Is to assess for underlying lung disease: DLCO usually reduced;volumes and flows normal

•CT angiogram to assess lung parenchyma and possible PH

•V/Q scan ± pulmonary angiogram to rule out thromboembolic disease

•serology: ANA positive in 30% of patients with primary pulmonary HTN;other serologic markers can

be used in the appropriate clinical setting

•routine blood work: biochemistry, CBC, TSH, liver function tests, possible HIV test

Treatment

•treatment depends on classification (see Table 19, R1S)

Multldelector Computed Tomography for Acute

Pulmonary Embolism (PIOPEDIITrial)

ItIM 2006;354:2317-232!

Study: Hulticeitre. prospective study

Population:S24 patients with clinicallysaspected

acute PE

Measurements Accuracy of multideiector CIA alone

and combined with venous-phase imaging.

Outcomes: Diagnosis o!PE.

Results: ))3o!824 patients had adequate CTAs for

interpretation. PE was diagnosed in 192 of the 824

patients.Sensitivity was 831(150 of 181 patients.

951Cl 0.76 0.92) and specificity was961(56)

of 592 patents.951Cl 0.93-0.9)). However,the

predictive value of CTA-CTV varied when clinical pretest probablitywas taken into account. PPV of CTA for

high, intermediate and low clinical probability were

961(951Cl 0.78-0.99).921(951Cl 0.84-0.96).and

581(951Cl 0.40-0.73).respectively. NPV of CTA for

high, intermediate, andlowclinical probability were

601(951Cl 0.32-0.83),891(951Cl 0.82-0.93).and

961(951Cl 0.92-0.98) respectively.

Conclusion:CIA iseffective for diagnosing or

deluding PE in accordance with assessment of

clinical pretest probab lity.When clinical probability

is inconsistent with imaging results,further

investigations are required torule out PE.

Prognosis

•morbidity and mortality are high but depend on underlying condition

•survival decreases to approximately 1 yr if severe pulmonary HTN (with rapid progression of

symptoms, frequent syncope, and advanced \V HO functional class), or right heart failure

Pulmonary Embolism

Definition

• mechanical obstruction of the pulmonary vasculature leading to obstruction of blood flow

• can be classified as acute,subacute, or chronic depending on presentation of symptoms relative to

time after initial event

an acute PH can also be classified as massive,sub-massive, and low-risk PH

ri

Etiology and Pathophysiology

• lower extremity deep vein thrombi are the source of most clinically recognized PHs

• less common causes include fat emboli,septic emboli,amniotic fluid emboli, tumour thrombi, and air

emboli

• thrombi often start in calf, but must propagate into proximal veins to create a sufficiently large

thrombus for a clinically significant PH

L J

+

R20 Rcspirology Toronto Notes 2023

Epidemiology

• one of the most common causes of preventable death in the hospital

• VTE affects approximately 1-2 in 1000 adults per vr with approximately one third of first V I E

presentations being due to PE

D-dimer is elevated in patients with

increased age.recent surgery.CA.

inflammation,infection,pregnancy,

and severe renal dysfunction.It has

good sensitivity and negative predktive

value,but poor specificity and positive

predictive value

Risk Factors

• stasis

• immobilization: paralysis, stroke, bed rest, prolonged sitting during travel, immobilization of an

extremity after fracture

• obesity, CHE

• chronic venous insufficiency

• endothelial cell damage

postoperative injury,trauma

• hypercoagulable states

• underlying malignancy (particularly adenocarcinoma)

• CA treatment (chemotherapy, hormonal)

• exogenous estrogen administration (oral contraceptive pill, hormone replacement therapy)

pregnancy, post-partum

• prior history of DVT/PE, family history

• nephrotic syndrome

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

antithrombin/protein C/protein S, antiphospholipid antibody, hyperhomocysteinemia, increased

Factor VIII levels, and myeloproliferative disease

• increasing age

Classic ECG finding of PE is S1-03-T3

(inverted T3).but most commonly only

sinus tachycardia is seen

ClmkalPrediction tileforPulwonary Eabofisa

JItTj-JK;-osi200033:?6-420

els'Criteria

tiskFactors Posts

Coxal signs ofDVT

loBorelitlyalterable dagrass 10

I—obiizaio- orsirgerjc peeress 15

3.0

Jo. Investigations (if highly suspicious, go straight to CT pulmonary angiogram)

• see Emergency Medicine, ER33 PrenossPEDlfT 15

Hi >100 beKsri' -

Heooptps

atgaatq

15

Table 21. Common Investigations for Pulmonary Embolism 10

Investigation Purpose/Utility 10

Pulmonary Angiography (Gold Filling defect indicative of embolus:negative angiogram excludes clinically relevant PE

Standard)

CKaicalProbability

It*

(0-2)

ttencedaS(3-6)

Hrgtpfi)

31

More invasive,and harder to perform UtanCl,therefore done infrequently ::

Highly sensitive D-dimer result can exclude DVT/PE tf pretest probability is already low

Little valueif pretest probability is high

If D-dimer positive,will need further evaluation with compression UIS(for DVT) and/or CT (for PE)

D-Dimer 701

HoKalHb:HFtHy:st PE wAdy

JAMA 2006

CT Angiogram Both sensitive and specific for PE

Diagnosis and management uncertain for small filling defects

CT may identify an alternabve diagnosis if PE is not present

CT scanning of the proximal leg and pelvic veins can be done at the same time and may be helpful

Virchow's Triad

• Venous stasis

• Endothelial cell damage

• Hypercoagulable states

Venous Duplex ll/S or Doppler With leg symptoms

Positive test rules in proximal DVT

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 calf DVT

ECG Findings not sensitive or specific

Sinus tachycardia most common:may see non-specific ST segment andIwave changes

RV strain.RAD. right bundle branch block (RBSS).SI 03 13 with massive embolization

CXR Frequently normal;no specific features

Atelectasis (subsegmental).elevation of a hemidiaphragm

Pleural effusion:usuallysmall

Hampton's hump:cone-shaped area of peripheral opacification representing infarction

Westermark'ssign:dilatedproximal pulmonary artery with distal ol.gemia decreased vascular markings

(difficult to assess without prior films)

Dilatation of proximal pulmonary artery:rare

+

R21 Respirology Toronto Notes 2023

Table 21. Common Investigations for Pulmonary Embolism

Investigation Purpose/Utility

P Bile Out Criteria (PERC)

Prospective Multicentre Evaluationol the

hlaoiary Embolism Rule Out Criteria

JUrorcb Herns

’

.2008:6:772

•IgeesstbaSOyr

- Senrate less than100 bpm

- Ogteaogofc saturation >95 percent

•lote=op^

sis

•toestrogen use

•tojrotDflorPE

•Race ateral teg swelling

•to sa-geqr o- Uauma requring huspitalnation

mttc ttre past 4«k

krte PEcan probably be entluded without further

dagnostic testing dthe patient meets ail PERC

crpe-ittDthere is a onclmical suspicion for PE.

accordmgtietteflbe Wells’criteria or a Ion gestalt

arc-pep.ity deter— -ejbythe clinician prior to

dagrsstrctestingforPE.

V O Scan Very sensitive but low specificity

Order scan it:

CXR normal,no C0P0

Contraindication loCE (contrast allergy,renal dysfunction.pregnancy!

Avoid V/0 scan it:

CXR abnormal or C0P0

Inpatient

Suspect massive PE

Results:

Normal:excludes the diagnosis of PE

High probability: most likely means PE present unless pre-test probability is low

60% of V/O scans are nondiagnostic

Echocardiogram Useful to assess massive or chronic PE

Dependent on clinical status

ABC No diagnostic use in PE (insensitive and nonspecific)

May shovr respiratory alkalosis(due to hypenrent alien ) Evaluation of a Suspected Pulmonary

Embolism

Urndmcal probability olembolism

D-dimer (-ve) -» CT scan (+ve) ruled in

(-ve) -*

ruled out

Intermediate or high probability

CT pulmonary angiography scan

(-ve) •ruled out

(

*

ve)»ruled in

Notes:

• Use O-dimers only if low clinical

probability,otherwise, go straight

toCT

• If using V/O seans (CT contrast

allergy or renal failure):

• Negative V/O scan rules out the

diagnosis

• High probability V/O scan only

rules inthe diagnosis if high clinical

suspicion

• Inconclusive V/O scan requires leg

U/S to look for DVT or CT

Treatment

•admit for observation and stratify risk -in low-risk PE setting with no other indication

for hospitalization and low-risk of early adverse outcomes, patients may be sent home with

anticoagulation

•oxygen:supplemental oxygen should be administered to target an oxygen saturation S9() percent

•pain relief:analgesics if chest pain - narcotics or acetaminophen

•acute anticoagulation: therapeutic-dose SC LMVV H or fondaparinux or unfractionated heparin or oral

factor Xa inhibitors(rivaroxaban, apixaban, edoxaban) or direct thrombin inhibitors (dabigatran) -

start ASAP

anticoagulation stops clot propagation, prevents new dots,and allows endogenousfibrinolytic

system to dissolve existing thromboemboli over months;get baseline CBC,1NR, aPTT ± renal

function ± liver function

for SC LMWH:dalteparin 200 U/kg once daily, enoxaparin 1 mg/kg BID, or fondaparinux 5-10

mg once daily - no lab monitoring - avoid or reduce dose in renal dysfunction

for IV heparin:bolus of 75 U/kg (usually 5000 U)followed by infusion starting at 20 U/kg/h -aim

for aPTT 2-3x control

•long-term anticoagulation

• for most nonpregnant patients who do not have renal insufficiency or active cancer,first-line is

direct oral anticoagulants (rivaroxaban, apixaban, edoxaban, or dabigatran) rather than warfarin

• if using warfarin instead ofDOAC:start the same day as LMWH/heparin - overlap warfarin with

LMWH /heparin for at least 5 d and until INR in target range of 2-3 for at least 2 d ( use for patients

with severe renal insufficiency)

LMWH instead of warfarin for pregnancy, active cancer,or high bleeding risk patients

•IV thrombolytic therapy

if patient has massive PE (hypotension or clinical right heart failure) and no contraindications

hastens resolution of PE but may not improve survival orlong-term outcome and doubles risk of

major bleeding

• interventional thrombolytic therapy

massive PE may be treated with catheter-directed thrombolysis by an interventional radiologist

catheter-directed thrombolysis is not recommended oversystemic thrombolysis

•1VC filter:routine use is not indicated; use if recent proximal DVT and absolute contraindication to

anticoagulation

•duration oflong-term anticoagulation: individualized,however generally

• if reversible cause for PE (e.g.surgery, injury, pregnancy,etc.):3-6 mo

• if PE unprovoked: 6 mo to indefinite

• if ongoing major risk factor (active cancer, antiphospholipid antibody, etc.): indefinite

Workup for Idiopathic Venous

Thromboembolism

Thrombophilia workup: recurrent or

idiopathic DVT/PE. age <50. FMHx.

unusual location,massive

Malignancy workup:12% of patients with

idiopathic VTE will have a malignancy

The Useof Unfractionated Heparin

Should Be Limited to:

• Patients with severe renal

dysfunction (CrCI <30 ml/min)

in whom LMWH and novel oral

anticoagulation should be avoided

• Patients at elevated risk of bleeding

that may need rapid reversal of

anticoagulation

• Patients who receive thrombolytic

Thromboprophylaxis therapy

•mandatory for most hospital patients: reduces DVT, PE.all-cause mortality, cost-effective

•start ASAP

•continue at least until discharge or recommend extending for 35 d postoperatively, if major

orthopaedic surgery

r n

c.J

Sri landra-s 10M Resorology Trials table for mote

jr~at o- 0‘EPSTEIN-CHOiCE which details the

eicacj of *< aroiaOanw.ASA in patients v/ith VTE

ir.Q co-Dieted a 6-12 mo course of anticoagulation

tirercTf.

+

R22 Respiredogy Toronto Notes 2023

Table 22. VTE Risk Categories and Prophylaxis (see Hematology, H36)

DirectOral Antimagulaas Comparedwib

VitaminK Antagonists (VICAsI for AcuteVeoMS

Thromboembolism:Evidence fromPhase 3Trials

Bood 2014:124:1968-1975

Study:Meta-anaysrs ofachase3 -j-ej-adart-ped

Risk Group Prophylaxis Options

low Thrombosis Risk

Medical patients:fully mobile

Surgery:<30 min.fully mobile

No specific prophylaxis

frequent ambulation trials

Population:27023 jaientsirii VTE

Intervention:OOJtCs reiaisVKAs

Outcomes:Cveralefficacy.safey sena.ardretcr cal

bench!torthetreafciedofaccSsymncscVIE

Results:RacurrentHIacxedrID1

;r OOSC recoents

compa-tdwi'Ji22%nVXA reepeds|58030.56% 0

0.77-1.06).TreatneSnthaDMsynercy reducedbe

risk olmajor bleedng(M03155%Cl0.4S0.83).

Conclusions DOlCsandi'

lisfa.eas- arefecy

in thebeacment of acu#syopfcmaxKitbonnet,

treahnentwithaDOJCsgcficartly reducesBensksof

major heeding.

Moderate ThrombosisRisk

Most general,gynaecologic,urologic surgery

Sick medical patents

LMWH

Low dose unfractionated heparin

fondaparinux

High ThrombosisRisk

Arthroplasty,hip fracture surgery

Major trauma,spinal cord injury

IMWH

fondaparinux

Warfarin (INR 2 3)

Dabrgatran

Apixaban

Rhraroxaban

Low dose unfraclionated heparin

Scleroderma is the most likely collagen

vascular disease to lead to pulmonary

involvement which can indudeILD and

pulmonary HTN High Bleeding Risk

Neurosurgery,intracranial bleed TED stockings'

.pneumatic compression devices

Active bleeding LMWH or low dose heparin when bleeding risk decreases

Horner’s Syndrome

Ptosis. Miosis.Anhidrosis

Pulmonary Vasculitis

Table 23. Pulmonary Vasculitis

Disease Definition Pulmonary Features Extra Pulmonary Features Investigations Treatment

Granulomatosis with

Polyangiitis (ERA.

previously Wegener's

Granulomatosis)

(see Nephrology.NP25.

NP26.and NP29)

Systemic vasculitis of medium

and small arteries,most

common pulmonary vasculitis

Focal necrotizing lesions of

arteries and veins:mayhave

nasal,sinus,and ear disease:

crescentic glomerulonephritis

CXR/CT:nodules,cavities,and

alveolar opacities

c-ANCA (positive in90% of

cases)

Corticosteroids and

cyclophosphamide or rihuimab

Plasma Exchange (FLEX)is

also used often in cases of

pulmonary hemorrhage,severe

renal failure.or concomitant

anti-GBM

Prognosis with treatmentis

generally good (65-90% achieve

full remission)

Necrotizing granulomatous

lesions of the respiratory

tract,which may lead to

tracheal and/or bronchial

stenosis,nodules.ILD.or

alveolar hemorrhage

PR3

Tissue confirmation

Urinalysis:look for abnormal

sedimentation

Life-threatening systemic

vasculitis involving thelongs,

pericardium and heart kidneys,

skin,andPNS (mononeurits

multiplex)

Eosinophilic

Granulomatosis with

Polyangutis (EGPA.ChurgStrauss)

Multisystem disorder

characterized by allergic

rhinitis,asthma,andprominent

peripheral eosinophilia

Asthma (prodromal phase,

usually occurs before other

systemic features)

Eosinophilic infiltrates in

smali-and- medium sized

vessels

CXR can often be normal

(30-60%) but can see transient. Cyclophosphamide (Use five

patchy opacities

Peripheral eosinophilia is the

most common finding

p-ANCA.myeloperoxidase

(MPO) may be positive

Biopsy involved tissue

CXR:may see alveolar

infiltrates

EUSA test with anti-GBM

antibodies

Renal biopsy/indirecl

immunofluorescence shows

linear staining

Corticosteroids

factor Score to determine need)

With treatment.90% of patients

have clinical remission

Anti-GBM Disease

(Goodpasture's)

(seeNephrology.NP24)

A disorder characterized by

diffuse alveolar hemorrhage

and glomerulonephritis caused

by anti-GBM antibodies,which

cross-readwith basement

membranes of the kidney

and lung

See Rheumatology.RH11.RH8.

and RH14

Alveolar hemorrhage,which

may present withdyspnea,

cough,hemoptysis

May follow influenza

infection

Anemia

Acute renal failure

Acutely:corticosteroids,

plasmapheresis,

immunosuppressive therapy

Severe cases:bilateral

nephrectomy

Systemic lupus

Erythematosus.

Rheumatoid Arthritis.

Scleroderma

Pulmonary Edema

r i

L J

• see Cardiology and Cardiac Surgery,C42

+

R23 Rcspirology Toronto Notes 2023

Diseases of the Mediastinum and Pleura

Mediastinal Masses Differential of an Anterior

Compartment Mass

• see General and Ihoracic Surgery.(iS13 4 %

Thymoma

Thyroid enlargement (goitre)

Teratoma

Tumours (lymphoma,parathyroid,

esophageal,angiomatous)

Mediastinitis

• most common causes:postoperative complications of cardiovascular or thoracic surgical procedures

Acute

• etiology

perforation of esophagus or trachea -vomiting (Boerhaave’

ssyndrome), penetrating trauma,

foreign body, instrumentation, erosion (e.g. carcinoma,infection)

direct extension of infection -dental,lung, pleura, pericardium,lymph nodes, paraspinous,

pancreatic

postoperative (sternotomy or mediastinoscopy)

primary mediastinal infections (e.g. inhalational anthrax)

• signs and symptoms

fever,substernal pain; often a dramatic and acute onset ofsymptoms,with irritability,

restlessness, and a sense of impending doom

pneumomediastinum, mediastinal compression

Hamman’

ssign (auscultatory “crunch” during cardiac systole)

• treatment

antibiotics (IV vancomycin + 3rd gen cephalosporin), drainage, ± surgical closure of perforation

Mediastinal Components

• Anterior sternum to pericardium

and great vessels.Indudes:thymus,

extrapericardiat aorta and brandies,

great veins,lymphatic tissues

• Middle:pericardium (anteriorty).

posterior pericardial reflection,

diaphragm,thoracic inlet Indudes:

heart intrapericardial great vessels,

pericardium,trachea

• Posterior:posterior pericardial

reflection,posterior border of

vertebral bodies,first rib to the

diaphragm.Includes:esophagus,

vagus nerve,thoracic duct

sympathetic chain,azygous venous

system

Pleural Effusions

Definition

• excess amount of fluid in the pleural space

Etiology

• disruption of normal equilibrium between pleural fluid formation/entry'and/or pleural fluid

absorption/exit

• pleural effusions are classified as transudative or exudative

distinguish clinically using Light’

s Criteria (98% sensitivity and 83% specificity for identifying

exudative pleural effusions)

Starting'shypothesis:The rate

of passive fluid movement across

a capillary waB is governed by the

gradients of hydrostatic pressure and

oncotic pressure across the same

capillary wall

Table 24. Laboratory Values in Exudative Pleural Effusion

Light's Criteria Modified Light's Criteria

Protein -Pleural/Serum

LDH -Pleural/Serum

Pleural LDH

Exudate = any one criterion

MIS >0.5

>0.6 >0.6

>2/3 upper limit of H serum LDH >0.45 upper limit of N serum LOH

Ann Intern Med1979:77:507-513

Chest1997:111:970-980

Transudative Pleural Effusions

• pathophysiology: alterations toStarling forces affects the rates of formation and absorption of pleural

fluid

• etiology

CHI'

:usually bilateral, right-sided more than the left, can occasionally be isolated right-sided

cirrhosis leading to hepatic hydrothorax (diaphragmatic deficit allows fluid into chest cavity)

« nephrotic syndrome, protein losing enteropathy

pulmonary embolism (may cause transudative but more often causes exudative effusion)

peritoneal dialysis with transdiaphragmatic flow, hypothyroidism, urinothorax

Transudative effusions are usualy

bilateral,not unilateral

Exudative effusions can be bilateral or

unilateral

Exudative Pleural Effusions

• pathophysiology:increased permeability of pleural capillaries or lymphatic dysfunction r

+

R2-I Respirology Toronto N'

otcs 2023

Table 25. Exudative Pleural Effusion Etiologies

Etiology Examples

Appearance of Pleural Fluid

• Bloody:trauma, malignancy,

traumatic tap

• White:empyema, chylous,or

chyliform effusion

• Black: aspergillosis, amoebic liver

abscess

• Yellow-green:rheumatoid pleurisy

• Viscous: malignant mesothelioma

• Ammonia odour: urinothorax

• Food particles: esophageal rupture

Infectious Parapneumonic effusion (associated withbacterial pneumonia,or other process such as lung abscess)

Empyema:bacterial,fungal.IB

IB pleuritis

Viral infection (rare)

Fungal

Parasitic

lung carcinoma (35%)

lymphoma (10%)

Metaslases:breast (25%). ovary,kidney,other

Mesothelioma

Malignancy

Myeloma

Collagen vascular diseases:RA.SIE

Pancreatitis

Benign asbestos related effusion

Pulmonary embolism

Post-coronary artery bypass grafting or cardiacinjury

Drug reaction

Inflammatory

Subphrenic abscess (sympathetic effusion)

Pancreatic pseudocyst with fistula into pleuralspace (associated with elevated pleural fluidamylase)

Meigs'

syndrome (ascites and hydrothorai associated with an ovarian fibroma or other pelvic tumour)(can also

be a transudate)

Intra-Abdominal

Intra-Thoracic Esophageal perioralion (associated with elevatedpleural fluid amylase)

Hemothorax:rupture of a blood vessel,conn-onlyby trauma or tumours

Pneumothorax:spontaneous,traumatic

Chylothorax (thoracic duct leak)

Iatrogenic

Trauma

Other Drug-induced

Hypothyroidism (can also be transudate)

Signs and Symptoms

• often asymptomatic

• dyspnea: varies with size of effusion and underlying lung function

• pleuritic chest pain,shoulder pain ( referred pain from the phrenic nerve, C3-C5, which innervates the

diaphragm)

• inspection:ipsilateral decreased expansion; when accumulated rapidly, trachea can deviate away from

effusion

• palpation:decreased tactile fremitus

• percussion:dullness

• auscultation:decreased breath sounds;bronchial breathing and egophony just above fluid level,

sometimes pleural friction rub if inflammatory cause and minimal fluid

Role of CT in Pleural Effusion

• To assessfor fluid loculation. pleural

enhancement, thickening and

nodules, parenchymal abnormalities,

and adenopathy

• Can provide clues to help distinguish

benign from malignant effusion

• May not distinguish empyema from

parapneumonic effusion

Features of Mesothelioma

• Multiple pleural nodules

• Circumferential pleural thickening

>1 cm

• Mediastinal pleural involvement

Investigations

. CXR

must have >200 m L of pleural fluid for visualization on PA film

• PA:blunting of lateral costophrenic angle

• lateral:>50 mL leads to blunting of posterior costophrenic angle

• dense opacification of lower lung fields with concave meniscus as fluid accumulates

• decubitus:fluid will layer out unless it is loculated

• supine:fluid will appear as general haziness over lung field

• CT: helpful in differentiating parenchymal from pleural abnormalities; identifying loculation.

measuring density of fluid (higher density may indicate a hemothorax); contrast can detect pleural

enhancement indicative of empyema and may identify underlying lung pathology causing effusion

• VIS: detectssmall effusions and can guide thoracentesis

• thoracentesis:indicated if pleural effusion is a new and concerning finding, if patient is unstable,and/

or if patient has pneumonia and there is a concern about infected parapneumonic effusion;order

blood work (serum LDH,glucose, protein, albumin) at the same time for comparison

risk of re-expansion pulmonary edema if >1.5 L of fluid is removed in one shot through a closed

Imaging Features of Empyema

• Parietal pleural thickening

• Pleural enhancement

• Concurrent thickening and

enhancement of both the visceral

and parietal pleural (split pleural

sign)

tap

• inspect for colour, character, presence of pus, and odour of fluid

send fluid for analysis (see T able 26)

• pleural biopsy: indicated if suspect IB, mesothelioma, or other malignancy (and if cytology nondiagnostic)

+

R25 Rcspirology Toronto Notes 2023

Table 26. Analysis of Pleural Effusion

Measure Purpose

Always order:

Protein,LDH Transudate vs.eudate

LDH especially high (>1000 IU/L)in empyema,rheumatoid,malignancy

Protein especiallyhighin 16.myeloma

Gram Stain.liehl-Neelsen Stain (T6).Culture Looking for specific organisms lean add ZieM-Neelsen Stain if 16 suspected)

Neutrophils vs.lymphocytes (lymphocytic effusion inIB.cancer,lymphoma.RA)

Eosinophilic (seen in pneumothorax,hemothorax,drug reactions,pulmonary embolism,

eosinophilic granulomatosis with polyangutis.asbestos-related,malignancy,parasitic,

occasionally IB)

High R 6C count:mostly traumatic,malignancy.PE with infarction.IS.hemothorax

Malignancy

Low (fluidiserum <0.5) inrheumatoid.16.empyema,malignancy,esophageal rupture

Normally about 7.6

Very low (<7.0) inempyema,TB.rheumatoid,malignancy,esophageal rupture

Complicated Parapneumonic Effusion

(needs drainage if any of these are

present):

• Loculation

• >1/2 hemithorax of fluid

. pH <7.2

• Glucose<2.2 mmol/L

. LDH>1000

• Gram stain or culture positive

• Frank pus

Cell Count Differential

Cytology

Glucose Empyema (always needs drainage)

Frank pus on tap

May or may notbe loculated,and will

often fulfill many of the criteria of a

ComplicatedParapneumonic Effusion

pH

May order (depending onclinical suspicion):

Albumin Albumin gradient for higher specificity assessment for exudate (compared to Light's criteria

alone)

Pancreatitis,esophageal perforation,malignancy

Collagen vascular disease

Chylothorax from thoracic duct leakage,mostly due to trauma,lung CA.or lymphoma

Distinguish between chylothorax and chyliform effusion (latter seen in inflammation,e.g.16.

Amylase

Rheumatoid Factor.ANA,Complement

Triglycerides

Cholesterol,chylomicrons

RA)

Treatment

• thoracentesis

• tube drainage if required

• early tissue plasminogen activator (tPA)/deoxyribonudease ( DNase) instillation to improve drainage

of infected effusions

• treat underlying cause

• consider indwelling pleural catheter or pleurodesis in refractory'chronic effusions

• consultation with thoracic surgery for potential surgical management

When possible,organism-directed

therapy,guided by culture sensitivities

or local patterns of drug resistance

should be utilized

Complicated Parapneumonic Effusion

General and '

• see Ihoracic Surgery,GS17

Empyema

• see General and Ihoracic Surgerv. GSI7

Atelectasis

• see General and Ihoracic Surgery.(IS11

Pneumothorax

• see General and Ihoracic Surgery.GS17

Asbestos-Related Pleural Disease

Etiology and Pathophysiology

• non-malignant manifestations of asbestos exposure:

• BAPE

Need to Rule Out Life-Threatening

Tension Pneumothorax

If pneumothorax with:

• Severe respiratory distress

• Tracheal deviation to contralateral

» exudative effusion, typically -10 yr after exposure, often resolves on its own

• pleural cytology is needed to distinguish from mesothelioma or pleural extension of other

malignancies side r m

iJ

• Distended neck veins (» JVP)

• Signs of hemodynamic instability

(eg.hypotension)

• asbestosis

low lobe 1LD (appearsthe same as 1PE)

• round atelectasis

commonly seen peripherally, due to asbestos-pleural disease

• calcified pleural plaques and/or pleural thickening

• marker of exposure; usually an asymptomatic radiologic finding

Do not perform CXR

Needs immediate treatment

See Emergency Medicine,ERT1and ER22

+

R26 Respirologv Toronto Notes 2023

Mesothelioma

Etiology and Pathophysiology

• primary malignancy of the pleura

• decades after asbestos exposure (even with limited exposure)

• smoking not a risk factor, but asbestos exposure and smoking synergistically increase risk of lung

cancer

Signs and Symptoms

• chest pain, dyspnea, cough, bloody pleural effusion, and weight loss

• there can be associated paraneoplastic syndromes (e.g. hypercalcemia, hemolytic anemia,

hypoglycemia)

Investigations

• CT thorax

• biopsy (pleuroscopic or open)

• needle biopsy may seed needle tract with tumour

Treatment

• use of multidisciplinary team with trimodal treatment (e.g. chemotherapy, radiation,surgical

resection)

• palliation is often needed because of poor prognosis

Respiratory Failure

Definition

• failure of respiratory system to maintain normal gas exchange (oxygen and carbon dioxide

homeostasis)

• hypoxemia (PaO> <60 mmHg), hypercapnia (PaC02 >50 mmHg)

• acute vs.chronic (compensatory mechanisms activated)

Signs and Symptoms

• signs of underlying disease

• hypoxemia:restlessness, confusion, cyanosis, coma, cor pulmonale (if chronic)

• hypercapnia: confusion, headache, dyspnea,drowsiness, asterixis, warm periphery, plethora,

increased ICP (secondary to vasodilatation)

Investigations

• ABGs

• CXR and/or Cl'

• pulmonary function tests (for chronic respiratory failure)

Hypoxemic Respiratory Failure

Definition

• PaO:decreased, PaCOi normal or decreased

Treatment

• reverse the underlying pathology

• oxygen therapy: maintain oxygenation (ifshunt present,supplemental 02 is less effective) using

O’

delivery systems (see Anesthesia, A10)

• ventilation, BiPAP,and PEEP/CPAP (seeAnesthesia, All): positive pressure can recruit alveoli and

redistribute pulmonary edema fluid

• improve cardiac output:± hemodynamic support (fluids, vasopressors, inotropes) (increases O’

delivery), reduces 0’

requirements

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R27 Respirology Toronto Notes 2023

Table 27. Approach to Hypoxemia

Ventilation, BiPAP, Increasing

Cardiac Output

Type of

Hypoxemia

Settings PaCOr AaO; Oxygen

Therapy and PEEP

1. tow FiOi No change

No change

High altitude

2. Hypoventilation Drug overdose,obesity, t

hypoventilation

syndrome

Nor a N Improves

Improves

No change

Improves with

ventilation

N

3. Physiologic AROS. pneumonia

Shunt ^ V/0

mismatch with

lowV

4. Anatomic Shunt Ventricular septal delect N o r a

(Right to loft)

5. low Mixed Shock

Venous Or Content

6. Dillusion

Impairment

Nor a t Less ellective Improves No change

Can worsen by

increasing shunt

Can worsen by reducing Improves

cardiac output

Improves with positive No change or

pressure

t No change Can worsen

Improves or no

change

Improves

a t

IIP. emphysema N t

worsens

'Where "N" » withinnormal limits.A-aOr

*

Alveolar-arterial gradient

Reprinted with permission from Or.IanFraser

Hpercapnic Respiratory Failure

Definition

• PaCO:increased, PaO:decreased

Dead Space

• Ventilation without perfusion

• The opposite of shunt

Pathophysiology

• increased CO:production:fever,sepsis,seizure, acidosis, carbohydrate load

• increased dead space (normal or increased minute ventilation, low alveolar ventilation):COPD,CP,

chest wall disorder, dead space ventilation (rapid shallow breathing)

inefficient gas exchange results in inadequate CO:removal in spite of normal or increased minute

ventilation

• hypoventilation (low minute ventilation)

restrictive processsuch as chest wall disorder (e.g.severe kyphoscoliosis)

central:brainstem stroke, hypothyroidism,severe metabolic alkalosis, drugs (e.g.opiates,

benzodiazepines)

neuromuscular: myasthenia gravis,Guillain-Barre, phrenic nerve injury,muscular dystrophy,

polymyositis

muscle fatigue

Causes of Hypercapnia

• Low total ventilation

• High dead space ventilation

• High COvproduction

In chronic hypercapnia, supplemental O2

may worsen hypoxemia by worsening

V/O mismatch,Haldane effect,and/or

decreasing respiratory drive (in order of

physiologic importance): but do not deny

oxygen if the patient is hypoxic

Treatment

• reverse the underlying pathology

if PaCO:>50 mmHg and pH <7.35 consider noninvasive or mechanical ventilation

• correct exacerbating factors

• nasotracheal/endotracheal tube suction: clearance of secretions

• bronchodllators:reduction of airway resistance

• antibiotics:treatment of infections

• reverse medications that may be contributing (e.g. narcotics)

• maintain oxygenation (see above)

• diet: increased carbohydrates can increase PaCO:in those with mechanical or limited alveolar

ventilation; high lipids decrease PaCO:

In COPD patients with chronic

hypercapnia ("COJ retainers"),provide

supplemental oxygen to achieve target

SaOa from 88 92%

Acute Respiratory Distress Syndrome

Definition

• clinical syndrome characterized by severe respiratory distress, hypoxemia, and noncardiogenic

pulmonary edema

•

'

1 he Berlin Criteria for ARDS

• acute onset

within 7 d of a known clinical insult or of patient noticing new or worsening of respiratory

symptoms

usually occurs within 72 h of presumed trigger

bilateral opacities consistent with pulmonary edema on either CT or CXR

• not fully explained hv cardiac failure/fluid overload, but patient may have concurrent heart failure

• objective assessment of cardiac function (e.g echocardiogram) should be perfumed if no clear risk

factors

Acute Lung Injury

ALI is an outdated term that has the

same definition as ARDS but with a

PaOj/FiOj <300. The Berlin Definition

removed ALI and replaced It with the

term mild ARDS

ri

1J

+

R28 Rcspirology Toronto Notes 2023

Etiology

• direct lung injury

• airway: aspiration (gastric contents,drowning), pneumonia, inhalation injury (oxygen toxicity,

nitrogen dioxide,smoke)

circulation: embolism (fat,amniotic fluid), reperfusion injury

• indirect lung injur>’

• circulation:sepsis,shock, trauma, blood transfusion, pancreatitis

neurogenic: head trauma, intracranial hemorrhage, drug overdose (narcotics,sedatives, tricyclic

antidepressants)

Pathophysiology

• disruption of alveolar capillary membranes > leaky capillaries -> interstitial and alveolar pulmonary

edema -> reduced compliance. V/Q mismatch,shunt, hypoxemia, pulmonary HTN

Categorization of ARDS as Mild.

Moderate or Severe - The Berlin

Criteria

AIDS Severity PaO.F.O , Mortality

l«n»|H r (95.

» Cl|

Mild 200300

100 200

27 (24-30|%

32 (29-34) •

«5 (A2 48)%

Moderate

Serere < 100

MtJinHjOKIMMIOOl

MIU »17.307:JMMM1

Clinical Course

A. Exudative Phase

• first 7 d of illness after exposure to ARDS precipitant

• alveolar capillary endothelial cells and type 1 pneumocy tes are injured, resulting in loss of normally

tight alveolar barrier

• patients develop dyspnea, tachypnea, increased work of breathing

these result in respiratory fatigue and eventually respiratory failure (see Hypoxemic Respiratory

Failure, R26 )

B. Fibroproliferative Phase

• after day 7

• may still experience dyspnea, tachypnea,fatigue, and hypoxemia

• most patients clinically improve and are able to wean off mechanical ventilation

• some patients develop fibrotic lung changes 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, R35)

• treat underlying disorder (e.g.antibiotics if infection present)

• mechanical ventilation using low tidal volumes (<6 mL/kg) to prevent barotrauma

use optimal amount of PEEP to keep airways open and allow the use of lower FiOi

may consider using prone ventilation, ± inhaled nitric oxide,short term paralytics (<48 h) or

ECMO (extracorporeal membrane oxygenation) if conventional treatment is failing

• fluids and inotropic therapy (e.g.dopamine, dobutamine) if cardiac output inadequate

• pulmonary-arterial catheter now seldom used for monitoring hemodynamics

• mortality: 30-40%, usually due to non-pulmonary complications

• sequelae of ARDS include residual pulmonary impairment,severe debilitation, polyneuropathy and

psychological difficulties, which gradually improve over time

• most survivors eventually regain near-normal lung function, often with mildly reduced diffusion

capacity

Risk Factors for Aspiration

Pneumonia

Categories Examples

Decreased level o< Alcoholism

consciousness

Upper 61 tract disoeders Drsphagia.esoptiageal

disorders

Intubation, nasogastric

tube,feeding tube

neurologic conditions Dementia.Parkinson'

s

disease

Protracted vomiting

Mechanical

instrumentation

Others

Neoplasms

Lung Cancer

• see (

icncr.il and Ihnr.tcic Surgery.(iSU

Approach to the Solitary Pulmonary Nodule

• sec Medical 1 mayinn. Lung Abnormalities,MI7

• see General and ’

thoracic Surgery, GS13

r -t

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R29 Rcspirology Toronto Notes 2023

Sleep-Related Breathing Disorders

Hypoventilation Syndromes

Definition

•group of syndromes characterized by hypoventilation during sleep, though daytime hypercapnia may

also be a feature

•superimposed sleep apnea may be present

•categories of hypoventilation syndromes include: medical disorders, lung parenchymal or airway

disease (typically severe), chest wall disorder (deformity such as kyphoscoliosis), neurologic disorder

(brainstem lesions), respiratory muscle weakness (neuromuscular disease, myopathy), medications

(opiates and othersedatives),obesity-hypoventilation syndrome (Pickwickian syndrome:BM1 >30

kg/m 2and no other cause of hypoventilation identified), congenital central alveolar hypoventilation

syndrome, idiopathic hypoventilation syndrome

Treatment

•management of the underlying condition

•usually PAP therapy (frequently BiPAP, which delivers ventilation in addition to airway splinting)

Normal Respiratory Changes during

Sleep

. Tidal volume decreases,leading to

decreased minute ventilation

• PaCOi increases (due to decreased

minute ventilation)

• Pharyngeal dilator muscles relax

causing increased upper airway

resistance

Sleep Apnea

Definition

• episodic decreases in airflow during sleep

• quantitatively measured by the Apnea-Hypopnea Index (AH1)

= # of apneas and hypopneas per hour

ofsleep

• sleep apnea generally accepted to be present if AH1 S5 events/h

• AH1: Mild OSA 5-15 events/h, Moderate 15-30 events/h, Severe >30 events/h

• Apnea:reduction in airflow >90%

from baseline,lasting for >10s

. Hypopnea:reduction in airflow

z30% from baseline,lasting for >10 s.

associated with oxygen desaturation

>3% or EEG arousal

. Hyperpnea:period of increased

ventilation,typically in thecontext of

resumption inbreathing,following an

apnea or hypopnea

• Obstructive apnea: absent airflow

despite respiratory effort due to

upper airway occlusion

• Central apnea:absent airflow,due

to absent or reduced respiratory

effort

• Mixed apnea:absent airflow,

with features of both central and

obstructive events

Classification

• obstructive sleep apnea

caused by transient, episodic obstruction of the upper airway

absent or reduced airflow despite persistent respiratory effort

• central sleep apnea (see Neurology, N49)

hypercapnic CSA caused by transient, episodic decreases in CNS drive to breathe, typically seen

in patients with sleep hypoventilation syndromes (see Hypoventilation Syndromes)

hypocapnic CSA, most commonly Cheyne-Stokes breathing, typically seen in patients with

congestive heart failure and sometimes stroke;characterized by a crescendo-decrescendo pattern

of alternating apnea and hyperpnea

• some patients exhibit a combination of obstructive, central and, mixed apneas (sometimes referred

to as‘complex sleep apnea"). Typically this involves ventilatory overshoot following an obstructive

apnea, resulting in hypocapnia,loss of respiratory drive, and consequently a central apnea

SLEEP TESTING

Treatment of AdultObstructiveSleep Apaeiwith

Positive Airway Pressure:AnAmericanAcademy

of Sleep Medicine Systematic Review, MetaAnalysis,and GRADE Assessment

JDim SleepMeil 2019:15:301 33d

Purpose:Toprovide Supporting evidence for the

clinical practice guidelines for the treatment of OSA in

adults usingPAP.

Methods: Systematic review including ltdstudies

comparing use of PAP withno treatment and studies

comparing differentPAPmodalities.

Conclusions:Tire data demonstrated thatPAP

compared to no treatmentresultsina clinically

signibcanlreduction in disease severity,sleepiness,

blood pressure,motor vehicle accidents,and

improvement in sleep-related quality of lifeinadults

with OSA.

Polysomnography

• sleep study, usually in-laboratory with technologist in attendance

• evaluatessleep stages and arousals (using EEG, EGG,EMG), airflow, ribcage and abdominal

movement, ECG,SaOa, limb movements,snoring, body position, and video recording

• indications:

evaluation forsuspected sleep disordered breathing in a patient with compatible symptoms or

risk factors

evaluation for non-respiratory causes of excessive daytime sleepiness

evaluation ofselected cases of insomnia and abnormal behaviours during sleep

titration of PAP therapy, to determine optimal settings

assessment of objective response to other interventions (e.g. oral appliances for sleep apnea,

positional therapy)

Home Sleep Apnea Testing

• done in the home, unattended

• evaluates a limited number of parameters primarily focused on the diagnosis of OSA; EEG monitoring

typically not included

• indication: evaluation forsuspected OSA, in patients withoutsignificant cardiopulmonary

comorbidities

+

R30 Respirology Toronto Notes 2023

OSA

Risk Factors

• obesity, craniofacial abnormalities,crowded oropharynx (including enlarged tonsils, large tongue),

short/wide neck (neck circumference >17 inches(>43 cm) for men and >16 inches(>40.6 cm) for

women), nasal obstruction

• more common in males than females (pre-menopause)

Signs and Symptoms

• airway obstruction:snoring, apneas,choking and gasping spells(may be witnessed by a bed partner)

• sleep fragmentation: nocturnal awakenings, nocturia, unrefreshing sleep, daytime somnolence,

irritability, depression, memory loss, morning headaches

Complications

• increased risk of:hypertension, cardiovascular disease (e.g.CAD,CHF, arrhythmia),stroke, motor

vehicle collisions, polycythemia, pulmonary hypertension, type 2 DM

Treatment

• modifiable factors:weight loss, decreased alcohol/sedatives, treatment of nasal congestion (usually

modest effect),avoidance of supine sleep

• CPAP very effective but can be limited by compliance

• oral appliances typically less effective at reducing AH1 but better tolerated by some patients

• surgical intervention can be helpful in select patients (e.g. tonsillectomy, tongue base and jaw

procedures, tracheostomy)

CSA

Risk Factors

• hypercapnic CSA: underlying disorder causing sleep hypoventilation syndrome (see Hypoventilation

Syndromes, R29 )

• non-hypercapnic CSA (mostly Cheyne-Stokes breathing): congestive heart failure, atrial fibrillation,

high altitude

Signs and Symptoms

• typically those of underlying medical condition

• those with hypercapnia typically have daytime somnolence:seen less frequently in non-hypercapnic

CSA

Complications

• hypercapnic CSA:may have complications of chronic hypoxemia including cor pulmonale

• hypocapnic CSA: higher mortality but not clear whether this is due to Cheyne-Stokes breathing,or if

Cheyne-Stokes breathing is a marker of severe heart disease

Treatment

• both hypercapnic and non-hypercapnic CSA:treatment of underlying medical conditions, especially

optimization of congestive heart failure in Cheyne-Stokes breathing

• hypercapnic CSA:typically benefit from BiPAP

• hypocapnic CSA: has not been shown to benefit from CPAP or BiPAP; clinical trials of adaptive servoventilation (ASV) are ongoing, but one study showed a signal for harm

Introduction to Intensive Care

Intensive Care Unit Basics

• goal is to stabilize critically ill patients: hemodynamic, respiratory, cardiac instability, or need for

close monitoring

Lines and Catheters

n

LJ

• arterial lines

• monitor beat-to-beat blood pressure variations,obtain blood for routine ABCs

common sites:radial and femoral arteries

• central venous catheter (central line)

administer IV fluids, monitor CVP, insert pulmonary artery catheters

administer total parenteral nutrition and agents too irritating for peripheral line (e.g.

vasopressors, chemotherapy)

common sites:internal jugular vein,subclavian vein, femoral vein

+

R31 Rcspirology Toronto Notes 2023

• pulmonary arterial catheter

balloon guides the catheter from a major vein to the right heart

• measures PCWP via a catheter wedged in distal pulmonary artery

• PCWP reflects the LA and LV diastolic pressure (barring pulmonary venous or mitral valve

disease)

indications ( now used infrequently due to associated complications)

diagnosis of shock, primary pulmonary H'

l

'N, valvular disease, intracardiac shunts, cardiac

tamponade, PL

assessment of hemodynamic response to therapies

differentiation of high- vs. low-pressure pulmonary edema

management of complicated Ml, multiorgan system failure and/orsevere burns, or

hemodynamic instability after cardiac surgery

absolute contraindications

tricuspid or pulmonary valve mechanical prosthesis

right heart mass (i.e. thrombus or tumour)

tricuspid or pulmonary valve endocarditis

Intensive vs.ConventionalGlucose Control in

Critically IIIPatients

NEJU 2009:360:1283-1297

Purpose:ID assess whether intensive glucose control

improves mortality in critically inpatients.

Study: Prospective,randomned controlled trial.

Population: $104 patients eapetted to regoue ICU

treatment lot 3 or more consecutne days.

Intervention:Patients were randonned to insulin

therapy regimens with intensive (blood glucose 4.5 -6

mM)or conventional (blood glucose10 mM or less)

glucose control taigets.Intravenous insulin therapy

was used to maintain blood glucose intaiget range.

Primary Outcome:Oeatb from any cause within 90 d

alter landomiiation.

Results the odds ratio for death m the intensive

control group was1.14195 « Cl1.02-1.28:P'0.02) and

this effect did not differ between surg: cal and medical

patents.Severe hypoglycemia (Piood glucose <2.2

irII) was significantly more common in the intensive

management group (6.9H vs.0.SV P

‘

0.001).

Conclusion: Intensive insulin therapy m ICU palients

increased moitably compaiedtoblood glucose

targetrgof <10 mM with a number needed toharm

of 38.

Table 28. Useful Equations and Cardiopulmonary Parameters

Equations and Cardiopulmonary Parameters

BSA -[HI (cm) * Wt (leg) - 60|/100

SV - CO / HR

Cl- CO / BSA

PCWP - LVE0P

SVI - Cl / HR

RV Ejection Fraction - SV / RVEDV

PP - sBP -dBP

MAP -1/3 sBP '

2/3 dBP - dBP <1/3 PP

SVRI *[|MAP -RAP) 801/Cl

P:F ratio - PaOt / FlOp

BSA - body surface mica: Cl » cardiac Index:CO e cardiac output: JBP - diastolic blood pressure;HR - heart rale;IVEDP•left ventricular end

diastolic pressure:

MAP •mean arterial pressure: PCWP *

pulmonary capillary wedge pressure:PP - pulse pressure:RAP - right atrial pressuie:RVEDV

-right

ventricular end diastolic voluaie:sBP

- systolic blood pressure:SV = stroke volume:SVI

- stroke volume index:SVRI

- systemic vascular resistance

index

Organ Failure

Table 29. Types of Organ Failure

Type of Failure Clinical Features Treatment

Treat underlying cause [e g. lung disease,shunt. V/0

mismatch, drug related, caidiac)

Manage mechanical ventilation settings

Supplemental oxygen

Treat underlying cause |e.g.myocardial ischemia.IV lailure.

bradycardia,tachycardia,blood loss,adrenal insufficiency)

Correct volume status

Vasopressots

Inotiopes

Intra aortic balloon pump

Treat underlying cause (e.g.thrombocytopenia,drug-related,

immune-related. DIC)

Transfusion of blood products,dotting factors

Treat underlying cause (e.g.viral hepatitis, drug related.

metabolic)

lactulose

liveitransplant

Respiratory Failure

[we lleipitatoiffdilute, R 26)

Hypoxemia

Hypercapnia

Cardiac Failure

(see Cardiology and Cardiac

Surgery,C401

Hypotension

Decreased urine output

Altered mental status

Arrhythmia

Hypoxia

Coagulopathy

(see Hematoloov. H34 and

H57)

liver Failure

(sec Gastroenterology. G40)

Increased INR or PIT

Low platelet count

Bleeding,bruising

Elevated transaminases,bilirubin

Coagulopathy

Jaundice

Altered mental status (encephalopathy)

Hypoglycemia

Elevated creatinine

Reduced urine output

Signs of volume overload (e.g. CHE. effusions) Diuretics

Dialysis

Causes of SHOCK Renal Injury

(see Nephrology. NP20)

Treat underlying cause (e.g.shock. drug-related,obstruction)

Correct volume and electrolyte status,eliminate toxins Spinal (neurogenic). Septic

Hemorrhagic

Obstructive (c .g. tension pneumothorax,

cardiac tamponade. PE)

Cardiogenic (e.g. arrhythmia. Ml)

Shock AnaphylaKtic

Definition

• see Emergency .Medicine, ER3

• inadequate tissue perfusion potentially resulting in end organ injury

• categories of shock

hypovolemic: hemorrhage, dehydration, vomiting, diarrhea, interstitial fluid redistribution

cardiogenic: myopathic (myocardial ischemia ± infarction), mechanical,arrhythmic,

pharmacologic

obstructive: massive PL (saddle embolus), pericardial tamponade, constrictive pericarditis,

increased intrathoracic pressure (e.g. tension pneumothorax)

distributive:sepsis, anaphylaxis, neurogenic, endocrine, toxins

->

• Shock:Clinical Correlation

• Hypovolemic:patients have cool

extremities due to peripheral

vasoconstriction

• Ca rdiogenic: patients usually have

signs of left-sided heart failure

• Obstructive: varied presentation

• Distributive: patients have warm

extremities due to peripheral

vasodilation

+

R32 Rcspirology Toronto Notes 2023

Table 30. Changes Seen in Different Classes of Shock

Hypovolemic Cardiogenic Obstructive Distributive

Systemic Inflammatory Response

Syndrome (SIRS):generalized

inflammatory reaction caused by

infectious and noninfectious entities,

manifested by two or more of:

• Body temperature >38"C or <36"C

• Heart rate >90/min

• Respiratory rate >20/min or PaCOu

<32 mmHg

. WBC >12000 cclls/ml or <4000 cells/

mlor >10% bands

HR t. N. or

*

t or

*

t t

BP 4 « *

JVP a t t r

Extremities Cold Cold Warm

Bilateral crackles on chest Depending on cause,may Look for obvious signs of

see pulsus paradoxus. infection or anaphylaxis

Kussmaul's sign,or

tracheal deviation

Not Cold

Other Look for visible

hemorrhage or signs of

dehydration

exam

Treatment

• treat underlying cause (hypovolemia is the most common cause)

• treatment goal is to return critical organ perfusion to normal (e.g. normalize BP)

• common treatment modalities include:

fluid resuscitation (NOT in cardiogenic shock)

• inotropes (e.g. dobutamine), vasopressors (e.g. norepinephrine), vasopressin

revascularization or thrombolyticsfor ischemic events

needle decompression or tube thoracostomy forsuspected tension pneumothorax

Quick SOFA (qSOFA) Criteria

• Respiratory ratei22/mln

• Altered mentation

• Systolic blood pressure <100 mmHg

Sepsis Goal Directed Resuscitation lor Patients with

Early ScpticShock

ItlM 2014:371:1496-1406

Study: Prospective.random ized controlled trialpopulation: 1600 patients in Australia and New

Zealand presenting tothe emergency department

witb early septic shock.

Intervention Patents were random zed to receive

early goal directed therapy (EGDT|or usual care.

Outcome: The primary outcome wasalkaase

mortality within 90 d ol randomization.

Results: Ihe rate ol death did not significantly

differ between patients treated with ECOI oi

usual care (absolute risk difference ESDI vs.usual

care

--03%,95% Cl -4.1 to 3.6%:P-0.90).EG01

treated patients received more intravenous fluids,

vasopressor infusions,red bipod cell transfusions,

and dobutamine|P<0.000t lot all).Survival lime,

in- hospital mortality, duration ol organ support,and

length nf hospitalstay did notsign ilicaetly d iff er

between patients randomized to EGOI nr usual care.

Conclusions: EGOI did not improveall-cause

mortalityal 90 d in patients presentingto the

emergency department with early seplx shock.

•the leading cause of death in noncoronary ICU settings is multi-organ failure due to sepsis

•the predominant theory is that sepsis is attributable to uncontrollable immune system activation

Definitions

•sepsis:life threatening organ dysfunction caused by dysregulated host response to infection (Table 31)

•septic shock: a subset of sepsis, where sufficient circulatory and/or cellular/metabolic abnormalities

substantially increase mortality. Clinically defined as sepsis with persisting hypotension requiring

vasopressors to maintain MAP 265 mmHg and having a serum lactate 22 mmol/L ( 18 rng/dl.) despite

adequate lluid resuscitation

Signs and Symptoms

•new guidelines recommend the use of quick SOFA (qSOTA) criteria and SOFA score to replace SIRS

criteria

•in patients with suspected infection, bedside application of qSOFA criteria identifies individuals with

high likelihood of poor outcomes, including prolonged ICU stay and/or death

•a positive qSOFA (>2 criteria) should prompt application of the SOFA score, and further evaluation of

possible infection and organ dysfunction

•in the context of suspected infection, a SOFA score 22 reflects an overall mortality risk of 10%

•the absence of 22 criteria on either qSOFA or SOFA score should not delay or defer investigation or

treatment of infection or any other aspect of care deemed necessary by the practitioners

Corticosteroids in Sepsis: An Updated Systematic

Review and Meta-Aoalysis

till Caic Med 2018:46 1411 1420

Purpose: Addressthe efficacy and safety of

corticosteroids m critically ill patents witti sepsis.

Methods:MEDLINE.EMBASE. CENTRAL,and LILACS

were searched foe Rtls comparing any corticosteroid

to placebo or no corticosteroid in critically ill children

and adults with sepsis.

Results: 42 RCTs including 10194 patients.

Corticosteroids may achieve a small reduction

oc no reduction in the relative cskof dying in the

short-term (relative risk. 0.93;95% Cl 0.84-103;

1.8 % absolute risk reduction;95% Cl 4.1% reduction

to 0.8% Increase!,and possibly achieve a small effect

on long-term mortality based on moderate certainly

(relative risk,0.94:95% Cl 0.89-1.00;22% absolute

risk reduction:95% Cl 4.1% reduchon to oo effect).

Conclusions: In critically ill patients vrth sepsis,

corticosteroids possibly result In a small reduction

in mortality while possibly increasing the nsk of

neuromuscularweakness.

Table 31. Sequential (Sepsis-Related) Organ Failure Assessment (SOFA) Score

Score

System 0 1 2 3 4

Respiratory

PriO/ FiO;.mmHg

(kPa)

>400(53.3) <400 (53.3) <200 (26.7) with <100 (13.3) with

respiratory support respiratory support

<300 (40)

Coagulation

Platelets,xIOVpl >150 <150 <100 <50 <20

liver

Bilirubin, pmolfl

(mqi'dt )

<20 (1.2) 20-32 (1.2-1.9) 33-101(2.0-5.9) 102-204 (6.0-11.9) >204 (12.0)

Cardiovascular MAP >70 mmHg MAP *70 mmHg Dopamine 5.1-Wor Dopamine >15

'

or

epinephrine <0.1k>r epinephrine >0.1a or

norepinephrine <0.k norepinephrine >0.1a

Oopamme ‘5a or

dobutamine (any

dosep

Central Nervous System

Glasgow coma scale 15

score

1314 1012 69 < 6

L J

Renal

Creatinine.|imol/L

(mg/dl)

Urine output,ml/d

<110 (1.2) 110-170 (1.2-1.9) 171-299 (2.0-3.4) 300-440 (3.5-4.9) >440 (5.0)

<

500 < 200

11 +