Chapter 3. Respiratory medicine
The breathless patient: the general approach 56
Is this patient’s breathlessness due to his heart or his lungs?56
Introduction
This chapter explains the basic principles underlying these two areas and then applies them to the assessment and management of the types of respiratory cases that you will encounter on a day-to-day basis: asthma, COPD and pneumonia.
The Breathless Patient: The General Approach
Is this patient’s breathlessness due to his heart or his lungs?
The two most important and most difficult questions in a breathless patient are always:
• is this cardiac or respiratory breathlessness?
• is this a pulmonary embolus?
Differentiating the causes of breathlessness can be very difficult, and the history and examination will not always provide an answer. Symptoms and signs are shared by many of the common respiratory and cardiac conditions. Thus a patient with LVF and a patient with acute asthma will both have nocturnal breathlessness and severe wheeze. Ankle swelling is characteristic of congestive heart failure, but it can also be a complication of severe COPD. The difficulties are often age related. If a young person presents with a history of intermittent wheeze, breathlessness and cough, the diagnosis is almost certain to be asthma; but what about the obese, wheezy, 70-year-old smoker with previous myocardial infarcts and chronic venous disease in both legs? Why is the patient short of breath? COPD? Pulmonary oedema? Pulmonary embolus?
What tests will be needed to make the right diagnosis?
It can be helpful to remember a few ground rules about the investigation of patients with unexplained breathlessness.
• In breathlessness caused by LVF:
— the chest X-ray will show pulmonary oedema
— the ECG is abnormal, showing ischaemia, strain or an arrhythmia
— a cardiac echogram will confirm poor left ventricular function
• In breathlessness caused by pulmonary emboli:
— the diagnosis is often missed, usually because it is not considered
— risk factors are usually present (recent surgery, phlebitic legs, etc.)
— when in doubt, anticoagulate and scan the lungs to confirm later
Principles of emergency treatment
The principles of emergency treatment are set out in Box 3.1 below. It must be recognised, however, that on occasions in a critically ill patient with unexplained breathlessness it may be appropriate to cover a number of diagnostic options until the picture becomes more clear and the results of further tests become available.
Box 3.1
1. Correct the immediate and life-threatening problems
| — Hypoxia | Oxygen Ventilation |
| — Acidosis | Correct high arterial carbon dioxide |
| — Hypotension | Fluids ± inotropic support |
2. Treat the cause
| — Pulmonary oedema | Diuretics Vasodilators |
| — Bronchoconstriction | Bronchodilators Steroids |
| — Pulmonary embolism | Anticoagulants |
| — Pneumonia | Antibiotics |
| — Tension pneumothorax | Intercostal drain |
3. Prevent further attacks
| — Asthma | Education |
| — Pulmonary oedema | Review previous cardiac therapy |
| — Pulmonary embolism | Warfarin |
Respiratory Failure
Normal ventilation is a process in which fresh air is brought through the airways to the alveoli, where it is in intimate contact with blood in the pulmonary capillaries. Gas exchange occurs across the alveolar-capillary interface: oxygen passes from the alveoli into the blood and carbon dioxide passes from the blood into the alveoli. We measure blood gas partial pressures to assess the efficiency of this two-way traffic: the arterial pO2 tells us about oxygenation; the arterial pCO2 indicates how well the lungs are venting carbon dioxide.
Type I and Type II Respiratory Failure
The lungs are more efficient at venting carbon dioxide than they are at oxygenating blood. As a result, during the development of respiratory failure, problems with oxygenation occur well before carbon dioxide starts to build up. When things start to go wrong, the patient compensates for lesser degrees of carbon dioxide retention by increasing ventilation and blowing off the build-up of carbon dioxide. Thus, if you look at the blood gases in a case of acute asthma, you will find that, in the early stage of an attack, carbon dioxide levels in the blood are often lower than normal.
Unfortunately, this compensatory mechanism does not work at all well for problems with oxygenation. You will find, for example, that arterial oxygen levels decrease early on in an attack of asthma. Several conditions have a similar pattern of hypoxia without carbon dioxide retention: this pattern is termed ‘Type I’ respiratory failure (→Fig. 3.1 and Box 3.2). (Look at ward blood gas results in some of the conditions mentioned in Box 3.2– in Type I respiratory failure the arterial pO2 is less than 8kPa, with a normal or low carbon dioxide at 4kPa or less. You need to remember that these figures apply to patients whose gases are measured while they are breathing room air; once oxygen is given to patients with Type I respiratory failure, the pO2 increases.)
Box 3.2
• The early part of an attack of asthma
• The thin breathless emphysematous patient
• Pneumonia
• Pulmonary oedema (LVF)
• Pulmonary embolism
With more advanced disease in which the compensatory mechanism of trying to blow off carbon dioxide has ‘worn out’, carbon dioxide retention occurs in addition to hypoxia. This is Type II respiratory failure (pO2 < 8kPa, pCO2 > 6kPa while not receiving oxygen; →Fig. 3.1). Examples are listed in Box 3.3; the patient in Case study 3.1 has Type II respiratory failure.
Box 3.3
• Severe life-threatening asthma (Type I failure progresses to Type II failure)
• The obese oedematous patient with severe COPD
• Respiratory centre depression in a severe drug overdose
• Obesity/hypoventilation syndrome
Case Study 3.1
A 68-year-old non-smoking woman was admitted because of increasing drowsiness following a fall at home.The emergency doctor thought she had probably had a stroke.
She and her husband led ‘separate lives’ at home but he said that she had become increasingly immobile and had taken to sleeping in an armchair over the previous 3 years. Her only medication was a mild diuretic. After a fall in her bedroom she had not been able to get up and became increasingly difficult to rouse.
On admission she was drowsy and uncooperative; she was morbidly obese and deeply cyanosed. Her respiratory rate was five breaths per minute and she was wheezy; her legs, thighs and abdomen were grossly oedematous.There was no evidence of a head injury or any focal neurological signs. Her chest film was normal. Her arterial gases showed a pO2 of 4.5kPa, a pCO2 of 16kPa and a pH of 7.1. A diagnosis of severe Type II respiratory failure due to a combination of obesity/hypoventilation syndrome and asthma was made.
The anaesthetists declined to ventilate her and attempts at NIV (→ p. 78; non-invasive ventilation in COPD, ) were only partially successful. Intravenous doxapram infusion, 24% oxygen and a combination of twice daily high-dose frusemide and aminophylline were started.With considerable difficulty she was nursed in a sitting position. On this regimen she had a marked diuresis with reduction of her oedema, although with a negative deficit of 10L she still weighed 150kg. She became increasingly alert and started to cough up purulent sputum. She slowly mobilised and lost weight over several weeks on the continuing care ward.
Hypoxia and hypercapnia: the blood gases
Carbon dioxide is a central nervous system depressant, its build up (termed hypercapnia) leads to a cycle of confusion, lack of cooperation, increasing drowsiness and hence further carbon dioxide retention. Hypoxia impairs the function of the heart, brain and kidneys. The combination of excessive carbon dioxide and the tissue hypoxia causes an acidosis that produces its own damaging effects on major organ function. (The pH in the blood gas results reflects the degree of tissue acidosis. A pH of less than 7.3 in respiratory failure indicates a major problem and a pH of less than 7.25 requires urgent and aggressive intervention to improve gas exchange.)
Principles of treatment
Before vital organ function is compromised, the blood gases must be corrected, at the simplest level by giving additional oxygen and in more complex cases by assisting or even replacing normal respiratory efforts. The introduction of new forms of ‘non-invasive’ respiratory support (i.e. the patient does not need endotracheal intubation), now means that selected patients with quite severe respiratory failure can be managed on the Acute Medical Unit with a ‘half-way house’ type of ventilation. This approach does not have the implications of full ITU treatment with the problems of endotracheal tubes, weaning, hospital-acquired infection and so forth.
Pulse oximetry
The oximeter measures the oxygen saturation in the arterial blood. The range of values for a normal saturation is small: thus a saturation of 97% is seen in the healthy population, whereas a saturation of 90% can indicate impending respiratory failure. The pulse oximeter is invaluable in recognising early respiratory failure, particularly when readings are taken on admission, before the patient has been given oxygen. You must remember, however, that the oximeter only measures oxygen saturation – it will tell you nothing about the level of carbon dioxide or the degree of acidosis.
Why and when do we do blood gases?
Oxygen saturations will be low in all cases of respiratory failure. Only the blood gases will tell you whether this is Type I or Type II respiratory failure. In acute asthma, for example, there is a world of difference between the patient with hypoxia and a normal pCO2 and the patient who is similarly hypoxic but, having passed from acute asthma to near exhaustion, is now retaining carbon dioxide. If you are in doubt about the severity of the patient’s condition, examine the blood gases. As a general rule, in Acute Medical Unit patients, arterial blood gases must be checked when the oxygen saturations are less than 92% with the patient breathing room air (you will see patients with severe Type II respiratory failure who have been given unlimited oxygen on their way in to hospital: the oxygen saturations look wonderful at 97%, but the gases reveal grossly increased levels of carbon dioxide).
Acute Severe Asthma
Mechanisms
Who gets acute severe asthma and why?
Any patient with asthma may have an acute attack, but those who are at particular risk of dying from acute asthma are:
• chronic severe asthma sufferers
• non-compliant with therapy and follow-up
• those who have previous acute/near-fatal attacks
• poor at recognising the severity of their asthma
• exposed to a high allergic load with a strong history of allergy
• normally requiring regular oral steroids
• those with a history of brittle asthma/frequent AED attendances
• those with serious psychosocial problems
• inappropriately prescribed beta blockers and NSAIDs
The number of acute exacerbations per year in which asthma treatment has to be intensified is a useful marker of the severity and control of the underlying asthma. The patient in Case Study 3.2 had been getting attacks of nocturnal breathlessness for months, but had not appreciated their significance.
Case Study 3.2
A 38-year-old man had had asthma for 30 years. Contrary to medical advice his only treatment was occasional inhaled salbutamol. He described chronic sleep disturbance from early morning wheezing, but even the presence of frequent symptoms did not dissuade him from the view that ‘normal people like him’ should not need to rely on inhalers. His asthma worsened over 2 weeks in spite of oral steroids.After a day of exposure to building dust and grass cuttings he became severely breathless and collapsed. He was admitted after his wife dialled 999.
The patient was too breathless to speak and unable to tolerate a mask.The peak flow could not be recorded. He was clammy with quiet breath sounds and a pulse rate of 160. He was given high-flow oxygen, nebulised bronchodilators and i.v. steroids. Emergency blood gases with the patient breathing oxygen showed a pO2 of 5.6kPa, a pCO2 of 16kPa and a pH of 6.9. A portable chest film showed no sign of a pneumothorax.
The patient was transferred immediately from the Acute Medical Unit to ITU and ventilated for 48h. His peak flows thereafter slowly improved on 40mg of prednisolone and nebulised salbutamol. He continued to have early morning wheezing for the next four mornings which required extra nebulisers before his symptoms slowly improved. He was transferred to the chest unit.
Three major factors narrow the airways in acute asthma:
• airway muscle contraction
• thickening of the airway wall with inflammatory cells
• airway clogging by thickened secretions
Without inhaled steroid treatment, the patient’s airways will have been chronically inflamed (→Case Study 3.2). Uncontrolled airway inflammation in asthma is a potent cause for persistent symptoms and repeated severe attacks.
What goes wrong during an attack?
As an attack develops, breathing becomes progressively more difficult because the patient has to drag and push air through increasingly narrow tubes. Air becomes trapped behind the blocked tubes so that the lungs over-inflate, making the work of breathing even harder. There are two consequences as the asthma attack progresses:
• gas exchange worsens
• the muscles used for breathing start to fatigue
The abnormal gas exchange, if uncorrected, goes through two phases.
1. Early in an attack of asthma, a combination of necessity and fear drives breathing sufficiently hard to blow off carbon dioxide. At this point, the levels of carbon dioxide in the blood are normal or low. In contrast, oxygen uptake is impaired and there is hypoxia, even at this early stage.
The patient in Case Study 3.2 had already passed this stage by the time he was admitted to hospital.
2. Later, as breathing tires, carbon dioxide builds up, oxygen levels continue to decrease and the patient’s condition becomes critical. The increase in carbon dioxide, which can be rapid and dramatic, now causes a sudden and dangerous decrease in the blood pH. If this is unchecked, a respiratory arrest will follow.
The implications for emergency management are to identify the patients who are at risk:
• those who are tiring (history, observation and blood gases)
• those with severe airway narrowing (peak expiratory flow rate)
• those with hypoxaemia (oxygen saturation) and a build-up of carbon dioxide (blood gases)
Assessment of Acute Severe Asthma
History
It is unusual for the patient to overestimate the severity of their attack. Patients like that in Case Study 3.2 who are panicking and uncooperative are far more likely to be doing so because of impending asphyxia than because of over-anxiety.
Examination
The signs of severe asthma must be recognised:
• a pulse rate of more than 110 beats/min
• a respiratory rate of more than 25 breaths/min
• the patient is too breathless to complete a sentence in one breath
• a PFR between a third and a half of their best or their predicted
A common sequence leading to respiratory arrest is of a desperately breathless patient who becomes ashen, clammy and quietly ‘cooperative’. The chest becomes quiet, the pulse slows and respiratory efforts become increasingly feeble. You may have seen patients who are poor at perceiving the severity of their own attacks, and noted how they can pass from the severe to the life-threatening stage with little apparent fuss.
The signs of life threatening asthma are any one of:
• oxygen saturations of less than 92%
• cyanosis
• a silent chest with feeble respiratory effort and exhaustion
• increasing confusion or a reduction in consciousness level/sudden collapse
• a bradycardia or arrhythmia
• hypotension
• PFR less than one-third of their best or their predicted
• PaO2 < 8.0kPa (if the PaCO2 is also > 6.0kPa the asthma is very severe)
Peak flow rate
The PFR is the simplest and most important objective way to assess acute asthma and to monitor the effectiveness of treatment (→Fig. 3.2). It must be measured in every case; most patients can produce a reading. However, even the observation that the patient is ‘too breathless to do a peak flow’ is a clear indication of the severity of the asthma.
It is important to try and find out how the patient is when at their best. There is a world of difference between an admission peak flow of 250L/min in a steroid-dependent asthmatic patient who never blows better than 275L/min, and a peak flow of 250L/min in a previously ‘mild’ asthmatic individual who is used to peak flows of 550L/min. This information may be available in their hospital case notes, GP records and in home peak-flow diaries. The best ever peak flow is not necessarily the same as the predicted peak flow, but both values are useful to decide the current state of the patient’s asthma. To know the predicted PFR you will need a table giving the normal value for a person of the same height, age and sex. These tables should be freely available on the Acute Medical Unit.
• An initial PFR of less than 50% of the predicted value or, if available, 50% of their best ever PFR reading indicates severe asthma. Peak flows down to one-third of these values indicate life-threatening asthma. As a rough guide, acute severe asthma is associated with PFR readings of less than 300L/min for most males and less than 200L/min for most females.
• The change in PFR with emergency treatment predicts the likely course of events.
• The subsequent PFR chart shows the level of asthma control and stability. Peak flows seesaw as an attack resolves (Fig. 3.2). Patients are particularly vulnerable during the morning dips in PFR, which occur during the first 2–3 days after an acute attack.
Nursing the Patient with Acute Severe Asthma
The balance between resuscitation and communication will depend on your initial assessment. A patient with an unrecordable peak flow, a pulse rate of 140 beats/min and an oxygen saturation of 75% will not welcome a discussion on preventative inhalers. He will, however, be terrified by his suffocating breathlessness and will be desperate for your reassurance that he is not going to stop breathing and die (→Box 3.4). There will be excellent educational opportunities, before the patient is discharged, and while the attack is fresh in the patient’s mind. Your approach will be tailored to the individual patient. There will be an obvious difference between the communication issues in a case of chronic asthma with repeated admissions to hospital and the case of a new asthmatic presenting with their first attack. There will also be sometimes surprising similarities, not least in the most basic of requirements: the understanding and practical use of inhalers.
Box 3.4
• I will measure your PFR; we will treat you and we will see how it improves.
• The hard work of breathing will lessen with treatment.
• You will regain control of your breathlessness soon.
• We will stay with you until the treatment works.
• We will sort things out for you – try and relax if possible.
• Find your most comfortable position.
• Slow your breathing rate.
• Take deep slow breaths through the mask.
• Allow the nebuliser to do its work.
• If the mask is too claustrophobic we can use oxygen tubing to your nostrils.
• The nurses and doctors will be here near you at all times.
• Call us if your breathing seems to be getting more difficult.
• Don’t worry about all the noises from the monitors and drips.
• The oximeter shows that you are getting enough oxygen into your lungs.
• Steroid side-effects will be minimised by the short course that you need.
Critical nursing tasks during the acute attack
Give reassurance and support
Take the patient through the ways in which each aspect of his treatment acts to bring the attack to an end and enables him to regain control of his breathing (→Box 3.4).
Explain
Explain the importance of effective, continuous oxygen therapy. Show the patient how to use the nebuliser and how to perform a peak flow reading. Explain how the patient can get immediate assistance from the staff.
Minimise the work of breathing
Provide effective and timely asthma medication. Sit the patient up in his most comfortable position (this will often involve the patient wanting to sit up, either leaning over a bed table or on the edge of the bed).
▪ Pulse rate
▪ Respiratory rate
▪ PFR
▪ Oxygen saturation (preferably before oxygen is started)
▪ Ability to complete a sentence
▪ Blood pressure (may be increased by anxiety)
▪ Urine dip stick (for steroid-induced diabetes)
▪ Sputum colour (wallpaper glue sputum is common in asthma)
▪ Temperature (a sign of respiratory infection)
▪ Inhaler technique (critical for future management)
Monitor the patient’s progress
This may need to be continuous for the critical first hour or so. Beware of an increasing pulse rate, decreasing peak flow and a tiring patient. Do not be falsely reassured by a normal oxygen saturation if the patient looks awful. Just before a respiratory arrest, many asthmatic patients become quiet, clammy and cooperative.
Plan to prevent this happening again
Identify why this attack occurred. Start a re-evaluation of the patient’s long-term management that can be taken over by appropriate follow-up arrangements.
Management of Acute Severe Asthma
Initial emergency treatment
• Bronchodilators (to increase airway calibre). Nebulised salbutamol 5mg combined, if there are life-threatening features, with nebulised ipratropium 0.5mg.
• Corticosteroids (to reduce airway inflammation). Intravenous (i.v.) hydrocortisone 100mg and/or 40–50mg oral prednisolone.
• Oxygen (to correct gas exchange). High-flow oxygen at 40–60% and oxygen-driven nebulisers. The target oxygen saturations are 94–98%.
Subsequent treatment
If there is no improvement by 15min:
• repeat the salbutamol and ipratropium
• consider a single dose of i.v. magnesium sulphate 1.2–2g over 20min
• continue to give nebulised salbutamol every 15min (alternatively use a special nebuliser to give continuous salbutamol at 10mg/h)
• consider i.v. aminophylline 5mg/kg over 20min. Particular care is needed in choosing the doses, especially if the patient has been taking theophyllines as his usual asthma therapy. Start an infusion of aminophylline 0.5 to 0.7mg/kg/hour over 24h. Check daily theophylline levels
Assessing response
Following the PFR and oximetry. The key to assessment lies in a measurement of PFR. This is done on admission and, while the patient is in the unstable phase, at 15-min intervals. Thereafter, measure the PFR before and after bronchodilator treatment at least four times per day. Oximetry is monitored with the aim of keeping the oxygen saturations above 94%.
Repeating the blood gases. During the first few critical hours, you may need to use the arterial blood gases if there is any doubt about the patient’s progress. The purpose of the blood gas measurement is to identify an increase in the PaCO2 (and a fall in the pH). Thus the blood gases should be repeated 1h after the start of treatment (or earlier) if:
• poor blood gases on admission (pO2 < 8.0kPa, with a normal or high pCO2)
• saturations cannot be kept above 92%
• the patient’s condition deteriorates
Transfer to Intensive Therapy Unit? If the patient is tiring, confused or drowsy, if the PFR is deteriorating or unchanged and the patient feels worse, and particularly if the pCO2 is increasing and the pH is decreasing, you should prepare to move the patient to the ITU (→Case Study 3.2). Respiratory arrest, when it complicates acute asthma, occurs with alarming speed and always poses a major challenge to the resuscitation team. With proper assessment and by monitoring the response to treatment, you can avoid this complication.
Non-invasive ventilation? CPAP/Bi PAP are of unproven value in acute severe asthma and should only be considered in an ITU setting.
A good response to treatment.
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