Indications to chest radiograph in preoperative adult assessment: recommendations of the SIAARTI-SIRM commission.
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Biomedical subjects
Publications and source records attributed to E Calderini.
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An index (IS), quantitating the departure of the inspiratory flow profile (IFP) from the rectangular one, i.e. the optimal profile (IS=0), was computed from pneumotachograms recorded in 26 normal, anesthetized subjects breathing spontaneously through the endotracheal tube (ETT) or face mask (FM) with or without added resistances (R) and in 27 awake subjects breathing through the mouth and FM in the supine and seated posture at rest and during exercise (40 W) on a cycloergometer, through the nose and FM, and through the mouthpiece (MP). During anesthesia, IS decreased with R both while breathing through the ETT (DeltaIS=-0.037+/-0.006 (SE); P<0.001) and FM (DeltaIS=-0.054+/-0.008; P<0.001). This indicates that (a) the change of IFP towards the optimal shape is reflex in nature and related to the dynamic inspiratory load, and (b) tracheobronchial mechanoreceptors and inspiratory muscles are involved in this response. The reflex is also operative in awake subjects, since IS decreased whenever the inspiratory dynamic load was increased, as on turning from seated to supine posture (DeltaIS=-0.024+/-0.003; P<0.001), shifting from mouth to nose breathing (DeltaIS=-0.034+/-0.003; P<0.05), from rest to mild exercise (DeltaIS=-0.066+/-0.005; P<0.001). The different IS value between FM and MP breathing (DeltaIS=0.036+/-0.004; P<0.001) indicates, however, that other factors, likely behavioral, also affect the IFP.
OBJECTIVE: Air leaks around the mask are very likely to occur during noninvasive ventilation, in particular when prolonged ventilatory treatment is required. It has been suggested that leaks from the mask may impair the expiratory trigger cycling mechanism when inspiratory pressure support ventilation (PSV) is used. The aim of this study was to compare the short-term effect of two different expiratory cycling mechanisms (time-cycled vs flow-cycled) during noninvasive inspiratory pressure support ventilation (NIPSV) on patient-ventilator synchronisation in severe hypoxemic respiratory failure. STUDY POPULATION: Six patients with acute lung injury (ALI) due to acquired immunodeficiency syndrome (AIDS)-related opportunistic pneumonia were enrolled in the protocol. INTERVENTION: Each subject was first studied during spontaneous breathing with a Venturi oxygen mask (SB) and successively submitted to a randomly assigned 20' conventional flow-cycling (NIPSVfc) or time-cycling inspiratory pressure support ventilation (NIPSVtc). The pre-set parameters were: inspiratory pressure of 10 cm H2O, PEEP of 5 cm H2O for the same inspired oxygen fraction as during SB. A tight fit of the mask was avoided in order to facilitate air leaks around the mask. The esophageal pressure time product (PTPes) and tidal swings (delta Pes) were measured to evaluate the patient's respiratory effort. A subjective "comfort score" and the difference between patient and machine respiratory rate [delta RR(p-v)], calculated on esophageal and airway pressure curves, were used as indices of patient-machine interaction. RESULTS: Air leaks through the mask occurred in five out of six patients. The values of PEEPi (< 1.9 cm H2O) excluded significant expiratory muscle activity. NIPSVtc significantly reduced PTPes, delta Pes, and delta RR(p-v) when compared to NIPS-Vfc [230 +/- 41 (SE) vs 376 +/- 72 cm H2O.s.min-1; 8 +/- 2 vs 13 +/- 2 cm H2O; 1 +/- 1 vs 9 +/- 2 br.min-1; respectively] with a concomitant significant improvement of the "comfort score". CONCLUSIONS: In the presence of air leaks a time-cycled expiratory trigger provides a better patient-machine interaction than a flow-cycled expiratory trigger during NIPSV.
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The aim of this study was to assess the mechanical characteristics of the respiratory system in patients with acquired immune deficiency syndrome (AIDS) and acute respiratory distress syndrome (ARDS) caused by Pneumocystis carinii pneumonia (PCP). In 12 mechanically ventilated patients, total respiratory system mechanics was assessed using the technique of rapid airway occlusion during constant flow inflation, and was partitioned into lung and chest wall components using the oesophageal balloon technique. We measured interrupter resistance (Rint), which mainly reflects airway resistance, additional resistance (deltaR) due to viscoelastic behaviour and time constant inequalities, and static elastance (Est). In addition, the static inflation volume-pressure (V-P) curve was assessed. In eight patients, computed tomography scans were performed within 2 days of the assessment of respiratory mechanics. Compared to values reported in the literature for normal subjects, Est and deltaR were markedly increased in AIDS patients with PCP, whilst Rint exhibited a relatively smaller increase. These changes, which involved only the lung and airways, were mainly due to the reduction of ventilated lung units, but additional factors were involved to cause independent modifications of lung stiffness, airway calibre, and viscoelastic properties. The changes in Rint, deltaR, and Est were similar to those observed in other studies on patients with ARDS of different aetiologies. At variance with common observations in the latter patients, none of the AIDS patients with PCP exhibited an inflection point on the static inflation V-P curve, suggesting little or no alveolar recruitment during lung inflation. This finding could be related to the distinctive histopathology of Pneumocystis carinii pneumonia. Indeed, computed tomography revealed homogeneous diffuse interstitial and alveolar infiltration rather than the dense, dependent opacities observed in other studies on acute respiratory distress syndrome of different aetiologies.
METHODS: One hundred and five ASA I-II patients, scheduled for elective surgical procedures were studied in order to evaluate the effect of different surgical postures on physiological pulmonary dead space (VDphys/ VT) and arterial to end-tidal carbon dioxide gradient [P(a-Et)CO2]. Patients were divided into four groups according to their position on the operating table: supine position (acting as control group, n = 33), 20 degree Trendelenburg position (n = 24), lateral position (n = 24) and prone position with convex saddle frame (n = 24). Physiologic dead space was measured using Enghoff modification of Bohr equation. Arterial CO2 partial pressure was measured by blood gas analysis and end tidal CO2 was measured by means of an infrared CO2 analyser. All measurements were performed 20 minutes after general anaesthesia induction, with patients mechanically ventilated by a constant inspiratory flow (TV = 8 ml kg-1, RR = 10-14, EIP = 10%) in order to reach a steady state end tidal CO2 ranging between 32 and 36 mmHg; afterwards surgery started. RESULTS: Arterial blood pressure showed a mean decrease of about 5-10% compared to baseline values, but no significant differences in arterial pressure decrease were found between the four groups. A significant VDphys/VT increase in postures other than supine was observed, unless it was statistically significant in lateral and prone position only; while P(a-Et)CO2 was higher in all postures compared to supine. Changes of intrapulmonary gas and blood distribution due to patients' posture are probably responsible for the observed physiologic dead space and CO2 gradient differences. CONCLUSIONS: In conclusion, the clinical practice of predicting PaCO2 from EtCO2 must be tempered by recognition of the potential magnitude of P(a-Et)CO2 gradient, which is higher than normal during general anaesthesia and further increased when positioning the patient other than supine.
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Tracheal (Ptr) and esophageal (Pes) pressure and flow were measured in 12 supine anesthetized paralyzed normal subjects aged 16-22 yr. The subjects were ventilated with a fixed inflation volume (range 0.57-0.62 liter) and with different constant flows ranging between 0.24 and 1.12 l/s. A rapid airway shutter (closing time 10-15 ms) was used to briefly occlude (0.4-0.9) the airways at end inspiration for 33-44 consecutive breaths. At each flow level, Ptr and Pes records obtained during end-inspiratory occlusions were ensemble averaged to allow for the cardiac artifacts. The interrupter resistances of the chest wall and respiratory system were assessed as the rapid fall in Pes and Ptr with occlusion divided by the flow preceding the occlusion. Interrupter resistances of both the chest wall and lung were independent of flow and averaged 0.4 +/- 0.1 and 1.5 +/- 0.4 (SD) cmH2O.s.l-1, respectively. The contribution of the chest wall to the total interrupter resistance was approximately 27% at flows < or = 1 l/s.
The utility of laparoscopic cholecystectomy in reducing postoperative pain and patient's hospital discharge is already known. Nevertheless peritoneal gas insufflation required by surgical procedure can modify respiratory homeostasis during general anesthesia. The aim of this study was to evaluate the effect of laparoscopic cholecystectomy on pulmonary dead spaces and alveolar gas exchange during inhalation anesthesia compared with traditional laparotomic cholecystectomy. With the approval of Hospital Ethical Committee, thirty-one patients undergoing isoflurane general anesthesia for laparoscopic (CL-S, n = 16) and open (CL-T, n = 15) cholecystectomy were prospectively evaluated in order to asses modifications in physiological (VDphy/VT), anatomical (VDan/VT) and alveolar (VDalv/VT) dead space to tidal volume ratio, arterial to end-tidal carbon dioxide partial pressure difference [P(a-Et)CO2] and alveolar to arterial oxygen partial pressure difference (A-aDO2). Patients, 21-64 years-old, ASA I-II, had no cardiopulmonary diseases. The CL-S group required peritoneal insufflation of carbon dioxide with an intraabdominal pressure (IAP) of about 10-14 mmHg and antitrendelenburg positioning (15-20 degree). Expired gas measurements and arterial blood gas sample for pulmonary dead spaces and arterial to alveolar CO2 and O2 gradient calculation were performed 20 min after a steady state condition. VDphy/VT, VDalv/VT, P(a-Et)CO2 and A-aDO2 increased significantly in the CL-S compared to the CL-T group (p < 0.05). No differences were found in the VDan/VT. These results can be explained by analteration of the ventilation to perfusion ratio (VA/Q) with an increase of high VA/Q regions due to the antitrendelenburg positioning with a redistribution of blood flow towards basal zones.(ABSTRACT TRUNCATED AT 250 WORDS)
Nasal pressure support ventilation (NPSV) has been shown to be useful in the treatment of acute and chronic pulmonary failure. However, little is known about respiratory muscle activity during NPSV in stable patients with COPD. The aim of this study was to test the effect of two levels (10 and 20 cm H2O) of NPSV on diaphragmatic activity, in a group of seven stable, severe COPD patients (FEV1 20 percent +/- 7 of pred, FEV1/FVC 35 percent) with hypercapnic respiratory insufficiency. Since these patients had an intrinsic PEEP (PEEPi) of 2.6 +/- 1.3 cm H2O, we also investigated the effect of adding 5 cm H2O external PEEP (PEEPe) during NPSV. Blood gases, ventilatory pattern by inductive plethysmography, integrated electromyogram of the diaphragm (Edi), transdiaphragmatic pressure (Pdi), and the diaphragmatic pressure time product (PTPdi) were recorded during randomized 15-min runs of both levels of NPSV with and without the addition of PEEPe. Minute ventilation did not change with the application of NPSV, but a significant decrease in breathing frequency with a parallel increase in tidal volume was observed, so that blood gas determinations improved at the higher levels of support. A marked statistically significant reduction in diaphragmatic activity, as assessed by a decrease in Pdi swings, PTPdi, and Edi, was detected at the levels of 10 and 20 cm H2O; a further significant decrease in these values was observed when PEEPe was added. PEEPi decreased significantly only with the application of PEEPe, resulting in a small increase in end-expiratory lung volume. We conclude that NPSV improves diaphragmatic function in patients with severe stable COPD; this effect may be enhanced by the applications of external PEEP.
With the use of the technique of rapid airway occlusion during constant flow inflation, respiratory mechanics were studied in eight anesthetized paralyzed supine normal humans during zero (ZEEP) and positive end-expiratory pressure (PEEP) ventilation. PEEP increased the end-expiratory lung volume by 0.49 liter. The changes in transpulmonary and esophageal pressure after flow interruption were analyzed in terms of a seven-parameter "viscoelastic" model. This allowed assessment of static lung and chest wall elastance (Est,L and Est,W), partitioning of overall resistance into airway interrupter (Rint,L) and tissue resistances (delta RL and delta RW), and computation of lung and chest wall "viscoelastic constants." With increasing flow, Rint,L increased, whereas delta RL and delta RW decreased, as predicted by the model. Est,L, Est,W, and Rint,L decreased significantly with PEEP because of increased lung volume, whereas delta R and viscoelastic constants of lung and chest wall were independent of PEEP. The results indicate that PEEP caused a significant decrease in Rint,L, Est,L, and Est,W, whereas the dynamic tissue behavior, as reflected by delta RL and delta RW, did not change.
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Pulmonary and chest wall mechanics were studied in 18 anesthetized paralyzed supine humans by use of the technique of rapid airway occlusion during constant-flow inflation. Analysis of the changes in transpulmonary pressure after flow interruption allowed partitioning of the overall resistance of the lung (RL) into two compartments, one (Rint,L) reflecting airway resistance and the other (delta RL) representing the viscoelastic properties of the pulmonary tissues. Similar analysis of the changes in esophageal pressure indicates that chest wall resistance (RW) was due entirely to the viscoelastic properties of the chest wall tissues (delta RW = RW). In line with previous measurements of airway resistance, Rint,L increased with increasing flow and decreased with increasing volume. The opposite was true for both delta RL and delta RW. This behavior was interpreted in terms of a viscoelastic model that allowed computation of the viscoelastic constants of the lung and chest wall. This model also accounts for frequency, volume, and flow dependence of elastance of the lung and chest wall. Static and dynamic elastances, as well as delta R, were higher for the lung than for the chest wall.
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Recent work has demonstrated the ability of continuous positive airway pressure (CPAP) to relieve dyspnea during exercise in patients with severe chronic obstructive pulmonary disease (COPD). The present study examined the effects of CPAP (7.5-10 cmH2O) on the pattern of respiratory muscle activation and its relationship to dyspnea during constant work load submaximal bicycle exercise [20 +/- 4.8 (SE) W] in eight COPD patients (forced expiratory volume in 1 s = 25 +/- 3% predicted). Tidal volume, respiratory rate, minute ventilation, and end-expiratory lung volume increased with exercise as expected. There was no change in breathing pattern, end-expiratory lung volume, or pulmonary compliance and resistance with the addition of CPAP. CPAP reduced inspiratory muscle effort, as indicated by the pressure-time integral of transdiaphragmatic (integral of Pdi.dt) and esophageal pressure (integral of Pes.dt, P less than 0.01 and P less than 0.05, respectively). In contrast, the pressure-time integral of gastric pressure (integral of Pga.dt), used as an index of abdominal muscle recruitment during expiration, increased (P less than 0.01). Dyspnea improved with CPAP in five of the eight patients. The amelioration of dyspnea was directly related to reductions in integral of Pes.dt (P less than 0.001) but inversely related to increases in integral of Pga.dt (P less than 0.01). In conclusion, CPAP reduces inspiratory muscle effort during exercise in COPD patients. However, the expected improvement in dyspnea is not seen in all patients and may be explained by more marked increases in expiratory muscle effort in some individuals.
The effects of inspiratory flow rate and inflation volume on the resistive properties of the total respiratory system were investigated in 16 anesthetized paralyzed humans by using the technique of rapid airway occlusion during constant flow inflation. This allowed measurement of the intrinsic resistance (Rmin,rs) and of the effective additional resistance (delta Rrs) as the result of viscoelastic pressure dissipations within the pulmonary and chest wall tissues. We observed that 1) at fixed inflation volume, Rmin,rs increased linearly with increasing flow although delta Rrs decreased according to an exponential function; 2) at fixed inflation flow, Rmin,rs decreased with increasing inflation volume although there was a concomitant increase in delta Rrs. This behavior could be explained in terms of a spring-and-dashpot model incorporating 1) the standard resistance and elastance and 2) a spring-and-dashpot in parallel with standard elastance, reflecting the stress adaptation units within the thoracic tissues.