A, B, C, D, E is still the way to approach any patient, including one with respiratory failure (Box 4.1)
Box 4.1 Approach to a patient with respiratory failure A
• relieve any upper airway obstruction
• administer oxygen
• count respiratory rate
• treat wheezing, fluid, consolidation or pneumothorax
• assess oxygen saturations and arterial blood gases
• consider if ventilatory support is required early and if so, what method
• fluid therapy
• treat any associated severe sepsis (see Chapter 7) D
• assess conscious level as this affects treatment options E
• full history and examination once A, B and C are stable
1. A 30-year-old lady is admitted with acute severe asthma. Her vital signs are as follows: BP 100/60 mmHg, pulse 130, RR 40 per minute with poor respiratory effort, temperature 37°C and she is drowsy. Her arterial blood gases on 10 litres per minute reservoir bag mask show: pH 7-15, PaCO2 9-0 kPA (70 mmHg), PaO2 7 kPA (54 mmHg), bicarbonate 22 mmol/l, BE - 5. What is your management?
2. Later on ICU the same patient develops hypotension (60/30 mmHg). The patient is paralysed and the ventilator is set to 12 breaths per minute. The inspiratory to expiratory ratio is 1:4, tidal volumes are 600 ml, and peak airway pressures are 45 cm H20. She is on volume-controlled ventilation. What are the possible causes of the hypotension and what is your management?
3. A 50-year-old man is admitted with an exacerbation of his COPD. His arterial blood gases on 28% oxygen (Venturi mask) show: pH 7-3, PaCO2 8-0 kPA (62 mmHg), PaO2 7 kPA (54 mmHg) bicarbonate 29 mmol/l, BE + 3. What is your management?
4. A 40-year-old man with no past medical history is admitted with a severe pneumonia. His vital signs are: BP 120/70 mmHg, pulse 110, RR 40 per minute, temperature 38°C and he is alert. His arterial blood gases on 15 litres per minute via a reservoir bag mask show: pH 7-31, PaCO2 4-0 kPA (31-mmHg), PaO2 6 kPA (46 mmHg), bicarbonate 14 mmol/l, BE - 8. What do you do?
5. You are called to see a 70-year-old man who is 2 days post-laparotomy. He has developed a cough with green phlegm and fever. His respiratory rate is increased (30 per minute) and his arterial blood gases on 10 litres per minute simple face mask show: pH 7-3, PaCO2 8-0 kPA (62 mmHg), PaO2 7-6 kPA (58 mmHg), bicarbonate 29 mmol/l, BE + 4. What is your management?
6. A 60 kg 25-year-old lady with Guillain—Barré syndrome has been undergoing twice-daily forced vital capacity (FVC) measurements and treatment with intravenous immunoglobulin. Her FVC has fallen below 1 litre and her arterial blood gases on air now show: pH 7-3, PaCO2 7-5 kPA (58 mmHg), PaO2 10 kPA (77 mmHg), bicarbonate 27 mmol/l, BE + 3. Her respiratory rate is 28 per minute. What do you do?
7. A 60-year-old man is admitted with acute severe left ventricular failure. He has been given 100 mg intravenous frusemide, salbutamol nebulisers, and a small dose of intravenous diamorphine. His arterial blood gases on 10 litres per minute oxygen via a reservoir bag mask show: pH 7-15, PaCO2 7 kPA (54 mmHg), PaO2 9 kPA (70 mmHg), bicarbonate 18 mmol/l, BE - 8. His blood pressure is 180/90 mmHg and his respiratory rate is 38 per minute. What is your next step?
8. A 50-year-old lady is admitted with breathlessness. On examination she has an unrecordable blood pressure (which is 80 systolic by palpation). Her pulse is 110 per minute, RR 36 per minute, and she is alert. The chest sounds clear. The ECG shows sinus tachycardia with right heart strain and her chest x ray film is normal. The arterial blood gases on 15 litres per minute via a reservoir bag mask show: pH 7-25, PaCO2 3-0 kPA (23 mmHg), PaO2 12 kPA (92 mmHg), bicarbonate 10 mmol/l, BE - 12. What is the diagnosis and what is your management?
9. A 70-year-old man with COPD is admitted in extremis. He has been more breathless for a few days. He responds to painful stimuli only, his blood pressure is 130/60 mmHg, pulse 120 per minute and arterial blood gases on air show: pH 7-1, PaCO2 14-0 kPA (108 mmHg), PaO2 6 kPA (46 mmHg), bicarbonate 20 mmol/l, BE - 4. What is your management?
10. A 30-year-old man arrives with pleurisy. There seems to be no obvious explanation for this and he has had a previous DVT. Calculate the A-a gradient using the arterial blood gas sample taken whilst the patient is breathing air. pH 7-5, PaCO2 4-0 kPa (30-7 mmHg) bicarbonate 24 mmol/l, BE 0, PaO2 10-0 kPa (77 mmHg).
11. Your team is treating a patient with acute respiratory distress syndrome (ARDS) associated with pneumonia. He may need ventilation if his condition worsens. His physiology is stable apart from a respiratory rate of 30 per minute. Your boss has asked you to calculate the A-a gradient daily so that his progress can be charted. Yesterday's A-a gradient was 47 kPA. Today he is breathing 60% oxygen and his arterial blood gases show: pH 7-35, PaCO2 5-6 kPA (43 mmHg), bicarbonate 22.5 mmol/l, BE - 1, PaO2 10-0 kPA (77 mmHg). What is the A-a gradient today?
1. The arterial blood gases show a respiratory acidosis with hypoxaemia. Nine per cent of people with an attack of acute severe asthma have respiratory failure; 1% patients with asthma have a fatal or near fatal attack each year. Previous life-threatening attacks increase the risk of death from asthma. Initial management here is to ensure there is no upper airway obstruction, administer the highest concentration of oxygen possible (15 litres per minute via a reservoir bag mask) and treat her breathing with medication to relieve lower airway obstruction. The initial assessment of breathing should include looking for clinical signs of a pneumothorax, which can occur in asthma. The ICU team should be contacted immediately. A large bore intravenous cannula should be inserted and fluid given quickly (for example, 1-2 litres 0-9% saline stat) because the patient is likely to be dehydrated and needs imminent intubation. We can assume she is drowsy because of hypercapnia and hypoxaemia, but a bedside blood glucose estimation followed by a formal neurological examination should be performed once A, B and C are stable.
2. Patients with severe asthma who have just been intubated require long expiratory times because of severe airway obstruction. This limits the respiratory rate, otherwise stacking or "gas trapping" occurs. The expiratory time can be lengthened by reducing the respiratory rate or decreasing the inspiratory time (by increasing the inspiratory flow rate) or a combination of the two. Suitable settings would be 6-8 breaths per minute with an inspiratory to expiratory ratio of 1:4 or longer. The ventilator should be set to a pressure limit to prevent barotrauma and with peak airway pressures not exceeding 35-40 cm H20. This is slightly complicated by the fact that peak pressures in acute severe asthma do not necessarily reflect alveolar pressures but the pressures needed to overcome bronchial obstruction. An appropriate tidal volume should be < 10 ml kg-1. After excluding pneumothorax and volume depletion in this case, consider stacking as a cause of hypotension. The ventilator should be disconnected and the patient allowed to passively exhale - this can take several seconds and a prolonged wheeze can be heard by placing an ear near the end of the endotracheal tube. If this is the cause, the blood pressure will return to normal within seconds. PEEP is not usually of benefit in acute severe asthma as patients already have significant intrinsic or auto-PEEP.
3. The arterial blood gases show a respiratory acidosis with hypoxaemia. Initial management includes an assessment of his airway, medical treatment of his lower airway obstruction, and any other lung pathology that may have triggered his breathlessness (for example, pneumonia or pneumothorax). His oxygen should be increased using a 35% Venturi mask to get the PaO2 to around 8-0 kPA (60 mmHg). Intravenous fluid should be started for dehydration. If there is no prompt improvement of his respiratory acidosis with medical therapy, non-invasive ventilation should be started. Oxygen therapy is given through the ventilator mask, titrated to arterial blood gases.
4. This man is at risk of further physiological deterioration. He has hypoxaemic respiratory failure despite a high concentration of oxygen. His respiratory rate is 40 per minute. There is also a metabolic acidosis which could indicate hypoperfusion. In this situation, non-invasive CPAP in a critical care area could be tried. This will improve oxygenation and can reduce the work of breathing. However, intubation is indicated within hours if there is no improvement. Intravenous fluids should be administered to treat hypoperfusion, improve oxygen delivery, and aid the expectoration of secretions.
5. The arterial blood gases show a respiratory acidosis with hypoxaemia. Postoperative chest infections and respiratory failure often involve atelectasis (owing to the effects of supine position, general anaesthesia, and difficulty in taking a deep breath from poor pain relief). Retained secretions may be the result of an inability to cough properly. Therefore, close attention should be paid to improving analgesia to allow deep breaths and proper coughing. The acute pain team can be consulted, who may suggest epidural analgesia. Physiotherapy also has an important role to play and in some cases acute physiotherapy can significantly improve respiratory function. Humidified oxygen therapy is indicated in this circumstance as this aids the expectoration of secretions. The oxygen concentration should be increased. Antibiotics should be commenced and blood and sputum cultures sent. If these measures do not help, the ICU should be contacted for advice on further respiratory support.
6. There is a respiratory acidosis. This patient needs intubation both to support ventilation and to protect the airway from aspiration because of the profound muscle weakness seen in patients with Guillain-Barre syndrome. Up to 30% patients with this syndrome admitted to hospital require mechanical ventilation. There is evidence of ventilatory failure (high PaCO2 and increased respiratory rate) as a result of increasing respiratory muscle weakness as indicated by the falling FVC. Closer examination may reveal a patient who is using accessory respiratory muscles and has a cough, which is bovine in nature. Neurological examination may reveal poor bulbar function. Monitoring oxygen saturations and arterial blood gases in this condition are of little help when deciding when to institute respiratory support. Arterial blood gases follow the condition rather than precede it. Autonomic neuropathy can accompany Guillain-Barre syndrome, leading to tachycardia and hypotension, which also require close observation, especially during anaesthesia and intubation, which can precipitate an asystolic cardiac arrest from profound vagal stimulation. Plasmapheresis is useful in severe or rapidly progressing cases.
7. The arterial blood gases show a mixed respiratory and metabolic acidosis with a lower than expected PaO2. After his airway has been assessed and oxygen increased to 15 litres per minute, the breathing and circulation are treated in the following way: preload is reduced by sitting the patient up and giving small doses of intravenous diamorphine. Frusemide is a pulmonary vasodilator as well as a diuretic and has a quick onset of action in acute severe left ventricular failure. Around 1 mg kg-1 frusemide is given in the first instance and an intravenous nitrate infusion (a vasodilator) can be commenced, titrated to effect and blood pressure. If the patient does not improve, a further dose of frusemide (1-2 mg kg-1) is administered. After this, non-invasive CPAP is indicated to improve both left ventricular and respiratory function. This is appropriate in alert patients with a moderate respiratory acidosis. If the patient deteriorates or fails to improve, intubation is indicated.
8. The airway is fine, as the patient is alert and talking. Breathing and circulation are abnormal. She is extremely breathless but the chest x ray film is normal and the chest sounds clear. Is this because of shock alone? Her arterial blood gases show a lower than expected PaO2 (the A-a gradient is 41-2 assuming an FiO2
of 0-6) and a metabolic acidosis from hypoperfusion. The diagnosis is massive pulmonary embolism. Treatment is to give a high concentration of oxygen (for example, 15 litres per minute via a reservoir bag mask), fluid challenges, and thrombolysis. Intravenous thrombolysis should be considered in pulmonary embolism causing shock and is as effective as surgical embolectomy. Newer literature suggests thrombolysis is safe and effective in "sub-massive" pulmonary embolism as well.
9. The arterial blood gases show a severe respiratory acidosis with a metabolic acidosis and hypoxaemia. Management is to secure the airway by intubation, administer enough oxygen to get the PaO2 to around 8-0 kPA (62 mmHg), treat his exacerbation of COPD and any precipitating infection, and give intravenous fluid. Breathless patients who have been unwell for a few days are often dehydrated and general anaesthesia can cause vasodilatation which also leads to hypovolaemia. This patient has a base deficit of - 4 suggesting hypoperfusion. An unresponsive patient is not appropriate for non-invasive ventilation. However, before the patient is intubated, further information should be sought as to the severity of the patient's chronic lung disease. Has a discussion already taken place about intubation and ventilation between the patient and his specialist? Do the next of kin have information about what the patient would want in these circumstances? What was his quality of life beforehand and what is his anticipated quality of life after potential discharge from ICU?
10. A-a gradient in kPA = 20 - (3-5/0-8) - 10 = 5.0. This is above normal for this patient - this could indicate a pulmonary embolism given the history.
11. A-a gradient in kPA = 0-6 x 95 - (5-6/0-8) - 10-0 = 40. His physiology is stable, the PaCO2 is satisfactory and the A-a gradient is improving rather than worsening.
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