Understanding COPD and the Hypoxic Drive to Breathe
Published: 21 September 2016
Published: 21 September 2016
Lung Foundation Australia estimates that approximately 1.2 million Australians have some form of chronic obstructive pulmonary disease (COPD) – the umbrella term used for emphysema, chronic bronchitis and chronic asthma (review lung sounds).
This number incorporates the whole spectrum of COPD, from those who have advanced disease, to others who perceive their mild symptoms to be a sign of low fitness or normal ageing.
Given the wide variation in the presentation of patients with COPD, it is important that nurses have highly developed critical thinking and evaluation skills to ensure their patients are managed appropriately. The lack of these skills can increase the risk of a patient developing hypercapnia and requiring supplemental oxygen therapy.
Hypercapnia develops when an increased level of carbon dioxide is present in the bloodstream.
So why do some people with COPD retain carbon dioxide, and how can a nurse recognise hypercapnia in those who do?
Let’s head back to the text books for a moment…
Carbon dioxide (CO2) is the waste product of metabolism and is expelled from the body during exhalation. CO2 is also one of the gasses that can cross the blood-brain barrier. In the cerebrospinal fluid, it combines with water to produce carbonic acid which in turn separates to form hydrogen ions. The concentration of hydrogen ions in a solution is known as the pH.
Stay with me…
As the arterial level of carbon dioxide changes, this results in a change seen with the pH of the cerebrospinal fluid. This triggers a reaction in the central chemoreceptors located near the medulla. These sensory receptors are responsible for regulating respiratory function – breathing – and monitoring the levels of arterial carbon dioxide.
An increase in the arterial carbon dioxide level leads to an increase in the depth and rate of respiration, and the person breathes faster. A reduction in the arterial carbon dioxide level leads to reduced depth and rate of respiration, and the person breathes more slowly.
The disease process of COPD ultimately leads to chronically high arterial levels of carbon dioxide and low levels of oxygen. Over time, the central chemoreceptors become less sensitive to these changes. The stimulus for ventilation is then managed by the peripheral chemoreceptors located in the carotid bodies and the aortic arch. These receptors are stimulated by low arterial levels of oxygen, transmitting messages to the respiratory centre in the medulla. This leads to an increased respiratory rate and depth, with a low arterial oxygen level, and a reduced depth and rate with a high arterial oxygen level.
This short video provides a quick overview of the role of the brainstem, chemosensors and baroreceptors in the control and regulation of breathing.
From here, we can see what happens when inappropriate levels of oxygen are given to a ‘CO2 retainer‘. Arterial oxygen levels increase from what may be normal for that individual, leading to a reduction in the depth and rate of respirations, which will increase the arterial level of carbon dioxide. This is known as hypercapnia.
In a patient with COPD, the oxygen saturation level of the haemoglobin (SaO2) level may not reflect ‘normal’ values. It is important that you communicate with your patient and their family as much as possible to help you understand their premorbid respiratory function. Assess whether breathlessness, sputum production or persistent cough is normal for your patient. Involve the multidisciplinary team to create a care plan that defines SaO2 targets, as well as management for when the value falls outside of the limits.
Careful monitoring of the patient with COPD is essential. If supplemental oxygen is required, small changes to the rate of administration can have dramatic effects in those who have a hypoxic drive to breathe. The patient with COPD who becomes drowsy and appears to fall asleep after commencing oxygen therapy or having the flow rate changed, should be managed by immediately removing the supplemental oxygen, assessing Glasgow Coma Scale (GCS) and respiratory function against previous assessments, and following your organisation’s policies on patient deterioration appropriately.
The base nursing skills of communication, assessment, planning and evaluation are vital in caring for the patient with COPD. If you think it is challenging to care for a patient with COPD, imagine having COPD. Talk openly with your patient and their family. Ask them questions about their condition and allow them to understand how you are managing it in hospital. You might just learn something a textbook can’t teach you.
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