Chronic obstructive pulmonary disease (COPD) is progressive and not fully reversible. It is characterised by increasing airflow obstruction, predominantly caused by smoking, although exposure to occupational dusts, chemicals and air pollution are also considered risk factors (Brashers and Huether, 2014). COPD is the second most common respiratory disease in the UK, with 1.2 million people (2% of the population) suffering from the condition (Snell et al, 2016). Airflow obstruction occurs as a result of airway and parenchymal damage, caused by chronic inflammation (National Institute for Health and Care Excellence (NICE), 2010). Exacerbations of COPD are common, where symptoms become pronounced and unstable compared with those on a daily basis, characterised by rapid dyspnoea and hypoxaemia (Clancy and McVicar, 2009).
Pathophysiology of COPD
The clinical forms of COPD are chronic bronchitis and emphysema, although guidelines discourage differentiation between the two forms when making a diagnosis (NICE, 2010). Chronic bronchitis is defined as hypersecretion of mucus and a productive cough over 3 months of the year for at least 2 consecutive years (Brashers and Huether, 2014). Bronchitis occurs as a result of the inhalation of irritants which cause airway inflammation, leading to bronchial oedema, bronchospasm and increased mucous in the epithelium. Impaired ciliary function impedes the clearance of mucous, resulting in frequent infections and mucous plugging (Colbert et al, 2009; Brashers and Huether, 2014). Chronic inflammation results in hypertrophied bronchial smooth muscle and progression of inflammation to other airways; this leads to narrowing of the airways, which worsens during the expiration phase when airways are constricted (Brashers and Huether, 2014).
Progression of the disease
As the disease progresses, expiration becomes difficult because of the loss of elastic recoil and reduced volume of air that can be expired from the lungs. This results in air trapping and over-inflation of the lungs (Clancy and McVicar, 2009), a feature of emphysema. As a result, patients breathe at a higher functional residual capacity. Emphysema is defined as the abnormal permanent enlargement of gas-exchange airways and destruction of alveolar walls through the breakdown of elastin within the septa. This results in large air spaces within the lung parenchyma and adjacent pleurae, impaired gas exchange, ventilation-perfusion mismatch and hypoxaemia (Brashers and Huether, 2014).
Challenges of assessment
The assessment of COPD is challenged by the absence of a single test or symptom (NICE, 2010); therefore, in the prehospital environment, the identification and subsequent assessment is often reliant on the patient giving an accurate history and confirming a pre-existing diagnosis of the condition, in order to differentiate from other respiratory complaints (NICE, 2010).
One study found that ambulance personnel may only be aware of a diagnosis of COPD in 58% of cases (Durrington et al, 2005). Many patients are aware of their diagnosis owing to the resulting disability and impaired quality of life, while those with severe progression may have an individualised care plan available to assist with assessment (Association of Ambulance Chief Executives (AACE), 2016). However, it is estimated that millions of people with COPD are undiagnosed as a result of its gradual onset and a lack of recognition of its symptoms (Department of Health and Social Care (DHSC), 2011). This highlights the importance of an accurate and well-evidenced assessment by paramedics, particularly given that earlier recognition of the illness is linked to improved outcomes (DHSC, 2011).
Prehospital treatment
Patients with COPD will usually present to the ambulance service when they suffer an acute exacerbation of COPD. There are 100 000 acute COPD admissions in England annually (Davidson et al, 2016). The most common symptoms are as follows (NICE, 2010):
An initial assessment should comprise a focused respiratory assessment (Blaber and Harris, 2011), encompassing relevant clinical observations such as oxygen saturation monitoring. Signs of hypoxia, circulation deficiency and altered level of consciousness indicate failing ventilation and a clear requirement for transfer to a hospital.
Importance of controlled oxygen
Prehospital treatment of acute exacerbation of COPD focuses on the accurate assessment of the disease at the individual's current stage, and reversal of underlying cause with oxygen therapy, ventilation therapy and treatment with bronchodilators such as salbutamol and ipratropium bromide (AACE, 2016). Recent evidence has highlighted the importance of controlling oxygen therapy in the prehospital environment, to maintain target saturations of 88–92% (Davidson et al, 2016). Uncontrolled oxygen therapy increases the level of acidosis and mortality of patients with acute COPD. One study showed a 78% reduction in mortality of patients with confirmed COPD, where oxygen was titrated correctly in the prehospital phase (Austin et al, 2010). This further highlights the importance of early recognition.
Acute respiratory failure
While patients experiencing a mild exacerbation may be able to use standby medication to manage their condition at home, patients with unstable or more severe symptoms require transfer to hospital for future care (Table 1) (NICE, 2010; AACE, 2016). In severe cases of COPD, hyperinflation results in a mechanical disadvantage of the respiratory muscles. Elastic and resistive loads on the respiratory muscles increase, which may cause ventilatory failure; this combined with tissue acidosis further impairs ventilatory muscle function (Osadnik et al, 2017). Risk factors for the development of acute respiratory failure in COPD exacerbations are listed in Table 2 (Davidson et al, 2016). Acute respiratory failure complicates around 20% of exacerbations (Davidson et al, 2016) and is further defined as type 1 or type 2, depending on the aetiology (Table 3).
| Marked dyspnoea |
| Tachypnoea |
| Purse lip breathing |
| Use of accessory respiratory muscles at rest |
| Acute confusion |
| New-onset cyanosis |
| New-onset peripheral oedema |
| Marked reduction in activities of daily living |
| Infection |
| Mucosal oedema |
| Bronchospasm |
| Sputum retention |
| Excessive oxygen therapy |
| Sedation |
| Pneumothorax |
| Pulmonary embolism |
| Left ventricular failure |
| Type 1 | Type 2 |
|---|---|
| Inadequate gas exchange | Reduction in minute ventilation |
| Causes decrease in oxygen supply to tissue (hypoxaemia) | Causes increased carbon dioxide in the blood (hypercapnoea) |
| Causes include atelectasis, pneumonia and pulmonary oedema | Presents as hypoventilation |
| Leads to systemic acidosis | |
| Exacerbated by acute illness, e.g. chest infection |
Type 1 respiratory failure
Type 1 respiratory failure is primarily due to inadequate gas exchange, resulting in a decrease in oxygen supply to tissues; this is known as hypoxaemia (Brashers and Huether, 2014). Causes of type 1 respiratory failure include atelectasis, pneumonia and pulmonary oedema (Higgins and Guest, 2008). Although patients in respiratory failure with COPD may have some accompanying hypoxaemia, the primary cause of acidosis is usually hypercapnic (type 2) respiratory failure.
Type 2 respiratory failure
Type 2 respiratory failure is due to increased levels of carbon dioxide in the blood, with or without hypoxia, known as hypercapnia. This is primarily caused by reduced minute ventilation (the volume of gas inhaled and exhaled over a period of time), and presents as hypoventilation in the patient (Higgins and Guest, 2008). The reduced excretion of carbon dioxide results in systemic acidosis. Respiratory acidosis is defined as a pH <7.35 and a PCO2 >6.5 kPa (Davidson et al, 2016). Type 2 respiratory failure is usually seen in COPD, and is exacerbated by acute illness, such as a chest infection.
Non-invasive ventilation in COPD
UK guidelines suggest non-invasive ventilation (NIV) as the preferred treatment for persistent type 2 respiratory failure during exacerbations of COPD (NICE, 2010; Davidson et al, 2016) when pharmacological and oxygen therapy have failed to improve the patient's condition. A recent Cochrane review found that NIV was beneficial in reducing the risk of mortality by 46% on average, and the risk of requiring intubation by 65% (Osadnik et al, 2017).
NIV is a method of ventilatory support that does not require endotracheal intubation; therefore, avoiding some of the significant risks associated with intubation and sedation of patients with COPD, such as damage to tissue structures, ventilator-acquired pneumonia, and difficulty weaning patients from ventilators once the ventilatory failure is resolved. Advantages include the ability to apply it for short, intermittent durations, in addition to the ability for patients to eat, drink and continue to be involved in decisions regarding their care, as sedation is not required (Osadnik et al, 2017).
Some ambulance services have introduced NIV within their scope of practice for the treatment of acute respiratory failure (Mullen, 2013; South East Coast Ambulance Service NHS Foundation Trust, 2018). At the time of writing, one ambulance service is undertaking a pilot randomised controlled trial of prehospital NIV for acute respiratory failure (Fuller et al, 2018).
Indications for NIV in COPD
Recent guidelines for NIV treatment in hospital advocate the requirement of arterial blood gas (ABG) measurement prior to starting NIV (Davidson et al, 2016). However, considering the absence of ABG measuring in most UK prehospital practices, other indications for commencement of NIV by paramedics should be sought to assist with decision making. British Thoracic Society guidelines highlight the difficulty in predicting whether patients with COPD will develop hypercapnia during an acute exacerbation, and suggest they be considered at risk until the results of ABGs are available (O'Driscoll et al, 2017). Current hospital guidelines suggest that the patient should be able to protect and maintain their own airway, and be conscious and cooperative, with a primary diagnosis of COPD exacerbation (Royal College of Physicians (RCP), 2008). One prehospital trial of NIV developed a protocol of indications based upon the patient's initial presentation, using signs and symptoms such as increased respiratory rate, reduced oxygen saturation levels and accessory muscle usage (Cheskes et al, 2013). Current UK ambulance service guidelines are less prescriptive, advocating NIV as a clinical consideration when standard oxygen and pharmacological therapy fail to improve ventilation (AACE, 2016). There is a clear requirement for more guidance or protocols surrounding indications for NIV in the prehospital setting, which could be developed on a trust-specific basis as a standard operating procedure.
While the benefit of prehospital NIV as a treatment for acute pulmonary oedema is recognised (O'Driscoll et al, 2017), a recent systematic review highlighted the lack of UK-based evidence for NIV treatment of acute COPD. However, despite the need for further research, international trials have identified that prehospital treatment with NIV was more effective than standard treatment, and that it prevented intubation and deterioration in patients (Pandor et al, 2015).
Types of NIV
Continuous positive airway pressure
Continuous positive airway pressure (CPAP) is provided via a simple face mask with a tight seal over the patient's mouth and nose. The resistance to breathe against enables a reduced respiratory effort by increasing positive end-expiratory pressure (PEEP) above atmospheric air pressure. This extra pressure acts as a splint and prevents further development of atelectasis (Clancy and McVicar, 2009), in addition to opening collapsed alveolar structures (Mullen, 2013).
CPAP is oxygen driven; therefore, the increased oxygen therapy improves the patient's fraction of inspired oxygen levels. Some ventilators used within UK ambulance services already feature CPAP as a ventilatory mode, although many patients have their own portable units. Other benefits of CPAP include its portability, ease of use, and ability to immediately withdraw treatment should the patient suffer adverse effects (Mullen, 2013).
Non-invasive pressure-support ventilation
Unlike CPAP, non-invasive pressure-support ventilation (NIPSV) requires a ventilator unit, programmed with both expiratory and inspiratory pressures (Mas and Masip, 2014). Bi-level positive airway pressure ventilation (BIPAP) is an example of NIPSV used in UK hospitals and is delivered by a face or nasal mask. When the patient begins inspiration, the ventilator assists this with pressure support using a decelerated flow, keeping inspiratory positive airway pressure (IPAP) constant and lowering carbon dioxide levels (Credland, 2013). When the patient's expiratory effort finishes or decreases below a target pressure, the pressure support is discontinued, and pressure drops to a predetermined expiratory positive airway pressure (EPAP) or PEEP (Mas and Masip, 2014). This assists in maintaining airway patency during expiration and increases oxygen levels (Credland, 2013). BIPAP results in an overall reduction in respiratory effort compared with CPAP, owing to the constant IPAP (Nava and Hill, 2009), while hypercapnia is reversed and improved alveolar ventilation reverses respiratory acidosis (Credland, 2013). Therefore, it is favoured in many studies for the treatment of type 2 respiratory failure, secondary to exacerbation of COPD (Mas and Masip, 2014).
Risks of NIV
NIV is not without risks. The resulting elevation of pressure in the alveoli may result in barotrauma, while hyperinflation increases the risk of pneumothorax (Clancy and McVicar, 2009). Patients should be carefully monitored throughout for signs of further deterioration, such as reducing consciousness, airway compromise, vomiting, haemodynamic instability or ineffective ventilation. In the case of adverse effects, consideration should be given as to whether to withdraw treatment (Davidson et al, 2016).
Invasive mechanical ventilation
Treatment failure of NIV occurs in 20–40% of patients (Credland, 2013). Therefore, hospital guidelines have advocated early development of an ongoing management plan to address this when commencing NIV therapy (RCP, 2008; NICE, 2010). A decline in level of consciousness, hypotension, uncorrected hypoxaemia or no change in respiratory rate indicate treatment failure and invasive mechanical ventilation (IMV) should be considered where appropriate (RCP, 2008; Credland, 2013). As previously stated, there are often significant complications associated with IMV in this patient group, leading to poorer outcomes and increased rates of mortality.
Conclusion
COPD is a common respiratory disease affecting a significant proportion of the population. Exacerbation of the illness accounts for thousands of hospital admissions each year. Current UK prehospital management of acute exacerbation of COPD focuses on pharmacological management and oxygen therapy as a first-line treatment.
While this is appropriate, international evidence suggests that NIV during prehospital treatment of patients with acute respiratory failure is beneficial in improving patient outcome and avoiding treatment escalation in hospital. NIV is used by some ambulance services in the UK; however, its use is not widespread. Further UK research into its use is needed before it is likely to be introduced as a widespread treatment in paramedic practice.