COPD, ARDS and Resp Failure

Question 2

COPD - definition

Answer 2

A progressive disorder characterised by airway obstruction – FEV1 is <80% predicted and FEV1/ FVC ratio is <0.7 with little or no reversibility.

COPD vs asthma – COPD is more likely if age of onset is >35 years, disease is smoking (passive or active) or pollution related, there is chronic dyspnoea, sputum production and minimal diurnal or day to day variation in FEV1.

COPD includes the following:

• Chronic bronchitis – defined clinically as cough and sputum production on most days for 3 months of 2 consecutive years. Symptoms will improve if patients stop smoking.
• Emphysema – defined histologically as enlarged air spaces and destruction of alveolar walls.

Question 3

COPD - patients

Answer 3

Patients can be divided into 2 categories from the end of the bed:

• Pink puffers – emphysema – increased alveolar ventilation, a near normal PaO2 and a normal or low CO2. They are breathless, not cyanosed and may progress to type 1 respiratory failure.
• Blue bloaters – chronic bronchitis – decreased alveolar ventilation with a low PaO2 and a high PaCO2. They are cyanosed but not breathless and patients may go on to develop cor pulmonale. Their respiratory centres are insensitive to CO2 and rely on hypoxic drive to maintain their respiratory effort – beware when giving supplementary oxygen and keep SaO2

Question 4

COPD - clinical features

Answer 4

• Symptoms – there is persistent cough, sputum, dyspnoea and wheeze with no or little variation.
• Signs – tachypnoea, use of accessory muscles for respiration, hyperinflation, decreased cricosternal distance (<3cm), hyperresonant percussion, quiet breath sounds, wheeze, cyanosis or cor pulmonale.

Question 5

COPD - complications

Answer 5

Acute exacerbations ± infection, polycythaemia, respiratory failure, cor pulmonale (leading to oedema and raised JVP), pneumothorax (from a ruptured bullae) or lung carcinoma.

Question 6

COPD - investigations

Answer 6

• Bloods – FBC and CRP, ABG – low O2 and high CO2.
• CXR – hyperinflation (>6 anterior ribs), flat hemidiaphragms, large central arteries, decreased peripheral vasculature or bullae.
• ECG – RA and RV hypertrophy (cor pulmonale).
• Lung function – obstructive picture and air trapping.

Question 7

COPD - management - general

Answer 7

Smoking cessation, dietary advice and supplements (BMI is low), encourage exercise, mucolytics can help chronic productive cough, screen for depression, give influenza and pneumococcal vaccinations, give pulmonary rehabilitation and advise against air travel if FEV1 <50% or PaO2 <6.7 kPa.

Question 8

COPD - management - mild

Answer 8

FEV1 50-80% predicted – can give a short acting anticholinergic e.g. Ipratropium Bromide or short acting inhaled β2 agonist e.g. Salbutamol or Terbutaline as required.

Question 9

COPD - management - moderate

Answer 9

FEV1 30-49% predicted – regular antimuscarinic e.g.Tiotropium or a long acting β2 agonist e.g. Salmeterol or Formoterol with inhaled corticosteroids e.g. Beclometasone especially if FEV1 is <50% and patients has >2 exacerbations per year.

Seretide inhaler – a combination of salmeterol and beclometasone.

Symbicort inhaler – a combination of budesonide (corticosteroid) and formoterol.

Question 10

COPD - management - severe

Answer 10

Severe – FEV1 <30% predicted – combine a long acting β2 agonist, an inhaled steroid and an anticholinergic and refer to a specialist. Consider a steroid trial and/or home nebulisers.

Question 11

COPD - steroid trial

Answer 11

Give 30mg Prednisolone per 24 hours for 2 weeks and if FEV1 increases by 15% COPD is responsive to steroids and the patient may benefit from long term corticosteroid therapy.

Question 12

COPD - long term oxygen therapy

Answer 12

Trials have shown that if PaO2 was maintained >8 kPa for 15 hours a day the 3 year survival rate is increased by 50%.

Guidelines suggest that LTOT should be given to the following – clinically stable non-smokers with a PaO2 <7.3 kPa despite maximal therapy, if PaO2 is between 7.3 and 8 kPa and there is pulmonary hypertension and cor pulmonale or can be given to terminal patients.

Question 13

COPD - indications for referral

Answer 13

Unclear diagnosis, rapid decline in FEV1, cor pulmonale, bullous lung disease (to assess for surgery), <40 year pack year history or frequent infections (? Bronchiectasis).

Question 14

ARDS - definition

Answer 14

ARDS or acute lung injury is caused by direct injury or occurs secondary to severe systemic illness e.g. sepsis.

Lung damage and release of inflammatory mediators cause increased capillary permeability and non-cardiogenic pulmonary oedema often accompanied by multi organ failure.

Question 15

ARDS - causes

Answer 15

• Pulmonary causes – pneumonia, gastric aspiration, inhalation injury, vasculitis or contusion (bruise).
• Other causes - shock, septicaemia, haemorrhage, multiple transfusions, disseminated intravascular coagulation (DIC), pancreatitis, acute liver failure, trauma, head injury, malaria, fat embolism, burns, obstetric events (e.g. eclampsia or amniotic fluid embolus) and drugs or toxins (aspirin or heroin).

Question 16

ARDS - features and diagnosis

Answer 16

• Clinical features – cyanosis, tachypnoea, tachycardia, peripheral vasodilation and bilateral fine crackles.
• Diagnosis – the following 4 criteria should be present – acute onset, chest x-ray showing bilateral infiltrates, pulmonary capillary wedge pressure <19 mmHg and refractory hypoxaemia.

Question 17

ARDS - investigations

Answer 17

FBC and CRP, Us and Es, LFTs, amylase, clotting, blood cultures, ABG, chest x-ray to look for pulmonary infiltrates and pulmonary artery catheter to measure the capillary wedge pressure.

Question 18

ARDS - management

Answer 18

Admit to ITU and give supportive therapy whilst treating the underlying cause.

• Respiratory support – continuous positive airway pressure (CPAP) may be sufficient in early ARDS but most patients will require mechanical ventilation. Remember to use a low to medium peak expiratory end pressure (PEEP) due to reduced lung compliance in ARDS and an increased risk of pneumothorax. Indications for ventilation are PaO2 <8.3 on 60% oxygen or PaCO2 >6 kPa.
• Circulatory support – invasive haemodynamic monitoring with an arterial line and Swan-Ganz catheter aids the diagnosis and is helpful in monitoring PCWP and cardiac output. Maintain CO with inotropes e.g. 2.5-10 μg/kg/min dobutamine IVI, vasodilators and blood transfusions.
• Sepsis – identify organisms and treat accordingly but avoid nephrotoxic abx e.g. gentamicin.
• Other – enteral nutritional support and possibly steroids (their role is controversial).

Question 19

ARDS - prognosis

Answer 19

Mortality is high between 50-75% and varies with patient age, cause of ARDS (pneumonia 86% and trauma 38%) and number of organs involved (3 organs for >1 week is always fatal).

Question 20

Respiratory failure - definition

Answer 20

Respiratory failure occurs when gaseous exchange is inadequate resulting in hypoxia.

It is defined as a PaO2 <8 kPa and subdivided into 2 groups – type 1 and type 2 according to the PaCO2 level.

Question 21

Respiratory failure - type 1

Answer 21

Normal or low PaCO2 – caused primarily by a ventilation perfusion (V/Q) mismatch e.g. in pneumonia, pulmonary oedema, PE, asthma, emphysema or fibrosing alveolitis or ARDS.

Question 22

Respiratory failure - type 2

Answer 22

PaCO2 >6 kPa – caused by alveolar hypoventilation with or without mismatch. Causes:

• Pulmonary disease – asthma, COPD, pneumonia, pulmonary fibrosis or sleep apnoea.
• Reduced respiratory drive – caused by sedative drugs, CNS tumour or CNS trauma.
• Neuromuscular disease – cord lesion, diaphragm paralysis, poliomyelitis, myasthenia gravis or Guillian Barre or thoracic wall disease – flail chest or kyphoscoliosis.

Question 23

Respiratory Failure - Clinical Features

Answer 23

Of the underlying cause with symptoms of hypoxia with or without hypercapnia.

• Hypoxia – dyspnoea, restlessness, agitation, confusion, central cyanosis. If respiratory failure is long standing it can cause polycythaemia, pulmonary hypertension or cor pulmonale.
• Hypercapnia – headache, peripheral vasodilation, tachycardia, bounding pulse, tremor or flap, papilloedema, confusion, drowsiness and possibly coma.

Question 24

Respiratory Failure - Investigations

Answer 24

Aim to identify the underlying cause – FBC, CRP, Us and Es, ABG, chest x-ray, sputum and blood cultures if the patient is febrile and spirometry (for COPD, neuromuscular disease or GB).

Question 25

Respiratory Failure - Management

Answer 25

• Type 1 – treat underlying cause, give 35-60% oxygen or assisted ventilation if PaO2 <8kPa on 60%.
• Type 2 – the respiratory centre may be relatively insensitive to CO2 and respiration could be driven by hypoxia. Treat the underlying cause and give controlled oxygen therapy – start at 24% and re-check ABG for rising PaCO2. If this fails patient may require intubation and ventilation.

Question 26

Oxygen - Nasal Cannulae

Answer 26

May be preferred by patients but oxygen delivery is imprecise and may cause nasal soreness.

The flow rate is 1-4L/min providing an oxygen concentration of 24-40%.

Question 27

Oxygen - Face Mask

Answer 27

Deliver a variable amount of oxygen depending on the rate of inflow. They are less accurate than Venturi masks and there is a risk of CO2 accumulation of low flow rates.

Question 28

Oxygen - Venturi Mask

Answer 28

Provide a precise % of O2 at high flow rates. Masks are colour coded – blue provides 24% (use this in COPD patients), white 28%, yellow 35%, red 40% and green 60%.

Question 29

Oxygen - Non-rebreathe Mask

Answer 29

Have a reservoir bag and deliver high concentrations of O2 – 60-90% determined by the inflow (10-15L/min) and the presence of flap valves on the side.

Question 30

Promoting Oxygenation

Answer 30

Treat anaemia, improve cardiac output and give chest physiotherapy.