The Dept of Anaesthesia & Intensive Care, CUHK thanks

for an unrestricted education grant
Intensive Care Nephrology - beyond BASIC courses: London (June), Singapore (July)
Click here for details
Asian Intensive Care Conference, Hong Kong, November 21-22nd 2013

COPD

Chronic obstructive lung disease

Definitions

Chronic bronchitis: daily productive cough for at least 3 months of the year for 2 consecutive years

Emphysema: anatomical alteration of the lung characterised by an abnormal enlargement of the airspaces distal to the terminal and respiratory bronchioles associated with destructive changes of the alveolar walls and capillary membranes

NB Most patients with COPD have features of both disease processes.

Pathophysiology

- primary pathophysiological change in lung mechanics is airflow obstruction leading to expiratory flow limitation. Results from loss of elastic recoil pressure and airway narrowing.
- airway resistance is increased by mucosal oedema and hypertrophy, secretions, bronchospasm, airway tortuosity and turbulence and loss of lung parenchymal elastic tissues supporting small airways
- expiratory flow limitation cannot be overcome by increased expiratory effort because this tends to compress the airways - a tendency which is exaggerated in patients with COPD
- if a patient with COPD needs to breath harder the only way he can do so is to increase inspiratory flow and increase lung volume. In fact, during exercise the patient increases both end-expiratory volume and inspiratory flow: both are critically dependent on inspiratory muscle action. (Increase in lung volume makes respiratory muscles less efficient because of shortened fibre length and mechanical disadvantage).
- ie although the load is essentially expiratory the compensation is essentially inspiratory
- combined with high respiratory drive (which exists in patients with acute respiratory failure and COPD) and poor mechanical advantage may result in inspiratory muscle fatigue. (Fatigue = inability of muscles to continue to develop the amount of tension generated before fatigue, no matter what the degree of stimulation)
- thought that development of inspiratory muscle fatigue is of central pathophysiological importance in the development of acute respiratory failure in these patients
- intrinsic PEEP opposes inspiratory muscles
- other factors exacerbating decreased neuromuscular competence:

depressed drive eg sedative induced, hypothyroidism

muscle weakness eg secondary to hypokalaemia and hypophosphataemia (latter present in approx 20% of patients with acute respiratory failure and COPD; exacerbated by methylxanthines, beta agonists, corticosteroids and diuretics)

malnutrition

- additional causes of increased load:

increased resistive load eg bronchospasm, upper airway obstruction

increased lung elastic load: eg pulmonary oedema, pneumonia, atelectasis

increased chest wall elastic load: eg obesity, pleural effusion, pneumothorax, abdominal distension

increased minute ventilation loads: even if work of each breath remains constant an increase in respiratory rate increases the load. Minute ventilation requirements increased by excess CO₂ production (eg excessive carbohydrate feeding, fever) and increased V_D/V_T (eg PE, hypovolaemia, shallower breathing)

- management of these patients should be directed towards decreasing load and increasing neuromuscular competence
- pulmonary capillary bed loss from alveolar destruction and hypoxic pulmonary vasoconstriction lead to pulmonary hypertension, secondary vascular changes and ultimately cor pulmonale. Increased hypoxia during acute respiratory failure increases PA pressure and may precipitate RVF
- combination of airway obstruction, parenchymal disease and pulmonary circulatory disturbance leads to extensive V/Q mismatching and increased hypoxaemia
- shunting also increases hypercarbia
- increased dead space
- dynamic hyperinflation of lung

Clinical features

usually have a history of cigarette smooking
cough
dypsnoea
wheeze
prolonged expiration
barrel-chest
cyanosis
± signs of pulmonary hypertension and cor pulmonale

Investigations

CXR

Image
hyperinflation (characteristically on PA CXR dome of diaphragm is below 10th interspace posteriorly).
increased bronchial and peribronchial markings (chronic bronchitis).
patchy areas of hyperlucency and fibrosis, flat hemidiaphragms, attenuated vascular markings (empysema)

Lung function tests

FEV₁/FVC < 0.75
decreased PEFR and FEV₁
increased residual volume (chronic bronchitis),
increase in residual volume and total lung capacity with decreased diffusing capacity for carbon monoxide (emphysema)

Acute respiratory failure

Aetiology

viral infection
bacterial infection: especially H. influenzae, Strep pneumoniae. Other organisms include Pseudomonas aeruginosa, Strep. viridans, Moraxella catarrhalis, Mycoplasma pneumoniae
congestive cardiac failure: chronic hypoxia results in pulmonary hypertension and subsequent right heart strain and hypertrophy. RV muscle fibres interdigitate with those of the LV and thus RV dysfunction in patients with COPD may be associated with LV dysfunction
pulmonary embolus
sputum retention
pneumothoraces and bullae
sedation

Management

Drugs

antibiotics for those with purulent sputum
- antibiotics probably more useful in patients with severe disease (eg those who require admission to ICU0
- choice of agent should be based on local resistance patterns
- many recommend cephalosporins, azithromycin or clarithromycin , or fluoroquinolones
systemic corticosteroids
- reduce need for mechanical ventilation or death
- shorten length of hospital stay
- optimal duration of treatment unknown
  - GOLD report recommended 10 day course
  - 8 week course not superior to 2 weeks
  - 10 day course superior to 3 days
b ₂ agonists
ipratropium bromide
- some but not all data suggests combination with beta agonists better than either alone
± aminophylline: reports of benefits are conflicting
avoid sedatives unless ventilated
± diuretics

Oxygen

no clear consensus regarding how much oxygen to give
the argument for restricting the amount of oxygen the patient receives is based on the assumption that chronically hypercarbic patients are dependent on hypoxic respiratory drive. There is no good evidence to support this
the argument for completely correcting the patient's hypoxia is based on the fact that hypoxia can kill and the premise that the rise in Pco₂ often seen in these patients is not due to hypoventilation.

Physiotherapy

GOLD report concluded that physical methods may be beneficial in patients producing >25 ml/day of sputum or with lobar atelectasis
no evidence that postural drainage alters outcome

Artificial ventilation

Indications

largely subjective
the following are ominous:
- respiratory rate > 36
- use of all accessory muscles
- thoracoabdominal paradox
- even minor mental state changes
- patient's subjective sense of exhaustion
ABG used only to confirm clinical assessment

Mode of ventilation

Non-invasive
- decreases need for invasive ventilation and may be associated with improved outcome
- CPAP alone can reduce work of breathing in COPD during weaning and during sleep
- BiPAP weaning may be better than weaning on pressure support via an ETT
Invasive
- aim is to support ventilation while reversible components improve, to allow respiratory muscles to rest and recover without wasting and to minimize dynamic hyperinflation
- use low tidal volumes (8-10 ml/kg), low minute ventilation (£ 115 m//kg) and long expiratory times in SIMV mode. High inspiratory flows allow short inspiratory time and therefore longer expiratory time for any given respiratory rate but use is controversial. Has been shown to reduce dynamic hyperinflation and alveolar pressure and improve gas exchange
- if higher minute ventilation is required for excessive hypercapnic acidosis the degree of dynamic hyperinflation and its effects should be determined before increasing ventilation
- if dynamic hyperinflation is significant discourage spontaneous ventilation with heavy sedation. However if it is not excessive spontaneous ventilation should be encouraged. Low level CPAP may reduce the work of breathing in spontaneous breathing modes by facilitating triggering (NB avoid PEEP in controlled ventilation)

Weaning

flow-based algorithm for inspiratory to expiratory cycling in pressure support mode may not be suitable for some patients with COPD. Many older ventilators cycle from inspiration to expiration in pressure support mode when the inspiratory flow rate falls to 25% of the peak inspiratory flow rate. This tends to occur early in patients with COPD with the result the ventilator cycles while the patient is still trying to breath in. A cut-off of 5% which is used in some newer ventilators may circumvent this problem

Prognosis

60-75% of patients with COPD and acute respiratory failure are successfully weaned however 1 year survival is only 32-50%. NB these studies are relatively old and the ventilators used relatively basic
prognostic factors with regard to weaning:

FEV₁ when well

premorbid exercise tolerance

severity of dyspnoea (premorbid)

serum albumin

age, sex, co-existing illness, Po2, Pco2, ECG findings, cause of respiratory failure not related to weaning outcome

prognostic factors with regard to 1 year survival:

FEV₁

premorbid exercise tolerance

? serum albumin

? cor pulmonale

? severity of dyspnoea

NB once the patient has been weaned duration of ventilation not related to 1 year survival