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PubMed1995

Titration of tidal volume and induced hypercapnia in acute respiratory distress syndrome.

Mechanical ventilation may promote overdistension-induced pulmonary lesions in patients with acute respiratory distress syndrome (ARDS). The static pressure-volume (P-V) curve of the respiratory system can be used to determine the lung volume and corresponding static airway pressure at which lung compliance begins to diminish (the upper inflection point, or UIP). This fall in compliance may indicate overdistension of lung units. We prospectively studied 42 patients receiving mechanical ventilation with an FIO2 of 0.5 or more for at least 24 h. According to the Lung Injury Score (LIS), 25 patients were classified as having ARDS (LIS > 2.5), while 17 patients constituted a non-ARDS control group. The P-V curve was obtained every 2 d. Mechanical ventilation initially used standard settings (volume-control mode, a positive end-expiratory pressure [PEEP] adjusted to the lower inflection point on the P-V curve, and a tidal volume [VT] of 10 ml/kg). The end-inspiratory plateau pressure (Pplat) was compared to the UIP, and VT was lowered when the Pplat was above the UIP. In the range of lung volume studied on the P-V curves (up to 1600 ml), a UIP could be shown in only one control patient (at 23 cm H2O). By contrast, a UIP was present on the P-V curve obtained from all patients with ARDS, corresponding to a mean airway pressure of 26 +/- 6 cm H2O, a lung volume of 850 +/- 200 ml above functional residual capacity and 610 +/- 235 ml above PEEP.(ABSTRACT TRUNCATED AT 250 WORDS)

Case-Control Studies↗

PubMed1990

Diagnostic value of maximal exercise tidal volume.

Though breathing pattern is frequently analyzed during clinical exercise testing, there is little information regarding its usefulness in the differential diagnosis of impaired exercise tolerance. This study tested the hypothesis that differences in peak tidal volume during exercise between patients with different cardiorespiratory diseases are related largely to differences in severity of respiratory mechanical impairment (vital capacity), not to differences in disease state. Patients with chronic obstructive pulmonary disease, restrictive lung disease, bronchial asthma, and heart disease (mitral valve disease or left ventricular dysfunction) were studied. Subjects selected had one and only one of the above diagnoses. All subjects performed maximal (symptom-limited) incremental exercise on a cycle ergometer. Multiple linear regression of all subjects (n = 30) in all four groups showed a significant correlation between VTmax and VC: VTmax = 0.55, VC -0.09 L (r = 0.827, p less than 0.0001). The VTmax/VC (x 100) was (mean +/- SD) 44 +/- 15, 54 +/- 11, 56 +/- 11, and 54 +/- 12 for the COPD, RLD, BA and HD patients respectively. There was no significant difference between any of the groups. We concluded that differences in VTmax between different patients are related largely to differences in VC (ie, differences in severity of respiratory mechanical impairment), not to differences in disease state. Measurement of VTmax or the VTmax/VC ratio has little value in the differential diagnosis of exertional dyspnea.

Aged↗

PubMed2000

Compliance is nonlinear over tidal volume irrespective of positive end-expiratory pressure level in surfactant-depleted piglets.

Between the lower and the upper inflection point of a quasistatic pressure-volume (PV) curve, a segment usually appears in which the PV relationship is steep and linear (i.e., compliance is high, with maximal volume change per pressure change, and is constant). Traditionally it is assumed that when positive end-expiratory pressure (PEEP) and tidal volume (V T) are titrated such that the end-inspiratory volume is positioned at this linear segment of the PV curve, compliance is constant over VT during ongoing ventilation. The validity of this assumption was addressed in this study. In 14 surfactant-deficient piglets, PEEP was increased from 3 cm H(2)O to 24 cm H(2)O, and the compliance associated with 10 consecutive volume increments up to full VT was determined with a modified multiple-occlusion method at the different PEEP levels. With PEEP at approximately the lower inflection point, compliance was minimal in most lungs and decreased markedly over VT, indicating overdistension. Compliance both increased and decreased within the same breath at intermediate PEEP levels. It is concluded that a PEEP that results in constant compliance over the full VT range is difficult to find, and cannot be derived from conventional respiratory-mechanical analyses; nor does this PEEP level coincide with maximal gas exchange.

Animals↗

PubMed1999

Effect of frequency and tidal volume on pleural pressure in rabbits during high frequency ventilation.

Regional effects of the chest wall on airway pressure transmission were studied during high frequency ventilation in anesthetized rabbits. We measured airway pressure (Paw), esophageal pressure (Pes), and costal pleural pressure (Ppl) by a rib capsule and flow and volume with a calibrated pneumotachograph. Using a closed circuit, pressures and flow were measured at varying frequencies (2-80 Hz) and tidal volumes (2-20 ml). Mean Pes and Ppl increased with flow amplitude above 100-250 ml/s, whereas mean Paw decreased, consistent with air trapping. Paw, Pes, and Ppl amplitudes increased monotonically with flow amplitude except above 400-500 ml/s, where the Ppl amplitude decreased suddenly. The latter occurring simultaneously with a sudden fall in mean Paw indicated airway flow limitation in costal regions. Flow instabilities during flow limitation were consistent with the large increase in the phase difference between Paw and Ppl and its variability, with frequency. By contrast, the phase difference between Paw and Pes and its variability were relatively small. These differences in Pes from Ppl responses might be caused by a difference in the impedance of the airway-mediastinum pathway or a direct transmission of tracheal pressure oscillations to the esophagus. The former suggests that constraints offered by the mediastinum and rib cage resulted in nonuniform ventilation during high frequency ventilation.

Animals↗

PubMed1998

Evaluation of respiratory inductive plethysmography in controlled ventilation: measurement of tidal volume and PEEP-induced changes of end-expiratory lung volume.

STUDY OBJECTIVE: To determine the accuracy of respiratory inductive plethysmography (RIP) with a respiratory monitor (Respitrace Plus; NIMS Inc., Miami) operating in the DC-mode for the measurement of tidal volumes (VT) and positive end-expiratory pressure (PEEP)-induced changes of end-expiratory lung volume (deltaEELV) in patients with normal pulmonary function, acute lung injury (ALI), and COPD during volume-controlled ventilation. DESIGN: Prospective comparison of RIP with pneumotachography (PT) for assessment of VT and with multibreath nitrogen washout procedure (N2WO) for determination of deltaEELV as reference methods. SETTING: Mixed ICU at a university hospital. PATIENTS: Thirty-one sedated and paralyzed patients: 12 patients with normal pulmonary function mechanically ventilated after major surgery, 10 patients with respiratory failure due to ALI, and 9 patients with a known history of COPD ventilated after surgery or because of respiratory failure due to bronchopulmonary infection. INTERVENTIONS: Stepwise increase of PEEP from 0 to 5 to 10 cm H2O and reduction to 0 cm H2O again. On each PEEP level, N2WO was performed. MEASUREMENTS AND MAIN RESULTS: The baseline drift of RIP averaged 25.4+/-29.1 mL/min but changed over a wide range even in single patient measurements. Determination of VT for single minutes revealed that 66.5% and 90.0% of all values were accurate within a range of +/-10% and +/-20%, respectively. The deviation for VT measurements between RIP and PT in patients with COPD was significantly (p<0.05) higher compared to patients with ALI or normal pulmonary function. The difference of deltaEELV between RIP and N2WO was 11.6+/-174.1 mL with correlation coefficients of 0.77 (postoperative and COPD patients) and 0.86 (ALI patients). However, just 25.8% and 46.2% were precise within +/-10% and +/-20%, respectively. deltaEELV determination in COPD patients differed more between RIP and N2WO than in the other groups, but this was not significant. CONCLUSION: In a mixed group of patients undergoing controlled ventilation, RIP using the Respitrace Plus monitor was not consistently precise enough for quantitative evaluation of VT and EELV when compared to our reference methods. This was most evident in patients with COPD. For long-term volume measurements, a better control of the baseline drift of RIP should be achieved.

Aged↗

PubMed2003

Influence of tidal volume on pulmonary NO release, tissue lipid peroxidation and surfactant phospholipids.

Mechanical stress during ventilation may cause or aggravate acute lung injury. This study investigates the influence of low vs. high tidal volume (V(t)) on factors known to play key roles in acute lung injury: nitric oxide release, eNOS and iNOS gene expression, lipid peroxidation (LPO), and surfactant phospholipids (PL). Isolated rabbit lungs were subjected to one of three ventilation patterns for 135 min (V(t)-PEEP): 6 ml/kg-0 cm H(2)O. 12 ml/kg-0 cm H(2)O 6 ml/kg-5 cm H(2)O, 12 ml/kg-0 cm H(2)O, and 6 ml/kg-5 cm H(2)O resulted in comparable peak inspiratory pressure (PIP). This allowed comparing low and high V(t) without dependence on PIP. Ventilatory patterns did not induce changes in pulmonary artery pressure, vascular permeability (K(f,c)), PIP or pulmonary compliance. High V(t) in comparison with both of the low V(t) groups caused an increase in BALF-nitrite (30.6+/-3.0* vs. 21.4+/-2.2 and 16.2+/-3.3 microM), BALF-PL (1110+/-19* vs. 750+/-68 and 634+/-82 microg/ml), and tissue LPO product accumulation (0.62+/-0.051* vs. 0.48+/-0.052 and 0.43+/-0.031 nmol/mg), *P<0.05 each. Perfusate nitrite and BALF-PL composition (assessed by use of 31P-NMR spectroscopy and MALDI-TOF mass spectrometry) did not differ among the groups. High V(t) ventilation reduced eNOS gene expression but did not affect iNOS expression. The increased release of NO and the accumulation of LPO products may represent early lung injury while elevated BALF-PL may reflect distension-induced surfactant secretion.

Animals↗

PubMed1996

Positive end-expiratory pressure prevents the loss of respiratory compliance during low tidal volume ventilation in acute lung injury patients.

STUDY OBJECTIVE: To study the effect of positive end-expiratory pressure (PEEP) on the decay of respiratory system compliance (Cpl,rs) due to low tidal volume (VT) ventilation in acute lung injury (ALI) patients. SETTING: General ICU in a university hospital. PARTICIPANTS: Eight ALI patients with a lung injury score greater than 2.5. INTERVENTION: Pressure-controlled ventilation (PCV) and volume-controlled ventilation (VCV), with an average VT of 8.5 +/- 0.4 mL/kg, were applied at three levels of PEEP (5, 10, and 15 cm H2O). Before each PCV and VCV period, lung volume history was standardized by manual hyperinflation maneuvers. MEASUREMENTS: We measured Cpl,rs at time 0 (start), 10, 20, and 30 (end) min from the beginning of each PCV and VCV period. Gas exchange and hemodynamic data were collected at end. RESULTS: At PEEP 5 and 10 cm H2O, we observed a progressive Cpl,rs decay with both PCV and VCV modes. At PEEP 5 cm H2O, we detected a higher Cpl,rs decrease during PCV, due to a higher Cpl,rs at start, compared with VCV. At PEEP 15 cm H2O, Cpl,rs did not decrease significantly. Cpl,rs values measured at end as well as oxygenation and hemodynamic data did not differ between PCV and VCV. At PEEP 15 cm H2O, PCV provided lower PaCO2 than VCV. CONCLUSIONS: A PEEP of at least 15 cm H2O was needed to prevent Cpl,rs decay. The progressive Cpl,rs loss we observed at lower PEEP probably reflects alveolar instability.

Adult↗

PubMed1983

Bilateral vocal cord paralysis for 26 years with respiratory failure. Timing of restoration of tidal volume and serum electrolytes after tracheostomy.

A 31-year-old man had respiratory failure caused by bilateral vocal cord paralysis. He had had limited exercise tolerance since the age of five years, when he had had poliomyelitis. Respiratory failure was present for at least three months. Following relief of the upper airway obstruction by tracheostomy, the patient's tidal volume increased from 200 ml to 500 ml in two days, his carbon dioxide tension fell from 75 to 38 mm Hg, and his arterial bicarbonate level decreased from 39.8 to 25.6 mEq/L in five days. The patient is currently doing well with a permanent tracheostomy.

Adult↗

PubMed1992

Reduced tidal volume increases 'air hunger' at fixed PCO2 in ventilated quadriplegics.

The act of breathing diminishes the discomfort associated with hypercapnia and breath-holding. To investigate the mechanisms involved in this effect, we studied the effect of tidal volume (VT) on CO2-evoked air hunger in 5 high-level quadriplegic subjects whose ventilatory capacity was negligible, and who lacked sensory information from the chest wall. Subjects were ventilated at constant frequency with a hyperoxic gas mixture, and end-tidal PCO2 was maintained at a constant but elevated level. VT was varied between the subjects' normal VT and a smaller VT. Subjects used a category scale to rate their respiratory discomfort or 'air hunger' at 30-40 sec intervals. In 4 of 5 subjects there was a strong inverse relationship between breath size and air hunger ratings. The quality of the sensation associated with reduced VT was nearly identical to that previously experienced with CO2 alone. We conclude that afferent information from the lungs and upper airways is sufficient to modify the sensation of air hunger.

Adult↗

PubMed1984

CO2 elimination as a function of frequency and tidal volume in rabbits during HFO.

CO2 elimination (VCO2) was monitored during high-frequency oscillation (HFO) over a frequency (f) range of 2-30 Hz in anesthetized and paralyzed rabbits to determine whether effective gas exchange could be achieved in this species, to determine the f and tidal volume (VT) dependence of gas exchange in this species, and to compare these results with those from dog and human studies. We were able to produce VCO2 levels during HFO that exceeded normal steady-state levels of CO2 production with VT's less than the total dead space volume. VCO2 was related to f in a curvilinear fashion, whereas in some rabbits VCO2 became independent of f at higher frequencies. This curvilinear relationship between f and VCO2 is similar to data from humans but contrasts with the linear relationship found in dogs. Evidence is presented indicating frequency-dependent behavior of gas exchange is correlated with a frequency-dependent decrease in respiratory system resistance. We propose that the frequency-dependent mechanical properties of the rabbit lung may also account for the species differences in HFO gas exchange.

Animals↗

PubMed1999

Exacerbation of acute pulmonary edema during assisted mechanical ventilation using a low-tidal volume, lung-protective ventilator strategy.

STUDY OBJECTIVES: To assess the magnitude of negative intrathoracic pressure development in a patient whose pulmonary edema acutely worsened immediately following the institution of a low-tidal volume (VT) strategy. DESIGN: Mechanical lung modeling of patient-ventilator interactions based on data from a case report. SETTING: Medical ICU and laboratory. PATIENT: A patient with suspected ARDS and frank pulmonary edema. INTERVENTIONS: The patient's pulmonary mechanics and spontaneous breathing pattern were measured. Samples of arterial blood and pulmonary edema fluid were obtained. MEASUREMENTS: A standard work-of-breathing lung model was used to mimic the ventilator settings, pulmonary mechanics, and spontaneous breathing pattern observed when pulmonary edema worsened. Comparison of the pulmonary edema fluid-to-plasma total protein concentration ratio was made. RESULTS: The patient's spontaneous VT demand was greater than preset. The lung model revealed simulated intrathoracic pressure changes consistent with levels believed necessary to produce pulmonary edema during obstructed breathing. A high degree of imposed circuit-resistive work was found. The pulmonary edema fluid-to-plasma total protein concentration ratio was 0.47, which suggested a hydrostatic mechanism. CONCLUSION: Ventilator adjustments that greatly increase negative intrathoracic pressure during the acute phase of ARDS may worsen pulmonary edema by increasing the transvascular pressure gradient. Therefore, whenever sedation cannot adequately suppress spontaneous breathing (and muscle relaxants are contraindicated), a low-VT strategy should be modified by using a pressure-regulated mode of ventilation, so that imposed circuit-resistive work does not contribute to the deterioration of the patient's hemodynamic and respiratory status.

Adult↗

PubMed2007

Measurement of pulsatile tidal volume, pressure amplitude, and gas flow during high-frequency percussive ventilation, with and without partial cuff deflation.

OBJECTIVE: With a high-frequency percussive ventilator and a mechanical lung model, to measure tidal volume (V(T)), pulsatile pressure amplitude (difference between peak and nadir pulsatile pressure [DeltaP];), and mean airway pressure (P (aw)) at various pulsatile frequencies, pulsatile inspiratory-expiratory ratios (I:E(p)), and pressures (measured at the interface between the pulse-generator and the endotracheal tube [P(vent)]). METHODS: With the endotracheal tube inside an artificial trachea, we manipulated the high-frequency percussive ventilation settings and adjuncts, including pulsatile frequency, I:E(p), and P(vent) by manipulating pulsatile flow. We also studied the effects of partially deflating the endotracheal tube cuff. We measured P (aw), pulsatile pressure amplitude at the carina (DeltaP(c)), and pulsatile V(T) at the carina. With the cuff partly deflated, we measured the fraction of inspired oxygen (F(IO(2))) in the gas efflux above and below the cuff. RESULTS: Increasing the pulsatile frequency from 300 cycles/min to 600 cycles/min and changing the I:E(p) from 1:3 to 1:1 significantly reduced V(T) (p < 0.001). P (aw) and DeltaP(c) were unaffected by the change in pulsatile frequency or I:E(p), except when we did not preserve the pulsatile flow. The measured V(T) range was from 19.1 mL (at 600 cycles/min) to 47.3 mL (at 300 cycles/min). Partial cuff deflation did not significantly reduce P (aw) or DeltaP(c), but it did significantly reduce V(T) and F(IO(2)). CONCLUSION: During high-frequency percussive ventilation, the pulsatile frequency is inversely related to V(T). Partial cuff deflation reduces the delivered F(IO(2)).

Air Pressure↗

PubMed1994

Rapid shallow breathing (frequency-tidal volume ratio) did not predict extubation outcome.

This was a prospective study of 52 patients that were extubated in our medical intensive care unit. Rapid shallow breathing, represented by a ratio of frequency to tidal volume (f/VT) of more than 105, was evaluated either on continuous positive airway pressure or pressure support prior to extubation as a marker of extubation outcome. Twelve out of 13 patients (92 percent) with rapid shallow breathing (f/VT ratio > 105) were successfully extubated. Out of 9 extubation failures only 1 patient had a f/VT ratio more than 105 (11 percent). A measured f/VT ratio of less than 105 had a sensitivity and specificity of 72 and 11 percent, respectively, for extubation success. Patients who had unsuccessful outcomes were ventilated for a significantly more prolonged period (9.6 +/- 6.8 d vs 4.6 +/- 3.9 d, unpaired t test, p = 0.004). We conclude that the presence of rapid shallow breathing during a weaning trial with the patient on partial ventilatory support does not necessarily preclude successful extubation.

Adolescent↗

PubMed2005

Mathematical modelling to centre low tidal volumes following acute lung injury: a study with biologically variable ventilation.

BACKGROUND: With biologically variable ventilation [BVV--using a computer-controller to add breath-to-breath variability to respiratory frequency (f) and tidal volume (VT)] gas exchange and respiratory mechanics were compared using the ARDSNet low VT algorithm (Control) versus an approach using mathematical modelling to individually optimise VT at the point of maximal compliance change on the convex portion of the inspiratory pressure-volume (P-V) curve (Experimental). METHODS: Pigs (n = 22) received pentothal/midazolam anaesthesia, oleic acid lung injury, then inspiratory P-V curve fitting to the four-parameter logistic Venegas equation F(P) = a + b[1 + e-(P-c)/d]-1 where: a = volume at lower asymptote, b = the vital capacity or the total change in volume between the lower and upper asymptotes, c = pressure at the inflection point and d = index related to linear compliance. Both groups received BVV with gas exchange and respiratory mechanics measured hourly for 5 hrs. Postmortem bronchoalveolar fluid was analysed for interleukin-8 (IL-8). RESULTS: All P-V curves fit the Venegas equation (R2 > 0.995). Control VT averaged 7.4 +/- 0.4 mL/kg as compared to Experimental 9.5 +/- 1.6 mL/kg (range 6.6 - 10.8 mL/kg; p < 0.05). Variable VTs were within the convex portion of the P-V curve. In such circumstances, Jensen's inequality states "if F(P) is a convex function defined on an interval (r, s), and if P is a random variable taking values in (r, s), then the average or expected value (E) of F(P); E(F(P)) > F(E(P))." In both groups the inequality applied, since F(P) defines volume in the Venegas equation and (P) pressure and the range of VTs varied within the convex interval for individual P-V curves. Over 5 hrs, there were no significant differences between groups in minute ventilation, airway pressure, blood gases, haemodynamics, respiratory compliance or IL-8 concentrations. CONCLUSION: No difference between groups is a consequence of BVV occurring on the convex interval for individualised Venegas P-V curves in all experiments irrespective of group. Jensen's inequality provides theoretical proof of why a variable ventilatory approach is advantageous under these circumstances. When using BVV, with VT centred by Venegas P-V curve analysis at the point of maximal compliance change, some leeway in low VT settings beyond ARDSNet protocols may be possible in acute lung injury. This study also shows that in this model, the standard ARDSNet algorithm assures ventilation occurs on the convex portion of the P-V curve.

Algorithms↗

PubMed2006

Intraoperative tidal volume as a risk factor for respiratory failure after pneumonectomy.

BACKGROUND: Respiratory failure is a leading cause of postoperative morbidity and mortality in patients undergoing pneumonectomy. The authors hypothesized that intraoperative mechanical ventilation with large tidal volumes (VTs) would be associated with increased risk of postpneumonectomy respiratory failure. METHODS: Patients undergoing elective pneumonectomy at the authors' institution from January 1999 to January 2003 were studied. The authors collected data on demographics, relevant comorbidities, neoadjuvant therapy, pulmonary function tests, site and type of operation, duration of surgery, intraoperative ventilator settings, and intraoperative fluid administration. The primary outcome measure was postoperative respiratory failure, defined as the need for continuation of mechanical ventilation for greater than 48 h postoperatively or the need for reinstitution of mechanical ventilation after extubation. RESULTS: Of 170 pneumonectomy patients who met inclusion criteria, 30 (18%) developed postoperative respiratory failure. Causes of postoperative respiratory failure were acute lung injury in 50% (n = 15), cardiogenic pulmonary edema in 17% (n = 5), pneumonia in 23% (n = 7), bronchopleural fistula in 7% (n = 2), and pulmonary thromboembolism in 3% (n = 1). Patients who developed respiratory failure were ventilated with larger intraoperative VT than those who did not (median, 8.3 vs. 6.7 ml/kg predicted body weight; P < 0.001). In a multivariate regression analysis, larger intraoperative VT (odds ratio, 1.56 for each ml/kg increase; 95% confidence interval, 1.12-2.23) was associated with development of postoperative respiratory failure. The interaction between larger VT and fluid administration was also statistically significant (odds ratio, 1.36; 95% confidence interval, 1.05-1.97). CONCLUSION: Mechanical ventilation with large intraoperative VT is associated with increased risk of postpneumonectomy respiratory failure.

Aged↗

PubMed2001

Implementation of a low tidal volume ventilation protocol for patients with acute lung injury or acute respiratory distress syndrome.

The ARDS (acute respiratory distress syndrome) Network study found 22% lower mortality in acute lung injury and ARDS patients ventilated with low tidal volumes (V(T)) than in those ventilated with traditional V(T) ventilation. Several points should be considered when using the low V(T) protocol for clinical practice. Prior to implementation, hemodynamic and acid-base status, minute ventilation, and adequacy of sedation should be assessed to minimize the potential for intolerance. The volume-preset, assist-control mode is recommended for better control of V(T), and the respiratory rate should be increased as V(T) is reduced, so as to maintain minute ventilation and prevent acute hypercapnia. When unavoidable, hypercapnia should be induced slowly. Ventilator inspiratory flow (V(I)) and trigger sensitivity settings should be optimized to limit the increase in work of breathing and dyspnea. When dyspnea results in double-triggered breaths, V(T) can be titrated to 7-8 mL/kg, provided end-inspiratory plateau pressure is < or = 30 cm H(2)O. In severe acidosis (pH < 7.15) V(T) also can be increased. However, every effort should be made to maintain plateau pressure and V(T) goals by buffering severe acidosis and treating patient-ventilator asynchrony with sedation. Evaluation for weaning should occur when adequate oxygenation can be maintained on 40% oxygen and a positive end-expiratory pressure of 8 cm H(2)O. Pressure support levels between 5 and 20 cm H(2)O (above 5 cm H(2)O positive end-expiratory pressure) are used for weaning and titrated to keep the respiratory rate < 35 breaths/min. Pressure support levels should be weaned aggressively, as long as the protocol's weaning tolerance criteria can be maintained.

Acute Disease↗

PubMed1998

Respiratory system compliance decreases after cardiopulmonary resuscitation and stomach inflation: impact of large and small tidal volumes on calculated peak airway pressure.

The purpose of the present study was to evaluate respiratory system compliance after cardiopulmonary resuscitation (CPR) and subsequent stomach inflation. Further, we calculated peak airway pressure according to the different tidal volume recommendations of the European Resuscitation Council (7.5 ml/kg) and the American Heart Association (15 ml/kg) for ventilation of an unintubated cardiac arrest victim. After 4 min of ventricular fibrillation, and 6 min of CPR, return of spontaneous circulation (ROSC) after defibrillation occurred in seven pigs. Respiratory system compliance was measured at prearrest, after ROSC, and after 2 and 4 l of stomach inflation in the postresuscitation phase; peak airway pressure was subsequently calculated. Before cardiac arrest the mean (+/- S.D.) respiratory system compliance was 30 +/- 3 ml/cm H2O, and decreased significantly (P < 0.05) after ROSC to 24 +/- 5 ml/cm H2O, and further declined significantly to 18 +/- 4 ml/cm H2O after 2 l, and to 13 +/- 3 ml/cm H2O after 4 l of stomach inflation. At prearrest, the mean +/- S.D. calculated peak airway pressure according to European versus American guidelines was 9 +/- 1 versus 18 +/- 3 cm H2O, after ROSC 12 +/- 2 versus 23 +/- 4 cm H2O, and 15 +/- 2 versus 30 +/- 5 cm H2O after 2 l, and 22 +/- 6 versus 44 +/- 12 cm H2O after 4 l of stomach inflation. In conclusion, respiratory system compliance decreased significantly after CPR and subsequent induction of stomach inflation in an animal model with a wide open airway. This may have a significant impact on peak airway pressure and distribution of gas during ventilation of an unintubated patient with cardiac arrest.

Airway Resistance↗

PubMed1999

Aspiration of dead space allows normocapnic ventilation at low tidal volumes in man.

OBJECTIVE: Aspiration of dead space (ASPIDS) improves carbon dioxide (CO2) elimination by replacing dead space air rich in CO2 with fresh gas during expiration. The hypothesis was that ASPIDS allows normocapnia to be maintained at low tidal volumes (VT). DESIGN: Prospective study. SETTING: Adult intensive care unit in a university hospital. PATIENTS: Seven patients ventilated for neurological reasons were studied. All patients were clinically and haemodynamically stable and monitored according to clinical needs. INTERVENTIONS: ASPIDS implies that, during expiration, gas is aspirated through a catheter inserted in the tracheal tube. Simultaneously, a compensatory flow of fresh gas is injected into the inspiratory line. ASPIDS was achieved with a computer/ventilator system controlling two solenoid valves for aspiration and injection. RESULTS: At the basal respiratory rate of 12.6 breaths min-1, with ASPIDS VT decreased from 602 to 456 ml, as did the airway pressures to a corresponding degree. PaCO2 and PaO2 remained stable. At a frequency of 20 breaths min-1, with ASPIDS VT was further reduced to 305 ml with preserved normocapnia. ASPIDS did not interfere with the positive end-expiratory pressure (PEEP) level. No intrinsic PEEP developed. All patients remained stable. No haemodynamic or other side effects of ASPIDS were noticed. CONCLUSION: The results of this study suggest that ASPIDS may be a useful and safe modality of mechanical ventilation that limits alveolar pressure and minute ventilation requirements while keeping PaCO2 constant.

Adult↗