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Objective: To examine patient-ventilator interaction during pressure support ventilation in critically ill patients when they were ventilated: (1) by a new system (Vision, Respironics) which uses the flow waveform as a method of triggering and cycling; and (2) by a new generation ventilator (Evita 4, Drager) which uses the traditional flow triggering (2 l/min) and cycling criterion (25% of peak flow)., Design: Prospective clinical and bench study., Methods: Twelve mechanically ventilated patients were studied at three levels of pressure support, applied randomly with both ventilators. The two systems of triggering were further studied at controlled levels of dynamic hyperinflation and respiratory drive using an active lung model., Results: Patients' breathing patterns, respiratory effort, and arterial blood gases were not affected by the type of ventilator. The flow waveform method of triggering was more sensitive to patient effort than the flow triggering, resulting in less ineffective effort but a greater number of auto-triggerings. At controlled levels of dynamic hyperinflation and inspiratory effort the simulated patient effort needed to trigger the ventilator was considerably less with the flow waveform method of triggering than that with the flow triggering. The flow waveform method of cycling resulted in mechanical breaths with similar characteristics to those that used the traditional flow criterion of breath termination., Conclusions: We conclude that the flow waveform method of triggering improves the ventilator function and decreases the patient effort during the triggering phase. This system is highly sensitive, but under certain circumstances may be unstable.

Background: Proportional assist ventilation (PAV) has been shown to maintain better patient-ventilator synchrony than pressure support ventilation (PSV); however, its clinical advantage regarding invasive ventilation of COPD patients has not been clarified., Objectives: To compare the effect of PAV and PSV on respiratory parameters of hypercapnic COPD patients with acute respiratory failure (ARF)., Methods: Nine intubated hypercapnic COPD patients were placed on the PAV or PSV mode in random sequence. For each mode, four levels (L1-L4) of support were applied. At each level, blood gases, flow, tidal volume (VT), airway pressure (Paw), esophageal pressure (Pes) (n = 7), patient respiratory rate (fp), ventilator rate (fv), missing efforts (ME = fp - fv) were measured., Results: We found increases in ME with increasing levels of PSV but not with PAV. PO2 and VT increased whereas PCO2 decreased significantly with increasing levels of PSV (p < 0.05). With PAV, PCO2 decreased and VT increased significantly only at L4 whereas PO2 increased from L1 to L4. Runaways were observed at L3 and L4 of PAV. The pressure-time product (PTP) was determined for effective and missing breaths. The mean total PTP per minute (of effective plus missing breaths) was 160 +/- 57 cm H2O/s.min in PSV and 194 +/- 60 cm H2O/s.min in PAV., Conclusion: We conclude that in COPD patients with hypercapnic ARF, with increasing support, PSV causes the appearance of ME whereas PAV develops runaway phenomena, due to the different patient-ventilator interaction; however, these do not limit the improvement of blood gases with the application of both methods., (Copyright 2003 S. Karger AG, Basel)

Patients with brain damage, in contrast to normal subjects, exhibit a significant ventilatory undershoot when brief hypocapnic hypoxia is terminated abruptly by hyperoxia. This has been attributed to an impairment of activation of short-term potentiation, a brain stem mechanism promoting breathing stability. We hypothesized that in these patients theophylline, a drug that stabilizes breathing, may affect short-term potentiation. Eight stable patients with brain damage and 10 normal adults were studied. Activation of short-term potentiation was examined by brief exposure to hypoxia followed by hyperoxia after pretreatment with placebo or theophylline. Both in patients and normal subjects at the end of hypoxia ventilation increased to a similar magnitude with and without theophylline. In normal subjects independent of pretreatment, when hypoxia was terminated abruptly by hyperoxia, ventilation declined slowly to baseline without an undershoot, indicating activation of short-term potentiation. In patients with placebo, ventilation upon switching to hyperoxia exhibited a significant undershoot. This undershoot was significantly attenuated by theophylline, although compared with normal subjects, a slight hypoventilation was observed. We conclude that in patients with brain damage, theophylline largely prevents the hyperoxic drop of ventilation, presumably by affecting the activation of short-term potentiation. This may underlie the beneficial effect of theophylline on breathing stability.

Bronchodilators represent one of the most important therapeutic weapons for the treatment of airway obstructive diseases and the inhaled route of administration is very often employed due to the greater drug availability and reduced magnitude of side effects. During acute exhacerbations, it is not unfrequent that the elastic and resistive loads imposed on the ventilatory pump overcome the force sustainable by the respiratory muscles and the patient requires ventilatory assistance, in order to relieve fatigue and to optimize alveolar gas exchange. During these episodes, inhaled bronchodilators, far from being discontinued, sometime must be administered during mechanical ventilation, that, in hypercapnic ventilatory failure can be frequently applied noninvasively with a good rate of success. While in the current literature there are a lot of data about inhaled drug administration during invasive mechanical ventilation, very few data are available on the topic of aerosol therapy during noninvasive mechanical ventilation. With the present paper we want to analyze the rationale, the feasibility and the current data dealing with the administration of inhaled drugs during noninvasive mechanical ventilation.

The pattern of lung emptying was studied in 10 mechanically-ventilated patients with acute respiratory distress syndrome. At four levels of positive end-expiratory pressure (PEEP) (0, 5, 10 and 15 cmH2O) tracheal (Ptr) and airway pressures (Paw), flow (V') and volume (V) were continuously recorded. Tidal volume was set between 0.5-0.6 L and V'/V curves during passive expiration were obtained. Expired volume was divided into five equal volume slices and the time constant (taue) and effective deflation compliance (Crs(eff)) of each slice was calculated by regression analysis of V/V' and postocclusion V/Ptr relationships, respectively. In each slice, the presence or absence of flow limitation was examined by comparing V'/V curves with and without decreasing Paw. For a given slice, total expiratory resistance (Rtot) (consisting of the respiratory system (Rrs), endotracheal tube (Rtube) and ventilator circuit (Rvent)) was calculated as the taue/Crs(eff) ratio. In the absence of flow limitation Rrs was obtained by subtracting Rtube and Rvent from Rtot, while in the presence of flow limitation Rrs equaled Rtot. The taue of the pure respiratory system (taue(rs)) was calculated as the product of Rrs and Crs(eff). At zero PEEP, taue(rs) increased significantly towards the end of expiration (52+/-31%) due to a significant increase in Rrs (46+/-36%). Application of PEEP significantly decreased Rrs at the end of expiration and resulted in a faster and relatively constant rate of lung emptying. In conclusion, without positive end-expiratory pressure the respiratory system in patients with acute respiratory distress syndrome deflates with a rate that progressively decreases, due to a considerable increase in expiratory resistance at low lung volumes. Application of positive end-expiratory pressure decreases the expiratory resistance, probably by preventing airway closure, and as a result modifies the pattern of lung emptying.

Objective: During assisted mechanical ventilation, changes in ventilator settings may acutely affect the respiratory motor output via the mechanoreceptor reflex feedback system, thus interfering with patient management. This feedback system in mechanically ventilated patients with parenchymal lung injury remains largely unexplored. To investigate this, the early response of respiratory motor output to varying ventilator settings was determined in 13 sedated patients with acute lung injury., Design: During assist/control and pressure support (PS) ventilation changes in (1) tidal volume (V(T)) at fixed inspiratory flow (V'(I)), (2) V'(I) at fixed V(T) and (3) PS level were employed and the response of respiratory motor output was followed for two breaths after the change. Respiratory motor output was assessed by total pressure generated by the respiratory muscles (Pmus), computed from esophageal pressure (Pes)., Results: Neural expiratory time increased with increasing V(T) and PS, while it remained constant with V'I changes. Neural inspiratory time (T(I)n) increased with decreasing V'(I) and PS, but was not affected by V(T) changes. None of the changes in ventilator settings influenced significantly the rate of rise of Pmus, used as an index of respiratory drive. The changes in respiratory timing resulted in significant changes in breathing frequency, which increased with decreasing V(T) and PS and increasing V'(I). The time integral of Pmus, an index of respiratory effort, increased with increasing T(I)n. These acute responses were not related to the severity of deterioration of respiratory system mechanics., Conclusions: We conclude that alterations in commonly used ventilator settings induce acute changes in respiratory timing, without affecting the respiratory drive. These changes, probably mediated via mechanoreceptor reflex feedback, are dependent on the type of the alteration in the ventilator settings.

Objectives: To test the effect of two different inspiratory flow rates on the bronchodilation induced by beta2-agonists administered by metered dose inhaler (MDI)., Patients: Ten patients with acute exacerbation of chronic obstructive pulmonary disease and receiving mechanical ventilation with constant inspiratory flow (V'I)., Design: Patients received four puffs of salbutamol (100 microg/puff) with either low V'I (0.6 l/s) or high V'I (1.2 l/s) administered with an MDI adapted to inspiratory limb of the ventilator circuit using an aerosol cloud enhance spacer. After a 6-h washout patients were crossed-over to receive the drug by the alternative mode of administration., Measurements and Results: Static and dynamic airway pressures, intrinsic positive end-expiratory pressure, and minimum and maximum inspiratory resistance values showed a significant decrease after salbutamol. These changes were not affected by the inspiratory flow rate and were evident 15, 30, and 60 min after administration. Heart rate, static end-inspiratory respiratory system compliance, and the difference between minimum and maximum inspiratory resistance were unchanged after salbutamol., Conclusions: Salbutamol delivered by MDI and spacer device induces significant bronchodilation in mechanically ventilated patients with chronic obstructive pulmonary disease, but the magnitude of the effect is not affected by the inspiratory flow rate. These results do not support flow rate manipulations when bronchodilators are administered during controlled mechanical ventilation.

Objective: In mechanically ventilated patients with ARDS, determination of the lower (LIP) and upper (UIP) inflection points of the static pressure-volume curve (P-V) is crucial for planning ventilatory strategies. Recently, a simple new method was proposed for measuring the P-V curve by inflating the lung with constant low flow [14]. We hypothesized that during low flow inflation LIP and UIP might be determined using the pressure-time curve (P-T) instead of P-V., Methods: Eleven paralyzed patients with ARDS were studied. During volume control ventilation the patients were allowed to reach passive functional residual capacity (FRC) and then ventilator frequency, inspiratory to total breath duration ratio and tidal volume (VT) were set to 5 breaths/ min, 80% and 500 or 1,500 ml, respectively. With these settings, constant inspiratory flow (V'I) was administered for 9.6 s and ranged, depending on VT, between 0.05 and 0.15 l/s. P-V and P-T were obtained at two levels of positive end-expiratory pressure (PEEP; 0 and 10 cm H2O), with V'I being achieved either fast (< 0.1 s, minimum delay) or slowly (0.4 s, maximum delay)., Results: With minimum flow delay for a given experimental condition, the shape of the P-T did not differ from that of P-V. In all cases P-T correctly identified the presence of LIP and UIP, which did not differ significantly between P-T and P-V. With maximum flow delay, compared to P-V, the initial part of P-T was significantly shifted to the left. P-T did not identify the presence of UIP and LIP in one and two cases, respectively., Conclusions: Provided that constant flow is given relatively fast, P-T accurately determines the shape of P-V, as well as the LIP and UIP. Flow delay causes a leftward shift of the initial part of P-T, masking the presence of LIP and UIP in some cases.

In mechanically ventilated patients the flow pattern during bronchodilator delivery by metered-dose inhaler (MDI) could be a factor that might influence the effectiveness of this therapy. In order to test this the effect of two different inspiratory flow patterns on the bronchodilation induced by beta2-agonists administered via MDI and spacer in a group of mechanically ventilated patients with chronic obstructive pulmonary disease (COPD) was examined. Eighteen mechanically ventilated patients with COPD, were prospectively randomized to receive two (n=8, protocol A) or six (n=10 protocol B) puffs salbutamol (100 microg x puff(-1)) either under pressure control (decelerating flow pattern) or under volume control (square wave flow pattern). With both modes, tidal volume and inspiratory time were identical. Salbutamol was administered via an MDI adapted to the inspiratory limb of the ventilator circuit using an aerosol cloud-enhancer spacer. After a 6-h washout, patients were crossed over to receive the same dose of salbutamol (200 or 600 microg, respectively in protocols A and B) by the alternative mode of administration. Static and dynamic airway pressures, minimum (Rint) and maximum (Rrs) inspiratory resistance and the difference between Rrs and Rint (deltaR) were measured before and at 15, 30 and 60 min after salbutamol. Independent of the dose, salbutamol caused a significant decrease in dynamic and static airway pressures, Rint and Rrs. These changes were not influenced by the inspiratory flow pattern and were evident at 15, 30 and 60 min after salbutamol. It is concluded that salbutamol delivered via metered dose inhaler and spacer device, induces significant bronchodilation in mechanically ventilated patients with chronic obstructive pulmonary disease, the magnitude of which is not affected by the inspiratory flow/time profile.

All patients with bronchial asthma are at risk of developing severe episodes of airway narrowing that do not respond to the usual medical treatment, a life-threatening situation referred to as status asthmaticus. In some cases, ventilatory failure occurs, necessitating mechanical ventilation to support gas exchange and to unload the respiratory muscles, giving time for other therapeutic interventions to improve the functional status of the patient. Mechanical ventilatory support poses additional risks to the patients, due to interaction between the pathophysiology of the disease and the process of mechanical ventilation. Dynamic hyperinflation, a cardinal feature of the pathophysiology, may cause serious complications during mechanical ventilation. Setting the ventilator, such as to minimize the dynamic hyperinflation, is a key point in the management of mechanically ventilated patients with status asthmaticus. Strategies to reduce dynamic hyperinflation, such as hypoventilation (permissive hypercapnia), increase of expiratory time and promotion of patient-ventilator synchrony are mandatory and significantly decrease the morbidity and mortality of the disease. Continuous monitoring of the effectiveness of these strategies, as well as the functional status of the patient, is crucial in order to limit complications associated with mechanical ventilation and to identify the time that weaning can start.