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Mechanisms of Pulmonary Gas Exchange Abnormalities During Experimental Group B Streptococcal Infusion

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Mechanisms of Pulmonary Gas Exchange Abnormalities During Experimental Group B Streptococcal Infusion 003 I -3998/85/1909-0922$02.00/0 PEDIATRIC RESEARCH Vol. 19, No. 9, I985 Copyright 0 1985 International Pediatric Research Foundation, Inc. Printed in (I.S. A. Mechanisms of Pulmonary Gas Exchange Abnormalities during Experimental Group B Streptococcal Infusion GREGORY K. SORENSEN, GREGORY J. REDDING, AND WILLIAM E. TRUOG ABSTRACT. Group B streptococcal sepsis in newborns obtained from GBS (5, 6). Arterial Poz fell by 9 torr in association produces pulmonary arterial hypertension and hypoxemia. with the increase in pulmonary arterial pressure (4). In contrast, The purpose of this study was to investigate the mecha- the neonatal piglet infused with GBS demonstrated both pul- nisms by which hypoxemia occurs. Ten anesthetized, ven- monary arterial hypertension and profound arterial hypoxemia tilated piglets were infused with 2 x lo9 colony forming (7). These results suggest that the neonatal pulmonary vascula- unitstkg of Group B streptococci over a 30-min period. ture may respond to bacteremia differently from that of adults. Pulmonary arterial pressure rose from 14 ? 2.8 to 38 ? The relationship between Ppa and the matching of alveolar 6.7 torr after 20 min of the bacterial infusion (p< 0.01). ventilation and pulmonary perfusion, a major determinant of During the same period, cardiac output fell from 295 to arterial oxygenation during room air breathing (8), has not been 184 ml/kg/min (p< 0.02). Arterial Po2 declined from 97 studied in newborns. The predictable rise in Ppa with an infusion 2 7 to 56 2 11 torr (p< 0.02) and mixed venous Po2 fell of group B streptococcus offers an opportunity to delineate the from 39.6 2 5 to 28 2 8 torr (p< 0.05). The multiple inert relationship between pulmonary gas exchange and pulmonary gas elimination technique was used to detect increases in hernodynamics and to understand the cause of hypoxemia during shunt and alterations in ventilation-perfusiou matching. sepsis in the neonate. Newborn animals are likely to have some Intrapulmonary shunt did not increase during or after the degree of intrapulmonary shunt (9). A rise in Ppa and PVR infusion with group B streptococci. However, there was a might increase shunt, if the rise in PVR is produced by constric- significant increase (p <. 0.05) in the SD of pulmonary tion of relaxed pulmonary vessels located within well-ventilated blood flow, an index of VA/Q mismatching, 20 min after regions of the lung (lo),rather than by vessels that are constricted initiation of the infusion of bacteria. All the above changes in regions of alveolar hypoxia. The altered relationship between reverted toward baseline during the 2-h period following resistance to flow in shunt and nonshunt associated areas would discontinuation of the infusion. We conclude that the hy- result in increased flow to shunt vessels. poxemia occurring in the early phase of group B strepto- This study tested the hypothesis that arterial hypoxemia asso- coccal sepsis does not develop solely because of increased ciated with the acute rise in Ppa during the early stages of GBS shunt, but rather is produced by a decline in cardiac output sepsis in newborns is caused primarily by an increase in intra- in conjunction with mismatching of pulmonary perfusion pulmonary shunt. to alveolar ventilation. (Pediatr Res 19: 922-926, 1985) MATERIALS AND METHODS Abbreviations Animal preparation and monitoring. Ten piglets, age 10-20 GBS, Group B streptococcal days and mean weight 3.2 kg (weight range 2.6-4.2 kg) were Ppa, pulmonary arterial pressure PVR, pulmonary vascular resistance anesthetized with intravenous pentobarbital (25 mg/kg) and studied in the supine position. Supplemental doses of pentobar- Qp, pulmonary blood flow bital (5 mg/kg) were administered hourly to maintain anesthesia VA/Q, ventilation-perfusion ratio P,02, mixed venous Po2 throughout the study. Core temperature, measured with a rectal temperature probe, was maintained at 38 a 0.5" C with a radiant warmer. A triple lumen catheter was placed into the right atrium via the left external jugular vein and a no. 5 Fr. balloon-tipped thermodilution catheter (Edwards Laboratories, Santa Ana, CA) Neonatal GBS infection produces septicemia, shock, and ar- was introduced into the right external jugular vein and positioned terial hypoxemia (I). While the constellation of clinical findings, under fluoroscopy in the left branch pulmonary artery for meas- risk factors, and incidence rate of early onset GBS sepsis have urement of pulmonary arterial and capillary wedge pressures and been previously reported (2, 3), the pathophysiologic events blood sampling. A polyethylene catheter (PE-160) was intro- producing arterial hypoxemia have not been well studied. Pul- duced into the right internal carotid artery for systemic arterial monary hypertension has been reported in an adult experimental blood sampling and monitoring blood pressure and heart rate. A model infused with live GBS (4) or with polysacchride toxin metal tracheostomy tube was inserted, secured, and connected to a nonrebreathing valve (1 1) and a heated 2.5 liter mixed Rece~vcdFebruary 10. 1085: accepted April 24, 1985. expired gas collection chamber. Tidal volume and minute ven- Reprints W~llia~nE. Truog. M.D.. Associate Professor of Pediatrics. Division of tilation were measured with a hot-wire anemometer inserted into Neonatal and Respiratory Diseases. University of Washington School of Medic~ne. Seattle, WA 98 195. the end of the gas collection chamber (12). The anemometer was Supported in part by NIH HL01205 RCDA (W.E.T.). NIH HL19187 (Pediatric calibrated before each sampling period over the tidal ~0lume Pulmonry SCOR). and a grant from the Washington Lung Association (G.J.R.). range of 20-40 ml, in 5-ml increments, with a signal variation 922 STREPTOCOCCAL SEPSIS AND GAS EXCHANGE 923 of <2.0%. Mean and phasic pressures were recorded from the using a least squares technique for best fitting ofthe data provided aorta, pulmonary artery, and trachea on a four channel polygraph the value offractional Q, perfusing 50 theoretical lung compart- recorder (Hewlett-Packard, Waltham, MA). Signals were aver- ments, each with a unique V,/Q ratio (14, 17). aged electronically. Ventilation-perfusion matching in the lung was assessed using Q, was determined in triplicate using the thermodilution tech- the SD Q, as an indicator of the closeness of matching of nique (Edwards Laboratories) (13). Values were averaged to ventilation and perfusion (18, 19). A narrow or small SD C?, obtain the recorded Q,. If a >lo% discrepancy among the three indicates blood flow tightly constrained to well ventilated areas; values was recorded, a fourth value was also obtained. PVR was an enlarged SD Q, implies substantial pulmonary blood flow to calculated from the formula: lung regions with a wider distribution of V,/Q; thus perfusion is less tightly matched to alveolar ventilation. For analysis of SD PVR = Ppa-Ppcwp/Q, Q,, Q, is the fraction of Q, where.Q, = Q, - Q, with Q, equal to where Pcwp is pulmonary capillary wedge pressure. total pulmonary blood flow, and Q, equal to flow to areas ofzero Following instrumentation, animals were paralyzed with pan- ventilation. curonium bromide (0.3 mg/kg). Supplemental doses of pancu- Study protocol. An intravenous infusion of group B strepto- ronium bromide were administered hourly to maintain paralysis. cocci (total dose of 2 x lo9 colony forming units per kilogram) The animals were ventilated with room air using a tidal volume was infused over 30 min. Hemodynamic measurements, arterial of 15 ml/kg with a large animal volume ventilator (Harvard blood gas tensions, pH, and inert gas samples were obtained Apparatus, Millis, MA). Positive end expiratory pressure was not before, 20 min after the onset of the infusion, and at 20 min, I used. Hyperinflations were delivered 15 rnin prior to each sam- h, and 2 h after discontinuing the bacterial infusion. pling period to inhibit development ofatelectasis. The respiratory Stat~strcs.Statistical analysis was performed using analysis of rate was initially adjusted to maintain Pamz between 30-40 torr; variance and Newman-Keuls' multiple-range test (20).The level no changes were made in minute ventilation once the protocol of significance was p < 0.05. Data are presented as mean _t 1 began. Blood gas tensions were measured within 5 min of sam- SD. pling and the results were corrected to the animal's temperature. Prepurution of huctcriu. Group B 8-hemolytic streptococci RESULTS (type 111) were inoculated into Todd Hewitt broth and incubated at 32" C for 18 h prior to each animal experiment. The broth Mean pulmonary arterial pressure increased immediately upon culture was centrifuged at 4 x gat 3" C for 30 min. The bacterial initiation of the infusion of GBS and reached a maximum val~~e pellet was resuspended in 10 ml phosphate-buffered saline. Bac- within 5 rnin after the onset ofthe infusion. Mean Ppa increased terial concentration of the resuspended solution was determined from a baseline value of 14.2 k 2.8 to 37.6 2 6.7 torr, (p< 0.0 I) by measurement of the optical density with comparison to a after infusing bacteria for 20 min (Fig. 1). Mean Ppa then previously determined plot of bacterial colony forming units to returned toward preinfusion values after discontinuing the infu- optical density. sion. Assessrncnt of shllnt and ventilation p(~r/i:sionmatching. The Q, fell to 65% of baseline values 20 min after beginning the multiple inert gas elimination technique (14) was employed to infusion (p< 0.02) (Fig. 1). This occurred uniformly in every determine pulmonary ventilation-perfusion relationships. This animal. Heart rate was increased 20 rnin after beginning the technique employs a continuous intravenous infusion ofsix inert gases ofwidely varying solubility in blood. Each exhibits a linear relationship between partial pressure and concentration in blood.
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