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respiratory Flashcards

1
Q

ards

A

diffuse alveolar damage (capillary) char by rapid onsef of severe life threatening respiratory insufficiency, cyanosis and severe arterial hypoxemia that is refractory to o2 therapy

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2
Q

xray- ARDS

A

diffuse alveolar infiltration

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3
Q

causes of ARDS

A

diffuse alveolar damage infection, chemical injury, physical injury, inhaled irritants, hematologic, pancreatitis, cabg

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4
Q

emphysema

A

abn permanent enlargement airways distal to terminal bronchiole. + obstruction of their walls without obvious fibrosis. enlargement without destruction equals overinflation

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5
Q

xray emphysema

A

hyperinflation

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6
Q

s/s emphysema

A

pink puffer- airway resistance increased, low elastic recoil, severe dyspnea, scant sputum

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7
Q

chronic bronchitis symptoms

A

mild dyspnea, copious sputum and cough, cor pulmanale common, increased airway resistance, normal elastic recoil, blue bloater

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8
Q

chronic bronchitis

A

chronic overinflation- air trapped, lung expands because air trapped in

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9
Q

xray chronic bronchitis

A

prominent vessels, large heart

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10
Q

bronchiolar and bronchial injury leads to

A

infection, bronchospasm, hypersecretion of mucous leads to reversible obstruction of bronchioles and small bronchi with repeated injury leads to chronic bronchitis, with destruction of alveolar walls leads to chronic bronchitis and emphysema

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11
Q

obstructive diseases PFTs

A

decrease fev/fvc, decreased fev1

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12
Q

obstructive disorders

A

emphysema, osa, asthma, obesity, bronchiectasis, chronic bronchitis

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13
Q

emphysema

A

damage at acinar level

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14
Q

bronchitis

A

damage at bronchial level

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15
Q

fev/fvc levels and severity

A

> 80% mild, 50-79% mod, 30-49% severe, < 30 very severe

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16
Q

copd+ air trapping equals

A

v/q mismatch

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17
Q

emphysema

A

abnormal permanent enlargement of air spaces enlargement and destruction of alveolar walls with loss of elasticity and air trapping.

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18
Q

chronic bronchitis

A

inflammation and thickening mucous membrane with accumulation of mucous and pus leads to obstruction

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19
Q

bronchiectasis

A

perm dilation bronchi and bronchioles, secondary to permanent muscle and elastic tissue secondary to chronic necrotizing infections

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20
Q

ex of bronchiectasis

A

cystic fibrosis, severe pneumonia, bronchial obstruction

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21
Q

anesthesia and copd

A

assess changes in symptoms, avoid smoking,

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22
Q

adenocarcinoma

A

originates in epithelial tissues that line body cavities and glands

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23
Q

squamous cell

A

originates in columnar epithelial cells-skin, digestive tract, lungs

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24
Q

non small cell ca

A

epithelial cell insensitive to chemo (80% lung ca)

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25
Q

small cell

A

usually in lungs, sensitive to chemo

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26
Q

presentation lung ca

A

couhing, smoker (90%), hemoptysis, sob, pain with breathing, fever

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27
Q

where are lung tumors normall located

A

proximal/central bronchi

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28
Q

when bronchial lumen is filled with tumor

A

gas exchanging units distal dont function, atelectasis, secretion trapping and pooling, infection, scarring

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29
Q

anesthetic implications airway tumor

A

expect higher airway pessure, dual lumen tube, airway recruitment maneuver, higher fio2

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30
Q

s/s upper airway tumors

A

slow onset, dyspnea, voice changes, swallowing trouble, stridor, hemoptysis, stertor

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31
Q

risks of upper airway tumors

A

smoking, tobacco chewing, HPV

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32
Q

anesthesia implications

A

DIFFICULT AIRAY

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33
Q

which mediastinum tumors are more likely to be malignant?

A

anterior then posterior

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34
Q

problem with mediastinum tumors

A

strutures can be compressed, cardiac tamponade, compression great vessels

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35
Q

SVC syndrome

A

direct compression SVC, causes backup in venous drainage, results in edema to tiddue whose venous drainage returns to heart via SVC

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36
Q

S/S svc syndrome

A

dilation collateral veins neck, edema/cyanosis face, edema conjunctiva, evidence increased ICP, dyspnea

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37
Q

asthma char by

A

airway inflammation, airflow obstruction, bronchial hyperreactivity

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38
Q

s/s asthma

A

dyspnea, wheezing, chest tighness, cough

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39
Q

atopic asthma

A

most common, type I ige hypersensitivity reaction, starts in childhood, triggered by allergens

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40
Q

non-atopic

A

no history allergen, inflammation assoc. hyperirritability

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41
Q

patho atopic astha

A

intitial exposure allergen stim. secretion inflammatory cytokines, trigger the b cells to produce ige which coat the mast cells.

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42
Q

early phase atopic asthma

A

bronchoconstriction, increase mucous production, vasodilation with increased vascular permeability

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43
Q

late phase atopic asthma

A

epithelial damage and additional inflammation and airway constriction

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44
Q

repeated exposure to allergen with atopic results in

A

goblet cell hyperplasia, subepithelial collagen dep, increased capillary network, smooth muscle hypertrophy

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45
Q

b2 adrenergic agonists

A

albuterol, terbutaline (short acting) formoterol, salmeterol (long acting

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46
Q

mech action B2 adrenergic

A

bind to b2 receptors of the lungs directly and relax smooth muscle of the airway by increasing concentration camp

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47
Q

ipratorpium bromide

A

antimuscarinic vasodilating agent

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48
Q

leukotriene receptor antagonists

A

montelukast, zafirlukast,zileuton

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49
Q

ga may trigger asthma exacerbation by

A

alteration diaphragmic function, impaired coughing ability, decreased mucociliary function, stim/irritation airway by ETT

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50
Q

most significant predictors of bronchospasm in asthma

A

proximity and severity of most recent asthma attack

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51
Q

pt with asthma can

A

those who are well controlle, have peak flow meter >80% of predicted are at avg risk surgery

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52
Q

intermittent asthma

A

day: no more then 2x/wk, night: no more than 2x/month

pef>80% predicted

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53
Q

mild persistent asthma

A

day: more than 2x per week but not daily, night- more than 2x/month
pef > 80% predicted

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54
Q

moderate persistent asthma

A

daily, night>1 night per week, exacerbation effects adls, fev 60-80% predicted

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55
Q

severe persistent asthma

A

day/night continuous symptoms with frequent exacerbations, severe limitations adl, fev<60% predicted

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56
Q

what needs to be avoided in asthmatics

A

nonselective beta blockers, nsaids, histamine releasing drugs, premed with steroids, antihistamines

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57
Q

propofol is a

A

bronchodilator

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58
Q

ketamine and respiratory

A

smooth muscle relaxant and decreased airway resistance

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59
Q

manifestations bronchospasm

A 
high inflation pressure with intermittent + pressure vent
expiratory upsloping on capno
prolonged expiration
decreased o2 sat
expiratory wheezing
decreased breath sounds
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60
Q

tx bronchospasm

A 
100% o2
increase anesthesia
beta agonist (albuterol)
anticholinergic inhaled (ipratropium)
lidocaine IV
epi
corticosteroids
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61
Q

rigid bronch

A 
trachea/prox/central airways
GA
straight hollow tube
direct intubation with rigid telescope
constant diameter
vent support
ability to analyze expired gas
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62
Q

uses rigid bronch

A 
large endotracheal or endobronchial tumor
foreign body removal
massive hemoptysis
stent placement
laser surgery
viscous secretions
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63
Q

flexible bronch

A 
most common
visualize down to segmental bronchi
LA, concious sedation or GA
suction, irrigated, biopsy channel
spont vent maintained
64
Q

indications flexible bronch

A 
clearing secretions
cold saline for hemoptysis
staging tumors
place stents
bracytherapy
65
Q

contraindications bronch

A 
arrhythmia
refractory hypoxemia
recent mi
creatinine>3
plt <50,000
SVC obstruction
pulm HTN
unstable neck
66
Q

r main bronchus

A

1-2.5cm long, internal diameter 10-16mm

67
Q

rul

A

apical, anterior, posterior bronchus

68
Q

rml

A

lateral, medial bronchus

69
Q

rll

A

sup. bronchus, medial basalar, anterior, lateral, posterior

70
Q

right bronchial tree 2 classifications

A

Jackson Huber, Boyden

71
Q

Boyden

A

RUL: B1-B3
RML B4-B5
RLL B6-B10

72
Q

Jackson Huber

A

RUL: as listed before

73
Q

L main bronchus

A

4-5cm long, internal diameter 8-14mm

74
Q

LUL

A

upper divison, apical/posterior, anterior

75
Q

linuala bronchus

A

superior segmental bronchus, inferior segmental bronchus

76
Q

left lower lobe

A

superior, anteromedial bronchi, lateral basal bronchi, posterior basal bronchi

77
Q

pulm edema on chest xray

A

kerly B or septal lines, bat wing pattern, increased heart size

78
Q

CHF xray

A

cardiomegaly, alveolar edema, kerley lines, bat wing

79
Q

pneumonia

A

airspace opacity, lobar consolidation, interstitial opacity, indistinct borders

80
Q

pleural effusion

A

costophrenic angle blunting, depression of diaphragm

81
Q

pneumo

A

air with lung markings in least dependent part of chest, upright most likely seen at apices

82
Q

emphysema xray

A

diffuse hyperinflation, flattening diaphragm

83
Q

donor pre-op

A

pao2/fi02>300, clear xray, neg bronchoscope, <20years

84
Q

cross clamp time

A

ischemia time starts

85
Q

obstructive lung disease anesthesia implications

A

I:E ratio 1:4 or 1:5, check autopeep, avoid hyperinflation, permissive hypercapnia, bronchodilator.

86
Q

pulmonary hypertension greater in OLD or RLD?

A

RLD

87
Q

COPD has

A

air trapping, large reserve volume, longer expiratory time

88
Q

restrictive lung disease

A

normal flows, pulmonary hypertension secondary to right vent. hypertrophy, decreased compliance

89
Q

anesthesia implications restrictive lung disease

A

nitric oxide (inhaled), epoprosternol (inhaled or IV, low volume vent (stiff lung) increased RR, minimal peep (autopeep not a concern)

90
Q

superative lung disease

A

large reserve volume from air trapping
purulent secretions
mucous plugs

91
Q

superative lung disease anesthesia implications

A

avoid hyperinflation, nitric oxide, aggressive pulmonary toilet

92
Q

pulmonary vascular disease

A

severe pulmonary hypertension, right ventricular hypertrophy, high pulmonary vascular resistance, hyperdynamic left ventricle, with low pre load, low volumes (total lung complicance

93
Q

anesthesia implications pulm vasc disease

A

low volume ventilation (stiff lung) higher RR, minimal peep, nitric oxide

94
Q

recipient ventilation

A

OLV or CPB, OLV test, PA clamp test

95
Q

possible CPB sites for lung transplant

A

CV site-aorta bypass, fem-fem bypass, bicaval cannulation

96
Q

after lung implanted what need to do

A

intraoperative bronch, avoid volume overload, avoid reperfusion injury keep pa<5mm HG at reperfusion (nitric oxide, epoprostenol), low pee, low fio2, low pressures less than 25mm HG

97
Q

primary grafy dysfunction

A

acute reperfusion injury, severe form of ALI, early post transplant (72 hours)
non cardiogenic pulmonary edema:

98
Q

s/s primary graft dysfunction

A

diffuse alveolar infiltrates, normal PCWP, refractory hypoxemia

99
Q

treatment primary grafy dysfunction

A 
protective ventilation PCV<25, VT6ml/kg, 
nitric oxide
lowest possible fi02
diuresis, avoid fluid overload
surfactant instillation
100
Q

prevention primary graft dysfunction-

A

retrieve donor lungs at low pressure, flush lungs with perfadex, keep short ischemia times, avoid fluid overload, epoprostenol prior to reperfusion, protective ventilation

101
Q

dynamic hyperinflation

A

occurs on lung tx recipienct with COPD have increased airay resistance with expired airflow obstruction, significant air trapping with large residual volume

102
Q

prevention dynamic hyperinflation

A

I:E ratio 1:4 or 1:5, transient disconnection from vent if autopeep produces hypotension
bronchodilator
permissive hypercapnia

103
Q

treatment dynamic hyperinflation

A

DLT and independent lung vent

104
Q

normal pvr

A

50-300dne/sec/cm

105
Q

pap normal

A

10-20

106
Q

paop normal

A

5-15

107
Q

vascoconstriction pulm vasculatre effects

A

co2, hypoxia, endothelin

108
Q

vasodilation of pulmonary vasculature

A

NO, prostacyclin

109
Q

characteristics of pulm hypertension

A

PAP> or = 25mm HG, progressive disorder with highly variable course

110
Q

PH leads to

A

PH+ right ventricl hypertrophy to rright ventricular failure

111
Q

group 1 PAH

A

idiopathic, hereditary, drugs/toxins, connective tissue, HIV, portal HTN, congenital heart disease. disease that localizes to small pulm muscular arterioles

112
Q

group 2 pah

A

LV systolic/diastolic dysfunction, mitral/aortic valve disease, cardiomyopathy, pericarditis,

113
Q

group 3

A

lung disorders/hypoxia (OSA, COPD, ILD)

114
Q

group 4 ph

A

chronic thromboembolic disease

115
Q

group 5 misc.

A

hematologic, systemic, metabolic

116
Q

what causes pulm hypertension

A

increased flow alone does not b/c the pulmonary vasculature vasodilates in response. increased venous pressure alone does not however a chronic increase of both can cause increased pulmonary vascular resistance

117
Q

pulmonary hypertension patho

A

proliferative vasculopathy characterized by vasoconstriction, cell proliferation, fibrosis and thrombosis

118
Q

pathological findings PH

A

intimal hyperplasia and fibrosis, medial hypertrophy, thromi of small pulm arteries and arterioles

119
Q

all types ph have

A

vascular remodeling and increased PVR

120
Q

genetic predisposition to ph

A

abnormal BMPR2 then 2nd hit, increased flow, k channel dysfunction, drugs, inflammatory mediators, then activates disease process increased endothelin, decrease NO and prostacylclin

121
Q

s/s ph

A

nonspecific= initially exertional dyspnea, lethargy, fatigue.
later- peripheral edema, exertional chest pain, exertional syncope, anorexia, abd pain

122
Q

ortner’s syndrome

A

cough, hemoptysis, hoarseness

caused by compression of left recurrent laryngeal nerve by a dilated main pulmonary artery

123
Q

clincial findings PH

A

increased intensity pulmonic sound, right ventricular hypertrophy(prominent A wave, left parasternal heave, murmurs

124
Q

systemic venous hypertension s/s

A

increased JV pressure, 3rd heart sound, peripheral edema, hepatomegaly, pleural effusion

125
Q

diagnosis pulm htn requires

A

pap > 25

126
Q

diagnosis pulm arterial hypertension requires

A

r heart cath

mean pap>25, pcwp >15, chornic lung disease absent or mild, venous thromboemolic dz absent

127
Q

cxr showing pah

A

enlargement central pulm arteries, right ventricle enlargement

128
Q

ekg

A

rvh right axis deviation, incomplete r bbb

129
Q

Cor pulmonale

A

hypertrophy, dilation and or impaired function of the right ventricle that is associated with lung, vasculature, upper airay and chest wall

130
Q

most common causes cor pulmonale

A

copd, ipf, osa

131
Q

COPD leads to

A

chonic hypoxemia, acidosis, pulmonary artery vasoconstriction, increased PAP, intimal fibrosis and hypertrophy of medial smooth muscle layer of pulm arteries leading to chronic ph leading to cor pulmonale and right heart failure

132
Q

progression of pulmonary hypertension can be reversed with copd after increased papwith treatement

A

true

133
Q

gold standard for diagnosis cor pulmonale

A

right heart cath

134
Q

end stag cor pulmonale s/s

A

cardiogenic shock s/s

135
Q

tx cor pulmonale

A

decrease RV pressure, decrease RV afterload, improve RV contractility

136
Q

treatment pulmonary hypertension

A

treat the cause- o2, diuretics, vasodilators, ccb, acei, prostacyclin, nitric oxide, transplant

137
Q

phophodiesterase inhibitors

A

inhibit nitric oxide degredation

138
Q

ex phosphodiesterase inhibitor

A

sildenafil, milnone

139
Q

sildenafil

A

decreases PAP, PVR, synergistic with NO

140
Q

mirinone

A

decreases PVR, PAP, SVR

141
Q

endothelin-1

A

neurohormone that cuases pulmonary vasoconstriction, smooth muscle proliferation and fibrosis, stimulates endothelin receptors A & B
A:vasoconstriction
B: vasodilation

142
Q

endothelin receptor antagonist- nonselective and selective

A

nonselective- bosentan

A selective: sitaxsentan, ambrisentan

143
Q

CCB and pulm htn

A

chornic tx pulm HTN

144
Q

ph preop

A

optimize- o2 administration, bronchodilation, antibiotics, steroids, vasodilators, inotropes

145
Q

anesthesia goals for PH: maintain

A

preload, svr, contractility, co, NSR

146
Q

prevent with ph and anesthesia

A

myocardial ischemia, hypotension, increased PVR

147
Q

Increased PVR caused by

A

hypoxia, hypercarbia, acidosis, pain, low lung volumes, overdistaention

148
Q

ketamine and pulm htn

A

controversial due to ?raise pvr

149
Q

propofol and pulm htn

A

use, decrease svr, decrease venous return, decrease contractility

150
Q

etomidate

A

no effect pvr, maintain hemodynamics

151
Q

nitrous oxide and PH

A

depression of myocardial contractility, icreased PVR and RAP. caution

152
Q

vent managment with ph

A

high o2 concentration, moderate lung volumes, rates sufficient to achieve hypocarbia and low levels peep

153
Q

hypertensive crisis and pulm htn

A 
magnesium- smooth muscle relaxant
inhaled NO
milrinone
dypiridamone
inhaled prostacylcin
154
Q

risks nitric oxide

A

methemoglobinemis, arboyhemoglobinemia, rebound HTN requires close circuit

155
Q

prostacyclins

A

potent pumonary and systemic vasodilators with antiplatelet properties.

156
Q

esoprostenol

A

iv, decreases pvr, increases co, improves exercise tolerance

157
Q

post op risk with pulm. htn

A

risk of acute pulmonary vasospasm, pe, arrhythmia, fluid shifts, increses symp tone and increased pulm vascular tone

advanced bioscience (2 decks)

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