back to basics review: respirology in under two hours jennifer block, md, frcpc april 15, 2009

Back to Basics Review:Respirology in Under Two Hours

Jennifer Block, MD, FRCPC

April 15, 2009

The Plan...

• Spirometry

• Asthma

• COPD

• Sleep Apnea

• Pleural Effusion

Spirometry

1. Take as deep a breath as possible2. Blast out the air into spirometer3. Continue exhaling for several more seconds

UpToDate

RVTLC

Interpretation

• Upper Airway Abnormalities

• Obstructive Lung Disease

• Restrictive Lung Disease

Upper Airway Abnormalities

ERJ 2005; 26: 948-968

Normal Restrictive Obstructive Fixed Intrathoracic Extrathoracic Variable

Obstructive Lung Disease

• FEV1/FVC is <70%

• “scooped out”

• lung volumes may show hyperinflation

ERJ 2005; 26: 948-968

Restrictive Lung Disease

• TLC < 5th percentile predicted

• normal FEV1/FVC ratio

ERJ 2005; 26: 948-968

Asthma

• Pathophysiology

• Diagnosis

• Chronic Management

• Acute Management

Asthma: Definition

• paroxysmal or persistent symptoms (dyspnea, chest tightness, wheeze, cough)

• variable airflow limitation and airway hyper-responsiveness

• due to inflammation

Asthma

Comprehensive Asthma Management

• Suspect asthma and confirm diagnosis

• Education

• Assess severity

• Avoid / control triggers and environmental modification

• Medications for chronic disease

• Assess control

• Management plan for exacerbation

• Regular follow-up

• If FEV1 is low, try to increase it using a short-acting

bronchodilator (reversibility)

• ≥12% and ≥180 ml improvement in FEV1 from baseline 15

minutes after the use of an inhaled short-acting

bronchodilator

Asthma Diagnosis

• If FEV1 is normal, try to see if airways are hyperresponsive

by giving an irritant (methacholine challenge)

Asthma Diagnosis

Comprehensive Asthma Management

• Suspect asthma and confirm diagnosis

• Education

• Assess severity

• Avoid / control triggers and environmental modification

• Medications for chronic disease

• Assess control

• Management plan for exacerbation

• Regular follow-up

Asthma Management

Relievers – Short Acting Beta-Agonists

• SABAs for acute relief• ‘rescue’ medication used prn• MDI salbutamol (Ventolin) • dry powder terbutaline (Bricanyl)

Asthma Management

Inhaled Corticosteroids (ICS)

• Anti-inflammatory ICS mainstay of therapy

– Prevent symptoms, improve PFTs, decrease hyper-responsiveness, reduce morbidity

Inhaled Corticosteroids – How do they work?

• Like steroids produced endogenously by adrenal cortex

• Anti-inflammatory – inhibit production of cytokines, which:

– reduces eosinophil infiltration– inhibits macrophage function– reduces production of leukotrienes

Dosing Guide

Drug Low Daily Dose (μg)

Medium Dose (μg)

High Daily Dose (μg)

Fluticasone(Flovent)

≤250 251-500 >500

Budesonide(Pulmicort)

≤400 401-800 >800

Beclomethasone(Qvar)

≤250 251-500 >500

Ciclesonide(Alvesco)

≤200 201-400 >400

ICS Adverse Effects

• thrush• dysphonia

• osteoporosis• growth velocity• glaucoma • cataracts• adrenal insufficiency

Asthma Management

Long Acting β2-Agonists (LABAs)

• add if not controlled by moderate dose ICS

• better than doubling ICS

• “not recommended as maintenance monotherapy”

• doesn’t replace SABAs

• salmeterol (Serevent), formoterol (Oxeze)

Combination LABA / ICS Products

– Salmeterol/fluticasone (Advair) MDI and diskus

– Budesonide/formoterol (Symbicort) turbuhaler

Leukotriene Receptor Antagonists (LTRAs)

• Second or third choice medication or in patients who can’t take ICS

• Montelukast (Singulair)

• Oral medication

• Use in patients with:

– symptoms despite LABA/ICS

– ASA sensitivity, nasal polyps

– exercise-induced asthma

IgE Antagonists: Omalizumab (Xolair)

• Monoclonal antibodies block action of IgE on mast cell

• Effective if IgE levels are only slightly elevated (500-1200)

• Monthly injection

• Extremely expensive $45,000/year

• Use if frequent need for oral steroids despite optimum conventional Rx and patient has drug plan or $$$

Comprehensive Asthma Management

• Suspect asthma and confirm diagnosis

• Education

• Assess severity

• Avoid / control triggers and environmental modification

• Medications for chronic disease

• Assess control

• Management plan for exacerbation

• Regular follow-up

Assess Control

Comprehensive Asthma Management

• Suspect asthma and confirm diagnosis

• Education

• Assess severity

• Avoid / control triggers and environmental modification

• Medications for chronic disease

• Assess control

• Management plan for exacerbation

• Regular follow-up

Asthma Exacerbation

• ABC’s– include RR, O2 sats, assess work of breathing, wheezing

• history: – diagnosis– triggers– previous exacerbations/admissions/intubations– treatment history

• identifiable trigger

• short-acting beta-agonists ie. salbutamol (Ventolin)

• short-acting anti-cholinergics ie. ipratropium (Atrovent)

• systemic anti-inflammatory therapy– oral = prednisone– intravenous = solumedrol

• very severe: MgSO4, intubation, anesthetic

Asthma Exacerbation

COPD

• Contrast from asthma

• Definition

• Pathophysiology

• Diagnosis

• Chronic Management

• Acute Management

COPD Definition

• respiratory disorder largely caused by smoking characterized

by:

- progressive, partially reversible airway obstruction

- hyperinflation

- systemic manifestations

- increasing frequency and severity of exacerbations

COPD Risk Factors

• Host Factors:

- genetics (alpha-1-antitrypsin deficiency)

- bronchial hyper-responsiveness

• Environmental Factors:

- smoking

- childhood viral infections

- occupational & environmental exposures

Pathophysiology - Airflow Obstruction

• alveoli and support structures are destroyed– decreased elastic recoil– lack of tethering gives airway collapse

• airway compression by adjacent overdistended lung units

• mucosal inflammation and secretions

Pathophysiology - Hyperinflation

• expiratory flow limitation in COPD gives air trapping

• end-expiratory lung volumes are increased

• further hyperinflation with exercise (increased RR, decreased expiratory time)

• decreased inspiratory capacity a major cause of dyspnea

COPD Diagnosis

• do not screen asymptomatic individuals

• assess symptomatic patients with spirometry

• post-bronchodilator FEV1/FVC ratio less than 0.7

COPD StagePost-bronchodilator FEV1

(% predicted)

mild ≥ 80

moderate 50 - 79

severe 30 - 49

very severe < 30

COPD Management

BMJ 2008; 336: 598-600.

Education - Effects of Smoking on FEV1

Education

“Tobacco is the only legal consumer product that kills

one third to one half of those who use it as intended

by its manufacturers, with its victims dying on

average 15 years prematurely”

- World Health Organization

Canadian Tobacco Use Monitoring Survey (CTUMS)

•telephone survey with 9547 respondents performed in first six months of 2007•19% population current smoker (male>female)

– 15% of youth age 15-19 [vs. 28%]– 24% of adults age 20-24 [vs. 34%]

Smoking in Canada

What Can You Do?

• smoking cessation advice– even brief advice increases chances of patients quitting– www.gosmokefree.ca– www.smokershelpline.ca

• nicotine replacement therapy– many different types– any form of NRT increases chances of quitting vs.

control

Other Prevention

• vaccination:– flu vaccine yearly– pneumococcal vaccine q5years

COPD Management

Short-Acting Bronchodilators

• Even patients with “fixed” airflow obstruction can have good clinical response to bronchodilators even if FEV1 changes very little

• Reduces hyperinflation, reduces dyspnea and increases exercise capacity

Short-Acting Bronchodilators

• anti-cholingergics: ipatropium (Atrovent)– bitter taste– dry mouth– glaucoma if sprayed into eye– urinary retention

• β2-agonists: salbutamol (Ventolin)– tachycardia, palpitations– sleeplessness, tremor

• improves PFTS, dyspnea and exercise performance

COPD Management

Long-acting anti-cholinergic

• tiotropium (Spiriva)

• once a day

• blocks M3 muscarinic receptors in bronchial smooth muscle

• improves:– PFTs, dyspnea, exercise capacity, QOL– decreases exacerbations– maybe more improvement than LABA

Long-acting β2-agonist (LABA)

• salmeterol (Serevent) and formoterol (Oxeze)

• twice daily

• more sustained improvement in PFTs, dyspnea and QOL

compared with SABA– effect on exercise capacity not clear– decrease exacerbation

COPD Management

Dyspnea – Downward Spiral of Deconditioning

Respiratoryimpairment

Dyspnea during moderate exertion

Abstentionfrom exercise

Physical deconditioning

Dyspnea during mild exertion

Furtherabstention

Furtherdeconditioning

Dyspneaduring ADL

*

* = stay at home. Depression, oxygen

therapy etc.

Pulmonary Rehabilitation

– Exercise + psychosocial support

– Aerobic exercise + strength training

– improves dyspnea, endurance, QOL

– trend to decreasing mortality

– need a maintenance program

www.lungchicago.org www.altru.org

COPD Management

Combination LABA / ICS Products

– Salmeterol/fluticasone (Advair) MDI and diskus

– Budesonide/formoterol (Symbicort) turbuhaler

– add to therapy if patient has persistent dyspnea or recurrent exacerbations

– improve PFTs, QOL, decrease exacerbations

– no ICS monotherapy

COPD Management

Indications for long term oxygen therapy

• pO2 on room air of≤ 55 mmHg< 60 mm Hg if evidence of

– Polycythemia– Cor pulmonale– Right heart failure

• Mortality benefit

COPD Management

Surgery

• Lung Volume Reduction Surgery- benefits patients with upper lobe (heterogenous)

emphysema and poor exercise capacity

• Lung Transplantation- single or double lung- non-smoker- generally age<60 without significant cardiac, renal,

hepatic disease- post-transplant survival is 5 years on average- death from infection (early) and chronic rejection (later)

COPD Management

End of Life Issues

• Empathetic, realistic conversations about illness• Opportunity to express wishes re: intubation

• Dyspnea- morphine po, sc, iv or - morphine nebulized 5 mg in 2 ml normal saline q4h- benzodiazepines

• Cough- opioids (codeine, morphine)

• Secretions- scopolamine

What Decreases Mortality?

Non-Pharmacologic• Smoking cessation Yes• Flu shot No• Pneumonia vaccine No• Pulmonary Rehab ?

Pharmacologic

• Oxygen Yes

• Systemic Steroids No

• Antibiotics No

• SABA (Ventolin) No

• Anti-cholinergics No

• Theophylline No

• Inhaled Steroids No

• LABAs No

• Combo ICS/LABA No

Acute exacerbations of COPD

• Definition: Anthonisen criteria. Require 2 of:– Increased dyspnea– Increased volume of sputum– Increased purulence of sputum

• Over 50% are associated with an infection

Acute exacerbations of COPD

• Treatment:

– ABCs

– O2 sat monitoring and oxygen prn

– history and p/e to rule out other causes of dyspnea

– CXR, ABG, sputum C&S

– short-acting bronchodilators: salbutamol + ipatropium

– systemic steroids: prednisone 30-40 mg/d x 10-14 days

– antibiotics if purulent sputum

– NIPPV

No modifying factors Macrolide Doxycycline

COPD w/o recent rx New macrolide Doxycycline

COPD w/ recent rx Resp fluoroquinolone Cephalosporin or amox/clav plus macrolide

Macro-aspiration Amox/clav Respiratory fluoroquinolone

plus plus

Macrolide Metronidazole or clindamycin

CTS/CIDS Guidelines for Management of CAP 2000

Outpatients

Ward Admission Respiratory fluoroquinolone Cephalosporin plus Macrolide

Intensive Care Unit Respiratory fluoroquinolone Macrolide plus plus 3rd gen Cephalosporin 3rd gen Cephalosporin or or b-lactam/b-lactamase inhibitor b-lactam/b-lactamase inhib

CTS/CIDS Guidelines for Management of CAP 2000

Inpatients

Not all that Wheezes...

• is asthma or COPD

• can also be heard in patients with bronchiectasis, cystic fibrosis, pulmonary edema

Obstructive Sleep Apnea Syndrome

• Snoring, witnessed apneas

• Morning headache, daytime sleepiness

• Sleep study = Polysomnography

– EEG to stage sleep– Electro-oculography– EKG– Oronasal airflow– Respiratory effort– SpO2

Obstructive Sleep Apnea Syndrome

• Respiratory Disturbance Index (RDI):– normal <5/hour– mild 5-15/hour– moderate 16-30/hour– severe >30/hour

• Treatment:– weight loss, avoid sedatives– positional therapy (off supine)– CPAP– oral appliance, tracheostomy less common

Pleural Effusion

Unit 1 – Integrative Lecture: Lung Cancer – J. Block

Pleural Fluid Accumulation

• In normal pleural space, the rate of fluid formation is balanced by the rate of removal

• Rate of fluid formation is determined by the Starling equation which describes a semi-permeable membrane

– hydrostatic forces push water out of vessel

– osmotic forces pull water back into vessel

• Pleural effusion is due to abnormalities in one of these processes

• Cell count and differential• Gram stain• Culture• AFB• Cytology

• LDH• Total protein• Glucose • pH

Pleural Effusion Evaluation

Unit 1 – Integrative Lecture: Lung Cancer – J. Block

Light’s Criteria•pleural fluid protein/serum protein > 0.5•pleural fluid LDH / serum LDH > 0.6•pleural fluid LDH > 2/3 upper limit normal LDH

Any of these three criteria means fluid is EXUDATE

Pleural Effusion Evaluation

Unit 1 – Integrative Lecture: Lung Cancer – J. Block

Many!

Transudate = heart, liver, kidney

Exudate = infectious inflammatory malignant movement from abdomen iatrogenic

Pleural Effusion Etiology

Unit 1 – Integrative Lecture: Lung Cancer – J. Block

• If exudate with no determined cause, you want to rule-out malignancy

repeat thoracentesisCT chest with contrastpleuroscopy or VATSbronchoscopyfollow and repeat

Pleural Effusion Etiology

Unit 1 – Integrative Lecture: Lung Cancer – J. Block

Most places, patients admitted for symptomatic thoracentesis +/- tube drainage and attempt at pleurodesis (talc)

In Ottawa, patients mostly receiving Pleurx catheters to allow home drainage

Malignant Pleural Effusions

Unit 1 – Integrative Lecture: Lung Cancer – J. Block

The Plan...

• Spirometry

• Asthma

• COPD

• Sleep Apnea

• Pleural Effusion