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Respiratory assessment and monitoring 

Respiratory assessment and monitoring
Chapter:
Respiratory assessment and monitoring
Author(s):

Heather Baid

, Fiona Creed

, and Jessica Hargreaves

DOI:
10.1093/med/9780198701071.003.0004
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date: 09 May 2021

Respiratory assessment

If an actual or potential respiratory abnormality is identified during a general ABCDE assessment (see Respiratory assessment and monitoring p. [link]) or while monitoring the patient, a more detailed and focused respiratory assessment can provide further information to guide clinical management. Patients with dyspnoea or acute respiratory failure will often also manifest systemic signs and symptoms, including altered consciousness, cardiovascular compromise, and gastrointestinal dysfunction.

Focused health history

Subjective information about the respiratory history can be taken from the patient if they are awake, or from other sources (e.g. family, caregivers, or patient notes).

Respiratory symptom enquiry

Check whether the patient has recently experienced any of the following:

  • cough (productive)

  • haemoptysis

  • dyspnoea (acute, progressive)

  • wheeze

  • chest pain

  • fever/night sweats

  • sleep apnoea.

Focused physical assessment

  • Respiratory rate over 1 min (normal range, 10–20 breaths/min).

  • Obvious signs of discomfort or distress.

  • Inability to lie flat or cough due to respiratory distress.

  • Inability to complete full sentences.

  • Oxygen therapy.

  • Fluid assessment (see Respiratory assessment and monitoring p. [link]).

  • Respiratory-focused assessment (see Table 4.1).

Table 4.1 Respiratory-focused assessment

Normal

Abnormal

Inspection

  • Pink, moist mucous membranes

  • Mucoid sputum

  • Symmetrical

  • breathing pattern

  • Midline trachea

  • Pallor or cyanosis

  • Dry mucous membranes

  • Mucopurulent, purulent, blood in sputum

  • Respiratory asymmetry

  • Dyspnoea/tachypnoea

  • Accessory muscle use

  • Chest wounds, drains, scarring

  • Tracheal deviation

Palpation

  • Bilateral chest expansion

  • Non-tender

  • Unilateral and/or reduced expansion

  • Subcutaneous emphysema

  • Fremitus

  • Localized pain across chest

Percussion

Tympanic/resonant in all zones

Dull/hyper-resonant in all or some zones

Auscultation

  • Patent airway

  • Normal breath sounds throughout chest

  • Stridor

  • Abnormal breath sounds, wheeze, crackles, pleural rub, diminished breath sounds

Normal breath sounds

  • Tracheal—heard over the trachea as very loud, harsh, and high-pitched. Inspiration duration < expiration duration.

  • Bronchial—heard over the manubrium as loud, harsh, and high-pitched. Inspiration duration = expiration duration.

  • Bronchovesicular—heard below the clavicles, between the scapulae as medium-pitched. Inspiration duration = expiration duration.

  • Vesicular—heard over areas of lung tissue as soft and low-pitched. Inspiration duration > expiration duration.

If the trachea is not in the midline it may be deviated toward the site of injury, as in the case of lung collapse, or away from the site of injury, as in pneumothorax. Note that tracheal deviation is a late sign of respiratory pathology.

Respiratory landmarking

Any abnormal findings during the health history and physical assessment should be documented and reported according to the specific area of the chest where the abnormality was identified (see Figure 4.1).


Figure 4.1 Posterior, anterior, and lateral landmarking of the thorax.

Figure 4.1 Posterior, anterior, and lateral landmarking of the thorax.

(Reproduced from Thomas J & Monaghan T, Oxford Handbook of Clinical Examination and Practical Skills, 2014, with permission from Oxford University Press.)

Abnormal percussion sounds

  • Dullness—indicates a solid structure, a consolidated or collapsed area of lung, or a fluid-filled area, which produces a dull note on percussion.

    • Causes include pleural effusion, infection, and lung collapse.

  • Hyper-resonance—indicates a hollow structure, which produces a hyper-resonant note on percussion.

    • Causes include pneumothorax.

Abnormal breath sounds

  • Wheeze—indicates airway restriction which is typically heard on expiration. An inspiratory wheeze indicates severe airway narrowing. High-pitched when produced in small bronchioles, and low-pitched when produced in larger bronchi. Monophonic (i.e. single pitch) when heard in an isolated area, and polyphonic (i.e. multi-pitched) when heard throughout the lung area.

    • Causes include bronchoconstriction, airway inflammation, secretions, and obstruction.

  • Crackles—indicate instability of airways collapsing on expiration. Fine crackles can be heard in small airways, and coarse crackles can be heard in larger airways.

    • Causes include pulmonary oedema, secretions, atelectasis, and fibrosis.

  • Pleural rub—indicates inflammation of the parietal and visceral layers of the pleura. Stiff creaking sound heard throughout inspiration and expiration.

    • Causes include pleurisy.

  • Diminished or absent breath sounds—indicate lack of ventilation and/or respiration.

    • Causes include pneumothorax, pleural effusion, gas trapping, and collapse.

Causes of key abnormalities

  • Consolidation—pneumonia.

  • Collapse—post-operative, mucus plugs.

  • Pleural effusion—transudate (heart failure), exudate (neoplasm), empyema.

  • Pneumothorax—bullae rupture, trauma (penetrating chest injury).

  • Bronchiectasis—tuberculosis, allergic reaction, cystic fibrosis.

Laboratory investigations

See Respiratory assessment and monitoring p. [link] for normal values of the following blood tests, which are relevant to check for a respiratory review:

  • full blood count (FBC)

  • C-reactive protein (CRP)

  • urea and electrolytes (U&E).

Further reading

Broad MA et al. Cardiorespiratory Assessment of the Adult Patient: a clinician’s guide. Churchill Livingstone Elsevier: Edinburgh, 2012.Find this resource:

Heuer AJ and Scanlan CL (eds). Wilkins’ Clinical Assessment in Respiratory Care 7th ed. Elsevier Mosby: Maryland Heights, Missouri, 2014.Find this resource:

Jarvis C. Physical Examination and Health Assessment, 6th edn. Saunders Elsevier: St Louis, MO, 2012.Find this resource:

Respiratory monitoring

Specific respiratory monitoring may be indicated during the care of a critically ill patient. An understanding of the indications and practices associated with these monitoring devices will ensure accuracy of the results. In addition to the respiratory monitoring described in this section, the following systems will provide further support for the respiratory assessment and care of the patient: chest X-ray, mechanical ventilation waveform analysis and blood gas analysis (see Respiratory assessment and monitoring p. [link]).

Pulse oximetry

This provides continuous, non-invasive measurement of oxygen saturation in arterial blood (SpO2). Pulse oximetry is used to assess for hypoxaemia, to detect variations from the patient’s oxygenation baseline (e.g. due to procedures or activity level), and to support the use of oxygen therapy.

Method

A probe is placed over a digit, earlobe, cheek, or the bridge of the nose. It emits light at two specific wavelengths—red and infrared. Light passes through the tissue and is sensed by a photodetector at the base of the probe. Most of the emitted light is absorbed by skin (including pigment), bone, connective tissue, and venous vessels (baseline measurement). This amount is constant, so the only relevant fluctuations are caused by increases in blood flow during systole. The peaks and troughs of the pulsatile and baseline absorption for each wavelength are detected and the ratios of each are compared. This provides the ratio of oxyhaemoglobin to total haemoglobin (i.e. the saturation). Oxygen content dissolved in plasma is 3% and that bound to haemoglobin is 97%.

Pulse oximetry measures the oxygen content bound to haemoglobin, not the oxygen content dissolved in the blood. Consequently an anaemic patient may still have an oxygen saturation of 100%.

It also does not identify whether the patient is making any respiratory effort, oxygen consumption, or carbon dioxide retention.

Limitations

  • Accuracy is within 2% only when the SpO2 is ≥ 70%.

  • Haemoglobin abnormality—for example, carboxyhaemoglobin (as a result of carbon monoxide poisoning or smoke inhalation) or methaemoglobinaemia (due to local anaesthetics, antibiotics, or radio-opaque dyes).

  • Impaired peripheral perfusion—due to hypothermia, hypovolaemia, peripheral vascular disease, or vasoconstriction (distal to blood pressure cuff).

  • Heart rate abnormality—weak, arrhythmia, absent.

  • Impaired light absorption—due to nail polish, high bilirubin concentration, high levels of ambient light (e.g. sunlight, phototherapy, surgical lamp).

  • Motion artefact—tremor, shivering, ill-fitting probe.

Ongoing care

  • Attach the probe securely.

  • Confirm that there is a clear pulsatile waveform.

  • Set alarm limits—individualized to the patient.

  • Observe the probe site 4-hourly for pressure ulceration.

  • Confirm abnormal readings with other assessment findings, such as arterial blood gas (ABG).

Capnography

This provides a measurement of carbon dioxide (CO2) with a continuous waveform at the end of expiration—that is, end-tidal CO2 (ETCO2). Capnography is used to assess the adequacy of ventilation, to detect oesophageal intubation (i.e. very little or no CO2 is detected), to indicate disconnection from the ventilator, and to diagnose circulatory problems, such as pulmonary embolus (a sudden fall in ETCO2).

Method

Most analysers utilize infrared absorption spectroscopy, whereby the infrared light is absorbed by CO2 at a specific wavelength (4.3 millimicrons). Since the amount of light absorbed is proportional to the concentration of CO2 gas molecules, the concentration of CO2 can be determined by comparing the measured absorbance with the absorbance of a known standard. The CO2 concentration is expressed as a partial pressure in kPa.

A large difference between ETCO2 and PaCO2 may represent an increase in the dead space to tidal volume ratio, poor pulmonary perfusion, auto-positive end expiratory pressure (auto-PEEP), or intra-pulmonary shunting.

A progressive rise in ETCO2 may represent hypoventilation, airway obstruction, or increased CO2 production due to an increase in metabolic rate.

Limitations

The ETCO2 approximates to PaCO2 only if the patient shows cardiorespiratory stability and is normothermic. It is not so reliable in patients with respiratory failure—for example, ventilation/perfusion mismatch or significant gas trapping (e.g. asthma).

Capnogram

There are four phases (see Figure 4.2).


Figure 4.2 The normal capnogram.

Figure 4.2 The normal capnogram.

(Reproduced from Singer M and Webb A, Oxford Handbook of Critical Care, Third Edition, 2005, with permission from Oxford University Press.)

Phase 1

Gas is sampled during the start of expiration from the anatomical and sampling device dead space. The concentration of CO2 should be negligible. However, if the CO2 level is significant this indicates re-breathing of exhaled gas. The commonest causes are failure of the expiratory valve to open during mechanical ventilation, or an inadequate amount of fresh gas in the reservoir of a non-rebreathing face mask.

Phase 2

Gas is sampled from the alveolar gas. The concentration of CO2 rapidly rises.

Phase 3

This is known as the alveolar plateau, and it represents the CO2 concentration in mixed expired alveolar gas. There is normally a slight increase in CO2 concentration as alveolar gas exchange continues during expiration. Airway obstruction or a high rate of CO2 production will increase the slope. The gradient during Phase 3 depends on the rate of alveolar gas exchange. A steep gradient can indicate ventilation/perfusion mismatch.

Phase 4

As inspiration begins there is a rapid fall in the concentration of CO2.

Peak flow meter

This provides a measurement of peak expiratory flow rate (PEFR). Peak flow is used to assess the trends in airway obstruction, but the accuracy of the results is dependent on patient effort. As it is a measure of airflow it cannot detect restrictive ventilatory defects, such as those caused by pulmonary fibrosis, as these reduce lung volume but do not affect airflow.

Method

The patient is required to take a full breath in and produce a rapid forced maximal expiratory puff into the single-use mouthpiece attached to the meter. The result is recorded in L/min and is interpreted according to the patient’s age, gender, and height. Peak flows can be checked twice daily, preferably at the same time.

Pneumonia

Definition

Pneumonia is an inflammation of the lung, which is characterized by exudation into the alveoli. It can be classified anatomically as lobar or by aetiology (see Box 4.1).

Causes

Pneumonia can be caused by any of over 100 microorganisms. Therefore the treatment should be started before the causative organism has been identified. Box 4.2 lists some of the most common causative organisms.

Assessment findings

  • The clinical findings are often referred to as consolidation.

  • Expansion is reduced on the affected side.

  • There is percussion dullness over the area of consolidation.

  • Breath sounds are bronchial.

  • Added sounds are crackles.

  • Tachypnoea and central cyanosis.

  • Fever, sweats, and rigors.

  • Cough and sputum.

Management

  • Chest X-ray.

  • ABG and pulse oximetry.

  • FBC, serum creatinine, U&E, and LFTs.

  • Blood cultures prior to administering antimicrobial therapy.

  • Sputum microscopy, culture, and sensitivity.

  • Bronchoalveloar lavage may be used for patients who are immunocompromised, those who do not respond to antimicrobial therapy, or those from whom a sputum sample cannot be obtained.

  • Urinary Legionella antigen.

  • Antimicrobial therapy.

  • Monitor haemodynamics (see Respiratory assessment and monitoring p. [link]).

  • Monitor electrolytes and treat imbalances (see Respiratory assessment and monitoring p. [link]).

  • Monitor fluid status and treat imbalances (see Respiratory assessment and monitoring pp. [link] and [link]).

  • Oxygen therapy (see Respiratory assessment and monitoring p. [link]).

  • Adherence to infection prevention and control.

  • Ventilator-associated pneumonia care bundle (see Box 4.3 and p. [link]).

Further reading

BRITISH Thoracic Society (BTS). BTS Guidelines for the Management of Community Acquired Pneumonia in Adults. BTS: London, 2009.Find this resource:

Department of Health. High Impact Intervention: care bundle to reduce ventilator-associated pneumonia. Department of Health: London, 2010.Find this resource:

Melsen WG, Rovers MM and Bonten MJ. Ventilator-associated pneumonia and mortality: a systematic review of observational studies. Critical Care Medicine 2009; 39: 2709–18.Find this resource:

National Institute for Health and Care Excellence (NICE). Technical Patient Safety Solutions for Ventilator-Associated Pneumonia in Adults. PSG002. NICE: London, 2008. Respiratory assessment and monitoringwww.nice.org.uk/guidance/psg002Find this resource:

Pleural effusion

Definition

This is a collection of fluid in the pleural space. It is the result of excessive fluid accumulating between the thin layers of tissue that line the lungs and thorax. Pleural fluid is normally a clear pale yellow colour. A large amount of purulent drainage indicates an empyema.

Causes

Transudate may be caused by cardiac failure, kidney disease, hypoalbuminaemia due to chronic liver disease, or hypothyroidism. The fluid has similar protein levels to those found in normal pleural fluid, with no evidence of blood, inflammation, or infection.

Exudate may develop as a result of pneumonia, neoplasm, tuberculosis, or pulmonary infarction. The fluid contains increased levels of protein, blood, or evidence of inflammation or infection.

Empyema is pus in the pleural space, and it may develop as a result of pneumonia, lung abscess, bronchiectasis, or tuberculosis.

Assessment findings

  • Trachea displaced away from a massive effusion.

  • Expansion reduced on the affected side.

  • Percussion dullness over the area of fluid.

  • Breath sounds reduced or absent.

  • Added sounds bronchial above the effusion due to compression of overlying lung.

  • Tachypnoea and central cyanosis.

  • Fever.

  • Cough.

  • Pleuritic pain.

Management

  • Chest X-ray.

  • Ultrasound examination.

  • ABG and pulse oximetry.

  • FBC, serum creatinine, U&E, and LFTs.

  • Treatment for pleural effusions will require management of the underlying cause (e.g. antimicrobial therapy for pneumonia, diuretics for cardiac failure).

  • Monitor haemodynamics (see Respiratory assessment and monitoring p. [link]).

  • Monitor electrolytes and treat imbalances (see Respiratory assessment and monitoring p. [link]).

  • Monitor fluid status and treat imbalances (see Respiratory assessment and monitoring pp. [link] and [link]).

  • Oxygen therapy (see Respiratory assessment and monitoring p. [link]).

  • Adherence to infection prevention and control.

Large, infected, or inflamed pleural effusions often require drainage to improve symptoms and prevent complications. Various procedures may be used to treat pleural effusions, including the following:

  • Thoracentesis—to remove large amounts of pleural effusion or for diagnostic purposes.

  • Pleurodesis—an irritant (e.g. talc, doxycycline) is injected through a chest tube into the pleural space. The irritant creates an inflammatory response that causes the surfaces of the pleura and chest wall to adhere, sealing the space and thus preventing further fluid collection.

  • Tube thoracotomy (chest drain)—a plastic tube is inserted into the pleural space via a small incision made in the chest wall. The tube is attached to suction and may remain in situ for several days (see Figure 4.3).


Figure 4.3 Chest drain.

Figure 4.3 Chest drain.

(Reproduced from Tubaro M et al. The ESC Textbook of Intensive and Acute Cardiac Care (2011), with permission from the European Society of Cardiology.)

Nursing care of a chest drain

A chest drain has three functions:

  • to drain fluid and/or air

  • to prevent additional air from entering the chest

  • to facilitate lung re-expansion using suction.

Monitor the appearance of drained fluid and record measurements hourly. If a chest drain was indicated for a pneumothorax, drainage of fluid is less likely.

Use of a water seal prevents air from entering the chest tube and the patient’s lungs. Fluctuation of the water in the tubing on inspiration and expiration is normal, and if not present this could indicate kinked, blocked tubing or a fully reinflated lung. Bubbling of the water indicates that air is escaping from the pleural cavity (e.g. in the case of a pneumothorax). New bubbling could indicate a new undiagnosed pneumothorax or disconnection of the tubing. It is possible to distinguish between an air leak and a pneumothorax by clamping the tubing close to the chest wall, which will stop the bubbling if the air is caused by a pneumothorax, but the bubbling will continue if it is due to a loose connection or a disconnection.

Clamping of a chest tube should only be performed to identify the cause of an air leak and on medical orders.

Removal of a chest tube can be undertaken at the bedside with the patient in bed, using an aseptic non-touch technique. Two sutures are usually inserted—the first to assist later closure of the wound after drain removal, and the second (a stay suture) to secure the drain which needs to be removed. Care must be taken to avoid air entering the pleural cavity. Clamping prior to removal is not recommended on the basis of the latest evidence. The patient should be instructed to exhale while the tube is being removed. Once the tube has been removed the closure suture should be tied and an occlusive dressing applied. The patient should be monitored for signs of respiratory distress. Disposal of the chest drain must include safe disposal of the fluid (absorbent gels can be used to avoid spillage of the contents).

Further reading

Frazer C. Managing chest tubes. MedSurg Matters! 2012; 21: 9–12.Find this resource:

Maslove DB et al. The diagnosis and management of pleural effusions in the ICU. Journal of Intensive Care Medicine 2013; 28: 24–36.Find this resource:

Pneumothorax

Definition

A pneumothorax occurs when there is air in the pleural space surrounding the lungs, and it requires a chest tube to allow the air to escape. Similarly, a haemothorax occurs when blood collects within the pleural cavity. A tension pneumothorax occurs when there is communication between the lung and the pleural space. Air is able to enter during inspiration, but is prevented from exiting on expiration. As a result the accumulation of air in the pleural space will cause displacement of the mediastinum and obstruction of blood vessels, and will restrict ventilation.

Causes

The causes can be classified as spontaneous or traumatic (see Table 4.2).

Table 4.2 Causes of pneumothorax

Spontaneous

  • Subpleural bullae rupture—usually in tall young males

  • Emphysema bullae rupture—usually in middle-aged or elderly patients with generalized emphysematous changes

  • Iatrogenic—central venous catheter insertion, high positive airway pressures with mechanical ventilation

Traumatic

  • Rib fracture

  • Penetrating chest wall injury

  • Pleural aspiration

Assessment findings

  • Trachea displaced away from a massive pneumothorax.

  • Subcutaneous emphysema.

  • Expansion is reduced on the affected side.

  • Percussion is hyper-resonant over the area of pneumothorax.

  • Breath sounds reduced or absent.

  • Tachypnoea and central cyanosis.

Management

  • Chest X-ray.

  • ABG and pulse oximetry.

  • FBC, serum creatinine, U&E, and LFTs.

  • Tube thoracotomy (chest drain)—a plastic tube is inserted into the pleural space via a small incision made in the chest wall. The tube is attached to suction and may remain in situ for several days.

  • Monitor haemodynamics (see Respiratory assessment and monitoring p. [link]).

  • Monitor electrolytes and treat imbalances (see Respiratory assessment and monitoring p. [link]).

  • Monitor fluid status and treat imbalances (see Respiratory assessment and monitoring pp. [link] and [link]).

  • Oxygen therapy (see Respiratory assessment and monitoring p. [link]).

  • Adherence to infection prevention and control.

Further reading

British Thoracic Society (BTS). Pleural Disease Guideline. BTS: London, 2010.Find this resource:

Haynes D and Baumann M. Management of pneumothorax. Seminars in Respiratory and Critical Care Medicine 2010; 31: 769–80.Find this resource:

Asthma

Definition

Asthma is a chronic respiratory condition with the following features:

  • reversible airway obstruction (depending on the severity, this can be complete or partial) (see Table 4.3)

  • airway inflammation

  • airway hyper-responsiveness to various stimuli.

Table 4.3 Levels of severity of acute asthma exacerbations

Moderate asthma

  • Increasing symptoms

  • PEF > 50–75% of best or predicted

  • No features of acute severe asthma

Acute severe asthma

Any one of the following:

  • PEF 33–50% of best or predicted

  • respiratory rate ≥ 25 breaths/min

  • heart rate ≥ 110 beats /min

  • inability to complete sentences in one breath

Life-threatening asthma

Any one of the following in a patient with severe asthma:

Clinical signs

Measurements

Altered conscious level

PEF < 33% of best or predicted

Exhaustion

SpO2 < 92%

Arrhythmia

PaO2 < 8 kPa

Hypotension

’Normal’ PaCO2 (4.6–6.0 kPa)

Cyanosis

Silent chest

Poor respiratory effort

Near-fatal asthma

Raised PaCO2 and/or requiring mechanical ventilation with raised inflation pressures

Reproduced from British Thoracic Society and Scottish Intercollegiate Guidelines Network, British guideline on the management of asthma, Thorax 2014; 69: i1–192, with permission from the BMJ Publishing Group Ltd.

An exacerbation of asthma is an acute event characterized by a worsening of the patient’s respiratory symptoms that exceeds normal day-to-day variations. It is typified by cough, wheeze, dyspnoea, chest tightness, and decreasing expiratory flow.

Status asthmaticus is a medical emergency that can be identified by failure to respond to nebulized bronchodilators (see Box 4.4).

Reproduced from BTS British Guidelines on Management of Asthma, with permission from Publishing Company (BTS 2012).

A patient may have more than one cause of airway obstruction—for example, COPD and asthma often coexist.

Causes

Both genetic and environmental factors have been implicated in the aetiology of asthma. Immunoglobulin E (IgE) appears to be involved in the characteristic airway inflammation and hyper-responsiveness, with the allergens in the local environment determining the level of antibody response.

Triggers for asthma can be non-specific (e.g. exercise, air temperature, pollutants), specific allergens (e.g. animal dander, house mite, pollen), or an alteration in airway control (e.g. beta blockers, aspirin).

Assessment findings

  • Accessory muscle use.

  • Decreased PEFR.

  • Expansion reduced bilaterally (hyperinflated chest).

  • Breath sounds diminished or absent.

  • Added sounds—expiratory/inspiratory wheeze.

  • Tachypnoea and central cyanosis.

  • Cough and sputum.

Management

  • ABG and pulse oximetry.

  • Peak flow.

  • β‎2-agonist bronchodilators—in most cases nebulized salbutamol or terbutaline given in high doses acts quickly to relieve bronchospasm, with few side effects. Repeat doses of β‎2-agonists at 15- to 30-min intervals, or give continuous nebulization of salbutamol at 5–10 mg/h if there is an inadequate response to initial treatment. Reserve the intravenous route for patients in whom the inhaled route is unreliable.

  • Steroid therapy—steroid tablets are as effective as injected steroids, provided that they can be swallowed and retained. Use prednisolone 40–50 mg daily or parenteral hydrocortisone 400 mg daily (100 mg 6-hourly).

  • Anticholinergic therapy—nebulized ipratropium bromide with a β‎2-agonist produces significantly greater bronchodilation than a β‎2-agonist alone. Add nebulized ipratropium bromide (0.5 mg 4- to 6-hourly).

  • Magnesium sulfate—use a single dose of IV magnesium sulfate for patients with life-threatening or near-fatal asthma who have not shown a good initial response to inhaled bronchodilator therapy (1.2–2 g IV infusion over 20 min).

  • Some patients with life-threatening near-fatal asthma who show a poor response to initial therapy may gain additional benefit from IV aminophylline (5 mg/kg loading dose over 20 min unless on maintenance oral therapy, followed by an infusion of 0.5–0.7 mg/kg/h). If given to patients taking oral aminophylline or theophylline, blood levels should be checked on admission and daily.

  • Monitor haemodynamics (see Respiratory assessment and monitoring p. [link]).

  • Monitor electrolytes and treat imbalances (see Respiratory assessment and monitoring p. [link]).

  • Monitor fluid status and treat imbalances (see Respiratory assessment and monitoring pp. [link] and [link]).

  • Oxygen therapy (see Respiratory assessment and monitoring p. [link]).

  • Adherence to infection prevention and control.

  • Mechanical ventilation strategies for asthma:

    • limit airway pressures (i.e. low tidal volumes)

    • extend expiratory time

    • low respiratory rate

    • minimize intrinsic PEEP

    • permissive hypercapnia (higher risk of hypoxia and barotrauma).

Further reading

British Thoracic Society (BTS). British Guideline on the Management of Asthma: a national clinical guideline. BTS: London, 2014.Find this resource:

Chronic obstructive pulmonary disease (COPD)

Definition

Around 900 000 people in the UK are known to have COPD, with a further 2 million people remaining undiagnosed.1 The Global Initiative for Chronic Obstructive Lung Disease (GOLD)2 has established an internationally recognized definition of COPD as a common but preventable disease, characterized by persistent airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases. Exacerbations and comorbidities contribute to the overall severity in individual patients.

An exacerbation of COPD is an acute event characterized by a worsening of the patient’s respiratory symptoms that exceeds normal day-to-day variations. Exacerbations are often precipitated by a viral upper respiratory tract infection, heart failure, or retained secretions.

Causes

The chronic airflow limitation that is characteristic of COPD is caused by a mixture of small airways disease (obstructive bronchiolitis) and parenchymal destruction (emphysema). Chronic inflammation causes structural changes and narrowing of the small airways. Destruction of the lung parenchyma, also by inflammatory processes, leads to the loss of alveolar attachments to the small airways and decreases lung elastic recoil. In turn these changes reduce the ability of the airways to remain open during expiration.

Assessment findings

  • Accessory muscle use.

  • Barrel-shaped chest.

  • Expansion reduced bilaterally (hyperinflated chest).

  • Breath sounds diminished or absent.

  • Added sounds—expiratory wheeze.

  • Tachypnoea and central cyanosis.

  • Cough and sputum.

Management

  • Chest X-ray.

  • ABG and pulse oximetry.

  • Peak flow.

  • FBC, serum creatinine, U&E, and LFTs.

  • Sputum microscopy, culture, and sensitivity.

  • β‎2-agonist bronchodilators—in most cases, nebulized salbutamol or terbutaline given in high doses acts quickly to relieve bronchospasm, with few side effects. Repeat doses of β‎2-agonists at 15- to 30-min intervals or give continuous nebulization of salbutamol at 5–10 mg/h if there is an inadequate response to initial treatment. Reserve the intravenous route for patients in whom the inhaled route is unreliable.

  • Steroid therapy—steroid tablets are as effective as injected steroids, provided that they can be swallowed and retained. Use a dose of 30–40 mg prednisolone per day for 10–14 days.

  • Anticholinergic therapy—nebulized ipratropium bromide with a β‎2-agonist produces significantly greater bronchodilation than a β‎2-agonist alone. Add nebulized ipratropium bromide (0.5 mg 4- to 6-hourly).

  • Antibiotic therapy.

  • Monitor haemodynamics (see Respiratory assessment and monitoring p. [link]).

  • Monitor electrolytes and treat imbalances (see Respiratory assessment and monitoring p. [link]).

  • Monitor fluid status and treat imbalances (see Respiratory assessment and monitoring pp. [link] and [link]).

  • Oxygen therapy, taking into consideration the patient’s normal PCO2 and PO2 (see Respiratory assessment and monitoring p. [link]).

  • Chest physiotherapy.

  • Adherence to infection prevention and control.

  • Mechanical ventilation strategies for COPD:

    • limit airway pressures (i.e. low tidal volumes)

    • extend expiratory time

    • low respiratory rate

    • minimize intrinsic PEEP

    • permissive hypercapnia (higher risk of hypoxia and barotrauma).

The decision to ventilate a patient with an exacerbation of COPD must take into consideration the stage of lung disease, the aggressive treatment, and the weaning process, together with the wishes of the patient.

References

1 Health Care Commission. Cleaning the Air: a national study of chronic obstructive pulmonary disease. Commission for Health Care Audit and Inspection: London, 2006.Find this resource:

2 Global Initiative for Chronic Obstructive Lung Disease (GOLD). Global Strategy for Diagnosis, Management, and Prevention of COPD. GOLD: 2015.Find this resource:

Further reading

Ward NS and Dushay KM. Clinical concise review: mechanical ventilation of patients with chronic obstructive pulmonary disease. Critical Care Medicine 2008; 36: 1614–19.Find this resource:

Wildman MJ et al. Implications of prognostic pessimism in patients with chronic obstructive pulmonary disease (COPD) or asthma admitted to intensive care in the UK within the COPD and asthma outcome study (CAOS): multicentre observational cohort study. British Medical Journal 2007; 335: 1132.Find this resource:

Pulmonary oedema

Definition

Pulmonary oedema is an accumulation of fluid in the interstitial space of the lung tissue. This excess fluid will impair gas exchange at the alveolar–capillary membrane.

Causes

Fluid accumulation within the lung itself has either a cardiogenic cause (failure of the heart to remove fluid from the lung circulation) or a non-cardiogenic cause (direct injury to the lung parenchyma) (see Table 4.4).

Table 4.4 Cardiogenic and non-cardiogenic causes of pulmonary oedema

Cardiogenic causes

Non-cardiogenic causes

Cardiogenic shock

Chest trauma (smoke inhalation)

Cardiac failure (left ventricle)

Oxygen toxicity

Myocardial infarction

Sepsis

Post-cardiac arrest

Multiple transfusions

Pancreatitis

Liver disease

Assessment findings

  • Added sounds—crackles.

  • Tachypnoea and central cyanosis.

  • Cough and sputum.

Management

  • Chest X-ray.

  • ABG and pulse oximetry.

  • FBC, serum creatinine, U&E, and LFTs.

  • Nitrate—sublingually or by infusion.

  • Diuretic—furosemide IV 0.5–1.0 mg/kg.

  • Morphine—IV 5 mg.

  • Monitor haemodynamics (see Respiratory assessment and monitoring p. [link]).

  • Monitor electrolytes and treat imbalances (see Respiratory assessment and monitoring p. [link]).

  • Monitor fluid status and restrict fluids (see Respiratory assessment and monitoring pp. [link] and [link]).

  • Oxygen therapy (see Respiratory assessment and monitoring p. [link]).

  • Adherence to infection prevention and control.

  • Non-invasive ventilation strategies for pulmonary oedema:

    • continuous positive airway pressure (CPAP) with high-level PEEP.

Further reading

Salman A, Milbrandt E and Pinksy M. The role of noninvasive ventilation in acute cardiogenic pulmonary oedema. Critical Care 2010; 14: 303.Find this resource:

Pulmonary embolism (PE)

Definition

Embolization of a venous thrombosis to the lungs will lead to pulmonary artery occlusion, obstruction of the pulmonary circulation, and sudden death. The effect of the obstruction will cause inflammatory changes, which will lead to pulmonary hypertension and subsequent coronary oedema. In addition, the obstruction will cause a ventilation/perfusion mismatch, leading to hypoxaemia.

Causes

Most pulmonary embolisms result from lower limb, pelvic, or inferior vena cava thrombus. Patients are at higher risk if they manifest any or all three of Virchow’s triad—venous stasis, hypercoagulability, or vein wall injury. Immobility is the main cause.

Assessment findings

  • Pulmonary embolism can often occur without any symptoms.

  • Sudden dyspnoea.

  • Pleuritic chest pain.

  • Haemoptysis.

  • Tachypnoea and central cyanosis.

  • Signs of venous thromboembolism (VTE).

  • Signs of right ventricle dysfunction (e.g. jugular venous distension).

Management

  • Chest X-ray.

  • ABG and pulse oximetry.

  • D-dimer.

  • FBC, serum creatinine, U&E, and LFTs.

  • ECG.

  • Anticoagulation.

  • Inferior vena cava filter if anticoagulation is contraindicated.

  • Thrombolysis.

  • Embolectomy if thrombolysis is contraindicated.

  • Monitor haemodynamics (see Respiratory assessment and monitoring p. [link]).

  • Oxygen therapy (see Respiratory assessment and monitoring p. [link]).

  • Adherence to infection prevention and control.

  • VTE assessment and prophylaxis.

Further reading

British Thoracic Society Standards of Care Committee, Pulmonary Embolism Guideline Development Group. D-Dimer in Suspected Pulmonary Embolism: a statement from the British Thoracic Society Standards of Care Committee. British Thoracic Society: London, 2006.Find this resource:

Miller A and Boldy D. Pulmonary embolism guidelines: will they work? Thorax 2003; 58: 463.Find this resource:

Tuberculosis (TB)

Definition

TB is a contagious bacterial infection that mainly affects the lungs, although the pathogen Mycobacterium tuberculosis can infect other parts of the body, such as the gastrointestinal tract, cerebrospinal fluid, and other organs.

Exposure is through aerosol droplets from coughing, sneezing, or speaking. Duration and intimacy of contact determine the likelihood of transmission. Four outcomes are possible following exposure—immediate clearance of bacteria, primary disease, latent infection, and reactivation disease. Latent infection refers to the presence of TB without the disease.

Causes

Medical conditions that predispose to TB include HIV, diabetes, chronic renal failure, and chronic pulmonary disease. Social factors such as homeless shelters, prisons, population density, and poverty are associated with an increased risk of TB.

Assessment findings

  • Productive and prolonged cough.

  • Chest pain.

  • Haemoptysis.

  • Fever, chills, and night sweats.

  • Weight loss and appetite loss.

  • Fatigue.

Management

  • Chest X-ray.

  • ABG and pulse oximetry.

  • FBC, serum creatinine, U&E, and LFTs.

  • Sputum microscopy, culture, and sensitivity for acid-fast bacilli (AFB).

  • Antiviral therapy (e.g. isoniazid, rifampicin, pyrazinamide, ethambutol).

  • Corticosteroid therapy.

  • Monitor haemodynamics (see Respiratory assessment and monitoring p. [link]).

  • Monitor electrolytes and treat imbalances (see Respiratory assessment and monitoring p. [link]).

  • Monitor fluid status and treat imbalances (see Respiratory assessment and monitoring pp. [link] and [link]).

  • Oxygen therapy (see Respiratory assessment and monitoring p. [link]).

  • Adherence to infection prevention and control.

Generally, patients with confirmed or suspected TB are cared for in isolation. If available, the ventilation for the room should be set to negative pressure, and the doors must be kept closed to achieve this.

If the patient is intubated or ventilated and a closed suction system is in use, masks do not need to be worn. However, high-filtration masks (e.g. FFP3) must be worn whenever the closed system is disconnected (e.g. when changing filters, catheter mounts, tubing, or suction apparatus, or for chest physiotherapy). Masks can be removed 30 min after the procedure has been completed. If the patient is not fully ventilated and a closed circuit cannot be maintained (e.g. on CPAP or T-piece), carers must wear high-filtration masks in the room at all times unless the patient is considered no longer infectious.

Further reading

World Health Organization. Policy on TB Infection Control in Health-Care Facilities, Congregate Settings and Households. World Health Organization: Geneva, 2009.Find this resource:

National Institute for Health and Care Excellence (NICE). Tuberculosis: clinical diagnosis and management of tuberculosis, and measures for its prevention and control. NICE: London, 2011. Respiratory assessment and monitoring https://www.nice.org.uk/guidance/cg117

Interstitial lung disease

Definition

There are a number of similar diseases that affect the lung tissue, and these are grouped under the umbrella term interstitial lung disease. This group of diseases is classified in this way to distinguish them from obstructive airway diseases.

  • Pulmonary fibrosis—injury to the epithelial surface that causes inflammation if prolonged, leading to fibrosis.

  • Granulomatous lung disease—accumulation of T lymphocytes, macrophages, and epithelioid cells organized into discrete structures known as granulomas.

The lung tissue involved includes alveoli, alveolar epithelium, capillary endothelium, and the spaces between these structures.

Interstitial lung disease can be considered a comorbidity, which will have acute and chronic phases as well as exacerbating any new lung pathologies.

Causes

Interstitial lung disease may be caused by inhaled substances (e.g. asbestosis), medications (e.g. amiodarone, chemotherapy), connective tissue disease (e.g. sarcoidosis), or infection (pneumonia), or it may be idiopathic.

Assessment findings

  • Finger clubbing.

  • Expansion reduced.

  • Added sounds—fine inspiratory crackles.

  • Tachypnoea and central cyanosis.

  • Fatigue.

Management

Management will not reverse fibrosis, but rather the goals are to remove the agents that are causing injury and to suppress the inflammatory process.

  • Chest X-ray.

  • ABG and pulse oximetry.

  • FBC, serum creatinine, U&E, and LFTs.

  • Sputum microscopy, culture, and sensitivity.

  • Glucocorticoids to suppress inflammation, 0.5–1 mg/kg daily.

  • Monitor haemodynamics (see Respiratory assessment and monitoring p. [link]).

  • Monitor electrolytes and treat imbalances (see Respiratory assessment and monitoring p. [link]).

  • Monitor fluid status and treat imbalances (see Respiratory assessment and monitoring pp. [link] and [link]).

  • Oxygen therapy (see Respiratory assessment and monitoring p. [link]).

  • Adherence to infection prevention and control.

Further reading

King T. Interstitial lung diseases. In: A Fauci et al. (eds) Harrison’s Principles of Internal Medicine, 17th edn. McGraw-Hill Companies, Inc.: London, 2008. pp. 1643–50.Find this resource:

Acute respiratory distress syndrome (ARDS)

Definition

The 2012 Berlin definition of ARDS3 changed the terminology and diagnostic criteria that had previously been used (see Table 4.5). For example, the phrase ‘acute lung injury’ is no longer to be used, and ARDS is now categorized as mild, moderate, or severe.

Table 4.5 The Berlin definition of acute respiratory distress syndrome (ARDS)3

Acute respiratory distress syndrome

Timing

Within 1 week of known clinical insult or new or worsening respiratory symptoms

Chest imaging

Bilateral opacities that are not fully explained by effusions, lobar or lung collapse, or nodules

Origins of oedema

Respiratory failure that is not fully explained by cardiac failure, fluid overload, or hydrostatic oedema

Oxygenation

  • Mild

PaO2/FiO2 < 200 mmHg or < 300 mmHg with PEEP or CPAP > 5 cmH2O

  • Moderate

PaO2/FiO2 < 100 mmHg or < 200 mmHg with PEEP > 5 cmH2O

  • Severe

PaO2/FiO2 < 100 mmHg PEEP > 5 cmH2O

ARDS is defined as a type of acute, diffuse, inflammatory lung injury that leads to increased pulmonary vascular permeability and loss of aerated lung tissue.

The clinical presentation consists of hypoxaemia, bilateral lung opacities, increased physiological dead space, and decreased lung compliance. The acute phase is characterized by diffuse alveolar damage (i.e. oedema, inflammation, or haemorrhage).

Causes

Patients at clinical risk of developing ARDS include those with:

  • pneumonia

  • aspiration of gastric contents

  • lung contusion

  • inhalational injury

  • non-pulmonary sepsis

  • multiple trauma

  • massive transfusion

  • pancreatitis.

Sepsis precipitates ARDS in up to 40% of cases, and the risk increases if shock, organ dysfunction, or systemic inflammatory response is present. Early detection of patients with sepsis who are at risk of developing ARDS is an important preventive strategy.

Assessment findings

See the Berlin definition of ARDS in Table 4.5.

Management

  • Chest X-ray.

  • ABG and pulse oximetry.

  • FBC, serum creatinine, U&E, and LFTs.

  • Monitor haemodynamics (see Respiratory assessment and monitoring p. [link]).

  • Monitor electrolytes and treat imbalances (see Respiratory assessment and monitoring p. [link]).

  • Monitor fluid status and treat imbalances (see Respiratory assessment and monitoring pp. [link] and [link]).

  • Oxygen therapy (see Respiratory assessment and monitoring p. [link]).

  • Adherence to infection prevention and control.

  • Ventilator-associated pneumonia care bundle (see Box 4.3).

    • consider I:E ratio change with prolonged inspiratory time

    • consider prone positioning (see Respiratory assessment and monitoring p. [link])

  • Consider airway pressure release ventilation (APRV) (see Respiratory assessment and monitoring p. [link]).

  • Consider extracorporeal membrane oxygneation (ECMO) (see Respiratory assessment and monitoring p. [link]).

  • Mechanical ventilation strategies for ARDS:

    • pressure control mode (in volume-controlled ventilation, gas is delivered preferentially to more compliant areas of lung with a risk of overstretch)

    • protective lung ventilation (see Respiratory assessment and monitoring p. [link])

    • tidal volumes 6–8 ml/kg

    • maintain plateau pressure < 30 cm H2O

    • high amounts of PEEP

Lung-protective strategies are the only supportive therapy that has been shown to improve survival in ARDS patients. Therefore they should be used for patients who have or are at risk of developing ARDS. It can be combined with an open lung approach in patients with moderate to severe ARDS (i.e. higher PEEP and recruitment manoeuvres). The ventilation strategy chosen should be modified in patients with obstructive lung disease in order to prevent dynamic hyperinflation (e.g. patients with COPD or asthma).

  • Severe ARDS: early administration of neuromuscular blocking agent (see Respiratory assessment and monitoring p. [link])

  • Steroids—research inconclusive

Reference

3 The ARDS Definition Task Force. Acute respiratory distress syndrome: the Berlin definition. Journal of the American Medical Association 2012; 307: 2526–33.Find this resource:

Further reading

deHaro C et al. Acute respiratory distress syndrome: prevention and early recognition. Annals of Intensive Care 2013; 3: 11.Find this resource:

National Heart, Lung, and Blood Institute (NHLBI) ARDS Network. Respiratory assessment and monitoringwww.ardsnet.org