DR SANJENA MITHRA, FY1

ASTHMA AND COPD

Objectives

Differentiate severity of acute asthma exacerbations

Pathophysiology of Asthma and COPDDiscuss CXR and ABGType 1 vs Type 2 respiratory failure

5 mins – pretest10 mins – case 110 mins – case 25 mins – end of session testfeedback

Pretest

Define asthma What constitutes COPD?Briefly outline the pathophysiology of asthmaDescribe 4 differences in the airways of acute and

chronic asthmatics.How can you categorise severity of acute asthma

attacks?List 4 classes of drug used to treat Asthma/COPDWhat are their mechanisms of action and side effects?How can you determine severity of COPD?Compare type 1 and type 2 respiratory failure

Take a history from this patient who is short of breath…

Cough +/- sputumChest pain (pleuritic)WheezeSMOKINGAllergies, PetsForeign travelHistory of DVT, PE*Compliance with

meds*

Weight lossHaemoptysis

AtopyFamily historyExercise toleranceDiurnal variation

Complications:OedemaSOBOERecurrent infectionsFever

CASE 1- Summary

28 year old lady presents to A&E after becoming short of breath whilst visiting friends. She was feeling well during the day and had been to work. Non-smoker

PMH: Asthma since childhood – Salbutamol PRNInhaler currently not relieving symptoms; SOB worse

over last 2 hours. Chest starting to feel tight, she is getting lightheaded.

On examination: T 36.2BP 124/71 HR 90RR26 96% sats on air

Alert, talking in full sentences but distressed. CVS and Abdo – NADResp – widespread wheeze, no crackles, no friction rub

What are your differentials for this patient and why? Acute asthma exacerbation (non-life threatening) PE Inhaled foreign body Allergic reaction Anxiety

Pathophysiology Define asthma 4 characteristics of acute and chronic asthma

Asthma

ASTHMA – chronic, inflammatory disease of the airways resulting in variable, often reversible airflow obstruction and airway hyperresponsiveness.

Acute asthma airway changes- Airway constriction, microvascular leakage /

oedema, vasodilation, mucus hypersecretion IgE mediated inflammatory response. Cross-

linking of IgE results in degranulation of mast cells, histamine release and inflammatory cell infiltration

Chronic asthma airway changes– airway remodelling Subepithelial fibrosis, smooth muscle

hyperplasia / hypertrophy, goblet cell hyperplasia, new vessel formation

Investigations

What investigations would you like to do? Bedside: Peak flow – 45% of best Bloods: ABG, FBC, U&E, CRP Imaging: CXR

ABG: pH 7.46 pCO2 4.1 pO2 10.3 HCO3 26

Respiratory Acidosis

Respiratory Alkalosis

Metabolic Acidosis

Metabolic Alkalosis

pH ↓ pH ↑ pH ↓ pH ↑

Primary problem: pCO2 ↑

Primary problem:pCO2 ↑

Primary problem: HCO3 ↓

Primary problem:HCO3 ↑

Compensation:HCO3 ↑

CompensationHCO3 ↓

Compensation:pCO2 ↓

Compensation:pCO2 ↑

Reading Chest X-RaysRIP...ABCDE

Adequacy:-Rotation (symmetry of clavicles)-Inspiration (ribs)-Penetration (vertebral bodies)-Mention central lines, NG tubes, pacemakers etc

-Airway: is the trachea central?-Boundaries and Both lungs: lung borders, consolidation, hazy etc-Cardiac: Heart size-Diaphragm-Everything else: soft tissue mass, fractures

What investigations would you like to do? Bedside: Peak flow – 45% of best Bloods: ABG, FBC, U&E, CRP Imaging: CXR

Allergic bronchopulmonary aspergillosis: refractory asthma with fever, cough and sputum. Eosinophilia and raised IgE

Acute severe asthma

How would you like to manage this patient?Immediate

A to E Salbutamol 5mg via oxygen driven nebuliser Repeat obs (SpO2, HR, RR) and PEF to assess for

progression of severity and risk to life If clinically stable and PEF >75%, can repeat

Salbutamol nebs and consider oral prednisolone 40-50mg

Moderate PEF >50-75% SpO2 >92%

No features of severe

Acute Severe PEF 33-50%

RR >25SpO2 >92%

HR >110Cannot complete

sentences

Life threatening33-92-CHEST

PEF <33%SpO2 <92%

Cyanosis/Confusion,

Hypotension, Exhaustion, Silent chest, Tachycardia

Senior help (ITU,

anaesthetics)

O SHIT!• O2 to maintain sats 94-98%• Salbutamol 5mg via O2 driven

nebs• Hydrocortisone IV/oral

prednisolone• Ipratropium via O2 driven nebs• Consider Magnesium Sulphate

IV

ABG, CXR

Salbutamol 4 puffs, then 2 puffs every 2

minsSalbutamol 5mg via O2 driven nebuliser

If life threatening features present

Repeat salbutamol nebs, give oral

prednisolone 40-50mg

Long term management

Long term Conservative: Follow up by GP, check inhaler

technique, refer to chest clinic/asthma liaison nurse Medical: If PEF <50% on admission, can consider

prednisolone, adequate inhaler supply Stepwise treatment of asthma

Communication

Please explain to Mr X how to correctly use his inhaler

Check understanding If you haven’t used it for a while, spray in the air to check it

works Shake it As you breathe in, simultaneously press down on the inhaler Continue to breathe deeply Hold your breath for 10 seconds or as long as you comfortably

can, before breathing out slowly. If you need to take another puff, wait for 30 seconds, shake your

inhaler again then repeat Advise on using a spacer

Chronic Management of Asthma

Case 2 – Summary

A 64 year old gentleman presents to A&E with increasing SOB over the last 3 days. This is associated with a cough productive of thick, green sputum.

Gets SOB normally after about 5-10 mins walking on the flat PMH: “asthma” SH: 50 cigarettes a day for the past 40 years. On examination he is alert but visibly SOB

T 37.7RR 25 HR 110 O2 sats 89% on air, you notice he is using his accessory muscles to breathe.

Resp: hyperinflated chest, diffuse coarse crepitations, widespread wheeze, reduced air entry bilaterally

CVS: JVP raised, ankle oedema (non-pitting)Abdo SNT

Case 2

What are your differentials for this patient and why? Acute infective exacerbation of COPD Pneumonia Cor pulmonale Bronchiectasis

Pathophysiology Define COPD clinically Histopathology? Pathophysiology?

Definitions

COPD: Umbrella term encompassing chronic bronchitis (chronic cough and sputum production on most days for at least 3 months per year for 2 years) and emphysema (pathological diagnosis of permanent destructive enlargement of distal air spaces)

Chronic bronchitis: airway narrowing due to bronchiole inflammation, mucosal oedema and mucus hypersecretion

Emphysema: Destruction and enlargement of alveoli that reduces elastic recoil and results in bullae.

Investigations

What investigations would you like to do? Bedside: ECG, sputum culture Bloods: ABG, FBC, U&E, CRP, blood cultures Imaging: CXR Special tests: ECHO, α1-antitrypsin levels

ABG: assess the oxygenation Checking for respiratory failure- failure to fully

oxygenate the blood passing through the lungs giving rise to hypoxia +/- hypercapnea.

ABG pH 7.29 pCO2 6.8 pO2 7.9 HCO3 25

Respiratory failure

Type 1- hypoxia with low or normal pCO2 – anything that impairs gas exchange Atelectasis, pulmonary oedema, pneumonia,

pneumothoraxType 2 – hypoxia with hypercapnea – alveolar

hypoventilation Same causes for a respiratory acidosis COPD, neuromuscular disorders (GBS, MND), CNS

depression (drugs, brainstem injuries)

Initial management – infective exacerbation of COPD

How would you like to manage this patient?Immediate

A to E Maintain sats 88-92% (titrate to ABG) Corticosteroids (oral/IV) Empirical antibiotics Salbutamol 5mg and Ipratropium via O2 driven

nebulisers Consider need for NIV – if

desaturating/decompensating Admit, chest physiotherapy

Flow volume loops - Spirometry

FEV1/FVC

Determines the severity of COPD Describes the proportion of a person’s vital capacity

(maximum air expelled after maximum inhalation) that can be expired in the first second.

Normal ~ 70% Mild 50-70% Moderate 30-50% Severe <30%

Management

Long term Conservative – smoking cessation, pulmonary

rehabilitation, flu vaccination, Spirometry Medical – LTOT (only if not smoking),

bronchodilators, steroids (can consider if more than 2 infective exacerbations/year), prophylactic antibiotics

Surgical – Transplant, lobectomy, bullectomyLTOT criteria

PaO2 <7.3 kPa on air during period of clinical stability PaO2 7.3-8.0 kPa and signs of secondary

polycythaemia, nocturnal hypoxaemia, peripheral oedema or pulmonary hypertension

Drugs 1

Bronchodilators: Beta-2 agonists – Short acting/Long acting

(Salbutamol/Salmeterol) MOA: increases cAMP production in the lung which

decreases calcium concentration Effect: Smooth muscle relaxation, bronchial dilatation S/e: tachycardia, sweating, tremor

Anticholinergics: Ipratropium (Atrovent), Tiotropium (Spiriva) MOA: Anti-muscarinic. Ipratropium is non-selective,

Tiotropium is selective (M3) s/e: dry mouth, sedation, skin flushing, tachycardia

Drugs 2

Methyxanthines Theophylline, Aminophylline MOA: Phosphodiesterase antagonists – raise intracellular cAMP levels.

Works well with beta-2 agonists s/e: narrow therapeutic window

Leukotriene receptor antagonists Montelukast, Zafirlukast s/e: GI upset, drowsiness

Corticosteroids Prednisolone, Beclamethosone MOA: upregulates intracellular proteins after binding with receptor

and causes expression of anti-inflammatory agents s/e: weight gain, immunosuppression, skin thinning, bruising,

osteoporosis, cataracts

Pretest

Define asthma What constitutes COPD?Briefly outline the pathophysiology of asthmaDescribe 4 differences in the airways of acute and

chronic asthmatics.How can you categorise severity of acute asthma

attacks?List 4 classes of drug used to treat Asthma/COPDWhat are their mechanisms of action?How can you determine severity of COPD?Compare type 1 and type 2 respiratory failure

Take home message

33-92 CHESTFocussed history taking: Symptoms, red flags,

complicationsStructure your answers

Questions?