Acute respiratory failure in a 68-year-old man

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Problem 53 Acute respiratory failure in a 68-year-old man

Having just finished congratulating yourself for managing your last case so well, you are called to see a 68-year-old man brought into the emergency department by ambulance with severe dyspnoea. He is accompanied by his wife, who states that he has had increasing shortness of breath overnight with some symptoms of an upper respiratory tract infection for the last day or so. Over this time he has also had increasing wheeze and a dry cough with ‘tightness’ of his chest. He has become somewhat agitated this morning.

He is in obvious respiratory distress, unable to utter more than one or two words at a time.

This man obviously needs urgent assessment and treatment. You only have time to elicit the essential parts of the history while you rapidly examine the patient and start the appropriate management.

Q.1

What are the major differential diagnoses to consider immediately?

The patient’s breathing is so laboured that he is unable to answer any of your questions.

Q.2

What are the main points of further information that you would like to elicit from his wife and ambulance officers?

The man’s wife tells you that he has ‘pretty bad’ emphysema. He has no known history of cardiovascular disease.

His medications are:

• Salbutamol inhaler: 2 puffs prn (1–3 times on a typical day).

• Salmeterol: 2 puffs metered dose inhaler bd.

• Fluticasone: 500 µg metered dose inhaler bd.

• Ipratropium bromide: 2 puffs metered dose inhaler bd.

He has smoked heavily for most of his life, but has reduced his current cigarette consumption to about five a day. He does not drink and has no known allergies.

The ambulance officer states that haemoglobin oxygen saturation (measured by pulse oximetry, SpO₂) has been around 80% throughout the journey, and that he has been wheezing loudly. He has been given 5 mg nebulized salbutamol in the ambulance.

As you examine the patient, you observe that on 6 L/min of oxygen by face mask, his SpO₂ is 78%. He seems irritable, obviously dyspnoeic, and grasping the sleeve of your designer shirt, he utters ‘help …’.

You persist with the examination. His respiratory rate is 30 breaths per minute with a prolonged expiratory phase. The pulse rate is 110 bpm and regular. His temperature is 36.5°C and the blood pressure 110/75 mmHg. He is well hydrated and peripheral perfusion is adequate. His peripheral pulses are all present and of good volume. In the semi-recumbent position his jugular venous pulsation (JVP) is 3–4 cm above the base of the neck. Both heart sounds appear normal and there are no murmurs. His trachea is in the midline. He is barrel-chested and there are reduced breath sounds throughout. There is a diffuse expiratory wheeze and the percussion note is normal, there are no crepitations. His abdomen is soft and non-tender. His calves are normal and there is no pedal or sacral oedema.

Q.3

What investigations should be performed straight away?

An electrocardiogram is performed which shows a sinus tachycardia. His arterial blood gas (ABG) results are as follows:

Investigation 53.1 Arterial blood gas analysis

PaO₂	48 mmHg
PaCO₂	70 mmHg
pH	7.24
Bicarbonate	29 mmol/L

Q.4

What does his arterial blood gas show?

You adjust his oxygen therapy carefully. He is too dyspnoeic for a peak expiratory flow rate (PEFR) measure. You order an urgent mobile chest X-ray and go on to administer emergency medications to treat this man’s condition.

Q.5

What should you do immediately with his supplemental oxygen therapy?

Q.6

Outline your options for administering supplemental oxygen to his man.

A chest X-ray is performed and is shown in Figure 53.1.

Figure 53.1

Q.7

What does the X-ray show? What is your diagnosis?

Q.8

Describe in detail what you would use to treat this man.

The patient starts to improve, but he is still struggling. You call the intensive care team, who admit him to the intensive care unit (ICU). He receives close monitoring of his gas exchange. He is placed on BPAP (bi-level positive airway pressure ventilation by non-invasive face mask) to support his ventilation. A radial arterial line is inserted to monitor blood gases.

The patient responds almost instantaneously with BPAP, reporting a marked reduction in dyspnoea. Oxygen therapy is carefully monitored and adjusted in the ICU. Bronchodilators are continued and he is commenced on a course of oral prednisolone beginning with 50 mg daily. His blood gases stabilize with improvement in his respiratory condition, achieving almost his baseline level of function over several days with PaO₂ 65 mmHg on 1 L/minute via nasal cannulae, PaCO₂ 53 mmHg, pH 7.38, bicarbonate 28 mmol/L.

He is discharged after 7 days in hospital to complete a 10-day course of prednisolone (dose to be tapered according to clinical progress), a programme for respiratory rehabilitation and to discontinue smoking, and follow-up appointments in the respiratory medicine clinic with pulmonary function testing.

Answers

A.1 In the absence of an obvious external cause (e.g. chest trauma, upper airways obstruction), the vast majority of cases of acute shortness of breath in adults will be due to one of four conditions:

• Exacerbation of chronic obstructive pulmonary disease (COPD) or asthma.

• Pneumonia/lower respiratory tract infection or irritation (such as aspiration).

• Pulmonary embolism.

• Pulmonary oedema (it is important to look for the underlying causes, e.g. myocardial ischaemia or cardiac arrhythmia, and non-cardiogenic causes).

Spontaneous pneumothorax, while much less common than the conditions above, is also an important diagnosis to consider.

Anaemia and metabolic acidosis may also cause tachypnoea and, along with pulmonary embolism, should be sought particularly in patients with normal-appearing plain chest radiograph.

A.2 You will need to have:

• A brief account of what has happened since the onset of his illness, including his condition on arrival of the ambulance officers and any treatment given so far. It is important to know the current trend of his condition (e.g. rapidly deteriorating, stable, improving, etc.) and response to treatment, as this can give you important clues to the diagnosis and vital information on the urgency and aggressiveness of intervention required.

• A ‘problem list’ of his active and inactive medical conditions.

• A list of his current medications.

• Information about any allergies.

A.3 The most important immediate investigations are:

• Arterial blood gas (ABG) analysis.

• Mobile chest X-ray.

All are quick to perform, and can be done while the patient is being examined and treated.

ABGs provide results within minutes, can be done in many emergency departments and intensive care units, and provide information on blood gases, acid–base status, most vital electrolytes (including sodium, potassium, chloride, bicarbonate, ionized calcium), blood glucose, and haemoglobin. All of these parameters are important in the assessment of any acutely unwell patient and can immediately influence the course of treatment.

ABGs performed on room air are not necessary, and should not be performed in patients requiring supplemental oxygen to maintain adequate SpO₂.

Complete blood picture, full electrolyte panel and cardiac enzymes should also be requested, but results may take some time to become available.

A.4 The ABGs show severe hypoxaemia. His acid–base status cannot be fully determined with the information available; however, the ABG result is consistent with acute on chronic respiratory acidosis.

The presence of a low arterial blood pH indicates the PaCO₂ is acutely raised. As a rough guide, for every acute increase in PaCO₂ of 10 mmHg, pH falls by approximately 0.07, and bicarbonate increases by about 1 mmol/L. In ‘chronic’ hypoventilation, compensatory mechanisms can bring the pH almost back to normal (takes about 2–3 days), with bicarbonate increasing by approximately 3 mmol/L for every 10 mmHg increase in PaCO₂.

Working backwards accordingly, it can be estimated that this man’s baseline ‘chronic’ PaCO₂ would be around 50 mmHg, and bicarbonate around 27 mmol/L. In addition to acute respiratory acidosis, he also has chronic respiratory acidosis with metabolic compensation.

Insufficient results have been provided for calculation of his anion gap; however, this is always important to calculate in order to detect a concurrent wide anion-gap metabolic acidosis (e.g. from ingested toxins, lactataemia from ischaemic bowel, alcoholic/starvation/diabetic ketoacidosis, etc.).

A.5 A major error in this patient would be to reduce the supplemental oxygen therapy. Patients do not lose their ‘hypoxic drive’ (if this phenomenon actually exists) unless they have lost their hypoxia! His PaO₂ is 48, i.e. he is definitely still hypoxaemic, and this is contributing to his agitation and confusion.

• Titrate the O₂ up, aiming for a SpO₂ of around 90–94%, regardless of what is happening with his PaCO₂.

• Haemoglobin oxygen saturation (SaO₂) is more important as a clinical end point for titration of supplemental oxygen therapy than PaO₂. This is so for three main reasons. First of all, SaO₂ is a much greater determinant of the actual amount of oxygen in arterial blood being delivered to tissues than PaO₂, where blood oxygen content = (1.36 × Hb × SaO₂) + (0.0031 × PaO₂). Secondly, SaO₂ can be monitored almost continuously and non-invasively using SpO₂ (pulse oximetry). Thirdly, the haemoglobin–oxygen dissociation curve is ‘shifted to the right’ by both acidosis and high PaCO₂, meaning that for any given PaO₂, the SaO₂ is lower. Therefore while the PaO₂ may appear satisfactory at around 60 mmHg, SaO₂ will be <90%, and therefore arterial oxygen content insufficient. For example, with pH 7.24 and PaCO₂ 70 mmHg, a PaO₂ of 60 mmHg will produce SaO₂ of around 85%, and PaO₂ of 55 mmHg will produce SaO₂ of around 81%. Clearly, a PaO₂ of 55–60 mmHg is inadequate for such a patient.

• Hypercapnia needs to be followed clinically (rate and depth of respiration, signs of hypercapnia such as drowsiness, vasodilatation, bounding pulses, asterixis) and with periodic ABGs. Remember that good SpO₂ readings do not mean that the patient’s ventilation is adequate – alveolar ventilation is monitored by the PaCO₂. An arterial line should be inserted to allow frequent ABG analysis. If PaCO₂ is either increasing or elevated with associated respiratory acidosis, ventilatory support in the form of non-invasive mechanical ventilation (NIV, including bi-level positive airway pressure – BPAP) or invasive ventilation (involving induction of anaesthesia and endotracheal intubation) may be needed to control this, not a reduction in supplemental oxygen (unless SaO₂ is greater than 94%).

• Nasal cannulae can be used with oxygen flow rates of up to 6 L/min, although many patients experience discomfort and drying of nasal mucosa with flow rates greater than 4 L/min. Pure oxygen from the nasal cannulae is mixed with room air during inspiration and hence the actual inspired concentration of oxygen (fraction of inspired oxygen, FiO₂) can vary depending on nose versus mouth breathing, as well as several other factors such as the patient’s rate and depth of respiration. As a rough guide, nasal cannulae increase the inspired oxygen percentage by approximately 3 for every L/min of oxygen flow (e.g. inspired oxygen of around 28% at 2 L/min).

• If nasal cannulae are insufficient, a face mask (called medium capacity O₂ mask (MCOM)) can be used, with a minumum oxygen flow of 6 L/minute. MCOMs can deliver up to around 50% inspired oxygen, with the same caveats as discussed above with nasal cannulae.

• Non-rebreather masks with 15 L/min oxygen flow can deliver close to 100% inspired oxygen (provided the patient is inspiring at a rate slower than 15 L/min); however, the oxygen is not humidified, and inadequate humidification of inspired gases leads to abnormal mucociliary function.

• Venturi masks can be useful in controlling the FiO₂ in these patients more reliably than nasal cannulae and ordinary MCOMs. Venturi masks deliver gas at a predetermined percentage of oxygen directly to the patient by utilizing the entrainment of a high (and fixed) volume per minute of room air with a fixed flow rate of oxygen. This removes the variability in room air entrainment inherent in gas delivery methods where rate of inspiration is greater than rate of gas delivery.

• ‘High flow humidified oxygen circuits’ (HFOs) also provide accurate control of FiO₂ by delivering a high volume of gas per minute, thereby minimizing entrainment of room air during inspiration. Because the gas they deliver is humidified, they are the preferred method of providing a high FiO₂ to patients beyond the acute setting.

A.7 The chest X-ray shows flattening of the diaphragms consistent with ‘gas trapping’, which reflects the inability of gas to escape from the lungs due to airways obstruction. The lung fields are clear, with no evidence of alveolar consolidation or oedema.

This man is having an exacerbation of his COPD.

He is starting to succumb to respiratory fatigue, and hence hypoventilate. The work of breathing is becoming too much for him. This is reflected by his climbing PaCO_2, as the carbon dioxide in his alveoli is not being ‘washed out’ due to inadequate ventilation.

• Remember that cough and wheeze can also be due to pulmonary oedema (‘cardiac asthma’).

Those with low tidal volumes may not have prominent crepitations or wheeze, due to the low volumes of gas reaching the alveoli and low air flows. Thus, the absence of crepitations does not exclude cardiogenic pulmonary oedema, and a lack of wheeze does not exclude airways disease.

Chest tightness is a symptom commonly described by patients with bronchoconstriction as well as patients with cardiac angina.

For these reasons, acute pulmonary oedema (which may have been precipitated by cardiac ischaemia or infarction) was an important differential diagnosis in this man’s presentation, and thus the emergent importance of a CXR and ECG.

• Beta-2 adrenergic agonists are indicated. The conventional way to use them is to nebulize 2.5–5 mg of salbutamol, diluted to a total of 3 mL with normal saline (to make up an appropriate volume for nebulization), repeated continuously up to three doses in a row (takes about 15 minutes each). The maximal response is usually reached after three continuous doses.

• Ipratropium bromide is also useful, suggested to be particularly so for COPD, at a nebulized dose of 250–500 µg every 4–6 hours.

• If the patient’s ventilatory status is poor, the dose of nebulized medication actually reaching the airways (rather than being nebulized into the environment for the medical and nursing staff to breathe) may be markedly reduced. Undiluted nebulized salbutamol and continuous nebulized salbutamol can be used; however, there is doubt over the effectiveness of these techniques.

• All parenterally administered sympathomimetics and methylxanthines (such as aminophylline) are less effective and more hazardous than the inhaled bronchodilators discussed above, and are nowadays rarely used.

• A common mistake is to continue aggressive nebulized or parenteral beta-2 adrenergic agonists in an attempt to completely eliminate wheeze and dyspnoea. In exacerbations of chronic airways disease and asthma, acute mucosal inflammation with oedema and increased mucus production are often significant contributors to airflow limitation. Maximal bronchodilatation is still the goal; however, airflow limitation with wheeze can still be present when this has been achieved. Time for the precipitating event (such as airway irritation or infection) to resolve and airway inflammation to settle (assisted by corticosteroids) is needed before baseline airway patency can be achieved. In the meantime oxygen, bronchodilator therapy and ventilatory assistance are continued as required to support the patient through the exacerbation. Continuing administration of beta-2 adrenergic agonists can lead to significant toxicity with hypokalaemia, tachyarrhythmias, lactic acidosis, tremor and hypoxaemia (beta-2 mediated pulmonary vascular dilatation and consequent ventilation–perfusion mismatch) among their prominent adverse effects.

• Continuous or bi-level positive airway pressure (CPAP and BPAP) are both modalities of ‘non-invasive’ ventilatory (NIV) support (non-invasive means not requiring endotracheal intubation). NIV utilizes a ventilator machine with a face (or nose) mask to apply pressure during inspiration and expiration. NIV is a vital component of the management of acute exacerbation of COPD, where important contraindications (most notably the need for immediate endotracheal intubation) are not present. When used correctly, NIV can reduce the need for intubation, which is associated with a higher incidence of ventilator-related complications and poorer patient outcome. ‘Gas trapping’ (gas not exhaled before the next inspiratory breath due to airflow limitation) creates an elevated intrathoracic pressure which must be overcome by the patient’s respiratory muscles before air will actually enter the lungs (via a pressure gradient). This ‘threshold work of breathing’ is countered by NIV at the onset of inspiration. Patients often report an immediate improvement in their symptoms on correct application of NIV. NIV can also assist inspiration, thereby helping them to achieve better alveolar ventilation and hence a lower PaCO₂.

• A short course of systemic corticosteroids starting with 40–60 mg of oral prednisolone or equivalent daily, preferably given in the mornings, and tapered over 7–10 days should be given. Longer courses have been shown to be of no further benefit. Parenteral corticosteroids have not been found to be more effective than orally administered therapy provided that patient is capable of taking oral medication.

• Inhaled corticosteroids (in addition to systemic corticosteroids) may also be helpful, and doses required are around 500–1000 µg of budesonide nebulized every 15–30 minutes. Dose-dependent, rapid-onset non-genomic effects take place within minutes and include vasoconstriction which can reduce hyperaemia in inflamed mucosa and may potentiate the effect of adrenergic bronchoconstrictors. Clinical evidence, however, is not yet sufficient for their use to be included in management guidelines.

• A course of immunosuppressive glucocorticoids can result in the emergence of infectious agents such as fungi, Pneumocystis and Mycobacterium tuberculosis (TB). Those with a suspicion of latent (or even active) TB should be referred to the appropriate clinic for further assessment and advice.

• Antibiotics are not always indicated in acute exacerbations of COPD as non-infectious and viral LRTI may be responsible. When antibiotics are commenced empirically, patients with COPD require broader-spectrum coverage (including Pseudomonas). Typical antibiotics used for empirical cover include one of either ticarcillin (± clavulanic acid), piperacillin (± tazobactam), cefepime, or a carbapemen (e.g. meropenem) along with a macolide (e.g. azithromycin) to cover bacterial organisms of ‘atypical’ pneumonia (e.g. Legionella, Mycoplasma). Outcomes in severe Streptococcus pneumoniae pneumonia may also be improved by the addition of a macrolide antibiotic to ‘standard’ antibiotic cover for pneumococcus. Newer-generation quinolones such as moxifloxacin provide an important alternative for patients with contraindication to beta-lactam antibiotics, as well as some coverage for ‘atypical’ bacterial organisms.

• Mucolytics and chest physiotherapy have been shown to be ineffective in acute exacerbation of COPD.

Revision Points

In acute respiratory failure:

• Hypoxia is the enemy.

• It is never correct to reduce oxygen supplementation when severe hypoxaemia and tissue hypoxia are present.

• The minimum amount of oxygen should be used to achieve adequate tissue oxygenation in patients with chronic hypercapnoeic respiratory failure. The usual target in these patients is SaO₂ (measured on ABG and monitored clinically using pulse oximetry, SpO₂) of 90–94%, while also ensuring adequate cardiac function. It is not correct to conclude that arterial oxygen content is adequate by looking at the PaO₂. Many factors alter the haemoglobin-oxygen dissociation relationship (including acid–base status and PaCO₂), and haemoglobin-oxygen saturation (SaO₂) is a much greater determinant of blood oxygen content than PaO₂.

• Not all people with a diagnosis of COPD are ‘CO₂ retainers’ with ‘hypoxic drive’.

Fatigue from sustained and severely elevated work of breathing is a common cause for rising PaCO₂ in patients with acute severe exacerbation of COPD; however, a loss of ‘hypoxic drive’ (hypoxia replacing hypercapnia as a stimulus to breath) is often blamed, resulting in an inappropriate reduction in supplemental oxygen even in the presence of hypoxaemia. Nonetheless, oxygen supplementation in patients with chronic hypercapnoeic respiratory failure can result in an increase in hypercapnia. The Haldane effect (haemoglobin binding to oxygen as hypoxaemia is treated results in displacement of CO₂ bound to haemoglobin, thus releasing CO₂ into plasma) and V/Q (ventilation–perfusion) mismatch due to oxygen induced reduction in pulmonary vasoconstriction are important causes of hypercapnia which have been found in these patients. The significance of ‘hypoxic drive’ in COPD exacerbations is yet to be conclusively demonstrated. The most important cause from a clinical standpoint remains the inability to sustain such a high work of breathing.

• A common mistake is to interpret wheeze and evidence of airflow limitation as inadequate bronchodilator therapy, and beta-2 adrenergic agonist toxicity can contribute significantly to the patient’s deterioration. Airflow limitation caused by acute mucosal inflammation, oedema and increased mucus production takes time to resolve, requires the inciting event to be removed and is expediated by corticosteroids.

• A course of corticosteroid, particularly if prolonged, places the patient at risk of developing opportunistic infection and adrenal suppression. TB is an important consideration. Pneumocystis infection can emerge even after the cessation of steroid treatment.

• The presence of chronic lung disease, immunosuppresive steroid therapy and previous courses of antibiotics and hospital admissions must be taken into consideration when deciding empirical antibiotic therapy for patients with suspected bacterial infective exacerbation of COPD.

Issues to Consider

• What are the normal physiological mechanisms behind respiratory drive?

• What forms of ventilatory assistance are useful in this situation, and how are they used? What are the indications for ventilatory assistance?

Further Information

www http://www.goldcopd.org. Global strategy for the diagnosis, management and prevention of COPD, Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2010

www http://www.thoracic.org/clinical/copd-guidelines/resources/copddoc.pdf. American Thoracic Society/European Respiratory Society Task Force. Standards for the diagnosis and management of patients with COPD 2004

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