Mark A Rodrigues and Emily R McCall-Smith
Station 3.1: Acute exacerbation of asthma
You are the junior doctor working in the emergency department. You are asked urgently to review Mr Cannon, a 23-year-old asthmatic, who has presented with breathlessness and wheeze.
‘The patient is maintaining their airway and no stridor is audible.’
No additional airway support is required at present, but remember the patient could deteriorate quickly.
Look at the work of breathing: nasal flaring, use of accessory muscles. Is the patient able to complete sentences? Often patients with respiratory distress fix their rib cage and shoulder girdle by supporting themselves on straight arms and grasping the sides of the bed
Perform a respiratory exam, particularly assessing for chest wall movement, air entry into the lungs, and additional sounds (crackles or wheeze) on auscultation. Also look for signs of a pneumothorax by assessing the percussion note. Tracheal deviation, displacement of the apex beat away from the side of the pneumothorax and haemodynamic instability are clinical findings indicating a pneumothorax is under tension. This is a medical emergency, requiring urgent needle decompression
‘RR 35/min, oxygen saturations are 89% on room air. The patient is using his accessory muscles and unable to speak in full sentences. On auscultation, there is symmetrical chest wall movement, lung fields are resonant throughout, with reduced air entry at the base of the lungs, and a widespread bilateral polyphonic wheeze.’
You start the patient on high-flow oxygen via a non-rebreather mask (to maintain saturations between 94% and 98%). You prescribe 5 mg of salbutamol to be nebulized with oxygen.
‘The patient’s heart rate is 134 bpm, with a BP of 145/95 mmHg and CRT of 2 seconds. There is no evidence of heart failure or valvular disease on cardiovascular exam.’
No cardiovascular support is required at present.
‘The patient is GCS 15 (E4, M6, V5). His blood sugar is 4.8 mmol/L.’
ABG: Perform if (a) the SpO2 is<92% or (b) if there are any features of life-threatening asthma. Patients are likely to be hypoxic. The PaCO2 is likely to be low (due to hyperventilation), causing a respiratory alkalosis (low H+/high pH). However, if a patient becomes exhausted, their respiratory rate will reduce, and the PaCO2 will go from low to normal to high (indicating a near-fatal exacerbation)
Peak flow: This helps measure the severity of an asthma attack (Table 3.1), as well as the response to treatment. It is most useful if measured as a percentage of a patient’s previous best, but it can also be measured as a percentage of predicted (which is based on height, sex and age)
‘The patient’s peak flow is 40% of his usual best. ABG on air shows hypoxaemia and a respiratory alkalosis (PaO27 kPa, PaCO23.1 kPA, H+28 nmol/L (pH 7.55), and HCO320.3 mmol/L). CXR shows hyperinflation. The lungs are clear, no pneumothorax. ECG shows sinus tachycardia. Bloods are normal.’
Initial Management 
Salbutamol: 5 mg nebulized with oxygen should be given as soon as possible. These can then be given ‘back-to-back’, i.e. every 10 minutes if the initial response is poor. Only consider IV beta-2 agonists for those who are unable to undergo inhaled therapy
Corticosteroids: 40 mg prednisolone (oral) or 200 mg hydrocortisone (IV) if unable to swallow. Corticosteroids should be given in all cases of acute asthma. Oral corticosteroids are as effective as IV corticosteroids if the patient can absorb them. Continue for at least 5 days or until recovery
‘The patient is starting to improve. Airway is patent and RR is now 20/min. Oxygen saturations are now 95% on 2 L of nasal cannula oxygen. There is still expiratory wheeze; however, air entry has improved. HR is 118 bpm and BP is 120/80 mmHg. Peak flow is now 60% of predicted. Repeat ABG on 2 L oxygen shows PaO215 kPa, PaCO23.8 kPA, H+30 nmol/L (pH 7.52), and HCO323.1 mmol/L.’
|Parameter||Value||Normal range (units)|
|H+||30 nmol/L||35–45 (nmol/L)|
|PaO2||15 kPa on 2 L of nasal cannula oxygen||>10 (kPa) on air|
|PaCO2||3.8 kPa||4.7–6.0 (kPa)|
|HCO3||23.1 mmol/L||22–26 (mmol/L)|
Continue 40 mg of prednisolone for at least 5 days. The dose does not need to be tapered down, unless the patient is on maintenance corticosteroid treatment or has been on corticosteroid treatment for>3 weeks
Handing over the Patient
‘Mr Cannon is a 23-year-old gentleman who presented this evening with a life-threatening exacerbation of asthma.
He was acutely breathless, with a RR 35/min, saturations of 89% on air, widespread wheeze in the lung field, and poor basal lung entry. He has been treated with oxygen, 2×5 mg salbutamol nebulizers back to back, ipratropium bromide, and prednisolone, and is responding well.
Current observations are RR 20/min, SpO2 95% on 2 L of O2. HR is 118/min and BP is 120/80 mmHg. Peak flow is 60% of predicted, and ABG shows a respiratory alkalosis. He has been reviewed by the HDU registrar who is happy with ward level management at present.
He is being transferred to the ward on 2-hourly salbutamol nebulizers and 6- hourly ipratropium. CXR shows hyperexpanded lungs, and bloods are normal. Please could you review him in one hour and check his peak flow again within 30 minutes.’
Station 3.2: Exacerbation of COPD
You are the junior doctor working in the medical assessment unit. Your next patient is Mrs Johnson, an acutely breathless 67-year-old lady with a history of COPD. She normally controls this with inhalers alone, and has no home nebulizers or long-term oxygen therapy. She says she is more breathless and wheezy but her sputum has not changed in colour.
‘The airway is patent.’
No additional airway support is currently required.
‘RR 30/min, oxygen saturations are 82% on 2 L oxygen, with increased work of breathing. Resonant lung fields. There is good bilateral air entry with widespread inspiratory wheeze. No crepitations.’
You give oxygen via a Venturi mask and nebulized salbutamol and ipratropium. You also perform an arterial blood gas.
Perform a cardiovascular exam, looking at the JVP and listening to the lung bases for evidence of heart failure, and assessing the heart sounds for evidence of valvular disease, all of which can cause dyspnoea
‘HR 84 bpm, BP 122/74 mmHg. Mrs Johnson has warm peripheries with a CRT<2 seconds. She has good volume peripheral pulses. CV exam reveals normal HS, no murmurs, and no evidence of heart failure.’
Secure IV access and take bloods.
‘She is alert but finding it difficult to speak in sentences. Her blood sugar is 9.5 mmol/L.’
ABG: One of the most important investigations in an exacerbation of COPD. It allows assessment of the degree of oxygenation (PaO2) and ventilation (PaCO2). Check within 20 minutes of starting or changing flow of oxygen. Aim for a PaO2>6.6 kPa and H+<55 (pH>7.25). If this is achieved, increase the oxygen to achieve PaO2>7.5 kPa. Aim for oxygen saturations of 88–92%. If possible, compare to a baseline, e.g. clinic ABG result
CXR: To exclude other causes of dyspnoea, especially a pneumothorax. Look for areas of consolidation. This is a priority investigation and may need to be a portable CXR if the patient is not stable enough to go to the X-ray department
‘ABG (on 2 L/min oxygen) PaO26.0 kPa, PaCO23.1 kPa, H+33 nmol/L (pH 7.48), HCO3−26 mmol/L. WCC 8.6×109/L. CRP is 12 mg/L. Renal function is normal. CXR shows hyperinflated lungs with coarsening of the background markings in keeping with COPD. No consolidation or pneumothorax. ECG: sinus rhythm.’
|Parameter||Value||Normal range (units)|
|Haemoglobin||150 g/L||Men: 135–177 (g/L)|
Women: 115–155 (g/L)
|CRP||12 mg/L||0–5 (mg/L)|
|Urea||4.5 mmol/L||2.5–6.7 (mmol/L)|
|Creatinine||112 μmol/L||79–118 (μmol/L)|
|eGFR||>60 mL/min||>60 (mL/min)|
|Sodium||140 mmol/L||135–146 (mmol/L)|
|Potassium||4.5 mmol/L||3.5–5.0 (mmol/L)|
|PaO2||6 kPa on air||>10 (kPa) on air|
|PaCO2||3.1 kPa||4.7–6.0 (kPa)|
|HCO3||26 mmol/L||22–26 (mmol/L)|
|H+||33 nmol/L||35–45 (nmol/L)|