Respiratory emergencies: the acutely breathless patient

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Chapter 8 Respiratory emergencies

the acutely breathless patient

Craig Hore, John Roberts

GENERAL PRINCIPLES

Exclude airway compromise, which may be subtle, as the cause of acute breathlessness. Management of airway problems always comes first. Dyspnoea is a sensation which has multiple aetiologies and can be difficult to assess.

There may be several reasons why the patient with comorbidities experiences dyspnoea. This patient may require comprehensive treatment strategies to optimise their condition and thus relieve their symptoms.

Initial goals in assessment and management are:

1. To identify and treat life-threatening abnormalities of gas exchange, acute onset or deterioration of hypoxia and hypercarbia.
2. To commence non-invasive ventilation in the form of bi-level positive airway pressure (BiPap) or continuous positive airway pressure (CPAP) where indicated.
3. To identify when intubation and ventilation is required and initiate this therapy.
4. To identify and commence specific treatment to relieve respiratory distress based on initial history and examination.
5. To formulate a plan of investigation and management of cases where the exact cause of respiratory distress is unknown or uncertain.

Triage all patients presenting with a respiratory system emergency to a monitored acute bed. Obtain IV access. Arterial blood gases (ABGs), chest X-ray (CXR) and BiPap services should be available.

OXYGEN THERAPY

(Craig Hore)

Delivery of oxygen is one of the most common therapies in the emergency department and an important component of resuscitation. Acute hypoxaemia is immediately life-threatening and the ‘first-line drug’ for hypoxaemia is oxygen! It is a safe drug: the complications of oxygen therapy are concentration- and time-dependent, uncommon and take time to develop. Other aspects of oxygen delivery may also need to be improved in the hypoxaemic patient, especially cardiac output, haemoglobin, tissue perfusion and reducing tissue O2 requirements.

Table 8.1 The haemoglobin–oxygen (Hb–O2) dissociation curve

SaO2 (%) PaO2 (mmHg) Level
98 100 Arterial blood
90 60  
75 40 Venous blood
50 26  
∼33 ∼20 Tissue

SaO2, oxygen saturation; PaO2, partial pressure of oxygen in arterial or venous blood or tissue

Note: When SaO2 ≈ 60–90%, there is a linear relationship between SaO2 and PaO2.

Essentially, oxygen should be delivered to all patients who have acute respiratory failure to maintain a partial pressure (PaO2) of 60–80 mmHg (or a PaO2 > 55 mmHg in chronic respiratory failure). The lowest fraction of inspired oxygen (FiO2) that provides an acceptable PaO2 should be chosen. Choosing the right mode of delivery is also important.

Oxygen delivery systems

Simple delivery systems

These are variable performance systems—the FiO2 delivered not only depends upon the oxygen flow rate, but also on the rate and depth of respiration. The FiO2 delivered by various systems can be estimated (Table 8.2).

Table 8.2 Estimation of the fraction of inspired oxygen (FiO2) achieved by simple delivery systems

Flow rate (L/min) FiO2
2 (nasal prongs) 0.25
3 (nasal prongs) 0.28
4 (nasal prongs) 0.30
6 0.40
8 0.45
15 0.65
15 (reservoir mask)∗ 0.70

∗ If a double wall supply is used, a flow rate of 30 L/min and FiO2 up to 0.90 can be achieved.

Nasal prongs. These are easy to use and usually well tolerated by the patient, allowing them to eat, drink and talk without interrupting oxygen delivery. They are ineffective if the patient has blocked nasal passages or is an obligate mouth breather. Flow rates > 4 L/min can lead to mucosal drying and are less well tolerated.

Hudson mask. A simple and easy way to deliver oxygen but delivery is variable (see above). Flow rates < 4 L/min are not recommended as rebreathing can occur.

Entrainment systems

Venturi masks. This system uses the Bernoulli effect to entrain a fixed amount of air to mix with oxygen. This is an example of a fixed performance system—the FiO2 delivered is more independent of patient factors. Nonetheless, it may vary in patients with very high peak inspiratory flow rates. One commonly used system delivers the following options: 24/28/35/40/50/60% oxygen. The lower concentrations are especially useful for patients with chronic obstructive pulmonary disease (COPD) and CO2 retention.

Partial rebreathing systems

Reservoir masks. These can achieve a higher FiO2 than simple masks but it is essential to keep the reservoir inflated with O2. This can require high flow rates. This is a good initial choice for most conscious, unwell, hypoxaemic patients in the emergency department.

Anaesthetic circuits. Mentioned for completeness; rarely used in the emergency department setting.

Non-rebreathing systems

Resuscitation bags (e.g. Laerdal, Baxter). The commonly used bags are self-inflating, and have a series of one-way valves and a reservoir bag. The aim is to keep the reservoir bag at least 75% inflated with O2. An FiO2 of close to 100% can be delivered if 15 L/min O2 is used and the reservoir bag is inflated (50% without a reservoir bag). There is a growing trend to use disposable, single-use bags to help overcome the problem of incorrect assembly and sterilisation. The ability to use a bag–mask system is a vital skill that should be learned and mastered early!

Gas-driven inflating valves (e.g. Oxy-viva).

Others

• Positive pressure ventilators
• Non-invasive positive pressure ventilation (e.g. CPAP, biPAP)
• Hyperbaric oxygen (HBO) therapy

Other delivery systems are dealt with in more detail in other chapters of this text.

INVESTIGATIONS IN RESPIRATORY EMERGENCIES

(Craig Hore)

Arterial blood gases: oxygenation and ventilation

Arterial blood gases (ABGs) reflect oxygenation (PaO2), ventilation (PaCO2) and acid–base status. The last is dealt with in more detail in Chapter 27, ‘Metabolic disorders’.

Oxygenation

Remember that, even for ‘normal’ lungs, the PaO2 varies with the following parameters.

The inspired O2 concentration (FiO2). Never take ABGs, or try to interpret ABGs, without noting the FiO2. If room air, this is 21% (i.e. FiO2 = 0.21).

Age. PaO2 falls with age. As a rough guide to what to expect at a given age, use the following estimation:

image

Altitude. PaO2 falls by ∼ 3 mmHg for each 1000 feet (∼300 m) above sea level. Temperature. For each degree Celsius rise (or fall) in temperature, the PaO2 will rise (or fall) by ∼ 5%.

pH. For each 0.1 decrease (or increase) in pH, the PaO2 will increase (or decrease) by ∼ 10%.

Do not take oxygen off a hypoxic patient to perform ABGs. Perform the ABGs with the patient on oxygen and note the FiO2. The A-a gradient (the difference between alveolar and arterial oxygen pressure, PA-aO2) is calculated from the alveolar gas equation:

image

PAO2 is the alveolar oxygen tension and R is the respiratory quotient (usually 0.8). The partial pressure of inspired oxygen (PiO2) is determined by the atmospheric pressure, which varies with altitude. Usually, it is assumed that the patient is breathing at sea level, that atmospheric pressure is 760 mmHg and that the water vapour pressure is 47 mmHg. There is usually a small difference between the PAO2 and the PaO2—the A-a gradient or PA-aO2.

• PA-aO2 < 15 mmHg is normal.
• PA-aO2 = 20–30 mmHg reflects mild pulmonary dysfunction.
• PA-aO2 > 50 mmHg reflects severe pulmonary dysfunction. Note that pulmonary embolism is only one of many causes of an increased PA-aO2.

The gradient varies with age: add 3 for each decade over the age of 30 years.

The PAO2 can also be quickly estimated using one of the following rules of thumb:

• If breathing room air,

image

• If breathing supplemental O2,

image

The causes of hypoxia

There are four main types of hypoxia:

1. stagnant hypoxia resulting from decreased cardiac output
2. anaemic hypoxia resulting from decreased haemoglobin
3. histotoxic hypoxia resulting from decreased oxygen-binding capacity
4. hypoxaemic hypoxia resulting from decreased O2 saturation.

The take-home message from this list is that the patient can be ‘hypoxic’ with a normal O2 saturation. Perhaps the most obvious example is histotoxic hypoxia resulting from CO poisoning.

Acute respiratory failure is generally associated with hypoxaemic hypoxia. The problem is getting the oxygen from the lungs into the capillaries. Ventilation/perfusion (V/Q) mismatch is the commonest cause. At one extreme of V/Q mismatching, there is normal ventilation, but abnormal perfusion (dead space ventilation). This mismatching affects the exchange of O2, resulting in hypoxaemia. Hypercarbia occurs to a lesser extent as CO2 diffuses more easily than O2. The classic example is pulmonary embolism. At the other extreme, there is normal blood flow but abnormal ventilation (shunt). This is most commonly a result of venous admixture where capillary blood and alveolar gas do not equilibrate, such as when blood is flowing through a consolidated lung. The larger the shunt, the less responsive it is to supplemental O2.

Ventilation

Hypercarbia (↑PaCO2)

The commonest cause of hypercarbia is alveolar hypoventilation. This can be due to a variety of problems, e.g. airway obstruction, narcotics, CNS disorders, PNS disorders, chest wall disorders. Remember there are other uncommon causes of hypercarbia including: V/Q inequality (e.g. COPD, emphysema); increased CO2 production (e.g. hyperpyrexia, hypercatabolism, thyrotoxicosis, inappropriate carbohydrate load); and increased dead space (e.g. physiological—V/Q mismatch or ‘dead space ventilation’, equipment—long ventilator tubing and circuitry).

The clinical effects of hypercarbia

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