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Effects of Rapid Permissive Hypercapnia on P Intensive Care Med (1996) 22:182-191 Springer-Verlag 1996 J.-B. Thorens Effects of rapid permissive hypercapnia on P. Jolliet M. Ritz hemodynamics, gas exchange, and oxygen J.-C. Chevrolet transport and consumption during mechanical ventilation for the acute respiratory distress syndrome Received: 13 October 1994 Abstract Objective." To measure the p < 0.05), requiring an increase in Accepted: 23 November 1995 effects of rapid permissive hyper- FIO2 from 0.56 to 0.64 in order to capnia on hemodynamics and gas maintain an SaO2> 90%. PvO2 in- exchange in patients with acute creased (36.5_+5.7 to 43.2_+ respiratory distress syndrome 6.1 mmHg, p <0.05), while satura- (ARDS). tion was unmodified. The arterio- Design: Prospective study. venous 02 content difference was Setting." 18-bed, medical intensive unaltered. Oxygen transport (DO2) care unit, university hospital. increased (545+240 to 621 _+ Patients: 11 mechanically ventilated 274 ml/min/m 2, p < 0.05), while the ARDS patients. 02 consumption and extraction Intervention: Patients were sedated ratio did not change significantly. and ventilated in the controlled Venous admixture (Qva/Qt) in- mode. Hypercapnia was induced creased (26.3_+ 12.3 to 32.8+ 13.2, over a 30-60 min period by p < 0.05). decreasing tidal volume until pH Conclusions: These data indicate decreased to "7.2 and/or Ps0 increas- that acute hypercapnia increases ed by 7.5 mmHg. Settings were then DO2 and 02 off-loading capacity in maintained for 2 h. ARDS patients with normal plasma Results." Minute ventilation was lactate, without increasing 02 ex- reduced from 13.5_+6.1 to traction. Whether this would be 8.2+4.1 1/min (mean+SD), PaCO2 beneficial in patients with elevated increased (40.3 +6.6 to 59.3_+ lactate levels, indicating tissue 7.2 mmHg), pH decreased hypoxia, remains to be determined. ('7.40+0.05 to 7.26+0.05), and Ps0 Furthermore, even though hypercap- increased (26.3+2.02 to 31.1+ nia was well tolerated, the increase 2.2 mmHg) (p < 0.05). Systemic vas- in Qva/Qt, CI, and MPAP should cular resistance decreased (865-+454 prompt caution in patients with to 648_+265 dyne.s.cm -5, and car- severe hypoxemia, as well as in diac index (CI) increased (4+2.4 to those with depressed cardiac func- 4.'7 -+ 2.41/min/m 2) (p < 0.05). Mean tion and/or severe pulmonary systemic arterial pressure was un- hypertension. changed. Pulmonary vascular resistance was unmodified, and Key words Permissive hypercapnia. mean pulmonary artery pressure Mechanical ventilation Alveolar J.-B. Thorens (~) " P. Jolliet M. Ritz (MPAP) increased (29+5 to 32_+ hypoventilation Oxygen transport J.-C. Chevrolet Medical ICU, Division of Pneumology, 6 mmHg, p < 0.05). PaO2 remained Oxygen consumption DO2/VO2 University Hospital, 1211 Geneva 14, unchanged, while saturation relationship Hemoglobin Switzerland decreased (93 _+ 3 to 90 + 3 %, dissociation curve ARDS 183 Introduction tilated in the pressure-limited controlled mode, with decelerating flow and an inspiratory : expiratory ratio between 0.5 and 2.0 (Evita respirator, Drfiger Werk AG, Ltibeck, Germany). FIO 2 and positive It has been suggested that the tidal volume (VT) should end-expiratory pressure (PEEP) were set by the clinicians in charge be lowered during mechanical ventilation for the acute of the patients before measurements were taken. Hypercapnia was respiratory distress syndrome (ARDS) to minimize the induced over a 30-60 min period by decreasing tidal volume (VT). risk of ventilator-induced lung injury [1, 2]. This ap- The target values for arterial CO 2 tension (PaCO2) and pH were proach, known as controlled hypoventilation or per- determined by an increase of 40 mmHg in PaCO 2 resulting in a de- crease in pH of 0.2 [11], which, in turn, leads to a 7.5 mmHg in- missive hypercapnia, has been associated with a decrease crease in Ps0 [12]. The results of prior validation tests indicate that in mortality and fewer complications in patients with the magnitude of these expected changes was greater than the acute asthma and ARDS [3, 4]. However, even though variability of the measurement techniques used (see Measurements human exposure to severe hypercapnia seems not to have and Discussion). Thus, V r was reduced by increments of 100 ml serious side effects [4, 5], little is known about its conse- until either Ps0 increased by 7.5 mmHg (four patients) or pH decreased to 7.2 (seven patients), in arterial blood gas (ABG) quences on hemodynamics and the various aspects of O 2 samples analyzed every 15 min. Subsequently, no further changes in transport (DO2) and consumption (VO2) in ARDS pa- VT, respiratory rate, or PEEP were made during the protocol. If tients. In fact, these effects could theoretically have a necessary, FIO 2 was increased to maintain an SaO 2 of ___90%. favorable impact on some patients. Indeed, hypercapnia Tracheal suctioning was withheld. No modification of vasoactive or inotropic drugs treatment or fluid administration was made during induces a shift to the right in the oxyhemoglobin dissocia- the measurements. Mean systemic arterial pressure (MAP) and tion curve (ODC) [6], and has been shown in animal SaO 2 were continuously monitored via an indwelling arterial cathe- studies to raise cardiac output and lower systemic vascu- ter and pulse oximetry (N-200 pulse oximeter, Nellcor Inc., lar resistance (SVR) [7, 8]. These combined effects might Hayward, Calif.), respectively. Cardiac rhythm was continuously be beneficial if tissue hypoxia is present by increasing monitored. Patients were withdrawn from the study if there was a decline in SaO 2 of < 90% not compensated for by an increase in both DO 2 and peripheral O2 extraction. The present F102, a pH < 7.2, or a MAP < 60 mmHg, or if tracheal suctioning, study was conducted, first, to corroborate experimental fluid administration, or modification of vasoactive/inotropic drug data on hemodynamics and gas exchange during hyper- treatment was required. Hypercapnia was maintained for 2 h, after capnia in ARDS patients, and, second, to look for a which the patient was returned to baseline conditions by increasing possible benefit on oxygenation should tissue hypoxia be V T to its preprotocol level. Measurements were performed at baseline before starting hyper- present. capnia (baseline 1), after /h (PaCO 2 = 52.2+7.0mmHg) and 2 h (PaCO 2 -59.3+7.2 mmHg) of hypercapnia, and 1 h after return- ing to baseline conditions (baseline 2). As the difference between baseline and hypercapnia measurements was maximal at 2 h, only Material and methods those values will be reported (henceforth referred to as hypercap- nia). Patients Patients were included in the study if they met the criteria for Measurements ARDS, were intubated and mechanically ventilated, and were equipped with pulmonary and peripheral artery catheters. ARDS was defined according to recently published guidelines [9]: sudden Blood gases, oxyhemoglobin saturation, and Pso onset of respiratory failure, bilateral diffuse infiltrates on the chest X-ray, arterial oxygen tension/fractional inspired oxygen Arterial samples were withdrawn from the arterial catheter. Mixed (PaO2/FIO2)_<200mmHg, and pulmonary capillary wedge pres- venous samples were collected from the distal port of the sure < 18 mmHg). Systemic inflammatory response syndrome, sep- pulmonary artery catheter. All blood gas and hemoglobin satura- sis, severe sepsis, and septic shock were defined according to recent tion measurements were performed on an ABE 520 blood gas guidelines [10]. analyzer (Radiometer, Copenhagen, Denmark). In this analyzer, Patients were excluded if cerebral edema, postanoxic ence- PO 2, PCO> and pH are measured with specific electrodes, oxy- phalopathy, and/or intracranial hypertension were present, or if any hemoglobin saturation is measured by spectrophotometry, and Ps0 of the following conditions were present: systolic blood pressure is calculated from pH, PO2, and SO 2 [13]. A validation study to _<90mmHg, arterial oxygen saturation (SAO2)_<90%, arterial assess the measurement variability using this analyzer in the clinical pH_<7.3. setting had been previously conducted. Its goal was to determine if The study was approved by the Ethics Committee of our institu- the expected changes in the various determinants of blood 0 2 con- tion. Informed consent was obtained from next of kin. tent could be obscured by variations due to the measurement tech- nique. Ten sets of measurements were performed in ten patients presenting diverse blood gas and acid-base status, after appropriate calibration. The results are shown in Table 1. Protocol Patients were included as soon as possible after entry criteria were met. Sedation was maintained by a continuous infusion of either Oxygen transport and consumption variables midazolam or propofol. In order to prevent all respiratory muscle activity, muscle paralysis, if necessary, was achieved by intermittent DO 2 was computed as DO 2 (ml/min/m 2) - CI • CaO 2 • 10, where bolus injections of pancuronium bromide. All patients were ven- CI = cardiac index (ml/min/m2), and CaO 2 - arterial oxygen con- 184 Table 1 Assessment of blood gas analyzer measurement variabili- baseline 1 and hypercapnia. Additional blood samples were ty. (Sat oxyhemoglobin saturation) withdrawn at baseline I to determine the various parameters needed to compute the Apache II score. Arterial blood Coefficient of variation (%)a pH 0.4 Statistics PCO 2 (mmHg) 1.1 Ps0 (mmHg) 1.3 All results are reported as mean_+ 1 SD and were analyzed by a one- PO 2 (mmHg) 1.5 way analysis of variance for repeated measures (ANOVA). Signifi- Sat (%) 0.2 cance between the three time points was determined by Fisher's pro- a Mean coefficient of variation of ten sets of ten measurements tected least significance test.
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