The British Thoracic Society Guidelines Nursing Essay

My colleague and I were called to attend an elderly gentleman who was suffering from severe shortness of breath (SOB). On arriving at the location we entered the house to find a gentleman in his seventies sat in a chair having severe breathing problems. He appeared cyanosed around his lips; he had signs of recession and was leaning forward in his chair. He was unable to communicate verbally due to the severity of his condition. The patient’s wife informed us that her husband had Asthma and Chronic Obstructive Pulmonary Disease (COPD) and had been having difficulty breathing all day. My colleague (a Paramedic) and I quickly established that the patient needed urgent medical intervention. As my colleague attached the monitoring equipment (see annex 1), I administered oxygen and prepared a nebuliser with Salbutamol. We established the patient’s oxygen saturation levels were less than 50%, and he was tachycardic. His condition had not improved despite the oxygen and salbutamol. We moved the patient to the ambulance as soon as we were able. Once inside the ambulance my colleague administered Ipratropium Bromide (Atrovent) to the nebuliser as the patient had deteriorated. We obtained further observations (Appendix 1) and ascertained the patient’s condition to be deteriorating further, he was showing signs of severe exhaustion, and he was no longer able to sit up so was sat back on the stretcher. His colour deteriorated and his respiratory effort was poor with reduced air entry bilaterally. At this point my colleague administered Adrenaline (Epinephrine) via an Intra muscular injection. We left the scene and headed to hospital under emergency driving conditions and provided the receiving hospital with a pre alert call. On our arrival we were directed to the resuscitation area where hospital staff were awaiting our arrival, a full clinical handover was given out and as we left the patient he was in a critical condition.

I checked on this patient later in our shift and found him to have improved slightly and he was able to communicate verbally. He stayed in hospital for several days before being discharged home.


As with many of the jobs we attend I had very mixed emotions, the initial excitement and adrenaline rush associated with receiving and responding to emergency situations was quickly replaced with apprehension and a certain amount of nervousness as we attended the patient. A sense of urgency was apparent throughout the job. Both my colleague and I felt under pressure from the onset as we both acknowledged the severity of the situation. I was confident in both my own and my colleague’s ability and knew that although we were both worried for the patient we had to appear relaxed and confident in order to reassure the patient who appeared distressed and anxious and was obviously afraid. I felt helpless and worried at certain times during the job as we were doing everything possible to help the patient but our efforts seemed frustratingly ineffective against the frighteningly rapid deterioration in the patient’s condition. I was left with a sense of hope as I left the hospital and felt happy and relieved when I found the patient had improved and had later been discharged.


Good Points

Overall the job went well and the patient made a good recovery.

We recognised immediately that the patients condition was time critical.

All interventions were carried out in a timely manner.

My colleague and I worked well as a team and recognised each others strengths.

All policies, procedures and guidelines were followed.

As I was working with a paramedic the patient received a higher level of care than would have been available if I had been the senior clinician.

Bad Points

As the patient is known COPD, the likelihood of further episodes is high.

The patient had been deteriorating over several hours but refused to call for assistance. Earlier intervention could have prevented the patient reaching a life threatening stage.

The patient often runs out of medication including inhalers.

No Peak Flow was recorded.

Capnography was not used.


Asthma is a common inflammatory disease of the airways associated with episodes of reversible over-reactivity of the airway smooth muscle. The mucous membrane and muscle layers of the bronchi become thickened and the mucous glands enlarge, reducing airflow in the lower respiratory tract. The walls swell and thicken with inflammatory exudate and an influx of inflammatory cells, especially eosinophils (Waugh and Grant 2010, p.256). Waugh and Grant (2010) also go on to state that during an asthma attack, spasmodic contraction of bronchial muscle (Bronchospasm) constricts the airway and there is excessive secretion of thick sticky mucus, which further narrows the airway. The bronchospasm and mucus secretion lead to Inspiration being normal but only partial expiration being achieved.

There are two clinical categories of asthma, Atopic (childhood onset, Extrinsic) and Non-atopic (adult onset, intrinsic) (Waugh and Grant 2010). Asthma patients generally live normal lives, often using medication such as inhaled anti inflammatory and bronchodilator agents to regulate the condition. Both Caroline (2008) and Sanders (2010) state that Asthma characteristically occurs in acute attacks of variable duration and that between attacks patients may be relatively asymptomatic.

In the United Kingdom asthma is classified due to its severity. This enables prehospital professionals to plan and implement the most appropriate treatment and transport regime for the patient (Caroline 2008). According to the British thoracic society (2011) there are four levels of severity moderate exacerbation, acute severe, life threatening and near fatal (See appendix 2).

Our patient was suffering from life threatening asthma and our treatment of him was carried out in line with the guidelines provided by JRCALC (2006) and the BTC (2012). On reaching the hospital our patient was handed over to the staff in the Emergency Department (ED), it was at this point that the patient had further tests to ascertain the severity of his condition; although I do not intend to gain a full understanding of these tests and the results of the tests will have no direct relevance to my treatment of the patient. I feel that by having a basic understanding of the results I will have more confidence and greater professional credibility when dealing with ED Staff of various levels. I have taken many patients to hospital and witnessed the Arterial Blood Gas (ABG) sample being taken during the initial examination stage but I have not had an understanding of the results once the test has been completed.

Because of the cost and risk to the patient, ABG analysis must be performed when clinically indicated, ABG analysis is indicated if the patient’s symptoms, medical history, physiological examination, or laboratory data suggest significant abnormalities in respiratory or acid-base status (Wilkins, Dexter and Heuer 2010). A table of clinical findings that may indicate the need to obtain an ABG sample can be seen in Annex 3.

Shortly after arriving at the hospital the patient had a sample of blood taken from an artery in his wrist, the purpose of this sample was to enable an ABG reading to be obtained so that a rapid biochemical evaluation could be carried out to guide diagnosis and further management of the patient. It is important to adopt a systematic approach to interpreting results of arterial blood gases, preceded by a brief history and focussed clinical examination (Cowley, Owen and Bion 2013). The systematic approach referred to involves six steps

Assess Oxygenation.

Assess pH.

Assess sHCO- and the base excess

Assess PaCO²

Review additional analytes

Re assess

However, Woodrow (2004) suggests that to have a basic understanding of the results in order to determine the severity of a patient’s condition, only three areas need to be analysed.

Ph Level.

Respiratory Function (Oxygen/carbon dioxide saturation).

Metabolic measures (bicarbonate, base excess).

Assess Oxygenation.

The Normal range for the partial pressure of oxygen in the plasma (PaO2) is 11.5 – 13.5kPa. (Woodrow 2004). Assessment of the basic blood gas measurements reflecting oxygenation involves interpreting data that identify PaO2, the amount of oxygen bound to Haemoglobin (HB) (SaO2), and the total content of oxygen in the arterial blood (CaO2) (Wilkins, Dexter and Heuer 2010) The oxygenation levels or respiratory function relate to the arterial oxygen tension (PaO2) which is the partial pressure of oxygen in arterial blood and the inspired oxygen concentration expressed as a fraction (FiO2) which is termed the PaO2/FiO2 ratio or P/F ratio. This is a useful index for determining the presence and severity of impaired alveolar gas exchange and is easier to calculate than alternative indices, such as the alveolar-arterial gradient (Cowley, Owen and Bion 2013). A healthy individual would be expected to have a P/F ratio above 50, with lower values signifying impaired gas exchange. Patients with acute lung injury or acute respiratory distress syndrome have values below 40 and 26.7 respectfully (Cowley, Owen and Bion 2013).

Assess pH

Following the handover of a patient to ED staff and once the ABG results have been obtained, nursing staff and doctors often refer to a patient as "Acidotic" or "Alkalotic". The pH is a measure of the hydrogen ion (H+) concentration in an environment. (Peate and Dutton 2012) The pH scale is a negative logarithm. A logarithm presents large numbers in a few, more easily managed, figures. A negative logarithm similarly represents small numbers, with many decimal points, in a more manageable and safer form (Woodrow 2004). The pH scale rages Between 1 (absolute acid) to 14 (Absolute alkali). The normal pH range in blood should be 7.35 to 7.45 (Waugh and Grant 2010) Our patient was having severe breathing difficulties, Peate and Dutton(2012) indicate that If the CO2 increases in the body because of poor respiration then the patient will become acidotic. In comparison, if the patient had been suffering from his kidneys not functioning properly then there would be an increase in alkalinity due to the removal of the bicarbonate ion decreasing. Peate and Dutton(2012) conclude that the overall pH process is much more complex but their examples are given as an example of the control of the cellular environment. Slight changes in pH affect enzyme activity, while acidity increases oxygen dissociation from haemoglobin (the Bohr Effect) and impairs cardiac contraction. Blood pH below 7.0 or above 8.0 makes survival very unlikely (Woodrow 2004). Woodrow goes on to say that Acidosis occurs more often than Alkalosis, but both are life threatening, complications are cumulative as blood pH moves progressively further from the normal range.

Assess sHCO- and the base excess.

This relates to metabolic Acid base disturbance. The contribution of any respiratory acid-base disorder to the sHCO3 concentration and base excess is removed by the analyser. (Cowley, Owen and Bion 2013). As this has little relevance to the patient in question I feel that further discussion is not required and that an awareness of its presence in the results is adequate.

Respiratory Function.

In order to assess respiratory function, three areas need to be analysed, the arterial partial pressure of carbon dioxide (PaCO2), partial pressure of arterial oxygen (PaO2) and the saturation of haemoglobin by oxygen (SaO2) (Woodrow 2004).

The PaCO2 should be assessed next according to Cowley, Owen and Bion (2013), in order to identify any ventilator component in the acid-base disturbance, a raised PaCO2 value will contribute towards an acidosis, and a low towards alkalosis. In the UK gases are almost always measured in Kilopascals (kPa). The normal range for PaCO2 4.5 - 6.0 kPa with less than 4.5kPa referred to as hypocapnia or respiratory alkalosis and a reading of more than 6.0kPa is referred to as hypercapnia or respiratory acidosis (Woodrow 2004). The presence of a normal PaCO2 value, or normal values on pulse oximetry, does dot rule out respiratory failure, particularly in the presence of supplemental oxygen (Cowley, Owen and Bion 2013). Many patients that we take in to hospital who require an ABG test have been on supplemental oxygen prior to hospital arrival so a normal reading might be seen with these patients.

In respiratory problems, abnormal blood gas values often reflect respiratory acidosis with PaCO2 elevated above 6.0kPa (Type II respiratory failure). The hydration of excess CO2 in the body results in carbonic acid which in turn increases the acidity in the blood. If a patient has ventilator difficulty they will not be able to blow off CO2 during expiration (Peate and Dutton 2012).

The SaO2 normal value is about 97%. Differences between SaO2 and the reading achieved using a pulse oximetry probe (SpO2), in practice are very similar (Woodrow 2004). Woodrow goes on to say that the relationship between PaO2 and SaO2 is complex and factors such as Hb levels should be considered in order to obtain a true result.


Sanders (2010) states that approximately 5.2 million people are living with asthma in the UK. It is responsible for 1400 deaths per annum (1 death every hour). In addition, confidential inquiries into asthma deaths have often concluded that fatality could have been avoided through better routine and emergency care, avoiding delay in getting help during the final attack or by taking prescribed medication. Caroline (2008) agrees and adds two thirds of the deaths were in the over 65 age group, and that women are more likely to die from the disease than men.

In my opinion this job was one of the most interesting jobs that I have attended. Not often do we as clinicians see an asthma patient deteriorate to such a level that they require the full range of drugs available to us. As an Advanced Emergency Technician looking to become a paramedic this job required me to think about what interventions would be required at the next level. As the job developed I was able to see a range of paramedic drugs used as they were intended and although the patient showed little improvement whilst in our care, our interventions enabled staff at the hospital to help promote the patients recovery. The ABG results obtained from the patient in question were key in guiding the ED staff towards a diagnosis and the treatment plan to be taken. By carrying out this reflection my understanding of ABG analysis and the results it provides is basic and although I understand the results are far more complex than what I have included in this reflection the basic understanding I now have will give me confidence when conversing with the doctors and nursing staff who attend any of the patients I deal with in the future.

I feel that without our intervention this patient would have been one of the 1400 deaths in that year.

Action Plan

I have developed an action plan to assist me with any further incidents of this nature. The plan is as listed below.






Annex 1 (PRF)

Annex 2

British Thoracic Society Guidelines

(British Thoracic Society 2012)

Annex 3


Past Medical History

Physical Examination

Laboratory Data

Chest Radiograph

Acute Dyspnoea.

Chest Pain.


Cough, Fever Sputum consistent with pneumonia.

Headache, Blurred vision consistent with Carbon Monoxide poisoning

History of COPD.

History of Cystic Fibrosis

History of Pulmonary Fibrosis.

History of exposure to dust known to affect the lung.

History of Ketoacidosis.

History of chronic renal failure.

Significant smoking history.


Diffuse crackles or wheezing.

Severe Tachypnoea or abnormal breathing.

Significant use of accessory muscles.

Unexplained confusion.

Evidence of chest trauma.

Digital Clubbing.

Unexplained Polycythaemia.

Severe electrolyte abnormalities.

Diffuse infiltrates.


Significant atelectasis.


Large pleural effusion.

Enlarged Heart.

Lobar consolidation.

(Wilkins, Dexter and Heuer 2010)