Fig. 1. Airway pressure, flow, volume and transdiaphragmatic pressure in a patient at 2 levels of pressure support. Note marked increase in ventilator rate as PSV decreased from 15 to 12 cmH2O. Patient rate, as judged from diaphragmatic pressure, did not increase. The increase in patient effort, resulting from lower assist, caused better synchrony between patient and ventilator; ventilator is now triggered with every effort as opposed to every 5th or sixth breath. In addition, the reduction in ventilator TI, due to better synchrony, resulted in a much smaller VT. The change in pattern from deep slow breathing to rapid shallow breathing, due to better synchrony, is often misinterpreted as respiratory distress. Arrows in panel A indicate new inspiratory efforts occurring during ventilator cycles triggered by earlier efforts.
.An increase in ventilator rate, even of a large magnitude, following a decrease in level of assist need not reflect distress. It is necessary first to establish that the increase in ventilator rate is not due to improved synchrony and reduction or loss of ineffective efforts (Fig.1). This can be done non-invasively by inspecting the Paw and flow tracings  for evidence of extra efforts that did not produce new ventilator cycles (these can occur during expiration [i.e., the traditional ineffective efforts] or during an inflation phasetriggeredby an earlier effort(Fig. 1A)). These extra efforts should be added to the ventilator rate to arrive at what actually happened to the patient's rate. Even if the patient's RR increased following a reduction in assist, it should not be presumed that the patient is developing distress, unless there are other manifestations of distress. Particularly with PSV, a reduction in assist, with a consequent increase in inspiratory effort, promotes better synchrony between end of ventilator cycle and end of nTI. Extension of inflation into nTE is reduced, resulting in reduction of nTE (via built-in reflexes) and an increase in RR, independent of distress .
7. A spontaneous sudden increase in ventilator rate at the same PSV level need not reflect distress, particularly in the absence of other manifestations of distress. It could simply be the result of improved synchrony associated with a physiologic increase in inspiratory output related to awakening from sleep, subsidence of sedative effect, increase in metabolic rate due to movement, etc.
8. Recurrent central apneas almost invariably signify overassist in a patient with a short mechanical time constant (RC).
9. Recurrent central apneas and ineffective efforts are more likely to occur during sleep because of sleep related downregulation of respiratory output. Central apneas result in sleep fragmentation , and it is also quite possible that non-synchrony between patient and ventilator, of which ineffective efforts are only one expression (others being trigger delay and extension of inflation into nTE), may disrupt sleep. Sleep fragmentation has several undesirable effects, including decrease in ventilatory response to hypercania and hypoxia , decreased respiratory muscle endurance  and increased metabolic rate , all factors that can adversely affect weaning. Furthermore, sleep deprivation decreases host immunity with predisposition for systemic infections [54, 55].
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