The most common reason that patients require admission to an intensive care unit (ICU) is for support of their respiratory system. Over the last decade, almost half of all patients admitted to ICU in Australia and New Zealand required mechanical ventilation;¹ a statistic of 41% in 2008.² Failure or inadequate function of the respiratory system occurs as a result of direct or indirect pathophysio-logical conditions. The process of mechanical ventilation may also injure a patient’s lungs, further impacting functioning of the respiratory system. Preventing or minimising ventilator-associated lung injury is therefore also a primary goal of patient care. Chapter 13 described the relevant anatomy and physiology and assessment and monitoring practices for a patient with life-threatening respiratory dysfunctions. This chapter describes the incidence, pathophysiology, clinical manifestations and management of common respiratory disorders that result in acute respiratory failure, specifically pneumonia (including discussion of respiratory epidemics), asthma, chronic obstructive pulmonary disease (COPD), acute lung injury (ALI), pneumothorax and lung transplantation. Discussion of oxygenation and ventilation strategies to support respiratory function during a critical illness is presented in Chapter 15.

Incidence of Respiratory Alterations

Respiratory diseases are common and affect significant numbers of the population in Australia, accounting for almost half of all hospital admissions.³ These diseases are also the most common illness responsible for emergency admission to hospital, the most common reason to visit a general practitioner and represent the most commonly reported long-term illnesses in children.⁴ Despite these findings, the incidence of respiratory alterations is difficult to quantify as the number of patients who require admission to hospital as a result of respiratory disease represent a small proportion of the total number affected. Further, patients who require admission to ICU as a result of respiratory disease represent only a fraction of all hospital admissions.^5,⁶

Data presented in Table 14.1 ⁷ illustrates the total number of patients (adults and children) admitted to hospital as a result of a range of respiratory diseases. While it is difficult to determine the number of patients in each diagnostic group who required admission to ICU as part of their management, ICU admissions account for around 4% of all overnight hospital admissions.⁵ Infective processes (influenza and pneumonia), COPD and asthma represent the three largest groups of hospital admissions. Conditions such as adult respiratory distress syndrome (ARDS), pneumothorax, pulmonary embolus and pulmonary oedema are relatively small. It should be noted, however, that these conditions often evolve throughout the course of an illness⁶ and may not therefore be included as the reason for admission. Common respiratory-related ICU presentations are discussed in the following sections.

TABLE 14.1 Incidence of respiratory alterations in Australia 2007–2008 ⁷

Disorder	Hospital admissions
Disorder	n	%
Adult Respiratory Distress Syndrome	202	0.06
Asthma	37,641	10.40
COPD (acute exacerbation)	56,249	15.54
Influenza and pneumonia	70,232	19.41
Lung transplantation	91	0.03
Pneumothorax	3,177	0.88
Pulmonary embolus	9,234	2.55
Pulmonary oedema	902	0.25
Total	177,728	49.11

Respiratory Failure

Respiratory failure occurs when there is a reduction in the body’s ability to maintain either oxygenation or ventilation, or both. It may occur acutely, as observed in pneumonia and ARDS or it may exist in chronic form, as observed in asthma and COPD. Respiratory failure, and the disorders that cause it, are responsible for a high proportion of death and disability throughout the world.⁶

Aetiology of Respiratory Failure

For the respiratory system to function effectively, the rate and depth of breathing is controlled by the brain, the chest wall must expand adequately, air needs to flow easily through the airways and effective exchange of gases needs to occur at the alveolar level. Conditions that impact on one or more aspects of the normal physiological functioning of the respiratory system can cause respiratory failure, for example:

• decreased respiratory drive may be caused by brain trauma, drug overdose or anaesthesia/sedation

• decreased respiratory muscle strength may be caused by Guillain–Barré syndrome, poliomyelitis, myasthenia gravis or spinal cord injury

• decreased chest wall expansion may be caused by postoperative pain, rib fractures or a pneumothorax

• increased airway resistance may be caused by asthma or COPD

• increased metabolic oxygen requirements may be caused by severe sepsis

• decreased capacity for gas exchange may be caused by impairment in either ventilation (e.g. pulmonary oedema, pneumonia, acute lung injury, COPD) or pulmonary perfusion (e.g. pulmonary embolism), or a combination of the two.

Importantly, respiratory failure can be an acute or chronic condition. While acute respiratory failure (ARF) is characterised by life-threatening alterations in function, the manifestations of chronic respiratory failure are more subtle and potentially more difficult to diagnose. Patients with chronic respiratory failure often experience acute exacerbations of their disease, also resulting in the need for intensive respiratory support.⁶

Pathophysiology

Respiratory failure occurs when the respiratory system fails to achieve one or both of its essential gas exchange functions: oxygenation or elimination of carbon dioxide, and can be described either as type I (primarily a failure of oxygenation) or type II (primarily a failure of ventilation).⁶

Type I Respiratory Failure

A patient with type I (‘hypoxaemic’) respiratory failure presents with a low PaO₂ and a normal or low PaCO₂. Hypoxaemic respiratory failure may be caused by a reduction in inspired oxygen pressure (e.g. such as extreme altitude), hypoventilation, impaired diffusion or ventilation-perfusion mismatch. Most major respiratory alterations cause this type of failure, usually as a result of hypoventilation due to alveolar collapse or consolidation, or a perfusion abnormality.⁶

When there is mismatch between ventilation and perfusion in the lungs, exchange of gases is impaired and hypoxaemia ensues (see Figure 14.1):⁶

• In some cases, there may be reduced ventilation to a certain area of lung tissue (e.g. pulmonary oedema, pneumonia, atelectasis, ARDS). A severe form of mismatch known as intrapulmonary shunting occurs when adequate perfusion exists but there are sections of lung tissue that are not ventilated. In these alveoli, the oxygen content is similar to that of the mixed venous blood and the CO₂ is elevated.

• In other instances, ventilation may be adequate but perfusion is impaired (e.g. pulmonary embolus). In its severe form, this is known as dead space ventilation as the lungs continue to be ventilated but there is no perfusion, and therefore no gas exchange. In this situation, the alveolar oxygen content is similar to that of the inspired gas mixture and the CO₂ is minimal ⁶ (see Chapter 13 for further discussion).

FIGURE 14.1 Ventilation-perfusion mismatches.⁶ Ventilation-perfusion (V/Q) ratio displays the normal balance (star) between alveolar ventilation and vascular perfusion allowing for proper oxygenation. When ventilation is reduced, the V/Q ratio decreases, in the most extreme case resulting in pure shunt, where V/Q = 0. When perfusion is reduced, the V/Q ratio increases, in the most extreme case resulting in pure dead space, where V/Q = infinite (∞). (published with permission)

Type II Respiratory Failure

Conversely, a patient with Type II respiratory (‘hypercapnoeic/hypoxaemic’) failure presents with a high PaCO₂ as well as a low PaO₂. This failure is caused by alveolar hypoventilation, where the respiratory effort (or minute ventilation) is insufficient to allow adequate exchange of oxygen and carbon dioxide. This may be caused by conditions that affect respiratory drive such as neuromuscular diseases, chest wall abnormalities or severe airways disease (e.g. asthma or COPD).

Clinical Manifestations

Patient presentations in acute respiratory failure can be quite diverse and are dependent on the underlying pathophysiological mechanism (e.g. hypercapnoea and/or hypoxaemia), the specific aetiology and any comorbidities that may exist.⁶ Specific clinical manifestations for the clinical disorders discussed in this chapter are provided in each section. Dyspnoea is the most common symptom associated with ARF; this is often accompanied by an increased rate and reduced depth of breathing and the use of accessory muscles. Patients may also present with cyanosis, anxiety, confusion and/or sleepiness.⁴

A systematic approach to clinical assessment and management of patients with ARF is crucial, given the large number of possible causes. Clinical investigations to assess the cause of respiratory failure vary depending on the suspected underlying aetiology and the progression of disease. Continuous monitoring of oxygen saturation using pulse oximetry, arterial blood gas (ABG) analysis and chest radiograph assessment are used in almost all cases of respiratory failure.⁸ Other more specialised tests such as computed tomography (CT) of the chest and microbiological cultures may be used in specific circumstances.⁹ With ABG analysis, the measurement of PaO₂, PaCO₂, Alveolar–arterial (A–a) PO₂ difference and the patient response to supplemental oxygen are key elements in determining the cause of ARF (see Chapter 13).

Practice tip

Respiratory failure:

Type I (‘hypoxaemic’) = low PaO₂ and normal or low PaCO₂

Type II (‘hypercapnoeic’) = high PaCO₂ and low PaO₂

Independent Nursing Practice

The primary survey (airway, breathing and circulation) and immediate management form initial routine practice.¹⁰ Frequent assessment and monitoring of respiratory function, including a patient’s response to supplemental oxygen and/or ventilatory support, is the focus. Patient comfort and compliance with the ventilation mode, ABG analysis and pulse oximetry guide any titration of ventilation. The key goals of management are to treat the primary cause of respiratory failure, maintain adequate oxygenation and ventilation and prevent or minimise the potential complications of positive pressure mechanical ventilation.

Maintaining Oxygenation and Ventilation

The therapeutic aim is to titrate the fraction/percentage of inspired oxygen (FiO₂) to achieve a PaO₂ of 65–70 mmHg and to maintain minute ventilation to achieve PaCO₂ within normal limits where possible.⁶ Oxygen is not a drug, therefore it does not require prescription for use. Nursing staff in ICU are therefore commonly responsible for titration of oxygen therapy to maintain a specific PaO₂ or SpO₂, and the alteration of respiratory rate and/or tidal volume to maintain a specified PaCO₂. One concern that often arises, particularly with patients who require high concentrations of oxygen, is the risk of oxygen toxicity. The link between prolonged periods of oxygen concentrations approaching 100% and oxidant injuries in airways and lung parenchyma has been established, although mostly from animal research. Although it remains unclear how these data apply to human populations, most consensus groups have argued that FiO₂ values less than 0.4 are safe for prolonged periods of time and that FiO₂ values of greater than 0.8 should be avoided if possible⁶ (see Chapter 15 for further discussion of oxygenation).

Ventilator-associated lung injury is also a concern when managing patients with acute respiratory failure. A lung can be injured when it is stretched excessively as a result of tidal volume settings that generate high pressures, often referred to as barotrauma or volutrauma. The most common injury is that of alveolar rupture and/or air in the pleural space (pneumothorax).⁶ An approach known as ‘lung protective ventilation’ aims to minimise overdistension of the alveoli through careful monitoring of tidal volumes and airway pressures. This method should be considered for all ventilated patients. The approach may result in tolerance of higher PaCO₂ than normal in patients presenting with acute lung injury or ARDS (see Chapter 15 for further discussion).

Development of ventilator-associated respiratory muscle weakness has been reported as a significant issue when the respiratory muscles are rendered inactive through adjustment of ventilator settings and administration of pharmacotherapy. While it is not yet possible to provide precise recommendations for interventions to avoid this, clinicians are advised to select ventilator settings that provide for some respiratory muscle use.¹¹

Prevention or minimisation of complications associated with positive pressure mechanical ventilation remains a major focus of nursing practice. These complications may relate to the patient–ventilator interface (artificial airway and ventilator circuitry), infectious complications such as ventilator-associated pneumonia (VAP) or complications associated with sedation and/or immobility. Some common complications and the appropriate management strategies are briefly outlined in Table 14.2 ^6,¹²^–¹⁴ and discussed further in Chapter 15.

TABLE 14.2 Complications of mechanical ventilation and associated management strategies

Patient–ventilator interface complications
Airway dislodgement/disconnection	Endotracheal tube (ETT) or tracheostomy tube is secured to optimise ventilation and prevent airway dislodgement or accidental extubation.
Circuit leaks	Cuff pressure assessmentCircuit checksExhaled tidal volume measurement
Airway injury from inadequate heat/humidity	Maintain humidification of the airway using either a heat-moisture exchanger or a water-bath humidifier.
Obstructions from secretions	Assess the need for suctioning regularly and suction as required.
Tracheal injury from the artificial airway	Assessment of airway placement and cuff pressure (minimal occlusion method)
Infectious complications
Ventilator-associated pneumonia (VAP)	Hand washing Appropriate antibiotic therapy Ventilator Care Bundle: • Elevating head of bed to 30–45 degrees • Daily sedation vacation and assessment of readiness to extubate • Peptic ulcer disease prophylaxis • Deep vein thrombosis prophylaxis Minimising interruptions to ventilator circuit (e.g. closed suctioning technique) Drainage of sub-glottic secretions Aerosolised antibiotics for patients who are colonised Weaning and discontinuation of ventilatory support as soon as possible Nurse-led weaning protocols

Complications associated with immobility/sedation Gastrointestinal dysfunction Prokinetic medicationConstipation – bowel therapy regimen Muscle atrophy Passive limb movements, foot splints (see Chapter 6) and early activity/mobility (see Chapter 4) Pressure ulcers Pressure-relieving mattresses, regular repositioningAssessment of risks and management of any pressure ulcers by wound care specialists, nutrition advice

Collaborative Practice

A patient with ARF requires extensive multidisciplinary collaboration between nurses, physiotherapists, specialist medical staff, speech and occupational therapists, dietitians, social workers, radiologists and radiographers. Patients may require additional oxygen delivery through an adequate haemoglobin level for oxygen transportation and a cardiac output sufficient to supply oxygenated blood to the tissues.⁶ At times this may require blood transfusion and/or the use of vasoactive medications (see Chapters 11 and 20).

Chest physiotherapy is a routine activity for managing patients with ARF. This involves positioning, manual hyperinflation, percussion and vibration and suctioning. The evidence base for these techniques is limited, however, with a systematic review not demonstrating an improvement in mortality.¹² Guidelines for physiotherapy assessment have enabled identification of patient characteristics for treatments to be prescribed and modified on an individual basis.¹³ Table 14.3 ^6,^13,¹⁵ outlines a number of collaborative practice issues for patients with respiratory failure, particularly those who may require prolonged mechanical ventilation.

TABLE 14.3 Collaborative practices for patients with respiratory failure

Long-term patient management	Best practice
Timing of tracheostomy insertion	Where mechanical ventilation is expected to be 10 days or more, tracheostomy should be performed as soon as identified. Early tracheostomy is associated with less nosocomial pneumonia, reduced ventilation time and shorter ICU stay.
Weaning protocols	Specific plan is patient dependent; better outcomes are achieved when there is an agreed and well communicated weaning plan (see Chapter 15)
Nutrition	Consider adequate nutrition for physiological needs – important to not overfeed as this increases CO₂ production and need to have balance of vitamins and minerals
Swallow assessment	Assess for dysphagia
Mobilisation	Sitting out of bed, mobilising (see Chapter 4)
Communication	Communication aids, speaking valves
Activities	Activity plan/routine, entertainment (TV/Films), visitors, outings
Sleep	Clustering cares, reducing stimuli to promote sleep (see Chapter 7)
Family support	Importance of providing physical, emotional and/or spiritual support to family members (see Chapter 8)
Tracheostomy follow-up	Outreach team: follow-up care by nurses experienced in tracheostomy care can prevent complications and improve outcomes
End-of-life decisions in ARF	see Chapter 5

Medications

Medications commonly prescribed in respiratory failure include inhalation steroids and bronchodilators, intravenous steroids and bronchodilators, antibiotic therapy, analgesia and sedation to maintain patient–ventilator synchrony, but may also involve nitric oxide, glucocorticoid or surfactant administration. A patient’s condition, comorbidities and the above-mentioned pharmacological therapy may also be supported with inotropic and other resuscitation therapies (see Chapter 11). As the use of medications will vary depending on the underlying cause of respiratory failure, these are discussed in each section respectively.

Special Considerations

Respiratory failure in patients who are pregnant, elderly or have comorbidities require specific attention to avoid clinical deterioration. Respiratory physiology and the respiratory tract itself are altered during pregnancy; this may result in exacerbation of preexisting respiratory disease or increased susceptibility to disease (see Chapter 26). Upper airway mucosal oedema may increase the likelihood of upper respiratory tract infection. Lung function and lung volume are also altered, compensated by an increase in respiratory drive and minute ventilation. The impact of these alterations on chronic conditions such as asthma/COPD and acute illness are explored in the subsequent sections. The impact on the fetus of infection, hypoxia and drug therapy is an important consideration.⁶

The elderly have ageing organs and systems and other comorbidities that may exacerbate their respiratory dysfunction. Drug metabolism and excretion is slowed, complicating drug dosing and response.¹⁶ Metabolism of anaesthetic agents is slower due to the diminished physio-logy of ageing organs. Common comorbidities may also be present, including obesity, heart disease, diabetes, and renal impairment or muscle wasting. Pneumonia is a common presentation in the elderly and is often exacerbated by chronic lung conditions.⁶

Comorbidities add to the complexity of managing a patient’s primary condition and increase the risk of additional organ dysfunction or failure. Chronic respiratory conditions can have a significant impact on the severity of respiratory infections, while cardiovascular and renal disease impact on disease severity and the management of many respiratory alterations. Other factors such as smoking and alcohol use, living conditions and lifestyle impact on the predisposition and clinical course of an illness.

Post-anaesthesia Respiratory Support

Short-term respiratory support may be required after major surgery, in cases of extended anaesthesia, preexisting comorbidities and/or diminished physical reserve (e.g. elderly, patients with obstructive sleep apnoea). Most patients requiring ventilation in the early postoperative period have had cardiothoracic surgery, and so much of the available research relates to this patient group (see also Chapter 12).

Preoperative assessment and management is a key factor in preventing respiratory complications. This involves optimising physical condition and nutritional status, planning the timing of surgery to reduce the likelihood of preexisting respiratory infection and patient education regarding the importance of respiratory support, including postoperative mobilisation and physiotherapy. Patients with suspected or confirmed chronic conditions require a thorough diagnostic work-up prior to surgery to determine the best management strategy in the postoperative period.¹⁷

The key focus in management of postoperative ventilation is to limit ventilation time, as prolonged ventilation time is associated with poor outcome. Once a patient has reached normothermia, is haemodynamically stable, responsive and has adequate analgesia, weaning of ventilation is commenced. Rapid and/or nurse-led weaning protocols are often implemented to minimise delays in the weaning process. Anaesthetic care in these patients includes use of short-acting or regional anaesthesia (e.g. epidural analgesia) to minimise respiratory depression.¹⁸

Pneumonia

Pneumonia is infection of the lung. Depending on the type and severity of the infection and the overall health of the person, it may result in ARF. Pneumonia can be caused by most types of microorganisms, but is most commonly a result of bacterial or viral infection. In critical care the key distinctions in assessing and managing a patient with pneumonia relate to the specific aetiology or causative organism. This section reviews the aetiology, pathophysiology, clinical presentation and management of two types of pneumonia:

• community-acquired pneumonia (CAP)

• ventilator-associated pneumonia (VAP)

The issue of epidemic or pandemic respiratory disease as a result of viral infections is included in the following Respiratory pandemics section.

Pathophysiology

The normal human lung is sterile, unlike the gastrointestinal tract and upper respiratory tract which have resident bacteria. A number of defence mechanisms exist to prevent microorganisms entering the lungs, such as particle filtration in the nostrils, sneezing and coughing to expel irritants and mucus production to trap dust and infectious organisms and move particles out of the respiratory system. Infection occurs when one or more of these defences are not functioning adequately or when an individual encounters a large amount of microorganisms at once and the defences are overwhelmed.⁶ An invading pathogen provokes an immune response in the lungs, resulting in the following pathophysiological processes:

• alteration in alveolar capillary permeability that leads to an increase in protein-rich fluid in the alveoli; this impacts on gas exchange and causes the patient to breathe faster in an effort to increase oxygen uptake and remove CO₂

• mucous production increases and mucous plugs may develop which block off areas of the lung, further reducing capacity for gas exchange

• consolidation occurs in the alveoli, filling with fluid and debris; this occurs particularly with bacterial pneumonia where debris accumulates from the large number of white blood cells involved in the immune response.⁶

Aetiology

Pneumonia is caused by a variety of microorganisms, including bacteria, viruses, fungi and parasites. In many cases, the causative organism may not be known and current practice in many cases is to initiate antimicrobial treatment as soon as possible, based on symptoms and patient history, rather than waiting for microorganism culture results.¹⁹ The true incidence of pneumonia is not well known as many patients do not require hospitalisation. Different ages and characteristics of the patient are often associated with different causative organisms. Viral pneumonias, especially influenza, are most common in young children, while adults are more likely to have pneumonia caused by bacteria such as Streptococcus pneumoniae and Haemophilus influenzae. Pneumonia is a particular concern among elderly adults as they experience an increase in the frequency and severity of pneumonia.⁶

Table 14.4 ⁷ outlines the principal diagnoses of patients hospitalised with pneumonia in Australia during 2007–2008. This information reflects the high proportion of viral pneumonia and the large number of cases where the causative organism may not be known.

TABLE 14.4 Principal diagnoses of patients hospitalised with pneumonia in Australia during 2007–2008

Principal Diagnosis	Hospitalisations
Principal Diagnosis	n	%
Pneumonia due to identified influenza virus	1668	2.4
Influenza, virus not identified	1429	2.0
Viral pneumonia, not elsewhere classified	1899	2.7
Pneumonia due to Streptococcus pneumoniae	1331	1.9
Pneumonia due to Haemophilus influenzae	1029	1.5
Bacterial pneumonia, not elsewhere classified	3184	4.5
Pneumonia due to other infectious organisms, not elsewhere classified	292	0.4
Pneumonia, organism unspecified	59,389	84.6
Total	70,232	100.0

Community-acquired Pneumonia

Clinical assessment, especially patient history, is important in distinguishing the aetiology and likely causative organism in patients with community-acquired pneumonia (CAP). Specific information regarding exposure to animals, travel history, nursing home residency and any occupational or unusual exposure may provide the key to diagnosis.⁹ Personal habits such as smoking and alcohol consumption increase the risk of developing pneumonia and should be explored. Many patients admitted to hospital or ICU with CAP have comorbidities, suggesting that those who are chronically ill have an increased risk of developing ARF. The most common chronic illnesses involved are respiratory disease (including smoking history, COPD/asthma), congestive cardiac failure and diabetes mellitus.^6,²⁰ Table 14.5 outlines aspects of the clinical history associated with particular causative organisms in CAP.^6,^9,²¹

TABLE 14.5 Clinical history/comorbidities associated with particular causative organisms in CAP

Condition	Causative organisms
Individual factors
Alcoholism	Streptococcus pneumoniae (including penicillin-resistant), anaerobes, gram-negative bacilli (possibly Klebsiella pneumoniae), tuberculosis
Poor dental hygiene	Anaerobes
Elderly	group B streptococci, Moraxella catarrhalis, H. influenzae, L. pneumophila, gram-negative bacilli, C. pneumoniae and polymicrobial infections
Smoking (past or present)	S. pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, Aspergillus spp.
IV Drug use	S. aureus, anerobes, M. tuberculosis, S. pneumoniae
Comorbidities
COPD	S. pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, Aspergillus spp.
Post influenza pneumonia	S. pneumoniae, S. aureus, H. influenzae
Structural disease of lung (e.g., bronchiectasis, cystic fibrosis)	P. aeruginosa, P. cepacia or Staphylococcus aureus
Sickle cell disease, asplenia	Pneumococccus, H. influenzae
Previous antibiotic treatment and severe pulmonary comorbidity, (e.g. bronchiectasis, cystic fibrosis, and severe COPD)	P. aeruginosa
Malnutrition related diseases	Gram-negative bacilli
Environmental exposure
Air conditioning	Legionella pneumophila
Residence in nursing home	S. pneumoniae, gram-negative bacilli, H. influenzae, S. aureus, Chlamydia pneumoniae; consider M. tuberculosis. Consider anaerobes, but less common.
Homeless population	S. pneumoniae, S. aureus, H. influenzae, Cryptococcus gattii: caused by inhalation of spores while sleeping, associated with red gum trees (Australia, Southeast Asia, South America)
Suspected bioterrorism	Anthrax, tularaemia, plague
Animal exposure
Bat exposure	Histoplasma capsulatum
Bird exposure	Chlamydia psittaci, Cryptococcus neoformans, H. capsulatum
Rabbit exposure	Francisella tularensis
Exposure to farm animals or parturient cats	Coxiella burnetii (Q fever)
Travel history
Travel to southwestern USA	Coccidioidomycosis; hantavirus in selected areas
Travel to southeast Asia	Severe acute respiratory syndrome (coronavirus), Mycobacterium tuberculosis, melioidosis
Residence or travel to rural tropics	Melioidosis (Burkholderia pseudomallei)
Travel to area of known epidemic	Avian influenza (H5N1), Swine influenza (H1N1) and SARS (coronavirus)

The Australian CAP study collaboration ²⁰ examined episodes of CAP in which all patients underwent detailed assessment for bacterial and viral pathogens. Aetiology was identified in 46% of episodes, with the most frequent causes being Streptococcus pneumoniae (14%), Mycoplasma pneumoniae (9%) and respiratory viruses (15%). Mechanical ventilation or vasopressor support was required in 11% of cases.

Diagnosis of CAP

Routine screening of patients with suspected pneumonia continues to rely on microscopy and culture of lower respiratory tract specimens, blood cultures, detection of antigens in urine and serology. Methods for detection of antigens are now widely available for several pneumonia pathogens, particularly S. pneumoniae, Legionella and some respiratory viruses.²² Culture of respiratory secretions may be limited due to difficulty in obtaining sputum samples. For this reason, nasopharyngeal aspirates or swabs may be taken as part of the routine screening for CAP.²³

Severity assessment scoring

International guidelines recommend a severity-based approach to management of CAP. CURB65, CRB65 and the Pneumonia Severity Index (PSI) are the most widely recommended systems that produce scores and assess severity based on patient demographics, risk factors, comorbidities, clinical presentation and laboratory results.⁶ Recent evaluation found no significant differences between these systems in their ability to predict mortality.²⁴ The Australian CAP Collaboration team devised and validated the SMART-COP scoring system for predicting the need for intensive respiratory or vasopressor support in patients with CAP. The acronym relates to the factors: low Systolic blood pressure, Multilobar chest radiography involvement, low Albumin level, high Respiratory rate, Tachycardia, Confusion, poor Oxygenation and low arterial pH.²⁵

Hospital-acquired and Ventilator-associated Pneumonia

Hospital-acquired or nosocomial pneumonia is defined as pneumonia occurring more than 48 hours after hospital admission.⁹ It is the second-most common nosocomial infection and the leading cause of death from infection acquired in-hospital. Ventilator-associated pneumonia (VAP) is a nosocomial pneumonia in patients who are mechanically ventilated. The incidence of VAP is reported at 10–30% among patients who require mechanical ventilation for greater than 48 hours.²⁶

Critically ill ventilated patients commonly experience chest colonisation as a result of translocation of bacteria from the mouth to the lungs via the endotracheal tube (ETT). This may lead to clinical signs of infection, or the patient may remain colonised without an infective process. The patient’s severity of disease, physiological reserve and comorbidity influence the development of infection.⁶ Most cases (58%) of VAP are associated with infection involving gram-negative bacilli such as Pseudomonas aeruginosa and Acinetobacter spp. A high number of cases (20%) are associated with gram-positive Staphylococcus aureus. Many cases of VAP are associated with multiple organisms.⁶ As in CAP, the presence of comorbidities and other risk factors influence the causative organism.

Diagnosis and treatment of VAP

VAP can be difficult to diagnose, as clinical features can be non-specific and other conditions may cause infiltrates on chest X-ray (CXR). However, it is often suspected when there are new infiltrates observed on CXR or when clinical signs of infection begin to develop, e.g. new onset of pyrexia, raised white blood cell counts, purulent sputum and a difficulty in maintaining adequate oxygenation.⁶ Specific risk factors associated with increased mortality in VAP have been identified over the last decade. The most widely-recognised risk factor is the provision of appropriate antibiotic treatment, which has reduced mortality and the rate of complications. Timeliness of antibiotic admini-stration is an independent risk factor for mortality; mortality was increased where administration of antibiotics was delayed for more than 24 hours after diagnosis.²⁶ When VAP is suspected there are two treatment strategies, although a systematic review did not demonstrate any differences in mortality, length of ICU stay or length of ventilation period:¹⁹

• Clinical Strategy: involves treatment of patients with new antibiotics, based on patient risk factors and the local microbiologic and resistance patterns. Therapy is adjusted based on culture results and the patient’s response to treatment.

• Invasive Strategy: involves collection and quantitative analysis of respiratory secretions from samples obtained by bronchoalveolar lavage (BAL) to confirm the diagnosis and causative organism. Antibiotic therapy is then guided by specific protocols.

Clinical Manifestations

Symptoms for pneumonia are both respiratory and systemic. Common characteristics include fever, sweats, rigours, cough, sputum production, pleuritic chest pain, dyspnoea, tachypnoea, pleural rub, inspiratory crackles on auscultation, plus radiological evidence of infiltrates or consolidation. Cough is the most common finding and is present in up to 80% of all patients with CAP.^6,⁹

Collaborative Practice

Early recognition of pneumonia and timely administration of antibiotic therapy are key aspects for patient management. The most important aspect of management in VAP is prevention and this is a key emphasis in the care of all mechanically-ventilated patients. One approach in encouraging the implementation of VAP prevention was the combination of four aspects of patient management into one evidence based guideline, known as the Ventilator Care Bundle: elevating the head of bed to 30–45 degrees, daily sedation vacation and assessment of readiness to extubate, peptic ulcer disease (PUD) prophylaxis and deep vein thrombosis (DVT) prophylaxis.²⁷ Effectiveness of this strategy and implementation issues have been further evaluated, with some additional perspectives offered. While it is apparent that daily spontaneous awakening and breathing trials are associated with early liberation from mechanical ventilation and VAP reduction, the strategies included for DVT and PUD prophylaxis do not directly affect VAP reduction. Semi-recumbent positioning has been associated with a significant reduction in VAP but is difficult to maintain in ventilated patients.¹⁴ It has been suggested that other methods to reduce VAP, such as oral care and hygiene, chlorhexidine in the posterior pharynx and specialised endotracheal tubes (continuous aspiration of sub-glottic secretions, silver-coated), should be considered for inclusion in a revised Ventilator Bundle more specifically aimed at VAP prevention.¹⁴

Development of VAP is attributed in part to aspiration of oral secretions that are colonised by a variety of bacteria. Maintenance of oral hygiene is therefore a key element in the care of mechanically-ventilated patients.⁶ Oral mucosa and dental plaque may also be colonised with bacteria and the use of an oral antiseptic solution (e.g. Chlorhexidine) may further reduce the risk of developing VAP.²⁸

Supportive ventilation is a key focus for managing patients with pneumonia. In some instances this may include increased oxygen delivery and positive end expiratory pressure (PEEP) to maintain oxygenation and prevent alveolar collapse. Chest physiotherapy assists in the prevention of VAP ²⁹ and remains a key component of management of all ventilated patients. However, its contribution towards improving mortality in patients with pneumonia is unclear.³⁰ Upright positioning and early mobilisation are important elements of both prevention and management of pneumonia. The effectiveness of additional strategies, such as use of beds with a continuous lateral rotation or a vibration function to assist in the removal of secretions is yet to be shown.³¹ See Chapter 15 for further discussion.

Medications

Antibiotic administration is fundamental to a patient’s clinical progress. As noted earlier, the importance of accurate and timely administration of antibiotics directly impacts on patient outcome. In particular, the first dose of antibiotics is required as soon as possible after the diagnosis of pneumonia has been made. Studies where the first dose of antibiotic therapy was delayed showed an increase in mortality.³² Antibiotic cover for pneumonia depends on the causative organism and sensitivity to drugs (see Table 14.6 ⁶). Review of antibiotic prescribing practices in Australia and New Zealand has shown that prescription of antibiotics in pneumonia is consistent with current guidelines.³³

TABLE 14.6 Preferred antimicrobial agents in pneumonia ⁶

Type of infection	Preferred agent(s)
Community-acquired pneumonia
Streptococcus pneumoniae	PCN-susceptible: Penicillin G, amoxicillin, clindamycin, doxycycline, telithromycinPCN-resistant: cefotaxime, ceftriaxone, vancomycin, and fluoroquinolone
Mycoplasma	Doxycycline, macrolide
Chlamydophila pneumoniae	Doxycycline, macrolide
Legionella	Azithromycin, fluoroquinolone (including ciprofloxacin), erythromycin (rifampicin)
Haemophilus influenzae	Second- or third-generation cephalosporin, clarithromycin, doxycycline, β-lactam/β-lactamase inhibitor, trimethoprim/sulfamethoxazole, azithromycin, telithromycin
Moraxella catarrhalis	Second- or third-generation cephalosporin, trimethoprim-sulfamethoxazole, macrolide doxycycline, β-lactam–β-lactamase inhibitor
Neisseria meningitidis	Penicillin
Streptococci (other than S. pneumoniae)	Penicillin, first-generation cephalosporin
Anaerobes	Clindamycin, β-lactam–β-lactamase inhibitor, β-lactam plus metronidazole
Staphylococcus aureus Methicillin-susceptible Methicillin-resistant	Oxacillin, nafcillin, cefazolin; all rifampin or gentamicin Vancomycin, rifampicin or gentamicin
Klebsiella pneumoniae and other Enterobacteriaceae (excluding Enterobacter spp.)	Third-generation cephalosporin or cefepime (all aminoglycoside) carbapenem
Hospital-acquired infections
Enterobacter spp.	Carbapenem, β-lactam–β-lactamase inhibitor, cefepime, fluoroquinolone; all + aminoglycoside in seriously ill patients
Pseudomonas aeruginosa	Anti-pseudomonal β-lactam + aminoglycoside, carbapenem + aminoglycoside
Acinetobacter	Aminoglycoside + piperacillin or a carbapenem

Special Considerations

Pneumonia is a leading cause of maternal and fetal morbidity and mortality. It also increases the likelihood of the complications of pneumonia, including requirement for mechanical ventilation. Bacterial pneumonia is the most common type experienced in pregnancy although diagnosis is often delayed as a result of the reluctance to obtain a chest X-ray. Management is similar to a non-pregnant patient with antibiotic therapy adjusted to consider the impact on the fetus.⁶

CAP is a major cause of morbidity and mortality in elderly patients. Streptococcus pneumoniae is the most common causative organism, with an increase in drug-resistance being reported more widely in the over-65 age group. Treatment of elderly patients with pneumonia is similar to younger patients, with emphasis on supportive care, prevention of sepsis and management of preexisting chronic conditions. Immunisation with pneumococcal and influenza vaccines is beneficial in the prevention of pneumonia in elderly patients.³⁴

Respiratory Pandemics

Serious outbreaks of respiratory infections that spread rapidly on a global scale are termed pandemics. Their spread is so rapid because the infection is usually associated with emergence of a new virus where the majority of the population has no immunity. These infections are characterised by extremely rapid ‘transmission with concurrent outbreaks throughout the globe; the occurrence of disease outside the usual seasonality, including during the summer months; high attack rates in all age groups, with high levels of mortality particularly in healthy young adults; and multiple waves of disease immediately before and after the main outbreak’.³⁵ Several severe respiratory infections have progressed to become pandemics in recent years; these have been associated with the Coronavirus and Influenza viruses. Prediction of the interval between pandemics is difficult, but occurrence is likely to continue and therefore requires that the health care community be well prepared.

Severe Acute Respiratory Syndrome

In 2002–03 an outbreak of a novel Coronavirus occurred in China and rapidly spread throughout the world. The infection was highly virulent with over 8000 cases reported and a mortality rate of 11%. The infection was called Severe Acute Respiratory Syndrome (SARS) due to the severity of the disease, characterised by diffuse alveolar infiltrates, resulting in about 20% of patients requiring respiratory support. The SARS outbreak provoked a rapid and intense public health response coordinated by the World Health Organization (WHO), resulting in a cessation of disease transmission within ten months.³⁵

Influenza Pandemics

Epidemics of influenza occur regularly and are associated with high morbidity and mortality. Incidence is usually highest in the young, while mortality is highest in the elderly population. Those with preexisting respiratory conditions such as asthma or COPD experience particularly high morbidity and mortality. In contrast, when influenza occurs on a pandemic scale it has been shown to affect greater numbers of younger and otherwise healthy people.

A feature of the influenza virus that explains why it continues to be associated with epidemic and pandemic disease is its high frequency of antigenic variation. This occurs in two of the external glycoproteins and is referred to as antigenic drift or antigenic shift, depending on the extent of the variation. The result of this is that new viruses are introduced into the population, and due to the absence of immunity to the virus, a pandemic of influenza results.⁶

Pandemics of influenza were observed a number of times in the twentieth century, and were believed to have involved viruses circulating in humans that originated from influenza A viruses in birds. The ‘Spanish influenza’ pandemic of 1918–19 resulted in the death of over 50 million people worldwide and remains unprecedented in its severity.³⁵

The first reported infection of humans with avian influenza viruses occurred in Hong Kong in 1997, with six recorded fatalities. The increased virulence of this disease was observed in the acuity of those affected by the outbreak of the highly pathogenic avian influenza virus (H5N1) in 2004–2005.³⁵ Most patients presented with non-specific symptoms of fever, cough and shortness of breath. In many patients this progressed rapidly to ARF requiring ventilation and other supportive measures. The majority of people affected (90%) were less than 40 years of age with case fatality rates highest in the 10–19-year-old age group.³⁶

The most recent influenza pandemic declared by WHO occurred in 2009 when a novel H1N1 influenza A virus emerged in Mexico and the USA. This virus contained genes from avian, human and swine influenza virus and affected millions of people worldwide.³⁷ Patients typically presented with nonspecific flu-like symptoms, however in a quarter of patients this was accompanied by diarrhoea and vomiting. The disease spread globally with millions of cases reported and resulted in over 16,000 deaths by March 2010.³⁸

Australia and New Zealand communities had a high proportion of cases of H1N1 influenza-A infection, with 856 patients being admitted to ICU; 15 times the incidence of influenza A in other recent years. Infants (aged 0–1 years) and adults aged 25–64 years were at particular risk; others at increased risk were pregnant women, adults with a BMI over 35 and indigenous Australian and New Zealand populations. Australian and New Zealand Intensive Care Society (ANZICS) investigators prepared a report based on the Australian and New Zealand experience to assist those in the northern hemisphere to better prepare for their winter influenza season.³⁹

The emergence of novel swine-origin influenza A virus was not anticipated and it is unlikely, given the limitations of current knowledge, that future pandemics can be predicted. The threat of pandemic disease from avian influenza remains high with the rapid evolution of H5N1 viruses; however the direction this will take is unpredictable. Priorities for prevention and management of future influenza pandemics therefore involve development of an international surveillance and response network for early detection and containment of the disease, local preparation for controlling the spread of the infection and further development of vaccines and antiviral agents.³⁸

Influenza Vaccinations

Influenza vaccines are formulated annually based on current and recent viral strains. Success in protecting an individual against influenza requires that the virus strains included in the vaccine are the same as those currently circulating in the community. Vaccines are commonly effective in 70–90% in preventing influenza in healthy adults younger than 65 years of age. Efficacy appears lower in elderly persons. Health care workers are a key target group for the influenza vaccine, at the very least to reduce absenteeism over what is often the busiest period for most hospitals and health services ³⁵ and to reduce the risk of nosocomial influenza in hospitals.⁴⁰

Isolation Precautions and Personal Protective Equipment

Key aspects of infection control in an epidemic or pandemic situation focus on limiting opportunities for nosocomial spread and the protection of health care workers. Guidelines for institutional management of these infections involve designing and implementing appropriate isolation procedures and recommending appropriate personal protective equipment (PPE). The impor-tance of adequate PPE was highlighted particularly in the SARS epidemic where there was overrepresentation of health care workers who became patients infected with the virus.³⁵

Specific infection control guidelines are usually developed for individual institutions, based on government recommendations for management of staff, appropriate PPE and isolation procedures. Table 14.7 summarises the recommendations from the Australian⁴¹ and New Zealand⁴² governments.

TABLE 14.7 Recommendations for personal protective measures in respiratory pandemics

Section	Protective measure
Staff management	Assessment of staff at increased risk of complications from the specific infection should be redeployed if possibleMonitoring health care workers for signs of illness and management with antivirals as a priority
Personal protection: basic measures	Hand hygiene, social distancing, safe cough/sneeze etiquette, and good ventilation
Personal Protective Equipment	Gloves Gowns/aprons Eye protection Masks: a range of masks are available to provide respiratory protection to workers in medium to high-risk situations. Two options are available: • Surgical mask: designed to contain droplet spread from the wearer but offers a degree of protection from external infection • P2 or N-95 particulate masks: provide a higher degree of filtration or respiratory protection, when appropriately worn and handled

In all settings, it is important to ensure that staff members are familiar with respiratory protection devices. In areas or situations where respirators (P2 or N-95 masks) are used, a fit-testing program ensures understanding of how the devices work and maximal safety. During the SARS epidemic, infection of staff members through inappropriate or ineffective use of these masks occurred, and infection due to failure to wear adequate eye protection was also reported.⁴³

Acute Lung Injury

Acute lung injury (ALI) is a generic term that encompasses conditions causing physical injury to the lungs. Acute respiratory distress syndrome (ARDS) is a severe form of ALI as a result of bilateral and diffuse alveolar damage due to an acute insult, and is the predominant form of ALI observed in ICU.⁶

Aetiology

ARDS is a characteristic inflammatory response of the lung to a wide variety of insults. Approximately 200,000 patients are diagnosed annually in the USA with ARDS, accounting for 10–15% of ICU admissions.⁴⁴ Commonly associated clinical disorders can be separated into those that directly or indirectly injure the lung⁹ (see Table 14.8).

TABLE 14.8 Direct and indirect causes of acute lung injury ⁹

Direct lung injury	Indirect lung injury
• Pneumonia • Aspiration of gastric contents • Pulmonary contusion • Fat, amniotic fluid, or air embolus • Near drowning • Inhalational injury (chemical or smoke) • Reperfusion pulmonary oedema

• Sepsis

• Multiple trauma

• Cardiopulmonary bypass

• Drug overdose

• Acute pancreatitis

• Transfusion of blood products

The most common cause of indirect injury resulting in ALI/ARDS is sepsis, followed by severe trauma and haemodynamic shock states. Transfusion-related ALI (TRALI) is not common but is observed in ICU. ARDS arising from direct injury to the lung is most commonly seen in patients with pneumonia. An individual’s risk of developing ARDS increases significantly when more than one predisposing factor is present.⁶

Pathophysiology

Inflammatory damage to alveoli from inflammatory mediators (released locally or systemically) causes a change in pulmonary capillary permeability, with resulting fluid and protein leakage into the alveolar space and pulmonary infiltrates. Dilution and loss of surfactant causes diffuse alveolar collapse and a reduction in pulmonary compliance and may also impair the defence mechanisms of the lungs.⁴⁵ Intrapulmonary shunt is confirmed when hypoxaemia does not improve despite supplemental oxygen administration.⁶ The characteristic course of ARDS is described as having three phases:^6,⁴⁵

1. Oedematous phase: involves an early period of alveolar damage and pulmonary infiltrates resulting in hypoxaemia. This phase is characterised by migration of neutrophils into the alveolar compartment, releasing a variety of substances including proteases, gelatinases A and B, and reactive nitrogen and oxygen species that damage the alveoli. Further damage is caused by resident alveolar macrophages and release of proinflammatory cytokines that amplify the inflammatory response in the lung. Significant ventilation–perfusion (intrapulmonary shunt) mismatch evolves causing hypoxaemia.

2. Proliferative phase: begins after 1–2 weeks as pulmonary infiltrates resolve and fibrosis and remodelling occurs. This phase is characterised by reduced alveolar ventilation and pulmonary compliance and ventilation–perfusion mismatch. Reduced compliance (stiff lungs) causes further atelectasis in the mechanically ventilated patient as alveoli are damaged by increased volume and/or pressure on inspiration.

3. Fibrotic phase: the final phase where alveoli become fibrotic and the lung is left with emphysema-like alterations.

Diagnosis

A standardised definition of ARDS was first described in 1988, with three clinical findings; hypoxia, decreased pulmonary compliance and diffuse infiltrates observed on a chest X-ray. The Murray Lung Injury Score was developed as a method for clarifying and quantifying the existence and severity of the disease.⁴⁶ The American-European Consensus Conference on ARDS provided the following definition:

• acute onset of arterial hypoxaemia (PaO₂:FiO₂ ratio < 200)

• bilateral infiltrates on radiography without evidence of left atrial hypertension or congestive cardiac failure.

The spectrum of disease was also acknowledged and the term ALI was introduced to describe patients with a less severe but clinically similar form of respiratory failure (PaO₂:FiO₂ ratio <300).⁴⁷ It has been suggested that these definitions require review as they include such a broad, heterogenous group of patients that has limited investigation of appropriate management strategies. This may also be because the interventions studied were ineffective, but it is just as likely that the broadly inclusive definition of ARDS captures a heterogeneous group of patients that respond differently to current therapies.⁴⁸

Clinical Manifestations

While no specific test exists to determine whether a patient has ARDS, it should be considered in any patient with a predisposing risk factor who develops severe hypoxaemia, reduced compliance and diffuse pulmonary infiltrates on a chest X-ray.⁴⁴ ARDS usually occurs 1–2 days following onset of a presenting condition and is characterised by rapid clinical deterioration. Common symptoms include severe dyspnoea, dry cough, cyano-sis, hypoxaemia requiring rapidly-escalating amounts of supplemental oxygen and persistent coarse crackles on auscultation.⁶

Assessment

A patient with ARDS requires ongoing monitoring of oxygenation and ventilation through ABG analysis and pulse oximetry and monitoring of PaCO₂ to assess permissive hypercapnia. Monitoring of ventilatory pressures and volumes ensures that additional lung injury is prevented. As many patients with ARDS require cardiovascular support, assessment of haemodynamics and peripheral perfusion is important to ensure oxygen delivery to cells is achieved.⁶

Collaborative Practice

The key principles of management are treatment of the precipitating cause and providing supportive care during the period of acute respiratory failure.^6,⁴⁵ Mortality rates from ARDS have decreased over time; this is not attributed solely to the use of low tidal volume ventilation promoted by the ARDS Network group, but to other advances in critical care.⁴⁴ Specific strategies include cautious fluid management, adequate nutrition, prevention of ventilator-associated pneumonia, prophylaxis for deep venous thrombosis and gastric ulcers, weaning of sedation and mechanical ventilation as early as possible, and physiotherapy and rehabilitation (similar to ARF management). Management involves a coordinated collaborative approach including supportive ventilation, patient positioning and medication administration.

Ventilation Strategies

The key focus of ventilation in ARDS is the prevention of refractory hypoxaemia rather than reversing it after it develops. The use of small tidal volumes and adequate levels of PEEP, along with careful attention to fluid status and patient–ventilator synchrony, may be sufficient to maintain oxygenation at an appropriate level while minimising further damage from barotrauma and nosocomial pneumonia.^6,⁴⁷ The use of rescue therapies is controversial as none to date have reduced mortality when studied in large heterogeneous populations of patients with ARDS. Some therapies however demonstrated improved oxygenation, which may be an important goal in many patients who experience severe hypoxaemia. The key focus of rescue ventilatory strategies is alveolar recruitment, including higher levels of PEEP, use of airway pressure release ventilation (APRV), high-frequency oscillatory ventilation (HFOV) and high-frequency percussive ventilation (HFPC) (see Chapter 15). If hypoxaemia is severe, extracorporeal life support may also be considered. As there is no evidence to support the use of one strategy over another, the choice of therapy is often based on equipment availability and clinician expertise. An evidence based approach is likely to involve lung-protective ventilation (volume and pressure limitation with modest PEEP) requiring permissive hypercapnia and permissive hypoxaemia.⁴⁹

Prone Positioning

Use of prone positioning in patients with ARDS was described almost 30 years ago as a means of improving oxygenation. This improvement is largely due to the effect that the prone position has on chest wall and lung compliance. The result is a more homogenous ventilation of the lungs and improved ventilation–perfusion matching.⁶ Investigation into the effectiveness of this as a therapy in ARDS has noted improvement in oxygenation, but no corresponding improvement in mortality. It is therefore recommended as a rescue therapy for the patient at risk of death from hypoxia, rather than as a routine treatment.⁵⁰ See Chapter 15 for further discussion.

Medications

A number of non-ventilatory strategies may form part of the treatment of patients with ARDS. Neuromuscular blocking agents (NMBAs) are used to promote patient–ventilator synchrony, especially when non-conventional modes of ventilation are used. Improvements in oxygenation are usually observed and may be attributed to reduction in oxygen consumption and improved chest wall compliance. The use of NMBAs, however, is also associated with an increased risk of myopathy, so any benefits gained should be weighed against known risks.⁵¹

Inhaled nitric oxide (iNO) therapy may be used to improve oxygenation through selective vasodilation of the pulmonary blood vessels, promoting improvement in ventilation–perfusion matching. Despite the lack of evidence regarding its effectiveness in improving outcomes of patients with ARDS, its use is reasonably widespread. Improvement in oxygenation should be observed within the first hour of treatment to support its ongoing use.⁵¹ Some groups have reported the use of iNO to be harmful and recommend that it not be used, given the lack of evidence demonstrating reduction in mortality.⁵²A similar effect, in terms of pulmonary vasodilation, has been achieved using inhaled prostacyclines and this remains under investigation as an alternative therapy.⁵¹

A number of medications are currently being investigated to treat ARDS in acute and subacute exudative phases. These include agents that target the disrupted surfactant system (exogenous surfactant therapy), oxidative stress and antioxidant activity (antioxidants), neutrophil recruitment and activation, expression and release of inflammatory mediators (corticosteroids), activation of the coagulation cascade (immunomodulating agents and statins), and microvascular injury and leak (beta₂-agonists).⁵³ The use of low-dose corticosteroids has been associated with improved outcomes for patients with ARDS,⁵⁴ although its use remains controversial and further investigation is recommended.

Special Considerations

ALI and ARDS occur in pregnancy usually as a result of aspiration pneumonitis, sepsis or pneumonia. Management of ventilation is similar to the non-pregnant patient, although consideration of the impact on the fetus is important in medication usage and ventilatory management.⁶ Elderly patients who develop ARDS are likely to experience an increased severity of disease, yet have a mortality rate comparable to other patients. Development of other organ dysfunction depends on the presence of chronic conditions such as renal and cardiovascular diseases.⁵⁵

Asthma and Chronic Obstructive Pulmonary Disease

Asthma is defined as a respiratory condition where airflow limitation may be fully or partially reversible either spontaneously or with treatment.⁵⁶^–⁵⁸ COPD is a respiratory condition defined by a largely fixed airflow limitation. The partial airway responsiveness to therapy in COPD results in a clinical overlap between COPD, asthma and chronic bronchitis. A non-proportional Venn diagram (see Figure 14.2), originally used by the American Thoracic Society⁵⁹ and now in the Australian and New Zealand expert guidelines^60,⁶¹ depict this overlap between conditions. It is not uncommon for people with an obstructive lung disease to share clinical characteristics for more than one respiratory condition, although the dominant clinical symptom is usually indicative of the underlying condition.⁶² It is however important to differentiate between COPD and asthma as they have different management and illness trajectories.⁵⁶

FIGURE 14.2 Overlap between asthma, emphysema and bronchitis.^60, ^{p. S10}

Pathophysiology

Asthma is a complex syndrome influenced by genetic and environmental factors.⁶³ Altered airway physiology and airway wall remodelling in asthma are consequences of inflammatory processes.⁶⁴ While initial symptoms can occur at any age, most patients exhibit episodes of wheezing and obstruction before the age of six.^65,⁶⁶ The increasing incidence of disease burden in children may be attributable to a greater awareness and diagnosis of the condition, with the overall differences in global prevalence now becoming less.⁶⁷

In contrast, COPD is a systemic, permanent and progressive condition with a number of mechanisms involved in its development. Smoking is the cardinal risk factor and continuation is the most significant determinant for disease progression.^60,⁶⁸ The concept of ‘pack years’ is used to quantify smoking, and is independent of whether an individual is a current or reformed smoker.⁶⁹ A history of more than 20 pack years of smoking is a significant risk factor for the development of COPD.⁷⁰ Continued smoking accelerates the decline of respiratory function in susceptible individuals.^71,⁷² However, less than 15% of smokers actually develop clinically-significant COPD^68,^73,⁷⁴ suggesting that other factors are also involved, including environmental and occupational pollutants, genetic predisposition, hyper-responsive airways and respiratory infections.^68,⁷⁵^–⁷⁹ Disease progression in susceptible individuals is most likely to be dependent on the synergistic effects of these factors.

Ventilation abnormalities in COPD result from airway inflammation, bronchoconstriction, increased mucus secretion and oedema. Perfusion abnormalities arise from hypoxic-induced vasoconstriction of the capillary beds. Pulmonary ventilation/perfusion (V/Q) abnormalities, and hyperinflation contribute to increased pulmonary vascular resistance (PVR), and respiratory muscle fatigue.⁸⁰ Increased PVR and hypoxaemia require the heart’s right side heart to work harder, over time resulting in hypertrophy, remodelling and cor pulmonale.^81,⁸² The incidence of right ventricular hypertrophy approximates 40% for patients with moderate levels of COPD (i.e. FEV₁ <1000 mL).⁶⁰ The left ventricle may also be compromised by hyperinflation, which generates an increased work of afterload.⁸³ Heart disease is therefore a frequent concomitant condition with COPD⁸⁴^–⁸⁶ (see Chapter 11 for further discussion). Impaired ventilation and perfusion leads to hypoxaemia and mechanical dysfunctions, with the primary cause of adverse lung mechanics being hyperinflation.

Hyperinflation has two components: static and dynamic.⁸³ Loss of elastic recoil (static hyperinflation) and incomplete expiratory airflow (dynamic hyperinflation) leads to air trapping and a reduced inspiratory capacity.^87,⁸⁸ The effects of incomplete and prolonged expiration accounts for increased work of breathing, dyspnoea and reduced exercise tolerance experienced by people with COPD.⁸⁹^–⁹⁵ Severity of COPD promotes hyperinflation of the lungs, and hyperinflation is a catalyst for hypoventilation.⁹⁶

COPD is also a systemic condition that has an effect on the skeletal muscles, the intercostals and diaphragm.⁹⁷^–⁹⁹ Bloodflow is diverted from lower limb muscles to meet the oxygen requirements of these respiratory muscles; a phenomenon referred to as circulatory steal.⁸² Use of supplemental oxygen to hypoxaemic patients with COPD has been found to reduce dynamic hyperinflation, dyspnoea and improve exercise tolerance;^88,⁹⁷ reduce PVR;^76,^86,¹⁰⁰ reduce ventilatory requirements and circulating lactate levels.¹⁰¹ The systemic limitations that arise with COPD are therefore profound and complex.¹⁰² These inter-relationships are illustrated in Figure 14.3.

FIGURE 14.3 The systemic interrelationships in COPD.^102, ^{p. 148}

Clinical Manifestations

With asthma and COPD, a patient may present with wheeze, cough and/or dyspnoea. History and physical assessment are fundamental to determining the severity of presentation. Presence of diminished or silent breath sounds, central cyanosis, an inability to speak, an altered level of consciousness, an upright posture and diaphoresis indicate a life-threatening case.⁵⁸ Chest pain or tightness may be present. Underestimation of severity is associated with higher mortality.⁵⁸ Recent longitudinal datasets for Australia and New Zealand highlight a trend in reduced ICU admissions following an exacerbation of asthma and an improved health outcome.¹⁰³ Conversely, studies in patients with COPD identified poorer 12 month health outcomes following an ICU admission for hypercapnoeic respiratory failure.^104,¹⁰⁵

Assessment and Diagnostics

Communication with patients that builds trust, through honesty and effective intervention, contributes considerably to the de-escalation of panic and fear in patients presenting with hypoxaemia. Creating a calm and trusting environment is paramount for those struggling for breath. Forward-planning for potential deterioration and constant assessment of respiratory, cardiovascular and neurological systems are fundamental in determining optimal clinical progress for these patients. Where possible, diagnostic tests and procedures involve peak flow monitoring, spirometry, radiology and ABGs.⁵⁸

The ‘gold standard’ for diagnosing COPD is spirometry.^60,^75,¹⁰⁶ While there is no gold standard in the diagnosis of asthma, spirometry is the lung function test of choice.¹⁰⁴ In Australia, respiratory function tests are usually performed according to standard principles.¹⁰⁷ Values obtained are expressed at body temperature, ambient pressure, saturated with water vapour (BTPS), in absolute units (L or L/sec) and as a percentage of predicted normal values. The carbon monoxide pulmonary diffusing capacity (TLCO), may be measured using the single breath technique modified by Krogh. Diffusing capacity indicates the available surface area for gas exchange, and is reduced with emphysema but can be normal with asthma.¹⁰⁸ The TLCO can be a directly measured value or as a percentage of predicted normal for age, sex, height and weight. A number of reference tables of predicted normal values enable comparison with population norms.¹⁰⁹ A continuing lack of consensus remains for differentiating asthma and COPD.⁷¹ The most commonly used criterion in Australia and New Zealand is airway reversibility in response to bronchodilator therapy: <15% reflects COPD; >15% reflects asthma.^60,¹¹⁰

Collaborative Practice

Contemporary management of asthma follows an asthma management plan, to minimise the acute exacerbation and any subsequent respiratory arrest. Many presentations will be managed in the emergency department (see Chapter 22 for further discussion). For patients requiring ventilatory support, a case series noted that patients were better managed with noninvasive ventilation (NIV), as mechanical ventilation was associated with significant mortality and morbidity¹¹¹ from hyperinflation and aggravation of bronchospasm.⁵⁸ Contemporary management of COPD has advocated a care plan for patients in the community setting. This has an effect on prompting patients to recognise a change in their symptoms and seek appropriate care. However, improving symptom recognition does not reduce health care utilisation.¹¹² Patients with COPD managed with NIV in a timely manner have a reduced length of hospital stay, reduced need for endotracheal intubation and reduced mortality rate.¹¹³ There are published guidelines on the prevention, identification and management of asthma⁵⁶ and COPD.⁶¹

Medications

Administration of oxygen and beta-agonists (salbutamol) are first-line therapies. Nebulised salbutamol is the preferred route, with IV administration considered for patients not responding to nebulised medication.⁵⁸ See Table 14.9 for key medications used in the treatment of asthma.

TABLE 14.9 Key medications in an acute episode of asthma ⁵⁸

Pneumothorax

Pneumothorax describes air that has escaped from a defect in the pulmonary tree and is trapped in the potential space between the two pleura. A pneumothorax normally resolves with treatment. A pneumothorax is termed persistent if the air leak lasts for more than five days,¹¹⁴ while one reappearing on the same side after seven days is termed reoccurring.¹¹⁵ A pneumothorax can arise spontaneously, from disease or from traumatic injury and can be life-threatening.

A tension pneumothorax involves significant and progressive respiratory or haemodynamic compromise that is quickly offset by decompression.¹¹⁶ A patient with a tension pneumothorax can present with symptoms similar to asthma, i.e. ‘respiratory distress, wheeze, tachycardia, tachypnoea, desaturation, hyper-expansion, agitation and decreased air entry.’^117, ^{p. 525} Fortunately, tension pneumothorax is a far less common condition, and the patient is more likely to report additional chest pain. The actual incidence of a tension pneumothorax is relatively unexamined but it is more likely to occur in a ventilated patient where a pneumothorax has been missed on assessment.¹¹⁷

Pathophysiology

If the pleural defect functions as a one-way valve, air enters the pleural cavity on inspiration but is unable to exit on expiration, leading to increasing ipsilateral intrapleural pressure. This causes further lung collapse, diaphragmatic depression, and (dependent on mediastinal distensibility) contralateral lung compression.¹¹⁷

Clinical Manifestations

Severe presentations are identified by history and clinical examination (respiratory distress, cyanosis, tachycardia, tracheal shift and unilateral movement of the chest). They are also detected on CXR with a translucent appearance of the air and absence of lung markings ¹¹⁸ (see Chapter 13 for interpretation of CXR).

Collaborative Practice

Insertion of a thoracic underwater seal drain allows the collapsed lung to re-expand. This is facilitated with mechanical ventilation if required. If a haemothorax is present, suction on the underwater seal drain (20–60 mmHg) will expedite drainage and re-expansion of the lung.¹¹⁸

No differences in short- and long-term health outcomes were reported between insertion of an underwater seal drainage system and simple aspiration of the air for patients with a spontaneous pneumothorax.¹¹⁹ Treatments for pneumothorax where there is concomitant lung disease, e.g. cystic fibrosis, identified a paucity of data to guide practice.¹²⁰

Pain management and facilitation of respiratory care with oxygen therapy, non-invasive or invasive ventilation, positioning and deep-breathing and coughing, and the monitoring of the chest tube and drainage for presence of air-leak and serous drainage, are key to recovery without development of further complications.¹²¹ Drainage system connections need to be tight and supported to prevent drag on the patient. Evidence is available for the development of clinical practice guidelines on thoracostomy.¹²¹ Chapter 12 discusses chest tube management in more detail.

Medications

Management of pain associated with chest trauma is guided by the presence of any comorbidities. Epidural or intravenous opioids are the most effective pain management strategies (see Table 14.10).¹²¹

TABLE 14.10 Common medications prescribed with chest injury: pneumothorax

Pulmonary Embolism

Deep vein thrombosis (DVT) and pulmonary embolism (PE) are two aspects of the disease process known as venous thromboembolism (VTE).¹²² Certain factors lead to higher incidence: immobilisation (due to long bone, pelvic and spinal fractures) and closed head injury in particular (see Table 14.11 for a list of risk factors).¹²³ Most PE originate in the lower limbs, pelvic veins or inferior vena cava. Three predisposing risk factors for thrombosis are venous stasis, vein wall injury and hypercoagulability of blood. Clinical risk factors are immobility, surgery, trauma, malignancy, pregnancy or thrombophilia. PE may have no clinical consequence or it may be catastrophic, causing sudden death,¹²³ and is responsible for 10% of in-hospital deaths.¹²⁴ The morbidity and costs associated with VTE are also significant. An evidence-based clinical practice guideline has been published to address this significant health issue¹²² and addresses the risks and benefits of treatments for medical, surgical and oncology patients. Further, VTE guidelines for patients with heparin-induced thrombocytopenia; pregnancy and childbirth are outlined with a listing of the publications to support the level of evidence for the clinical management guidelines.

TABLE 14.11 Risk factors for venous thromboembolism (VTE)¹²³

Primary hypercoaguable states (thrombophilia)	Secondary hypercoagulable states
Antithrombin III deficiency Protein C deficiency Protein S deficiency Resistance to activated protein C (inherited factor V Leiden mutation) Hyperhomocysteinaemia Lupus anticoagulant (antiphospholipid antibody)

Clinical Manifestations

Pulmonary artery obstruction causes release of vasoactive agents from accumulating platelets, with subsequent raised pulmonary vascular resistance and acute pulmonary hypertension. The arterial obstruction causes severe shunting and life-threatening hypoxaemia. Symptomatic patients present with dyspnoea (most common), pleuritic chest pain and haemoptysis. The physical signs of tachypnoea, fever, tachycardia and right ventricular dysfunction may also be present. If a massive PE has occurred, the patient exhibits hypotension with pale, mottled skin and peripheral and/or central cynanosis.¹²⁴

Assessment and Diagnostics

Investigations to confirm VTE include compression ultrasonography for a suspected DVT, pathology test for elevated levels of D-dimer in plasma ¹²⁵ and a ventilation-perfusion (V/Q) isotope scan, computed tomographic (CT) and pulmonary angiography (helical CT) scan for PE.¹²²

Collaborative Practice

Current and ongoing treatment modalities for PE are selected according to the patient’s individual circumstances. In general, options include medications and percutaneously inserted vena caval filters.¹²⁶

To prevent VTE, prophylactic interventions include hydration and early mobilisation that, depending on the need for patient admission are not always possible in the critical care setting. Mechanical measures of prophylaxis aim to reduce venous stasis via external compression. Commonly employed measures include knee- or thigh- length graduated compression stockings and/or intermittent pneumatic compression and/or venous foot pumps. Clinical practice guidelines are published to support evidence-based care.¹²⁴ Two Cochrane systematic reviews have established that combined modalities reduce the incidence of DVT but the effect on PE remains unknown.^127,¹²⁸

Medications

Table 14.12 outlines the key medications recommended and prescribed for patients with PE. Risk reductions for DVT postsurgery have been reported following the use of prophylactic medications.¹²⁹ Studies continue to postulate the efficacy of novel versus standard medication administration for VTE with only preliminary conclusions available.^130,¹³¹

TABLE 14.12 Medications for pulmonary embolism

Lung Transplantation

Transplantation is a life-saving and cost-effective form of treatment that enhances the quality of life for people with chronic respiratory disease. Lung transplantation is facilitated by organ donation from patients with brain death or donation after cardiac death.¹³² Donation after cardiac death has the potential to significantly increase the number of organs available for lung transplantation.¹³² In 1985, 13 lung transplant procedures were reported worldwide.¹³³ In subsequent years, the number of recipients worldwide has steadily increased to be in excess of 2700 annually.¹³⁴ Patients have received lung transplants in Australasia since the early 1990s. Lung transplantation can be either single or double, depending on a patient’s underlying disease state. In the postoperative period, clinicians need to carefully balance fluid management to optimise respiratory function without causing haemodynamic compromise or renal dysfunction. As severe pain, particularly for transverse thoracotomy incisions, can compromise recovery significantly, effective analgesic regimens to facilitate physiotherapy are critical.

Indications

The two generally-accepted criteria for lung transplantation in patients with end-stage pulmonary or pulmonary vascular disease are a poor prognosis (less than 50% chance of surviving 2 years) and poor quality of life.¹³⁵ In terms of quality of life, prospective lung transplant recipients usually struggle to perform activities of daily living, may be oxygen-dependent and have New York Health Authority functional class III or IV symptoms. As a result, most patients presenting for surgery are at risk of being debilitated and may be malnourished or overnourished, and therefore require specific interventions by health team members.

Description

The four possible forms of lung transplantation, indications for each form of surgery and salient nursing implications are outlined in Table 14.13. Currently, lung transplantation takes two main forms: bilateral sequential lung transplantation (BSLTx) and single-lung transplantation (SLTx). BSLTx is the most common form of lung transplantation and confers a survival advantage over and above SLTx. However the advantage of SLTx over BSLTx is that twice as many people receive life-saving surgery. For SLTx recipients with COPD, there is an increase in the complexity of postoperative respiratory management, and for this reason some centres may perform BSLTx for patients with COPD. SLTx is also utilised for patients with idiopathic pulmonary fibrosis (IPF) and other forms of interstitial lung disease (ILD) who have a high waiting list mortality.¹³⁶

TABLE 14.13 Comparison of the four standard lung replacement techniques, including their common indicators ¹³⁵

Clinical Manifestations

Postoperative nursing and medical management common to all forms of lung transplant recipients involves intensive clinical monitoring similar to that for heart transplant recipients, with a focus on the stabilisation and optimisation of haemodynamic, respiratory and renal status. Great skill by clinicians is required to manage this complex interplay. Respiratory dysfunction can develop due to severe allograft dysfunction secondary to ischaemia-reperfusion injury, pulmonary oedema, hyperacute rejection and pulmonary venous or artery anastomotic obstruction. Other major complications in the early postoperative period that affect respiratory management include severe pain, diaphragmatic dysfunction, acute rejection and infection. Patients who receive a SLTx for COPD are at risk of developing pulmonary dynamic hyperinflation, requiring independent lung ventilation. Haemodynamic function can be compromised in the early postoperative phase due to cardiac and respiratory problems; renal and gastrointestinal dysfunction is also prevalent. Long-term respiratory complications include airway anastomotic problems (stricture and dehiscence), suboptimal exercise performance, and chronic rejection manifesting as bronchiolitis obliterans syndrome. The most important aspects of these complications are discussed below in relation to nursing practice, and Table 14.14 provides a summary.

TABLE 14.14 Possible causes of low cardiac output in first week after lung transplantation

Cardiovascular

Hypovolaemia

Haemorrhage

Hypothermia

Acute myocardial infarction

Pulmonary venous or arterial anastomosis obstruction (embolism, clot, stitch, torsion)

Pulmonary embolism (thrombus or air)

Non-specific left ventricular dysfunction

Arrhythmias

Coronary artery air embolism

Pulmonary

Pulmonary dynamic inflation of native lung in single-lung transplantation

Pneumothorax

Oversized pulmonary allograft

Other

Sepsis/infection (especially line or occult gut)

Sedatives

Analgesics (especially epidural)

Transfusion reaction

Anaphylaxis

Hyperacute rejection (rare)

Respiratory Dysfunction

Respiratory dysfunction within the first 24–48 hours postoperatively is usually caused by primary graft dysfunction (PGD), a syndrome characterised by non-specific alveolar damage, lung oedema and hypoxaemia.¹³⁷ Primary graft dysfunction may be aggravated by factors associated with the donor (e.g. trauma, mechanical ventilation, aspiration, pneumonia and hypotension), cold ischaemic storage,¹³⁷ inadequate preservation and disruption of pulmonary lymphatics. Clinical signs of PGD range from mild hypoxaemia with infiltrates on chest X-rays to severe ARDS requiring high-level ventilatory support, pharmacological support and ECMO.¹³⁸ Australian researchers have shown a decrease in the severity and incidence of PGD following the implementation of an evidence-based guideline for managing patients’ respiratory and haemodynamic status postoperatively.¹³⁹ The guideline directs clinicians to minimise crystalloid fluids, use vasopressors as the first-line treatment to maintain blood pressure if cardiac output is adequate and use ARDSNet principles for ventilatory support.^139,¹⁴⁰ Respiratory dysfunction beyond 72 hours is likely to be due to infection or hemidiaphragm paralysis secondary to phrenic nerve damage. Although BSLTx is usually performed without cardiopulmonary bypass, for those patients who require cardiopulmonary bypass for surgery, it is recognised that there is a higher incidence of PGD but management principles are essentially the same.

Nursing practice

Severity of allograft dysfunction is assessed by ABG analysis, respiratory function and patient comfort, chest X-ray, bronchoscopy and haemodynamic parameters. A careful balance in the management of haemodynamic, respiratory and renal status is vital in the first 12 hours, and their optimisation should be achieved with inotropes (e.g. adrenaline, noradrenaline) and limited and judicious use of colloid fluids to ensure adequate end-organ perfusion without causing pulmonary overload. Fluid management should aim to keep filling pressures low to normal in light of a recent retrospective review that found a high CVP (>7 mmHg) was associated with prolonged mechanical ventilation and high mortality.¹⁴¹ Importantly, there was no evidence of renal complications associated with these low filling pressures.¹⁴¹ Fluid resuscitation should include products to correct anaemia and preoperative low plasma protein levels.¹⁴²

For patients who have required intraoperative cardiopulmonary bypass, high doses of inotropes are often needed to overcome a transient relative hypovolaemia. Additionally, gentle rewarming measures are needed to re-establish normothermia in order to prevent haematological and peripheral perfusion impairments associated with hypothermia. Slow rather than rapid rewarming, and close monitoring of CI, CVP and PAWP should minimise the development of pulmonary oedema at this time. For patients with allograft dysfunction accompanied by high pulmonary pressures, inhaled NO is useful in decreasing high pulmonary pressures and intrapulmonary shunting.^143,¹⁴⁴ Ongoing nursing assessments of MAP, CI, PAP, PAWP, CVP and urine output guide and evaluate haemodynamic therapeutic interventions (see Chapter 9).

To assess the causes and progress of allograft dysfunction, chest X-rays provide vital information about line placement, ETT position, lung expansion, lung size, position of the diaphragm and mediastinum and the presence of pneumothorax, oedema and atelectasis.¹⁴⁵ Allograft dysfunction due to ischaemia-reperfusion injury appears on chest X-rays as a rapidly-developing diffuse alveolar pattern of infiltration that is greater in the lower regions,¹⁴² most commonly seen on the first postoperative day but may occur up to 72 hours following surgery. The presence of rapidly worsening pulmonary infiltrates (especially if associated with low cardiac indices) should however prompt urgent echocardiography to assess cardiac function and pulmonary venous anastamosis patency. Beyond 72 hours, alveolar and interstitial infiltration may indicate either acute rejection or an infective process.¹⁴⁶ This information is combined with other respiratory and haemodynamic data to inform appropriate collaborative interventions.

Commonly, ventilatory settings and respiratory weaning are guided by pH rather than CO₂ levels. A modest degree of hypercarbia is anticipated postoperatively and resolves over time. Given that low-volume ventilation has a positive impact on lung recovery and long-term outcomes in patients with adult respiratory distress syndrome (ARDS),¹⁴⁷ it has now been recommended that SLTx and BSLTx recipients receive similar settings to prevent barotrauma while providing adequate ventilation.¹⁴² In SLTx recipients, ventilation perfusion mismatches can also be improved by inhaled NO and by positioning patients regularly with the allograft uppermost.

Allograft dysfunction can develop in SLTx recipients with a remaining native COPD lung who are ventilated via a single-lumen ETT, due to gas trapping in the overdistensible native lung, a condition known as pulmonary dynamic hyperinflation (PDH) (see Figure 14.4). Any condition that lowers the compliance of the allograft can lead to PDH in these patients. Nurses need to be aware of the patients who can potentially develop PDH and to remain hypervigilant, as early signs and opportunities to stabilise patients’ haemodynamic and respiratory status quickly can be easily missed. Initial presentation of PDH is usually a set of ABGs showing inadequate ventilation (hypercarbia and hypoxaemia). However, this pattern of ABG values must not be responded to with increases in respiratory rate, tidal volume or PEEP, as these actions will exacerbate the degree of native lung hyperinflation; rather, minute ventilation must be reduced.¹⁴⁸

FIGURE 14.4 Mechanism of pulmonary dynamic hyperinflation: distribution of inspiratory gas

Other common presenting cues of PDH include a haemodynamic profile of cardiac tamponade, tracheal deviation, obvious hyperinflation of the native lung with or without mediastinal shift on chest X-ray, decreased air entry to the allograft on auscultation and pneumothorax. The early stages of PDH in a patient with a left SLTx for COPD can be seen on the chest X-ray in Figure 14.5. Immediate management of the condition requires attempts to minimise hyperinflation with altered ventilatory settings and bronchodilators. If this fails, a skilled physician is required to administer an anaesthetic, insert a dual-lumen ETT, check the position of each lumen’s position and cuff with an intubating bronchoscope. Secure placement of the tube is paramount, to avoid slight movement of the position and consequent displacement of correct cuff placement (see Figure 14.6 for correct positioning of a dual-lumen ETT).

FIGURE 14.5 Chest X-ray of patient with left single lung transplant for COPD who has developed PDH

FIGURE 14.6 Correct positioning of double-lumen endotracheal tube for pulmonary dynamic hyperinflation

Independent lung ventilation is then established to ensure that the native lung receives no PEEP and a minimal tidal volume and rate (e.g. four breaths of 100 mL/min).¹⁴⁸ The allograft may require high levels of PEEP to provide adequate ABGs. Ongoing assessment of respiratory function determines the timing of weaning from the dual-lumen ETT and independent lung ventilation to a single-lumen ETT and standard ventilatory practice. If PDH is not recognised until the patient has a cardiac arrest, the single-lumen ETT should be pushed into the bronchus of the transplanted lung in order to selectively ventilate the allograft until the patient’s condition is stable, when a dual-lumen ETT can be safely inserted.

Patients with allograft dysfunction are always assessed by doctors for the emergence of rejection and pulmonary infection via bronchoscopy (using transbronchial biopsy and bronchoalveolar lavage) in critical care. Evidence of rejection will be treated with changes in the immunosuppression regimen and appropriate ventilatory and haemodynamic support. Many patients with rejection in the immediate postoperative period may not exhibit classic signs of rejection such as abrupt onset of dyspnoea, cough and chest tightness while mechanically ventilated. Subtle changes in respiratory effort, gas exchange and minute ventilation may be the only signs to alert the nurse to respiratory dysfunction secondary to rejection or infection during mechanical ventilation.

Classic clinical signs of pulmonary infections include a low-grade fever, increasing dyspnoea and sputum production, cough and infiltrates on a chest X-ray. Hypotension, a reduced cardiac index and subtle changes in respiratory parameters during mechanical ventilation noted above may also be present. Pulmonary infections may be acquired through nosocomial, community or donor means, with recipient-colonised and opportunistic infections prevalent. Regardless of the means of acquisition, all infections are treated promptly with specific antibiotic, antifungal or antiviral therapies. The risk of developing CMV and Pneumocystis carinii in lung transplant recipients is somewhat higher than in heart transplant recipients, so prophylactic therapies for both infections are provided. Clinicians play an important role in preventing the transmission of infection between patients and cross-contamination within patients. Meticulous hand-washing between patients and between procedures, as well as minimising traffic into and out of patient care areas, are important measures in reducing infection rates.¹⁴⁹

Pain

All recipients of lung transplantation can experience severe pain afterwards due to the incisions and chest drains. However, recipients of BSLTx in particular experience extremely severe postoperative pain secondary to the transverse sternotomy (clam-shell incision) and presence of four chest tubes. The recent use of a minimally invasive thoracotomy rather than transverse sternotomy for patients with obstructive respiratory illnesses may also reduce the postoperative pain experienced by recipients. Ideally, all lung transplant recipients should receive epidural analgesia; however, the insertion of an epidural catheter at the time of surgery may be contraindicated due to preoperative anticoagulation therapy. In these circumstances, epidural analgesia should be instituted as soon as appropriate after surgery. Higher failure rates of transition from epidural to oral analgesia have been reported in lung transplant recipients than in other thoracotomy patients,¹⁵⁰ and in our experience it is not uncommon for BSLTx recipients to require opiate analgesia for a month after surgery in order to perform activities of daily living and physiotherapy.

Nursing practice

Consultation with pain services to ensure that patients receive optimal analgesic regimens should be an integral component of patients’ postoperative management (see Chapter 19). Paracetamol is beneficial in relieving mild to moderate pain, and may be used as an adjunct to centrally-acting analgesics for moderate to severe pain.¹⁵¹ The use of non-steroidal antiinflammatory drugs should be avoided, due to their detrimental effects on renal and gastrointestinal function.¹⁵¹

The nursing management of intercostal chest tubes is similar to that for cardiac surgical patients ¹⁵² (see Chapter 12), with a few additional considerations. Recipients of SLTx have one apical and one basal chest tube, whereas BSLTx recipients have four chest tubes: two apical and two basal. Both BSLTx and HLTx recipients have one pleural space, so the amount and consistency of drainage from basal tubes will vary depending on patient positioning. Apical chest tubes are removed prior to basal tubes. Once lung expansion is optimal and any pneumothoraces have resolved, the apical tubes are removed. Basal chest tubes are removed once drainage is considered minimal in volume (approximately 250 mL/day) and serous in nature.

Haemodynamic Instability

As noted earlier, all lung transplant patients can experience haemodynamic compromise and renal impairment postoperatively as a result of managing respiratory function. Potential causes of a low cardiac output are outlined in Table 14.14. Patients with pulmonary hypertension must be carefully managed in the early postoperative period because of impaired cardiac output and changes in right ventricular dynamics. Prior to surgery, prolonged periods of a high right ventricular afterload lead to right ventricular thickening and stiffness, accompanied by limited wall motion of the left ventricle.¹⁵³

Nursing practice

During arousal from anaesthesia and patient activity, fluctuations in oxygenation and systemic and pulmonary pressures exacerbate haemodynamic instability.^154,¹⁵⁵ When weaning from mechanical ventilation, as ventilation pressures fall, increases in preload may precipitate acute pulmonary oedema, even days after surgery.¹⁵⁴ Conversely, if the patient is hypovolaemic at the time of weaning, right ventricular outflow obstruction may occur.¹⁴² These potential events confirm that careful titration of fluid and inotropic therapies, guided by frequent, accurate monitoring of invasive haemodynamic parameters, is required in patients with preoperative pulmonary hypertension.

Renal and Gut Dysfunction

Reasons for renal dysfunction in LTx recipients in the early postoperative phase are similar to those for heart recipients. The situation is, however, compounded in lung recipients due to aminoglycoside and NSAID use preoperatively, the high number of patients with diabetes and a requirement for ‘dry’ lungs postoperatively. Fortunately, the use of interleukin-2 receptor antibody drugs can assist in lowering the doses of calcineurin inhibitor agents to offer some early protection to the kidneys without inducing acute rejection.¹⁵⁶

Nursing practice

Routine management of gut function is an important aspect of nursing practice, including the prevention of constipation (see Chapter 19). For patients receiving surgery for cystic fibrosis, pancreatic enzyme supplements are required postoperatively. As these patients are invariably debilitated preoperatively, enteral feeds that do not require pancreatic enzyme supplements should be commenced as soon as possible after surgery, as these supplements cannot be administered via enteral feeding tubes. Further specific information on managing patients with cystic fibrosis is available.¹⁵⁷

Psychosocial Care

In the early postoperative period, corticosteroids, sedatives, sleep deprivation and persistent pain contribute to acute organic brain syndrome ¹³⁵ (see Chapter 7). Rejection episodes can be emotionally demanding, and the requirement for higher doses of corticosteroids can lead to irritability, insomnia, profound depression, mania or psychosis.¹³⁵

Although LTx surgery offers recipients relief from shortness of breath and increased exercise tolerance, many patients have to continue managing other aspects of their underlying disease (e.g. cystic fibrosis). Thus, the burden of living with a chronic illness remains. Conversely, some recipients experience wellness for the first time in their life, and this can alter family and relationship dynamics. In circumstances where lung function deteriorates after initial success, patients and families experience feelings of devastation and hopelessness. Counselling services are essential in both the preoperative and the postoperative phase.^135,¹⁵⁸^–¹⁶⁶

Long-term Sequelae

Long-term sequelae for lung transplant recipients include renal impairment, hypertension and increased risk of malignancies, similar to those with heart trans-plantations. Further information about long-term complications specific to lung transplantation, such as bronchiolitis obliterans syndrome and other non-pulmonary complications, is available.¹³⁵

Summary

Respiratory alterations, whether a primary disruption or a secondary complication of comorbidity, are the primary reason for ICU admission. Vigilant assessment, monitoring and being responsive to a deteriorating state are central to critical care nursing practice. Contemporary approaches to respiratory support focus on preserving a patient’s respiratory function, including NIV, using less controlled ventilation when appropriate and consideration of weaning from mechanical ventilation at the earliest opportunity. The current evidence base supports strategies to prevent VAP, using daily checklists or care bundles.

Case study

Frances is a thirty-six-year-old female. She presented to her local general practitioner (GP) with an 11-day history of cough, fever and shakes, and a 5-day history of expectorating tenacious yellow–green sputum, decreased appetite and mild right-sided chest pain with increasing dyspnoea and a hoarse voice. Her GP organised for the ambulance to transport Frances directly to the Emergency Department (ED) of the nearest major public hospital. A peripheral intravenous line was inserted and the patient was continuously monitored during transportation to the hospital.

Upon arrival at the ED, Frances was assessed as a Triage Category 2 patient and a baseline assessment was determined:

• CNS: GCS 15, Temperature 38.6 °C

• CVS: HR 135/min, sinus tachycardia, BP 150/78 mmHg, brisk capillary refill

• RESP: RR 40/min, shallow rapid breathing, appears tired. SpO₂ 95% while receiving oxygen at 6 L/minute via Hudson Mask, improving to 98% with increased flow to 8 L/minute.

Investigations revealed:

• U&E: Na⁺ 132 mmol/L, K⁺ 3.2 mmol/L, BGL 8.5 mmol/L, Cr 99 µmol/L, eGFR >90, bHCG <0.5

• FBE: Hb 130 g/L, WCC 12.89 x 10⁹/L, Neut 174 x 10 ⁹/L

• INR: 1.8

• CXR: Right middle lobe pneumonia

• Pending: Legionella urinary antigen, atypical serology and respiratory polymerase chain reaction (PCR) testing.

Frances’ past history included hirsutism, polycystic ovaries (PCOS), pre-eclampsia and depression. She had no known allergies. At the time of presentation to the ED her regular medications were sertraline and spironolactone (for PCOS). She reported that she lived with her partner and that she had been at home on annual leave from her employment for the past three weeks. Further, she reported that she had not been exposed to any exotic pets or undertaken recent overseas travel.

An additional peripheral intravenous line was inserted in ED. The clinical impression was pneumonia secondary to possible H1N1 Influenza A (swine flu). The decision was made to transfer Frances directly to ICU where an arterial line was promptly inserted for monitoring, followed by an elective endotracheal intubation for respiratory distress. She was administered morphine and midazolam sedation. Ceftriaxone, azithromycin, vancomycin and oseltamivir were commenced. A central venous catheter was inserted for fluid administration and inotropic therapy if required. The aim was to maintain a mean arterial blood pressure (MAP) > 70 mmHg. Her first arterial blood gas showed a respiratory acidosis with metabolic compensation (FiO₂ 1.0, PO₂ 197 mmHg; PCO₂ 42 mmHg; pH 7.33; BE-9; bicarbonate 22 mmol/L and SaO₂ 99%).

By day 1 of her ICU stay, Streptococcus had been identified in the blood cultures. Legionella was not detected. Frances remained under respiratory isolation precautions pending PCR results. Ventilation settings were FiO₂ 0.3, rate 18, V_T 500 mL, PEEP 5 cmH₂O, pressure support 10 cmH₂O. A noradrenaline infusion was commence to maintain a MAP >70mmHg. Ongoing enteral feeding and prophylactic VTE management had commenced.

By day 2 of ICU, the PCR repeat testing again returned a negative result and respiratory isolation precautions were ceased. Following 39 hours of intubation, Frances was extubated and maintained an oxygen saturation greater than 96% with FiO₂ 0.5 and humidification. Within the next ten hours Frances was re-intubated as she was visibly exhausted with an increased work of breathing, and an increased respiratory rate from 24 to 35 breaths/minute. Further, a reduced GCS and increasing FiO₂ requirement (0.8) to maintain her oxygen saturation supported the need for assisted ventilation. Prior to reintubation her ABG result was PO₂ 55 mmHg, PCO₂ 48 mmHg, pH 7.35, BE 0.9, HCO₃⁻ 26 mmol/L and SaO₂ 98%.

On day 3 of ICU, Frances’ oxygenation began to deteriorate with changes in positioning. Blood-stained sputum was being suctioned via the ETT. A computed tomography angiogram (CTA) of the pulmonary vasculature was undertaken and excluded pulmonary embolus as a cause for the hypoxaemia. It did show that that there was bibasal and right upper lobe consolidation. There was no evidence of goitre. An echocardiogram bubble study reported that there was no shunt. The plan was to reduce the PEEP to reduce the shunting and by day 4 of ICU the hypoxaemia had resolved.

On day 9 of ICU, following an additional 161 hours of intubation, Frances was extubated again and received high flow oxygen via nasal prongs. During the next 3 hours Frances complained of difficulty breathing with no apparent increase in her work of breathing or alterations in arterial blood gases. An audible stridor and bovine cough developed despite administration of nebulised adrenaline, intravenous steroids and application of BiPAP. Frances was re-intubated; a Grade 1 airway was evident with oedematous epiglottis and vocal cords sighted. On day 10 of ICU percutaneous tracheostomy (size 8) was inserted.

By day 12 of ICU, following an additional 81 hours of ventilation, Frances was successfully breathing via a tracheostomy-shield and oxygenation was adequate. Frances was transferred to the ward on day 15 of her admission following more than 24 hours of successful breathing via a tracheostomy shield. Antibiotic therapy continued while on the ward and her tracheostomy was removed later that day. Frances remained haemodynamically stable and her health continued to rapidly improve so that three days later Frances was discharged home to convalesce with her family.

Frances attended a clinical review in the ambulatory care department four weeks after her ICU discharge. Her recovery had progressed to the point that she reported being able to walk two kilometres (her baseline tolerance was five kilometres). On examination her lung fields were clear, her oxygen saturation was 98% on room air and her CXR was clear indicating full resolution of the pneumonia. Her blood pressure remained elevated at 150/70 mmHg and she was advised to remain on amlodipine and consult her GP for further follow-up and repeat prescriptions. Frances was discharged from the ambulatory care clinic following this clinical review, with ongoing care to be provided by her GP. Frances experienced pneumonia post an initial viral illness. Her plan for the future was to include annual Influenza vaccination in her health maintenance plan, and timely consultation with healthcare workers with any development of unusual respiratory symptoms.

Research vignette

Tiruvoipati R, Lewis D, Haji K, Botha J. High-flow nasal oxygen vs high-flow face mask: A randomized crossover trial in extubated patients. Journal of Critical Care 2010; 25(3): 463–8.

Abstract

Critique

This article is a well-written and readable research study. It is also the first to report a scientific comparison between these two often-employed oxygen-delivery modalities in clinical practice. The article’s liberal use of tables and headings allows for ease of understanding and the ability to locate specific information.

This clinical enquiry was a randomised controlled study. Each study participant had a stabilisation period and following this, proceeded to be randomised to either protocol A or B. The stabilisation period became the control period for each participant and increased the strength of the study design. The merit of this experimental design is that extraneous variables are controlled for. Extraneous variables may be antecedent or intervening. Examples of antecedent variables include age, gender, socioeconomic status and premorbid health status. These data provide a baseline to confirm similarity between groups prior to assessment of an effect of the intervention.¹⁶⁷ Intervening variables may occur during the course of the study and are unrelated to the clinical trial but may influence the dependent variables. For example a media report on the merit of clinical research may influence the public’s attitude to participation in a clinical trial.

The study was well conducted. The researchers were transparent in their handling of data and reporting of all those initially recruited into this study via the CONSORT statement.¹⁶⁸ The duration of ventilation prior to extubation report wide confidence intervals. This could suggest that a wide profile of patients were enrolled into this study. Due to this trial being a prospective evaluation undertaken in the local setting it is possible to generalise the applicability of findings across the population in Australia and New Zealand. Outcome measures were a combination of quantifiable data such as arterial blood gas analysis and vital signs in addition to subjective measures i.e. the nurse’s report of the patient’s comfort and tolerance for the flow delivery system using the visual analogue scale (VAS). The VAS is a ubiquitous, valid and sensitive measure in a range of age groups.¹⁶⁹

Certain limitations were apparent within the study. The recruitment period of time for the study is unreported. It is not reported whether random number generation was responsible for the creation of the randomisation sequence (n = 50) or whether this was undertaken by the recruiters. The researchers had identified their study’s limitations. This could not be a double- or even single-blind study as the patient participating and their nurse were aware of which high-flow modality was being used. Further, it is thought,¹⁷⁰ but remains unclear, what window of time with one high-flow set up before change over to the alternative strategy is a sufficient length of time to wash out one intervention before measuring the clinical, self report and bedside observer patient data.

There are a number of recognised factors that influence gas exchange such as skeletal muscle conditioning, haematological profile and diffusion capacity. Variability of these factors was offset by the trial design as each participant was their own control in this study’s design. However, it was unclear whether patient positioning was consistent within and between the study’s participants. Patient positioning could influence the level of alertness, airway clearance and gas exchange. It would need to be assumed when interpreting these data that the temperature/humidity of the inspired gas with each intervention was consistent across the sample. The function of airway mucosa and temperature of inspired gas has been long established.¹⁷¹

The sample size was small (n = 44) and the risk of drawing conclusions based on a small sample size risks a Type II error. These results support the researchers’ contention that a larger sample size is required. Power calculations to determine equivalence between interventions exist.¹⁷² It is unclear how many bedside nursing staff participated in this study and if any and/or regular staff in-service education occurred to achieve inter-rater reliability of their reports of the patients’ tolerance with these two high-flow modalities. Each high-flow set up was trialled in 30-minute episodes. How frequently the bedside nurse observed the patient’s tolerance of the high-flow set up may have been variable. Interestingly the utility of nasal-delivered high flow oxygen therapy in generating a positive airway pressure has been examined and reported in healthy subjects as proportional to rates of gas flow and reduced pressure in mouth breathers in Australia and New Zealand in healthy subjects¹⁷³ and ICU patients¹⁷⁴ albeit with small sample sizes. This study is important, as it is the first randomised trial that compares two popular high flow delivery systems and highlights that further generation of evidence is vital to support our clinical decision making in everyday practice.

Learning activities

1. A patient has severe ARDS following aspiration pneumonia. Their FiO₂ is 1 and PaO₂ 60 mmHg. Core temperature is 40°C and the only medications are antibiotics. Any activity including suctioning causes profound desaturation. What additional measures could be implemented to minimise this effect?

2. What is your understanding of ARDS?

3. List the interventions required for a nurse to safely care for a patient with a provisional diagnosis of a novel infectious disease.

4. Describe and compare the differences between a simple, persistent and reoccurring pneumothorax.

5. At the commencement of your shift you undertake a respiratory assessment of your patient. List the parameters that should be examined.

Online resources

American Association for Respiratory Care. http://www.aarc.org/.

ARDS Network. http://www.ardsnet.org.

Asian Pacific Society of Respirology. http://www.apsresp.org/.

Asthma Foundation. http://www.asthmaaustralia.org.au/.

Australian & New Zealand Society of Respiratory Science. http://www.anzsrs.org.au/.