrees or more vertical
L: 45 degrees

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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

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19
Q

Both lungs have how many bronchopulmonary segments and how many generations?

A

10 bronchopulmonary segments

20-25 generations (bifurcations)

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20
Q

diaphragm innervation

A

C3,4,5

C3,4,5, keep diaphragm alive:

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21
Q

External and internal intercostals role during respiration

A

external intercostals help with forced inhalation

internal intercostals help with forced expiration

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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)

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23
Q

humans have how many alveoli by age 9? how many meters squared is this?

A

300 million

60-80 meters squared

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24
Q

distance from front incisors to carina

A

26 cm
(incisors to larynx 13cm)
(larynx to carina 13cm)

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25
Q

2 zones of lungs

A

conducting zone

respiratory zone

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26
Q 
conducting zone
gas exchange
where it starts to where it ends
type of cells here (3)
blood supply (name 3 arteries)
diameter
A

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

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27
Q 
respiratory zone
gas exchange
where it starts to where it ends
type of cells
blood supply
diameter
A

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.

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28
Q

anatomic dead space and 3 ways its estimated

A

made up of conducting zone. estimated by
150ml in 70kg 6’ man
1/3 TV
1ml/lb or 2ml/kg IBW

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29
Q

Mechanics of Breathing: Inspiration

A

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

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30
Q

Mechanics of Breathing: Expiration

A

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

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31
Q

Mechanics of Breathing: Accessory Muscles for inspiration and expiration

A

inspiratory: sternocleidomastoid, scalene lift
expiratory: rectus, internal/external obliques, transversus abdominus

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32
Q

you see (+) intrathoracic pressure only during

A

exhalation or autopeep

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33
Q

trans pulmonary pressure

A

difference between intrapleural and intra alveolar pressures and it determines size of lungs. a higher transpulmlonary pressure corresponds to a larger lung

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34
Q

what actually sends signal to DRG

A

medulla

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35
Q

neuronal control of lungs via

A

medulla and pons in brainstem. pons modifies medulla output but signal comes from medulla

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36
Q

Medullary control: DRG

A

stimulates inspiration, pacer for breathing via external intercostals and diaphragm.

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37
Q

Medullary control: VRG

A

stimulates inspiration/expiration. helps with forced inspiration/expiration via accessory muscles and internal intercostals.

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38
Q

Pons: Pneumotaxic Center

A

decreases TV for fine control of TV. located high in pons

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39
Q

Pons: apneustic center and 2 factors that limit it

A

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

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40
Q

central chemoreceptors

A

respond to H+ ion levels (also pH)

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41
Q

peripheral chemoreceptors

A

respond to CO2 (also pH and hypoxemia)

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42
Q

normal stimulus to breathe is

A

hypercapnea

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43
Q

cranial nerve X

A

carries aortic arch and lung stretch signals to DRG

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44
Q

cranial nerve IX

A

carries carotid body signals to DRG

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45
Q

parasympathetic control of airway

A 
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
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46
Q

sympathetic control of airway

A

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

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47
Q

TV equation for men and women

A

based on IBW

men: 50kg + 2.3 * (ht(in)-60)
women: 45.5kg + 2.3* (height(in)-60)

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48
Q

residual volume

A

cannot be measured with spirometry. whats left in lung after forced exhalation

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49
Q

4 capacities of lung

A

inspiratory capacity
vital capacity (everything you can control)
FRC (where all O2 comes from when not ventilating)
TLC

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50
Q

inspiratory capacity (IC)

A

IRV+Vt

3L + 500ml = 3.5L

51
Q

Vital Capacity (VC)

A

IRV+Vt+ERV

52
Q

Functional Residual Capacity (FRC)

A

RV+ERV

1.2L + 1.1 L = 2.3L

53
Q

Total Lung Capacity (TLC)

A

IRV+Vt+ERV+RV

54
Q

FRC definition and positions that effect it

A 
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
Q

normal tidal breathing brings in _____ml of fresh air into respiratory zone

A

350mL (21% is O2).

this is in addition to the 2 liters in FRC

56
Q

each exhalation is approximately _____ of gas containing ______ CO2

A

350mL

5-6%

57
Q

how many mL of O2 diffuse from alveoli to blood versus how much CO2 diffuses from blood to alveoli?

A

250mL O2 versus
200mL CO2
this is why RQ is .8 (200/250)

58
Q

types of thoraces(?) (7)

A 
pneumothorax (air)
tension pneumo (air under pressure)
hemothorax (blood)
peffusion (excess serous fluid)
empyema or pyothorax (pus)
fibrothorax (organized blood clot)
chlyothorax (lymph)
59
Q

compliance equation

A

change in volume over change in pressure

60
Q

static compliance

A

compliance of lung and chest wall with no air movement. ex) Pplat
airway resistance doesnt play a role in this calculation

61
Q

reasons for decreased static compliance

A

fibrosis, obesity, edema, vascular engorgement, ARDS, external compression, atelectasis

62
Q

(static compliance) Cst=

A

TV/(Pplat-PEEP)

normal value 60-100mL/cmH2O

63
Q

reasons for reduced dynamic compliance

A

bronchospasm, tube kinking, mucous plugs, increased RR, anything that increases airway resistance

64
Q

dynamic compliance

A

compliance of lung and chest wall during a breath

65
Q

dynamic compliance calculation

A

=TV/(Ppeak-PEEP)

normal 50-100mL/cmH2O

66
Q

elastic recoil of lung and part that plays largest role

A

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
Q

greatest airway resistance is where?

A

medium size bronchi

68
Q

reynolds number and significance

A 
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
Q

laminar, turbulent, transitional flow numbers

A

<2000 laminar
>4000 turbulent (big airways)
2000-4000 transitional flow

70
Q

Poiseulles Law and significance

A 
resistance to flow
R=8nL/R^4
R=resistance
N=viscosity
L=length
R=radius
71
Q

Zone 1

A

alveolar>arterial>venous pressure

VQ>1, worst

72
Q

Zone 2

A

arterial>alveolar>venous pressure

VQ=1

73
Q

Zone 3

A

arterial>venous>alveolar
VQ: .8
alveoli have greatest compliance and perfusion, zone where PA cath tip should be placed

74
Q

Zone 4

A

arterial>interstitial>venous>alveolar
VQ<1
pedema/fluid buildup

75
Q

as far as zones and art v venous

A

arterial should always be >venous

76
Q

closing volume

A

volume above residual volume where small airways close

77
Q

closing capacity

A

absolute volume of gas in lung when small airways close (CV+RV)
increased by supine position, pregnancy, obesity, COPD, CHF, aging

78
Q

if CV>FRC,

A

airway closure occurs during tidal breathing causing poorly ventilated or unventilated alveoli and intrapulmonary shunting

79
Q

HGB consist of

A

4 protein subunits, 2 alpha and 2 beta
4 heme subunits
iron-porphyrin compound

80
Q

each gram of HGB binds how much O2

A

1.34 mL

81
Q

left shift of OxyHGB dissociation curve “left loves”

A 
increased affinity of HGB for O2, higher saturation for given PO2
decreased temp
decreased CO2
increased pH
decreased 2,3 diphosphoglycerate
82
Q

right shift of OxyHGB dissociation curve “right release”

A

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
Q

haldane effect

A

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
Q

bohr effect

A

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
Q

Oxyhemoglobin P50

A

26-28mmHg

PaO2 at which 50% of HGB is saturated

86
Q

HGB affinity at SaO2 of:
50%
70%
90%

A

27mmHg at 50%
40mmHg at 70%
60mmHg at 90%

87
Q

DLCO
why we use it
results and what they mean
how its performed

A

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
Q

CO2 is transported in blood in 3 ways

A

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
Q

carbonic anhydrase and CO2

A

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
Q

hamburger shift

A

HCO2 leaves RBCs and chloride enters to maintain electrical neutrality. this is also called a chloride shift

91
Q

hypoxic hypoxia

A

generally an issue within the lungs

decrease of FiO2 (

92
Q

hypoxic hypoxia clinical examples

A 
high altitudes
O2 equipment error
drug OD
COPD
PFibrosis
PE
atelectasis
congenital heart disease
93
Q

circulatory hypoxia and examples

A

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
Q

hemic hypoxia and examples

A

reduced HGB content/function
examples: anemia, carboxyhgbemia, methemoglobinemia.
supplemental O2 will have minimal effect, will increase PaO2 but not O2 carrying capacity

95
Q

methemoglobinemia reasons

A

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
Q

demand/histotoxic hypoxia and clinical examples

A

increased O2 consumption or inability to utilize O2
examples: fever, seizures, cyanide toxicity
supplemental O2 will help

97
Q

HPV and MOA, why it happens and what its affected by (4 things)

A

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
Q

HPV effect of CO2/acidosis on pulmonary vasculature

A

increased PCO2 = vasoconstriction (acidosis)

decreased PCO2=vasodilation

99
Q

HPV is reduced or eliminated by

A

elevated FiO2

volatile agents above 1 mac down regulate HPV

100
Q

causes of dead space (increased V/Q)

A 
pembolism
hypovolemia
cardiac arrest
shock
anything that causes decrease in pBF
101
Q

causes of shunts (decreased V/Q)

A 
mucus plugging
ETT in R or L mainstem
atelectasis
PNA
pedema
anything that causes alveoli to collapse or fill
102
Q

anatomical dead space definition

A

air that is present in airway that never reaches alveoli and therefore never participates in gas exchange

103
Q

alveolar dead space definition

A

air found within alveoli that are unable to function, such as those affected by disease or abnormal BF

104
Q

physiologic dead space =

A

anatomical dead space + alveolar dead space. (represents all of air in respiratory system that is not being used for gas exchange)

105
Q

Deadspace Bohrs equation

A

=VT[(PaCO2-PeCO2)/PaCO2]
PaCO2-PeCO2 gradient usually 2-5. increases with VQ mismatch
“PaCOPeCOPaCO”

106
Q

venous admixture definition

A

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
Q

mixed venous definition

A

oxygen tension (PVO2) represents overall balance between O2 consumption (VO2) and O2 delivery (DO2)

108
Q

factors that lower PVO2

A

decrease CO
increase O2 consumption
decreased HGB concentration

109
Q

absolute shunt

A

supplemental O2 won’t do shit hunni.
VQ=0
hypoxia unresponsive to supplemental O2

110
Q

shunt like alveoli

A

low VQ, have low PO2 and high PaCO2. think venous blood, will stay the same

111
Q

deadspace like alveoli

A

high VQ, have high PO2 and low PCO2

think atmospheric air, will stay same

112
Q

URI sx (10)

A 
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
Q

allergies sx (histamine mediated) (8)

A 
sneezing
ash or boggy mucosa
itchy/runny nose
conjunctivitis
wheezing
hives
possible swollen lips, tongue, eyes or face
dry, red, cracked skin
114
Q

ficks law of diffusion equation

A

Vgas=DAdeltaP/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
Q

alveolar gas equation, alveolar oxygen tension (PAO2)

A 
=(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
Q

Alveolar Arterial O2 Tension Gradient P(A-a)O2

A

=PAO2-PaO2
normal value 5-15
increases with age, obesity, supine position, heavy exercise (because decreases I time)

117
Q

PaO2=

A

102-(age/3)

118
Q

Arterial/Alveolar Oxygen Tension (A/a) Ratio

A

=PAO2/PaO2
good indicator of overall gas exchange
normal >75%

119
Q

Arterial Oxygen Content CaO2

A 
=(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
Q

CaO2-CvO2

A

CaO2 20mL O2/100mL blood
CvO2 15mL O2/100mL blood
(CaO2-CvO2) = about 5mL of/100mL blood used

121
Q

DO2 (oxygen delivery)

A

DO2=QT * CaO2
QT=CO
5L/min * 200mL/min=1000mL min of O2 delivery at baseline so we have excess/ reserve

122
Q

Fick Equation of Oxygen consumption VO2

A

=Qt* (CaO2-CvO2)

5L/min*(200mL-150mL)=250mL/min

123
Q

CO2/Alveolar Ventilation. PaCO2=

A

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
Q

PF Ratio

A 
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)

N932 Pathophysiology (4 decks)

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