First Aid Respiratory

Front 1

conducting zone of respiratory tree

Back 1

brings air in and out, humidifies, filters air

anatomic dead space

nose, pharynx, trachea, bronchi, bronchioles, and terminal bronchioles

smooth muscle is present from bronchi to respiratory brochioles. Airways resistance is most due to the secondary bronchioles

Front 2

respiratory zone of respiratory tree

Back 2

participates in gas exchange

consists of the respiratory bronchioles, alveolar ducts, and alveoli

Front 3

type 1 pneumocytes

Back 3

thin squamous cells, for gas exchange

97% of alveolar surfaces

Front 4

type 2 pneumocytes

Back 4

secrete pulmonary surfactant - decrease alveolar surface tension, dipalmitoyl phosphtatidylcholine

cuboidal

proliferate during lung damage

lethacin-to-shingomyelin ratio >2 in amniotic fluid indicates lung maturity of fetus

Front 5

lethacin-to-sphingomyelin ratio

Back 5

> 2 in amniotic fluid indicates lung maturity in fetus

Front 6

clara cells

Back 6

nonciliated columnar with secretory granules - secretes a component of surfactant (GAG), degrade toxins, act as reserve cells

Front 7

T/F goblet cells are present throughout the respiratory tract

Back 7

FALSE

found only until the terminal bronchioles

Front 8

where do you find pseudostratified ciliated columnar epithelium?

Back 8

extend to respiratory bronchioles

Front 9

gas exchange barrier

Back 9

endothelial cell of capillary

basement membrane

type 1 pneumocyte - epithelial cell

Front 10

bronchopulmonary segment

Back 10

each has a tertiary bronchus and 2 arteries (1 bronchial and 1 pulm) in the center

arteries run with airways

veins and lymphatics run along boarders

Front 11

which lung is more common for inhaled objects?

Back 11

the right because the right main stem bronchous is more vertical and wider

Front 12

how many lobes does the right lung have? left lung?

Back 12

right - 3 lobes (10 segments)

left - 2 lobes + lingula - left has 2 lobes because heart takes up space, lingula represents the missing middle lobe (8-10 segments)

Front 13

most likley location for aspirated objects while upright? supine?

Back 13

when upright - lower portion of right inferior lobe

when supine - superior portion of right inferior lobe

right side- upper lobe

left side- lingula

Front 14

location of strictures passing through diaphragm

Back 14

T8 - IVC

T10 - esophagus + vagus nerve

T12 - aorta, thoracic duct, azygous (red, white, blue)

I ate (T8) ten (T10) eggs at twelve (T12)

I = IVC
eggs = esophagus
at = aorta

Front 15

diaphragm innervation

Back 15

C3,4,5 keeps diaphragm alive

Front 16

muscles of quiet breathing - inspiration and expiration

Back 16

inspiration - diaphragm

expiration - passive

Front 17

muscles of breathing during exercise - inspiration and expiration

Back 17

inspiration - external intercostals, scalene muscles, sternomastoids

expiration - rectus abdominus, internal and external obliques, transverse abdominis, internal intercostals

Front 18

Paradoxical breathing

Back 18

diaphragmatic fatigue, accessory muscles take over -> diaphragm no longer pushes down with inspiration -> organs are sucked up towards thorax -> abdomen contracts with inspiration

Front 19

collapsing pressure

Back 19

2(tension)/radius

tendency to collapse as radius decreases

Front 20

residual volume

Back 20

air left in lung after maximal expiration

cannot be measured by spirometry

Front 21

expiratory reserve volume

Back 21

air that can still be breathed out after normal breathing

Front 22

tidal volume (TV)

Back 22

air that moves in with each quiet inspiration

usually 500ml

Front 23

inspiratory reserve volume (IRV)

Back 23

air in excess of tidal volume that moves into lung during MAXIMAL inspiration

Front 24

vital capacity (VC)

Back 24

everything by residual volume

TV + IRV + ERV

Front 25

functional residual capacity (FRC)

Back 25

RV + ERV

volume in lungs after normal exhalation

Front 26

inspiratory capacity (IC)

Back 26

IRV + TV

Front 27

total lung capacity (TLC)

Back 27

IRV + TV + ERV + RV

Front 28

physiologic dead space

Back 28

physiologic dead space = anatomical dead space in conducting airways + functional dead space in alveoli

does not take part in gas exchange

Vd = Vt x (PaCO2-PeCO2)/PaCO2

Vt = tidal volume
PaCO2 = arterial PCO2
PeCO2 = expired air PCO2

Front 29

lung and chest wall determinants

Back 29

lung has tendency to collapse

chest wall has tendency to expand

at FRC they balance and system of pressure is atmospheric - airway and alveolar pressure is 0, intrapleural pressure is negative (prevents pneumothorax)

Historesis - inhalation will have a lower volume change for any given pressure change than expiration

Front 30

hemoglobin T vs R state

Back 30

T state - has low affinity for O2

R state - high affinity O2

increased Cl-, H+, CO2, 2,3-BPC and temperature favor the T form (shift curve right leading to increased O2 unloading)

Front 31

methemoglobin

Back 31

oxidized form of hemoglobin to Fe3+ (normal is Fe2+)

does not bind O2 well, has increased affinity for CN-

treat with METHylene blue

nitrates and nitrites can produce methemoglobin

Front 32

why can methemoglobin be useful in treating cyanide poisoning

Back 32

methemoglobin has high affinity for CN-, thus competes for binding, allowing cytochrome oxidase in mitochondria to function

give nitrites to oxidize hemoglobin to methemoglobin - binds CN-

then give thiosulfate to bind this -> excretion

Front 33

carboxyhemoglobin

Back 33

hemoglobin bound to Carbon monoxide

CO has a much higher affinity for hemoglobin than O2

causes a left shift in disassociation curve

decreases oxygen unloading

Front 34

what causes a right shift in the dissociation curve?

Back 34

CADET face right

CO2
Acid/Altitude
2,3-DPG (2,3-BPG)
Exercise
Temperature

increases in all factors besides pH shift the curve right

decreasing any of these factors except pH will shift left

Front 35

a shift to the right for the dissociation curve means what in terms of oxygen affinity?

Back 35

decreased affinity for O2 - facilitates unloading of O2 to tissue

Front 36

Fetal Hb has higher or lower affinity for O2 than Hb A

Back 36

higher affinity - disassociation curve shifted left
also has a lower affinity for 2,3-DPG which is partially why it has a higher affinity

Front 37

a decrease in PAO2 causes vasoconstriction or vasodilation in pulmonary arteries?

Back 37

vasoconstriction

different from what you expect in systemic artery, pulmonary artery constricts if low O2 and redirects blood to well ventilated areas

Front 38

normally O2, CO2, and N2O is perfusion or diffusion limited?

Back 38

usually perfusion limited

gas equilibrates early along length of capillary

diffusion can only increase if blood flow increases

Front 39

when does O2 become diffusion limited?

Back 39

emphysema or fibrosis

gas does not equilibrate completely before reaching end of capillary - poor diffusion across membrane

Front 40

cor pulmonale

Back 40

consequence of pulmonary hypertension - right ventricular heart failure

see jugular venous distension, edema, hepatomegally

Front 41

what is normal pulmonary artery pressure? what is considered pulmonary hypertension?

Back 41

normal 10-14mmHg.

hypertension > 25mmHg or > 35 during exercise

Front 42

Pulmonary hypertension

Back 42

presents with exertion angina, RV ischemia, exertional syncope
athlerosclerosis, medial hypertrophy, intimal fibrosis of pulmonary arteries
tx: prostaglandin (sildenafil)

Front 43

primary pulmonary hypertension causes

Back 43

due to mutation in BMPR2 gene which normally inhibits vascular smooth muscle prolif
tx: besenten -endothelien receptor antagonist -> decreases hypoxicvasoconstriction

Front 44

2ndary pulmonary hypertension causes

Back 44

due to:

COPD - destruction of lung parenchyma

mitral stenosis - increased resistance causes increased pressure

recurrent thromboemboli - decreases crosssectional area of pulmonary vascular bed

autoimmune disease - inflammation -> fibrosis -> medial hypertrophy

L->R shunt - high shear stress -> endothelial injury

sleep apnea - hypoxic vasoconstriction

high altitude - hypoxic vasoconstriction

Front 45

pulmonary vascular resistance

Back 45

PVR = P[pulmonaryartery] - P[L atrium]/Cardiac output

R = deltaP/Q

R = 8nl/(pi)r^4

lowest at FRC, increases with inhalation and exhalation

Front 46

cyanosis relationship to hemoglobin

Back 46

cyanosis results when deoxygenated Hb > 5g/dl

Front 47

O2 content of blood equation

Back 47

(O2 binding capacity x %sat) +dissolved O2

Front 48

T/F O2 content of arterial blood decreases as Hb, O2 sat, or arterial PO2 fall

Back 48

False: O2 content of arterial blood decreases as Hb decreases, BUT O2 sat and arterial PO2 does not

arterial PO2 decreases with lung disease because physiologic shunt lowers oxygen extraction ratio

Front 49

alveolar gas equation

Back 49

PAO2 = PIO2 - PACO2/R

approximately on room air = 150-PACO2/0.8

PAO2 = alveolar PO2
PIO2 = inspired PO2

PACO2 = alveolar PCO2

R = respiratory quotient = CO2 produced/O2 consumed


use this equation in calculating A-a gradient

Front 50

A-a gradient

Back 50

A-a gradient = PAO2 - PaO2

difference in PO2 between alveoli and arterial blood

should equal 10-15mmHg

increase in A-a gradient indicates hypoxemia - shunting, V/Q mismatch, fibrosis

normal in hypoxemic states due to high altitude and hypoventilation

Front 51

causes of hypoxemia

Back 51

hypoxemia is decrease in PaO2

normal A-a gradient
high altitude (less O2 total)
hypoventilation (can't blow off CO2, no O2 can bind)

increased A-a gradient
V/Q mismatch
Diffusion limitation
R-L shunt

Front 52

causes of hypoxia

Back 52

hypoxia is decreased O2 delivery to tissue

Normal A-a- gradient
decreased cardiac output
hypoxemia

Increased A-a gradient
anemia
cyanide poisoning
carbon monoxide poisoning

Front 53

causes of ischemia

Back 53

also causes O2 deprivation like hypoxemia and hypoxia

impeded artery flow
impaired venous drain

Front 54

V/Q mismatch

Back 54

ventilation should be matched to perfusion V/Q = 1, mismatched V/Q can be physiologic or due to pathology

normal:
apex of lung V/Q = 3 (wasted ventilation)
vase of lung V/Q = 0.6 (wasted perfusion)

both total ventilation and perfusion is highest at the base of the lung

Front 55

what does it mean V/Q = 0

Back 55

V/Q = 0 means airway obstruction (shunt) - 100% O2 doesnt help

Front 56

what does it mean V/Q is infinity

Back 56

V/Q is infinity in blood flow obstruction (physiologic dead space)

100% O2 will improve PO2 as long as some part of the lung is perfused

Front 57

why do you find TB in the apex of the lung more?

Back 57

heavily ventilated, by low perfusion means there is high O2 content

Front 58

how does exercise change V/Q ratio

Back 58

approaches 1 due to increased cardiac output and vasodilation of apical capillaries

Front 59

which part of the lung would you find PO2[alveolar] > PO2[arterial] > PO2[venous]

Back 59

apex (zone 1)

Front 60

how do PO2[alveoli], PO2[artery], PO2[venous] compare in zone 2 (middle of lung)

Back 60

PO2[artery] > PO2[alveoli] > PO2[venous]

Front 61

T/F the base of the lung has PO2[artery] > PO2[vein] > PO2[alveoli]

Back 61

True

Front 62

T/F the base of the lung has the lowest ventilation and highest perfusion compared to the apex of the lung

Back 62

FALSE

the base of the lung has the highest ventilation AND perfusion than the apex

Front 63

CO2 is transported from the tissues to the lungs via: 3 mech

Back 63

1. bicarbonate (90%)

2. bound the hemoglobin at N-terminus (not on heme) - favors T form

3. dissolved in blood

Front 64

Formation of bicarbonate

Back 64

catalysed by carbonic anhydrase within RBCs
CO2 + H2O ->H2CO3 -> H + HCO3 (all reversible)
Bicarbonate is exchanged with Cl- into bloodstream

Front 65

Haldane effect

Back 65

in lungs, oxygenation of hemoglobin releases H+ from hemoglobin

H+ shifts equilibrium to formation of CO2 to be exhaled from the lung

Front 66

Bohr effect

Back 66

in tissues, increased H+ from tissue metabolism shifts disassociation curve to the right -> unload O2 to tissues

Front 67

physiological response to high altitude

Back 67

1. Acute T in ventilation

2. Chronic T in ventilation

3. increased erythropoietin > increased hematocrit and hemoglobin (chronic hypoxia)

4. increased 2,3-DPG (binds to hemoglobin and releases O2)

5: . Cellular changes (increased mitochondria)

6. increased renal exerelion of bicarbonate to compensate for respiratory alkalosis

7. Chronic hypoxic pulmonary vasoconstriction results in RVH

Front 68

physiological response to exercise

Back 68

1. inc CO2 production

2. inc O2 consumption

3. inc ventilation rate to meet O2 demand

4. V/Q ratio from apex to base becomes uniform

5. inc pulmonary blood flow due to inc CO

6. dec pH (lactic acidosis)

7. no change in PaO2 and PaCO2 but increased venous CO2

Front 69

types of embolus

Back 69

FAT BAT

1. fat - associated with long bone fractures, liposuction

2. air

3. thrombus - most common from deep veins in leg (DVT)

4. bacteria

5. amniotic fluid - can lead to DIC

6. tumor

Front 70

virchow's triad

Back 70

predisposes to DVT

1. stasis
2. hypercoagulability
3. endothelial damage

Front 71

deep vein thrombosis

Back 71

virchow's triad

lead to pulmonary embolism

homan's sign - dorsiflexion of foot -> tender calf muscle

prevent with heparin

Front 72

COPD

Back 72

obstruction of air flow resulting in air trapping in the lung

hallmark is decreased FVC and FEV1 thats even more decreased compared to FVC-> decreased FEV1/FVC ratio < 80%

V/Q mismatch

types:
Chronic Bronchitis

emphysema

asthma

brochiectasis

Front 73

Chronic Bronchitis

Back 73

"blue bloater"

metaplasia/hypertrophy of mucus secreting glands in bronchioles

use reid index >50% (gland depth/total thickness of bronchial wall)

productive cough >3 consecutive months for > 2 years

early onset cyanosis, wheezing, crackles

Front 74

emphysema

Back 74

"pink puffer" - barrel chest

see increased elastase -> increased compliance

enlargement of air spaces and decreased recoil - destruction of alverolar wall

late onset hypoxemia, early onset dyspnea

exhale through pursed lips to increase airway pressure

centriacinar - smoking

panacinar - alpha1 antitrypsin deficiency (also liver cirrhosis)

paraseptal - see bullae that can rupture -> spontaneous pneumothorax (in young males)

Front 75

asthma

Back 75

bronchial hyperresponsiveness -> bronchoconstriction

smooth muscle hypertrophy

curschmann's spirals

triggered by drugs, allergens, stress

mucus plugging, pulsus paradoxus

test with methacholine challenge

Front 76

curschmann's sprial

Back 76

shed epithelium from mucous plugs form a spiral shape - found in sputum and tracheal washing

Front 77

bronchiectasis

Back 77

chronic necrotizing infection of bronchi - permanently dialated airways, purulent sputum, recurrent infection, hemoptysis

see with cystic fibrosis, bronchial obstruction, poor ciliary motility =Kartagener's snydrome

aspergillosis

Front 78

restrictive lung disease

Back 78

restricted lung expansion decreases lung volume

decreased FVC and TLC

FEV1/FVC > 80%

type 1: poor breathing mechanism - muscular, structural

type 2: interstitial lung disease (ARDS, neonatal respiratory distress syndrome, and others)

Front 79

interstitial lung disease types

Back 79

Acute respiratory distress syndrome

neonatal respiratory distress syndrome

pneumoconioses (coal miner's lung, silicosis, asbestose)

sarcoidosis - bilateral hilar lymphadenopathy,noncaseating granulomas, elevated ACE and Ca

idiopathic pulmonary fibrosis (repeated lung damage -> collagen -> decreased diffusion)

goodpasture's syndrome - AntiGBM, glomerulonephritis, diffuse alveolar hemorrhage

wergener's granulomatosis

eosinophlic granuloma (histiocytosis X)- malignant proliferation of langerhan cells

drug tox

Front 80

coal miner's lung

Back 80

pneumoconioses

results in cor pulmonale, caplan's syndrome

upper lobes effected

Front 81

silicosis

Back 81

foundries, sandblasting, mines

macrophages release fibrogenic factors in response to silica -> fibrosis

increased TB susceptability by damage to macrophage

upper lobes affected

see eggshell calcification of hilar lymph nodes

Front 82

asbestosis

Back 82

shipbuilding, roofing, plumbing

ivory white calcified pleural plaques

increased risk of bronchogenic carcinoma and mesothelioma

asbestos bodies - golden brown fusiform rod shaped like dumbells in macrophages

Front 83

neonatal respiratory distress syndrome

Back 83

surfactant deficiency -> increased surface tension and alveolar collapse

surfactant is produced by type II pneumocytes after 35th week gestation

maternal diabetes and c-section delivery (reduced release of fetal glucocorticoids)

test with lethicin-to-sphingomyelin ratio <1.5

low O2 tension increases risk of PDA

giving O2 risks retinopathy of prematurity

treatment: give mom steroids before birth, artificial surfactant after birth, thyroxine

Front 84

acute respiratory distress syndrome

Back 84

diffuse alverolar damage -> increased alveolar capillary perm -> protein leaks in to alveoli

see intra-alveolar hyaline membrane, bilateral white-out on CXR

many causes - most through neutrophil secretions damage, activation of coagulation cascade, or free radicals

Front 85

restrictive vs obstructive lung disease

Back 85

both have decreased FEV1 and FVC

obstructive FEV1 is more dramatically reduced, thus a lower FEV1/FVC ratio (less than 80%)

obstructive lung disease has increased lung volume (inc TLC, FRC, RV)

________

restrictive lung disease FEV1/FVC > 80%, decreased TLC

Front 86

sleep apnea

Back 86

stop breathing for at least 10 seconds during sleep

central sleep apnea - no respiratory effort, central signalling problem

obstructive - effort against an airway obstruction, microagnathia

obesity, loud snoring, systemic pulm htn, arrhythmia, sudden death

treat with CPAP, weight loss, surgery

Front 87

bronchial obstruction physical findings

Back 87

lack breath sounds over affected area

dec resonance and fremitus

tracheal deviation to side of lesion

Front 88

pleural effusion physical findings

Back 88

decreased breath sounds over site of effusion

dull resonance

decreased fremitis

Front 89

pneumonia physical findings

Back 89

still can have breath sounds over lesion

dull resonance

increased fremitis

Front 90

tension pneumothorax

Back 90

decreased breath sounds

hyperresonance

absent fremitis

tracheal deviation away from lesion

Front 91

lung cancer complications

Back 91

SPHERE

Superior Vena Cava syndrome
Pancoat's tumor
Horner's Syndrome
Endocrine (paraneoplastic)
Recurrent laryngeal symptoms
Effusion (pericardial, pleural)

Front 92

presentation of metastases to lung vs primary cancer in lung

Back 92

metastasis is most common - presents with dyspnea

primary cancer - presents with cough

look for "coin" lesion on x-ray

Front 93

squamous cell carcinoma of lung

Back 93

linked to smoking

centrally located - mass arising from bronchus

look for keratin pearls and intracellular bridges

paraneoplastic effect: parathyroid like activity, hypercalcemia (PTH-related peptide, TGF-beta, TNF, IL-1)

Front 94

adenocarcinoma of lung

Back 94

bronchial or bronchioalveolar - peripherally located

most common lung cancer in nonsmokers

bronchial - develops in site of prior injury

bronchioloalveolar can result in hypertrophic osteoarthropathy

arise from/look like clara cells or type II pneumocytes

Front 95

small cell (oat cell) carcinoma

Back 95

undifferentiated, centrally located - very aggressive

arise from enterochromafin cells (kulchitski cell) -> small dark blue cells

paraneoplastic effects: ectopic production of ACTH or ADH,

lambert eton associated: antibodies to presynaptic Ca channels at neuromuscular junction

treat with chemo, surgery doesnt work

Front 96

large cell carcinoma

Back 96

undifferentiated, peripherally located

pleomorphic giant cell with leukocyte fragments

treat with surgery, chemo doesnt work

Front 97

mesothelioma

Back 97

malignancy associated with asbestos

see pleural thickening and hemorrhagic pleural effusion

psammoma bodies

Front 98

carcinoid tumor of lung

Back 98

secretes serotonin - carcinoid syndrome (flushing, wheezing, diarrhea)
fibrous deposits in right heart valves may lead to tricuspid insufficiency, pulmonary stenosis, RHF

Front 99

pancoast tumor

Back 99

carcinoma that occurs in apex of lung and may affect sympathetic plexus -> horner's syndrome

ptosis, anhidrosis, ptosis (horny PAM)

Front 100

lobar pneumonia

Back 100

pnemococcus most frequent, Klebsiella possible

see intra-alveolar exudate -> consolidation, may involve entire lung

Front 101

bronchopneumonia

Back 101

s. aureus, H. influenza, Klebsiella, S. pyogenes

acute inflam infiltrate into adjacent alveoli - patchy distribution in more than 1 lobe

Front 102

interstitial pneumonia

Back 102

viruses (RSV, adenovirus), mycoplasma, legionella, chlamydia

diffuse patchy inflam in interstitial areas

multiple lobe involvement

more indolent

Front 103

lung abscess

Back 103

localized collection of pus in parenchyma - due to bronchial obstruction or aspiration

often S. aureus or anarobes, Klebsiella in alcoholics

air-fluid levels seen on CXR

Front 104

pleural effusion - 3 types

Back 104

transudate - low protein content due to CHF, nephrotic syndrome, hepatic cirrhosis

exudate - high protein content, cloudy, due to malignancy, pneumonia, collagen vascular disease, trauma

lymphatic - milky fluid with high triglicerides

Front 105

Surfactant

Back 105

produced by type II pneumocytes, decrease alveolar surface tension, increase compliance, decrease work of inspiration

Front 106

Important lung products

Back 106

prostaglandins - bronchodilation
histamine - bronchoconstriction
ACE -> angiotensin I -> angiotensin II -> inactivate bradykin
Kallikrein - activates bradykin (cough, angioedema)

Front 107

pH changes is stored blood and physiologic consequences

Back 107

stored blood has an increase in citrate -> H+ binds with 2,3-DPG which causes the transfused blood to have a high affinity for oxygen
can present problems for recipient as the added blood will not unload O2 as much
treat with inosine to restore 2,3-DPG

Front 108

superior vena cava syndrome

Back 108

obstruction of SVC that impairs blood drainage
often caused my tumor or thromboses
can raise intracranial pressure -> headache and dizziness -> increased risk of aneurysm/rupture of cranial arteries

Front 109

Pneumothorax

Back 109

unilateral chest pain, dyspnea, unilateral chest expansion, decreased tactile fremitus, hyperresonance, diminished breath sounds

spontaneous -- air in pleural space, rupture of apical blebs, trachea deviates toward affected lung

tension - trauma or lung infection, air enters pleural space but doesn't exit, trachea deviates away from lesion