It is a medical condition in critically ill or severely injured patients and is characterized by generalized inflammation in the lungs.
The distinctive feature of acute respiratory distress syndrome is the diffuse lesion of the cells that form the barrier of the microscopic alveoli of the lungs, the surfactant dysfunction, the activation of the innate immune response, and the dysfunction of the regulation of the body of the coagulation and bleeding.
In effect, acute respiratory distress syndrome affects the ability of the lungs to exchange oxygen and carbon dioxide with the blood through a thin layer of microscopic air sacs of the lungs known as alveoli.
The syndrome is associated with a mortality rate between 20 and 50%. The risk of death varies according to the severity, the age of the person, and the presence of other underlying medical conditions.
Although the terminology of “respiratory distress syndrome in adults” has sometimes been used to differentiate acute respiratory distress syndrome from “infant respiratory distress syndrome” in newborns. The international consensus is that “acute respiratory distress syndrome” is the best term because of acute respiratory distress.
The syndrome can affect people of all ages.
Signs and symptoms
The signs and symptoms of acute respiratory distress syndrome often begin within two hours of an inciting event but may occur after 1-3 days. Signs and symptoms may include difficulty breathing, rapid breathing, and a low oxygen level in the blood due to abnormal ventilation.
The diffuse involvement of the pulmonary system that results in acute respiratory distress syndrome generally occurs in the context of a critical illness.
Acute respiratory distress syndrome can be observed in cases of pulmonary (pneumonia) or severe systemic (sepsis) infection, following trauma, multiple blood transfusions, severe burns, severe inflammation of the pancreas (pancreatitis), drowning, or other aspiration events, reactions to medications or injuries by inhalation.
Some acute respiratory distress syndrome cases are related to large volumes of fluid used during post-traumatic resuscitation.
The diagnostic criteria for acute respiratory distress syndrome have changed over time as the understanding of physiopathology has evolved.
The international consensus criteria for acute respiratory distress syndrome were updated in 2012 and are known as the “Berlin definition.”
In addition to generally broadening the diagnostic thresholds, other notable changes from the previous consensus criteria of 1994 include discouraging the term “acute lung injury” and defining degrees of severity of acute respiratory distress syndrome according to the degree of decrease in oxygen content from the blood.
According to the Berlin definition of 2012, acute respiratory distress syndrome is characterized by the following:
- Acute onset lung injury within one week of apparent clinical insult and respiratory symptoms progression.
- Bilateral opacities in the chest images (chest x-ray or computed tomography) are not explained by another pulmonary pathology (effusion, pneumothorax, or nodules).
- Respiratory failure is not explained by heart failure or volume overload.
Decrease in pao2 / fio2 ratio (a decreased pao2 / fio2 ratio indicates reduced arterial oxygenation from available inhaled gas):
- Syndrome of mild acute respiratory distress: 201 – 300 mmHg (≤ 39.9 kph).
- Moderate acute respiratory distress syndrome: 101 – 200 mmHg (≤ 26.6 kph).
- Severe acute respiratory distress syndrome: ≤ 100 mmHg (≤ 13.3 kpa).
The Berlin definition requires a minimum positive final expiratory pressure (PEEP) of 5 cmH2O for consideration of the PaO2 / FiO2 ratio.
This degree of positive end-expiratory pressure can be administered non-invasively with continuous positive airway pressure to diagnose mild acute respiratory failure syndrome.
Keep in mind that the “Berlin Criteria” of 2012 modify the previous definitions of the 1994 consensus conference.
Radiological images have long been a criterion for diagnosing acute respiratory distress syndrome.
Although the original definitions of acute respiratory distress syndrome specified that correlative chest radiography findings were necessary for diagnosis, diagnostic criteria have been extended over time to accept computed tomography scanning and ultrasound findings. contributory
In general, radiographic findings of fluid accumulation (pulmonary edema) that affect both lungs and are not related to increased cardiopulmonary vascular pressure (as in heart failure) may suggest acute respiratory distress syndrome.
Sonographic findings suggestive of acute respiratory distress syndrome include the following:
- Previous subpleural consolidations.
- Absence or reduction of the pulmonary slip.
- “Protected spaces” of the normal parenchyma.
- Abnormalities of the pleural line (irregular thickened fragmented pleural line).
- Inhomogeneous distribution of B lines (a characteristic ultrasound finding that suggests an accumulation of fluid in the lungs).
Acute respiratory distress syndrome is a form of fluid accumulation in the lungs that is not explained by heart failure ( non-cardiogenic pulmonary edema ).
An acute injury typically causes it to the lungs and results in the flooding of the microscopic alveoli of the lungs responsible for the exchange of gases such as oxygen and carbon dioxide with capillaries in the lungs.
Additional common findings in acute respiratory distress syndrome include the partial collapse of the lungs (atelectasis) and low oxygen levels in the blood ( hypoxemia ).
The clinical syndrome is associated with pathological findings that include pneumonia, eosinophilic pneumonia, organized cryptogenic pneumonia, acute fibrinous organized pneumonia, and diffuse alveolar damage.
Of these, the pathology most commonly associated with acute respiratory distress syndrome is diffuse alveolar damage, characterized by diffuse inflammation of the lung tissue.
The tissue trigger usually results in an initial release of chemical signals and other inflammatory mediators secreted by local epithelial and endothelial cells.
Neutrophils and some T lymphocytes migrate rapidly into inflamed lung tissue and contribute to the amplification of the phenomenon. The typical histological presentation involves diffuse alveolar damage and hyaline membrane formation in the alveolar walls.
Although the trigger mechanisms are not fully understood, recent research has examined the role of inflammation and mechanical stress.
Inflammation, caused by sepsis, causes endothelial cell dysfunction, leakage of fluid from the capillaries, and affects the drainage of fluid from the lungs.
A high concentration of inspired oxygen often becomes necessary at this stage and can facilitate a “respiratory burst” in immune cells.
In a secondary phase, the dysfunction of the endothelial cells causes the cells and the inflammatory exudate to enter the alveoli.
This pulmonary edema increases the thickness of the layer that separates the blood in the capillary from the alveoli space, increasing the distance that oxygen must diffuse to reach the blood.
This impairs gas exchange and leads to hypoxia, an increase in breathing work, and finally induces healing of the lungs’ alveoli.
The accumulation of fluid in the lungs and the decrease in surfactant production by type II pneumocytes can collapse complete air sacs or be wholly filled with fluid.
This loss of aeration further contributes to the short circuit from right to left in acute respiratory distress syndrome. A traditional right-to-left shunt refers to blood passing from the right side of the heart to the left side without moving to the lung’s capillaries to get more oxygen (for example, as seen in a permeable foramen ovale).
In acute respiratory distress syndrome, a right lung to left shunt occurs inside the lungs since some blood from the right side of the heart will enter capillaries that can not exchange gas with damaged air sacs full of fluid and waste of acute respiratory distress syndrome.
As the alveoli contain progressively less gas, the blood flowing through the alveolar capillaries is progressively less oxygenated, which causes massive shunting within the lung.
The collapse of alveoli and small airways interferes with the standard gas exchange process. It is common to see patients with a PaO2 of 60 mmHg (8.0 kPa) despite mechanical ventilation with 100% inspired oxygen.
The loss of aeration can follow different patterns depending on the nature of the underlying disease and other factors. These are usually distributed to the lower lobes of the lungs in their posterior segments and correspond approximately to the initial infected area.
In sepsis or acute respiratory distress syndrome induced by trauma, infiltrates are usually more irregular and diffuse. The posterior and basal segments are always more affected, but the distribution is even less homogeneous.
The loss of aeration also causes essential changes in the mechanical properties of the lungs that are fundamental in amplifying inflammation and progression to acute respiratory distress syndrome in mechanically ventilated patients.
As the loss of aeration and the underlying disease progress, the final tidal volume grows to a level incompatible with life.
Therefore, mechanical ventilation is initiated to relieve the muscles responsible for breathing (respiratory muscles) of your work and protect the affected person’s respiratory tract.
However, mechanical ventilation may be a risk factor for developing or worsening acute respiratory distress syndrome.
In addition to the infectious complications derived from invasive ventilation with endotracheal intubation, positive pressure ventilation directly alters pulmonary mechanics during acute respiratory distress syndrome.
When these techniques are used, there is higher mortality by barotrauma.
In 1998, Amato et al. published an article that shows a substantial improvement in the outcome of ventilated patients with lower tidal volumes (tidal volumes, Vt) (6 ml · kg-1). This result was confirmed in a 2000 study sponsored by the National Institutes of Health.
Both studies were widely criticized for several reasons, and the authors were not the first to experiment with lower volume ventilation. Still, they increased the understanding of mechanical ventilation and acute respiratory distress syndrome.
This form of stress is thought to be applied by the transpulmonary pressure (gradient) (Pl) generated by the ventilator or, better yet, by its cyclical variations. The best result obtained in individuals ventilated with a smaller tidal volume can be interpreted as a beneficial effect of the lower PI.
The way Pl is applied to the alveolar surface determines the shear stress to the alveoli exposed.
The syndrome of acute respiratory distress is characterized by a generally heterogeneous reduction of the air space and, therefore, by a tendency towards a higher PI in the same tidal volume and towards more significant stress in less diseased units.
The heterogeneity of the alveoli in the different stages of the disease is further increased by the gravitational gradient to which they are exposed and the different perfusion pressures at which blood flows through them.
The different mechanical properties of the alveoli in acute respiratory distress syndrome can be interpreted as having variable time constants: the product of alveolar compliance resistance.
It is said that the slow alveoli are “kept open” by positive pressure at the end of expiration, a characteristic of modern respirators that maintains a positive force in the airways throughout the respiratory cycle.
A higher average pressure throughout the cycle delays the collapse of the diseased alveoli but must be weighed against the corresponding elevation in the Pl/plateau pressure.
Newer ventilatory approaches attempt to maximize mean airway pressure by their ability to “recruit” collapsed alveoli while minimizing shear stress caused by frequent openings and closures of aerated units.
Mechanical ventilation can worsen the inflammatory response in people with acute respiratory distress syndrome by inducing hyperinflation of the alveoli and increased shear stress with frequent openings and closures of collapsible alveoli.
The stress index is measured during assisted mechanical ventilation and controlled by constant flow volume without changing the ventilatory reference pattern.
The identification of the most stable portion of the inspiratory flow waveform (F) is adjusted to the corresponding part of the airway pressure waveform (Paw) in the following equation of power:
Paw = a × tb + c: Where the coefficient b-the stress index-describes the shape of the curve. The stress index shows constant compliance if the value is around 1, increases compliance during inspiration if the value is below one, and decreases if the value is above 1.
Ranieri, Grasso, et al. establish a strategy guided by the stress index with the following rules:
- The stress index was below 0.9, and the positive pressure at the end of expiration was increased.
- The stress index was between 0.9 and 1.1; no change was made.
- The stress index above 1.1 positive end-expiratory pressure decreased.
Alveolar hyperinflation in patients with focal respiratory distress syndrome ventilated with the Clinical Network protocol of acute respiratory distress syndrome is mitigated by a physiological approach for the positive fixation of the final expiratory pressure based on the measurement of the stress index.
If the underlying disease or the deleterious factor is not eliminated, the number of inflammatory mediators released by the lungs in acute respiratory distress syndrome can cause a systemic inflammatory response syndrome or sepsis if there is a pulmonary infection.
The evolution towards shock syndrome or multiple organic dysfunctions follows paths analogous to the pathophysiology of sepsis. This leads to altered oxygenation, which is the central problem of acute respiratory distress syndrome, as well as respiratory acidosis.
Respiratory acidosis in acute respiratory distress syndrome is often caused by ventilation techniques such as permissive hypercapnia, which attempts to limit ventilator-induced lung injury in acute respiratory distress syndrome.
The result is a critical illness in which the “endothelial disease” of severe sepsis or the systemic inflammatory response syndrome is worsened by pulmonary dysfunction, which further affects the supply of oxygen to the cells.
Acute respiratory distress syndrome is usually treated with mechanical ventilation in the intensive care unit.
Mechanical ventilation is usually administered through a rigid tube that enters the oral cavity and is secured in the airway (endotracheal intubation) or by tracheotomy when prolonged ventilation is required (≥2 weeks).
The role of non-invasive ventilation is limited to the very early period of the disease or to preventing the worsening of respiratory distress in individuals with atypical pneumonia, pulmonary hematomas, or patients with significant surgery who are at risk of developing acute respiratory distress syndrome.
The treatment of the underlying cause is crucial. Appropriate antibiotic therapy should be administered as soon as the microbiological culture results become available or clinical infection is suspected (whichever occurs first).
Empirical therapy may be appropriate if local microbiological surveillance is efficient. The origin of the infection, when treated surgically, should be eliminated. When sepsis is diagnosed, proper local protocols should be promulgated.
The general objective of mechanical ventilation is to maintain an acceptable gas exchange to satisfy the body’s metabolic demands and minimize adverse effects in its application.
Positive pressure parameters are used at the end of expiration to keep the alveoli open, the airway pressure (to promote the recruitment (opening) of easily collapsible alveoli and the predictor of hemodynamic effects), and the plateau pressure (better predictor of alveolar overdistension).
Previously, mechanical ventilation aimed to reach tidal volumes (tidal volumes) of 12-15 ml/kg (where the weight is the ideal body weight instead of the actual weight).
Recent studies have shown that high tidal volumes can overstretch the alveoli and produce volutrauma (secondary lung injury).
The Clinical Network of acute respiratory distress syndrome completed a clinical trial that showed an improvement in mortality when people with acute respiratory distress syndrome were ventilated with a tidal volume of 6 ml/kg compared to the traditional 12 ml/kg.
Low tidal volumes (Vt) can cause an allowable increase in carbon dioxide levels in the blood and collapse of the alveoli due to their inherent tendency to increase shunt within the lung.
The physiological dead space can not change since it is ventilation without perfusion. A shunt is a perfusion without ventilation.
Ventilation with low tidal volume was the primary independent variable associated with reducing mortality in the Clinical Network trial of acute respiratory distress syndrome t sponsored by the National Institutes of Health on tidal volume in respiratory distress syndrome sensitive.
The pressure of the plateau of less than 30cm H2O was a secondary objective, and subsequent analyzes of the data from the Clinical Network test of acute respiratory distress syndrome and other experimental data show that there does not appear to be a safe upper limit for pressure. Plateau.
Regardless of plateau pressure, people with acute respiratory distress syndrome fare better with low tidal volumes.
Ventilation of airway pressure release
No particular ventilator mode is known to improve mortality in acute respiratory distress syndrome.
Some doctors favor ventilation with the release of pressure in the airway when treating acute respiratory distress syndrome.
The well-documented advantages of ventilation with pressure release in the respiratory tract include:
- Decrease in airway pressure.
- Decreased minute ventilation, reduced ventilation of the dead space, and promotion of spontaneous breathing.
- Alveolar recruitment almost 24 hours a day.
- Decrease in the use of sedation.
- Almost elimination of neuromuscular block.
- Optimized results of arterial gas.
- Mechanical restoration of functional residual capacity.
- A positive effect on cardiac output (due to the negative inflection of the elevated baseline with each spontaneous breath).
- Increased organ and tissue perfusion.
- Potential for increased urine production secondary to renal perfusion.
A patient with acute respiratory distress syndrome, on average, spends between 8 and 11 days with a mechanical ventilator. Ventilation with pressure release in the airway can significantly reduce this time and conserve valuable resources.
Positive pressure at the end of expiration
In mechanically ventilated patients with acute respiratory distress syndrome, positive end-expiratory pressure is used to improve oxygenation. In acute respiratory distress syndrome, three populations of alveoli can be distinguished.
There are normal alveoli that are always inflated and participate in the exchange of gases, flooded alveoli that never, under any ventilation regime, can be used for gas exchange, and atelectasis or partially flooded alveoli that can be “recruited” to participate in the business of gases under specific ventilatory regimes.
The recruitable alveoli represent a continuous population, some of which can be recruited with minimal positive pressure at the end of expiration. Others can only be recruited with high levels of positive pressure at the end of expiration.
An additional complication is that some alveoli can only be opened with airway pressures higher than those needed to keep them open, hence the justification for maneuvers where the positive pressure at the end of expiration increases to very high levels for seconds or minutes before dropping a positive lot of expiratory pressure to a lower level.
Positive pressure at the end of expiration can be harmful; High Positive end-expiratory pressure increases the mean airway pressure and alveolar pressure, which can damage normal alveoli by overdistension, resulting in diffuse alveolar damage.
To compromise between the beneficial and adverse effects of positive pressure at the end of expiration.
The “best positive pressure at the end of expiration” used to be defined as “something” of cmH2O above the lowest inflection point in the sigmoid pressure-volume relationship of the lung.
Recent research has shown that the pressure of the LIP point is no better than any higher pressure since the recruitment of collapsed alveoli and, more importantly, the overdistention of the aerated units occurs throughout inflation.
Despite the discomfort of most of the procedures used to track the pressure-volume curve, some still use it to define the positive pressure at the end of the minimum expiration applied to their patients. Some new fans can automatically draw a pressure-volume curve.
The positive pressure at the end of expiration can also be established empirically. Some authors suggest performing a “recruitment maneuver”: a short time at a very high continuous positive pressure in the airways, such as 50 cmH2O (4.9 kPa), to recruit or open collapsed units with high-pressure distension before restoring previous ventilation.
At the end of expiration, the final level of positive pressure should be just before the drop in PaO2 or peripheral blood oxygen saturation during a reduction test.
First described by John Marini of St. Paul Regions Hospital, positive end-expiratory pressure or end-expiratory positive pressure is a potentially unrecognized contributor to end-expiratory positive pressure in intubated individuals.
Its contribution can be substantial when ventilating at high frequencies, particularly in people with obstructive lung disease such as asthma or chronic obstructive pulmonary disease.
The positive pressure at the end of intrinsic expiration has been measured in very few formal studies on ventilation in patients with acute respiratory distress syndrome, and its contribution is largely unknown.
Its measurement is recommended in treating people with acute respiratory distress syndrome, especially when using high-frequency ventilation (oscillatory / jet).
The position of the pulmonary infiltrates in acute respiratory distress syndrome is not uniform. Repositioning prone (upside down) may improve oxygenation by relieving atelectasis and improving perfusion.
If this is done early in treating severe acute respiratory distress syndrome, it confers a mortality benefit of 26% compared to passive ventilation.
Several studies have shown that lung function and outcome are better in people with acute respiratory distress syndrome who lost weight or whose wedge pressure was reduced by diuresis or fluid restriction.
Inhaled nitric oxide selectively widens the lung’s arteries, allowing greater blood flow to open the alveoli for gas exchange.
Despite an increase in oxygenation status, no evidence that inhaled nitric oxide decreases morbidity and mortality in people with acute respiratory distress syndrome.
In addition, nitric oxide can cause kidney damage and is not recommended as therapy for acute respiratory distress syndrome, regardless of severity.
No prospective controlled clinical trial has demonstrated a significant benefit in the mortality of exogenous surfactant in acute respiratory distress syndrome in adults.
Extracorporeal membrane oxygenation
Oxygenation by the extracorporeal membrane is mechanically applied with prolonged cardiopulmonary support.
There are two types of extracorporeal membrane oxygenation: venovenous, which provides respiratory and veno-arterial support, and respiratory and hemodynamic support.
People with acute respiratory distress syndrome who do not require cardiac support undergo venovenous extracorporeal membrane oxygenation.
Multiple studies have demonstrated the effectiveness of extracorporeal membrane oxygenation in acute respiratory failure.
Specifically, conventional ventilatory support versus extracorporeal membrane oxygenation for the acute respiratory failure trial demonstrated that a group referred to an extracorporeal membrane oxygenation center demonstrated a significantly higher survival than conventional treatment (63% to 47%).
Since acute respiratory distress syndrome is a severe condition that requires invasive forms of therapy, it is not without risks. The complications to consider include the following:
- Pulmonary: barotrauma (volutrauma), pulmonary embolism, pulmonary fibrosis, and pneumonia.
- Gastrointestinal: hemorrhage (ulcer), dysmotility, pneumoperitoneum, bacterial translocation.
- Cardiac: abnormal heart rhythms, myocardial dysfunction.
- Kidney: acute renal failure, positive fluid balance.
- Mechanical: vascular injury, pneumothorax (placing a catheter in the pulmonary artery), tracheal lesion/stenosis (the result of intubation and irritation by endotracheal tube.
- Nutritional: malnutrition (catabolic state), electrolyte deficiency.