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