Pulmonary Function
Anatomy
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In utero lung development
Begins-21-28 day gestation
Complete at 16 weeks
Approx. 15-26 divisions
Anatomy
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True alveoli @ 28 weeks
Continue past birth, with 20 mil @ birth
300 mil @ 10 yrs (peak)
Lung volume80% air
10% blood
10% solid tissue
Anatomy
 Alveolar-Capillary membrane
 5 Layers
alveolar epithelium
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basement membrane
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ground substance
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basal membrane
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capillary epithelium
Anatomy
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Bronchi
23 branches from trachea to alveoli
larger airways lined with ciliated columnar
epithelium
flatten in the alveoli
mucociliated esculator
Anatomy
 Alveoli Type I
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cover 90 %
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make up 50 %
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gas exchange
 Type II
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cover 10%
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make up 50 %
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lipoprotein- surfactant- decrease surface
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tension
Anatomy
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Bony Thorax
12 ribs
1-5 attach to sternum
6-10 fuse to costal cartilage arch
11-12 free floating
Lobe sections
R- 3 lobes, major & minor fissure 10 segs
L- 2 lobes, major fissure 8 segs
Anatomy
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Lymphatics
generally drain to ipsilateral hilum
from intralobar nodes
mediastinal nodes drain cephadal
exception- LLL may > R mediastinal
Nerves
none in parenchyma
rich in parietal pleura (painful chest tube)
Anatomy
 Blood supply
 2 fold
 pulmonary artery
 bronchial arteries off aorta
Pulmonary Function Tests
 Pre Operative Evaluation
 Measures
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lung volumes
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elasticity
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recoil
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complaince
Pulmonary Function Tests
 Blood Gases
 pO2
 pCO2 >43-45 severe functional loss
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i.e. > 50 %
 Volume measurements
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FEV1 normal > .8L ^ risks if less
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FEV1/FVC ratio
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obstructive- ratio low
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restrictive- ratio normal (both reduced)
Pulmonary Function Tests
 Exercise Testing
 DL CO- measures CO from alveoli to
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hemoglobin (affinity >200 times)
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<50% high risk of failure
 VO2-(max O2 consumption)
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<15 ml/min/kg high risk
 Vent/Perfusion scan functional segments
 Clinical- stair climb 1,wedge 2,lobe 3,lung
Surgical Incisions
 Types
 Post. Lat
 Axillary
 Ant. Lat
 Median sternotomy
 Thoracoabdominal
 Clamshell
 VATS
 Up to one quarter functional loss
Preoperative Risks
 Increased
 age
 smoking
 COPD
 asthma
 obesity
 diabetes
 poor nutritional state
Preoperative Treatment
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Smoking cessation- >2 wks, ideal > 4-6 wks
Bronchodialators
Antibiotics- Bronchitis
Steriods- short term
Incentive Spirometry training
DVT prophylaxis
Sub-q heparin or equal
Compression device
Consider- epidural, nerve blocks, PCA’s
Lung Cancer
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General
173,000 new yearly
14% all cancer
28% all cancer deaths (most freq)
decrease mortality in men 1991-1996
increase in women since 1987 > breast CA
lag in smoking cessation
Lung Cancer
 Survival
 Overall 5 year 14%
 Regional disease 20 %
 Distant disease 2 %
 Only 15% localized at time of dx
 Stage I & II– generally surgery
 Stage IIIA and up—generally XRT, chemo
Lung Cancer
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Etiology
cigarettes
alcohol
environmental
asbestos, radon,nickel, radiation,
arsenic, chromium, air pollution,
second-hand smoke
Lung Cancer
 Pathology
 R>L secondary to 55% lung on R
 Stages
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proliferation
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atypical nuclei
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stratification
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squamous metaplasia
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CA in situ
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invasive CA
Lung Cancer
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Types
Adeno CA 45%
peripheral, early mets, mucous cells
Bronchoalveolar CA <5%
subtype of adeno, best prognosis
Squamous Cell CA 30%
centrally located, later mets, local invade
Lung Cancer
 Types (cont)
 Large Cell CA 10%
 peripheral, early mets
 Small Cell CA 20%
 central, aggressive, early mets bone,
 brain, chemo (!), oat cell
Lung Cancer
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Metastasis
typically, lobar>hilar>mediastinal (ipsilat)
exception, LLL>contralateral mediastinum
hematologous spread
liver, adrenals, bone, brain, kidneys, lung
Lung Cancer
 Detection
 local symptoms
 cough, pnemonia, hemoptysis, rib pain,
 nerve involvement
 distant symptoms
 weight loss, bone pain, neurologic,
 paraneoplastic,
Lung Cancer
 Staging
 TNM
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adopted 1986
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revised 1997
Lung Cancer
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Special Circumstances
Superior Sulcus CA
Solitary pulmonary nodule
overall 33% CA
risk roughly age of patient
Molecular Markers
poor survival-DNA aneuploidy;
oncogenes KRAS, Her 2, p53 mutation
Respiratory Failure
 Clinical Assessment
 Distress
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>24 breaths/min
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accessory mm usage
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color
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O2 content difficult to tell
 Pulse Ox
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sat 90% approx pO2 of 60
Respiratory Failure
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Ventilatory Settings
Tidal Volume 12-15 ml/kg
PEEP +5 (starting)
Rate 10-12
Mode IMV
O2 % depends
Respiratory Failure
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Ventilator Weaning
pO2 > 70
stable BP
Cause corrected
NIF > 30
RR < 24
pH > 7.35
pCO < 50
Respiratory Failure
 Ventilators
 + pressure vents 1950’s Scandinavia
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polio
 Excellent support
 Negatives
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decrease venous return
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^ dead space
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^ work of breathing
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^ venous admixture
Respiratory Failure
 Ventilators
 favor flow to nongravity dependent
 portions of lung, ^ shunt
 O2 deficits not correctable with PPV
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 Fighting the vent
 hypercarbia, acidemia, CNS problems,
 low O2, pain, anxiety
Respiratory Failure
 Ventilator Modes
 PPV deliver TV without ^ MAP
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large TV- dec deadspace,atelectasis
 Control Mode Ventilation
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frequency and depth independent of
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patient’s response
 Assist Control Mode
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initiates breath whenever preset limit
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is hit by patient
Respiratory Failure
 Ventilator Modes (cont)
 Intermittent Mandatory Ventilation (IMV)
 PPV independent of patient
 no impedence to spontanous breath
 + gas flow
 SIMV
 synchronized to patient
 assist control w/ spontanous ventilation
 ^ work of breathing, demand flow