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Biomedical subjects

A Braschi

Publications and source records attributed to A Braschi.

At least 37 records · Page 2Linked to original sources
PubMed1999

Increased plasma levels of fibrinogen in acute and chronic ischemic coronary syndromes.

BACKGROUND: The aim of this study was to evaluate the pathophysiological role of fibrinogen in patients with chronic or acute ischemic coronary syndromes on the basis of epidemiological and clinical evidences showing the importance of fibrinogen as a risk factor for cardiovascular diseases and atherosclerosis progression. METHODS: We evaluated the behavior of plasma fibrinogen in 310 hospitalized patients with 1) acute myocardial infarction (n = 98); 2) unstable angina (n = 87); 3) chronic ischemic heart disease (n = 75); and 4) in controls without myocardial ischemia (n = 50). Fibrinogen was evaluated, by using the Clauss method, on day 1 and 5 during in hospital-stay and at 6-month follow-up in patients suffering from acute myocardial infarction. RESULTS: Plasma levels of fibrinogen were higher in patients with chronic ischemic heart disease (335.3 +/- 81.2 mg/dl, p < 0.001) and especially in patients with acute myocardial infarction (454.72 +/- 69.5 mg/dl, p < 0.00001) and unstable angina (382.6 +/- 101.3 mg/dl, p < 0.00025) in comparison with controls (271.28 +/- 62.4 mg/dl). Q wave myocardial infarction showed higher levels of fibrinogen than non-Q wave (461.3 +/- 95.8 vs 422.5 +/- 71.3 mg/dl, p < 0.02). Patients with acute myocardial infarction showed a further increase in fibrinogen on day 5 in comparison with entry levels (525.88 +/- 87.3 vs 454.7 +/- 69.5 mg/dl, p < 0.00001) regardless of the fibrinolytic treatment. Patients who died (n = 6) or had severe arrhythmias (n = 4) during in-hospital stay as well as those with post-infarction angina (n = 20) showed higher fibrinogen levels. CONCLUSIONS: Our results confirm the role of fibrinogen as a risk factor for ischemic heart disease, especially in patients with unstable angina and acute myocardial infarction. In the latter, elevated fibrinogen values seem also to be associated with a worsen prognosis during hospitalization.

Acute Disease↗
PubMed1998

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↗
PubMed1997

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↗
PubMed1997

ECMO and inhaled nitric oxide for cardiopulmonary failure after heart retransplantation.

Cardiopulmonary failure occurred in a 62-year-old patient a few hours after emergency cardiac retransplantation. Venoarterial extracorporeal membrane oxygenation was required to support biventricular dysfunction; thereafter, inhaled nitric oxide was given for residual hypoxemia and pulmonary hypertension. We report survival after venoarterial extracorporeal membrane oxygenation and inhaled nitric oxide treatment for both heart and lung failure in a heart recipient.

Extracorporeal Membrane Oxygenation↗
PubMed1997

Patient-ventilator interaction and inspiratory effort during pressure support ventilation in patients with different pathologies.

The aim of this study was to evaluate whether pressure support ventilation (PSV) requires different diaphragmatic efforts and patient-ventilator matching, according to the underlying disease. Four groups of patients requiring PSV were studied: Group A, recovering from an episode of acute respiratory failure due to adult respiratory distress syndrome (ARDS); Group B, with postsurgical complications; and two subsets of chronic obstructive pulmonary disease (COPD) patients, with "normal" static compliance of the respiratory system (Cst,rs) (Group C) or elevated Cst,rs (Group D). Ventilatory pattern, transdiaphragmatic pressure (Pdi), the pressure-time product of the diaphragm (PTPdi), static (PEEPi,stat) and dynamic intrinsic positive end-expiratory pressure (PEEPi,dyn), Cst,rs and resistance of the total respiratory system (Rrs) were recorded. The matching between patient and ventilator was analysed, recording the number of "ineffective efforts" (inspiratory efforts not efficient enough to trigger a new ventilator cycle, despite a positive deflection in Pdi). A satisfactory blood gas equilibrium arterial oxygen saturation (Sa,O2 > 93%, with a pH > 7.32) was obtained in the various groups with different levels of PSV. Minute ventilation was found to be significantly higher in Groups A and B, due to the longer expiratory time (tE) in the COPD groups. Group A (2 out of 7), Group B (3 out of 7), Group C (3 out of 5) patients showed sporadic "ineffective efforts". All Group D patients manifested continuous mismatching with the ventilator, so that the pressure-time product of the diaphragm per minute (PTPdi/min), reflecting the metabolic work of the diaphragm, was not different in the four groups. Tidal volume and the spontaneous inspiratory efforts were similar in the four groups, but the number of breaths delivered by the ventilator was significantly higher in Groups A and B. The application of different levels of pressure support ventilation in patients with acute respiratory failure due to different pathologies, led them to breathe with comparable pressure time product of the diaphragm. The majority of the patients showed mismatching with the ventilator, although this effect was more pronounced in the groups with chronic obstructive pulmonary disease.

Acute Disease↗
PubMed1997

[Inhaled nitrous oxide (NO) for the treatment of ARDS].

OBJECTIVE: To investigate the initial longterm effect of inhaled NO on hypoxemia in ARDS patients. DESIGN: Retrospective study. PATIENTS: Nine hypoxemic patients with ARDS (Murray Lung Injury Score, LIS, 2.8 +/- 0.3), treated with conventional mechanical ventilation. INTERVENTIONS: Continuous NO inhalation was started after a test of inhaled NO efficacy on gas exchange and hemodynamics. Long term effects of inhaled NO were evaluated daily in terms of arterial oxygenation and methemoglobin formation. RESULTS: The initial NO inhalation increased the PaO2/FiO2 from 141 +/- 64 mmHg to 216 +/- 70 mmHg (p < 0.0001) and decreased the mean pulmonary pressure from 38 +/- 7 mmHg to 32 +/- 5 mmHg (p < 0.01), the pulmonary venous admixture from 29 +/- 10% to 20 +/- 8% (p < 0.01) and the pulmonary vascular resistance from 325 +/- 97 dyne.s.cm-5 to 238 +/- 48 dyne.s.cm-5 (p < 0.01). Daily withdrawal of inhaled NO, which was administered for 14 +/- 16 days at 8 +/- 2 ppm, was associated with a decrease in PaO2/FiO2 by 61 +/- 32 mmHg (p < 0.0001). During prolonged NO inhalation the FiO2 was decreased, on average, by 0.34 +/- 0.19 (p < 0.01), the positive end-expiratory pressure by 4 +/- 2 cmH2O (p < 0.01) and the peak inspiratory pressure by 7 +/- 4 cmH2O (p < 0.01). Three patients died during the ICU stay. CONCLUSIONS: Our results confirm the interest for inhaled NO as an additional approach for the treatment of hypoxemia in ARDS. Inhaled NO seems to allow for a better control of gas exchange, rather than for a rapid reduction of the ventilatory support.

Adolescent↗
PubMed1996

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↗
PubMed1996

Bronchoalveolar lavage fluid composition in alveolar proteinosis. Early changes after therapeutic lavage.

In patients with idiopathic alveolar proteinosis, the alveoli are filled with materials rich in surfactant components, especially surfactant protein A (SP-A). The anomaly could be caused by either increased secretion, decreased clearance, or both. To clarify this point, we studied five patients who underwent therapeutic lavage and then were ventilated mechanically for 24 h. During the first 8 h of mechanical ventilation, a surfactant-depleted lung was lavaged at selected intervals, and the bronchoalveolar lavage fluid was analyzed. We observed that, after lavage, various surfactant components accumulated in the airways with different time courses. We also observed that SP-A increased until the second hour and then dropped rapidly, suggesting the existence of an efficient mechanism of removal. These findings suggest that idiopathic alveolar proteinosis might be caused by a primary defect in a slow mechanism of removal or by the presence of factor(s) that interfere with the clearance of surfactant and that can be removed by lavage. It seems clear, however, that an increased secretion rate is unlikely to be the major cause of idiopathic alveolar proteinosis.

Adult↗
PubMed1995

Elevated static compliance of the total respiratory system: early predictor of weaning unsuccess in severed COPD patients mechanically ventilated.

OBJECTIVE: To assess in a group of COPD patients mechanically ventilated for an episode of acute respiratory failure the respiratory mechanics with a simple and non invasive method at the bedside in order to evaluate if these parameters may be predictive of weaning failure or success. DESIGN: A prospective study. SETTING: Intensive care and intermediate intensive care units. PATIENTS: 23 COPD patients ventilated for acute respiratory failure and studied within 24 hours from intubation. METHODS: Using end-expiratory and end-inspiratory airway occlusion technique, we measured PEEPi, static compliance of the respiratory system (Crs, st) maximum respiratory resistance (Rrsmax) and minimum respiratory resistance (Rrsmin). MEASUREMENTS AND RESULTS: The weaned group (A) and the not weaned group (B) were not different regarding to static PEEPi (group A 8.5 +/- 4.0 vs group B 8.9 +/- 2.6 cmH2O), TO Rrsmax (22.4 +/- 5.3 versus 22.2 +/- 9.0 cmH2O/1/s) and to Rrsmin (17.6 +/- 5.5 versus 17.9 +/- 8.0 cmH2O/1/s), while a significant difference (p < 0.001) has been found in Cst, rs (62.7 +/- 17.% versus 111.6 +/- 18.0 ml/cm H2O). The threshold value of 88.5 ml/cmH2O was identified by discriminant analysis and provided the best separation between the two groups, with a sensitivity of 0.85 and a specificity of 0.87. CONCLUSION: Cst, rs measured non invasively in the first 24 h from intubation, provided a good separation between the patients who were successfully weaned and those who failed.

Acute Disease↗
PubMed1995

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↗
PubMed1995

Respiratory response and inspiratory effort during pressure support ventilation in COPD patients.

OBJECTIVE: Pressure Support Ventilation (PSV) is now widely used in the process of weaning patients from mechanical ventilation. The aim of this study was to evaluate the effects of various levels of PS on respiratory pattern and diaphragmatic efforts in patients affected by chronic obstructive pulmonary disease (COPD). SETTING: Intermediate intensive care unit. PATIENTS: We studied ten patients undergoing PSV and recovering from an episode of acute respiratory failure due to exacerbation of COPD. METHODS: Three levels of PSV were studied, starting from the lowest (PSb) one at which it was possible to obtain an adequate Vt with a pH > or = 7.32 and an SaO2 > 93%. Then, PS was set at 5 cmH2O above (PSb + 5) and below (PSb-5) this starting level. Ventilatory pattern, transdiaphragmatic pressure (Pdi), the pressure-time product of the diaphragm (PTPdi), the integrated EMG of the diaphragm, static PEEP (PEEPi, stat), dynamic PEEP (PEEPi, dyn), and the static compliance and resistance of the total respiratory system were recorded. RESULTS: Minute ventilation did not significantly change with variations in the level of PS, while Vt significantly increased with PS (PS-5 = 6.3 +/- 0.5 ml/kg vs. PSb = 10.1 +/- 0.9 [p < 0.01] and vs. PS + 5 = 11.7 +/- 0.6 [p < 0.01]), producing a reduction in respiratory frequency with longer expiratory time. The best values of blood gases were obtained at PSb, while at PSb-5, PaCO2 markedly increased. During PSb and PSb + 5 and to a lesser extent during PSb-5, most of the patients made several inspiratory efforts that were not efficient enough to trigger the ventilator to inspire; thus, the PTPdi "wasted" during these inefficient efforts was increased, especially during PS + 5. The application of an external PEEP (PEEPe) of 75% of the static intrinsic PEEP during PSb caused a significant reduction in the occurrence of these inefficient efforts (p < 0.05). Minute ventilation remained constant, but Vt decreased, together with Te, leaving the blood gases unaltered. The PTPdi per breath and the dynamic PEEPi were also significantly reduced (by 59% and 31% of control, respectively, p < 0.001) with the application of PEEPe. CONCLUSION: We conclude that in COPD patients, different levels of PSV may induce different respiratory patterns and gas exchange. PS levels capable of obtaining a satisfactory equilibrium in blood gases may result in ineffective respiratory efforts if external PEEP is not applied. The addition of PEEPe, not exceeding dynamic intrinsic PEEP, may also reduce the metabolic work of the diaphragm without altering gas exchange.

Acute Disease↗
PubMed1995

Simple method to measure total expiratory time constant based on the passive expiratory flow-volume curve.

OBJECTIVE: In intubated, mechanically ventilated patients, inspiration is forced by externally applied positive pressure. In contrast, exhalation is passive and depends on the time constant of the total respiratory system. The expiratory time constant is thus an important determinant of mechanical ventilation. The aim of this study was to evaluate a simple method for measuring the expiratory time constant in ventilated subjects. DESIGN: Prospective study using a lung simulator and ten dogs. SETTING: University hospital. SUBJECTS: Commercially available lung simulator and ten greyhound dogs. INTERVENTIONS: Different expiratory time constants were set on the lung simulator. In the dogs, the endotracheal tube was clamped to increase airways resistance by 22.5 cm H2O/(L/sec) and the lungs were injured with hydrochloric acid to decrease total respiratory compliance by 16 mL/cm H2O. This procedure resulted in a wide range of expiratory time constants. MEASUREMENTS AND MAIN RESULTS: Pneumotachography was used to measure flow and volume. The ratio of exhaled volume and peak flow was calculated from these signals, corrected for the limited exhalation time yielding the "calculated expiratory time constant" and compared with the actual expiratory time constant. The typical error was +/- 0.19 sec for the lung simulator and +/- 0.15 sec for the dogs. CONCLUSIONS: The volume and peak flow corrected for limited exhalation time is a good estimate of the total expiratory time constant in passive subjects and may be useful for the titration of mechanical ventilation.

Airway Resistance↗
PubMed1995

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↗
PubMed1995

[Current views on the use of vasodilators in pulmonary hypertension].

Vasodilators represent one of the main steps for the medical treatment of pulmonary hypertension; the rationale for their use is the reversibility of the pulmonary vasoconstriction, to be tested with a correct pharmacological trial. In this report the authors consider the use of calcium-channel blockers, prostaglandin and nitric oxide. Calcium blockers, the only drugs active when administered orally, provide a satisfactory clinical response in 25-30% of treated patients. Prostaglandins are active in a higher percentage of patients and can be infused in a domiciliary regimen with portable pumps even for long periods of time. Nitric oxide is the only selective pulmonary vasodilator; it is used in paediatric and adult cardiac surgery and in patients affected by respiratory distress syndrome, but its use is restricted to intensive care units and many cautions must be adopted. Finally some future therapeutic strategies are briefly reviewed: endothelin inhibitors, cGMP phosphodiesterase inhibitors etc.

Administration, Oral↗