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Biomedical subjects

P H Breen

Publications and source records attributed to P H Breen.

At least 19 recordsLinked to original sources
PubMed1996

Measurement of pulmonary CO2 elimination must exclude inspired CO2 measured at the capnometer sampling site.

OBJECTIVE: The pulmonary elimination of the volume of CO2 per breath (VCO2/br, integration of product of airway flow (V) and PCO2 over a single breath) is a sensitive monitor of cardio-pulmonary function and tissue metabolism. Negligible inspired PCO2 results when the capnometry sampling site (SS) is positioned at the entry of the inspiratory limb to the airway circuit. In this study, we test the hypothesis that moving SS lungward will result in significant inspired CO2 (VCO2[I]), that needs to be excluded from VCO2/br. METHODS: We ventilated a mechanical lung simulator with tidal volume (VT) of 800 mL at 10 breaths/min. CO2 production, generated by burning butane in a separate chamber, was delivered to the lung. Airway V and PCO2 were measured (Capnomac Ultima, Datex), digitized (100 Hz for 60 s), and stored by microcomputer. Then, computer algorithms corrected for phase differences between V and PCO2 and calculated expired and inspired VCO2 (VCO2[E] and VCO2[I]) for each breath, whose difference equalled overall VCO2/br. The lung and Y-adapter (where the inspiratory and expiratory limbs of the circuit joined) were connected by the SS and a connecting tube in varying order. RESULTS: During ventilation of the lung model (VT = 800 ml) with SS adjacent to the inspiratory limb, VCO2[E] was 16.8 +/- 0.4 ml and VCO2[I] was 1.1 +/- 0.1 ml, resulting in overall VCO2/br (VCO2[E] - VCO2[I]) of 15.7 +/- 0.4 ml. If VCO2[I] was ignored in the determination of VCO2/br, then the %error that VCO2[E] overestimated VCO2/br was 7.2 +/- 0.3%. This %error significantly increased (p < 0.05, Student's t-test) when VT was decreased to 500 mL (%error = 12.4 +/- 0.8%) or when SS was moved to the lungward side of a 60 mL connecting tube (VCO2[I] = 2.8 +/- 0.2, %error = 18.2 +/- 1.6) or a 140 mL tube (VCO2[I] = 5.9 +/- 0.3 mL, %error = 37.5 +/- 3.3). CONCLUSIONS: When the SS was moved lungward from the inspiratory limb, instrumental dead space (VDINSTR) increased and, at end-expiration, contained exhaled CO2 from the previous breath. During the next inspiration, this CO2 was rebreathed relative to SS (i.e. VCO2[I]), and contributed to VCO2[E]. Thus, VCO2[E] overestimated VCO2/br (%error) by the amount of rebreathing, which was exacerbated by larger VDINSTR (increased VCO2[I]) or smaller VT (increased VCO2[I]-to-VCO2/br ratio).

Capnography↗
PubMed1996

How does positive end-expiratory pressure decrease CO2 elimination from the lung?

Six chloralose-urethane anesthetized dogs (23 +/- 2 kg) underwent median thoracotomy (open pleural spaces) and constant mechanical ventilation with O2. We conducted measurements at baseline and during 25 min of ventilation with 3.3 cmH2O positive end-expiratory pressure (PEEP3) or 10.7 cmH2O PEEP (PEEP 11), including breath-by-breath values in the first 2 min after PEEP began. PEEP 11 immediately decreased pulmonary CO2 elimination per breath (VCO2,br, digital integration and multiplication of exhaled flow and FCO2) from 8.4 +/- 2.0 to 4.5 +/- 1.6 ml (P < 0.05) by significantly decreasing alveolar ventilation (VA) (29% increase in anatomical dead space (VDana) and generation of high VA/Q regions) and by decreasing alveolar PCO2 (PACO2) from 42.5 +/- 3.5 to 35.9 +/- 3.5 Torr (decreased CO2 transfer to the lung as electromagnetic aortic cardiac output (QT) decreased by 51%). The immediate dilution of alveolar gas and PACO2 by fresh gas as PEEP increased functional residual capacity by 1152 +/- 216 ml was offset by simultaneous decreased expiratory volume and, hence, CO2 accumulation. Compared to baseline, the 17% reduction in VCO2,br was sustained at 25 min after addition of PEEP 11 because VA remained depressed. Then, VCO2,br could only be restored to baseline if PACO2 sufficiently increased. However, CO2 transport was still in unsteady state at 25 min of PEEP. Peripheral tissue retention of CO2 and the significant increase in mixed venous PCO2 (PVCO2, 62.4 +/- 6.2 Torr) were not enough to normalize CO2 transfer to the lung and to sufficiently increase PACO2, especially during the continued depression in QT that occurred at higher PEEP. The sustained decrease in VCO2,br during PEEP was not mirrored by changes in end-tidal PCO2 (PETCO2).

Anesthesia, Inhalation↗
PubMed1996

How does experimental pulmonary embolism decrease CO2 elimination?

To test how large pulmonary embolism changes non-steady state CO2 kinetics, the right pulmonary artery (RPA) was occluded in 5 anesthetized, ventilated, thoracotomized dogs. By 1 min after RPA occlusion, CO2 volume exhaled per breath (VCO2,br) decreased from 9.3 +/- 2.8 to 7.0 +/- 2.6 ml and end-tidal PCO2 (PETCO2) decreased from 28.7 +/- 4.2 to 21.8 +/- 3.3 Torr. During the ensuing 70 min, VCO2,br increased back to baseline but PETCO2 was still 13% less than baseline. Both PaCO2 (41.5 +/- 1.7 to 55.1 +/- 8.1 Torr) and PvCO2 (48.2 +/- 1.9 to 62.8 +/- 6.5 Torr) steadily increased and approached equilibrium by 45 min of RPA occlusion. Cardiac output did not significantly change. In summary, RPA occlusion immediately decreased VCO2,br by 25%, due mostly to increased alveolar VD (VDalv). Then, VCO2,br recovered back to baseline as CO2 accumulated in tissues and lung. In contrast, elevated VDalv caused persistent decreased PETCO2, which did not detect recovery of VCO2,br nor increase in PaCO2 during RPA occlusion.

Animals↗
PubMed1996

Comparison of end-tidal PCO2 and average alveolar expired PCO2 during positive end-expiratory pressure.

The measurement of average alveolar expired PCO2 (PAECO2) weights each PCO2 value on the alveolar plateau of the CO2 expirogram by the simultaneous change in exhaled volume. PAECO2 can be determined from a modified analysis of the Fowler anatomic dead space (VDANAT). In contrast, end-tidal PCO2 (PETCO2) only measures PCO2 in the last small volume of exhalate. In conditions such as mechanical ventilation with positive end-expiratory pressure (PEEP), where the alveolar plateau can have a significant positive slope, we questioned how much PETCO2 could overestimate PAECO2. Accordingly, in six anesthetized ventilated dogs, we digitally measured and processed tidal PCO2 and flow to determine VDANAT. We determined PETCO2 and PAECO before and after the application of 7.6 cm H2O PEEP. Alveolar dead space to tidal volume fraction (VD/VT) was determined by [arterial PCO2- alveolar PCO2]/arterial PCO2, where alveolar PCO2 was determined by either PETCO2 or PAECO2. During baseline ventilation, PETCO2 was 3.4 mm Hg (approximately 11%) greater than PAECO2. Because PEEP significantly increased the slope of the alveolar plateau from 28 to 74 mm Hg/L, the difference between PETCO2 and PAECO2 significantly increased to 6.6 mm Hg (approximately 20% difference). The concurrent increase in VDANAT during PEEP decreased alveolar tidal volume and tended to limit the overestimation of PETCO2 compared to PAECO2. When alveolar PCO2 was estimated by PETCO2, alveolar VD/VT was 18%, compared to an alveolar VD/VT of 26% when alveolar PCO2 was estimated by PAECO2. This difference was significantly magnified during PEEP ventilation. The overestimation of PAECO2 by PETCO2 can result in a falsely high assessment of overall alveolar PCO2. Moreover, the use of PETCO2 to estimate alveolar PCO2 in the determination of the alveolar dead space fraction can result in falsely low and even negative values of alveolar dead space.

Anesthesia↗
PubMed1996

Carbon dioxide elimination measures resolution of experimental pulmonary embolus in dogs.

Patients with severe pulmonary embolism can suffer progressive hypercapnia refractory to supramaximal mechanical ventilation, and may require open-thoracic or transvenous emergency embolectomy in addition to anticoagulation and/or thrombolysis. The functional recovery of gas exchange would be signaled by an increase in pulmonary CO2 elimination and decrease in CO2 retention; such data could guide the course of operative embolectomy. Accordingly, we studied five chloralose-urethane anesthetized, mechanically ventilated dogs with open thoraces in which the right pulmonary arteries (RPAs) were reversibly occluded with cloth snares. After waiting for steady state, we abruptly released the snare to restore RPA perfusion and experimentally simulate resolution of pulmonary embolism. For 70 min we serially measure the CO2 volume exhaled per breath (VCO2,br), arterial, mixed venous, and end-tidal PCO2 (PACO2, PVCO2, PETCO2), cardiac output (QT), and the alveolar dead space fraction (VDalv/VTalv = [PaCO2 - PETCO2/PaCO2). RPA reperfusion caused VCO2,br to significantly and abruptly increase from 8.9 +/- 2.7 to 11.6 +/- 3.6 mL; 70 min later VCO2,br had returned to baseline. PaCO2 and PVCO2 steadily decreased during 70 min of RPA reperfusion. PETCO2 increased from 25 +/- 5 to 33 +/- 5 mm Hg immediately after RPA reperfusion, as VDalv/VTalv decreased from 54% +/- 10% to 32% +/- 12%, but PETCO2 was still significantly greater than baseline at 70 min of RPA reperfusion. QT did not significantly change. We conclude that intraoperative measurement of VCO2,br should immediately detect and follow the resolution of CO2 retention in the lung and peripheral tissues after RPA reperfusion. PETCO2 could not detect the decrease of VCO2,br back to baseline because PETCO2 does not measure exhaled volume or the PCO2 waveform.

Animals↗
PubMed1996

Protective effect of stroma-free methemoglobin during cyanide poisoning in dogs.

BACKGROUND: During fire exposure, cyanide toxicity can block aerobic metabolism. Oxygen and sodium thiosulfate are accepted therapy. However, nitrite-induced methemoglobinemia, which avidly binds cyanide, decreases oxygen-carrying capacity that is already reduced by the presence of carboxyhemoglobin (inhalation of carbon monoxide in smoke). This study tested whether exogenous stroma-free methemoglobin (SFmetHb) can prevent depression of hemodynamics and metabolism during canine cyanide poisoning. METHODS: In 10 dogs (weighing 18.8 +/- 3.5 kg) anesthetized with chloralose-urethane and mechanically ventilated with air, baseline hemodynamic and metabolic measurements were made. Then, 137 +/- 31 ml of 12 g% SFmetHb was infused into five dogs (SFmetHb group). Finally, the SFmetHb group and the control group (n = 5, no SFmetHb) received an intravenous potassium cyanide infusion (0.072 mg.kg-1.min-1) for 20 min. Oxygen consumption (VO2) was measured with a Datex Deltatrac (Datex Instruments, Helsinki, Finland) metabolic monitor and cardiac output (QT) was measured by pulmonary artery thermodilution. RESULTS: From baseline to cyanide infusion in the control group, QT decreased significantly (p < 0.05) from 2.9 +/- 0.8 to 1.5 +/- 0.4 l/min, mixed venous PCO2 (PvCO2) tended to decrease from 35 +/- 4 to 23 +/- 2 mmHg, PvO2 increased from 43 +/- 4 to 62 +/- 8 mmHg, VO2 decreased from 93 +/- 8 to 64 +/- 19 ml/min, and lactate increased from 2.3 +/- 0.5 to 7.1 +/- 0.7 mM. In the SFmetHb group, cyanide infusion did not significantly change these variables. From baseline to infused cyanide, the increases in blood cyanide (4.8 +/- 1.0 to 452 +/- 97 microM) and plasma thiocyanate cyanide (18 +/- 5 to 65 +/- 22 microM) in the SFmetHb group were significantly greater than those increases in the control group. SFmetHb itself caused no physiologic changes, except small decreases in heart rate and PvO2. Peak SFmetHb reached 7.7 +/- 1.0% of total hemoglobin. CONCLUSIONS: Prophylactic intravenous SFmetHb preserved cardiovascular and metabolic function in dogs exposed to significant intravenous cyanide. Blood concentrations of cyanide, and its metabolite, thiocyanate, revealed that SFmetHb trapped significant cyanide in blood before tissue penetration.

Animals↗
PubMed1996

Measurement of blood CO2 concentration with a conventional PCO2 analyzer.

OBJECTIVES: CO2 content can be determined from the Pco2 in an acidified (forces all CO2 into solution) and diluted blood sample. However, Pco2 concentrations measured in conventional blood gas analyzers are only correct for samples with a significant buffer capacity (such as whole blood), so that mixing with the Pco2 in the rinse solution and tubing walls does not significantly change the sample Pco2. This study describes a calibration method and validation data for the Radiometer Medical ABL2 CO2 electrode system to accurately measure unbuffered blood samples used in the determination of blood CO2 content (or other aqueous fluids). DESIGN: Prospective, criterion standard. SETTING: Laboratory. MEASUREMENTS AND MAIN RESULTS: Blood samples (0.4 mL) were acidified and diluted with 0.2 M lactic acid. After measuring Pco2, CO2 content was calculated using the CO2 solubility coefficient and the dilution factor of 20. CO2 content was determined in a series of sodium carbonate (Na2CO3) solutions spanning the physiologic range of CO2 content. Regression of the measured vs. the actual CO2 content data generated a straight line with a slope of 0.796 and y-intercept of 12.5 (r2 = .99; n = 48). These coefficients were successfully used to correct CO2 content determined in blood samples into which graduated amounts of sodium carbonate were added. CONCLUSIONS: This calibration procedure allows accurate measurement of Pco2 in aqueous samples using the Radiometer ABL2 electrode system, and should be applicable to other blood gas analyzers. Necessary syringes and chemicals are readily available, the method is fast and simple, and the sample volume is small. In the practice of critical care medicine, accurate Pco2 measurement in aqueous acidified and diluted blood provides direct determination of blood CO2 content (useful in calculations of modified Fick cardiac output or tissue CO2 production). Determinations of absolute CO2 content in blood requiring complex methodology are not necessary. In addition, accurate measurement of aqueous gastric Pco2 can help determine gastric pH, which is an important marker of tissue perfusion.

Blood Gas Analysis↗
PubMed1995

Effect of oxygen and sodium thiosulfate during combined carbon monoxide and cyanide poisoning.

In a canine model of combined carbon monoxide (CO) and cyanide (CN) poisoning, cardiac output (QT) and oxygen consumption (Vo2) decreased but recovered to baseline values by 15 min after toxic exposure; elevated blood CN and lactic acidosis persisted for at least another 10 min. Given the rapid spontaneous recovery after cessation of toxic exposure, we questioned the efficacy of usual treatment with oxygen (O2) and sodium thiosulfate (Na2S2O3) for CN poisoning. Accordingly, in seven dogs (26 +/- 3 kg, chloralose and urethane anesthesia), we sequentially administered CO by closed circuit inhalation (231 +/- 42 ml) and potassium CN by intravenous infusion (0.072 mg.kg-1.min-1 for 17 +/- 3 min). Fifteen minutes after toxic exposure, O2 breathing began and Na2S2O3 (150 mg/kg) was infused. Measurements were repeated 10 and 45 min after treatment. At the end of the CN infusion, QT decreased by 43% and Vo2 decreased by 51%, compared to baseline values. Both variables recovered to baseline by 15 min after stopping toxic exposure. Significant lactic (4.8 +/- 2.9 mM) acidosis (7.14 +/- 0.10) persisted for at least another 10 min. Treatment with oxygen and Na2S2O3 did not hasten the recovery of this lactic acidosis or decrease blood cyanide levels compared to nontreated dogs. However, after treatment, plasma thiocyanate significantly increased from 16.3 +/- 12.5 to 94.4 +/- 72.2 microM, as Na2S2O3 participated in the increased metabolism of cyanide to thiocyanate. We conclude that O2 and Na2S2O3 therapy should be continued during combined CO and HCN poisoning. Oxygen increases CO elimination and can enhance anti-CN treatment. After infusion or inhalation of CN, when most CN has already penetrated the intracellular compartment, postexposure sodium thiosulfate increased the metabolism of CN.

Animals↗
PubMed1995

Combined carbon monoxide and cyanide poisoning: a place for treatment.

During fires, victims can inhale significant carbon monoxide (CO) and cyanide (CN) gases, which may cause synergistic toxicity in humans. Oxygen therapy is the specific treatment for CO poisoning, but the treatment of CN toxicity is controversial. To examine the indication for treatment of CN toxicity, we have established a canine model to delineate the natural history of combined CO and CN poisoning. In seven dogs (24 +/- 3 kg), CO gas (201 +/- 43 mL) was administered by closed-circuit inhalation. Then, potassium CN was intravenously (i.v.) infused (0.072 mg.kg-1.min-1) for 17.5 +/- 3.0 min. Cardiorespiratory measurements were conducted before and after these toxic challenges. Despite significant CO poisoning (peak carboxyhemoglobin fractions [COHb] = 46% of total hemoglobin [Hb]; elimination t1/2 = 114 +/- 42 min) with attendant decrease in blood O2 content, CO had essentially little effect on any hemodynamic or metabolic variable. On the other hand, CN severely depressed most hemodynamic and metabolic functions. Compared to baseline values, CN caused significant (P < 0.01) decreases in cardiac output (6.4 +/- 2.0 to 3.1 +/- 0.5 L/min) and heart rate (169 +/- 44 to 115 +/- 29 bpm) and decreases in oxygen consumption (VO2) (133 +/- 19 to 69 +/- 21 mL/min) and carbon dioxide production (VCO2) (128 +/- 27 to 103 +/- 22 mL/min). However, these critical hemodynamic and metabolic variables recovered to baseline values by 15 min after stopping the CN infusion, except lactic acidosis which persisted for at least 25 min after the CN infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Exhaled flow monitoring can detect bronchial flap-valve obstruction in a mechanical lung model.

Flap-valve obstruction to expiratory flow (V) in a major bronchus can result from inspissated secretions, blood, or foreign body. During inhalation, increasing airway caliber preserves inspired V past the obstruction; during exhalation, decreasing airway diameter causes airflow obstruction and even frank gas trapping. We reasoned that the resultant sequential, biphasic exhalation of the lungs would be best detected by measuring exhaled V versus time. Accordingly, we designed an airway obstruction element in a mechanical lung model to examine flap-valve bronchial obstruction. A mechanical lung simulator was ventilated with a pressure-limited flow generator, where f = 10/min, tidal volume = 850 mL, and respiratory compliance = 40 mL/cm H2O. Airway V (pneumotachometer) and pressure (P) were digitally sampled for 1 min. Then, the circumference of the diaphragm in a respiratory one-way valve was trimmed to generate unidirectional resistance to expiratory V. Measurement sequences were repeated after this flap-valve was interposed in the right "main-stem bronchus." Integration of airway V versus time generated changes in lung volume. During flap-valve obstruction of the right bronchus, the V-time plot revealed preservation of peak expired flow from the normal lung, followed by retarded and decreased flow from the obstructed right lung. Gas trapping of the obstructed lung occurred during conditions of decreased expiratory time and increased expiratory resistance. Airway P could not differentiate between bronchial and tracheal flap-valve obstruction because P decreased abruptly in both conditions. The flow-volume loop displayed less distinctive changes than the flow-time plot, in part because the flow-volume loop was data (flow) plotted against its time integral (volume), with loss of temporal data. In this mechanical lung model, we conclude that bronchial flap-valve obstruction was best detected by the flow-time plot, which could measure the sequential emptying of the lungs.

Airway Obstruction↗
PubMed1995

Right atrial bypass model in the dog.

In gas exchange studies addressing the storage and transport of CO2 in dogs, a model in which cardiac output (QT) can be precisely controlled and measured would be beneficial. We identified problems with described extracorporeal circuits and implemented right atrial bypass (RAB) in dogs. In 6 anesthetized (chloralose and urethane), heparinized dogs (mean +/- SD, 24 +/- 4 kg) with open thorax, cannulas were inserted in both vena cavas to drain venous blood return to a reservoir (anaerobic bag or bubble oxygenator). A roller pump then drove blood through a heat exchanger back to the right atrial appendage. After 1.8 +/- 1.4 hour of RAB, physiologic variables remained within reference limits for dogs (QT, 1.5 +/- 0.3 L/min; blood pressure, 92 +/- 25 mm of Hg; arterial PCO2, 35 +/- 4 mm of Hg; PO2, 513 +/- 39 mm of Hg; pH, 7.39 +/- 0.08; and tissue CO2 production, 126 +/- 56 ml/min). To permit study of gas exchange, venous return (and thus, QT) and venous PCO2 and PO2 could be accurately regulated and measured over a wide range. Maintenance of native pulsatile lung perfusion and cardiogenic oscillations minimizes mismatching of pulmonary ventilation and perfusion and facilitates studies addressing pulmonary gas exchange. This RAB model is designed so that investigators can establish the preparation in a few hours.

Animals↗
PubMed1994

Capnometer transport delay: measurement and clinical implications.

The sidestream capnogram is delayed behind real time by transport delay (TD; time to aspirate gas through the sampling tubing) and by the dynamic response (DR) of the measurement cuvette. In six capnometers, we measured TD and DR by plunging the end of the sample tubing into a flask containing CO2 and then digitally analyzing the capnogram. TD ranged from 0.6 to 5.0 s and accounted for 89% or more of the total response time (TD + DR) of the capnometer. TD was generally not reported in the manufacturers' specifications. TD was further prolonged by low aspiration rates or by sampling tube extensions. During a series of quick breaths after endotracheal intubation, long TD can delay the appearance of CO2 and result in a false diagnosis of esophageal intubation. Also, long TD can prolong DR, which can result in underestimation of end-tidal PCO2 during rapid ventilation in pediatric anesthesia.

Blood Gas Monitoring, Transcutaneous↗
PubMed1992

Simple computer measurement of pulmonary VCO2 per breath.

Measurements of the volume of CO2 exhaled per breath (VCO2/br) are preferable to end-tidal PCO2, when the exhaled flow and CO2 waveforms may be changing during unsteady states, such as during alterations in positive end-expiratory pressure or alterations in cardiac output. We describe computer algorithms that determine VCO2/br from digital measurements of exhaled flow (including discontinuous signals common in anesthesia circuits) and CO2 concentration at the airway opening. Fractional concentration of CO2 is normally corrected for dynamic response and transport delay (TD), measured in a separate procedure. Instead, we determine an on-line adjusted TD during baseline ventilation. In six anesthetized dogs, we compared the determination of VCO2/br with a value measured in a simultaneous collection of expired gas. Over a wide range of tidal volume (180-700 ml), respiratory rate (3-30 min-1), and positive end-expiratory pressure (0-14 cmH2O), VCO2/br was more accurate with use of the adjusted TD than the measured TD (P less than 0.05).

Algorithms↗
PubMed1991

Can changes in end-tidal PCO2 measure changes in cardiac output?

In recent studies of cardiopulmonary resuscitation, an increase in end-tidal carbon dioxide tension (PETCO2) signifies an increase in cardiac output (QT) as spontaneous circulation resumes. We hypothesized that changes in QT might generally be measured by changes in PETCO2. In five pentobarbital-anesthetized dogs, we inflated percutaneously inserted vena cava balloons to impede venous return and to decrease QT (measured by pulmonary thermodulation). The PECTCO2 was measured at the airway opening by sidestream infrared capnometry. In 32 vena cava balloon inflation sequences during constant ventilation in five dogs, the percent decrease in PETCO2 directly correlated with the percent decrease in QT (slope = 0.73, R2 = 0.89, P less than 0.001). During decreased QT, reduced CO2 delivery to the lungs decreased alveolar PCO2 to cause part of the decrease in PETCO2. The remaining reduction in PETCO2 resulted from the increase in alveolar dead space (in turn due to lower pulmonary perfusion pressures during reduced QT), which diluted the CO2 from perfused alveolar spaces to further reduce PETCO2. During a sustained reduction in QT, increasing CO2 accumulation in the peripheral tissues and in venous blood began to restore CO2 delivery to the lung and PETCO2 toward baseline levels. Reciprocal changes occurred during increases in QT when the vena cava balloons were deflated. The linear relationship between changes in PETCO2 and QT in animals supports a decision to perform clinical studies necessary to determine whether a change in PETCO2 will be useful as a noninvasive, continuous monitor of a change in QT during anesthesia or intensive care.

Animals↗
PubMed1988

Treatment of canine aspiration pneumonitis: fluid volume reduction vs. fluid volume expansion.

The aspiration of gastric acid causes pulmonary edema and hypoxemia. One approach to the management of this syndrome is to raise cardiac output (Qt) and O2 delivery (QO2) to ensure tissue oxygenation (VO2) at the risk of increasing the edema. Another approach reduces the edema by reducing pulmonary microvascular pressure (Pmv) at the risk of reducing QO2 and VO2. We compared these approaches in 24 anesthetized, ventilated dogs with pulmonary wedge pressure (Ppw), a clinical approximation of Pmv, of 12.5 mmHg. Before and again 1 h after endobronchial instillation of 0.1 N HCl, we measured Qt, QO2, VO2, venous admixture, and in vivo extravascular lung liquid. The dogs were then randomly divided into four equal groups: 1) 12.5 mmHg Ppw, high Qt; 2) 7.5 mmHg Ppw, intermediate Qt; 3) 4.5 mmHg Ppw, low Qt; and 4) 4.5 mmHg Ppw plus dopamine, intermediate Qt. Measured values were followed for 4 more h, after which the lungs were excised to compare wet weight-to-body weight ratios (W/B). When plasmapheresis reduced Ppw at 1 h, edema did not increase further and W/B of groups 2 (21 +/- 3), 3 (18 +/- 3), and 4 (22 +/- 3) were significantly less than in group 1 (27 +/- 3) (P less than 0.001). Although Qt decreased with Ppw, increased hematocrit and reduced venous admixture maintained QO2 in group 2 but not in group 3. In group 4 an intermediate Qt maintained QO2 even at 4.5 mmHg Ppw but edema increased to the group 2 level presumably because Pmv rose with Qt on dopamine. VO2 remained constant over time in each group. These data demonstrate that canine HCl-induced pulmonary edema, measured in vivo or gravimetrically, is very sensitive to reductions in Pmv. Moreover, the lowest Pmv (and QO2) was well tolerated because an O2 supply dependency of VO2 was not observed.

Animals↗