PURPOSE: The purpose of this study was to determine the dynamic changes in right ventricular (RV) and left ventricular (LV) output during positive airway pressure inspiratory hold maneuvers so as to characterize the interaction of processes in creating steady-state cardiac output during positive pressure ventilation. MATERIALS AND METHODS: We examined the disparity of RV and LV outputs at 5 seconds (early) and 20 seconds (late) into a 24-second inspiratory hold maneuver in 14 subjects in the intensive care unit immediately following coronary artery bypass surgery. RV output was measured by the thermodilution technique, whereas LV output was measured by the arterial pulse contour method. RV and LV volumes were also measured by thermal and radionuclide ejection fraction techniques, respectively. RESULTS: As P(aw) was progressively increased from 0 to 20 cm H2O in sequential inspiratory hold maneuvers, both RV and LV outputs changed differently both at 5 seconds and 20 seconds into the inspiratory hold maneuvers. When expressed as change in cardiac output (L/min) for every cm H2O P(aw) increase relative to end-expiratory values, RV output increased at 5 seconds (0.05 +/- 0.15 L/min) then decreased at 20 seconds (-0.08 +/- 0.21, P < .05). LV output decreased slightly at 5 seconds (-0.14 +/- 0.22) and did not change from this minimal depressed level at 20 seconds (P < .05). Changes in RV and LV output were paralleled by changes in RV and LV end-diastolic volumes, respectively. CONCLUSION: Positive pressure inspiration induces time-dependent changes in central hemodynamics, which are dissimilar between RV and LV function. Initially, inspiration increases RV output but decreases LV output, such that intrathoracic blood volume increases. However, sustained inspiratory pressures induce proportionally similar decreases in both RV and LV outputs. Thus, the hemodynamic effects of positive pressure ventilation will depend on the degree of lung inflation, the inspiratory time, and when measurements are made within the ventilatory cycle. These data also suggest that positive pressure ventilation with up to 20 cm H2) P(aw) does not significantly impair ventricular performance in humans.

Aged↗

PubMed1997

Splanchnic buffering of metabolic acid during early endotoxemia.

PURPOSE: We sought to determine the sites of metabolic acid production and clearance during acute endotoxemia. MATERIALS AND METHODS: In 10 pentobarbital-anesthetized dogs, flow was measured (ultrasonic probes) for the protal vein, hepatic artery, and renal artery. Catheters were inserted into the hepatic vein, pulmonary artery, renal vein and portal vein. Measurements of blood gases and strong ions were obtained from each site during control conditions and after 30 minutes of intravenous infusion of 1 mg/kg of Escherichia coli endotoxin. The total metabolic acid flux across each organ was calculated using the standard base excess formula and the effective strong ion difference method. PaCO2 was maintained by controlled ventilation. RESULTS: Mean arterial pH decreased from 7.34 to 7.22 with acute endotoxemia. Although transvisceral pH gradients revealed net acid release, the source of this was purely respiratory (carbon dioxide). During early endotoxemia, the gut significantly increased metabolic acid uptake (36.60 +/- 6.60 mmol/h, P < .05). CONCLUSIONS: We conclude that during early endotoxemia in the dog, the gut is a major site of metabolic acid removal.

Acid-Base Equilibrium↗

PubMed1997

Tracheal gas insufflation improves ventilatory efficiency during metacholine-induced bronchospasm.

INTRODUCTION: Barotrauma and cardiovascular insufficiency are frequently encountered problems in patients with acute bronchospastic disease who require mechanical ventilation. Permissive hypercapnia is a recognized strategy for minimizing these adverse effects; however, it has potential risks. Tracheal gas insufflation (TGI) has been shown to increase carbon dioxide elimination efficiency and thus could permit mechanical ventilation at lower peak airway pressures without inducing hypercapnia. However, caution exists as to the impact of TGI on lung volumes, given that expiratory flow limitation is a hallmark of bronchospastic disease. PURPOSE: To examine these issues, we studied ventilatory and hemodynamic effects of continuous TGI as an adjunct to mechanical ventilation before and after methacholine-induced bronchospasm. MATERIALS AND METHODS: Ten anesthetized, paralyzed dogs were ventilated on volume-controlled mechanical ventilation during administration of continuous TGI (0, 2, 6, and 10 L/min) while total inspired minute ventilation (ventilator-derived minute ventilation plus TGI) was kept constant. In an additional step, with TGI flow of 10 L/min, total inspired minute ventilation was decreased by 30%. RESULTS: PaCO2 decreased (44 +/- 7 mm Hg at zero flow to 34 +/- 7 mm Hg at 6 L/min and 31 +/- 6 mm Hg at 10 L/min, respectively, P < .05), as did the dead space to tidal volume ratio at TGI of 6 and 10 L/min compared with zero flow. There were no significant changes in end-expiratory transpulmonary pressure, mean arterial pressure, or cardiac output. During the highest TGI flow (10 L/min), with a 30% reduction of total inspired minute ventilation, both PaCO2 and peak airway pressure remained less than during zero flow conditions. CONCLUSION: We conclude that TGI increases carbon dioxide elimination efficiency during constant and decreased minute ventilation conditions without any evidence of hyperinflation or hemodynamic instability during methacholine-induced bronchospasm.

Animals↗

PubMed1997

Tracheal gas insufflation during pressure-control ventilation: effect of using a pressure relief valve.

OBJECTIVES: Pressure-control ventilation minimizes alveolar overdistention by limiting peak airway pressure, but a consequence of this pressure limitation may be a reduction in tidal volume with subsequent hypercarbia. Tracheal gas insufflation (TGI) can be used in combination with pressure-control ventilation to augment CO2 elimination. During pressure-control ventilation with continuous TGI, we observed that peak airway pressure increased above the set inspiratory pressure. Based on this observation, we investigated the ability of the pressure-control ventilator circuit to compensate for continuous TGI and the effect of insertion of a pressure relief valve to eliminate over-pressurization. SETTING: University research laboratory. DESIGN: Using an artificial lung model, we studied the effects of continuous TGI with varying catheter flows (0, 2, 6, and 10 L/ min); ventilator frequencies (10 and 20 breaths/min); inspiratory duty cycles (0.33, 0.50, and 0.67); lung compliance (0.01, 0.02, and 0.04 L/cm H2O); and airway resistance (5, 20, and 50 cm H2O/L/sec) on: a) peak airway pressure; b) total inspiratory tidal volume; c) ventilator-derived tidal volume; and d) intrapulmonary pressure at end-exhalation (auto-PEEP). Tests were performed with and without a pressure relief valve whose threshold "pop-off" pressure was adjusted to match the set inspiratory pressure (35 cm H2O) for a total of 432 experimental conditions. MEASUREMENTS AND MAIN RESULTS: Our data demonstrate that pressure-control ventilation augmented with continuous TGI can increase peak airway pressure above set inspiratory pressure due to delivery of a higher than intended tidal volume. Predisposing conditions include catheter flow rates of 6 and 10 L/min, long inspiratory time, low compliance, and low resistance. With the pressure relief valve, peak airway pressure was maintained at the set inspiratory pressure and total inspiratory tidal volume remained constant. CONCLUSION: A pressure relief valve is a necessary adjunct to maintain peak airway pressure at set inspiratory pressure and keep total inspiratory tidal volume constant when continuous TGI is administered in conjunction with pressure-control ventilation.

Airway Resistance↗

PubMed1997

Low levels of nitric oxide as contaminant in hospital compressed air: physiologic significance?

OBJECTIVES: To determine whether the levels of nitric oxide found in hospital compressed air have a clinically relevant effect on oxygenation in intubated patients with normal lungs. DESIGN: Prospective study. SETTING: Cardiothoracic and surgical intensive care unit in a university hospital. PATIENTS: Twelve postoperative patients receiving mechanical ventilation. INTERVENTIONS: Pure nitrogen and oxygen were substituted for hospital compressed air as a source of blending for correct FIO2. MEASUREMENTS AND MAIN RESULTS: Hemodynamics and PaO2 were measured in nitrogen and oxygen used for blending oxygen during stable FIO2 levels. Inhaled nitric oxide was measured with a nitric oxide-chemiluminescence detector. There was no clinically relevant change in systemic hemodynamics. However, the PaO2 decreased significantly when nitrogen was used for blending. Inhaled nitric oxide levels varied from 2 to 550 parts per billion during use of hospital compressed air; no nitric oxide was detectable during use of nitrogen. CONCLUSIONS: The low concentration of nitric oxide in hospital compressed air improves oxygenation in patients with normal lungs receiving mechanical ventilation.

Blood Gas Analysis↗

PubMed1997

Left ventricular performance assessed by echocardiographic automated border detection and arterial pressure.

Automated echocardiographic measures of left ventricular (LV) cavity area are closely correlated with changes in volume and can be coupled with LV pressure (PLV) to construct pressure-area loops in real time. The objective was to rapidly estimate LV contractility from end-systolic relationships of cavity area (as a surrogate for LV volume) and central arterial pressure (Pa) (as a surrogate for PLV) in a canine model using automated algorithms. In eight anesthetized mongrel dogs, we simultaneously measured PLV, LV area, and Pa (fluid-filled catheter). End-systolic pressure-area relationships in terms of pressure-area elastance (E'es)] from pressure-area loops during inferior vena caval occlusions were determined during basal conditions (control), dobutamine infusion (5-10 micrograms.mg-1.min-1), and after bolus propranolol (2 mg/kg) with both PLV and Pa by semiautomated and automated iterative regression methods. E'es increased during dobutamine infusion and decreased after propranolol infusion in all animals and with all iterative methods. Estimates of Ees from Pa were closely correlated with E'es from PLV by both the semiautomated and automated methods (r = 0.93; P < 0.01). The relationship between E'es obtained from Pn for the two methods was also closely correlated. Although the automated methods displayed larger differences from the semiautomated iterative technique by Bland-Altman analysis, the change in E'es with all techniques during dobutamine infusion and after propranolol infusion was of similar magnitude and direction among the three techniques. Greater variability with the dobutamine runs was partially due to abnormally conducted ventricular beats that minimized the number of consecutive beats that could be used for these analyses. We conclude that on-line Pa recordings from fluid-filled catheters can be used with echocardiographic automated border detection to rapidly calculate E'es as a means to estimate LV contractility.

Algorithms↗

PubMed1997

Release of lactate by the lung in acute lung injury.

UNLABELLED: The pathogenesis of hyperlactatemia during sepsis is poorly understood. We have previously described an increase in lactate concentration across the lung in the dog during early endotoxemia. Accordingly, we sought to determine if the lung releases lactate in humans and what relation this has with lung injury. METHODS: We measured lactate concentrations across the lung and lung injury scores (LIS) in two groups of patients. Group 1 consisted of nine patients with acute lung injury (LIS > or = 2.0) and elevated lactate concentrations (> 2.0 mmol/L). Group 2 contained 12 patients with no acute lung injury (LIS scores < or = 1.5), with or without increased lactate concentrations. Simultaneous measurements of plasma lactate and blood gases were obtained from indwelling arterial and pulmonary artery catheters. Measurements of cardiac output were also obtained. Lactate measurements were done using a lactate analyzer (YSI; Yellow Springs, Ohio). RESULTS: For each patient with acute lung injury and hyperlactatemia, an arterial-venous lactate gradient existed demonstrating release of lactate by the lung. This gradient persisted after correction for changes in hemoconcentration across the lung. The lactate gradient across the lung was 0.4 +/- 0.2 mmol/L for group 1 vs 0.05 +/- 0.1 mmol/L for group 2 (p = 0.001). This corresponded to a mean pulmonary lactate flux of 231.3 +/- 211.3 vs 5.0 +/- 37.2 mmol/h (p = 0.001). The lactate flux and the arterial-venous lactate difference correlated with LIS both for the entire sample and for the subgroup with hyperlactatemia (r = 0.69, p < 0.01). Pulmonary lactate flux was not related to arterial lactate levels (r = 0.25). CONCLUSION: In patients with acute lung injury and hyperlactatemia, the lung is a major source of lactate and lactate flux correlates with LIS. This lactate flux could explain some of the hyperlactatemia seen in sepsis.

Adult↗

PubMed1997

Contamination of hospital compressed air with nitric oxide: unwitting replacement therapy.

BACKGROUND: Inhaled nitric oxide (NO) at levels between 5 and 80 ppm has been used experimentally to treat a variety of conditions. NO also is a common environmental air pollutant in industrial regions. As compressed hospital air is drawn from the local environment, we speculated that it may contain NO contamination, which, if present, would provide unwitting inhaled NO therapy to all subjects respiring this compressed gas. METHODS: NO levels were measured twice daily from ambient hospital air and compressed gas sources driving positive pressure ventilation from two adjacent hospitals and compared with NO levels reported daily by local Environmental Protection Agency sources. An NO chemiluminescence analyzer (Sievers 270B; Boulder, Colo) sensitive to > or =2 parts per billion was used to measure NO levels in ambient air and compressed gas. RESULTS: NO levels in ambient air and hospital compressed air covaried from day to day, and absolute levels of NO differed between hospitals with the difference never exceeding 1.4 ppm (range, 0 to 1.4 ppm; median, 0.07 ppm). The hospital with the highest usage level of compressed air had the highest levels of NO, which approximated ambient levels of NO. NO levels were lowest on weekends in both hospitals. We also documented inadvertent NO contamination in one hospital occurring over 5 days, which corresponded to welding activity near the intake port for fresh gas. This contamination resulted in system-wide NO levels of 5 to 8 ppm. CONCLUSION: Hospital compressed air contains highly variable levels of NO that tend to covary with ambient NO levels and to be highest when the rate of usage is high enough to preclude natural degradation of NO in 21% oxygen. Assuming that inhaled NO may alter gas exchange, pulmonary hemodynamics, and outcome from acute lung injury, the role of unwitting variable NO of hospital compressed air needs to be evaluated.

Air↗

PubMed1997

Right ventricular function in human sepsis: a thermodilution study.

STUDY OBJECTIVE: To assess the relations among right ventricular (RV) pressures and volumes in sepsis. DESIGN: Prospective study. SETTING: ICU. PATIENTS: Eighteen patients with sepsis who were in hemodynamically stable condition. INTERVENTION: Stepwise increases and decreases in RV end-diastolic volume (EDV) as induced by military antishock trousers (MAST) inflation of 0, 15, 30, 50 and then 0 mm Hg over 15-min intervals. MEASUREMENTS AND RESULTS: RV volumes and pressures were measured using a rapid response thermistor pulmonary arterial catheter based on RV ejection fraction (RVEF) calculations. RV EDV was estimated as stroke volume (SV)/RVEF, while RV end-systolic volume (ESV) was estimated as EDV-SV. Right atrial pressure (Pra) was taken as end-diastolic pressure, and pulmonary artery pressures (Ppa), both mean and end-systolic, were used as RV ejection pressures. MAST inflation to 15 mm Hg had no measurable effects on the measured variables. However, inflation to 30 and 50 mm Hg increased Pra, both mean and end-systolic Ppa, EDV, and ESV, whereas SV and RVEF remained unchanged. The relation between either Pra and EDV (r=0.33) or the change in Pra and EDV, mean or end-systolic Ppa and ESV (r=0.5 and 0.28, respectively), or the change in mean or end-systolic Ppa and ESV for both the group and individual subjects was poor. Furthermore, SV correlated poorly with EDV (r=0.32), while RVEF correlated better with both EDV and ESV (r=-0.41 and -0.69, respectively), although it showed no definable relation to mean or end-systolic Ppa. However, both absolute and relative changes in EDV corresponded closely with respective ESV values (r=0.93). CONCLUSIONS: During sepsis, RV EDV and ESV vary independently of changes in Pra and ejection pressure. These data can be explained by assuming that the RV is a highly compliant chamber during filling, such that changes in RV EDV do not alter RV wall stress (preload) or ejection efficiency (RVEF). Thus, changes in RV EDV should proportionally alter RV ESV. Furthermore, the slope of the ESV/EDV relation should be inversely proportional to ejection efficiency.

Adult↗

PubMed1997

The influence of high-frequency jet ventilation with varying cardiac-cycle specific synchronization on cardiac output in ARDS.

BACKGROUND: Previous studies have shown "beat-to-beat" variation in systemic BP with high-frequency jet ventilation (HFJV). However, it is not clear if such changes are paralleled by changes in cardiac output. OBJECTIVE: To characterize the effect of HFJV near or equal to the heart rate (HR) on beat-to-beat cardiac output in an adult human subject with ARDS. DESIGN: Case study. SETTING: ICU, university teaching hospital. PATIENTS: One patient with end-stage liver disease complicated by sepsis, severe pancreatitis, ARDS, and multisystem organ failure. METHODS: The patient was intubated, sedated, paralyzed, and ventilated with controlled mechanical ventilation (CMV). Ventilatory mode was then switched to HFJV at fixed frequencies (f) near but not equal to the HR (f= 100, 110, and 120 beats/min; HR=108/min). HFJV was then synchronized to the ECG such that f and HR were equal. Continuous cardiac output (COc) was monitored during change of ventilator mode from CMV to fixed-rate HFJV to synchronized HFJV, then followed through progressive delays in jet triggering within the cardiac cycle during the synchronous HFJV mode. COc was monitored by arterial pulse-contour analysis, allowing assessment of beat-to-beat changes in cardiac output. MEASUREMENTS AND MAIN RESULTS: A cyclic variation in COc equal to the beat frequency difference between f and HR was observed (harmonic interaction) during fixed-rate HFJV. This COc oscillation was abolished during synchronous HFJV. COc was significantly greater during systolic synchronous HFJV as compared to diastolic synchronous HFJV or fixed-rate HFJV (10.1 to 9.0 [p<0.05] and to 8.6 [p<0.05] L/min, systolic synchronous to diastolic synchronous and to fixed-rate HFJV, respectively). CONCLUSIONS: This study demonstrates instantaneous variations in cardiac output in a human subject with fixed rates of HFJV near to the HR in humans. These variations are abolished by synchronous HFJV but cardiac output was dependent on the timing of the HFJV inspiration in relation to the cardiac cycle. COc is a potentially valuable method to monitor sudden changes in cardiac output and facilitate attempts to maximize cardiac output during synchronized HFJV.

Adult↗

PubMed1997

Clinical applications of cardiopulmonary interactions.

The hemodynamic consequences of both spontaneous and positive-pressure ventilation may be profound and may have opposite effects on cardiovascular stability in differing patient populations. Thus, no firm rules apply as to the specific response that will be seen in all patients and under all conditions. Some generalities, however, are probably reasonable. In patients with markedly increased work of breathing, hypervolemia, or impaired LV pump function, the institution of mechanical ventilatory support can be lifesaving because of its ability to support the cardiovascular system, independent of any beneficial effects that mechanical ventilation may have on gas exchange. In patients with decreased pulmonary elastic recoil, increased pulmonary vascular resistance, hypovolemia, or airflow obstruction, the institution of mechanical ventilatory support may induce cardiovascular instability, which, if not corrected, can lead to total cardiovascular collapse. Similarly, withdrawal of ventilatory support invariably increases intrathoracic blood volume and LV afterload and can be thought of as a type of cardiovascular stress test. Patients who pass this test easily can usually be successfully weaned from mechanical ventilatory support, whereas those who fail often are not ready to be weaned. Some patients who fail weaning trials do so because of the cardiovascular effects of spontaneous ventilation, not because the work of breathing is too great. Identification of such patients early on may improve their treatment by directing supportive therapies toward cardiovascular rather than ventilatory endpoints. However, in many situations, it will be difficult to single out a primary process determining cardiovascular instability, because multiple factors are compounded to create the observed situation and the patient's response to initiation of ventilatory support or weaning. Thus, the clinician is left with a series of therapeutic options, which if depending on the patient's response, suggest specific origins of the ventilatory and cardiovascular dysfunction. In that regard, the initiation and withdrawal of ventilatory support can be seen as a ventilatory probe into the determinants of cardiovascular homeostasis in the ventilatory-dependent patient.

Heart↗

PubMed1996

The effect of managed care on ICU length of stay: implications for medicare.

OBJECTIVE: To determine whether insurance status (managed care vs traditional commercial and Medicare) influences resource consumption (as measured by length of stay [LOS]) in the intensive care unit (ICU). DESIGN: Retrospective analysis of the 1992 Massachusetts state hospital discharge database, using prospectively developed and validated risk-stratification models. SETTING: All nonfederal hospitals in Massachusetts. SUBJECTS: Of all adult hospitalizations where an ICU stay was incurred (n=104270), we selected those covered by 1 of 4 payer groups (n=88050): (1) commercial fee-for-service (patients aged <65 years); (2) commercial managed care (patients aged <65 years); (3) traditional Medicare (patients aged >/=65 years); and (4) Medicare-sponsored managed care (patients aged >/=65 years). MAIN OUTCOME MEASURE: Mean ICU LOS. ANALYSIS: The ICU LOS regression models were constructed using split-halves validation to adjust for differences in age, sex, severity of illness, diagnosis, discharge status, and payer. Separate models were constructed for those younger than 65 years and those aged 65 years or older. Robustness of the models was explored using goodness of fit and correlation. The effect of payer on hospital mortality was also explored using logistic regression. Observed minus predicted mean ICU LOS and mortality rates were correlated with managed care penetration at the hospital level. RESULTS: The ICU LOS models performed well (R2=0.84 and R2L [likelihood ratio statistic]=0.92 for the development set, and R2=0.83 and R2L=0.89 for the validation set). Significant covariables affecting LOS included age, severity of principal illness, comorbidity, reason for admission, and discharge status (P<.001 for each). Among the cohort younger than 65 years (n=27805), although unadjusted mean ICU LOS was shorter (2.9 vs 3.43 days; P<.05) for those covered by managed care organizations, payer status had no independent effect on ICU LOS (P=.48). Among those older than 65 years, there was neither a difference in unadjusted ICU LOS (3.94 vs 3.88 days; P>/=.05) nor an independent effect of payer on ICU LOS (P=.35). Unadjusted mortality was lower among managed care patients (3.9% vs 5.1% in patients aged <65 years [P<.05] and 8.7% vs 12.1% in patients aged > or = 65 years [P<.05]). Age, severity of principal diagnosis, comorbidity, and reason for admission significantly influenced mortality (P<.001). After controlling for these factors with the mortality model (R2L=0.92 and 0.89, C statistic [12 df]=8.45 and 17.58, and P=.75 and .13 [where a large P reflects good agreement] for the development and validation sets, respectively), payer continued to have a small but significant effect on mortality (odds ratios ranging from 1.67 at 0.1% probability of death to 1.11 at 30% probability of death.) Managed care penetration among the commercially insured varied across hospitals (n=82) from 0% to 68%. There was no correlation between managed care penetration and either ICU LOS (R2=0.04; P=.09) or mortality (R2=0.0; P=.88). CONCLUSIONS: Though patients covered under managed care consume fewer ICU resources, this appears to be primarily attributable to a difference in patient-related factors. Thus, as managed care case mix changes in the future to include sicker and older patients, the initial advantages of reduced resource consumption may diminish.

Adult↗

PubMed1996

Blood lactate levels are better prognostic indicators than TNF and IL-6 levels in patients with septic shock.

OBJECTIVE: Both serum levels of tumor necrosis factor-alpha (TNF alpha) and interleukin-6 (IL-6) and blood lactate levels in patients with septic shock have been shown to correlate with prognosis. The aim of the study was to define the relative predictive value of these measures. PATIENTS: 38 hospitalized patients with septic shock, including 18 survivors and 20 non-survivors. INTERVENTION: Blood TNF alpha (immunoradiometric assay), IL-6 (bioassay) and lactate (enzymatic method) levels were serially measured at the onset of septic shock and after 24 and 48 h. RESULTS: TNF alpha levels tended to be higher in the non-survivors than in the survivors at the onset of shock (204 +/- 392 vs 129 +/- 195 pg/ml, p = NS) but decreased similarly in both groups with time (p = 0.03). IL-6 levels at admission were highly variable (9656 +/- 19851 U/ml in the non-survivors and 69,222 +/- 248,804 U/ml in the survivors). Log IL-6 decreased similarly in both groups with time (p = 0.004). Admission blood lactate levels were higher in the non-survivors than in the survivors (6.11 +/- 4.78 mEq/l vs 3.49 +/- 2.00 mEq/l, p < 0.05) and decreased significantly with time in all patients (p = 0.024). However, this decrease was greater in the survivors than in the non-survivors (p = 0.003). CONCLUSION: These data indicate that the large variability in TNF alpha and IL-6 levels limit their prognostic significance in patients with septic shock. The predictive value of the trend in cytokine levels over time is not superior to that of trends in blood lactate levels.

Adult↗

PubMed1996

Left ventricular pressure-volume relations with transesophageal echocardiographic automated border detection: comparison with conductance-catheter technique.

Pressure-volume relations are important means used to assess left ventricular (LV) contractility; however, on-line volume acquisition has been limited to the invasive conductance catheter. The objective was to compare simultaneous measures of LV volume by transesophageal echocardiographic automated border detection (ABD) and conductance catheter and their respective pressure-volume relations during steady state and alterations in preload and contractility. Seven dogs had placement of high-fidelity pressure and conductance catheters, a vena caval balloon occluder, and a transesophageal probe. An automated Simpson's rule volume algorithm was used from the transverse four-chamber view. Inotropic modulation was induced with dobutamine in four dogs and propranolol in three. Relative changes in ABD volume were linearly related to conductance volume at steady state with group mean r = 0.93 +/- 0.03, standard error of estimate (SEE) = 10 +/- 2%. Changes in end-diastolic volume, end-systolic volume, and stroke work with caval occlusion were also significantly correlated:r = 0.93 =/- 0.04, SEE = 3.6 ml; r = 0.89 +/- 0.04, SEE = 3.8 +/- 1.9 ml; and r = 0.86 +/- 0.05, SEE = 40 +/- 21 mJ, respectively. The overall bias was for absolute ABD volume to be less. End-systolic and maximal elastance values by ABD were significantly higher than by the conductance method; baseline group average 4.97 +/- 0.92 mm Hg/ml versus 2.70 +/- 1.15 mm Hg/ml and 6.63 +/- 1.66 mm Hg/ml versus 3.20 +/- 1.37 mm Hg/ml (p<0.05), respectively. However, the direction and relative magnitude of changes in elastance with inotropic modulation were similar.

Analysis of Variance↗