R Respirology

Helen Cheung. Yehoshua Glei.cher and Lorraine Jensen, chapter editors

Doreen Ezeife and Nigel Tan, associate editors
Steven Wong, EBM editor
Dr. Matthew Binnie, staff editor

Approach to the Respiratory Patient . . . . . . . . 2 Introduction to Intensive Care ............ 33

Basic Anatomy Review ICU Basics
Differential Diagnoses of Common Presentations ICU Approach to Management
Pulmonary Function Tests (PFTs) Organ Failure
Chest X-Rays Shock
Arterial Blood Gases Infection/Sepsis
Common Drug Overdoses
Diseases of Airway Obstruction ........... 7
Asthma Common Medications ................... 37
Chronic Obstructive Pulmonary Disease (COPD)
Bronchiectasis Landmark Respirology Trials ............. 38
Cystic Fibrosis (CF)
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38
Interstitial Lung Disease {ILD) . 12
Unknown Etiologic Agents
Idiopathic Pulmonary Fibrosis (IPF)
Sarcoidosis
Known Etiologic Agents
Hypersensitivity Pneumonitis
Pneumoconioses
ILD Associated with Drugs or Treatments

Pulmonary Vascular Disease .............. 16

Pulmonary Hypertension
Pulmonary Embolism (PE)
Pulmonary Vasculitis

Diseases of the Mediastinum and Pleura ... 21

Mediastinal Masses
Mediastinitis
Pleural Effusions
Complicated Effusion
Empyema
Pneumothorax
Asbestos-Related Pleural Disease and
Mesothelioma
Pulmonary Edema

Respiratory Failure . . . . . . . . . . . . . . . . . . . . . 25
Hypoxemic Respiratory Failure
Hypercapnic Respiratory Failure
Acute Respiratory Distress Syndrome (ARDS)
Mechanical Ventilation

Neoplasms ............................ 28
Approach to the Solitary Pulmonary Nodule
Benign Lung Tumours
Malignant Lung Tumours

Sleep-Related Breathing Disorden ........ 32

Sleep Apnea

Toronto Notes 2011 Respirology Rl

R2 Respirology Approach to the Respiratory Patient Toronto Notes 2011

Respiration Pattern
Approach to the Respiratory Patient
Normal (inspiration and expiration)

Basic Anatomy Review
Obstructive (prolonged expiration)
Asthma, COPD

Bradypnea (slow respiratory rate)

Drug-induced respiratory depression
Diabetic coma (nonketotic)
Increased ICP

W\f\1\Mf\
Kussmaul's Breathing (fast and deep)
Metabolic acidosis
Exercise
Anxiety

Biot's/Ataxic
(irregular with long apneic periods)
Drug-induced respiratory depression
Increased ICP
Brain damage, especially medullary

Figure 1_ Lung Lobes and Bronchi

Cheyne-Stokes Breathing (changing
rates and depths with apneic periods)
Drug-induced respiratory depression
Brain damage (especially cerebral)
Differential Diagnoses of Common Presentations
CHF
Uremia
Table 1. Differential Diagnosis of Dyspnea Table 2. Differential Diagnosis of Chest Pain
Acute dvspnea lmjg-hgl Nggpleuritic eJmu:ilili.
Cardiac causes Pulmonary Pulmonary
Apneustic (prolonged inspiratory pause)
Pontine lesion
Ischemic heart disease Pneumonia Pneumonia
CHF exacerbation PE PE
Figure 2. Respiration Patterns in LVF with pulmonary edema Neoplastic Pneumothorax
Cardiac tamponade Cardiac Hemothorax
Normal and Disease States
Pulmonary causes Ml Neoplasm
Upper airway obstruction (anaphylaxis, foreign body) Myocarditis/pericarditis TB
Airway disease (asthma, COPD exacerbation, bronchitis) Esophageal Empyema
Parenchymal lung disease (ARDS, pneumonia) GERD Cardiac
Pulmonary vascular disease (PE, vasculitis) Spasm Pericarditis
Pleural disease (pneumothorax. tension pneumothorax) Esophagitis Dressier's syndrome
Respiratory control (metabolic acidosis, ASA, toxicity) Ulceration Gl
Psychiatric Achalasia Subphrenic abscess
Anxiety/psychosomatic Neoplasm Pancreatitis
Esophageal rupture MSK
Chronic dvspnea lwks-mpsl
Mediastinal Costochondritis
Cardiac causes
Lymphoma Fractured rib
Valvular heart disease
Thymoma Myositis
Decreased CO
Subdiaphragmatic Herpes zoster
Respiratory causes
PUD
Parenchymal lung disease (interstitial disease)
Gastritis
Pulmonary vascular disease (pulmonary HTN, vasculitis)
Biliary colic
Pleural disease (effusion)
Pancreatic
Gas exchange (infection, emphysema, fibrosis, etc.)
Vascular
Airway disease - asthma, COPD
Dissecting aortic aneurysm
Hematologic causes
MSK
Severe anemia
Costochondritis
Neuromuscular and chest wall disorders
Skin
Deconditioning, obesity, pregnancy
Breast
Ribs
'IbroDlo Nota 2011 Approach to the Respiratory Patiml RespirolCJBY R3

Tallie 3. Diffarentiel Dilanlllil of Hemoptysis Table 4. Diflerlllltiel Dieanosil af Caugh

AiiWIV' Dilllle AnoMy InlaiD
----t,
Acute or ciRni: bronchitis lrlllled smoka, Uls. fllrnBI ...II Cannan C.-..
ClnmG
Calh in Hul*re....-i.. l'llliant
Bnn:hiac.tasis AsJRian ICGIGI >!IIDIIIM will 110111111 CXJQ
llnlnchoganic CA Gastric con11nt1 {GBIDJ GERD
llnlnchial CIGilaid llmour lnl secretions
l'lllnclrwnl DiiiDI
Pnallllllllie
Farai!JI body
l'llmlul drip
Ast!m
l'oltilllll
l'olt-vial
*"
lB An., ..... ACE irlmitar
able Ullll ilduding pD8tnB&al*ll BDd ainusitis
...."""
Miscellaneous: Acute II" ch111nic lmlchitis
Gaadpesbn'a synd111me Bl'lllchiaclalis \'
Vascular
PE
a--.
..apallic pWIIICIIIY llamllsiderasis Neaplasm
Exbrnal campiiSiian by nad1 ar IIIBIS ilsion
AstiiJII
H-plpil
MDSt ccnrmon causa is bronc:flitis
10% of miiANt hernoplylis il fram
EIM1IId pgm11111ry vnus JIS8Ur&: COPD 1ha brtlnchilll rtarisa
Canaidlnd "lllllllllivlf" if
LVF PlnllcllrNI m.u >600 CQ'24 haur.
Mitralllanasis
Vasc!Er L.q lliJscels
MIIUI-u lniEnlitiall11111 disease Normal ClMid
. .ired coegiJatian CIIF

j
andclnalriasis Dlllt'llllad (1... ACE l1hlllbrl "
Mi!11a1 frum llill$*ld .l'linaBy.lld:ill, 5111 actlill, SE with ]lllliaiJn fllln llrir. <11&" >In"
<l:ABD <182" <tABD >192"
Telll 5. Diffarentiel Dilgnlllil of aullbing I__ lDPD>IPD
.
Galbam.tilll lllllilllllilllll IPD>DPD
Cyatic lbraais IBDIUC,all Elophlgaal CA
CShonyH.I.oi21XJ'i
fibrosis Dnlicnaans ll1',maml
Ch111nic pus irthe lung Lmti'l8 abuse Ilk Figura 3. Thrae Signs of Clubllinl
(broncliac1asis. abscess. Polyposis IDvas Dislase 1. Profile Angle (ABC > 176")
infectimm. elc.J Malignn 11mou111 lhalas3ania 2. Hyponychial Allgla (ABD > 192"1
CA (Jiinwy or mall) Ci111asil Other 111111ig11111Cias 3. Ptalangaal Depth Ratio {DPD:IPD > 1)
A-Vfililllll Hapallleallular carcinoma l'linary hypll1fl:tlli': CIStSOIIthlllpalhy Mi!llalfmm.w.M 2001;
Salilllly fibrous 111naur Df Canilc
Cyanotic CQ!lgerilal he.t disease
lnfa:tive endocaditis

Pulmonary Function Tests (PFTs)

useful in ditferentlatlng the pattern oflung disease (obstructive vs. restrictive) (Table 6)
assess lung volumes, flow rates, and dJffusJ.on capacity (see Figures 4a and 4b below)
note: normal values for FEV1 are approximately 20% of the predicted values (for age, sex and
height): race may a1fect predicted values
----t,
. ...
FEV1 - Forced ElcpinrtoryVol1111e ilone
811Cond
MMm - Maximal Mid-ExpiratDry Row
Rlt8
FVC- Forced
FEF- Fomed Expii"IIDry Flow Rita
FRC - Funcli111111l CIIPICitv
1LC - TDIII Lung CIIPICitv
vc - V"llll CaplJCity
RV - RIISidull Volume
Dco - Dillll&ion Clpacity of Clrbon
TlME Mai"IIIXida

Figure 4A. Salcompartmenta rsf Lua Volumes Figure 48. ExplratoiJ Row Volume CUr81
Mi!11a1 . ..... 51flactlill, SE'Niillla"Qer. with]lllliailnfllln llrir.

Obstructive Lung Disease

characterized by decreased flow rates (most marked during apiratlon), air trapping (.t.ncreased
RVITLC), and hyperinflation (increased FRC, TLC)
differential diagnosis includes asthma, chronic obstructive pulmonary disease (COPD), cystic
fibrosis (CF), bronchiolitis and bronchiectasis
Restrictive Lung Disease
characterized by decreased lung compliance and lung volumes
differential diagnosis includes interstitial. lung disease, pleural disease (e.g. pulmonary fibrosis),
neuromuscular disease, chest wall disease
R4 Respirology Approach to the Respiratory Patient Toronto Notes 2011

Table 6. Comparison of Lung Flow and Volume Parameters in Olmructive vs. Restrictive Lung Disease
-"(.., Obsbuclive llestriclive
Dftaion c.pacity of Carllon
Monaxlda (Dcol Flow Rates FEV,/FVC "" 'I' arN
Dca dacl'l- will!: Lung Volumes TLC
1. O.a.slld surfac1 na (1.g. RV
emphysema) RV/TlC
2. O.a.sad hemoglobin
3. disease Diffusion Capacity Dca
4. Pulmonary VISCUIIIr diu-
Ilea inc,__ wilb:
1. Asthma Pulmonary Function Tests IPFTs)
2. Pulmonary hllmorrfliQe
3. Polycylhemil
4. Increased pulmonary blood valume

Figura 5. Interpreting PFTs

Chest X-Rays
see also Diagnostic Medical hnaging, DM4
Table 7. CXR Patterns and Differential Diagnosis
Pattern Signs Common DDx
Consolidation Air bronchogram Ac!!m: water (pulmonary edema), pus (pneumonia), blood
("Airspace disene") Sihoullttllsign (hemorrhage)
Less visible blood vessels neoplasm (lymphoma), irAimrnatory (eosinophilic
pneumonia), granuloma {TB, fungal, sarcoid)
Reticular Increased pulmonary markilgs lnt!!IS!itiallung disease (IPF, CW, asbestos, drugs)
disease") {IPF)

Nodulll" Cavitay vs. nan-cavitary neoplasm (prinary vs. metastatic cancer),

infectious (TB, i1flammatory (Wegener's, RA)
No1tc;wili11y: abow + sarcoid (in HIV), Kaposi's sarcoma
Toronto Notes 2011 Approach to the Reapiratory Patient Respirolo8Y R5

Arterial Blood Gases

provides information on acid-base and oxygenation status
see also Nc;phroloif, NP16

Approach to Acid-Base Status

1. Is the pH acidemic (pH <7.35), alkalemic (pH >7.45), or normal (pH 7.35-7.45)?
2. What is the primary disturbance?
metabolic: change in HC03 and pH in same direction
respiratory: change in HC03 and pH in opposite direction
3, Has there been appropriate compensation? (Table 8)
metabolic compensation occurs over 2-3 days reflecting altered renal HC03 production and
excretion
respiratory compensation through ventilation control of PaC02 occurs immediately
inadequate compensation may indicate a second acid-base disorder

Tabla 8. Ex]lectad Compensation for Specific Acid-Basa Disorders

Diltwbuu:e PICD2 (mmltg] HCD, (mmltg)
llespil'llary Acidosis
Acut& '1'10 '1'1
Chronic 1' 10 1'3
Rapil'llary Alblasis
Acute ..J.-10 .J.-2
Chronic ..J.-10 .J.-5
Metlllbalic Acilalis .J.-1 .J.-1
Metlllbalic Albl1111il N-7 1-10

4. If there is metabolic acidosis, what is the anion gap and osmolar gap?
anion gap= [Na]-([Cl]+[HC03 ]); normal mmoUL
osmolar gap= measured osmolarity- calculated osmolarity= measured- (2[Na] +glucose
+urea); normal
5. If anion gap is increased, is the change in bicarbonate the same as the change in anion gap?
if not, consider a mixed metabolic picture \,
Nota: Mixed acid-base disturbances am
DIFFERENTIAL DIAGNOSIS OF RESPIRATORY ACIDOSIS still have a "normal pH"
characterized by increased PaC02 sewndary to hypoventilation
respiratory centre depression (decreased RR)
drugs (anesthesia, sedatives, narcotics)
.... ,.. ,

trauma
increased ICP Ventilltilll Failure
encephalitis
1hmk eant a....._-
1111.
'"Won"t a.......- (incruHd PaC02I
stroke
Won"tllre.thl
central apnea RaspiraiDiy clllllnl depra11ion
supplemental 0 2 in chronic C02 retainers (ie. COPD) Hypothyroidism
neuromuscular disorders {decrease TV) Slaep 1p1111
myasthenia gravis Can"tarulh
Guillain-Barre syndrome Neuromuscular disorders
poliomyelitis Airway obstruction
Parenchyrnlll di._a
muscular dystrophies
ALS
myopathies
chest wall disease (obesity, kyphoscoliosis)
airway obstruction (asthma, COPD) Anion Gllp M8tallolic: Ac:idollia
parenchymal disease !CARMEL
COPD Ketoacidosis
pulmonary edema ASA
pneumothorax Renal failurs {uremia)
Mrlhanol
pneumonia E1hylene glycol
interstitial lung disease (late stage) lactic acidosis
acute respiratory distress syndrome (ARDS)
mechanical hypoventilation (inadequate mechanical ventilation)
DIFFERENTIAL DIAGNOSIS OF RESPIRATORY ALKALOSIS \,
characterized by decreased PaC02 sewndary to hyperventilation Acidosis E- lfyperUiemia
hypoxemia AIUiosis Hypokalemia
pulmonary disease (pneumonia, edema, PE, interstitial fibrosis)
severe anemia
heart failure
high altitude
R6 Rupirology Approuh to the Reqlratory Patient 1'oroDio 2011

respiratory centre stimulation

CNS disorders
hepatic failure
Gram-negative sepsis
drugs (ASA. progesterone. theophylline. catecholamines, psychotropics)
pregnllllcy
anxiety
pain
mechanical hypervent!htion (excessive mechanical ventilation)

see NP16 for differential diagnosis of metabolic acidosis and alkalosis

,, I Calculation of A-8002 Gradient (Approach to Oxygenation Status)

A-aDOz: alveolar-arterial oxygen tension difference
Alllal.eulll cnygen gradient between the alveolus and the pulmonary capillaries
A-IID01 1ndtlll on Rllo11 Air approach includes:
lrliDilz = {150- 1.25 {PeC01)} -l'aOz 1. What Is the PaOz? (normal= 95-100 mmHg)
2. What is the A-aDOz gradient? (normal <15 mmHg)

100
......
.,. co
_ ,..---
A-aDOz = (alveolar) - Pa02(arterial) = [FiOz (Patm - PH20)- PaCOz.(RQ] -
on room air: FiOz = 0.21, Patm = 760 mmHg, PH20 = 47 mmHg. RQ = 0.8
at sea level: A-aD02 = [150- 1.2S(PaCOz)] - Pa02
the normal A-aD02 incre85eS with age
110 3. What ill the cause of the hypoxemia? (see Figure 7)
t_,..
!l!m
0
I. I PIIDz <!5 -H I

:i40
II<

20
/
I pM UO. T88'C
h:1811111d gradient(> 15 mmHal = luna dl-1
1Jaaa.ad lito
I Lung nurmll Ml Fldant (<15 mrmlg) = narmallunp I
20 40
pO, (rrrN!g)
110 10 lOCI .t
I Gi'IIIIDD'K.O, I

llnCIIIIIIId I'IICO,
Hypoventilation I LowFiO,

I

6. Oxn--1111 Dissacildian {e.g. high altitude)
Cum
I'IIO,ImpiVV8S 1'110, dDII not lmpl'll'le
V/0 mismllb:h Stull I Fi!Jlra 8)
Airway d l - {atlma. COPD) Atlilac11al&
lnllnlilill mg dii8111B lntraalvaalfilling
Alvvolar di- (e.g. pulmon.., edama, pneurnaria)
I'IM!onary YIISI:U diiiiiS8 lntracardiac shunt
Vucular 811.1nt wt1hln lunga

1. Appraaci!ID Hypaxamia

...
2
PaOz< j

0

L Pathaphysioloay af Shu.t
Toronto Notes 2011 Diseases of Airway Obstruction Respirolo8Y R7

Diseases of Airway Obstruction

Asthma
Definition
chronic, inflammatory disorder of the airways resulting in episodes of reversible bronchospasm
...... ,

causing airflow obstruction AirwBy m.trucllon (dec...-.! FEV1]
associated with reversible airflow limitation and airway hyper-responsiveness to endogenous or Asthma
exogenous stimuli COPO !chronic bronchitis, emphyse11111]
Bmnd1iac:tlsis
Epidemiology Cystic fibrosis
common {7-10% of adults), especially in children (10-15%)
most children with asthma improve significantly in adolescence
often family history of atopy (asthma. allergic rhinitis, eczema)
occupational asthma (organic allergies, isocyanates, animals, etc.)

Etiology and Pathophysiology

acute asthma: airway obstruction -+ Y /Q mismatch -+ hypoxemia -+ increased ventilation
-+ decreased PaCOz -+ increased pH and muscle fatigue -+ decreased ventilation, increased
PaCO:Jdecreased pH
IIIIFIIg
Triggers A good predictor of apotential
URTis, allergens (pet dander, house dusts, moulds), irritants (cigarette smoke. air pollution), lif&-1hl811bJning llttadr: is exc8S8ive
drugs {NSAIDs, beta-blockers), preservatives (sulphites, MSG), other (emotion/anxiety, cold air, consumption of short-IIC!ing
exercise, GERD) bebtz-agoni&bi.

Signs and Symptoms

dyspnea. wheezing, chest tightness, cough (especially nocturnal), sputum production ...... ',
..
symptoms can be paroxysmal or persistent Canbal cyanosis is not detectable until
1he Sa02 is < 85'llo.
Tabla 9. Important Signs and Symptoms in Acllta Asthma It ismor1 Hlily dltlctlld i1
polycytllemilllld len r111dily detecllble
Red F111111 llllpilllllry Dimlll in enarnil.
Fatigue NBSal tnlchual tug
Diminished ellpiratory effort lnabiity tD speak
Cyanosis Accessory muscle use, intercosbll indrawii"Cl
Silent chest Pulsus paradOlWS "-\.,
LDC
Asthma Tri-.1 (S.m.r"s Triad]
Adllptudlillm CM4J 11188; 161111 Suppi):S1-61 Ar1hmll
AS.NNSAID Uflllitivity
Tabla I 0. Risk Factors Indicating Poor Alth11111 Control Nasal polyps

Ominou1 ud
LDSS of cansciousll88s during astlma attack Night tirna symptoms > 1nighVwuuk
Frequent ER visits Silent chest
Prior intubation FEV1 or PEF {peak ellpiratory flaw) <611%
ICU admission Limited activiliss of daily living
Use af >Jiimllll/day
Adllptudlillm CM4J 11188; 161111 Suppi):S1-61

Tabla I I. Criteria for Datarmining whatllar Asthma is Wall Controllad

Daytime symptDms <4 dayflwk No astlma-flllatad absence from workfachool
Night-limesyn'1lloms <1 night/Wk Betaz-ilganistuse
Normal physical activity FEV, or PEF >90% of personal best
PEF diu mal variation <10.15% Mild, axacllltations
Adllptud frllm CM4J2005; 173111 S4

Investigations
Oz saturation
ABGs
decreased Pa02 during attack (V/Q mismatch)
decreased PaCOz in mild asthma due to hyperventilation
normal or increased PaC02 is an ominous sign as patient is no longer able to hyperventilate
(worsened airway obstruction or respiratory muscle fatigue)
PFTs (may not be possible during severe attack; do when stable)
spirometry: in asthmas will have increase in FEY1 > 12% with betaragonist, or >20% with
10-14 days of steroids, or >20% spontaneous variability
provocation testing: decrease in FEY1 >20% with methacholine challenge {to confirm
diagnosis when bronchodilator response not significant)
peakflow
R8 Respirology Diseaaes of Airway Obstruction Toronto Notes 2011

Treatment
environmental control: avoid triggers
patient education: features of the disease, goals oftreatment, self-monitoring
pharmacological therapy
symptomatic relief in acute episodes: short-acting beta2-agonist, anticholinergic
...llllizM.I'IIDIIII C.nnlllll Trill If bronchodilators, oral steroids, addition of a long acting
Etr.ctfl -Anflagllilt, long-term prevention of acute episodes: inhaled/oral corticosteroids, anti-allergic agent,
.-.... ... r.,.qiiBIIIII long-acting beta2 -agonist, methyhanthine, leukotriene receptor antagonists (LTRA)
Cllli:llllniR il Allllllllli:
BK/1999;319:17-90
SIQr-llcdQ blind, . .rniaJd, plll:ebg Guidelines for Asthma Management
cormlld. pnlll Qllllp. ndiclabll1udyMIII I
lallllw-up rl12 -a.
l'lllllnll: 226 cinicely llllbll pl1ilnls 11111111
41 !'. 58 feaU) Mill clnric llllliml
Rlqliria;lllllderQ" high
la!c:riol.
lhllrnnllan: l'ltilla Wlllllllldllrnillllllll IIIC8MI
lihlllllf1bUiast 10 1TQ PO qlls or placeo while

rlm*l corliCillllroids MSIIJ*Id, l11llilllinld,
111 ilmlsecllllllCUe)IMIIY 2-ks based 11111
lllndardizad cilical101111.
rnn.y Lowest1Diemld dose rl
ilhlled cOIIi:oA!oida.
11116:1'1tiems tdiJr.l maallluklst were lille
Short-acting on demand
Ill 1lp8f tlllir i._d corlicoilaroid do1111D
thosatakilg Environmental control and education
I47'J. vs. m., P=0.046). In eddition. b
1lkq II'IIIIIIIUklltwmlligriliCIIIIIy ls lblyiD Severity of asthma
4
reqlire clsc:ormrutili r1 tile llplrilg ]RfDcol due
1D fliur8 rl inCTIUid corlicoiiiiUid d011/rnc1111D
Vary mild
Symptom characteristics
)II(
Mikl
Modarall

s::f!Y
)14
Savara
)I

116llvs. :m, P=0.001,

tfoll=Bf. Subclinical Intermittent Persistent
c:.:IIUn: MWlJklst llows spCIIIIIv
gram llductioo in 11r1 dllllll r1 mlled Figura 9. Guidalinas for Asthma Managamant
corli:oaoidl RICILifld 1D lllliain clirical Sllhilty Adaip11dfnlmCM4.1 1999; 161111 5uRII):S161
il dvonic lllllrnllicl fllnw RlqLiq modal'lllll
1D hi;h dons.
Emergency Management of Asthma (see also E1neuencyMedidne, ER31)
l. inhaled betaragonist first line (MDI route and spacer device recommended)
2. add anticholinergic therapy
['\.., 3. ketamine and succinylcholine for rapid sequence intubation in life-threatening cases
Remember to step down therapy to 4. SC/IV adrenaline, IV salbutamol if unresponsive
lowest dosn which control symptoms 5. all patients admitted to ER for asthma exacerbations should be considered for corticosteroid
and signs of bronchoconrtriction.
therapy at discharge
...... ,
.. Chronic Obstructive Pulmonary Disease (COPD)
rMIIII'II PrDtP'el&ion llf CDPD
40s Chronic productiVI cough,
wheezinv occa&ionally
Definition
characterized by progressive development of irreversible airway obstruction
lOa 1st acum chlst ilness
2 subtypes (chronic bronchitis, emphysema): usually coexist to variable degrees in most patients
&as Dyspnea on axartion, incr.sing course: gradual decrease in FEY1 over time with episodes of acute exacerbations
amounbi af sputum production,
mora fraquant acuta
exacerbations Table 12. Clinical and Patll..ogic features of COPD
l.etll Hypoxamil cyanosis,
polycythemia [RBC.f,
hypercapnia (mominv hllldllchaf,
Dalinlll c:lilically as: Defiled pathaiDgicallr a:
hypoxemia. cor pulmollllle Prolllctive cough on most days for at least 3 Diation 111d destruction of air spaces distal to the tlmlilal bronchiole
conseartive months in 2successive yean without obvious fibrosis

.... ,

Obstruction is U! to niiTIIWilg ol1he airway lumen by
mucosal1hickening and excess mucus
Decreased elastic recoil of lung p!lrenchyma causes decreased
expiratory driving pressure, airway collapse, and air trapping
2typet;
Remember, first line 1herapy for CDPD is 1I Cantrildnll' (respiratOIY bronchioles predominantly affected)
&molting ce-lion Typical form seen in smolan, primarily affects upper lung mnes
2) Pa111cinu (respiratory brunchioles,aveolar lllcts. and
alvaolar sacs lifected)
Responsible for less than 1% of emphysema cases,
It' (alph&- deficiency), primarily affects IDWII' lobes
Chronic Ttutment for CDPD
CDPDEII
Corticostllroids [ilhlllllf
Oxyven
Prevention [vaccines, smokinq
cessationf
Dillltors (AChl's > blta2aqonists)
Experimenllll(surgery, roftumilut)
Rahllbiibltion
Toronto Notes 2011 Diseases of Airway Obstruction Respirolo8Y R9

Risk Factors 'lhl Aa:lrlr;ytf,._ Hilblry. - . ....

smoking is the most important risk factor (likelihood ratio of8.3) IIIIILII.,..III.__.... .. . , . . .
other risk factors include:

environmental factors: air pollution, occupational exposure .lAMA 2000; 238l14l:1853-67.

lllllly: Wlkenler case-MrD1 s1ultt.
treatable factors: alpha-1-antitrypsin deficiency, bronchial hyperactivity ,....._.:308 prient. will! knowncllunic
demographic factors: age, family history, male sex, history of childhood respiratory obs1R1:tive llli'nDfliiV tlseue ICII'OI;
infections, and low socioeconomic status crfll; and c:ormll.
'*-Iiiii: Yarious aspects of himy ltld
Signs and Symptoms lAd FfYJ
F1t <5111
MJ.yO.... S.niiMty, !piCiic:tymd
Tabla , 3. Clinical Prantation and Investigations for Chronic Bronchitis and Emphysema lillillood ratios (UIIID dil(lnosa CII'D.
Symptom Sign IIIV8IIigllian "--Il:
Branchitis Chronic procllctiw cough Cyanotic {2 to hypoxemia and hypei'CIIplia) PfT: (+IIR 1-1 II
(llue Bloater) Purulent sputum Peripheral edema from RVF {cor pulmonale) .V FEV1 .V FEV,JFVC SmoUd >40 pt.yaln , 1.6 (8.311 0.9 (0.811
Hemoptysis Crackles, wheezes N TLC, 1' or N IJro
Age >46 U (1.311 0.5 (OAI1
Mild dyspnea initially Prolonged expiration if obstructive CXR:
FIIKJI&ntly obese AP diamster nonnal Muirrunllr,<rv811 3J (2.81 1
OJ (0.811
1' bronchDVBSCUiar rmrtings heijlt <4cm
heart with cor pulmonale AI f:IIID!ed 0.3210.13*1"
Emp..,_.a Dyspnea{:!:: exertion) Pirtskin PfT: Stpnl& Ulsfur pllins put
(Pink Pulllrl Minimal cough Pursed-lip breathing .V FEV, .V FEV,JFVC hiRory ct COI'D
Techypnea Accessory muscle use 1' llC {hyperinflation) *Includes plsllis!DryctCOPD (+1117.3. -UI 0.51
Decreased exercise Cechectic app88111nce lle to anorexia and 1' RV {gas trapping)
tolerance increased work CJf breathing CXR:
Hyperinflation/barrel chest, hyperresonant 1' AP diameter ...... willl
percussion Flat hemidiaphragm (on lateral CXR)
Decreased breath sounds
Decreased diaphragmatic excursion
-v heart shadow
1' 1111nlsbrnal spiiC8
llbllllcM,._.., -1"11n.-:. ..
Iiiii Fan
Bullae .MI!ilfemMed2006; 144:39G-396
S1udy: Prolpectiw cohart lludy ct 211 plli8llll
-v vascular markings l'liGI CII'D {d current IIIII former 11111111111) who
want admillad ID IIIJIP!IIfor 11M1111IIliiC8Iblliall
Treatment of Stable COPD ct flli COPDor-.-,
prolong survival .._...._AI
CT.._.., (CTAjllld-.. ciX11pi'Ran
origiL
pllieal$ -Ned I

smoking cessation: nicotine replacement, bupropion (Zyban), varenicline (Champix) l&gi.

vaccination: influenza, Pneumovax"' llhlll: 2!111 of pllieols 111114iiQnollic crilaril for
home oxygen: to prevent cor pulmonale and decrease mortality if used >15 hrs/day PE {+ CTA +l.USI.
indications: Pa02 <55 mmHg; or <60 mmHg with cor pulmonale or polycythemia
holpibll!1j for COPD lllllllllllllio ct Lrlimvn
symptomatic relief (no mortality benefit) qinil25\.
bronchodilators: mainstay of current drug therapy, used in combination Thnlofl, Ill palilnb presenlilg 10 holililll will!
anticholinergics (e.g. ipratropium bromide, tiotropium bromide) CII'D 8liiQ8Ibrlion willloullll oiMM C...
- more effective than with fewer side effects
II wlich 1D use depends 111 pre-lest ct
- slower onset of action; take regularly rather than on pm basis lhlpelienl).
short acting beta2-agonists (e.g. salbutamol, terbutaline)
- rapid onset of action
- significant side effects at high doses (e.g. hypokalemia) MINMiilll'ldll ,._.. Vllllllian

-
long acting betaz-agonists (e.g. salmeterol, formoterol) larlilltmllllal . . . . . . hllll ..
theophylline - increases collateral ventilation, mucociliary clearance, and may reduce rta.lllic Dllltruclin
airway inflammation; used as 4th line
CocnelllflllllseS)stllev ZOOt; 3:Crol4104.
- side effects: nervous tremor, nausea/vomiting/diarrhea, tachycardia, arrhythmias, S1udy: Cacli11111 Sysllmltic 111\'iiW. 14RCTs.
sleep changes, headache, gastric acid, toxicity 758 adul pllieai$1Wil ctuonie
corticosteroids pulninlydiallllctfDIIIId acliS raspilltD!y
chronic use of systemic glucocorticoids should be avoided llillr8 due bJ 1 COPD8XIelllladion.
Uullllllicll Clll{lJMCIIIId
COPD airways are usually inflamed, but not generally responsive to steroids Nan-inivl pcllilivl wnllllion {NPPV)-
inhaled steroids shown to improve FEV1, reduce exacerbations, and possibly improve UMCiione.
mortality (TORCH study, NEJM 2007) ,_uy 0...... TnlllmentfliUt, martaily,Md
lnlchell irUIIion.
surgical treatment
llhlll: n. rilb ford pinmy IUDon'llwant
lung reduction surgery: resection of emphysematous parts oflung to improve ventilatory TICb:edMh M'I"V'UIII:Ialmmtfallrt{RR
function, associated with higher mortality in certain risk groups (FEV1 <20%) 0.481; rnorlaity (AA 0.521; IIIII ilblbllion usa(RII
lung transplant D.611.LqlllofhospilllslayMSIIiiiJjicanl
others _, l24 dlylsllarllt hit no diffltiiiCI
ICU lengll ct slay. There ila111'111111d ligJificant
patient education, eliminate respiratory irritants/allergens (occupational/environmental), improva1na in pll {waijd 111111n clfln1ce
exercise rehabilitation to improve physical endurance (WMDJO.D4I,I'ICOz (Wt;'ll 0.40 kf'l).111d
re.pillblrylll8 (WMD=-3.08 bpnj IWhil one
hell' poii-NimentMh M'l'v. CaQiicltiJns
asac:illld l'lilll!umnantWIIII nWced inlhl
NI'I'V lnlalmnurm (RII D.38l.
c...- fo'pllilnls in "''i*Y flikn
UID 1 COPD NPPV illllldiw
in lrelllmenl fliUt, llllllllj;y.llld need
for inblbaliaft wbln Ulld IS I filii line lrl8lnWit
lldjmct ID usull medalc:are.
RIO Rnpirology Diseaaes of Airway Obstruction Toronto Notes 2011

.....
ar.cti"S.IIIilll.._.n-.ltlw U..rl
1111 II Dillie II FEY,

.lAMA 1994; 272:14971505

......

1
llnhalad conieoslllnoids
rs;-
o,
S1udy: lllndolrizld. I*CibO I Rahabilillllion
t:anlralled, nUticenlnl trill wti1 rJ 5
I Long-ac:ting bronchadilalol$
yem.
l'ilil* 73,684 athe!wise bella!y Sllllim I Shan-acting bronchodilator$
hltwl111 the IIQIS al3511111 &0 "jllf1 Will I Ecklcatiorv'SeW-management
wti1 SJi!anwlry for l\lidlllcl al mild il
mod81118 14Winllllll FlV1:PiC
IIIII FIV1

themnllllldlttu,. at IQI risk fat ar iiMIIIII COPD
Ill il the am, S11Q11 ofCll'1l. Application rl Stage Mild
a:lJiioll rilril yialdad 1 inal Wly populltion
al lllllkllll Y1itb twidiiiiCa of llild tu
lllllllemllilwly abslnl:tion lme1111!114B ""
63\lllllel. I
diagnosis
[spuomelly)
+prevention
I RxAECOPD
Folow-up
II
...._..: Pllilnls wn111111amiad ID IICM
11111 rJ uul cni\ICI.ImDkiiiQ iniiiMinlion ltld
Figura 10. Guidalinas for COPD Managamant
inhaled 511111- Adlp\lldfnlmCanllllan ThcncieSocietyllec:ommendlticmsfar Mlnagement rJ C(I'[).I2003).Cin 2003; tSuppl A):I7A
Dlcn il FPI,-as
Ylll period. Acute Exacerbations of COPD
._11: Pllilnls illlla smoti1Q irGMn1ion
PlPi had deciDes in FlV1
definition
cere. FIV, resullnwre episode of increased dyspnea, coughing, increase in sputum volume or purulence
malt striking It 1 Ylitb ll111111 del:nue etiology: viral URTI, bacteria, air pollution, CHF, PE, Ml must be considered
r/34.3 ml il the UC llldmeen
of 11.2 111d 38.8 mL in the SIP IIIII SIA gRqlf,
management
IP<0.005j. Between 1yeulllll5 assess ABCs, consider assisted ventilation if decreasing LOC or poor ABGs
ye111, FlV1 decnd at simillr IIIII il d 1lne supplemental 0 2 (controlled FiO:J: target 88-92% Sa02 for C02 retainers
""'152.3-5&.2 ml/111. Howw., bronchodilators by nebulizer
111. . in the SIP group
sludy's5 short acting beta2 -agonists used concurrently with anticholinergics
11 fobrMqJ ex,erienced I C111T1llltiw decline il salbutamol and ipratropium bromide via nebulizers x 3 back-to-hack
FIV, rlonly72 ml i1111e sne systemic corticosteroids: IV solumedrol or oral prednisone
Ylitb ll:UIIIIIIIIive declne rJ 301 ml il tl1ase who
t:CIIIIiud 1D smab.lhl 111111 banllfit 11110Ci111d antibiotics: often used to treat precipitating infection
Ylitb Alruv8nt- -ible disconlilution, indications (2 out of 3): increased SOB, increased sputum, or increased sputum
111d 1herefult did not m,.ct111e lmtl-111m declne purulence (change in colour)
inFlV1
c:.llllan: S!liumnv is llllllllcliw tcrllllling post exacerbation: rehab with general conditioning to improve exercise tolerance
llll1llod for the dllaction ofrlv COPD. S1nii1cDJ ICU admission
inlrllvlnion pqpns ClllsigniiCIIdlt ltduce 1111 for life threatening exacerbations
il FIV1 in 1lis ,..u.tiaiL AlnMmt did not
impiCI111e bng.l!Jm declne illt'l1. ventilatory support
non-invasive: NIPPY, BiPAP
.... ,,
conventional mechanical ventilation

Prognosis in COPD
Remember to step down thenpy to complications
lowust dos whidl control $YRIPlDmllll'
signs of bronchoconstriction. secondary polycythemia due to hypoxemia
pulmonary hypertension due to reactive vasoconstriction 2 to hypoxemia
cor pulmonale from chronic pulmonary IITN
pneumothorax due to rupture of emphysematous bullae
CompllcdDns of COPD
prognostic factors
Chronic hypoxemia severity of airflow limitation (FEV1) is the single best predictor
PulmoniiiY hypartansion from development of complicating factors such as hypoxemia or cor pulmonale
vasoconstriction 5-year survival
Car pulmonat.
FEV1 <1 L =50%
FEY1 <0.75 L = 33%
BODE index for risk of death in COPD
Vlccblio1inCOPD
are. 2004; 125161:201120 greater score indicates higher probability that the patient will die from COPD; score can also
S1udy: Clnlll, randomilld, dldiiH!Iindlcl be used to predict hospitalization
trill. 10 point index consisting of four factors:
P11i1n11: 125 pUnll wti1 COPD, s1rltifild by
FIVI iniD mld.llllldllll811111 SMIII C[I'D.
body mass index (BMI): <21 ( +1 point)
obstruction (FEV1): 50-64% (+1), 36-49% (+2), <35% (+3)
lbil IMrily dyspnea (MMRC scale): walks slower than people of same age on level surface, stops
aiiMI mpilllury ihli, inbl1ll-f8lltld IIIII occasionally (+1), stops at 100 yards ora few minutes on the level (+2), too breathless to

-=
ID1II.
lnbn!l vaccilated
6.8 RIU111111-11111ad lllqlerienced
J)l1ieatJ illllll111
11CUb1 raspitllDiy p11

leave house or breathless when dressing/undressing (+3)
exercise capacity (6minute walk distance): 250-349 m (+1}, 150-249 m (+2), <149m (+3)

llpllillad 28., inbl1ll-ftllltBd IICUbl f8lliii1Dry

itlesses per 100 !Dent..,.rs IRR 0.24. p-0.005).
lli518duction i*j for lilldlgnJup!S of FlVI IMI.
Bronchiectasis
Nalftlct-SIIIIIon11111DIIInunt.riiiCidl
TllpirDy ima-.
Definition
c.ncluian: WI,_ wc:cinllion is allactivl il an irreversible dilatation of airways due to inflammatory destruction of airway walls resulting
ll!ducing 1lle IUIIber of ill'bnt-IIAaiBd illlesaes from persistently infected mucus
in C(l'[) pllilntl.lllt IIIII in Dllm ID.D 111pilllly usually affects medium sized airways
itless.
.P. aeruginosa is the most common pathogen
Toronto Notes 2011 Diseases of Airway Obstruction Respirolo8Y R11

T1ble 14. Etiology 1nd Pathophysiology of Bronchiechlsis Oni ......... COPDEDc. . . .

Obllruction Post-infection Impaired dele1181 {leads to int81farence of NUI#21103; 3U:2lill-25
lludy: lllndonizld, cb.lllll-blnd, pllcebo-
{181Uit& in dillllldion of bronchial walls) lhinage. clllJnic inflictions, and inflamrnlllion)
TllllOU!$ Pneumonia 147 Pltilllls lme... 6h 97% aU,
Foreign bodies TB CF m I\IDIMh COPD. llllhiBI
Thick ITIICUS Measles Def!!ctive leukocyte function z
Nth at least af the fllllwilv: Meent illCRIIIe
l{lUiunwUnl, aripUiiln
Pertussis Ciiary dysfunction (Kartagener's syndrome:
]Ulllence. ..cUsion em. also incbled alllllkiiJ
Allel'llic bronthopulmonary aspergillosis brunchiactasis, ii'IVIII'Ius)
lillur'{ af m1 irmlniblrllidlow
MAC (mycobacteria avium allltructiaa in lhl81 (FEVI,wt gJJOI. Excklliaal
indudld plllilnll Mh llllhm ar llrlpy, 181*11
Signs and Symptoms Gill IY lllfUid IIIII, ChlltlHIY consisllriwith
chronic cough, purulent sputum (but 10-20% have a dry cough), hemoptysis (can be massive), pneumonil cr Cit F.ml those reqliring admissiJn
1D hii!J1i1ll.
recurrent pneumonia. local crackles {inspiratory and expiratory), wheezes ...__:AI patients receMid IDdays of
clubbing l*l ill-.ledllllul8tol
often difficult to differentiate from chronic bronchitis a rar
iplmpiln biOmide 3D days. f'alieal1i-
11lllbnizsd 1D IDMI < mg pnldnilana x IDdlyl.
Investigations crplaba.
lllil 0utr:an-= llall(ile defined
PFTs: often demonstrate obstructive pattern but may be normal 11isit10 1 ar1Uin1D 81 far-DJ
CXR SOB Ytilll days.
nonspecific: increased markings, linear atelectasis, loss of volume in affected areas 1111111: Dill pnldni10111 sigJificlnlly fldiJCid lhl
specific: "tram tracking" - parallel narrow lines radiating from hilum, cystic spaces, Ill! afrellp1nt lJ dlys (2'l'J.vs. 43%,
honeycomb like structures l'r8dllilolll pmlllnged t11a tina tD rr41p11 D.04I.
high-resolution thoracic cr (diagnostic, gold standard): 1-.dlflpelje, weigltgain, 111d ilsormi WR
11111111 JliiiVIIInt il tha p!lldniiDna Q111141.
87-97% sensitivity, 93-100% specificity Canlbin: 1n C!l'llJlltiaratlll:lwgldfmm tilt
"signet ring": dilated bronchi with thickened walls where diameter bronchus > diameter of 81 Mh COPD 8XIC8rllltion, 110-dly of Dl'll
accompanying artery pl8lllilons orr. atmlll adllariage-JIIaclbo il
sputum cultures (routine + AFB)
serum Ig levels
sweat chloride if systic fibrosis suspected (upper zone predominant)

Treatment
vaccination: influenza and Pneumovax"'
antibiotics (oral, IV; inhaled) - routinely used for mild exacerbations, driven by sputum
sensitivity; rn.acrolides may be used chronically for an anti-inflammatory effect
inhaled corticosteroids - decrease inflammation and improve FEY1
oral corticosteroids for acute, major exacerbations
chest physiotherapy, breathing exercises, physical exercise
pulmonary resection: in severe cases where medical therapy fails

Cystic Fibrosis (CF) -----------------------------------------

see also Pediatrics, P94

Pathophysiology
chloride transport dysfunction: thick secretions from exocrine glands (lung, pancreas, skin,
reproductive organs) and blockage of secretory ducts

Clinical Features
results in severe lung disease, pancreatic insufficiency, diabetes and azospermia
other manifestations include meconium ileus in infancy, distal ileal obstruction in adults,
sinusitis, liver disease
usually presents in childhood with recurrent lung infections that become persistent and chronic
chronic lung infections
S. aureus: early
P. aeruginosa: most common
B. cepacia: worse prognosis but less common
Aspergillusfumigatus
Investigations
sweat chloride test
increased concentrations of sodium chloride and potassium (chloride >60 mmol/L is
diagnostic in children)
heterozygotes have normal sweat tests (and no symptoms)
PFTs
characteristic of obstructive airway disease
early: only small airways will be affected
late: characteristics of obstructive disease with airflow limitation, hyperinflation, gas
trapping, decreased DL00 (very late)
ABGs
hypoxemia, hypercapnia later in disease with eventual respiratory failure and cor pulmonale
CXR
hyperinflation, increased pulmonary markings (especially involving upper lobes)
Rl2 Rnpirology Diseases of Airway Obstruction/Interstitial LUJ18 Disease (ILD) Toronto Notes 2011

Treatment
chest physiotherapy and postural drainage
bronchodil.ators (salbutamol ipratropiurn bromide)
inhaled mucolytic (reduces mucus viscosity)
inhaled tobramycin
antibiotics (e.g. ciprofloxacin)
lung transplant

Prognosis
depends on: infections, FEV1, acute pulmonary exacerbations, lung transplant vs. non-lung
transplant

Interstitial Lung Disease (ILD)

Pathophysiology
inflammatory process in the alveolar walls thickening and possible destruction of pulmonary
vessels, and fibrosis of interstitium leading to:
decreased lung compliance {increased or normal FEV1/FVC)
decreased lung volumes (decreased TLC, decreased VC, decreased RV)
impaired diffusion (decreased DcJ
hypoxemia usually without hypercapnia due to V/Q mismatch
pulmonary HTN and cor pulmonale occur with advanced disease secondary to hypoxemia
and blood vessel destruction

Tabla 15. Causes of Interstitial Lung Disana Classified by Distribution

Uppar Lung Disaae l.awlr Lung DisaBH
Fanner'sl111g Bnn:hiolitis oblitenrls with pneumonia (BOOP)
It'
In lnllrslitial L.unv DiiHIII Think Ankylosing spondylitis Asbestosis
FASSTUI and BAD RASH Sarcoidosis Drugs (nilrofunr'IIDin, hythlazina, INH, amiodll'!lne, many chemo drugs)
(sea Table 15) Silicosis Rheumatologic diseese
1B Aspiration
Eosinophiic granuloma (histiocytosis) Sclerodenna
Neurofibromlllosis Hamman Rich pulmonay fibrosis)

Etiology
>100 known disorders can cause interstitial lung disease
majority due to unknown agents or cause
divided into 2 major categories: unknown etiology and known etiology

Tabla 16. Interstitial Lung Diaaas81

UNKNOWN EllOLOGY
ldioplllhic pumonaryfibrosis Other idiopalhic intarstitial pneumonias includilg:
Sarcoidosis NSIP (nonspecific pneumonial
Llrlgelhans-cell histiocytosis (histiocytosis XI LIP (lymphocytic interstitial pneumonia)
Lymphangioleiomyomatosis COP (cryptogenic organizing pneumonia AKA BOOP)
Pulmonary infiltrlllll6 eosinophilia (PIE syndromll6)
KNOWN EllOLOGY
ILD Altocimd Willi ILD Astocilted Willi Drup or Inherited Dilonlers
Sysle11ic RUIIItic Dilanln TrMimlllll Familial idiopathic pulmonfiY fibrosis
Scleroderma An1ibiotics {nilrofunntoinl Neurofibromatosis
Rheumatoid artlvilis An1i-inftarnnatory agents (methotrexatel Tuberous sclerosis
SLE Cardiova&c:ular drugs (amiodarona) Gaucher's di&ea&e
An1ineoplastic agents agents) A'"-'- F"l" o n1
Mixed connective tiss.te disease Ill"cit d1J ,....,,.r I IIIII . . n
1 gs Chronic eosinophilic pneumonia
Environment/Dc:alpati111 Altocilted ILD on Goodpasture's syndrome
Organic d.Jsls pneumonitis! ILD Astocillllld Wlllll'lllmonary Diffuse alveolar hemonhage
Fanner's lung YaiCIIItis Pulmonll'{ alveolar proteinosis
Air lung Wegener's granulomatosis
Bini brusder's lung Churg-Strauss syndrome
Inorganic d.Jsbl (pneiiTIOconiosis) Hype11anmivity
Silicosis Necrotizing sarcoid gnmulomatosis
Asbestosis lciopathic pulmonary hemosiderosis
Coal wortars' pneumoconiosis
Berylliosis
Gaseslfumes/Yipours
Toronto Notes 2011 Interstitial LUDg Disease (ILD) Respirolo8Y R13

Signs and Symptoms

SOB, especially on exertion
dry crackles
nonproductive cough
cyanosis
clubbing (especially in IPF and asbestosis)
features of cor pulmonale
note that signs and symptoms vary with underlying disease process
e.g. sarcoidosis is seldomly associated with crackles and clubbing
Investigations
CXR!high resolution CT
.... ',

decreased lung volumes, reticular, nodular, or reticulonodular pattern (nodular <3 mm), The CXR can be normal in up to 15% of
paliants wilh intarslitiallung dil81sa.
Kerley B lines, hilar/mediastinal adenopathy
diffuse ground-glass appearance early in disease progresses to honey-combing late in disease
DD.x: pulmonary fibrosis, interstitial pulmonary edema (CHF), PCP, TB (miliary),
sarcoidosis, pneumoconiosis, lymphangitic carcinomatosis \9,
DDx of cystic lesions: end-stage emphysema, pulmonary Langerhans-cell histiocytosis, Chlract.rim cr Rndi1111 in ILD
lymphangioleiomyomatosis "ground glass"- 81rly ILD
PFTs "hon-v combing" -IIIIIIILD, espiCiaUy
restrictive pattern: decreased lung volumes (VC and TLC) and compliance IPF
normal or increased FEV1/FVC (> 70-80%), Le. flow rates are often normal or high when
corrected for absolute lung volume
Dco decreased due to V/Q mismatch less surface area for gas exchange pulmonary
vascular disease
ABGs
initially may be normal
with progression of disease, hypoxemia and decreased PaC02 may be present
Other
bronchoscopy, bronchoalveolar lavage, lung biopsy
c-ANCA (Wegener's), anti-GBM (Goodpasture's), ESR, ANA (lupus), RF (RA), serum-
precipitating antibodies to inhaled organic antigens (hypersensitivity pneumonitis)

Unknown Etiologic Agents

Idiopathic Pulmonary Fibrosis (IPF)

Definition
a diagnosis of exclusion
also known as cryptogenic fi.brosing alveolitis or usual interstitial pneumonitis (UIP) \"'
DD:x: IPF Prwalence
Age 35-44: 2-7 per 100 000
nonspecific interstitial pneumonitis (NSIP) Age > 75: 175 per 1DO 000
desquamative interstitial pneumonitis (DIP)
lymphocytic interstitial pneumonitis (UP) - usually 2 to immune conditions such as mv,
Sjogren's, common variable immunodeficiency

Signs and Symptoms

commonly presents over age 50, incidence rises with age; males > females
dyspnea on exertion, nonproductive cough, constitutional symptoms, late inspiratory fine
crackles at lung bases, clubbing
Investigations
labs (nonspecific): ESR, ANA, RF
CXR: reticular or reticulonodular patter in lower lung, no hilar adenopathy, cystic or
honeycombing (late, poor prognosis)
high resolution CT: reticular markings, honeycombing (late), ground glass typically not
prominent in true IPF
biopsy: exclude granulomas, helpful if CT not classic
Treatment
02> steroids immunosuppressants
lung transplantation if refractory to medical therapy
mean survival of 3 to 5 years after diagnosis
R14 Rnpirology Interstitial L11l18 Diseue (ILD) Toronto Notes 2011

Sarcoidosis
Definition
idiopathic non-infectious granulomatous multi-system disease with lung involvement in 90%
characterized pathologically by non-caseating granulomas
proposed triggers include infectious, allergic. and environmental exposures (neither genetic nor
specific triggers have been established)

Epidemiology
typically affects young and middle-aged patients
higher incidence and more severe disease among black North Americans

Signs and Symptoms

can be asymptomatic or present with cough, dyspnea, fever, arthralgia, malaise, erythema
nodosum, chest pain
chest exam usually normal
common extrapulmonary manifestations
cardiac (arrhythmias, sudden death)
eye involvement (anterior uveitis)
skin involvement (skin papules, erythema nodosum, lupus pernio)
peripheral lymphadenopathy
arthralgia
hepatomegaly
less common extra-pulmonary manifestations involve bone, CNS and kidney
two acute sarcoid syndromes
Lofgren's syndrome: fever, erythema nodosum, bilateral hilar lymphadenopathy, arthralgias
Heerfordt-Waldenstrom syndrome: fever, parotid enlargement, anterior uveitis, facial nerve
palsy
Investigations
..... , CBC (cytopenias from marrow involvement)
serum lytes, creatinine, hypercalcemia, hypercalciuria due to vitamin D retention by granulomas

hypergammaglobulinemia. RF positive
Most common pmantation: elevated serum ACE (non-specific)
asymptomllic CXR finding
CXR: predominantly nodular opacities especially in upper lung zones hilar adenopathy
ABG: normal, or hypoxemia and hypocapnia
PFTs: normal, obstructive pattern, restrictive pattern with normal flow rates and decreased D00
ECG: to rule out arrhythmias
slit-lamp eye exam: to rule out uveitis

Diagnosis
biopsy
transbronchiallung biopsy or mediastinoscopic lymph node biopsy for granulomas
in -75% of cases, transbronchial biopsy shows granulomas in the parenchyma even ifthe
CXR is normal

Staging
radiographic. based on CXR
Stage 0: normal radiograph
Stage 1: bilateral hilar lymphadenopathy right paratracheallymphadenopathy
Stage II: bilateral hilar lymphadenopathy and diffuse interstitial disease
Stage III: interstitial disease only (reticulonodular pattern or nodular pattern)
Stage N: pulmonary fibrosis (honeycombing)

Treatment
85% of stage I resolve spontaneously
50% of stage II resolve spontaneously
steroids for symptoms, declining lung function, hypercalcemia. or involvement of eye, CNS,
kidney, or heart (not for abnormal CXR alone)
methotrexate or other irnmunosuppressives occasionally used

Prognosis
approximately 10% mortality secondary to progressive fibrosis oflung parenchyma
Toronto Notes 2011 Interstitial LUDg Disease (ILD) Respirolo8Y R15

Known Etiologic Agents

--------------------------------

Hypersensitivity Pneumonitis
also known as extrinsic allergic alveolitis
caused by intense/repeated inhalation and sensitization to certain organic agents
non-IgE mediated inflammation oflung parenchyma (acute, subacute, and chronic forms)
lymphocytic inflammation and granulomas present, airway centred
exposure usually related to occupation or hobby
Farmer's Lung (Thermophilic actinomycetes)
Bird Breeder's/Bird Fancier's Lung (Chlamydia psittaci in bird droppings)
Humidifier Lung (Aureobasidium pullulans)
Sauna Taker's Lung (Aureobasidium spp.)

Signs and Symptoms

acute presentation: ( 4-6 hours after exposure)
dyspnea, cough, fever, chills, malaise (lasting 18-24 hrs)
PFTs: modestly and transiently restrictive
CXR: diffuse infiltrates
type III (immune complex) reaction
subacute presentation: more insidious onset than acute presentation
chronic presentation
insidious onset
dyspnea, cough, malaise, anorexia, weight loss
PFTs: progressivdy restrictive
CXR: predominantly upper lobe, nodular/reticulonodular pattern
type IV (cdl mediated, ddayed hypersensitivity) reaction (see Rheumatology. R16)
in both acute and chronic reactions, serum precipitins may be detectable (neither sensitive nor
specific)

Treatment
goal is to prevent chronic fibrotic changes
early diagnosis: avoidance of further exposure is critical as chronic changes are irreversible
systemic corticosteroids can relieve symptoms in acute phase
steroids for persistent disease

Pneumoconioses
reaction to inhaled inorganic dusts 0.5-5 flM in size
no effective treatment, therefore key is exposure prevention through the use of protective equipment

Asbestosis
population at risk: insulation, shipyard, construction, brake linings, pipe fitters, plumbers
slowly progressive diffuse interstitial fibrosis from dose-related inhalation of asbestos
etiology: usually >10-20 yrs of exposure; may develop with shorter but heavier exposure;
','

typically prolonged interval (20-30 yrs) between exposure and clinical manifestations of disease Diaphragmatic plaques are highly
suggestive of asbestosis.
signs and symptoms
insidious onset
SOB on exertion usually first symptom with increased dyspnea as disease progresses
cough: paroxysmal, non-productive
fine end-respiratory crackles (increased at bases)
clubbing (much more likely in asbestosis than silicosis or coal workers' pneumoconioses), CXI Fillrutic l'iltl8m1
edema, jugular venous distention Albesto&is: IOWIII' > upper loba1
investigations: CXR Silicosis: upper > lower lobes
Coal: upper > lower lobes
lower > upper lobe
early: fibrosis with linear streaking
later: cysts and honeycombing
asbestos exposure can also cause pleural and diaphragmatic plaques ( calcification), pleural

effusion, round atelectasis Ramllmbar ID involvll occupatiollll

microscopic examination reveals ferruginous bodies: yellow-brown rod-shaped structures hHith at piiCI of work for da!ll
which represent asbestos fibres coated in macrophages collaction and traatmant plan.
Also cooosal re: worbr's insurance as
complications: asbestos exposure increases risk of bronchogenic CA and malignant per jurisdiction (e.g. WSIB in Ontario).
mesothelioma
risk oflung cancer dramatically increased for smokers
treatment:
removal from exposure
smoking cessation. proper nutrition, exercise
home oxygen PRN
treatment of respiratory infections, annual influenza and pneumococcal vaccinations
Rl6 Rnpirology Interstitial L11111 Disease (ILD)/Pulmonary Vucular Diseue Toronto Notes 2011

Silicosis
at risk population: sandblasters, rock miners, stone cutters, quarry and highway workers
etiology: generally requires >20 years exposure; may develop with much shorter but heavier
exposure
signs and symptoms: dyspnea, cough and wheezing
investigations: CXR
upper > lower lobe
early: nodular disease (simple pneumoconiosis),lung function usually normal
late: nodules coalesce into masses (progressive massive fibrosis)
when nodules become larger and coalesce into masses, disease has changed from simple
silicosis to complicated silicosis (progressive massive fibrosis)
possible hilar lymph node enlargement (frequently calcified), especially "egg shell calcification
complications: mycobacterial infection (e.g. TB)
treatment: prevention, removal from exposure, treat associated TB if present, supportive
measures (oxygen, bronchodilators),lung transplant
Coal Worker's Pneumoconiosis (CWP)
at risk population: coal workers, graphite workers
etiology: coal and silica, coal is less fibrogenic than silica
pathologic hallmark is coal macule:
coal dust surrounded by minimal tissue reaction and focal emphysema
found around respiratory bronchioles
simpleCWP
no signs or symptoms
CXR: multiple nodular opacities, mostly upper lobe
respiratory function well preserved
complicated CWP (also known as progressive massive fibrosis)
dyspnea
CXR: opacities larger and coalesce
course: few patients progress to complicated CWP
Caplan's syndrome: rheumatoid arthritis and CWP present as larger nodules
treatment: minimize future exposure, cardiopulmonary rehabilitation, follow periodically

ILD Associated with Drugs or Treatments

Drug-Induced
antineoplastic agents: bleomycin. mitomycin, busulfan, cyclophosphamide, methotrexate.
chlorambucil, BCNU (carmustine)
antibiotics: nitrofurantoin, penicillin, sulfonamide
cardiovascular drugs: arniodarone. tocainide
anti-inflammatory agents
gold salts
illicit drugs (heroin, methadone)
Radiation-Induced
early pneumonitis: approximately6 weeks post-exposure
late fibrosis: 6-12 months post-exposure
infiltration conforms to the shape and field of the irradiation

Pulmonary Vascular Disease

Pulmonary Hypertension
-------------------------------
Definition
mean pulmonary arterial pressure >25 mmHg at rest and >30 mmHg with exercise, or a systolic
pulmonary artery pressure of >40 mmHg at rest
in the past, pulmonary hypertension was classified as primary or secondary pulmonary
hypertension, but this classification was modified to a more clinically useful, treatment based
classification (Table 17)
Toronto Notes 2011 Pulmonary Vascular Disease Respirolo8Y R17

Table 17. Diagnostic Classification of Pulmonary Hypertension (WHO 1998)

Classification
Pulmonary arterial hypertension PriiiiiiY pulmonary spcndic vs. familial related to:
Collagen vascular disease (sderoderrna. SLE. RA)
Conganitlll sysbmic-toI'Jimonary siJJnts (Eisarmangar syndrome)
Portopulmonary
HIV infection
Drugs and toxins (e.g. anorexigens)
Pulmonary venous hypertension Left-sided atrial or venbicular heart disease (e.g LV dysfunction)
Lett-sided valvular heart disease (e.g. aortic stenosis, mitral stenosis)
Pulmonary Vllll!rocclusive diS811Se
Eminsic al cenlnll pulmonary veins (tumour, adenopathy,
fibrosing
Associated with disorders of the respiratury Parenchymal lung disease (COPD, interstitial fibrosis, cystic fibrosis)
system and/or hypoxemia Chronic alveolar hypoxia (c!Yonic high alveolar hypovenliation
disorders, sleep disordered bnlathing)
Due to chroric thl'lllrilotic ancVor embolic disease lh'omboembolic obstruction al proximal pulmonary aterias
al distal pulmti1Bry artarial - PE (throrrtus, foreign material,
tumour. schistosomiasis, in thrombosis, sickle cell disease)
Due to disordars directly afflicting tha lnllamrnatory (sarcoidosis, schistosomiasis)
pulmonary vasculature Pulmonary capillary heman!Jomatosis

Mechanisms of Pulmonary Hypertension

hlrVIIIIIIIIr ...... il
the approach is simplified as some causes could fall under more than one mechanism I'UrawyAllllill Hll
hypoxic vasoconstriction
1. &idenc:e far the UE of CCBIIIfbr I poliM
chronic hypoxia causes pulmonary vasoconstriction by a variety of actions on the VlllldiiiDr dlllange il ini1ad 1D pltilntl Mil
pulmonary artery endothelium and smooth muscle cells, such as: down regulation of I'AH.
endothelial nitric oxide synthase and alteration of voltage gated potassium channels leading 2. The p111ciN deinition lboutwta
to vasoconstriction I "pasitiw" fiiUk is Cllllllavll1ill. ThliltRI
causes: COPD, chronic alveolar hypoxia CIJI'IliiiiUS accordilg 111 the &lupeln Society al
decreased area of pulmonary vascular bed Canliology WIS tlllll1 poWw fiiUk C4ftltilutal
I Ill ofrne11n PAP pre- al10 mig ID
leads to a rise in resting pulmonary arterial pressure
causes: collagen vascular disease, HIV infection, drugs and toxins, thrombotic or embolic
'-llwl or 8!Pii1D 40 wmtOUT achlnge in
Clldilc output.
disease, inflammatory, pulmonary capillary hemangiomatosis, interstitial fibrosis, cystic
3. Belt IQIIIdllll use: NO or apopmslalal
fibrosis llll'lfltY!:In) Ulliop !best llllly JIR)filsl.
volume and pressure overload
4. Those who 1 "signific:llll" JeSI)OIIse las
significant hypertension only occurs with excessive volume overload, since pulmonary artery dallnnr.l by lhl CIDril in #ZIIIIauld ba
pressure will not rise in otherwise normal lung until pulmonary blood flow exceeds 2.5 times fllllld I:UiaultfMh I CCBiriflill*il.
the basal rate dilillllll, lmllldifilla 1111 good chaic8l, NOT
causes: congenital systemic to pulmonary shunts (e.g. VSD, ASD, PDA), portopulmonary .ap&miQ. E\lidlacallpsts 111111 patilnts
wil hiM! irnp!Md ..-..
hypertension, left-sided heart conditions, pulmonary veno-occlusive disease, extrinsic
compression of central pulmonary veins l!ldls:h 1111. MU::al T1Mpy Far
l\lmanlf\' Arterial Hypstnion. ACCP E\'ilenc:e-
BIIId Clinicell'rlctic:e GuidalnaL
Cllest126, .1Jti,2004.
IDIOPATHIC PULMONARY ARTERIAL HYPERTENSION [AKA PRIMARY
PULMONARY HYPERTENSION (PPH}]
Definition
pulmonary hypertension in the absence of a demonstrable cause (exclude left-sided cardiac
valvular disease, myocardial disease, congenital heart disease, and any clinically significant
parenchymal lung disease, systemic connective-tissue, or chronic thromboembolic disease)

Epidemiology
disease of young women (20-40 years); mean age of diagnosis is 36 years
most cases are sporadic; familial predisposition in 10% of cases, linked to mutations in BMPR2
may be associated with the use of anorexic drugs (e.g. Aminorex, Fenfluramine), also
amphetamines and cocaine

Signs and Symptoms

exertional dyspnea. fatigue, syncope, exertional chest pain, Raynaud's phenomenon
see Table 18
Prognosis
2-3 year mean survival from time of diagnosis
survival decreases to approximately 1 year if severe pulmonary HTN or right-heart failure
R18 Rnpirology Pulmonary VaKular Disease Toronto Notes 2011

Teble 18. Signs and Symptoms of Pulmonery Hypertension

Symptoms SiFS
Dyspnea Loud, palpable PZ
Fatigue RV hiiiMI
Substernal chest pain Right-sided S4 (due to RVHI
Syncope Systolic 11111111ur (TR)
Symptoms of underlying disease HRV failure: right sided S3, increased JVP, positive HJR, peripheral edema, TR

Investigations
CXR: enlarged central pulmonary arteries, cardiac changes due to RV enlargement (filling of
retrosternal air space)
ECG
RVH/right-sided strain and RA enlargement, rightward axis deviation
RIS ratio >1 in V1
increased P wave amplitude in lead II
incomplete or complete R bundle branch block (RVSP)
2-D echo doppler assessment of right ventricular systolic pressure
cardiac catheterization: direct measurement of pulmonary artery pressures
PFTs to rule out lung disease - DL.x, usually reduced
spiral CT to assess lung parenchyma and possible PE
V/Q scan pulmonary angiogram to rule out thromboembolic disease
serology: ANA positive in 30% of patients with primary pulmonary hypertension
Treatment
for primary pulmonary hypertension
anticoagulation in patients at increased risk for intrapulmonary thrombosis and
thromboembolism (anticoagulation of choice is warfarin, target INR approximately 2.0)
calcium channel blockers: nifedipine, diltiazem, NOT verapamil
vasodilators: oral (sildenafil, bosentan), parenteral (epoprostenol, treprostanil)
lung transplantation
for other forms of pulmonary hypertension
continuous oxygen therapy for patients who are hypoxic
treat underlying condition before irreversible damage occurs
phlebotomy for polycythemia (rarely required)
treatment of exacerbating factors: smoking, infection, sleep apnea
epoprostenol- beneficial in cardiomyopathy, and NYHA class III-IV symptoms
endothelin receptor antagonists (bosentan, sitaxentan)
phosphodiesterase inhibitors (sildenafil)

Pulmonary Embolism (PE)

,
----------------------------------

...... Definition
lodging of a blood clot in the pulmonary arterial tree with subsequent increase in pulmonary
V"rrchow'1 Trild vascular resistance and possible obstruction of blood supply to the lung parenchyma
VenO\IS slalil
Endothllilll Cllll damage Etiology and Pathophysiology
Hyparcoagulable llatai
one of the most conunon causes of preventable death in the hospital
proximal leg thrombi (popliteal, femoral or iliac veins) are the source of most clinically
recognized pulmonary emboli
CH:III'IIIIatan IIIII Ellballlm
83131:41&-20 thrombi often start in calf, but must propagate into proximal veins to create a sufficiently large
thrombus for a clinically significant PE
Willi Cdlllil
fewer than 30% of patients have clinical evidence ofDVT (e.g. leg swelling, pain or tenderness)
.U:flclll111 !'Villi always suspect PE if patient suddenly collapses 1-2 weeks after surgery
Clinical signJ of IIVT 3.0
ND 111111 ililly 111irr0w dilglais Risk Factors {Virchows Triad)
(usifG H&P, ClOI. Eail 3.0 stasis
lmndlilizltion or l1liiiiiY in
1118 pvviouls 4_.. 1.5 immobilization: paralysis, stroke, bed rest, prolonged sitting during travel, immobilization of
1.5 an extremity after fracture
llllltrlfl>100blmlmil 1.5 obesity, CHF
lllmDptylil 1.0 chronic venous insufficiency
Maligrlncy 1.0
endothelial cell damage
post-operative injury, trauma
IAJw 3'Jo hypercoagulable states
lnllmdiall 28% underlying CA (particularly adenocarcinoma)
1 78%
cancer treatment (chemotherapy, hormonal)
Simpliied Wels: >41elr. s4 Lrftelrlw PE
exogenous estrogen administration (OCP, HRT)
JWA2006 pregnancy; post-partum
prior history of DVT/PE, family history
nephrotic syndrome
Toronto Notes 2011 Pulmonary Vascular Disease Respirolo8Y R19

coagulopathies: Factor V Leiden, Prothrombin 20210A variant, inherited deficiencies of

antithrombin/protein C/protein S, antiphospholipid antibody, hyperhomocysteinemia, "-{_9,
increased Factor VIII levels, and myeloproliferative disease .......,.I'IIWim
increasing age Law r:/iniQi probl/llitf of enildimr:
Investigations (if highly suspicious, go straight to spiral CT) D-.._l+wi .. CT-I+VI! .. ruildil
see Emergency Medicine. Figure 13, ER35 {-\'tldeereased
Mid aut rulld IU:
D-dimer (products of thrombotic/fibrinolytic process)
llilllllratiltarxligllfll!blbiily:
ELISA better than latex agglutination
D-dimer results alone do not rule in or out DVT/PE cr ruled u
consider only in out-patients with low pretest probability I+VII dlcnlllld
Mldil
need to use in conjunction with leg Dopplers
Mlllr:
spiral CT scan with contrast is both sensitive and specific for PE Use I}Sas on1y t 1ow clra pabity.
diagnosis and management uncertain for small filling defects othiMist, go straight 'II spil'll CT
spiral CT may identify an alternative diagnosis if PE is not present flllivJVJI:IsCIIIs(CTOOIIInlltllllrgyorllflll
CT scanning of the proximal leg and pelvic veins can be done at the same time and may be flilllll:
Nlgllivl VJD ICIII Mls aut11!1 di1g1101il
helpful fl91 pnilllbityV/Ihw GJtt Mali il the
venous duplex ultrasound or doppler dilglois WhM high clinicll suspaJn
with leg symptoms lnc:oncwive uhound
positive test rules in proximal DVT fD look far DVT or CT
negative test rules out proximal DVT
without leg symptoms
positive test rules in proximal DVT .... ,

negative test does not rule out a DVT -patient may have non-occlusive or calfDVT
ECG Clllnic ECG finding of PE is S1 -03-13
(inverted T3J, but most commonly SH
findings not sensitive or specific only sinus tlldTyCIIIdia.
sinus tachycardia most common; may see non-specific ST segment and T wave changes
RV strain, RAD, RBBB, Sl-Q3-T3 with massive embolization
CXR
.._,,
frequently normal; no specific features
atelectasis (subsegmental), elevation of a hemidiaphragm Workup for ldioplthic VIE
pleural effusion - usually small 'l'hrQIDPhilill Wurkup: racumJII! or
idiopathic DVT/1'1:; age <50, +FHx.
Hampton's hump - cone-shaped area of peripheral opacification representing infarction unU&Ullllonlion, musiw.
Westennark's sign- dilated proximal pulmonary artery with distal oligemia/decreased M.. Worllllp: 12% of pldients
vascular markings (difiicult to assess without prior films) with idiopathic VTE will h11111 a
dilatation of proximal PA - rare malignancy.
V/Q scan (very sensitive but low specificity)
order scan if
CXR normal, no COPD
r.11G1U lllllllidl
contraindication to cr (contrast allergy, renal d)15function) Nil ilfrlm Mid 2001; 135:18-107
avoid V/Q scan if S1udy: Wliceme, piQipec:live.,. sludy.
CXR abnormal or COPD
lll'lf'gllley dlpnnlllls 114 tlrtilly Clll hal[itlls
inpatient
ill Clllldl.
suspect massive PE IEivlnlill: AWells ICOit was Ulld ID dallmila
results pllienl's pQt problblty !Pil'l rJ [IUimooary
normal- excludes the diagnosis ofPE lll'llolillllllld1hln al).dimtntwas Pllfand.
high probability- most likely means PE present, unless pre-test probability is low l'ltilniiMIIIaw I'll' IIIII 1 negllive
!Bit hid no fwtbar fiSiing IIIII the dilgnosl rl
60% ofV/Q scans are nondiagnostic pumon.y....IIIII Ml arrilded. AI Giber
echocardiogram jlllilnls 1-.d V,.Q IIIII Wnan-dilpllil:,
little diagnostic value IU Jildml Flrlllr
increased RVSP, RV hypokinesis, seen in massive PE aerill qiagllplly- dona
dependi'Q on tie palieniJ PIP llld ILIIO'scannillg
ABG !8Uil.
of NO diagnostic use in PE (insensitive and nonspecific) llllillls.-..: al(llmaoaryemballm
respiratory alkalosis (due to hyperventilation) 1111 1111 dMIDpment al1hrornbolntolic IMIIIIIII

Treatment laQIII: One r/751 palieniJ il whom PI:-
inilillly ruled aut dMiapld alii'DiriiDirmoic
admit for observation (patients with DVT only are often sent home on LMWH) Mill dllingfolbrtilp (0.11 [CI D.D\a71j]. One
oxygen: provide supplemental 0 2 if hypoxemic or short of breath rl1he 437 plliara Ylith nagdiw D-ciners llld low
pain relief. analgesics if chest pain - narcotics or NSAIDs claiclll'll' dmloped I"E duri1g follow up (Nf'V
acute anticoagulation: therapeutic-dose SC LMWH or IV heparin - start ASAP
CancUin: Malll(jnq pllierD Ylith IIIIS[IeCIId
anticoagulation stops clot propagation, prevents new clots and allows endogenous puftlonlly.....IIIIQII thabu rJ PTPd
fibrinolytic S}'5tem to dissolve existing thromboemboli over months D-dinlrltUII is llltllld die-tile rllldfor
get baseline CBC, INR, aPTT renal function liver function dilgnostic imlging.
for SC LMWH: dalteparin 200 U!kg once daily or enoxaparin 1 mg!kg bid- no lab
monitoring - avoid or reduce dose in renal d)15function
for IV heparin: bolus of75 U/kg (usually 5,000 U) followed by infusion starting at
20 U/kg/hr - aim for aPTT 2-3 times control
R20 Rnpirology Pulmonary VaKular Disease Toronto Notes 2011

Nnl.-y
EIQPm (NPED II Trill)
long term anticoagulation
warfarin - start the same day as LMWH/heparin - overlap warfarin with LMWH/heparin
NEJM 2006; 354(22):2317-27 for at least 5 days and until INR in target range of2-3 for at least 2 days
llldr. r.t.Jbtra, prolpllCtiv8 stut, Mtiglting LMWH instead of warfarin for pregnancy; active cancer, high bleeding risk
ICCII'IC'( cornpul8d tomogllphy llllgiogrlfbr
(CTA)It:lne 11'111 codined willlvenous plllll IV thrombolytic therapy
inlui'G ICTA-ClVl. if patient has massive PE (hypotension or clinical right heart failure) and no
Pllilnll: 824 patie!O. sMilll thauml contraindication&
lligibil far Aldy r11Ciiwld
1D Cllllfinn llluiiCI.- priiiiiCI rJ PE (Vft!IICIII, hastens resolution of PE but may not improve survival or long- term outcome and doubles
LVSfikM8r......_llld risk of major bleeding
IIUimoalry clli!ll-utraction !DSAI I interventional thrombolytic therapy
To cormn llbl8ncl. llliiiiiJ in whom
PE Will axdudld weralll.ed 3-611111111111 massive PE is preferentially treated with catheter directed thrombolysis by an interventional
lfbr errollnant M( dllthlWIII'III'IMIWid by radiologist
an outcam1 comrnilhle. All pllien1lllmllled IIIIo works better than IV thrombolytic therapy and fewer contraindications
Llldelwent dinic:IIIISSIISS1111111 af PE (including I
Willi ICIIIII prir Ill inlgilg_ IVC filter: only if recent proximal DVT + absolute contraindication to anticoagulation
a...n.: DiiQnon at pumanlfY mbaism duration oflong-term anticoagulation: individualized, however generally:
I l l * m rJ 824 petilnls had llllqlllll CTAs far if reversible cause for PE (surgery, injury, pregnancy, etc.): 3-6 months
idalpr8lllion. PE- ciiQilDIIId in 1!12 altha 824
pdierQ. SensiiM!y- m (150 111e1 pllillllll, ifPE unprovoked: 6 months to indefinite
M C1. and specificilv- 9K (567 if ongoing major risk factor (active cancer, antiphospholipid antibody, etc.): indefinite
rJ 5!12 Pllienls. 15'1. t11e
1111dicliw vatJa II CTA-ClVwied when clilical Thromboprophylaxis
pre-18Ct problbiily \'Ill- inlo ICCIUit P1'V
ri CTA far high, illlrrnedn and bw ciric:ll mandatory for most hospital patients: reduces DVT, PE, all-cause mortality, cost-effective
problbilitywn M (95'1. Cl 0.784JJ91, 112% startASAP
a.
(15'1. and 58\ (95\ Cl continue at least until discharge or at least 10 days if major orthopaedic swgery
IIIIIICIMir. NPV ri CTA Ia! hijl. ir111ndillll
and llw cllicll pmblbilyW111'116111 (M CL
0.32U3L 89!1. (M C1. 0.82.0.83L 11'111 9K 1M Tabla 19. VTE Risk Categories and Prophylaxis
Cl 0.!12.0.981llspeCtivelf-
c:.:IWn: CTA is atl8ctM for dilgnoling or Risk Gl'llllp Prophylaxis Opti-
mluding PE in KConiiiiCe willl.-tcl
clilical pral8ll pdllbility. Wll8n cia pmblbily Law th10111bnil rille:
is iiiCOIIIIiilaltwilll iniJilg 181UIIJ, bthlr Medical patients -fully mobile No specific prophylaxis
iMIIIigl1ialls 111181Prat Ill Ml aut PE. Surgery- < 30 mirutes, JUly mobile ambulation
Modal'lllll thrombosis rille
Most general, gynecologic, urologic surgety LMWH
Sick medical patients Low dose heparin
High thiOIIIbDiiS rille LMWH
Arthoplasty, hip fractura surgery Fondaparinux
Majarti'IIWI1a, spinal cord injury Warfarin (INR 2-JI
High bleeding risk:
Neurosurgery, inttaCI'IIlial bleed TED stockings, pneumatic compression devices
Actiw bleeding LMWH or low dose heparin when bleeding risk deCII!ISes

Pulmonary Vasculitis
Tabla 20. Pulmonary Vasculitis
Dilease Definition Extra-pulm111uy Felltllrel lnvatigations
WeQener's Granulomatesis Systamic Vllsculitis of medium Necrotizing Focal necratizing lesions CXR: nofllles and alveolar Corticosteroids il1d
end small artaries lesions of the uppll' and of wries end wins; Focal opacities cyclaplmsphamide
IDWII' respiratory tract glomerulonephritis c-ANCA
fiSSue confinnation
Clllrg-Strlluss Syndrome Multisystl!m disorder Asthma Life-threatening systemic No specific investigation, Corticosteroids
(Allergic Granulomatosis characterized by allergic rhinitis. Infiltrates vasculitis involving the peripheral eosinophilia is
and Angiitisl a&thma, and prominant lung&, pBricanlium il1d hllilt. the mo&t common finding
peripheral eosinophilia kittleys, skin, and PNS pANCA may be positive
(mononeuritis multiplex)
Goodputure's Syndrome Adisorder characterized by Hemoptysis Anemia CXII: may see alveolar Acutely:
diffuse alveolar hemorrhage and May folow an influelllll infiltrates Whemorrhage is corticosteroids,
glomarulonaih'itis caused by infection profuse plasmapheresis
anti-GBM antibodies, which EUSA test with anti-GBM rnmunosuppressive
cross-ntact with basement antibodies therapy
membranes of the kidney and Renal biopsy/indirect Severe cases: bilateral
lung
$ystlmic Lupus See Rheumatology
Erythemlbllul..
Rhaumlllllid Arthritis.
Sc:lamdanna
..... ,

Scleroderma is the most common

collaQen VB$CUiar .m-e to llffvc:t
the lung.
Toronto Notes 2011 Diseuea of the Mediastinum and Pleura Respirolo8Y R21

Diseases of the Mediastinum and Pleura

Mediastinal Masses
Definition
mediastinum structures that are bound by the thoracic inlet, diaphragm, sternum, vertebral
bodies and the pleura
can be broken down into 3 compartments: anterior, middle and posterior

Etiology and Pathophysiology

diagnosis is made by location and patient's age
anterior compartment (sternum to anterior border of pericardium) - more likely to be AnQrior
malignant
"Five TsD (see sidebar), lymphoma, lipoma, pericardia! cyst sr.
Thymoma
middle compartment (anterior to posterior pericardium) ThynJid enlll111ement (goiter}
pericardia! cyst. bronchogenic cyst/tumour, lymphoma, lymph node enlargement, aortic Tnmma
aneurysm lhoracic aonic an&UIV1Ill
llmOUI'$
posterior compartment (posterior pericardium to vertebral column) {lymphoma. pnthyraid, sophavalll.
neurogenic tumours, meningocele, enteric cysts, lymphoma, diaphragmatic hernias, angioma1Du5}
esophageal tumour, aortic aneurysm

Signs and Symptoms

50% asymptomatic (mainly benign); when symptomatic, 50% are malignant
chest pain, cough, dyspnea. recurrent respiratory infections
hoarseness, dysphagia. Homer's syndrome, facial/upper extremity edema (SVC compression)
paraneoplastic syndromes (e.g. myasthenia gravis (thymomas))

Investigations
CXR (compare to previous)
CT with contrast (anatomic location, density, relation to mediastinal vascular structures)
MRI - specifically indicated in the evaluation of neurogenic tumours
ultrasound (best for assessment of structures in close proximity to the heart and pericardium)
radionuclide scanning- 1311 (for thyroid), gallium (for lymphoma)
biochemical studies -thyroid function, serum calcium, phosphate, PTH, AFP, beta-hCG
biopsy (mediastinoscopy, percutaneous needle aspiration)

Management
depends on the diagnosis
decide ifthe lesion should be excised (e.g. symptomatic gowing benign masses or concerns of
malignancy)
resection via minimally invasive video assisted procedures (bronchogenic cysts, localized
neurogenic tumours)
exploration via sternotomy or thoracotomy
diagnostic biopsy rather than major operation if mass is likely to be a lymphoma. germ cell
tumour, or unresectable invasive malignancy
post-op radiotherapy/chemotherapy if malignant

Mediastinitis
most common causes of mediastinitis are postoperative complications of cardiovascular or
thoracic surgical procedures

Acute
etiology
complication of endoscopy (e.g. esophageal perforation providing entry point for infection)
esophageal or cardiac surgery
tumour necrosis
signs and symptoms
fever, substernal pain
pneumomediastinum, mediastinal compression
Hamman's sign (auscultatory "crunch" during cardiac systole)
treatment
antibiotics, drainage, surgical closure of perforation

Chronic
usually a granulomatous process or previous infection (e.g. histoplasmosis, TB, sarcoidosis,
syphilis)
R22 Rnpirology Diseases of the Mediastinum and Pleura Toronto Notes 2011

Pleural Effusions
Definition
excess amount of fluid in the pleural space (normally up to 25 ml)

Etiology
disruption of normal equilibrium between pleural fluid formation/entry and pleural fluid
absorption/exit
pleural effusions are classified as transudative or exudative - distinguish clinically using Light's
Criteria (Table 21)

Table 21. Laboratory Values in Transudative and Exudative Pleural Effusion ruahrs Criteria")
..... ,
Protain - plaUilll/sarum <0.5 >0.5
Tl'llnsud.m.. uffuaions are USUIIIIy
bilataral not unillllend LDH- pleuraVserum <0.6 >0.6
effusions can be bilatnl or Pleural LDH <2/3 upper limit af Nserum LDH >2/3 upper limit of Nserum LDH
unilateral RW, MIIC!JigOI'r.t, Luchlii'Gar PCetaLAnnllmMed1979; 77(41:507513

..... , Transudative Pleural Effusions

pathophysiology: alteration of systemic factors that affect the formation and absorption of
pleural fluid (e.g. increased capillary hydrostatic pressure, decreased plasma oncotic pressure)
All criblria fllr lnlnsudlllll must be etiology
fulliUad to be considnd alnlnsudativa
affusion. If any one of the criteria fllr CHF -usually right-sided or bilateral
llCIIdates is m11 - it is an llCIIdate. cirrhosis
nephrotic syndrome
pulmonary embolism (may cause transudative but more often causes exudative effusion)
peritoneal dialysis, hypothyroidism, CF, urinothorax
l.ljii'J tm.la: SIIIIMJ .. Spllllll*t
c:.,mlin . . . . al .. liii:Bicll
l'nMIIn U.IIIIID lllllblllh...,._l'llllnl Exudative Pleural Effusions
......... EUI!a pathophysiology: increased permeability of pleural capillaries or lymphatic dysfunction
IJI8It 1115; 107(61:161K-I etiology
llldr.l'lull fUd 1111 nafical reaJI1!s fur infectious
500 pllilla Mllllllllyzad ll1d tile liagnDitic
acancy's altha Light'sCrillria was 11sassad. parapneumonic effusion (associated with bacterial pneumonia, lung abscess)
lhe Light's crDril was can.,.lld 1D atbar empyema (bacterial, fungal. TB), TB pleuritis, viral infection
biacb.nclll nthods. malignancy
..... Sensitivly: 18%. Specflcty: 83\,lur
illl11flilg llllliiiiM plmllllllsians.
lung carcinoma (35%)
lymphoma (10%)
c:.,mlin Aulylil aiiJelts Crilllillllll metastases: breast (25%), ovary, kidney
... IIDdlllli:lll'lnnlln ... mesothelioma
........... EUI!a
inflammatory
/lelpido!lffolellcile 1998; 92(51:762765.
llldr.l'lllnl !'.lid snd mlllli:ll f1ICOids far collagen vascular diseases: RA, SLE
241 pulmonary embolism, after coronary artery bypass surgery
1lla l11' Critlria far axudlltiw pBnll intra-abdominal
ellu!ians was llllllyzed.lhe results were
subphrenic abscess
1u other poldlllll8lhodl for dillingui5hing
llllllllltM and lrmUIIIM planl esophageal perforation (elevated pleural fluid amylase)
allulions. pancreatic disease (elevated pleural fluid amylase)
..... Sefllitivly: m. Specificty: 71!. lor Meigs' syndrome (ascites and hydrothorax associated with an ovarian fibroma or other
ilenlf,<ilg wiiiNe plelnl elllsians.
pelvic tumour)
trauma
chylothorax: occurs when the thoracic duct is disrupted and chyle accumulates in the
pleural space, due to trauma, tumour
hemothorax: due to rupture of a blood vessel, commonly by trauma or tumours
other
pneumothorax (spontaneous, traumatic, tension)

Signa and Symptoms

often asymptomatic
dyspnea: varies with size of effusion and underlying lung function
pleuritic chest pain
inspection: trachea deviates away from effusion, ipsilateral decreased expansion
percussion: decreased tactile fremitus, dullness
auscultation: decreased breath sounds, bronchial breathing and egophony at upper level, pleural
friction rub
Toronto Notes 2011 Diseuea of the Mediastinum and Pleura Respirolo8Y R23

Investigations
CXR "-{.,
must have >200 ml of pleural fluid for visualization on PA film Ap,.._ of Pltural R.ud
lateral: >50 mlleads to blunting of posterior costophrenic angle Bloody- trauma. malignancy
PA: blunting oflateral costophrenic angle WMe - chylo1horax. empyema
Black- aspargHiosis, amoebic liver
dense opacification oflung fields with concave meniscus abscess
decubitus: fluid will shift unless it is loculated Ylllow-grun- rheumatoid pleurisy
supine: fluid will appear as general haziness Viscous- malignant mesothelioma
thoracentesis: indicated if pleural effusion is a new finding Ammonia odour - urinothorax
Food particles - esophageal rupture
risk of re-expansion pulmonary edema if> 1.5 L of fluid is removed
inspect for colour, character, and odour of fluid
analyze fluid (see Tables 21 and 22) ...... ,

pleural biopsy: indicated if suspect TB, mesothelioma, or other malignancy (and if cytology
negative) IDI1 of CT mP*lral Effusion
U/S: detects small effusions and can guide thoracentesis To ass111 for fluid locullltion, pleural
thickaning ltld nodules, pflf'llllCitymal
treatment depends on cause, drainage if symptomatic abnormalities and adenoplllhy
CT can be hdpful in differentiating parenchymal from pleural abnormalities Helps to distinvui.tl benign from
malignant effusion lllld transudativ1
Table 22. Analysis of Pleural Effusion from BXIIdative &ffu&ion
May not distinguish ampyema from
Meaure parapnaumonic effusion
Protein, LOH Tflllsudalll vs. axudalll (see Table 21) Featurn of Mllianllll Effnion
pleural nodules
G111111 stan. stan !TBI. culture Looking for specific organisms Nodular pleural tllicbning
Cell courrt dilfererrtial Neutrophil! vs. lymphocytes (lymphocytic effusion in TB, cancer, lymphDITI8, serositis! Featurn of E.xudri8 atu.iiDII
Cytology Malignancy, infection Loculation
Pleural thickaning
Glucose (lowl RA. lB. empyema, maliiJlllncy, esophageal rupture Pleural nodules
Extrapleural flit of increased density
Rheumatoid fllctor, ANA, complernerrt Collagen vascular disease
Amylase Pn:reatitis, esophageal perforation. malign111cy
pH Empyema < 7.2. TB and mesatheliama <7.3
Blood Mostly traumatic, malignancy, PE with infarction, 1B
Trig:erides Chylothorax from thoracic d.Jct leakage, mostly due to trauma, lung CA. or lyrrclhoma

Treatment
thoracentesis
treat underlying cause
..... ,,

Complicated Effusion Plaaral Effllaionl
Simple EffusiDn
persistent bacteria in the pleural space, but fluid is non-purulent pH > 7.2, LDH <112 serum, glucose
neutrophils, pleural fluid acidosis, and high LDH >2.2.
often no bacteria grown, since rapidly cleared from pleural space Camplicmd Elfnion
fibrin layer leading to loculation of pleural fluid pH <7.2, LDH > 112 serum, glucose
treatment: antibiotics and drainage, treat as an empyema <2.2. positive Gram sllin. Needs
drainllga.

Empyema
Definition
pus in pleural space or an effusion with organisms seen on a Gram stain or culture (ie. pleural
fluid is grossly purulent)
positive culture is not required for diagnosis ...._ , '

Etiology Whlll possibll, orvanism-diract.d
contiguous spread from lung infection (most commonly anaerobes), or infection through chest lllenpy, guided by culture
wall (e.g. trawna, surgery) or local pattllms af drug resistance
should be utilized.
Signs and Symptoms
fever, pleuritic chest pain
Investigations
CT chest
thoracentesis
PMNs (lymphocytes in TB) visible organisms on Gram stain
Treatment
antibiotic therapy for at least 4-6 weeks (rardy effective alone)
complete pleural drainage with chest tube
if loculated, more difficult to drain - may require surgical drainage
R24 Rnpirology Diseases of the Mediastinum and Pleura Toronto Notes 2011

Pneumothorax
Definition
twa ta lbD Out Ln-Thrllltanillll presence of air in the pleural space
Tllllion Pn-otllllru:
If pneumathom: with: Pathophysiology
Swm respiratory dislms increased intrapleural pressure reduces lung inflation
Trachell deviation to contralalend side
Distsndad nack veins !1' JVP)
Hypotension Etiology
traumatic- penetrating or non-penetrating chest injuries
Da not pufarm CXR.
twn imniNiata treatment. iatrogenic (central venous catheter, thoracentesis, mechanical ventilation with barotrauma)
See E!Dargancy Madjcjoa ER11 spontaneous (no history of trauma)
primary (no underlying lung disease)
spontaneous rupture of apical subpleural bleb oflung into pleural space
predominantly tall, healthy, young males
secondary (underlying lung disease)
rupture of subpleural bleb which migrates along bronchioalveolar sheath to the
mediastinum then to the intrapleural space
necrosis oflung tissue adjacent to pleural surfac:e (e.g. pneumonia, abscess, PCP,
lung CA, emphysema)

Signs and Symptoms

can be asymptomatic
acute-onset pleuritic chest pain, dyspnea
tachypnea, tachycardia
tracheal deviation (contralateral deviation in tension pneumothorax)
ipsilateral diminished chest expansion
decreased tactile/vocal fremitus
hyperresonant percussion note
ipsilateral diminished breath sounds

Investigations
CXR
small: separation of visceral and parietal pleura seen as fine crescentic line parallel to chest
wall at apex
large: increased density and decreased volume of lung on side of pneumothorax
see Dia&JlOstiC DM8

Treatment
small pneumothoraces (<20% with no signs of respiratory/circulatory collapse) resolve
spontaneously; breathing 100% oxygen accelerates resorption of air
small intercostal tube with Heimlich valve for most spontaneous pneumothoraces
large pneumothoraces or those complicating underlying lung disease require placement of a
chest tube connected to underwater seal suction
for repeated episodes: pleurodesis with sclerosing agent or apical bullectomy and abrasion
treat underlying cause (e.g. antibiotic for PCP)

Asbestos-Related Pleural Disease and

Mesothelioma
Etiology and Pathophysiology
benign manifestations of asbestos exposure
"benign asbestos pleural effusion
exudative effusion, typically -10 years after exposure, resolves
pleural plaques, usually calcified
marker of exposure; usually an asymptomatic radiologic finding
mesothelioma
primary malignancy of the pleura
decades after asbestos exposure (even light exposure)
smoking not a risk factor, but asbestos and smoking synergistically increase risk oflung
cancer

Signs and Symptoms

persistent chest pain, dyspnea, cough, bloody pleural effusion, weight loss
Toronto Notes 2011 Di1euea of the Mediastinum and Pleura/Respiratory Failure Respirolo8Y R25

Investigations
biopsy (pleuroscopic or open)
needle biopsy may seed needle tract with tumour

Treatment
resection (extrapleural pneumonectomy) requires careful patient selection; rarely successful
(average survival <1 year)

Pulmonary Edema
see Cardioloay and Cardiovascular C34

Respiratory Failure
Definition
to impairment of gas exchange between ambient air and circulating blood
hypoxemic (Pa02 <60 mmHg)
hypercapnic (PaC02 >50 mmHg)
acute vs. chronic (compensatory mechanisms activated)
Classification
airway obstruction: COPD, bronchiectasis, CF, asthma, bronchiolitis, upper airway obstruction
abnormal parenchyma: pneumonia, pulmonary edema, pulmonary fibrosis, acute respiratory
distress syndrome (ARDS), pleural effusion
hypoventilation without bronchopulmonary disease: CNS disorder (drugs, increased ICP, spinal
cord lesion, sepsis), neuromuscular (myasthenia gravis, Guillain-Barre, muscular dystrophies),
chest wall (kyphoscoliosis, obesity)

Signs and Symptoms

signs of underlying disease
hypoxemia: restlessness, confusion, cyanosis, coma, cor pulmonale
hypercapnia: headache, dyspnea, drowsiness, asterixis, warm periphery, plethora, increased ICP
(secondary to vasodilatation)

Investigations
serial ABGs
CXR and/or CI', bronchoscopy to characterize underlying cause if unclear

Hypoxemic Respiratory Failure

..._, I
Definition
Pa02 decreased, PaC02 normal or decreased c..... Df
1. Law Fi02
2. Hypgvantilation
Pathophysiology 3. Shunting
low inspired Fi02 (e.g. high altitude) 4. Low mixed venous O:r content
normal Fi02 5. V/Q mismatch
diffusion impairment: interstitial lung disease
V/Q mismatch: airway disease (asthma, COPD), alveolar disease (pneumonia, edema),
vascular disease (PE)
shunts: alveolar collapse, intra-alveolar filling (pneumonia, edema), intracardiac (R to L),
intrapulmonary (AVM)
low mixed venous saturation: anemia, low cardiac output, hypermetabolism

Treatment
reverse the underlying pathology
maintain oxygenation
enrichment of Fi02 (if shunt present, supplemental 0 2 is less effective)
positive pressure: use ofPEEP/CPAP can recruit alveoli and redistribute lung fluid
hemodynamic support: fluids, vasopressors, inotropes, reduction of 0 2 requirements
R26 Rnpirology Respiratory Failure Toronto Notes 2011

Table 23. Approach to Hypoxemia

.HD01 DIYII1111rapy Vllntilldi111, BiPAP lmprowd Clnlilc:
IIIII PEEP Output
1. LowFiDz Postop, high Nonnal, Low Normal Improves No chirlge No change
atitude
2. Hypoventilalion !ng overdose High Normal Improves Improves with No change
ventilation
3a. Shunt ARDS, Pneumonia Low, Nonnal Increased No change Improves (except if Improves
one-5ided)
3b. Sllmt Pulmonary HTN Nonnal, Low Ina-eased No change Worsens Worsens
(Right to Left)
4. low mixed venous Shock Low lncraased No change Worsens Improves
Dz content
5. V/0. miSITIII!ch COPD High. Nonnal lnCIIIIISed Improves with Often improv111 Improves
small11110unts
Reprinted with permission from Dr. 1111 Fraser

Hypercapnic Respiratory Failure

----------------------
...._,' PaC02 increased, Pa02 decreased

ea...a uf llypen;apnia
1. High lnspi111d C02 Pathophysiology
2. Low Total Ventilation increased C02 production: fever, sepsis, seizure, acidosis, carbohydrate load
3. High Oaadspac& V&ntilation alveolar hypoventilation: COPD, asthma., CF, chest wall disorder, rapid shallow breathing
4. High C02 Production hypoventilation
central: brainstem stroke, hypothyroidism, severe metabolic alkalosis, drugs (opiates,
...._,' benzodiazepines)
neuromuscular: myasthenia gravis, Guillain- Barre, phrenic nerve injury, muscular

dystrophy; polymyositis, kyphoscoliosis
In chronic hyparcapnia. IUJipiarn.nllll
02 may d&crwn the hypoxic driw tD muscle fatigue
breathe, but do not deny DXygen if the
plllient is hypoxic. Treatment
reverse the underlying pathology

..... ,'

ifPaC02 >50 rnmHg and pH is acidemic consider noninvasive or mechanical ventilation
correct exacerbating factors
NTT/ETT suction: clearance of secretions
In COPD pati&nbl wilh chronic
hyparc:apnia ("C0 2 llltainm"), provide bronchodilators: reduction of airway resistance
oxygen tD achieve target antibiotics: treatment of infections
from BB-9n.. maintain oxygenation (see above)
diet: increased carbohydrate can increase PaC02 in those with mechanical or limited
alveolar ventilation; high lipids decrease PaC02

Acute Respiratory Distress Syndrome (ARDS)

clinical syndrome characterized by severe respiratory distress, hypoxemia, and noncardiogenic
pulmonary edema
American-European Consensus Conference (1994) criteria for ARDS:
1. acute onset
2. bilateral infiltrates on CXR
3. PCWP 18 or no evidence of increased left atrial pressure
4. Pa02/Fi02

Etiology
may result from direct or indirect lung injury;
airway: aspiration (gastric contents, drowning), pneumonia, gas inhalation (oxygen toxicity,
nitrogen dioxide, smoke)
circulation: sepsis, shock, trauma, pancreatitis, DIC, blood transfusion, embolism (fat.
amniotic fluid), drug overdose (narcotics, sedatives, TCAs)
neurogenic: head trauma, intracranial hemorrhage

Pathophysiology
disruption of alveolar capillary membranes -+ leaky capillaries -+ interstitial and
alveolar pulmonary edema-+ reduced compliance, V/Q mismatch, shunt, hypoxemia,
pulmonary HTN
Toronto Notes 2011 Reapiratory Failure Respirolo8Y R27

Clinical Course
A. Exudative Phase
first 7 days of illness after exposure to ARDS precipitant
alveolar capillary endothelial cells and type I pneumocytes are injured. resulting in loss of
nonnally tight alveolar barrier
patients develop dyspnea, tachypnea, increased work of breathing
these result in respiratory fatigue and eventually respiratory failure
(see Hypoxemic Respiratory Failure, R25)

B. Proliferative Phase
day 7-21
may still experience dyspnea, tachypnea, fatigue, and hypoxemia
some patients develop fibrotic lung changes
most patients clinically improve and are able to wean off mechanical ventilation

C. Fibrotic Phase
some patients will enter a fibrotic phase that may require long-term support on supplemental
oxygen or even mechanical ventilation
if fibrosis present, associated with increased mortality

Treatment
based on ARDS network (see Landmark Respirology Trials, R38)
treat underlying disorder (e.g. antibiotics if infection present)
mechanical ventilation using low tidal volumes (<6 mllkg) to prevent barotrauma
use optimal amount of PEEP (positive end-expiratory pressure) to keep airways open and
allow the use oflower Fi02
may consider using prone ventilation, and/or inhaled nitric oxide, high frequency oscillator
or ECMO (extracorpeal membrane oxygenation) if conventional treatment is failing
fluids and inotropic therapy (e.g. dopamine, vasopressin) if cardiac output inadequate
pulmonary-arterial catheter now seldom used for monitoring hemodynamics
mortality: 30-4096, usually due to non-pulmonary complications
sequelae of ARDS include residual pulmonary impairment, severe debilitation, polyneuropathy
and psychologic difficulties, which gradually improve over time
most survivors eventually regain near-normal lung function, often with mildly reduced
diffusion capacity

Mechanical Ventilation
see Anesthesia, AIO
.... ,,


Definition Tr.ctleostornv should be considered
artificial means of supporting ventilation and oxygenation in pllliii'IIS who l'lqllil'l vllltila!Dr
mechanically ventilated patients may require some sedation and/or analgesia support for exlended periods of time
Shown to improva patient comfort
Indications and give patients a better ability to
general indications participalll in ruhllbilitlllion IIC!ivilies
hypoxemic respiratory failure
hypercapnic respiratory failure
specific indicators for mechanical ventilation
.... ,,

acute ventilation failure/acute respiratory acidosis .....,.. End Expimory I'NIIaur1
refractory hypoxemia [PEEPI
reduced level of consciousness Pf'IIIUI'I IIPPiild at 1h1 and of
ventillllion which opens up collapsad
facilitation of surgical procedures alveoli decreasing V/Q mismatch
Used with all invasive modes of
Ventilator Strategies wntillllion

,,
target tidal volume, respiratory rate, PEEP and ratio of inspiratory to expiratory time are all
determined based on the underlying reason for mechanical ventilation ....
hypoxemic respiratory failure: ventilator provides supplemental oxygen and helps improve V IQ
mismatch and decreases intrapulmonary shunt
hypercapnic respiratory failure: ventilator augments alveolar ventilation; may decrease the work Monilllring v.ntilllory ThlrPr
Pulse Oldmllly, end-tidal
of breathing, allowing respiratory muscles to rest concentrlllion
Regular art.rial blood QIIHI
Modes of Ventilation AH11111 tolemlce ragularty
assist-control ventilation (ACV) (often initial mode of ventilation)
every breath is delivered with a pre-set tidal volume
inspiration may be triggered by patient effort; if no effort is detected within a specified
...... ,,

amount of time the ventilator will initiate the breath
Management of pneumothorax in
paliii'IIS on mechanical ventilation -o
chest lube.
R28 Rnpirology Respiratory Failure/Neoplamu Toronto Notes 2011

synchronous intermittent mandatory ventilation (SIMV)

ventilator provides breaths at fixed rate and tidal volume
patient can breathe spontaneously between ventilator breaths
PEEP is still applied and therefore spontaneous breaths still supported
pressure support ventilation (PSV)
patient initiates all breaths and the ventilator supports each breath with a pre-set inspiratory
pressure
useful for weaning off ventilator
pressure control ventilation (PCV)
a minimum frequency is set and patient may trigger additional breaths above the ventilator
all breaths delivered at a preset constant inspiratory pressure
noninvasive ventilation (NIV)
achieved without intubation by using a nasal mask with:
BiPAP (bilevel positive airway pressure): a wave of increased pressure on inspiration and
lower constant pressure on expiration
CPAP (continuous positive airway pressure): constant pressure

Complications of Mechanical Ventilation

barotrauma
pneumothorax, tension pneumothorax, pneumomediastinum, subcutaneous emphysema,
ventilator-induced lung injury (from the use of high tidal volumes - can resemble ARDS)
ventilator associated[neumonia (nosocomial pneumonia)
patients intubate 72 hours are at high risk of acquiring pneumonia
common organisms include enteric Gram-negative rods, anaerobes, S. aureus
hypotension (decreased CO)
increased intrathoracic pressure with decreased venous return that usually responds to
intravascular volume repletion
stress ulcers
may be prevented with H 2-blocker prophylaxis
tracheal stenosis
laryngeal dysfunction

Neoplasms
Approach to the Solitary Pulmonary Nodule
',
also see Medical Imaging, DM7

Pulm-rv neoplasms mav pnsant as

solitary pulmo1111ry nocUe identified
Definition
incidantalv on 1 radiographic studv a round or oval, sharply circumscribed radiographic lesion up to 3-4 em, which may or
(-10% of cas11) or as s'(IIIIIIDmatic may not be calcified, and is surrounded by normal lung
disease (most casas). can be benign or malignant

Table 24. Diffarential Diagnosis for Benign vs. Malignant Solitary Nodule
',,
Beniga {70%) Mali.-nt{30'1'o)
grmu..ma {histoplasmosis, cocciditmyCosis, TB,IIlypical rnycobactelia) Branc:hoganic:
Cora1111 "--im Sign on Chnt CT
Fine striations 111111 mct.rxllin..ty Othar inf11ction1 (bacterial abscess, PCP. aspergilloma) Adenocercin011111
from 1 nodula in a spiculated fashion Baniga naaplums (hamarlllma, lipoma, fibroma) eel cerciloma
Highly associated with malignancv Ylscul (AV IIIIMorrnatian. pumonaryvarix) Large cell Cli'Cinoma
DIVIIopmnal (bronchogenic cyst) Small cell carcinoma
lnlla11matDry (Wegane(s gnmulomaiDsis, rhaumatoid nodule, sarcoidosis) Mllllllltic laions
',,
Othar {hematoma, infarct. pseudotumour, rounded atelectasis, lymph nodes, anyloidoma) Breast
Head and neck
Tminolagy Melanoma
"nodule" <3 em Calon
"IIIU1i" >3 em
Sarcoma
Germ celltumou11
Pulmonary can:inail

Investigations (see Figure 11)

CXR: always compare with previous CXR (see Table 25)
CT densitometry and contrast enhanced CT of thorax
sputum cytology: usually poor yield
biopsy (bronchoscopic or percutaneous) or excision (thoracoscopy or thoracotomy): if clinical
and radiographic features do not help distinguish between benign or malignant lesion
if at risk for lung cancer, biopsy may be performed regardless of radiographic features
if a biopsy is non-diagnostic, whether to observe, re-biopsy or resect will depend on the level
of suspicion
watchful waiting: repeat CXR and! or CT scan at 3, 6, 12 months
PET scan not yt:t routine but can help distinguish benign from malignant nodules
Toronto Notes 2011 Neoplasma Respirolo8Y R29

Table 25. CXR Characteristics of Benign vs. Malignant Solitary Nodule

<3 em, round, regular >3 em, irregular, spiculated

Smooth margin Ill-defined or notched margin
Calcified pattern: cenlnll, "popcorn" pattErn if Usually not calcified; if calcified, pattern is eccenbic, no
hamartoma, usually no cavillllion; if cavilled, sallillile lesions, cavitation with thick wall, may have
wall is smooth and thin, no other lung pathology plaurallllfusions, lymphadanoplthy
Doubling Time Doubles il < 1 month or >2 yan Doubles in > 1 month or <2 yean

Solitary pulmonary nodule

Check pliou CXR

Significant risk factor on Hx

Looks malignant or changed
I

...
Looks benign or unchanged

...
Repeat CXR in l-6 months

1
I
Changed Unchanged x 1 year

CT thorax+----------'

.J'
Infection
Cancar
I

Calcilicllion
No diagnosis
Repeat CXR avery 6 monthsx 1 year
...

Obsarve

I

Bronchoscopy Stage and treat Observe PET scan Transthoracic radla biopsy Follow with &erial CT
I I

...
Cancer

Stage and treat

...
Treat
1
Inflammatory

CIIU&e
...
Still no diagnosis growing

Biopsy or rnact for diagnosis

Figure 11. Evaluation of a Solitary Pulmonary Nodule

Benign Lung Tumours

----------------------
Epidemiology
less than 5% of all primary lung neoplasms
bronchial adenomas and hamartomas comprise 90% of the benign neoplasms of the lung
uncommon benign neoplasms of the lung include fibromas, lipomas,leiomyomas,
hemangiomas, papillomas, chondromas, teratoma and endometriosis

Signs and Symptoms

cough, hemoptysis, recurrent pneumonia. wheezing. atelectasis
can present as an asymptomatic solitary pulmonary nodule (see previous section)
Classification
bronchial adenomas
slow-growing, low-grade endobronchial tumours that rarely metastasize
may be carcinoids (90%}, adenocystic tumours, or mucoepidermoid
symptoms
systemic symptoms usually absent
patients may complain of chronic cough, wheezing or give a history of recurrent pneumonia
hemoptysis may be present
bronchial carcinoids
often in young adults; smoking not a risk factor
clinical presentation: follows a slow course, metastasizes late
carcinoid syndrome (flushing, diarrhea, cardiac valvular lesions, wheezing) is rarely
associated with pulmonary carcinoids
may cause paraneoplastic syndromes (see Table 27)
treatment and prognosis: amenable to resection; 5-year survival is 95%
atypical carcinoid: more aggressive form, tends to metastasize
hamartomas
composed of tissues normally present in lung (fat, epithelium, fibrous tissue and cartilage),
but they exhibit disorganized growth
peak incidence at age 60, more common in men, 10% of benign lung lesions [2nd to
infectious granuloma (80%)]
usually peripheral, clinically silent, and benign in behaviour
CXR: clustered "popcorn pattern of calcification is pathognomonic for hamartoma
RJO Rnpirology Neoplaama Toronto Notes 2011

Malignant Lung Tumours

----------------------------------------
Pathological Classification
bronchogenic cancer (90% of primary lung cancers, see Table 26)
classified into small OOllung cancer {SCLC) and non-SCLC (NSCLC, e.g. adenocarcinoma,
'
....
squamous cell, large cell), bronchioalvelolar cancer (BAC)
incidence of adenocarcinoma is increasing
MaliQillll! Mig tumours 111'11 the most lymphoma
common C81lse of cancer morlllity
throughout the wo!ld in both men 11111
secondary metastases: breast, colon, prostate, kidney, thyroid, stomach, cervix, rectum, testes,
women. bone, melanoma

Tabla 26. Characteristics of Bronchogenic Cancer

Ccl Type Incidence Carnlidion Loc:ation Histulogy
with 11110king
Adenocan:inorna M: 35% F: 40% Week Periphnl GlandLJar, mucin prarilcing Elrly, distant
SqUilllau& cell 30% Strong Cerml Keratin, intercellular bridge& Local irrva&ian and d&lilnt
carcinoma {SCCI spread. may cavitate
SCLC 25% Strong Cermal Oat cell, neuroendocrine Disseminated at pr888ntatian
Origin in endobronchial cells
lsge cell 11}-15% Strong Periphl!llll Anaplastic. undifferentiated Elrly. distant
carcinoma

Epidemiology
most common non-skin cancer in men and women
most common cause of cancer death in men and women
18% of all cancer related deaths

Risk Factors
cigarette smoking: 85% oflung cancer related to smoking
asbestos 5x increased risk, asbestos + smoker 80-90x increased risk
radiation: radon, uranium (especially if smoker)
arsenic, chromium, nickel exposure
genetic damage
parenchymal scarring: granulomatous disease, fibrosis, scleroderma
passive exposure to cigarette smoke
air pollution: exact role is uncertain
oHIV

Signs and Symptoms

cough {75%): beware of chronic cough that changes in character
dyspnea (60%)
chest pain (45%)
hemoptysis (35%)
other pain (25%)
dubbing (21 %)
constitutional symptoms: anorexia, weight loss, fever, anemia

Presentation by Location of Tumour Extension

lung, hilum, mediastinum, pleura: pleural effusion, atelectasis, wheezing
It'
pericardium: pericarditis, pericardia! tamponade
Hamar bu MAP of Ill ea..t
Al'lncout tumour compresses the esophageal oompression: dysphagia
CIIVical sympmhstic plexus causing phrenic nerve: paralyzed diaphragm
Harnar" syndrome: recurrent laryngeal nerve: hoarseness
Miosis superior vena cava syndrome:
Anhydrosis
Ptosis
obstruction of SVC causing neck and fadal swelling, as well as dyspnea and cough
other symptoms: hoarseness, tongue swelling, epistaxis, and hemoptysis
physical findings: dilated neck veins, increased number of collateral veins covering the
anterior chest wall, cyanosis, edema of the face, anns, and chest, Pemberton's sign
milder symptoms if obstruction is above the azygos vein
lung apex (Panooast tumour): Horner's syndrome, brachial plexus palsy (most commonly
C8 and Tl nerve roots)
rib and vertebrae: erosion
distant metastasis to brain, bone, liver, adrenals
paraneoplastic syndromes (see Table 27)
a group of disorders associated with malignant disease, not related to the physical effects of
the tumour itself
most often associated with SCLC
Toronto Notes 2011 Neoplasma Respirolo8Y R31

Tabla 27. Pllranaoplastic Syndromes

Clinicll Pnlsenlation "-{9,
213 of primary lung cancer is found in
Skllalll Clubbing. pulmonary NSCLC 1hs upparlung; 213 of rnabllbllaa occur
ostaoarthropathy (HPORl] in ltle lower lung (hemldoqenous spread
Dennatologic Acanthosis nigricans Bronchogenic cancer MCOndlry b) increated blood flow b)
DeiTTIIItomyositis Bronchogenic cancer 1111 ban of !he lung).
Endocrine (osteolysis or PTHrP) call cancer
Hypophosphllllmia cell cancer
Hypoglycemia Sarcama
Cushing's syndrome (ACTll) SCLC
Somato&tatinarna &yndro1118 Brom:lial carcinoid
SIADH SCLC
Neurumyuplllhic Lambsrt-E&tan syndroma SCLC
Polymyositis
Subacute cerebellar
Spinacaraballar degeneration
Pllriphllllll nauropathy
lluc:uluJllemirtologic NonbecteriBI endocarditis Bronchogenic cancer
Trousseau's &yndrome {migralllryltlrombophlebitis) NSCLC
OIC
lllnll Nephrotic &yndrume

Investigations
initial diagnosis
imaging: CXR, Cf chest + upper abdomen, PET scan, bone scan
cytology: sputum
biopsy: bronchoscopy, percutaneous, mediastinoscopy
staging work-up
blood work: electrolytes, LFTs, calcium, ALP
imaging: CXR, Cf thorax and upper abdomen, bone scan, neuroimaging
invasive: bronchoscopy, mediastinoscopy, mediastinotomy, thoracotomy
Staging/Treatment
Tabla 28. SCLC vs. NSCLC
Sllu Definition Tnlllmllllt Mldian Survinl
SCLC Umitad &taga Canfinad to single radiation part Radiation chama 1-2 yu;ll$
Extensive stage (one hemithorax and nodes) prophylactic to brain 6 months
Extension beyond a single radiation port Chemotherapy
Sllge (niM ISS) Treatment 5Year Survinl
NSCLC No invasion beyond kmg and nodas IJIIIjatiw Surgery -50%
No illVilsion beyond lung and ip5ilateral hilar Surgery + radiation 311%
Nodes positive
lilA Direct extension to chest wall, pleura, pericardium Chemotherapy + 15%
or ipsilateral mediastinal nodes positive radiation
fallowed by surgery
IIIB Advanced local involvement (1118lignant etrusian, Radiation chama 5%
1118jor structures), or contralateral nodes positive Surge!'(
IV Distant mslilstasis Palliatiw <2%

Therapy for Bronchogenic Cancer

surgery
surgery not usually performed since SCLC is generally non-curable
preferred treatment of stage I and II NSCLC is resection with a curative intent
advanced NSCLC (stage III and IV) is often palliated with chemotherapy and/or radistion
oontraindications:
spread to contralateral lymph nodes or distant sites
- patients with surgically resectable disease must undergo mediastinal node sampling
since Cf thorax is not accurate in 20-40% of cases
poor pulmonary status (e.g. unable to tolerate resection oflung)
perioperative mortality
6% if pneumonectomy
3% iflobectomy
..... ,,

1% if segmentectomy
Combination trealment may ba SL418rior,
chemotherapy (no role for chemo alone, only in combination with other treatments) giving better response l'llles.
cisplatin and etoposide
paclitaxel, vinorelbine, and gemcitabine are newer NSCLC therapies
new biologics, e.g. epidermal growth factor inhibitor (Gefi.tinib)
R32 Rnpirology NeoplasmaJSleep-Related Breathing Disorders Toronto Notes 2011

complications:
acute: tumour lysis syndrome, infection, bleeding, myelosuppression, hemorrhagic
cystitis {cyclophosphamide), card.iotoxicity {doxorubicin), renal toxicity {cisplatin),
peripheral neuropathy (vincristine)
chronic: neurologic damage, leukemia. additional primary neoplasms
radiotherapy
palliative care for end-stage disease
Prognosis of Bronchogenic Cancer
5 year survival rates for different subtypes:
squamous cell carcinoma 25%
adenocarcinoma 12%
large cell carcinoma 13%
SCLC 196 {poorest prognosis)
NSCLC {see Table 28)
greatest tendency to metastasize
70% present with extensive disseminated disease at initial diagnosis
limited-stage: 15-20% cure rate
extensive-stage treated: median survival of 6 months, but can live up to two years with a rare
cure (1%); untreated median survival is 2-3 months

BRONCHOALVEOLAR CARCINOMA
a type of adenocarcinoma that grows along the alveolar wall in the periphery
may arise at sites of previous lung scarring
clinical presentation: similar to bronchogenic cancer; late metastasis
treatment and prognosis: solitary lesions are resectable with a 60% 5-year survival rate; overall
survival rate is 25%

Sleep-Related Breathing Disorders

normal changes during sleep: tidal volume decreases, arterial C02 increases {due to decreased
minute ventilation), pharyngeal dilator muscles relax causing increased upper airway resistance
sleep-related breathing disorders: a group of disorders characterized by decreased air-flow
occurring only in sleep or worsening in sleep
affects 9% of men, 4% of women
sleep apnea
hypoventilation syndromes
primary alveolar hypoventilation: idiopathic
obesity-hypoventilation syndrome {Pickwickian syndrome)
respiratory neuromuscular disorders

Sleep Apnea
Definition
\, episodic decreases in airflow during sleep
quantitatively measured by the Apnea/Hypopnea Index (AHI) = # of apneic and hypopneic
Apneic- no breathing for <!10 seconds
events per hour of sleep
Hypopnllio - >50% 111duction in
for 0!1 0 seconds
sleep apnea generally accepted to be present ifAHI >15
Classification
obstructive (OSA)
caused by transient, episodic obstruction ofthe upper airway
absent or reduced airflow despite persistent respiratory effort
central {CSA)
caused by transient, episodic decreases in CNS drive to breathe
no airflow because no respiratory effort
Cheyne-Stokes Respiration {CSR): a form of CSA in which central apneas alternate with
hyperpneas to produce a crescendo-decrescendo pattern of tidal volUllle; seen in severe LV
dysfunction, brain injury, and other settings (Figure 2)
mixed {MSA)
features ofboth OSA and CSA
loss of hypoxic and hypercapnic drives to breathe secondary to "resuscitative breathing":
overcompensatory hyperventilation upon awakening from OSA induced hypoxia
Toronto Notes 2011 Sleep-Related Breathing Disorders/Introduction to Intensive Care Respirolo8Y R33

Risk Factors
for OSA: obesity, upper airway abnormality. neuromuscular disease, hypothyroidism,
alcohol/sedative use, nasal congestion, sleep deprivation
for CSA: LV failure, brain-stem lesions, encephalitis, encephalopathy, myxedema, high altitude

Signs and Symptoms

obtain history from spouse/partner
secondary to repeated arousals and fragmentation of sleep: daytime somnolence, personality
and cognitive changes, snoring
secondary to hypoxemia and hypercapnia: morning headache, polycythemia, pulmonary/
systemic HTN, cor pulmonale/CHF, nocturnal angina, arrhythmias
OSA typically presents in a middle-aged obese male snorer
CSA can be due to neurological disease

Investigations
Ceii-.I'UihArap"-nr.
sleep study (polysomnography) DMiruclill Slup,....
evaluates sleep stages, airflow, ribcage movement, ECG, SaOz, limb movements 1111 Codrn DIIIIIGtrA
indications m.iaua z
excessive daytime sleepiness lludr.I'Doled lllllysil ci 36 RCT1 (1718 peopej
nactJ1111I CI'N' with 1n inlciM Clldnll
unexplained pulmonary HTN or polycythemia cr al1l illlds with ob!INctM sleep
daytime hypercapnia ljii1IJL
titration of optimal nasal CPAP Cllcl111illnl: The 111e of CPAP showed siglificllll
i1 objei:INe llld 111bjec1Ne _ . .
assessment of objective response to other interventions
ilcbh.l cognitM blction.slllpi,_., n.ans
cl qwlily of lift,lllld lluwer --ua 1'111* llld
Treatment clallllc blood pre-. floPe who responded
modifiable factors: weight loss, decreased alcohol/sedatives, nasal decongestion, treatment of eqUII\'weiiiD CPAP IIIII Ollllll!lfilnces
underlying medical conditions llti'Dng p!lfnlcl far Dill ' - " '
OSA or MSA: nasal CPAP, postural therapy {i.e. no supine sleeping), dental appliance, participlllll on cnl applilnceswn men IW,1D
wilhdiiW hum lllerepy.
uvulopalatopharyngoplasty, tonsillectomy
CSA or hypoventilation syndromes: nasal BiPAP/CPAP, respiratory stimulants
(e.g. progesterone) in select cases
tracheostomy rarely required and should be used as last resort for OSA ---t,,
CPAP has bun lhown 1D raduca
Complications cardiavucular risk and cardiovascular
depression, weight gain, decreased quality oflife, workplace and vehicular accidents, cardiac ralatsd deaths in petiants with
obstructive lleep apnea.
complications (e.g. HTN), reduced work/social function

Introduction to Intensive Care

goal of the intensive care unit (ICU) is to provide stabilization in the setting of an acutely or
severely ill patient
hemodynamic, respiratory or cardiac instability, or widespread infection warrant ICU admission
ICUs are intended to reverse the abnormal physiology, contain the underlying problem and
create a favourable environment for recovery until the patient is stable enough to be transferred
features unique to ICU are:
high nurse to patient ratio
extensive invasive cardiopulmonary and other system support monitoring

ICU Basics
Lines and Catheters
arterial lines
used to monitor beat-to-beat blood pressure variations, obtain blood for routine ABGs,
common sites are femoral or radial lines
---t,,
A cathmr "Wlldgllll" in !he distal
central venous catheter (central line)
pulmolllll'f artery measures pressure
used to administer IV fluids, monitor central venous pressure, insert pulmonary artery transmilllld from the pulmonary venous
catheters, give parenteral nutrition, give agents which are too irritating to be given via a system. This is known as 1he p!Jmonary
peripheral line, when peripheral access is not possible capillary wedge prenure (PCWPI. The
PCWP reflectllleft atrial pressure (as
common sites include: internal jugular vein, subclavian vein, femoral vein
long u 1here is no pulmDilary venou&
pulmonary arterial catheter diseaseI and LV diastolic pressure (as
uses a balloon "sail" to guide the catheter from a major vein to the right heart long u 1here is no Vlllve di11811S8I.
"wedgedD in the pulmonary artery temporarily to take a variety of measurements PCWP is high in cardiog111ic shock and
rarely used due to associated complications low in hypovolemic shack.
SIIU!tl: l'Mil fmnliflls ti Afrlble. Iiiii Edilim.
R34 Rnpirology Introduction to Intensive Care Toronto Notes 2011

indications:
diagnosis of shod states, primary pulmonary hypertension (PPH), valvular disease,
intracardiac shunts, cardiac tamponade, and pulmonary embolism (PE)
assessing hemodynamic response to therapies
differentiation ofhigh- versus low-pressure pulmonary edema
monitoring and management of complicated MI
management of multiorgan system failure and/or severe bums
management of hemodynamic instability after cardiac surgery
absolute contraindications:
tricuspid or pulmonary valve mechanical prosthesis
right heart mass (thrombus and/or tumour)
tricuspid or pulmonary valve endocarditis

Table 29. Useful Equations and Cardiopulmonary Pa111m8ters

Body Surface Area (BSAI = [Ht (cml + Wt {kgl- 60V100
PCWP (Pulmonary Capillary Wedge Pressurel = LVEDP (Left End Diastolic Pressurel
Cardiac Index (CII = Cardiac Dutput!BSA
Slrokll VoiL111B lndax (SVII = CI/HBIIt Rate
RV Ejection Fnlction = SV/RVEDV
Systemic vascular resistance index (SVRI) = [(MAP- right alrial pressure (RAPU + 8D]ICI
P:F ratio =

ICU Approach to Management

llllllliw hdllhlpyllt:ritcllyiiPIIilnll the initial assessment of the critically ill patient focuses on life-threatening processes that require
NUif 2001; 345:135t-67
Studr.l'rol!lettive. llllllorrMzad cantrolad clinical immediate diagnostic and/or therapeutic intervention
outcome sUiy. management is based on the understanding of the pathophysiology of the disease process taking
1548 pQnl$ dmill8d bl111e M:U into consideration organ-system dependence
lllllmldial: Allllllissian. pilim were llf1lllllrtt
lllliunllll Ill ailhlll' iiDnlivl inUl u..py llf
aJaWalilnll thnpy. Those in 1hl inllniM grwp
t.d 111 irlulion sind l BG 8XCaldad 6.1 1JinOIA. Organ Failure
IIIII lllliroinld Ill kllp BG bllwHn
4.41116.IIIIIIJIIL respiratory failure (see Respiratory Failure, R25)
TID in lila CIIITIInlionlliiJliUp Will s1lllld m
ilsuliloltf HBG uceeded 1U,111d the itusm coagulopathy (see HematoloKY. H33)
wulldjllfld Ill 111tgat,._ coagulopathies commonly occur in acutely and severely ill patients
10.Dind11.111111D1'L monitor for:
l'lllwy D.au: 0111111 from l!?f cue dlling thrombocytopenia
M:Umy.
RMIIIII:35 plli&rD (4.R)bd inliMI inllniMI INR. PTT elevations
in lhiiCU, nil &3 palilnts (B.fi) in lila DIC (increase in fibrin degradation products and reduction in fibrinogen)
c:anwaliJnll This re,menls am. mmlily liver failure (see Gastroenterology. G34)
l'8lb:tiln (p=D.D41. lrDIIMI il.., llllnpy allo manifested by rise in transaminases, bilirubin, INR and hypoglycemia
reillced overal in-hospillll1n011111y,lowered delths
aiD llplis. ndi-GQII!fllikn. Mllllof111a renal failure (see NephroloKY NP19)
marllly bllllitwu - in lang my palilrD damage sustained by hypovolemia. nephrotoxins
1>5 dlySj. patients typically develop acute tubular necrosis (ATN)
Clllllbia1: 1rDniw ilsulin 111nvi in 1l1a M:U goal of treatment correct volume and electrolyte status, eliminate toxins
reillces II10IIDiy Ill' 32\ IIIII impiMs
marllly llld llllllllidily. common treatment modalities: diuretics, dialysis (early aggressive daily dialysis is key)

Shock
,,.. , see Emergency Medicine, ER3
Shoek: Cliniul Correlation inadequate tissue perfusion potentially resulting in end organ injury
categories of shod include
ltypowlllllic: patients have cool
8XIr8milies due to periphiJIIII hypovolemic: hemorrhagic, dehydration, vomiting, diarrhea, interstitial fluid
VIIIOCOIIItriction. redistribution
Cardiogenic: pelilllla usually hiM cardiogenic: myopathic (myocardial ischemia infarction), mechanical, arrhytlunic,
signs of left-sided heart fiiHure. pharmacologic
Dllllnlt:livll: varied pmenllltion. obstructive: massive PE (saddle embolus), pericardia! tamponade, constrictive
pericarditis, increased intrathoracic pressure (e.g. tension pneumothorax)
Distrib..-.: patients hllv8 wann
IXInlmiti8s dulto periphnl distributive: sepsis, anaphylactic reaction, neurogenic, endocrinologic, toxic
VIIIOdillrtion.
Toronto Notes 2011 Introduction to Intensive Care Respirolo8Y R35

Table 30. Changes Seen in Different Classes of Shock

Hypowlamil: Cardiogic Obstnlclivl DilllilutM
HR 'I',N,or..V
BP ""..v ..v ""..v ""..v
JVP ..v ..v
Extnmities Cold ""Cold "" Cold
Nor Warm
Other Look fur visible Bilateral crackles Depending on c111se, may see Look for obvious
hemorrhage or signs on chest exam paradDXUS, Kussmaul's signs of infection
of clahylhtion sign, or tracheal daviation or anaphylaxis

treatment should be directed at underlying etiology once it becomes clear

treatment goal is to return critical organ perfusion to normal (e.g. normalize BP)
common treatment modalities include:
fluid resuscitation
inotropes (e.g. dobutamine), vasopressors (e.g. norepinephrine), vasopressin
revascularization or thrombolytics for ischemic events

Infection/Sepsis
the leading cause of death in noncoronary ICU settings is multi-organ failure due to sepsis Efllcl oll......awilll Law 0.. of
treating sepsis is one of the biggest challenges faced by ICU staff as the underlying
IIGIIIIty ill'llilllll with 511* Shallt
pathophysiology of this condition is not fully understood JW4 211112; 288:8&271
the predominant theory is that sepsis is attributable to uncontrollable immune system activation lludy: l'lll:abo-QIOO"a..d, IIIJibrillld, daubltlbind
formal definitions for sepsis-related terms are as follows: M:ome Rlitf.
infection: pathologic process caused by the invasion of normally sterile tissue or fluid by 300 plllierQ Ql Mil
llpliclllock.
pathogenic or potentially pathogenic microorganisms l'lliun!IW111111111dantrlllipd111
bacteremia: the presence ofviable bacteria in the blood 11C8M li1lm HC (50 q&hllllll FC (50 mg Q24hl
Systemic In11ammatory Reaponae Syndrome (SIRS): clinical insults, including both .. pllcebo flll7
infectious and noninfectious entities that result in a generalized inflammatory reaction MllaryO..... 28-diY 111rviwl in pililru
relltite llhnll illiiJftGenc:y lnanresponden 111
manifested by two or more of the following: t:alticubaPn mroollliln llstj.
body temperature >38.50C or <35C llllaltl: (I the 229 nonresponden, 53% oiJ)IIieab
heart rate >90/min diedinlllenrllidgroup-63\inlhepiUJG
respiratory rate >20/min or PaCOz <32 mmHg GflllP. Tllil c:an.pands 111 I 15." llllliw risk
1llb:tion T111n- no ligliicn
WBC >12000 cells/mL or <4000 cells/mL or >10% bands diftarnca '*- IIAIUPI in the fiii)GIIders.
Sepsis: clinical syndrome defined by the presence of both infection and SIRS and is classified Cancbin: Corticostlroid lherlpy in 1lle ICU
by severity (see Table 31): JICb:IS 11'1J1111ilyMiiaut ldml
severe sepsis: sepsis associated with organ dysfunction, hypoperfusion or hypotension MDII.
septic shock: sepsis with arterial hypotension despite adequate fluid resuscitation
multiorgan dysfunction syndrome: sepsis in the presence of altered organ function such
that homeostasis cannot be maintained without intervention Cri:olllnldl far 'hllill .... Slflillllll
Slptic ShDck
Table 31. Clinical Manifestations of Sepsis
lsu1
Ganel'll Ylrilbles lludy: ,..... . . . Gf 151111domilld llld CJD
Fever ( >38"C) or Hypatherrnia ( <36"C) Arterial hypoxemia (PaO:IfiOz <300) mlomizad lllelfficaty 111
Wat008 moadl in patillds
Heart rate >90/rnin Acute oliguria (urine output <0.5
v.ilb -llplil and llplic shock.
sBP <90 mmHg. MAP <7D, ora sBP d8C111i1Se >40 rmtlg Creatinine increase > D.5 mlfdl llllaltl: Ovlnl1hn-no diffinnce in 2S-diry
Tachypnea Coagulation (INR > 1.5 or aPTT > 60 sees) al CIUIIIDOftllily. of live
Alll!red mental status Ileus (absent bowel sounds) 1rills 111111 used lonJ-tenn klw dole COiticollenids
fluid balance (>2D ml,\g over 24 hrs) Thl'lllltocytopenia (platelet count < 1OD,QOOILI )200lX) mg N)lliluw.ci I $ignifil:lnt benefit in
Hyperglycemia (BG >7.7 mmoL'l) in 1ha absanca of diaba!IJ5 Hyparbilirubinania (pli15ma tolill bilirubin >4 mg/dl or 70 mmoL'l) 28 dly lllllllllily IHil=0.80 95'Jo Cl 0.6HI.95).
Leukopenia (WBC <4,0DII/L) Leukocytosis (WBC > 12.0DII/L) IIIII from 1lis 111bgraup llsg llllclwud al9ificart
Normal \NBC count with >1II% immature fonns 1llb:tion ci IID'Iaity 11'111 inalll8d
TIDUI perfuliol Vllrilbla tiiDCk-..ibydly-.
Plasma C-reactive protein >2 SD above 1he nonnal value
Hyperlactatemia (>1mmoVLI Can&biaal: Thlllck allllannll bllllit
Decreased capillll'f refill or mDtdilg 111 ciJitilliiStlmJids ii2JIIis WHat!riiUid 111
tignificlnt Wily hllarogily. low dCIIIIIId
Table ..ptBd with permi11iall from lsvy MM, Fit MP. Mlrlhlll JC, Abmlm E, Arlgu& D, Cook D, Coh111 J, Opal SM, Vincant J.l, RlnRy G. 2001 SC{;MJESO.VACCP/ lonJ-tenn c:or1ico51enids 11111111o have signilicllt
ATS,ISIS lnlamonll Sepsillllllinitions Confnu:e.CIIUr:'I/Cire Mmle 2003; .bellefitlwplliei'D wi111$111$ia.lkMIM:c r.lher
- h is neecmd 111 ideolly patim with Sllllis
Basic Principles for the Management of Sepsis Ylflo 11M ldranll irdicialcy. Mo-. u.
identify the cause and source of infection: blood, sputum, urine Gram stain and C&S 1ini1D llllttrallmlri llld 1ha oplinal doll
initiate: empiric antibiotic therapy TIIJft r.lher 1rills.
monitor, restore and maintain hemodynamic function
R36 Rnpirology Introduction to Intensive Care Toronto Notes 2011

Early Goal Directed Therapy

... T......._.." early goal-directed therapy that involves adjustments of cardiac preload, afterload and
s-.s.,-.11111 S.plii:Sklct
NEJM 2001; 345(111:1368-77 contractility to balance oxygen delivery with demand provides significant outcome benefits
Studr. RCT rll)ltieols Mh - 181J1is or SIP1ic should be started immediately and completed within 6 hours of recognition of severe sepsis or
shock wf1o llrived II Ul emergency deparlmed
Wllllllllamiltd fD riCIM lllty-11011 dirlclld
septic shock
theApy or s1lndlld thenipy il the emergency patient should meet sms criteria and sBP <90 mmHg or lactate >4 mmolJL
depllllnant 1. supplemental oxygen intubation and mechanical ventilation
Ea!ty-goll diad 'dlerlvf Qllllisted 2. central venous and arterial catheterization
ri!Pdic tqatment god! in the inDIIIix rl
trnllrWil Specific god! Mill u labw:
3. if CVP <8 mmHg then crystalloidlcolloid fluid IV to maintain CVP 8-12 mmHg
CVP: 1-12 rrmig !Rid Mh llitta' Clyallbd 41' 4. MAP maintained 65-90 mmHg with the use of vasoactive agents
ailoidll 5. if central venous oxygen saturation (Scv02) <70% then
MAP: >65 TTrilg 1nd <90 mrnHg (llld transfusion of red cells until Hct >30%
mop111m11 oriiiiiiOdi1111nJ
SvciJZ: >70ll (lb(d Mil 11wfusiGri rl pRIICs IIIII if Scv02 <70% after transfusion then use inotropic agents
h8molacrit >30, - inmpie IQW).
supportive oxygenation and ventilation using lung-protective regimen
S1ml11111llerlpy in lbe eiTIIIQIIIcydl!)lllment early nutritional support: enteral route is used to preserve function of intestinal mucosal barrier
conlnd Df-mng MAP >65, CVP batw. control hyperglycemia with insulin to decrease infectious complications
8-12 ll1d llineiiiiJIIf >0.5 mWklltllr.
RMIIIII: 1hl in-llaspilll morldtyfor plliara
physiologic dose corticosteroid replacement therapy in patients with relative adrenal
lllignld ID alltMIMI dirlelld insufficiency (nonresponders to corticotropin stimulation test)
30.S.. c:ornpllai!D 46.W. in lhe sllndlnl nalieal consider in mechanically ventllated septic shock patients with organ dysfunction requiring
c:n IJUIIP 0.0091. PBtiln1J in lhl vasopressors, despite early goal-directed therapy and appropriate antibiotic therapy
direcled 1bnpy bill impnMd APACHE I
recombinant activated protein C may be considered in patients with severe sepsis or septic
-.1'91ar canlr'II-QlWirl Slbntion,
lower llc1lde conc:enbations, higher pH, and shock with an APACHE II score >25 despite early goal-directed therapy and appropriate
lawai boa dalicil antibiotic therapy
Cllllbil: EiltMIMI dirlelld thapy pnll'idal DVT/PE prophylaxis
aigniftart benafitJ ID plliiiD ID bolpitll
advanced care planning, including the communication of likely outcomes and realistic goals of
Mil or saplic sliock. l'IIMI!Dmls
hid inped mortlily ..t treatment with patients and families
lin:tion bltwlan 1Uld 72 hem.

Common Drug Overdoses

Table 32. Clinical Presentation and Management of Common Drug Overdoses
01118 0.,..18 Clinical Syndrome Specific Man11ement
AciWninaphen Nausea, vomiting,. RUQ pain, abnonnalli\ler Gastric lavage
enzymB& illd INR, jaWJdice, liver necro5is, Activirted charcoal <4 hrs post ingestion
coagulation defects N-acetytcysteine
Allpllelllmines KTN, tllchycanlia. 1Bchypn1111, anhythmia1, ML Activirted charcoal fur Drill ingestion
VBSUspasm, seizures, diaphoresis, parlllUid Agitatiowseizures: benZDdiazepines
psydlosis KTN: a-entagonists, vasodilators (nitroglycerin,
nifadipilel
Iron Nausea, vomiting,. Gl discomfort, Gl bleed, Whole bowel irrigation, especially Wabdominal x-ray
d'uwsiness, hypoglycemia. shuck, coma. evidence of pills
seizures, melllbolic acidosis. coagulopathy, Shock: Fluid resuscitation. vasopressors
cardiac failure, hepatotoxicity, renal Iron chelating: deferoxamine IV
insufficiency, achloridia
Tricydic: Antid.......-rta CNS: sedation, confusion, seizures, delirillll Prolonged QRS: alkalizing blood (pH 7.5-7.551, IV
Cardiovascular: wide complex MThythmias, sodium bicarbonate
hypDta'Jsion Seizur88: benzcdiiiZ8pines
Hypotension: fluid resuscitation, vasopressors
Salicyllta NausBII, vomiting,. tinnitus, vartigo, 1llchyp111111, Activirted charcoal <4 hrs post ingestion
noii-CII'diac pulrnonawy edema. altnd Alkalize blood with sodiJm bicarbonate
mental status, miKed respiratory alkalosis illd Consider hemodialysis Wpumonary edema, renal
metabolic acidosis insufficiency, sevaraly altered MS or plasma
salicyiBIB concenlnrtion > 100 mgfdl
Toronto Notes 2011 Common Medications Respirolo8Y R37

Common Medications
Tabla 33. Common Medications fur Respiratory DiSNsas
Drug Adult DoH lndicati- Sill Effects

saiiM!InoValmrol 1-2 puffs q4-6h 1111 Bronchodiatcr in IICU!e reversible airway CV (angina, flushing. palpitrions, tachycanlie, can precipitBte
[Vemolin1 ) Oight blue/navy), ob&tndion Afib), CNS (dii'Zin85&. headache, insomnia, nillly), Gl (dianflea.
terbulaline (Bricanyl8 ) nausea, vorriting), rasll, hypokllemie, paroxysmal bronchospasm
salmeterol [Serevent"), 1-2 pulls bid Maintenance tn!atrnent (p!MIItiJn of
farmDIEnil (Oxm1 ) bronchospasm) il chronic obstructiw lung
disease, aslhma
l:ombilltian flutic1110ne llllsalmeterol 1pull lid COPD and astlrna Common: CNS, headache, lizzinea
IAI!g.4Cting!Jia.Z (puiPie liscusl Resp: URll, IJ (NN. diarrhee. paiVdiscomfort oral candiliasis)
agonirtand inllalld Budesmdaand farrno1Brol
carticlllllllllid [Symticort") (red pufrer)
ANTICHOUNERGICS
bronide 2-3 puffs qid Bronchodialor used in COPD, bronclitis l'llpitllions, arDiiety, dii'Ziness, fltigue, headache, nausea, dry
(claar/IJ8en), and mucous memlnnes. urillry retention, increased IDxicity in
tiotropium bromide (Spiriva8 ) I pull qam combilation with other anticholinergic drugs
COmCOSlEROIDS
Inhaled fluticasana (Fiollant') 2-t pulls bid Maintanancatreltment ahsthma Headache, laver, MSK pllin, lJlH throat irrilltion, growth
[orangljpaach) velocity raduction in childrvr\l'adalascanl8, HPA axis
budesonide
2 puffs lid increased pneumonia risk in COPD
ciclasonila (Aivesco111)
1-t pulls 00
beclomethnona 1-t pulls bid (40 11111.
(QVAf!lll, Vancerir'J I-2 puffs bid (80 11111
Syanic pnldnisane [Apo-prednisme1 , mg per day PO Acute ilXICIIbation of COPD; severe. Endocrine (hirsutism, intolerance, Cushing's
Daltlscne") I25 mg q8h parsistant asthma. PCP syndrome, HPA axis supprassion), Gl (increased appetite,
rnethytpOOisolone PI (sodium succilate) lollding dose S'lzltus asthmaticus indigestion), acul (catncts. glaucoma), edema, AVN,
[Depj>-Mml8 , Soi11-MmJ8) 2nlj then O.S.I mflg q6h far osteoporosis, headache. psych (anxiety, insomnia), 111sy bnising
5days
ADJUNCT AGENTS thaaphylina (8ixophyllinlll, 5-13 mlll'kll/dlv PO in Treatment of symptoms oflftftble Gl upset, dianhea. r.vv, anxiety, headache, insomnia,
Theo-JM411 divided doses, max 900 m!Jday aiway obstructioll due Ia COPD muscle cmp, tremot tachycardia, M:s. anflytllnills,
Toxicity: persistant, repelitiv8 vorriling. seizuras
I.EIJIDTRIENE AlfllGDNISTS
montelutast [Sing!Mrl') 10 mg PO ctls. now only MilaIE Prophylaxis and chraric treatment of Headache, dizziness, fltigue, favat rash, dyspepsia,
as ooce daily slow release asthma symptoms

ANTIBIIJIICS - COMIIIINRY ACOUIRED PNEUMONIA

Maaulide l!l'fllromycin 250-5110mgPObidx7-IOd Alternate to doxycyclile or fliiiii'Dquinolone Gl (abdoninal pain, dianhea. WV), headache, jilllonged
azithramycin 500 mg PO OD x710 d
ar. vantricul antJytllnias. hepatic impairment
Gl (cianflea, NN. abda pail), renal flike. deafness
clarithramytin 250-5110 mg PO bid x7-10 d Headllche, rash, Glldianhea, NN. abnormal taste,
heartburn. abda paill, ir.:R!ISed BUN
Doqqdine 100mg PO tidx7-10d Alternate to macrolile or fllonxp.inolone Photosensitivity, rash, urticaria, nphylaxis. dianhee,
tooth ciscolouration in chikhn
Flu.....inDIIIIa levof'macil 500 mg PO OD x7-10 d Altemale to macrolile or doxycycline CNS [dizziness, fever, IVA), Gl (NN. cianhea,
maxilloxacil (Aveloxe) 400 mg PO OD X7d QT

ANTIBIIJIICS- HDSPIW ACOUIRED PNEUMONIA

3rd gen Cephalolparincaltriaxane (Rocaphil8 ) 12 g IV DO x710 d Combine with fluoroquinalana Rash, dianllea, eosinophilia, thrombocytosis, laukapania.
elevated tnmsaninases
Flu.....inDIIIIa ll'lllfllwlcil seaabow Combine with Jrd gen cephalosporin See above
moxilloxacin
Pipncillirt' Suspect Pseudomonas CNS (confusiat, Guwsineas), rash.
Tdit:tarl Hematokljjc platelelaggregation, plllllqed PT.
(Tamcil') positive Caorms)
VancDIIIJiil I g Pllidx 7-10 d Suspect MRSA CNS [chis, drug M), hemat!llogic [eosinaphia), rash,
(Vancocillll] interstitial nephritis, renal flilure, ototoxicity
Maaulide 5110 mg IV OD x2d, then Suspect l.ejjonella See above
5110mg POODx5 d Seeabava
2511-600 mg PO lid X7-10 d
ICU MEDICAliONS
norapirll!lhrile 0.5-30 jlQ!min IV Acute tr,otension Angina, lnl:s'dia. dyspnea. hyper}llypotEnsion, anllythmias
phenylephrine 0.5 !Wmin IV Severe See above
dab uta mine Inotropic support See above
Sllllllivlt/Anllgllil fentanyl (opioid class) SG-100 then Sedation analge$ia Bradycardia. respiratory depression, drowsiness, hypotension
5G-i.Dillitad
prupofol (anesthetic! 1-3 mw'ku then 0.3-5 PI Sedation analgesia A!ua.lndycanlia, lr,,otensian (good far ventilator sed!Din)
See Hectjous !Jseases, 1125 lor the
R38 Rnpirology Landmark Respirology Trials Toronto Notes 2011

Landmark Respirology Trials

Trill Results
Pneumonia NEJM 1978; 298:801-9 Interstitial lung disease subsets have different prognoses and response to
tntatrnll'll (e.g. desquamative but nat usual inlllrstitial pneumonia respond wall to
cDIIicDSIIIroids)
lung Health JAM4 1994; 272:1497-505 Aggressive slllDking intarvantion significantly decreases the ag&-ralated decline in
FEV1 in smokers with mild aiJWaYS obstruction
ARDS Network NEJM 2000; 342:1301-8 Mortality decreased in ARDS patients ventilated with a low tidal volume strategy
Emphysema NEJM 2003; 348:2059-73 lung volume reduction surgery benefits patients with upper lobe diseese and low
Treatment Trial exercise capacity
CPAP and Apnea NEJM 2005; 353:2025-33 CPAP ameliDrlltes symptoms of sleep apnea but does not affect martality in CHF
IB.CAP NEJM 2006; 355: 1763-71 Hilt! sLJYival rate in patients with earty stage lung cancer detected by low dose
CT screening
TORCH NEJM 2007; 356:775-89 Combination of inhaled steroids and lono-acting beta agonists improves COPD
symptoms, reduces exacerbations and shows atrend to lowers mortality
UPLIFT NEJM 2008; 359: 1543-54 TiCJtropilm inproves symptoms of COPD with fewer exacerbations. but do1111 not
affect FEV1 decline

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R40 Rnpirology

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