Respiratory failure

CRITICAL ILLNESS AND INTENSIVE CARE e II

 Muscular system: myasthenia gravis, muscular dystrophies, residual neuromuscular blockade following anaesthesia, diaphragmatic splinting (e.g. morbid obesity or abdominal pain).  Skeletal system: flail rib fracture, kyphoscoliosis.

Respiratory failure Rakesh Bhandary

Abstract Respiratory failure is a common clinical condition, and is associated with a 90-day mortality of approximately 40%. This article discusses the causes, pathophysiology, presentation and management of respiratory failure with reference to the identification and modification of risk in the perioperative period.

Pathophysiology of respiratory failure As discussed, respiratory failure can be caused by an abnormality in any component of the respiratory system. Furthermore, patients with hypoperfusion secondary to shock may present as respiratory failure. In health, ventilatory capacity (ability to breath without fatigue) greatly exceeds ventilatory demand (amount of breathing required to manage metabolic demand). Respiratory failure may result from a reversion of this relationship. The pathological processes involved in respiratory failure are:  diffusion impairment  ventilation/perfusion (V/Q) mismatch  shunt  alveolar hypoventilation. The first three are involved predominantly in hypoxic respiratory failure (unless the shunt is in excess of 60%), while alveolar hypoventilation is responsible for hypercapnic respiratory failure.

Keywords Failure; hypercarbia; hypoxaemia; respiratory; ventilatory

Definition Respiratory failure occurs when the respiratory system is unable to perform its basic function of gas exchange. Traditionally there are two types either of that may be acute or chronic:  Type I (hypoxaemic) respiratory failure, where the arterial oxygen level (PaO2) is below 8.0 kPa, whilst breathing room air. This is due to impaired gas diffusion across the alveolar-capillary membrane, shunt or ventilationeperfusion mismatch.  Type II (hypercarbic) respiratory failure, where the PaO2 is below 8.0 kPa, with a raised PaCO2, more than or equal to 6.5 kPa. These patients have ventilatory failure.

Clinical presentation Distinction between acute and chronic respiratory failure Acute type II respiratory failure develops over a minutes to days and is reflected by a respiratory acidosis with a pH below 7.3. Chronic type II failure develops over days to months. It is characterized by renal compensation with a near normal pH and raised serum HCO3 levels.

A careful assessment including history, examination and investigations should aim to elucidate cause and severity. Baseline respiratory reserve and relevant co-morbidities are important in predicting likely therapeutic requirements (e.g. mechanical ventilation). It should be noted that many signs (e.g. confusion in the elderly) are non-specific, but particular attention should be paid to the features in Table 1.

Causes of respiratory failure Respiratory failure can be precipitated by pathology in any of the components of the respiratory system, from the upper airway to the musculoskeletal system:  Airway obstruction: foreign body, tumour, bronchospasm, chronic bronchitis.  Pulmonary parenchyma: pneumonia, acute respiratory distress syndrome (ARDS), alveolar oedema, lobar collapse, pulmonary haemorrhage, atelectasis, interstitial lung disease.  Pleural pathology: pneumothorax, significant pleural effusion, haemothorax.  Vascular: pulmonary embolism, chronic thrombo-embolic pulmonary hypertension (CTEPH).  Central nervous system: sedative drugs, opiates, any condition causing coma, motor neurone disease.  Peripheral nervous system: Guillain-Barre syndrome, high spinal cord lesion, phrenic nerve lesion, poliomyelitis.

Specific investigations Arterial blood gas analysis in an unwell patient on room air is not usually necessary and should be avoided. The concentration of oxygen being administered should always be noted. The magnitude of the oxygen requirement helps determine the severity of the pathology. A chest X-ray should help to determine aetiology and disease severity, although the radiological picture may often lag behind the evolution and resolution of the disease process. It may also indicate the need for a therapeutic intervention such as thoracocentesis. Other investigations (e.g. CT Chest) may help clarify difficult diagnoses (see Chest imaging in ICU on pages 00e00 of this issue).

Management of respiratory failure A structured airwayebreathingecirculation approach should always be adopted in severely unwell patients. Many hospitals have a ‘track & trigger’ system for identifying and appropriately referring patients to critical care services.1

Rakesh Bhandary MBBS FRCA EDICM is a Consultant in Critical Care Medicine and Anaesthesia at University Hospital of North Tees, Stocktonon-Tees, UK. Conflicts of interest: none declared.

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Clinical features of respiratory system inadequacy Hypoxaemia

Hypercarbia

Neurological features

Anxiety Altered mental status Seizures Confusion

Cardiovascular features

Tachycardia Arrhythmias Bradycardia and hypotension (if severe)

Respiratory features

Tachyapnoea Accessory muscle use Cyanosis Diaphoresis

Somnolence & lethargy Asterixis Restlessness Slurred speech Headache Decreased conscious level Peripheral vasodilatation Tachycardia Arrhythmias Bounding pulses Signs of airway obstruction or narrowing (e.g. stridor, wheezing)

General features

Warm peripheries

Table 1

Methods include:  Humidification of inspired gases to avoid secretions from becoming tenacious.  Mucolytic agents, like cysteine analogues can reduce sputum viscosity.  Chest physiotherapy, either preventive or therapeutic, conventionally uses postural drainage, percussion & vibration or incentive spirometry to mobilize secretions and expand collapsed lung segments.

The management of respiratory failure includes general measures and focussed support in the form of CPAP, NIV or mechanical ventilation where appropriate. Supplemental oxygen Supplemental oxygen is always indicated in patients with acute respiratory failure. O2 is most effective when the main abnormality is V/Q mismatch. O2 can be administered via variable performance device (e.g. Hudson’s mask, nasal cannulae) or fixed performance devices (high flow mask with reservoir, high flow nasal cannulae, Venturi mask). A sub-group of COPD patients with chronic CO2 retention lose the hypercapnoeic stimulus to the respiratory centre. These patients are dependent on hypoxic respiratory stimulus and require titrated oxygen therapy rather than high flow oxygen.

Bronchodilators Bronchodilator therapy is often useful to improve airflow and reduce the work of breathing. Commonly used bronchodilators include b2 agonists, anticholinergics, and phosphodiesterase inhibitors. Steroids are often used in patients with a background of COPD or asthma, to reduce airway inflammation and hyper-reactivity of the bronchiae.

Antibiotics When possible, sputum and blood cultures should be obtained prior to commencing antimicrobial therapy. Appropriate antimicrobial agents should be commenced on an empirical basis. The choice of antibiotic often depends on hospital or community acquisition and patient factors (e.g. previous colonization, comorbidities). The spectrum of coverage should be narrowed as soon as microbiological reports are available. The Surviving Sepsis Campaign strongly recommends commencing antibiotic therapy as soon as possible, and always within an hour of diagnosis of severe sepsis and septic shock. A strong relationship exists between the delay in effective antimicrobial initiation following onset of septic shock and in-hospital mortality.2

Respiratory support If the above measures are ineffective and the patient is tiring, respiratory support can be provided using humidified high flow nasal oxygen, continuous positive airway pressure (CPAP), noninvasive ventilation (NIV), mechanical ventilation and much less commonly extracorporeal techniques like extracorporeal membrane oxygenation (ECMO) and extracorporeal carbon dioxide removal (ECCO2-R). These are complex, high-risk technologies, and are described more extensively in the mechanical ventilation article in this issue. High flow nasal cannulae (HFNC): HFNC system provides humidified, heated, high flow (up to 50 l/ min) oxygen through nasal cannulae Figure 1. It can provide titrated oxygen concentration of 30%e100%. HFNC improves mucociliary clearance and provides distending pressures similar to CPAP in the lower airways, although this effect is unpredictable. It can be used in patients as the first line of respiratory

Control of secretions Many patients with respiratory failure produce large quantities of bronchial secretions which are often infected. It is imperative that sputum retention is avoided as it often results in sputum plugging and hypoxia, segmental collapse and atelectasis, inadequate treatment of infection and superinfection.

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CRITICAL ILLNESS AND INTENSIVE CARE e II

support for hypoxaemic respiratory failure where CPAP is contraindicated (e.g. upper GI surgery, risk of aspiration) or the not tolerated. Continuous positive airway pressure (CPAP): CPAP provides a continuous positive pressure throughout the breathing cycle and is analogous to positive end expiratory pressure (PEEP). CPAP requires a facemask, nasal mask or a hood (or helmet) as an interface Figure 2. It is used primarily for patients with type I respiratory failure. CPAP improves oxygenation by recruitment of collapsed alveoli, thus reducing shunt. CPAP is particularly useful for post-surgical respiratory failure due to basal collapse/consolidation, acute cardiogenic pulmonary oedema and selected patients with chest trauma who remain hypoxaemic despite adequate analgesia. CPAP can be provided transiently outside the ICU with a simple CPAP circuit as shown in Figure 1 or in the ICU with CPAP bellows, NIV machine or ventilators with NIV mode.

Figure 2 A simple CPAP system for use on wards and A&E in an emergency. The PEEP depends on the flow of oxygen and there is no requirement for a PEEP valve.

Non-invasive ventilation (NIV): NIV provides mechanical respiratory support without tracheal intubation. NIV delivers a bilevel positive airway pressure (BiPAP). It can be delivered using modern ventilators on the ICU or portable NIV devices outside the ICU setting Figure 3. The interface used is normally a facial or nasal mask. A hood (or helmet) can be used, but it is less effective in terms of CO2 elimination.3 Although it has been used for a wide range of indications, including postoperative avoidance of intubation, and postextubation support, NIV is most beneficial in the management of selected patients with acute exacerbation of COPD,4 neuromuscular conditions or chest wall abnormalities and management of immunocompromised patients with respiratory failure, as the risk of ventilator associated pneumonia (VAP) is high in this patient sub-category (Table 2). While both NIV and CPAP have proven benefits in some clinical situations, they do not alter the outcome when used in respiratory failure secondary to ARDS or pneumonia. In these situations, NIV and CPAP may simply delay necessary intubation.5

Table 3 outlines the indications for intubation and mechanical ventilation. Ventilation strategy This is detailed in the mechanical ventilation article in this issue. Current recommendations6,7 include:  Limit tidal volume (VT) to 6 ml/kg.

Invasive mechanical ventilation Mechanical ventilation requires endotracheal intubation or tracheostomy, and sedation with or without muscle relaxants.

Figure 1 Nasal high flow system in use and the nasal cannulae e the system allows delivery of heated humidified of high flow oxygen. The flowmeter has maximum flow rate of 70 l/min.

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Figure 3 A modern portable NIV machine with facemask interface. These can be used to provide respiratory support in form of CPAP as well as BIPAP.

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Prerequisites, pros and cons of non-invasive ventilation Prerequisites for CPAP/NIV

C C C C C C

Contraindications

C C C C C C C C

Advantages of NIV/CPAP

C C C C C C

Problems with NIV/CPAP

C C C C C

Conscious Airway self maintained Co-operative Can tolerate periods without NIV/CPAP for chest physiotherapy, suction, oral feeds etc. Can tolerate tight fitting facemask, nasal mask or helmet interface device Able to cough up secretions Low GCS (<8/15) Inability to protect airway Inability to cough and expectorate effectively Copious respiratory secretions Recent facial or upper airway surgery Risk of aspiration (e.g. bowel obstruction) Uncooperative patient, confusion, agitation or coma Maxillofacial injuries Avoidance of tracheal intubation and associated complications especially ventilator associated pneumonia (VAP) Avoidance of sedation Natural airway defence is maintained Spontaneous coughing is not impaired Ventilatory support can be provided intermittently, to allow normal eating, drinking and communication Facilitates early mobilization Necrosis of skin over nasal bridge and face Air swallowing is common Claustrophobia with face mask Aspiration of gastric contents Cardiovascular instability

Table 2

Indications for endotracheal intubation and mechanical ventilation Airway control/establishing definitive airway

C C C C C

Protection of lungs from aspiration

C C C

Respiratory dysfunction

C C C C C C

Optimizing physiology

C C

Facilitating interventions

C C C C C

Inhalational burns Stridor/airway oedema Tumour causing airway obstruction Airway or facial trauma Cervical haematoma or oedema Bulbar dysfunction Decreased conscious level (GCS <8) Full stomach NIV/CPAP fails or is contraindicated (Table 2) Clinical deterioration Worsening blood gases despite optimal medical treatment Respiratory muscle fatigue Vital capacity (<15 ml/kg) Severe respiratory acidosis Controlling intracranial pressure Reducing oxygen consumption as in severe sepsis or anaemia (e.g. Jehovah’s witness) For surgical intervention To facilitate diagnostic intervention (e.g. MRI/CT in children, stereotactic brain biopsy) Post-cardiac arrest stabilization Therapeutic hypothermia Transferring critically ill patients

Table 3

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Complications relating to mechanical ventilation General problems C Complications associated with intubation or tracheostomy C Disconnection or accidental extubation C Failure of gas delivery or power supply C Mechanical faults Respiratory changes C Maldistribution of inspired gases C Collapse of distal lung segments C Decreased surfactant activity C Barotrauma C Ventilator associated lung injury C Ventilator associated pneumonia

Cardiovascular changes C Decreased venous return C Cardiovascular collapse C Peripheral oedema Others C Side effects of sedating agents and muscle relaxants C Venous thromboembolism C Ileus C Hepatic dysfunction C Fluid retention C Psychological trauma

Table 4

 Limit peak pressure to 35 cm/H2O.  Accept higher than normal PaCO2 (6e8 kPa) e permissive hypercapnea.  Accept lower than usual PaO2 (>8 kPa), or SpO2 > 90%.  Use higher levels of PEEP (5e15 cm/H2O) to improve alveolar recruitment.  Use ventilation modes which allow and support spontaneous respiratory effort.

Properative risk stratification and postoperative risk reduction strategies Postoperative pulmonary complications have a marked impact on morbidity and mortality from anaesthesia and surgery. The most important include atelectasis, hospital-acquired pneumonia, respiratory failure and exacerbation of pre-existing pulmonary disorders. A systematic review in 2006 suggested patient, intervention and laboratory investigation related factors associated with increased risk of postoperative respiratory complications for non-cardiothoracic surgeries.8 These are outlined in Table 5.

Problems with mechanical ventilation Invasive mechanical ventilation is associated with marked physiological changes and is associated with a number of diverse problems listed in Table 4.

Strategies to reduce postoperative respiratory complications Preoperative interventions should include optimization of medications to treat COPD, for example. Complex cases should be thoroughly reviewed in a preoperative assessment clinic or by a respiratory physician. The evidence regarding preoperative smoking cessation is unclear. Cessation over the 24 hours prior

Extracorporeal circulations used in respiratory failure Extracorporeal circuits are used in specialist centres as rescue therapies in severe respiratory failure, but a discussion of these is outside the scope of this article.

Risk factors for postoperative respiratory complications following non-cardiothoracic surgery Patient-related risk factors C C C C C C C C C C C C C C

Advanced age (>60 yrs) ASA grade >2 Congestive cardiac failure Partial or total functional dependence COPD Cigarette smoking Obstructive sleep apnoea Obesity Alcohol use Diabetes Asthma HIV infection Impaired sensorium Poor exercise tolerance

Procedure-related factors C C C C C C C C C C

Open aortic aneurysm repair Thoracic surgery Upper GI surgery Abdominal surgery Neurosurgery Vascular surgery Emergency surgery Prolonged surgery (>2.5 h) General anaesthesia Blood transfusion (>4 units)

Laboratory tests C C C C

Serum albumin <35 g/L Abnormal chest X-ray Blood urea >7.5 mmol/L Abnormal Spirometry (FEV1 < 60% of predicted or <1.2 L, FEV1:FVC ratio <70%)

Table 5

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to surgery improves oxygen delivery to the tissues and mitochondrial function. However, stopping in the 2 months prior may actually increase risk through airway hyper-reactivity and increased secretions. Only a few interventions have been shown to clearly or possibly reduce postoperative pulmonary complications. Lung expansion interventions (for example, incentive spirometry, deep breathing exercises, and continuous positive airway pressure) reduce pulmonary risk. Selective, rather than routine, use of nasogastric tubes after abdominal surgery and short-acting rather than long-acting intraoperative neuromuscular blocking agents may reduce risk. The evidence is conflicting or insufficient for epidural analgesia, and laparoscopic (versus open) operations, although laparoscopic operations reduce pain and pulmonary compromise as measured by spirometry. Similarly, while malnutrition is associated with increased pulmonary risk, routine total enteral or parenteral nutrition does not reduce risk. Enteral formulations designed to improve immune status (immunonutrition) may reduce the risk of postoperative pneumonia. Ultimately early detection of complications through clinicians’ awareness of risk, appropriate monitoring and vigilance is critical in improving outcomes in this important group of patients. A

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FURTHER READING Brun-Buisson C, Minelli C, Bertolini G, et al. Epidemiology and outcome of acute lung injury in European intensive care units. Results from ALIVE study. Intensive Care Med 2004; 30: 51e61. Zambon M, Vincent JL. Mortality rates for patients with acute lung injury/ARDS have decreased over time. Chest 2008; 133: 1120e7.

REFERENCES 1 Baruch M, Messer B. Criteria for intensive care unit admission and severity of illness. Surgery 2012; 30: 225e31. 2 Kumar A, Roberts D, Wood KE, et al. Duration of hypotension before initiation of effective antimicrobial therapy is the critical

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determinant of survival in human septic shock. Crit Care Med 2006; 34: 1589e96. Antonelli M, Pennisi MA, Pelosi P, et al. Non-invasive positive pressure ventilation using a helmet in patients with acute exacerbation of chronic obstructive pulmonary disease: a feasibility study. Anaesthesiology 2004; 100: 16e24. Ram FS, Picot J, Lightowler J, Wedzicha JA. Non-invasive positive pressure ventilation for treatment of respiratory failure due to exacerbations of chronic obstructive pulmonary disease. Cochrane Database Sys Rev 2004; 3: CD004104. Hess DR. Non-invasive ventilation for acute respiratory failure. Respir Care June 2013; 58: 950e69. The Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 2000; 342: 1301e8. Girard TD, Bernard GR. Mechanical ventilation in ARDS: a state-of-theart review. Chest 2007; 131: 921e9. Smetana GW, Lawrence VA, Cornell JE. Preoperative pulmonary risk stratification for noncardiothoracic surgery: systematic review for the American College of Physicians. Ann Intern Med 2006; 144: 581e95.

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Please cite this article in press as: Bhandary R, Respiratory failure, Surgery (2015), http://dx.doi.org/10.1016/j.mpsur.2015.07.013