Increased alveolar capillary hydrostatic pressure, as in left heart failure Heart failure (HF) Heart failure (HI) is a syndrome of ventricular dysfunction. Left ventricular failure leads to shortness of breath and fatigue; right ventricular failure leads to peripheral and. Learn more or hypervolemia
Increased alveolar capillary permeability, as in a predisposition to Acute Respiratory Distress Syndrome (ARDS)
Blood (as seen in diffuse alveolar hemorrhage Diffuse alveolar hemorrhage Diffuse alveolar hemorrhage is persistent or recurrent pulmonary hemorrhage. There are many causes, but autoimmune diseases are the most common. Most patients. Learn more occurs) or inflammatory exudates (as seen in pneumonia Overview of Pneumonia (Lung Inflammation) Pneumonia is an acute inflammation of the lungs caused by infections. The initial diagnosis is usually (Note. d. Red.: auscultatory or) based on a chest x-ray. Learn more or other inflammatory lung diseases occur)
ARDS is divided into 3 severity levels: mild, moderate, and severe, based on oxygenation defects and clinical criteria (see Table: Berlin definition of ARDS Berlin definition of ARDS Acute hypoxemic respiratory failure is high-grade arterial hypoxemia that cannot be reversed by O2 administration alone. Caused by an extended. Learn more ). Mild severity corresponds to the previous category of acute lung injury (ALI).
In ARDS, pulmonary or systemic inflammation leads to release of cytokines and other proinflammatory substances. Cytokines activate alveolar macrophages and cause neutrophils to migrate into the lungs. Neutrophils cause release of leukotrienes, oxidants, platelet activator, and proteases. These agents cause damage to the capillary endothelium and alveolar endothelial lining. There is a break in the barrier between the capillary space and the air-filled space. Edema fluid, proteins and cellular detritus spill into the airspace and interstitium, destroying the surfactant and thus leading to airway collapse, ventilation-perfusion mismatch, shunt formation, and pulmonary hypertension. Airway collapse is more common in dependent lung areas.
Among the causes of ARDS (see Table: Causes of ARDS Causes of ARDS Acute hypoxemic respiratory failure refers to high-grade arterial hypoxemia that cannot be reversed by O2 administration alone. Caused by an extended. Learn more can belong:
Direct lung injury (z. B, pneumonia, acid reflux)
Indirect lung injury (z. B. sepsis, pancreatitis, massive blood transfusion, non-thoracic trauma)
In both types of AHRF, flooded or collapsed air spaces do not allow inspired gas to enter, so blood passing through these alveoli remains at the mixed venous oxygen level, no matter how high the fractional inspired O2(F io 2). This constant admixture of deoxygenated blood into the pulmonary veins causes arterial hypoxemia. In contrast, hypoxemia resulting from ventilated pulmonary alveoli that have less ventilation than perfusion (d. h. a low ventilation-perfusion rate, as in asthma or chronic obstructive pulmonary disease or, to some extent, in ARDS), be controlled with supplemental O2.
Symptoms and complaints
Acute hypoxemia ( drop in oxygen saturation Drop in oxygen saturation Intensive care patients (as well as other patients) can experience hypoxia (oxygen saturation Learn more ) during their hospital stay even in the absence of respiratory disorders can lead to dyspnea, agitation and anxiety. This may be accompanied by confusion with alteration of consciousness. Other associated symptoms are cyanosis, tachypnea, tachycardia, and increased sweating. Cardiac arrhythmias and coma may eventually follow. Inspiratory opening of closed airways causes crackles detected during chest auscultation; crackles are typically diffuse but sometimes worse at the lung bases, especially in the left lower lobe. Jugular vein congestion results in cases of high PEEP or severe ventricular pump failure.
X-ray chest and ABGA
Clinical definition (see table: Berlin definition of ARDS Berlin definition of ARDS Acute hypoxemic respiratory failure is high-grade arterial hypoxemia that cannot be reversed by just giving O2. Caused by an extended. Learn more )
Hypoxemia is often first realized by pulse oximetry. Patients with low O2 saturation should have an arterial blood gas analysis and a lung x-ray taken. They should then be treated by O2 administration until test results are available.
Doesn’t this O2 administration lead to an increase in arterial O2 saturation> 90%, a right-left shunt is suspected. A previously unnoticed alveolar infiltrate on radiography, on the other hand, indicates fluid accumulation in the alveolar regions and is then more likely to be the cause than an intracardiac shunt. But at the onset of the disease, hypoxemia often occurs before changes are seen on x-ray.
Once an AHRF is diagnosed, the cause must be elucidated. Pulmonary and cardiac causes have to be taken into consideration. In some cases, a present known disorder (such as acute myocardial infarction, pancreatitis, or sepsis) is obviously the cause of this clinical situation. In other cases, the medical history is the key factor. Pneumonia may be a probable cause in immunocompromised patients. Acute alveolar hemorrhage is also possible in conditions after bone marrow transplantation or in collagenoses. Frequently, intensive care patients requiring resuscitation have received larger volumes of fluid. Consequences of ventricular pump weaknesses and fluid overload with the resulting image of an AHRF must be distinguished from those cases in which a "low-pressure AHRF" underlies (for example, due to sepsis or apneumonia).
Pulmonary edema due to high pressure must be assumed whenever a third heart sound can be auscultated, jugular venous congestion develops, peripheral edema is evident, and diffuse central infiltrates are present. Cardiomegaly and an unusually dilated vascular pedicle on chest X-ray are other signs. The diffuse, bilateral infiltrates in the context of ARDS are generally found more peripherally. Focal infiltrations, on the other hand, are usually caused by lobar pneumonia, atelectasis or pulmonary contusion. Even though echocardiography can show left heart failure, suggesting a cardiac cause, these findings are not specific because sepsis can also affect myocardial contractility.
When ARDS is diagnosed but the cause is unknown (z. B.: trauma, sepsis, severe pulmonary infection, pancreatitis), a review of medications and recent investigations, therapeutic measures, and clinical interventions may help uncover previously overlooked causes. This may also include contrast studies, air emboli, or transfusions. If no predisposing cause can be uncovered, some experts recommend bronchoscopy with bronchoalveolar lavage to rule out alveolar hemorrhage and eosinophilic pneumonia. If this procedure is unsuccessful, a lung biopsy is performed to rule out other disorders (z. B. exogenous allergic alveolitis, acute interstitial pneumonia).
Prognosis is highly variable and depends on a variety of factors, including respiratory failure etiology, disease severity, age, and chronic health status. In ALI/ARDS, the overall mortality rate was very high (40-60%) but has decreased to 25-40% in recent years. Reasons for this are probably the improvement of mechanical ventilation and the progress of sepsis therapy. However, mortality remains very high (> 40%) in patients with severe ARDS (d. h. those with a Pa O 2: F IO 2
However, residual pulmonary symptoms are more often found in patients with protracted and severe clinical courses. Pulmonary function returns to normal in most patients with ARDS after about 6-12 months. Numerous survivors have persistent neuromuscular weakness.
Mechanical ventilation when high flow O2 saturation is 90%
The underlying conditions must be considered, as described elsewhere on the website. AHRF is initially approached with high oxygen flow of 70-100% O2 using a non-rebreathing mask. If this reveals an O2 saturation of> 90% cannot be achieved, mechanical ventilation may need to be considered. The approach in each individual case depends on the individual circumstances.
Mechanical ventilation for cardiogenic pulmonary edema
Mechanical ventilation (see also Mechanical ventilation at a glance Mechanical ventilation at a glance Mechanical ventilation can be Noninvasive, using various types of face masks Invasive, involving endotracheal intubation Selecting the appropriate procedure. Learn more ) is useful in left heart failure in several ways. Positive inspiratory pressure reduces left and right ventricular preload and afterload and relieves work of breathing by decreasing the. This decreases the work of breathing, allowing redistribution of limited cardiac output independent of overloaded respiratory muscles. Expiratory positive airway pressure Mechanical aspects of ventilation Mechanical ventilation can be Noninvasive, with various types of face masks Invasive, involving endotracheal intubation Choosing the appropriate procedure. Learn More " [EPAP] or PEEP) results in redistribution of pulmonary edema and opening of collapsed alveoli.
Noninvasive positive pressure ventilation (NIPPV) Noninvasive positive pressure ventilation (NIPPV) Mechanical ventilation may be Noninvasive, with various types of face masks Invasive, involving endotracheal intubation Choosing the appropriate procedure. Learn more , both continuous positive pressure ventilation and bilevel ventilation, is useful in avoiding endotracheal intubation in many patients, as medical therapy often provides rapid improvement. The usual framework is an inspiratory positive airway pressure ("IPAP") of 10-15 cm H2O and an expiratory positive airway pressure ("EPAP") of 5-8 cm H2O.
In conventional mechanical ventilation, different ventilation modes can be selected. Controlled ventilation (A/C) is often used in acute situations. Full ventilatory support of the patient is often indicated here. Initially, a stroke volume of 6-8 ml/kg (based on ideal weight), a ventilation rate of 25/min, an F io 2 of 1.0 and a PEEP of 5-8 cm H2O are selected. Subsequently, the PEEP should be titrated out in increments of 2.5 cm H2O and meanwhile the F io 2 should be reduced into the non-toxic range. Pressure-assisted ventilation can also be used. PEEP levels are similar to those used during controlled ventilation. Airway pressure set at baseline should be selected to allow full recovery of respiratory muscles. This assessment must be made clinically based on respiratory rate and using accessory respiratory muscles. Typically, this requires pressure support of 10-20 cm H2O above PEEP.
Mechanical ventilation in ARDS
Nearly all patients with ARDS require mechanical ventilation. Only in this way can oxygenation be sufficiently improved and O2 consumption reduced by switching off respiratory muscle work. Goals are
Alveolar plateau pressures 30 cm H2O (taking into account factors that potentially reduce chest wall and abdominal compliance)
Tidal volume of 6 ml/kg estimated body weight to minimize further lung damage
F io 2 as low as allowed to maintain adequate SaO2, which should reduce O2 toxicity
PEEP ventilator settings Mechanical ventilation can be Noninvasive, using various types of face masks Invasive, involving endotracheal intubation Choosing the appropriate procedure. Learn more should be high enough to keep alveoli open and minimize F IO 2until plateau pressures of 28-30 cm H2O are achieved. Use of higher PEEP is most likely to reduce mortality in patients with moderate or severe ARDS.
NIPPV Noninvasive positive pressure ventilation (NIPPV) Mechanical ventilation can be Noninvasive, using various types of face masks Invasive, involving endotracheal intubation Choosing the appropriate procedure. Learn more – Ventilation is occasionally helpful in the treatment of ARDS. Compared with the approach to cardiogenic pulmonary edema, higher pressure support is required for a longer period of time. In addition, adequate oxygenation can often only be achieved with an EPAP of 8-12 cm H2O. This requires inspiratory pressures of> 18-20 cm H2O poorly tolerated. A satisfactory seal can rarely be established, and the mask is often poorly tolerated. Skin necrosis and insufflation of the stomach may occur. In addition, patients initially treated with NIPPV alone who eventually require intubation have often deteriorated more markedly by this time than those who have been previously intubated. The oxygen saturation may already have fallen into critical ranges. Intensive monitoring and a considered approach to each patient are critical for NIPPV.
Conventional mechanical ventilation for ARDS was previously focused on normalizing blood gas analysis values. It is now clear that ventilation with lower tidal volumes reduces mortality. Accordingly, in most patients, the ventilatory volume is set at 6 ml/kg ideal body weight ( Setting the ventilator in ARDS Setting the ventilator in ARDS Acute hypoxemic respiratory insufficiency refers to high-grade arterial hypoxemia that cannot be relieved by O2 administration alone. The cause is an extended. Learn more for determination). This setting necessitates an increase in ventilation rate up to 35/min to allow sufficient ventilation for adequate removal of CO2. Notwithstanding this, considerable respiratory acidosis often develops, but this is accepted for the sake of limiting ventilator-induced lung injury and is also usually relatively well tolerated, especially if the pH is ≥ 7.15. If pH drops below 7.15, bicarbonate infusion or tromethamine may be helpful. Hypercapnia can be the cause of dyspnea and also lack of patient coordination with the ventilator. Therefore, such patients should be given analgesics (z. B. Morphine) and appropriately high doses of sedatives (z. B. Propofol , initially 5 mcg/kg/min) should be given in increasing doses until the desired effect (possibly up to 50 mcg/kg/min) is achieved. There is a risk of hypertriglyceridemia, so triglyceride levels should be determined every 48 h. Sedation is preferred to neuromuscular blockade because blockade still requires sedation and can cause persistent muscle weakness.
PEEP ventilator settings Mechanical ventilation may be Noninvasive, with various types of face masks Invasive, involving endotracheal intubation Selecting the appropriate procedure. Learn more improves oxygenation in ARDS by increasing the volume fraction of the ventilated lung. This is possible by increasing recruitment of previously unventilated alveoli. This makes further ventilation feasible with lower F io 2. The optimal PEEP level and how to identify it have been discussed. Recently, recruitment maneuvers have been routinely used (z. B. Titration of PEEP to a maximum pressure of 35 to 40 cm) H2O and held for 1 min), followed by decremental PEEP titration, which has been associated with increased 28-day mortality (1 Treatment considerations Acute hypoxemic respiratory failure is high-grade arterial hypoxemia that cannot be reversed by mere O2 administration. The cause is an extended. Learn more ). Many physicians simply use the lowest amount of PEEP for this purpose, ensuring adequate arterial oxygen saturation and a nontoxic F io 2 level. In most patients, this moment is reached at a PEEP of 8-15 cm H2O, although sometimes patients with severe ARDS have a value of> Require 20 cm H2O. In these cases, special attention must be paid to whether other ways of optimizing O2 supply and minimizing O2 consumption can be found.
Best indicator of alveolar overdistension is determination of plateau pressure by end-inspiratory breath hold Mechanical aspects of ventilation Mechanical ventilation can be Noninvasive, with various types of face masks Invasive, involving endotracheal intubation Selecting the appropriate procedure. Learn more . This pressure should be determined every 4 h after each change in PEEP or tidal volume. Target is a plateau pressure of 30 cm H2O. Provided the value is above this and there is no problem with the chest wall (z. B. Ascites, pleural effusion, acute abdomen, chest trauma), the stroke volume should be reduced as much as possible in increments of 0.5-1.0 ml/kg, down to a minimum of 4 ml/kg. The respiratory rate is increased compensatorily to maintain the respiratory minute volume at approximately the same level. The waveform of the respiratory cycle should be observed to ensure that complete exhalation is provided. The ventilation rate can often be raised to 35/min during this process. Only then must residual gas in the lungs ("air trapping") be expected due to incomplete exhalation. If plateau pressure is less than 25 cm H2O and tidal volume is 6 ml/kg, increasing traction volume up to 6 ml/kg may be appropriate. Limiting for this increase should be a plateau pressure of 25 cm H2O. Some researchers believe pressure-controlled ventilation would better protect the lungs, but supporting data are lacking and it is the highest pressure rather than plateau pressure that is controlled. Because respiratory volume varies as the patient’s lung compliance develops, it is necessary with pressure ventilation to continuously check the respiratory volume and adjust inspiratory pressure to make sure the patient is not getting too high or too low a respiratory volume.