Splanchnic vascular capacitance and positive end-expiratory pressure in dogs

We have investigated the effect of positive end-expiratory pressure ventilation (PEEP) on regional splanchnic vascular capacitance. In 12 anesthetized dogs hepatic and splenic blood volumes were assessed by sonomicrometry. Vascular pressure-diameter curves were defined by obstructing hepatic outflow. With 10 and 15 cmH2O PEEP portal venous pressure increased 3.1 +/- 0.3 and 5.1 +/- 0.4 mmHg (P less than 0.001) while hepatic venous pressure increased 4.9 +/- 0.4 and 7.3 +/- 0.4 mmHg (P less than 0.001), respectively. Hepatic blood volume increased (P less than 0.01) 3.8 +/- 0.9 and 6.3 +/- 1.4 ml/kg body wt while splenic volume decreased (P less than 0.01) 0.8 +/- 0.2 and 1.3 +/- 0.2 ml/kg body wt. The changes were similar with closed abdomen. The slope of the hepatic vascular pressure-diameter curves decreased with PEEP (P less than 0.01), possibly reflecting reduced vascular compliance. There was an increase (P less than 0.01) in unstressed hepatic vascular volume. The slope of the splenic pressure-diameter curves was unchanged, but there was a significant (P less than 0.05) decrease in unstressed diameter during PEEP. In conclusion, hepatic blood volume increased during PEEP. This was mainly a reflection of passive distension due to elevated venous pressures. The spleen expelled blood and thus prevented a further reduction in central blood volume.     

Effects of positive end-expiratory pressure ventilation on cerebral venous pressure with head elevation in dogs.

Mechanical ventilation with positive end-expiratory pressure (PEEP) may prevent venous air embolism in the sitting position because cerebral venous pressure (Pcev) could be increased by the PEEP-induced increase in right atrial pressure (Pra). Whereas it is clear that there is a linear transmission of the PEEP-induced increase in Pra to Pcev while the dog is in the prone position, the mechanism of the transmission with the dog in the head-elevated position is unclear. We tested the hypothesis that a Starling resistor-type mechanism exists in the jugular veins when the head is elevated. In one group of dogs, increasing PEEP linearly increased Pcev with the dog in the prone position (head at heart level, slope = 0.851) but did not increase Pcev when the head was elevated. In another group of dogs, an external chest binder was used to produce a larger PEEP-induced increase in Pra. Further increasing Pra increased Pcev only after Pra exceeded a pressure of 19 mmHg (break pressure). This sharp inflection in the upstream (Pcev)-downstream (Pra) relationship suggests that this may be caused by a Starling resistor-type mechanism. We conclude that jugular venous collapse serves as a significant resistance in the transmission of Pra to Pcev in the head-elevated position.     

Epithelial and endothelial flux after bypass in dogs: effect of positive end-expiratory pressure

Cardiopulmonary bypass (CPB) causes lung injury that occasionally progresses to the adult respiratory distress syndrome (ARDS). We measured the effect of 10 cmH2O of positive end-expiratory pressure (PEEP) on small solute and protein flux in dogs 1 wk before and 2 h after the completion of CPB. As an index of alveolar epithelial permeability, the clearance from lung to blood of inhaled technetium-99m-labeled diethylenetriaminepentaacetic acid (99mTc-DTPA) was measured. To assess microvascular endothelial integrity, the rate of accumulation in the lung interstitium of intravascular 113mIn-transferrin was measured. The clearance half time (t 1/2) for 99mTc-DTPA in the study dogs declined from 18.8 +/- 1.9 min (mean +/- SE) at base line to 9.4 +/- 2.0 min during PEEP (P less than 0.05). Two hours after CPB, the t 1/2 was 8.1 +/- 1.6 min at base line and unchanged during PEEP. The 113mIn-transferrin rate of accumulation was unchanged by PEEP before CPB. After CPB, the index was 3.25 +/- 0.95 slope/min X 10(-3) (P less than 0.05). Of the five dogs with a significant slope, four showed a decrease in microvascular flux during PEEP, although for the group the mean change in slope was not significant (P = 0.10). We conclude that the application of PEEP does not increase 99mTc-DTPA clearance in lungs already injured by CPB, and may actually decrease the apparent microvascular protein flux in some cases.     

Expiratory flow limitation and intrinsic positive end-expiratory pressure in obesity

Breathing at very low lung volumes might beaffected by decreased expiratory airflow and air trapping. Our purposewas to detect expiratory flow limitation (EFL) and, as a consequence, intrinsic positive end-expiratory pressure(PEEP_i) in grossly obesesubjects (OS). Eight OS with a mean body mass index (BMI) of 44 ± 5 kg/m² and six age-matchednormal-weight control subjects (CS) were studied in different bodypositions. Negative expiratory pressure (NEP) was used to determineEFL. In contrast to CS, EFL was found in two of eight OS in the uprightposition and in seven of eight OS in the supine position. DynamicPEEP_i and mean transdiaphragmatic pressure (mean Pdi) were measured in all six CS and in six of eight OS.In OS, PEEP_i increased from 0.14 ± 0.06 (SD) kPa in the upright position to 0.41 ± 0.11 kPa inthe supine position (P < 0.05) anddecreased to 0.20 ± 0.08 kPa in the right lateral position(P < 0.05, compared with supine),whereas, in CS, PEEP_i wassignificantly smaller (<0.05 kPa) in each position. In OS, mean Pdiin each position was significantly larger compared with CS. Mean Pdiincreased from 1.02 ± 0.32 kPa in the upright position to 1.26 ± 0.17 kPa in the supine position (not significant) and decreasedto 1.06 ± 0.26 kPa in the right lateral position(P < 0.05, compared with supine),whereas there were no significant changes in CS. We conclude that in OS1) tidal breathing can be affectedby EFL and PEEP_i;2) EFL andPEEP_i are promoted by the supineposture; and 3) the increaseddiaphragmatic load in the supine position is, in part, related toPEEP_i.

     

Effects of positive end-expiratory pressure on the right ventricle

Transmural cardiac pressures, stroke volume, right ventricular volume, and lung water content were measured in normal dogs and in dogs with oleic acid-induced pulmonary edema (PE) maintained on positive-pressure ventilation. Measurements were performed prior to and following application of 20 cmH2O positive end-expiratory pressure (PEEP). Colloid fluid was given during PEEP for ventricular volume expansion before and after the oleic acid administration. PEEP significantly increased pleural pressure and pulmonary vascular resistance but decreased right ventricular volume, stroke volume, and mean arterial pressure in both normal and PE dogs. Although the fluid infusion during PEEP raised right ventricular diastolic volumes to the pre-PEEP level, the stroke volumes did not significantly increase in either normal dogs or the PE dogs. The fluid infusion, however, significantly increased the lung water content in the PE dogs. Following discontinuation of PEEP, mean arterial pressure, cardiac output, and stroke volume significantly increased, and heart rate did not change. The failure of the stroke volume to increase despite significant right ventricular volume augmentation during PEEP indicates that positive-pressure ventilation with 20 cmH2O PEEP decreases right ventricular function.     

Pulmonary vascular resistance after cessation of positive end-expiratory pressure

This report describes the pulmonary vascular response of infant lamb lung to abrupt cessation of positive end-expiratory pressure (PEEP) during volume-regulated continuous positive-pressure breathing (CPPB). In an intact, endobronchially ventilated preparation, the increase in left lung blood flow (QL) after abrupt cessation of 11 Torr left lung PEEP was found to be gradual, although peak airway pressure (Pmax) fell promptly from 36 to 14 Torr; 49% of the increase in QL occurred greater than 10 s after cessation of PEEP. Recruitment of zone I vasculature that had been created by balloon occlusion of the left pulmonary artery was found to occur promptly after balloon deflation. Isolated neonatal lamb lungs, perfused at constant flow rate, showed similar persistent elevation of pulmonary vascular resistance after cessation of 15 Torr PEEP, although Pmax fell abruptly from 39 to 12 Torr. This hysteresis was eliminated by calcium channel blockade with verapamil, and the magnitude of the change in pulmonary arterial pressure after either application or cessation of PEEP was reduced (25 and 26%, respectively). These observations suggest that, during CPPB, lung stretch alters neonatal pulmonary vascular tone or, by causing calcium channel-dependent lung volume hysteresis, modulates pulmonary vascular resistance. This interaction exaggerates the effect of airway pressure changes on pulmonary vascular resistance during mechanical ventilation.     

Effects of positive end-expiratory pressure on hepatic blood flow and performance

Positive end-expiratory pressure (PEEP) may impair extrapulmonary organ function. However, the effects of PEEP on the liver are unclear. We tested the hypothesis that at a constant cardiac output (CO), PEEP does not induce changes in hepatic blood flow (QL) and parenchymal performance. In splenectomized, close-chested canine preparations (group I, n = 6), QL was derived as hepatic outflow using electromagnetic flow probes (QLemf), and hepatic performance was defined by extraction and clearance of indocyanine green (ICG). In a noninvasive model (group II, n = 7), the effects of PEEP on hepatic performance alone were similarly analyzed. Measurements were taken during intermittent positive-pressure ventilation (IPPV1), after addition of 10 cmH2O PEEP to IPPV (PEEP1), during continued PEEP but after return of CO to IPPV1 levels by intravascular volume infusions (PEEP2), and after removal of both PEEP and excess blood volume (IPPV2). Phasic inspiratory decreases in QLemf present during positive-pressure ventilation were not increased during either PEEP1 or PEEP2. Mean QLemf decreased proportionately with CO during PEEP1 (P less than 0.05), but was restored to IPPV1 levels in a parallel fashion with CO during PEEP2. The ICG pharmacokinetic responses to PEEP were complex, with differential effects on extraction and clearance. Despite this, hepatic performance was not imparied in either group. we conclude that global QL reductions during PEEP are proportional to PEEP-induced decreases in CO and are preventable by returning CO to pre-PEEP levels by intravascular volume infusions. However, covarying changes in blood volume and hepatic outflow resistance may independently modulate hepatic function.