Neurally adjusted ventilatory assist

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Neurally adjusted ventilatory assist
Specialty pulmonary

Neurally adjusted ventilatory assist (NAVA) is a mode of mechanical ventilation. NAVA delivers assistance in proportion to and in synchrony with the patient's respiratory efforts, as reflected by an electrical signal. This signal represents the electrical activity of the diaphragm, the body's principal breathing muscle. [1]

The act of taking a breath is controlled by the respiratory center of the brain, which decides the characteristics of each breath, timing and size. The respiratory center sends a signal along the phrenic nerve, excites the diaphragm muscle cells, leading to muscle contraction and descent of the diaphragm dome. As a result, the pressure in the airway drops, causing an inflow of air into the lungs. [2]

With NAVA, the electrical activity of the diaphragm (Edi) is captured, fed to the ventilator and used to assist the patient's breathing in synchrony with and in proportion to the patients own efforts, regardless of patient category or size. As the work of the ventilator and the diaphragm is controlled by the same signal, coupling between the diaphragm and the SERVO-i ventilator is synchronized simultaneously. [3] [4] [5] [6] [7] [8] [9] [10] [11]

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Intermittent Mandatory Ventilation (IMV) refers to any mode of mechanical ventilation where a regular series of breaths are scheduled but the ventilator senses patient effort and reschedules mandatory breaths based on the calculated need of the patient. Similar to continuous mandatory ventilation in parameters set for the patients pressures and volumes but distinct in its ability to support a patient by either supporting their own effort or providing support when patient effort is not sensed. IMV is frequently paired with additional strategies to improve weaning from ventilator support or to improve cardiovascular stability in patients who may need full life support.

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There are many modes of mechanical ventilation. In medicine, mechanical ventilation is a method to mechanically assist or replace spontaneous breathing.

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<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.

References

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