Acute respiratory failure

Acute respiratory failure Straight to the point of care Last updated: Mar 30, 2022 Table of Contents Overview Summary Definition Theory Epidemiology Aetiology Pathophysiology Classification Case history Diagnosis Approach 9 History and exam 13 Risk factors 15 Investigations 18 Differentials 21 Criteria 22 Management 23 Approach 23 Treatment algorithm overview 26 Treatment algorithm 28 Emerging 36 Primary prevention 36 Secondary prevention 36 Patient discussions 36 Follow up 37 Monitoring 37 Complications 38 Prognosis 39 Guidelines 40 Diagnostic guidelines 40 Treatment guidelines 40 References 41 Images 49 Disclaimer 50 Acute respiratory failure Overview Summary Patients may present with shortness of breath, anxiety, confusion, tachypnoea, cardiac dysfunction, and cardiac arrest Central nervous system depression can occur as a result of lack of oxygenation of the blood and vital organs or excessive accumulation of carbon dioxide Pulse oximetry, chest x-rays, blood gas analysis, and end-tidal carbon dioxide monitoring (capnometry) are key diagnostic tests Management involves first ensuring that the upper airway is patent and clear of obstructions Supplemental oxygenation and ventilatory support are likely to be required, with immediate attention to the underlying cause or causes for respiratory failure Endotracheal intubation and mechanical ventilation are employed when other less invasive manoeuvres have failed This topic covers acute respiratory distress in patients over the age of 12 years Definition Acute impairment in gas exchange between the lungs and the blood causing hypoxia with or without hypercapnia (e.g., caused by acute decompensation of chronic pulmonary disease) Hypoxic respiratory failure (type I respiratory failure) is hypoxia without hypercapnia and with an arterial partial pressure of oxygen (PaO₂) of 50 mmHg) on room air at sea level This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Mar 30, 2022 BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice.bmj.com Use of this content is subject to our disclaimer ( Use of this content is subject to our) © BMJ Publishing Group Ltd 2022 All rights reserved OVERVIEW Acute respiratory failure results from acute or chronic impairment of gas exchange between the lungs and the blood causing hypoxia with or without hypercapnia Acute respiratory failure Theory THEORY Epidemiology Studies of acute respiratory failure in intensive care units in Europe report an incidence of 77.6 in 100,000 per year in Sweden, Denmark, and Iceland, 88.6 in 100,000 per year in Germany, and 149.5 in 100,000 per year in Finland; mortality rates were around 40%.[6] [7] [8] More recent incidence data are lacking from the literature In the US, the number of hospitalisations owing to acute respiratory failure increased from 1,007,549 in 2001 to 1,917,910 in 2009 During the same period, a decrease in mortality from 27.6% to 20.6% was observed Rates of mechanical ventilation (non-invasive or invasive) remained fairly stable over this 9-year period; however, the use of non-invasive ventilation did increase from 4% to 10%.[9] Mortality associated with acute respiratory failure is often related to a person’s overall health and the potential development of systemic organ dysfunction that can occur with acute illness Acute respiratory failure is often associated with pulmonary infections, the most common infection being pneumonia Pneumonia killed 808,694 children aged under years in 2017, accounting for 15% of all deaths of children aged under years.[10] The US Centers for Disease Control and Prevention reported that the US death rate from lower respiratory diseases in 2015 was 48.2 people in 100,000, and 17.8 people in 100,000 from influenza and pneumonia, with higher rates for older population groups.[11] Aetiology Respiratory causes include: • Acute exacerbation of asthma • Pulmonary embolism: thrombosis of pulmonary arteries that can occur as a result of hypercoagulable states, such as those induced by pregnancy, oral contraceptive pill use, inherited protein deficiencies (e.g., protein C, protein S, antithrombin III, factor V Leiden deficiencies), and autoimmune conditions (e.g., antiphospholipid syndrome, systemic lupus erythematosus) • Pulmonary oedema • Acute respiratory distress syndrome, including from COVID-19 infection • Pneumonia • Acute epiglottitis • Cardiogenic pulmonary oedema • Pulmonary trauma • Inhalation injury (with toxic fumes or gases including chlorine, smoke, carbon monoxide, hydrogen sulfide) • Upper/lower airway obstruction (e.g., foreign bodies, retropharyngeal abscess, epiglottitis, and swelling caused by acute allergy or anaphylaxis) • Pneumothorax • Chronic lung disease (e.g., COPD, cystic fibrosis, pulmonary fibrosis, chronic interstitial lung disease) • Bronchiectasis • Alveolar abnormalities (e.g., emphysema, Goodpasture's syndrome, granulomatosis with polyangiitis [formerly known as Wegener's granulomatosis]) • Chest wall abnormalities (e.g., kyphoscoliosis) • Malignancy • Decompensated congestive cardiac failure This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Mar 30, 2022 BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice.bmj.com Use of this content is subject to our disclaimer ( Use of this content is subject to our) © BMJ Publishing Group Ltd 2022 All rights reserved Acute respiratory failure Theory • Collagen vascular disease Non-respiratory causes include: • Poisons (e.g., chlorine gas, carbon monoxide) Traumatic causes include: • Blood loss (hypovolaemia with decreased pulmonary perfusion) • Direct thoracic injury (rib fractures, flail chest, penetrating lung injuries, penetrating pulmonary vasculature injuries, diaphragmatic injury with loss of diaphragm muscle function, pulmonary contusion with oedema and bleeding into lung tissue) • Spinal injury • Head injury with haemorrhagic mass effect and direct brain injury • Pulmonary contusion with intraparenchymal haemorrhage • Traumatic pulmonary emboli of marrow fat and cell elements secondary to major fractures Pathophysiology The respiratory system is responsible for oxygen and carbon dioxide exchange between the blood and the atmosphere Respiratory failure occurs when this exchange fails and metabolic demands for oxygen and body system acid-base stabilisation are not maintained, creating a ventilation-perfusion mismatch Failure of oxygen exchange results in the development of severe hypoxaemia (both type I and type II respiratory failure) with cellular anoxia and tissue asphyxia This can occur with all forms of lung disease, including: • Fluid filling of alveolar spaces • Collapse of alveolar spaces; • Re-distribution of blood flow from functioning alveolar units (shunting) • Loss of blood flow to alveolar tissue (e.g., pulmonary embolism); • Underlying loss of pulmonary tissue (e.g., emphysema, trauma, fibrosis); and This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Mar 30, 2022 BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice.bmj.com Use of this content is subject to our disclaimer ( Use of this content is subject to our) © BMJ Publishing Group Ltd 2022 All rights reserved THEORY • Hypovolaemia (from haemorrhage or dehydration) • Shock (septic and cardiogenic) • Severe anaemia (e.g., due to gastrointestinal haemorrhage, haemorrhage secondary to vascular or solid organ trauma) • Drug overdose (opioid and sedative medicines) • Neuromuscular disorders (e.g., Guillain-Barre, myasthenia gravis, muscular dystrophy, motor neuron disease, poliomyelitis) • Central nervous system disorders (e.g., infection, stroke, infiltrating cancers, mass cancers, brainstem lesions) • Spinal disorders (e.g., upper spinal canal mass with cord compression, cervical spinal stenosis, cervical spinal cord injury) • Bony spinal deformity (e.g., kyphoscoliosis, ankylosing spondylitis) • Right-to-left cardiac shunting (e.g., cyanotic congenital heart disease) • Toxins (e.g., botulism) Acute respiratory failure Theory THEORY • Thickening or fluid build-up at alveolar membranes that inhibits gas exchange (e.g., pneumonia) Chronic hypoxia in patients with chronic respiratory failure stimulates increases in the number of circulating red blood cells (erythrocytosis) Failure of carbon dioxide exchange results in hypercapnic respiratory failure (type II respiratory failure), causing increased carbon dioxide in arterial blood Carbon dioxide accumulation leads to carbonic acid accumulation within the tissues, resulting in respiratory acidosis Renal bicarbonate ion retention occurs to compensate for chronic respiratory acidosis Hypercapnic respiratory failure occurs with lung disorders that limit exchange of carbon dioxide from the blood to the atmosphere These lung disorders include: • Poor ventilatory muscle function, as occurs with neuromuscular disorders (e.g., Guillain-Barre, drug over-dose); • Obstruction of airways and alveoli (e.g., asthma, COPD, pulmonary oedema); • Secretions in the small airways and alveoli (e.g., COPD, cystic fibrosis); and • Chest wall abnormalities (e.g., traumatic flail chest, kyphoscoliosis) There are several factors that can trigger respiratory failure, including respiratory, non-respiratory, and traumatic factors Respiratory factors • Acute pulmonary vascular occlusion can result in ventilation-perfusion mismatch and respiratory failure due to insufficient blood flow to functioning alveoli Massive pulmonary artery embolisation may cause high right-sided after-load pressures leading to cardiac dysfunction and inability of the heart to circulate adequate blood volume • Pneumothorax can lead to respiratory failure if there is not enough lung reserve to compensate for the collapsed lung or lung segment This would typically occur in the setting of pre-existing pulmonary dysfunction Bilateral pneumothorax can cause catastrophic respiratory failure and rapid cardiac arrest • Fluid or blood accumulation in the pleural space (pleural effusion) may lead to compression of pulmonary tissues and loss of pulmonary function, causing respiratory failure Pleural effusions can occur secondary to infection, malignancy, trauma, cardiac failure, and collagen vascular disease, as well as many other conditions • Destruction or infiltration of alveoli reduces the surface area available for gas exchange Emphysema causes alveolar destruction, and the bullae that are formed occupy intra-thoracic space without contributing to gas exchange Respiratory failure results from acute or eventual loss of the baseline number of alveolar units Infiltration or filling of alveoli with fluid is a frequent cause of acute respiratory failure Conditions that cause alveolar filling include pneumonia, pulmonary oedema, and pulmonary haemorrhage Alveolar haemorrhage can occur with Goodpasture's syndrome, granulomatosis with polyangiitis (formerly known as Wegener's granulomatosis), and trauma Fluid-filling of alveoli leads to the inability of these alveoli to provide gas exchange with the blood Acute respiratory distress syndrome resulting from trauma, hypo-perfusion, or direct insult is a form of alveolar infiltration and injury • Acute upper airway obstruction (e.g., from foreign body aspiration, acute epiglottitis, anatomical abnormalities, anaphylaxis) can inhibit air flow into the lungs and cause respiratory failure Lower This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Mar 30, 2022 BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice.bmj.com Use of this content is subject to our disclaimer ( Use of this content is subject to our) © BMJ Publishing Group Ltd 2022 All rights reserved Acute respiratory failure Theory THEORY airway obstruction (e.g., from asthma, COPD, cystic fibrosis) is more common and involves constriction or mucous blockage of intermediate-size bronchioles • Pulmonary embolus can occur as a result of hypercoagulability from clotting cascade diseases or abnormalities • Exposure to toxic fumes can lead to damage of the upper airway, lower airway, or alveoli Industrial gases such as chlorine are an example The most common inhalation injury is smoke inhalation, where particulate matter and gases intermix and can cause upper airway and lower airway inflammation resulting in respiratory failure Toxic gases such as carbon monoxide and hydrogen sulfide are exchanged in the lungs, yet result in asphyxia by inhibiting the ability of the blood to effectively extract oxygen from the lungs, as well as causing cellular metabolic damage (cellular asphyxia) Non-respiratory factors • Poor perfusion of the brain, heart, and lungs (e.g., from haemorrhagic hypovolaemia, dehydration hypovolaemia, septic shock, cardiogenic shock, severe anaemia) can result in respiratory failure by reducing blood oxygenation and depressing central nervous system (CNS) respiratory centres • Ventilation with pulmonary gas exchange is dependent on diaphragm and chest wall muscle functioning Neurological disorders inhibiting respiratory muscle function limit ventilation and can cause respiratory failure Examples include Guillain-Barre syndrome and myasthenia gravis Muscular dystrophy results in muscle function abnormalities that limit ventilation and can result in respiratory failure • Opioid and sedative medicines decrease respiratory drive in the CNS, with resulting limited ventilatory effort • Injuries, disease, or insult of the CNS can result in loss of respiratory drive and secondary respiratory failure Examples include infiltrating and mass cancers of the CNS, head injury with haemorrhagic mass effect, direct brain injury, infections, primary CNS disorders, and stroke Traumatic factors • Direct thoracic injury may result in a number of abnormalities that can lead to respiratory failure • Direct brain injury can result in loss of respiratory drive • Spinal injury can result in loss of peripheral nerve function and inability to ventilate due to inadequate respiratory muscle function Classification Acute respiratory failure Acute respiratory failure is a life-threatening acute impairment of oxygenation or carbon dioxide (CO₂) elimination Respiratory failure may occur because of impaired gas exchange, decreased ventilation, or both The level of oxygen in the blood becomes dangerously low or the level of carbon dioxide becomes dangerously high Hypoxaemia occurs over a period of hours to days (less than days) Acute respiratory failure can develop quickly and may require emergency treatment.[1] This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Mar 30, 2022 BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice.bmj.com Use of this content is subject to our disclaimer ( Use of this content is subject to our) © BMJ Publishing Group Ltd 2022 All rights reserved Acute respiratory failure Theory THEORY Chronic respiratory failure Chronic respiratory failure is a life-threatening chronic impairment of oxygenation or CO₂ elimination Hypoxaemia occurs over a period of weeks to months (more than days) Chronic respiratory failure develops more slowly and lasts longer than acute respiratory failure.[2] Hypoxaemic respiratory failure Acute respiratory failure that causes a low level of oxygen in the blood without a high level of carbon dioxide Also known as type I respiratory failure.[3] This occurs when the PaO₂ is 80 mmHg) may produce headache, confusion, disorientation, coma, and seizure Patients with severe hypercapnia often appear comfortable and resting while actually progressively hypoventilating and developing severe respiratory acidosis and hypoxaemia secondary to decreased respiratory effort Friends/relatives may describe agitation, slurred speech, and tremor Examination findings An ABCDE assessment is essential for all patients This should be re-assessed regularly and include an evaluation of the airway patency and the patient's ability to protect the airway by checking the airway/gag reflex using a tongue depressor or laryngoscope blade DIAGNOSIS Respiratory distress is usually observed in patients with acute hypoxaemic respiratory failure (type I respiratory failure) Signs of this include tachypnoea (respiratory rate >24 breaths per minute in adults), use of accessory breathing muscles, and cyanosis Without rapid and effective intervention for hypoxaemic respiratory failure, encephalopathy, cardiac dysfunction, multi-system organ failure, and death can occur Hypercapnic respiratory failure (type II respiratory failure) is often more difficult to recognise than hypoxaemic respiratory failure because tachypnoea is often less profound, if present at all Early signs may be subtle and include agitation, slurred speech, asterixis, and decreased level of consciousness Failure to recognise and reverse acute hypercapnic respiratory failure can result in severe respiratory acidosis with subsequent myocardial depression, electrolyte imbalance, and multi-system organ failure Pulse oximetry Pulse oximetry is measured during the examination and provides non-invasive measurements of capillary oxygen saturation (SpO₂) using transmitted and absorbed light sources Low SpO₂ or temporarily decreasing SpO₂ can indicate impending respiratory failure Pulse oximetry can be limited by a number of factors including anaemia, nail polish, low perfusion to oximeter attachment site, and inaccuracy in readings.[15] This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Mar 30, 2022 BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice.bmj.com Use of this content is subject to our disclaimer ( Use of this content is subject to our) © BMJ Publishing Group Ltd 2022 All rights reserved Acute respiratory failure Diagnosis Blood gas analysis Arterial blood gases are required very early and should be obtained as soon as possible after an ABCDE assessment has been made Analysis provides sensitive measures of pulmonary function Low PaO₂ (50 mmHg]) in the presence of hypoxia (PaO₂