Acute respiratory distress syndrome

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Acute respiratory distress syndrome
Other namesRespiratory distress syndrome (RDS), adult respiratory distress syndrome, shock lung, wet lung
ARDSSevere.png
Chest x-ray
Specialty Critical care medicine
Symptoms Shortness of breath, rapid breathing, bluish skin coloration, chest pain, loss of speech [1]
Complications Blood clots, Collapsed lung (pneumothorax), Infections, Scarring (pulmonary fibrosis) [2]
Usual onsetWithin a week [1]
Diagnostic method Adults: PaO2/FiO2 ratio of less than 300 mm Hg [1]
Children: oxygenation index > 4 [3]
Differential diagnosis Heart failure [1]
Treatment Mechanical ventilation, ECMO [1]
Prognosis 35 to 90 % risk of death [1]
Frequency3 million per year [1]

Acute respiratory distress syndrome (ARDS) is a type of respiratory failure characterized by rapid onset of widespread inflammation in the lungs. [1] Symptoms include shortness of breath (dyspnea), rapid breathing (tachypnea), and bluish skin coloration (cyanosis). [1] For those who survive, a decreased quality of life is common. [4]

Contents

Causes may include sepsis, pancreatitis, trauma, pneumonia, and aspiration. [1] The underlying mechanism involves diffuse injury to cells which form the barrier of the microscopic air sacs of the lungs, surfactant dysfunction, activation of the immune system, and dysfunction of the body's regulation of blood clotting. [5] In effect, ARDS impairs the lungs' ability to exchange oxygen and carbon dioxide. [1] Adult diagnosis is based on a PaO2/FiO2 ratio (ratio of partial pressure arterial oxygen and fraction of inspired oxygen) of less than 300 mm Hg despite a positive end-expiratory pressure (PEEP) of more than 5 cm H2O. [1] Cardiogenic pulmonary edema, as the cause, must be excluded. [4]

The primary treatment involves mechanical ventilation together with treatments directed at the underlying cause. [1] Ventilation strategies include using low volumes and low pressures. [1] If oxygenation remains insufficient, lung recruitment maneuvers and neuromuscular blockers may be used. [1] If these are insufficient, extracorporeal membrane oxygenation (ECMO) may be an option. [1] The syndrome is associated with a death rate between 35 and 50%. [1]

Globally, ARDS affects more than 3 million people a year. [1] The condition was first described in 1967. [1] Although the terminology of "adult respiratory distress syndrome" has at times been used to differentiate ARDS from "infant respiratory distress syndrome" in newborns, the international consensus is that "acute respiratory distress syndrome" is the best term because ARDS can affect people of all ages. [6] There are separate diagnostic criteria for children and those in areas of the world with fewer resources. [4]

Signs and symptoms

The signs and symptoms of ARDS often begin within two hours of an inciting event, but have been known to take as long as 1–3 days; diagnostic criteria require a known insult to have happened within 7 days of the syndrome. Signs and symptoms may include shortness of breath, fast breathing, and a low oxygen level in the blood due to abnormal ventilation. [7] [8] Other common symptoms include muscle fatigue and general weakness, low blood pressure, a dry, hacking cough, and fever. [9]

Complications

Complications may include the following: [10]

Other complications that are typically associated with ARDS include: [9]

Causes

There are direct and indirect causes of ARDS depending whether the lungs are initially affected. Direct causes include pneumonia (including bacterial and viral), aspiration, inhalational lung injury, lung contusion, chest trauma, and near-drowning. Indirect causes include sepsis, shock, pancreatitis, trauma (e.g. fat embolism), cardiopulmonary bypass, TRALI, burns, increased intracranial pressure. [11] Fewer cases of ARDS are linked to large volumes of fluid used during post-trauma resuscitation. [12]

Pathophysiology

Micrograph of diffuse alveolar damage, the histologic correlate of ARDS. H&E stain. Hyaline membranes - intermed mag.jpg
Micrograph of diffuse alveolar damage, the histologic correlate of ARDS. H&E stain.

ARDS is a form of fluid accumulation in the lungs not explained by heart failure (noncardiogenic pulmonary edema). It is typically provoked by an acute injury to the lungs that results in flooding of the lungs' microscopic air sacs responsible for the exchange of gases such as oxygen and carbon dioxide with capillaries in the lungs. [13] Additional common findings in ARDS include partial collapse of the alveoli(atelectasis) and low levels of oxygen in the blood (hypoxemia). The clinical syndrome is associated with pathological findings including pneumonia, eosinophilic pneumonia, cryptogenic organizing pneumonia, acute fibrinous organizing pneumonia, and diffuse alveolar damage (DAD). Of these, the pathology most commonly associated with ARDS is DAD, which is characterized by a diffuse inflammation of lung tissue. The triggering insult to the tissue usually results in an initial release of chemical signals and other inflammatory mediators secreted by local epithelial and endothelial cells.[ citation needed ]

Neutrophils and some T-lymphocytes quickly migrate into the inflamed lung tissue and contribute in the amplification of the phenomenon. The typical histological presentation involves diffuse alveolar damage and hyaline membrane formation in alveolar walls. Although the triggering mechanisms are not completely understood, recent research has examined the role of inflammation and mechanical stress.[ citation needed ]

One research group has reported that broncho-alveolar lavage fluid in later-stage ARDS often contains trichomonads, [14] in an amoeboid form (i.e. lacking their characteristic flagellum) which makes them difficult to identify under the microscope. [15]

Diagnosis

A chest x-ray of transfusion-related acute lung injury (left) which led to ARDS. Right is a normal X-ray before the injury. Transfusion-related acute lung injury chest X-ray.gif
A chest x-ray of transfusion-related acute lung injury (left) which led to ARDS. Right is a normal X-ray before the injury.

Diagnostic criteria

Diagnostic criteria for ARDS have changed over time as understanding of the pathophysiology has evolved. The international consensus criteria for ARDS were most recently updated in 2012 and are known as the "Berlin definition". [16] [17] In addition to generally broadening the diagnostic thresholds, other notable changes from the prior 1994 consensus criteria [6] include discouraging the term "acute lung injury", and defining grades of ARDS severity according to degree of decrease in the oxygen content of the blood.[ citation needed ]

According to the 2012 Berlin definition, adult ARDS is characterized by the following: [ citation needed ]

The 2012 "Berlin criteria" are a modification of the prior 1994 consensus conference definitions (see history ). [10]

Medical imaging

Radiologic imaging has long been a criterion for diagnosis of ARDS. Original definitions of ARDS specified that correlative chest X-ray findings were required for diagnosis, the diagnostic criteria have been expanded over time to accept CT and ultrasound findings as equally contributory. Generally, radiographic findings of fluid accumulation (pulmonary edema) affecting both lungs and unrelated to increased cardiopulmonary vascular pressure (such as in heart failure) may be suggestive of ARDS. [18] Ultrasound findings suggestive of ARDS include the following:

Treatment

Acute respiratory distress syndrome is usually treated with mechanical ventilation in the intensive care unit (ICU). Mechanical ventilation is usually delivered through a rigid tube which enters the oral cavity and is secured in the airway (endotracheal intubation), or by tracheostomy when prolonged ventilation (≥2 weeks) is necessary. The role of non-invasive ventilation is limited to the very early period of the disease or to prevent worsening respiratory distress in individuals with atypical pneumonias, lung bruising, or major surgery patients, who are at risk of developing ARDS. Treatment of the underlying cause is crucial. Appropriate antibiotic therapy is started as soon as culture results are available, or if infection is suspected (whichever is earlier). Empirical therapy may be appropriate if local microbiological surveillance is efficient. Where possible the origin of the infection is removed. When sepsis is diagnosed, appropriate local protocols are followed.[ citation needed ]

Mechanical ventilation

The overall goal of mechanical ventilation is to maintain acceptable gas exchange to meet the body's metabolic demands and to minimize adverse effects in its application. The parameters PEEP (positive end-expiratory pressure, to keep alveoli open), mean airway pressure (to promote recruitment (opening) of easily collapsible alveoli and predictor of hemodynamic effects), and plateau pressure (best predictor of alveolar overdistention) are used. [20]

Previously, mechanical ventilation aimed to achieve tidal volumes (Vt) of 12–15 ml/kg (where the weight is ideal body weight rather than actual weight). Recent studies have shown that high tidal volumes can overstretch alveoli resulting in volutrauma (secondary lung injury). The ARDS Clinical Network, or ARDSNet, completed a clinical trial that showed improved mortality when people with ARDS were ventilated with a tidal volume of 6 ml/kg compared to the traditional 12 ml/kg. Low tidal volumes (Vt) may cause a permitted rise in blood carbon dioxide levels and collapse of alveoli [10] because of their inherent tendency to increase shunting within the lung. Physiologic dead space cannot change as it is ventilation without perfusion. A shunt is a perfusion without ventilation within a lung region.[ citation needed ]

Low tidal volume ventilation was the primary independent variable associated with reduced mortality in the NIH-sponsored ARDSNet trial of tidal volume in ARDS. Plateau pressure less than 30 cm H
2O was a secondary goal, and subsequent analyses of the data from the ARDSNet trial and other experimental data demonstrate that there appears to be no safe upper limit to plateau pressure; regardless of plateau pressure, individuals with ARDS fare better with low tidal volumes. [21]

Airway pressure release ventilation

No particular ventilator mode is known to improve mortality in acute respiratory distress syndrome (ARDS). [22]

Some practitioners favor airway pressure release ventilation when treating ARDS. Well documented advantages to APRV ventilation [23] include decreased airway pressures, decreased minute ventilation, decreased dead-space ventilation, promotion of spontaneous breathing, almost 24-hour-a-day alveolar recruitment, decreased use of sedation, near elimination of neuromuscular blockade, optimized arterial blood gas results, mechanical restoration of FRC (functional residual capacity), a positive effect on cardiac output [24] (due to the negative inflection from the elevated baseline with each spontaneous breath), increased organ and tissue perfusion and potential for increased urine output secondary to increased kidney perfusion.[ citation needed ]

A patient with ARDS, on average, spends between 8 and 11 days on a mechanical ventilator; APRV may reduce this time significantly and thus may conserve valuable resources. [25]

Positive end-expiratory pressure

Positive end-expiratory pressure (PEEP) is used in mechanically ventilated people with ARDS to improve oxygenation. In ARDS, three populations of alveoli can be distinguished. There are normal alveoli that are always inflated and engaging in gas exchange, flooded alveoli which can never, under any ventilatory regime, be used for gas exchange, and atelectatic or partially flooded alveoli that can be "recruited" to participate in gas exchange under certain ventilatory regimens. The recruitable alveoli represent a continuous population, some of which can be recruited with minimal PEEP, and others can only be recruited with high levels of PEEP. An additional complication is that some alveoli can only be opened with higher airway pressures than are needed to keep them open, hence the justification for maneuvers where PEEP is increased to very high levels for seconds to minutes before dropping the PEEP to a lower level. PEEP can be harmful; high PEEP necessarily increases mean airway pressure and alveolar pressure, which can damage normal alveoli by overdistension resulting in DAD. A compromise between the beneficial and adverse effects of PEEP is inevitable.[ citation needed ]

The 'best PEEP' used to be defined as 'some' cmH
2O above the lower inflection point (LIP) in the sigmoidal pressure-volume relationship curve of the lung. Recent research has shown that the LIP-point pressure is no better than any pressure above it, as recruitment of collapsed alveoli—and, more importantly, the overdistension of aerated units—occur throughout the whole inflation. Despite the awkwardness of most procedures used to trace the pressure-volume curve, it is still used by some[ who? ] to define the minimum PEEP to be applied to their patients. Some new ventilators can automatically plot a pressure-volume curve.[ citation needed ]

PEEP may also be set empirically. Some authors[ who? ] suggest performing a 'recruiting maneuver'—a short time at a very high continuous positive airway pressure, such as 50 cmH
2O (4.9 kPa)—to recruit or open collapsed units with a high distending pressure before restoring previous ventilation. The final PEEP level should be the one just before the drop in PaO
2 or peripheral blood oxygen saturation during a step-down trial. A large randomized controlled trial of patients with ARDS found that lung recruitment maneuvers and PEEP titration was associated with high rates of barotrauma and pneumothorax and increased mortality. [26]

Intrinsic PEEP (iPEEP) or auto-PEEP—first described by John Marini of St. Paul Regions Hospital—is a potentially unrecognized contributor to PEEP in intubated individuals. When ventilating at high frequencies, its contribution can be substantial, particularly in people with obstructive lung disease such as asthma or chronic obstructive pulmonary disease (COPD). iPEEP has been measured in very few formal studies on ventilation in ARDS, and its contribution is largely unknown. Its measurement is recommended in the treatment of people who have ARDS, especially when using high-frequency (oscillatory/jet) ventilation.[ citation needed ]

Prone position

The position of lung infiltrates in acute respiratory distress syndrome is non-uniform. Repositioning into the prone position (face down) might improve oxygenation by relieving atelectasis and improving perfusion. If this is done early in the treatment of severe ARDS, it confers a mortality benefit of 26% compared to supine ventilation. [27] [28] However, attention should be paid to avoid the SIDS in the management of the respiratory distressed infants by continuous careful monitoring of their cardiovascular system. [28]

Fluid management

Several studies have shown that pulmonary function and outcome are better in people with ARDS who lost weight or whose pulmonary wedge pressure was lowered by diuresis or fluid restriction. [10]

Medications

As of 2019, it is uncertain whether or not treatment with corticosteroids improves overall survival. Corticosteroids may increase the number of ventilator-free days during the first 28 days of hospitalization. [29] One study found that dexamethasone may help. [30] The combination of hydrocortisone, ascorbic acid, and thiamine also requires further study as of 2018. [31]

Inhaled nitric oxide (NO) selectively widens the lung's arteries which allows for more blood flow to open alveoli for gas exchange. Despite evidence of increased oxygenation status, there is no evidence that inhaled nitric oxide decreases morbidity and mortality in people with ARDS. [32] Furthermore, nitric oxide may cause kidney damage and is not recommended as therapy for ARDS regardless of severity. [33]

Alvelestat (AZD 9668) had been quoted according to one review article. [34]

Extracorporeal membrane oxygenation

Extracorporeal membrane oxygenation (ECMO) is mechanically applied prolonged cardiopulmonary support. There are two types of ECMO: Venovenous which provides respiratory support and venoarterial which provides respiratory and hemodynamic support. People with ARDS who do not require cardiac support typically undergo venovenous ECMO. Multiple studies have shown the effectiveness of ECMO in acute respiratory failure. [35] [36] [37] Specifically, the CESAR (Conventional ventilatory support versus Extracorporeal membrane oxygenation for Severe Acute Respiratory failure) trial [38] demonstrated that a group referred to an ECMO center demonstrated significantly increased survival compared to conventional management (63% to 47%). [39]

Ineffective treatments

As of 2019, there is no evidence showing that treatments with exogenous surfactants, statins, beta-blockers or n-acetylcysteine decreases early mortality, late all-cause mortality, duration of mechanical ventilation, or number of ventilator-free days. [29]

Prognosis

The overall prognosis of ARDS is poor, with mortality rates of approximately 40%. [29] Exercise limitation, physical and psychological sequelae, decreased physical quality of life, and increased costs and use of health care services are important sequelae of ARDS.[ citation needed ]

Epidemiology

The annual rate of ARDS is generally 13–23 people per 100,000 in the general population. [40] It is more common in people who are mechanically ventilated with acute lung injury (ALI) occurring in 16% of ventilated people. Rates increased in 2020 due to COVID-19, with some cases also appearing similar to HAPE. [41] [42]

Worldwide, severe sepsis is the most common trigger causing ARDS. [43] Other triggers include mechanical ventilation, sepsis, pneumonia, Gilchrist's disease, drowning, circulatory shock, aspiration, trauma —especially pulmonary contusion —major surgery, massive blood transfusions, [44] smoke inhalation, drug reaction or overdose, fat emboli and reperfusion pulmonary edema after lung transplantation or pulmonary embolectomy. However, the majority of patients with all these conditions mentioned do not develop ARDS. It is unclear why some people with the mentioned factors above do not develop ARDS and others do.[ citation needed ]

Pneumonia and sepsis are the most common triggers, and pneumonia is present in up to 60% of patients and may be either causes or complications of ARDS. Alcohol excess appears to increase the risk of ARDS. [45] Diabetes was originally thought to decrease the risk of ARDS, but this has shown to be due to an increase in the risk of pulmonary edema. [46] [47] Elevated abdominal pressure of any cause is also probably a risk factor for the development of ARDS, particularly during mechanical ventilation.[ citation needed ]

History

Acute respiratory distress syndrome was first described in 1967 by Ashbaugh et al. [10] [48] Initially there was no clearly established definition, which resulted in controversy regarding the incidence and death of ARDS.

In 1988, an expanded definition was proposed, which quantified physiologic respiratory impairment.

1994 American-European Consensus Conference

In 1994, a new definition was recommended by the American-European Consensus Conference Committee [6] [10] which recognized the variability in severity of pulmonary injury. [49]

The definition required the following criteria to be met:

If PaO
2:FiO
2 < 300 mmHg (40 kPa), then the definitions recommended a classification as "acute lung injury" (ALI). Note that according to these criteria, arterial blood gas analysis and chest X-ray were required for formal diagnosis. Limitations of these definitions include lack of precise definition of acuity, nonspecific imaging criteria, lack of precise definition of hypoxemia with regards to PEEP (affects arterial oxygen partial pressure), arbitrary PaO
2 thresholds without systematic data. [50]

2012 Berlin definition

In 2012, the Berlin Definition of ARDS was devised by the European Society of Intensive Care Medicine, and was endorsed by the American Thoracic Society and the Society of Critical Care Medicine. These recommendations were an effort to both update classification criteria in order to improve clinical usefulness and to clarify terminology. Notably, the Berlin guidelines discourage the use of the term "acute lung injury" or ALI, as the term was commonly being misused to characterize a less severe degree of lung injury. Instead, the committee proposes a classification of ARDS severity as mild, moderate, or severe according to arterial oxygen saturation. [16] The Berlin definitions represent the current international consensus guidelines for both clinical and research classification of ARDS.[ citation needed ]

Terminology

ARDS is the severe form of acute lung injury (ALI), and of transfusion-related acute lung injury (TRALI), though there are other causes. The Berlin definition included ALI as a mild form of ARDS. [51] However, the criteria for the diagnosis of ARDS in the Berlin definition excludes many children, and a new definition for children was termed pediatric acute respiratory distress syndrome (PARDS); this is known as the PALICC definition (2015). [52] [53]

Research directions

There is ongoing research on the treatment of ARDS by interferon (IFN) beta-1a to aid in preventing leakage of vascular beds. Traumakine (FP-1201-lyo) is a recombinant human IFN beta-1a drug, developed by the Finnish company Faron Pharmaceuticals, which is undergoing international phase-III clinical trials after an open-label, early-phase trial showed an 81% reduction-in-odds of 28-day mortality in ICU patients with ARDS. [54] The drug is known to function by enhancing lung CD73 expression and increasing production of anti-inflammatory adenosine, such that vascular leaking and escalation of inflammation are reduced. [55]

Aspirin has been studied in those who are at high risk and was not found to be useful. [1]

An intravenous ascorbic acid treatment was tested in the 2019 RCT, in people with ARDS due to sepsis and there was no change in primary endpoints. [56]

See also

Related Research Articles

<span class="mw-page-title-main">Respiratory failure</span> Inadequate gas exchange by the respiratory system

Respiratory failure results from inadequate gas exchange by the respiratory system, meaning that the arterial oxygen, carbon dioxide, or both cannot be kept at normal levels. A drop in the oxygen carried in the blood is known as hypoxemia; a rise in arterial carbon dioxide levels is called hypercapnia. Respiratory failure is classified as either Type 1 or Type 2, based on whether there is a high carbon dioxide level, and can be acute or chronic. In clinical trials, the definition of respiratory failure usually includes increased respiratory rate, abnormal blood gases, and evidence of increased work of breathing. Respiratory failure causes an altered mental status due to ischemia in the brain.

<span class="mw-page-title-main">Mechanical ventilation</span> Method to mechanically assist or replace spontaneous breathing

Mechanical ventilation or assisted ventilation is the medical term for using a machine called a ventilator to fully or partially provide artificial ventilation. Mechanical ventilation helps move air into and out of the lungs, with the main goal of helping the delivery of oxygen and removal of carbon dioxide. Mechanical ventilation is used for many reasons, including to protect the airway due to mechanical or neurologic cause, to ensure adequate oxygenation, or to remove excess carbon dioxide from the lungs. Various healthcare providers are involved with the use of mechanical ventilation and people who require ventilators are typically monitored in an intensive care unit.

<span class="mw-page-title-main">Tidal volume</span> Volume of air displaced between normal inhalation and exhalation

Tidal volume is the volume of air moved into or out of the lungs in one breath. In a healthy, young human adult, tidal volume is approximately 500 ml per inspiration at rest or 7 ml/kg of body mass.

<span class="mw-page-title-main">Pulmonary edema</span> Fluid accumulation in the tissue and air spaces of the lungs

Pulmonary edema, also known as pulmonary congestion, is excessive fluid accumulation in the tissue or air spaces of the lungs. This leads to impaired gas exchange, most often leading to dyspnea which can progress to hypoxemia and respiratory failure. Pulmonary edema has multiple causes and is traditionally classified as cardiogenic or noncardiogenic.

<span class="mw-page-title-main">Extracorporeal membrane oxygenation</span> Technique of providing both cardiac and respiratory support

Extracorporeal membrane oxygenation (ECMO), is a form of extracorporeal life support, providing prolonged cardiac and respiratory support to persons whose heart and lungs are unable to provide an adequate amount of oxygen, gas exchange or blood supply (perfusion) to sustain life. The technology for ECMO is largely derived from cardiopulmonary bypass, which provides shorter-term support with arrested native circulation. The device used is a membrane oxygenator, also known as an artificial lung.

<span class="mw-page-title-main">Pulmonary hemorrhage</span> Medical condition

Pulmonary hemorrhage is an acute bleeding from the lung, from the upper respiratory tract and the trachea, and the pulmonary alveoli. When evident clinically, the condition is usually massive. The onset of pulmonary hemorrhage is characterized by a cough productive of blood (hemoptysis) and worsening of oxygenation leading to cyanosis. Treatment should be immediate and should include tracheal suction, oxygen, positive pressure ventilation, and correction of underlying abnormalities such as disorders of coagulation. A blood transfusion may be necessary.

Positive end-expiratory pressure (PEEP) is the pressure in the lungs above atmospheric pressure that exists at the end of expiration. The two types of PEEP are extrinsic PEEP and intrinsic PEEP. Pressure that is applied or increased during an inspiration is termed pressure support.PEEP is a therapeutic parameter set in the ventilator, or a complication of mechanical ventilation with air trapping (auto-PEEP).

High-frequency ventilation is a type of mechanical ventilation which utilizes a respiratory rate greater than four times the normal value and very small tidal volumes. High frequency ventilation is thought to reduce ventilator-associated lung injury (VALI), especially in the context of ARDS and acute lung injury. This is commonly referred to as lung protective ventilation. There are different types of high-frequency ventilation. Each type has its own unique advantages and disadvantages. The types of HFV are characterized by the delivery system and the type of exhalation phase.

Ventilator-associated lung injury (VALI) is an acute lung injury that develops during mechanical ventilation and is termed ventilator-induced lung injury (VILI) if it can be proven that the mechanical ventilation caused the acute lung injury. In contrast, ventilator-associated lung injury (VALI) exists if the cause cannot be proven. VALI is the appropriate term in most situations because it is virtually impossible to prove what actually caused the lung injury in the hospital.

<span class="mw-page-title-main">Pulmonary contusion</span> Internal bruise of the lungs

A pulmonary contusion, also known as lung contusion, is a bruise of the lung, caused by chest trauma. As a result of damage to capillaries, blood and other fluids accumulate in the lung tissue. The excess fluid interferes with gas exchange, potentially leading to inadequate oxygen levels (hypoxia). Unlike pulmonary laceration, another type of lung injury, pulmonary contusion does not involve a cut or tear of the lung tissue.

<span class="mw-page-title-main">Diffuse alveolar damage</span> Medical condition

Diffuse alveolar damage (DAD) is a histologic term used to describe specific changes that occur to the structure of the lungs during injury or disease. Most often DAD is described in association with the early stages of acute respiratory distress syndrome (ARDS). DAD can be seen in situations other than ARDS (such as acute interstitial pneumonia) and ARDS can occur without DAD.

<span class="mw-page-title-main">Airway pressure release ventilation</span> Pressure control mode of mechanical ventilation

Airway pressure release ventilation (APRV) is a pressure control mode of mechanical ventilation that utilizes an inverse ratio ventilation strategy. APRV is an applied continuous positive airway pressure (CPAP) that at a set timed interval releases the applied pressure. Depending on the ventilator manufacturer, it may be referred to as BiVent. This is just as appropriate to use, since the only difference is that the term APRV is copyrighted.

Modes of mechanical ventilation are one of the most important aspects of the usage of mechanical ventilation. The mode refers to the method of inspiratory support. In general, mode selection is based on clinician familiarity and institutional preferences, since there is a paucity of evidence indicating that the mode affects clinical outcome. The most frequently used forms of volume-limited mechanical ventilation are intermittent mandatory ventilation (IMV) and continuous mandatory ventilation (CMV). There have been substantial changes in the nomenclature of mechanical ventilation over the years, but more recently it has become standardized by many respirology and pulmonology groups. Writing a mode is most proper in all capital letters with a dash between the control variable and the strategy.

Inverse ratio ventilation (IRV) is not necessarily a mode of mechanical ventilation though it may be referred to as such. IRV is a strategy of ventilating the lungs in such a way that the amount of time the lungs are in inhalation is greater than the amount of time they are in exhalation, allowing for a constant inflation of the lungs, ensuring they remain "recruited". The primary goal for IRV is improved oxygenation by forcing inspiratory time to be greater than expiratory time increasing the mean airway pressure and potentially improving oxygenation. Normal I:E ratio is 5:6, so forcing the I:E to be 2:1, 3:1, 4:1, is the source of the term for the strategy.

Within the medical field of respiratory therapy, Open lung ventilation is a strategy that is utilized by several modes of mechanical ventilation to combine low tidal volume and applied PEEP to maximize recruitment of alveoli. The low tidal volume aims to minimize alveolar overdistention and the PEEP minimizes cyclic atelectasis. Working in tandem the effects from both decrease the risk of ventilator-associated lung injury.

Prone ventilation, sometimes called prone positioning or proning, is a method of mechanical ventilation with the patient lying face-down (prone). It improves oxygenation in most patients with acute respiratory distress syndrome (ARDS) and reduces mortality. The earliest trial investigating the benefits of prone ventilation occurred in 1976. Since that time, many meta-analyses and one randomized control trial, the PROSEVA trial, have shown an increase in patients' survival with the more severe versions of ARDS. There are many proposed mechanisms, but they are not fully delineated. The proposed utility of prone ventilation is that this position will improve lung mechanics, improve oxygenation, and increase survival. Although improved oxygenation has been shown in multiple studies, this position change's survival benefit is not as clear. Similar to the slow adoption of low tidal volume ventilation utilized in ARDS, many believe that the investigation into the benefits of prone ventilation will likely be ongoing in the future.

<span class="mw-page-title-main">Pathophysiology of acute respiratory distress syndrome</span>

The pathophysiology of acute respiratory distress syndrome involves fluid accumulation in the lungs not explained by heart failure. It is typically provoked by an acute injury to the lungs that results in flooding of the lungs' microscopic air sacs responsible for the exchange of gases such as oxygen and carbon dioxide with capillaries in the lungs. Additional common findings in ARDS include partial collapse of the lungs (atelectasis) and low levels of oxygen in the blood (hypoxemia). The clinical syndrome is associated with pathological findings including pneumonia, eosinophilic pneumonia, cryptogenic organizing pneumonia, acute fibrinous organizing pneumonia, and diffuse alveolar damage (DAD). Of these, the pathology most commonly associated with ARDS is DAD, which is characterized by a diffuse inflammation of lung tissue. The triggering insult to the tissue usually results in an initial release of chemical signals and other inflammatory mediators secreted by local epithelial and endothelial cells.

Carolyn S. Calfee is a Professor of Medicine and Anaesthesia at the University of California, San Francisco. She works in intensive care at the UCSF Medical Center where she specialises in acute respiratory distress syndrome. During the COVID-19 pandemic Calfee studied why SARS-CoV-2 patients experienced such different symptoms.

<span class="mw-page-title-main">Proning</span> Nursing technique

Proning or prone positioning is the placement of patients into a prone position so that they are lying on their front. This is used in the treatment of patients in intensive care with acute respiratory distress syndrome (ARDS). It has been especially tried and studied for patients on ventilators but, during the COVID-19 pandemic, it is being used for patients with oxygen masks and CPAP as an alternative to ventilation.

The treatment and management of COVID-19 combines both supportive care, which includes treatment to relieve symptoms, fluid therapy, oxygen support as needed, and a growing list of approved medications. Highly effective vaccines have reduced mortality related to SARS-CoV-2; however, for those awaiting vaccination, as well as for the estimated millions of immunocompromised persons who are unlikely to respond robustly to vaccination, treatment remains important. Some people may experience persistent symptoms or disability after recovery from the infection, known as long COVID, but there is still limited information on the best management and rehabilitation for this condition.

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