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Biomedical subjects

G A Iotti

Publications and source records attributed to G A Iotti.

9 recordsLinked to original sources

Adaptive Support Ventilation (ASV).

Adaptive Support Ventilation is a novel ventilation mode, a closed-loop control mode that may switch automatically from a PCV-like behaviour to an SIMV-like or PSV-like behaviour, according to the patient status. The operating principles are based on pressure-controlled SIMV with pressure levels and SIMV rate automatically adjusted according to measured lung mechanics at each breath. ASV provided a safe and effective ventilation in patients with normal lungs, restrective or obstructive diseases. In cardiac surgery tracheal extrubation was faster in ASV patients then in controls. In the early weaning phase of acute ventilatory insufficiency the need of resetting ventilator parameters was decreased, suggesting potential benefit for patient care.

Critical Care↗

Closed-loop support of ventilatory workload: the P0.1 controller.

Conventional mechanical ventilation modes fail to provide a setting for direct control of a patient's ventilatory effort; however, with all modes clinicians may manipulate conventional controls to modulate the spontaneous respiratory activity of the patient. For instance, during pressure support ventilation the spontaneous respiratory activity can be decreased by increasing the pressure support level to achieve an adequate residual load for the respiratory muscles of the patient, neither too high nor too low. This choice is based on the clinical observation. A closed-loop controller can be envisaged to accomplish automatically, precisely, and on a breath-by-breath basis, this difficult task. The closed-loop controller should be based on the continuous and possibly noninvasive monitoring of a parameter that quantitatively reflects the patient's effort for ventilation. Occlusion pressure at 0.1 second (P0.1) can be the ideal parameter for that purpose. The authors have designed a noninvasive method for breath-by-breath monitoring of P0.1, and then a closed-loop control mode that automatically adapts the pressure support level to reach and maintain a user-set P0.1 and alveolar volume. This article discusses features and performance of this P0.1 control mode, fields of application, known limits, and possible future improvements.

Algorithms↗

Mechanical effects of heat-moisture exchangers in ventilated patients.

Although they represent a valuable alternative to heated humidifiers, artificial noses have unfavourable mechanical effects. Most important of these is the increase in dead space, with consequent increase in the ventilation requirement. Also, artificial noses increase the inspiratory and expiratory resistance of the apparatus, and may mildly increase intrinsic positive end-expiratory pressure. The significance of these effects depends on the design and function of the artificial nose. The pure humidifying function results in just a moderate increase in dead space and resistance of the apparatus, whereas the combination of a filtering function with the humidifying function may critically increase the volume and the resistance of the artificial nose, especially when a mechanical filter is used. The increase in the inspiratory load of ventilation that is imposed by artificial noses, which is particularly significant for the combined heat-moisture exchanger filters, should be compensated for by an increase either in ventilator output or in patient's work of breathing. Although both approaches can be tolerated by most patients, some exceptions should be considered. The increased pressure and volume that are required to compensate for the artificial nose application increase the risk of barotrauma and volutrauma in those patients who have the most severe alterations in respiratory mechanics. Moreover, those patients who have very limited respiratory reserve may not be able to compensate for the inspiratory work imposed by an artificial nose. When we choose an artificial nose, we should take into account the volume and resistance of the available devices. We should also consider the mechanical effects of the artificial noses when setting mechanical ventilation and when assessing a patient's ability to breathe spontaneously.

Filtration↗

Acute effects of inhaled nitric oxide in adult respiratory distress syndrome.

This study evaluated the dose-response effect of inhaled nitric oxide (NO) on gas exchange, haemodynamics, and respiratory mechanics in patients with adult respiratory distress syndrome (ARDS). Of 19 consecutive ARDS patients on mechanical ventilation, eight (42%) responded to a test of 10 parts per million (ppm) NO inhalation with a 25% increase in arterial oxygen tension (Pa,O2,) over the baseline value. The eight NO-responders were extensively studied during administration of seven inhaled NO doses: 0.5, 1, 5, 10, 20, 50 and 100 ppm. Pulmonary pressure and pulmonary vascular resistance exhibited a dose-dependent decrease at NO doses of 0.5-5 ppm, with a plateau at higher doses. At all doses, inhaled NO improved O2 exchange via a reduction in venous admixture. On average, the increase in Pa,O2, was maximal at 5 ppm NO. Some patients, however, exhibited maximal improvement in Pa,O2 at 100 ppm NO. In all patients, the increase in arterial O2 content was maximal at 5 ppm NO. The lack of further increase in arterial O2 content above 5 ppm partly depended on an NO-induced increase in methaemoglobin. Respiratory mechanics were not affected by NO inhalation. In conclusion, NO doses < or =5 ppm are effective for optimal treatment both of hypoxaemia and of pulmonary hypertension in adult respiratory distress syndrome. Although NO doses as high as 100 ppm may further increase arterial oxygen tension, this effect may not lead to an improvement in arterial O2 content, due to the NO-induced increase in methaemoglobin. It is important to consider the effect of NO not only on arterial oxygen tension, but also on arterial O2 content for correct management of inhaled nitric oxide therapy.

Administration, Inhalation↗

Unfavorable mechanical effects of heat and moisture exchangers in ventilated patients.

OBJECTIVE: To investigate the mechanical effects of artificial noses. SETTING: A general intensive care unit of a university hospital. PATIENTS: 10 patients in pressure support ventilation for acute respiratory failure. INTERVENTIONS: The following three conditions were randomly tested on each patient: the use of a heated humidifier (control condition), the use of a heat and moisture exchanger without filtering function (HME), and the use of a combined heat and moisture exchanger and mechanical filter (HMEF). The pressure support level was automatically adapted by means of a closed-loop control in order to obtain constancy, throughout the study, of patient inspiratory effort as evaluated from airway occlusion pressure at 0.1 s (P0.1). Patient's ventilatory pattern, P0.1, work of breathing, and blood gases were recorded. MEASUREMENTS AND MAIN RESULTS: The artificial noses increased different components of the inspiratory load: inspiratory resistance, ventilation requirements (due to increased dead space ventilation), and dynamic intrinsic positive end-expiratory pressure (PEEP). The additional load imposed by the artificial noses was entirely undertaken by the ventilator, being the closed-loop control of P0.1 effective to maintain constancy of patient inspiratory work by means of adequate increases in pressure support level. CONCLUSIONS: The artificial noses cause unfavorable mechanical effects by increasing inspiratory resistance, ventilation requirements, and dynamic intrinsic PEEP. Clinicians should consider these effects when setting mechanical ventilation and when assessing patients' ability to breathe spontaneously.

Adult↗

Closed-loop control of airway occlusion pressure at 0.1 second (P0.1) applied to pressure-support ventilation: algorithm and application in intubated patients.

OBJECTIVE: Airway occlusion pressure at 0.1 sec (P0.1) is an index of respiratory center output. During pressure-support ventilation, P0.1 correlates with the mechanical output of the inspiratory muscles and has an inverse relationship with the amount of pressure-support ventilation. Based on these observations, we designed a closed-loop control which, by automatically adjusting pressure-support ventilation, stabilizes P0.1, and hence patient inspiratory activity, at a desired target. The purpose of the study was to demonstrate the feasibility of the method, rather than its efficacy or even its influence on patient outcome. DESIGN: Prospective, randomized trial. SETTING: A general intensive care unit of a university hospital in Italy. PATIENTS: Eight stable patients intubated and ventilated with pressure-support ventilation for acute respiratory failure. INTERVENTIONS: Patients were transiently connected to a computer-controlled ventilator on which the algorithm for closed-loop control was implemented. The closed-loop control was based on breath by breath measurement of P0.1, and on comparison with a target set by the user. When actual P0.1 proved to be higher than the target value, the P0.1 controller automatically increased pressure-support ventilation, and decreased it when P0.1 proved to be lower than the target value. For safety, a volume controller was also implemented. Four P0.1 targets (1.5, 2.5, 3.5, and 4.5 cm H2O) were applied at random for 15 mins each. MEASUREMENTS AND MAIN RESULTS: The closed-loop algorithm was able to control P0.1, with a difference from the set targets of 0.59 +/- 0.27 (SD) cm H2O. CONCLUSIONS: The study shows that P0.1 can be automatically controlled by pressure-support ventilation adjustments with a computer. Inspiratory activity can thus be stabilized at a level prescribed by the physician.

Acute Disease↗

Respiratory mechanics by least squares fitting in mechanically ventilated patients: applications during paralysis and during pressure support ventilation.

OBJECTIVE: To evaluate a least squares fitting technique for the purpose of measuring total respiratory compliance (Crs) and resistance (Rrs) in patients submitted to partial ventilatory support, without the need for esophageal pressure measurement. DESIGN: Prospective, randomized study. SETTING: A general ICU of a University Hospital. PATIENTS: 11 patients in acute respiratory failure, intubated and assisted by pressure support ventilation (PSV). INTERVENTIONS: Patients were ventilated at 4 different levels of pressure support. At the end of the study, they were paralyzed for diagnostic reasons and submitted to volume controlled ventilation (CMV). MEASUREMENTS AND RESULTS: A least squares fitting (LSF) method was applied to measure Crs and Rrs at different levels of pressure support as well as in CMV. Crs and Rrs calculated by the LSF method were compared to reference values which were obtained in PSV by measurement of esophageal pressure, and in CMV by the application of the constant flow, end-inspiratory occlusion method. Inspiratory activity was measured by P0.1. In CMV, Crs and Rrs measured by the LSF method are close to quasistatic compliance (-1.5 +/- 1.5 ml/cmH2O) and to the mean value of minimum and maximum end-inspiratory resistance (+0.9 +/- 2.5 cmH2O/(l/s)). Applied during PSV, the LSF method leads to gross underestimation of Rrs (-10.4 +/- 2.3 cmH2O/(l/s)) and overestimation of Crs (+35.2 +/- 33 ml/cmH2O) whenever the set pressure support level is low and the activity of the respiratory muscles is high (P0.1 was 4.6 +/- 3.1 cmH2O). However, satisfactory estimations of Crs and Rrs by the LSF method were obtained at increased pressure support levels, resulting in a mean error of -0.4 +/- 6 ml/cmH2O and -2.8 +/- 1.5 cmH2O/(l/s), respectively. This condition was coincident with a P0.1 of 1.6 +/- 0.7 cmH2O. CONCLUSION: The LSF method allows non-invasive evaluation of respiratory mechanics during PSV, provided that a near-relaxation condition is obtained by means of an adequately increased pressure support level. The measurement of P0.1 may be helpful for titrating the pressure support in order to obtain the condition of near-relaxation.

Acute Disease↗

Noninvasive evaluation of instantaneous total mechanical activity of the respiratory muscles during pressure support ventilation.

OBJECTIVE: The measurement of esophageal pressure (Pes) is the conventional method for the evaluation of the forces applied to the respiratory system by the respiratory muscles. As an alternative to Pes measurement, we propose the calculation of the instantaneous net pressure applied by the respiratory muscles [Pmusc(t)]. DESIGN: Prospective, randomized study. SETTING: A general ICU of a university hospital. PATIENTS: Eight intubated patients submitted to pressure support ventilation for acute respiratory failure. INTERVENTIONS: Four different levels of pressure support were used to unload progressively the respiratory muscles. Pmusc(t) was calculated at all levels of pressure support and compared with Pes corrected for chest wall load as a reference. Pmusc(t) was further used to calculate inspiratory work of breathing, which in turn was compared with data obtained with the conventional method. MEASUREMENTS AND RESULTS: Airway pressure, airflow, and Pes were measured. Both for amplitude and for timing, Pmusc(t) showed good agreement with reference measurements. Work of breathing as calculated from Pmusc(t) agreed well with the measurement obtained with the conventional method (mean difference, 0.057 +/- 0.157 J). CONCLUSIONS: Noninvasive evaluation of Pmusc(t) allows extended monitoring of mechanical ventilation, which is particularly interesting for pressure preset ventilation modes.

Adult↗