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
2
Q
xray- ARDS
A
diffuse alveolar infiltration
3
Q
causes of ARDS
A
diffuse alveolar damage infection, chemical injury, physical injury, inhaled irritants, hematologic, pancreatitis, cabg
4
Q
emphysema
A
abn permanent enlargement airways distal to terminal bronchiole. + obstruction of their walls without obvious fibrosis. enlargement without destruction equals overinflation
5
Q
xray emphysema
A
hyperinflation
6
Q
s/s emphysema
A
pink puffer- airway resistance increased, low elastic recoil, severe dyspnea, scant sputum
7
Q
chronic bronchitis symptoms
A
mild dyspnea, copious sputum and cough, cor pulmanale common, increased airway resistance, normal elastic recoil, blue bloater
8
Q
chronic bronchitis
A
chronic overinflation- air trapped, lung expands because air trapped in
9
Q
xray chronic bronchitis
A
prominent vessels, large heart
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
11
Q
obstructive diseases PFTs
A
decrease fev/fvc, decreased fev1
12
Q
obstructive disorders
A
emphysema, osa, asthma, obesity, bronchiectasis, chronic bronchitis
13
Q
emphysema
A
damage at acinar level
14
Q
bronchitis
A
damage at bronchial level
15
Q
fev/fvc levels and severity
A
> 80% mild, 50-79% mod, 30-49% severe, < 30 very severe
16
Q
copd+ air trapping equals
A
v/q mismatch
17
Q
emphysema
A
abnormal permanent enlargement of air spaces enlargement and destruction of alveolar walls with loss of elasticity and air trapping.
18
Q
chronic bronchitis
A
inflammation and thickening mucous membrane with accumulation of mucous and pus leads to obstruction
19
Q
bronchiectasis
A
perm dilation bronchi and bronchioles, secondary to permanent muscle and elastic tissue secondary to chronic necrotizing infections
20
Q
ex of bronchiectasis
A
cystic fibrosis, severe pneumonia, bronchial obstruction
21
Q
anesthesia and copd
A
assess changes in symptoms, avoid smoking,
22
Q
adenocarcinoma
A
originates in epithelial tissues that line body cavities and glands
23
Q
squamous cell
A
originates in columnar epithelial cells-skin, digestive tract, lungs
24
Q
non small cell ca
A
epithelial cell insensitive to chemo (80% lung ca)
25
small cell
usually in lungs, sensitive to chemo
26
presentation lung ca
couhing, smoker (90%), hemoptysis, sob, pain with breathing, fever
27
where are lung tumors normall located
proximal/central bronchi
28
when bronchial lumen is filled with tumor
gas exchanging units distal dont function, atelectasis, secretion trapping and pooling, infection, scarring
29
anesthetic implications airway tumor
expect higher airway pessure, dual lumen tube, airway recruitment maneuver, higher fio2
30
s/s upper airway tumors
slow onset, dyspnea, voice changes, swallowing trouble, stridor, hemoptysis, stertor
31
risks of upper airway tumors
smoking, tobacco chewing, HPV
32
anesthesia implications
DIFFICULT AIRAY
33
which mediastinum tumors are more likely to be malignant?
anterior then posterior
34
problem with mediastinum tumors
strutures can be compressed, cardiac tamponade, compression great vessels
35
SVC syndrome
direct compression SVC, causes backup in venous drainage, results in edema to tiddue whose venous drainage returns to heart via SVC
36
S/S svc syndrome
dilation collateral veins neck, edema/cyanosis face, edema conjunctiva, evidence increased ICP, dyspnea
37
asthma char by
airway inflammation, airflow obstruction, bronchial hyperreactivity
38
s/s asthma
dyspnea, wheezing, chest tighness, cough
39
atopic asthma
most common, type I ige hypersensitivity reaction, starts in childhood, triggered by allergens
40
non-atopic
no history allergen, inflammation assoc. hyperirritability
41
patho atopic astha
intitial exposure allergen stim. secretion inflammatory cytokines, trigger the b cells to produce ige which coat the mast cells.
42
early phase atopic asthma
bronchoconstriction, increase mucous production, vasodilation with increased vascular permeability
43
late phase atopic asthma
epithelial damage and additional inflammation and airway constriction
44
repeated exposure to allergen with atopic results in
goblet cell hyperplasia, subepithelial collagen dep, increased capillary network, smooth muscle hypertrophy
45
b2 adrenergic agonists
albuterol, terbutaline (short acting) formoterol, salmeterol (long acting
46
mech action B2 adrenergic
bind to b2 receptors of the lungs directly and relax smooth muscle of the airway by increasing concentration camp
47
ipratorpium bromide
antimuscarinic vasodilating agent
48
leukotriene receptor antagonists
montelukast, zafirlukast,zileuton
49
ga may trigger asthma exacerbation by
alteration diaphragmic function, impaired coughing ability, decreased mucociliary function, stim/irritation airway by ETT
50
most significant predictors of bronchospasm in asthma
proximity and severity of most recent asthma attack
51
pt with asthma can
those who are well controlle, have peak flow meter >80% of predicted are at avg risk surgery
52
intermittent asthma
day: no more then 2x/wk, night: no more than 2x/month
| pef>80% predicted
53
mild persistent asthma
day: more than 2x per week but not daily, night- more than 2x/month
pef > 80% predicted
54
moderate persistent asthma
daily, night>1 night per week, exacerbation effects adls, fev 60-80% predicted
55
severe persistent asthma
day/night continuous symptoms with frequent exacerbations, severe limitations adl, fev<60% predicted
56
what needs to be avoided in asthmatics
nonselective beta blockers, nsaids, histamine releasing drugs, premed with steroids, antihistamines
57
propofol is a
bronchodilator
58
ketamine and respiratory
smooth muscle relaxant and decreased airway resistance
59
manifestations bronchospasm
```
high inflation pressure with intermittent + pressure vent
expiratory upsloping on capno
prolonged expiration
decreased o2 sat
expiratory wheezing
decreased breath sounds
```
60
tx bronchospasm
```
100% o2
increase anesthesia
beta agonist (albuterol)
anticholinergic inhaled (ipratropium)
lidocaine IV
epi
corticosteroids
```
61
rigid bronch
```
trachea/prox/central airways
GA
straight hollow tube
direct intubation with rigid telescope
constant diameter
vent support
ability to analyze expired gas
```
62
uses rigid bronch
```
large endotracheal or endobronchial tumor
foreign body removal
massive hemoptysis
stent placement
laser surgery
viscous secretions
```
63
flexible bronch
```
most common
visualize down to segmental bronchi
LA, concious sedation or GA
suction, irrigated, biopsy channel
spont vent maintained
```
64
indications flexible bronch
```
clearing secretions
cold saline for hemoptysis
staging tumors
place stents
bracytherapy
```
65
contraindications bronch
```
arrhythmia
refractory hypoxemia
recent mi
creatinine>3
plt <50,000
SVC obstruction
pulm HTN
unstable neck
```
66
r main bronchus
1-2.5cm long, internal diameter 10-16mm
67
rul
apical, anterior, posterior bronchus
68
rml
lateral, medial bronchus
69
rll
sup. bronchus, medial basalar, anterior, lateral, posterior
70
right bronchial tree 2 classifications
Jackson Huber, Boyden
71
Boyden
RUL: B1-B3
RML B4-B5
RLL B6-B10
72
Jackson Huber
RUL: as listed before
73
L main bronchus
4-5cm long, internal diameter 8-14mm
74
LUL
upper divison, apical/posterior, anterior
75
linuala bronchus
superior segmental bronchus, inferior segmental bronchus
76
left lower lobe
superior, anteromedial bronchi, lateral basal bronchi, posterior basal bronchi
77
pulm edema on chest xray
kerly B or septal lines, bat wing pattern, increased heart size
78
CHF xray
cardiomegaly, alveolar edema, kerley lines, bat wing
79
pneumonia
airspace opacity, lobar consolidation, interstitial opacity, indistinct borders
80
pleural effusion
costophrenic angle blunting, depression of diaphragm
81
pneumo
air with lung markings in least dependent part of chest, upright most likely seen at apices
82
emphysema xray
diffuse hyperinflation, flattening diaphragm
83
donor pre-op
pao2/fi02>300, clear xray, neg bronchoscope, <20years
84
cross clamp time
ischemia time starts
85
obstructive lung disease anesthesia implications
I:E ratio 1:4 or 1:5, check autopeep, avoid hyperinflation, permissive hypercapnia, bronchodilator.
86
pulmonary hypertension greater in OLD or RLD?
RLD
87
COPD has
air trapping, large reserve volume, longer expiratory time
88
restrictive lung disease
normal flows, pulmonary hypertension secondary to right vent. hypertrophy, decreased compliance
89
anesthesia implications restrictive lung disease
nitric oxide (inhaled), epoprosternol (inhaled or IV, low volume vent (stiff lung) increased RR, minimal peep (autopeep not a concern)
90
superative lung disease
large reserve volume from air trapping
purulent secretions
mucous plugs
91
superative lung disease anesthesia implications
avoid hyperinflation, nitric oxide, aggressive pulmonary toilet
92
pulmonary vascular disease
severe pulmonary hypertension, right ventricular hypertrophy, high pulmonary vascular resistance, hyperdynamic left ventricle, with low pre load, low volumes (total lung complicance
93
anesthesia implications pulm vasc disease
low volume ventilation (stiff lung) higher RR, minimal peep, nitric oxide
94
recipient ventilation
OLV or CPB, OLV test, PA clamp test
95
possible CPB sites for lung transplant
CV site-aorta bypass, fem-fem bypass, bicaval cannulation
96
after lung implanted what need to do
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
primary grafy dysfunction
acute reperfusion injury, severe form of ALI, early post transplant (72 hours)
non cardiogenic pulmonary edema:
98
s/s primary graft dysfunction
diffuse alveolar infiltrates, normal PCWP, refractory hypoxemia
99
treatment primary grafy dysfunction
```
protective ventilation PCV<25, VT6ml/kg,
nitric oxide
lowest possible fi02
diuresis, avoid fluid overload
surfactant instillation
```
100
prevention primary graft dysfunction-
retrieve donor lungs at low pressure, flush lungs with perfadex, keep short ischemia times, avoid fluid overload, epoprostenol prior to reperfusion, protective ventilation
101
dynamic hyperinflation
occurs on lung tx recipienct with COPD have increased airay resistance with expired airflow obstruction, significant air trapping with large residual volume
102
prevention dynamic hyperinflation
I:E ratio 1:4 or 1:5, transient disconnection from vent if autopeep produces hypotension
bronchodilator
permissive hypercapnia
103
treatment dynamic hyperinflation
DLT and independent lung vent
104
normal pvr
50-300dne/sec/cm
105
pap normal
10-20
106
paop normal
5-15
107
vascoconstriction pulm vasculatre effects
co2, hypoxia, endothelin
108
vasodilation of pulmonary vasculature
NO, prostacyclin
109
characteristics of pulm hypertension
PAP> or = 25mm HG, progressive disorder with highly variable course
110
PH leads to
PH+ right ventricl hypertrophy to rright ventricular failure
111
group 1 PAH
idiopathic, hereditary, drugs/toxins, connective tissue, HIV, portal HTN, congenital heart disease. disease that localizes to small pulm muscular arterioles
112
group 2 pah
LV systolic/diastolic dysfunction, mitral/aortic valve disease, cardiomyopathy, pericarditis,
113
group 3
lung disorders/hypoxia (OSA, COPD, ILD)
114
group 4 ph
chronic thromboembolic disease
115
group 5 misc.
hematologic, systemic, metabolic
116
what causes pulm hypertension
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
pulmonary hypertension patho
proliferative vasculopathy characterized by vasoconstriction, cell proliferation, fibrosis and thrombosis
118
pathological findings PH
intimal hyperplasia and fibrosis, medial hypertrophy, thromi of small pulm arteries and arterioles
119
all types ph have
vascular remodeling and increased PVR
120
genetic predisposition to ph
abnormal BMPR2 then 2nd hit, increased flow, k channel dysfunction, drugs, inflammatory mediators, then activates disease process increased endothelin, decrease NO and prostacylclin
121
s/s ph
nonspecific= initially exertional dyspnea, lethargy, fatigue.
later- peripheral edema, exertional chest pain, exertional syncope, anorexia, abd pain
122
ortner's syndrome
cough, hemoptysis, hoarseness
| caused by compression of left recurrent laryngeal nerve by a dilated main pulmonary artery
123
clincial findings PH
increased intensity pulmonic sound, right ventricular hypertrophy(prominent A wave, left parasternal heave, murmurs
124
systemic venous hypertension s/s
increased JV pressure, 3rd heart sound, peripheral edema, hepatomegaly, pleural effusion
125
diagnosis pulm htn requires
pap > 25
126
diagnosis pulm arterial hypertension requires
r heart cath
| mean pap>25, pcwp >15, chornic lung disease absent or mild, venous thromboemolic dz absent
127
cxr showing pah
enlargement central pulm arteries, right ventricle enlargement
128
ekg
rvh right axis deviation, incomplete r bbb
129
Cor pulmonale
hypertrophy, dilation and or impaired function of the right ventricle that is associated with lung, vasculature, upper airay and chest wall
130
most common causes cor pulmonale
copd, ipf, osa
131
COPD leads to
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
progression of pulmonary hypertension can be reversed with copd after increased papwith treatement
true
133
gold standard for diagnosis cor pulmonale
right heart cath
134
end stag cor pulmonale s/s
cardiogenic shock s/s
135
tx cor pulmonale
decrease RV pressure, decrease RV afterload, improve RV contractility
136
treatment pulmonary hypertension
treat the cause- o2, diuretics, vasodilators, ccb, acei, prostacyclin, nitric oxide, transplant
137
phophodiesterase inhibitors
inhibit nitric oxide degredation
138
ex phosphodiesterase inhibitor
sildenafil, milnone
139
sildenafil
decreases PAP, PVR, synergistic with NO
140
mirinone
decreases PVR, PAP, SVR
141
endothelin-1
neurohormone that cuases pulmonary vasoconstriction, smooth muscle proliferation and fibrosis, stimulates endothelin receptors A & B
A:vasoconstriction
B: vasodilation
142
endothelin receptor antagonist- nonselective and selective
nonselective- bosentan
| A selective: sitaxsentan, ambrisentan
143
CCB and pulm htn
chornic tx pulm HTN
144
ph preop
optimize- o2 administration, bronchodilation, antibiotics, steroids, vasodilators, inotropes
145
anesthesia goals for PH: maintain
preload, svr, contractility, co, NSR
146
prevent with ph and anesthesia
myocardial ischemia, hypotension, increased PVR
147
Increased PVR caused by
hypoxia, hypercarbia, acidosis, pain, low lung volumes, overdistaention
148
ketamine and pulm htn
controversial due to ?raise pvr
149
propofol and pulm htn
use, decrease svr, decrease venous return, decrease contractility
150
etomidate
no effect pvr, maintain hemodynamics
151
nitrous oxide and PH
depression of myocardial contractility, icreased PVR and RAP. caution
152
vent managment with ph
high o2 concentration, moderate lung volumes, rates sufficient to achieve hypocarbia and low levels peep
153
hypertensive crisis and pulm htn
```
magnesium- smooth muscle relaxant
inhaled NO
milrinone
dypiridamone
inhaled prostacylcin
```
154
risks nitric oxide
methemoglobinemis, arboyhemoglobinemia, rebound HTN requires close circuit
155
prostacyclins
potent pumonary and systemic vasodilators with antiplatelet properties.
156
esoprostenol
iv, decreases pvr, increases co, improves exercise tolerance
157
post op risk with pulm. htn
risk of acute pulmonary vasospasm, pe, arrhythmia, fluid shifts, increses symp tone and increased pulm vascular tone
