Abstract

The vast majority of patients receiving invasive mechani-cal ventilation in the intensive care unit (ICU) are put onassisted modes, with pressure support ventilation (PSV)being the most commonly used mode during weaning offthe machine [1]. The primary objectives of PSV are usual-ly to unload the respiratory muscles and to improve coor-dination between respiratory muscle contraction and ma-chine breaths [2, 3]. How can this be achieved? First, aswith all assisted modes, the ventilator initiates the deliveryof positive pressure at airway opening after sensing thetriggering signal. Each PSV cycle of flow delivery is trig-gered by the patient, and the physician simply sets the air-flow or airway pressure threshold, or “sensitivity,” whichtriggers the ventilator. Second, the PSV level determinesthe degree of respiratory muscle unloading. Third, duringPSV, airflow is the signal that causes the ventilator to cy-cle off, i.e., to stop generating a flow of gas.The preset triggering and cycling-off values are impor-tant determinants of patient-ventilator interactions [4, 5].In theory, the beginning and end of the inspiratory muscleeffort must coincide with the beginning and end of theventilator’s inspiratory phase, respectively. Often this isnot the case. To trigger the ventilator the inspiratory ef-fort developed by the patient must first generate a certainlevel of negative pressure to counterbalance the end-expi-ratory elastic recoil pressure of the respiratory system(i.e., intrinsic PEEP), if any. Then the preset trigger sensi-tivity must be reached. Two problems may occur at thispoint of the breathing cycle: ineffective triggering and au-totriggering. These stem from a number of factors actingalone or in combination, including intrinsic PEEP, weakneuromuscular drive, and suboptimal trigger sensitivity[4, 6, 7]. The clinical consequences of wasted inspiratoryefforts (ineffective triggering) are not completely under-stood but include an additional burden on the respiratorymuscles. Autotriggering causes unwanted respiratory rateincreases, hypocapnia, hyperinflation, muscle decondi-tioning, and patient discomfort. The switch from inspira-tion to expiration (cycling off) has received little researchattention. One reason for this is perhaps that until recentlyvery few ventilators allowed adjustment of the cycling-off signal for PSV: most machines had fixed nonmodifi-able flow thresholds (25% of the peak inspiratory flow oran inspiratory flow of 5 l/min, for instance). A few dataare available, however. In patients with airway obstruc-tion under PSV the inspiratory flow decay is less steepthan in nonobstructed individuals. As a result, some ob-structed patients begin active expiration (by recruitingtheir expiratory muscles) while the machine is still deliv-ering the inspiratory flow [8]. Thus the ventilator cyclesoff after the end of the patient’s inspiratory effort, aggra-vating the dynamic hyperinflation that is particularlycommon in patients with airway obstruction [9].Can technology help us to solve some of the problemsinherent in triggering and cycling off during PSV? In

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