Biomedical subjects

Santos E Cabreriza

Publications and source records attributed to Santos E Cabreriza.

At least 19 recordsLinked to original sources

PubMed2006

Ventricular diastolic stiffness predicts perioperative morbidity and duration of pleural effusions after the Fontan operation.

BACKGROUND: We validated the clinical relevance of ventricular stiffness by examining surgical morbidity in children with univentricular hearts undergoing Fontan operation. We hypothesized that ventricular stiffness affects Fontan morbidity, particularly duration of pleural effusions. METHODS AND RESULTS: Sixteen children with right ventricular (RV) (n =11) or left ventricular (LV) (n =5) dominance were studied intraoperatively at a median age of 3.3 years (1.8 to 5.1). Transesophageal long-axis echocardiograms and ventricular pressure by micromanometer provided end-diastolic pressure (P) area (A) relations during initiation and conclusion of cardiopulmonary bypass. Curve fitting to the equation P=alphae(betaA) defined the ventricular stiffness constant, beta. Changes in beta and clinical correlations were examined. Ventricular stiffness increased after bypass in patients with complete pre-bypass and post-bypass data (n =11, P=0.023, mixed models methodology). Pre-bypass beta correlated well with duration of chest tube (CT) drainage (r=0.90, n =16), net perioperative fluid balance (r=0.71, n=14), and length of stay (LOS) (r=0.81, n =16). CT duration and LOS also correlated significantly with post-bypass beta (r=0.77 for both, n=11), but insignificantly with preoperative catheterization pressures. CONCLUSIONS: Intraoperative beta predicts duration of CT drainage, net perioperative fluid balance, and LOS after the Fontan operation. These observations could improve risk stratification and clinical management of children at high-risk undergoing the Fontan operation.

Chest Tubes↗

PubMed2006

Effects of sequential biventricular pacing during acute right ventricular pressure overload.

Temporary sequential biventricular pacing (BiVP) is a promising treatment for postoperative cardiac dysfunction, but the mechanism for improvement in right ventricular (RV) dysfunction is not understood. In the present study, cardiac output (CO) was optimized by sequential BiVP in six anesthetized, open-chest pigs during control and acute RV pressure overload (RVPO). Ventricular contractility was assessed by the maximum rate of increase of ventricular pressure (dP/dt(max)). Mechanical interventricular synchrony was measured by the area of the normalized RV-left ventricular (LV) pressure diagram (A(PP)). Positive A(PP) indicates RV pressure preceding LV pressure, whereas zero indicates complete synchrony. In the control state, CO was maximized with nearly simultaneous stimulation of the RV and LV, which increased RV (P = 0.006) and LV dP/dt(max) (P = 0.002). During RVPO, CO was maximized with RV-first pacing, which increased RV dP/dt(max) (P = 0.007), but did not affect LV dP/dt(max), and decreased the left-to-right, end-diastolic pressure gradient (P = 0.023). Percent increase of RV dP/dt(max) was greater than LV dP/dt(max) (P = 0.014). There were no increases in end-diastolic pressure to account for increases in dP/dt(max). In control and RVPO, RV dP/dt(max) was linearly related to A(PP) (r = 0.779, P < 0.001). The relation of CO to A(PP) was curvilinear, with a peak in CO with positive A(PP) in the control state (P = 0.004) and with A(PP) approaching zero during RVPO (P = 0.001). These observations imply that, in our model, BiVP optimization improves CO by augmenting RV contractility. This is mediated by changes in mechanical interventricular synchrony. Afterload increases during RVPO exaggerate this effect, making CO critically dependent on simultaneous pressure generation in the RV and LV, with support of RV contractility by transmission of LV pressure across the interventricular septum.

Animals↗

PubMed2006

Left ventricular pacing site-timing optimization during biventricular pacing using a multi-electrode patch.

A 71-year-old man with class IV congestive heart failure and an infected pacemaker/implantable cardioverter defibrillator (ICD) underwent median sternotomy for removal of endocardial leads with a 15-mm vegetation. Cardiac output during biventricular pacing was optimized with an aortic flow probe, a multi-electrode left ventricular patch, and a randomized protocol assessing 54 combinations of pacing site and right ventricle-left ventricle delay. Results that were assessed with response surface methodology determined permanent epicardial lead position and timing. The difference between the best and worst site-timing combinations altered cardiac index by nearly 70%. This experience demonstrates potential importance of the epicardial approach to site-timing optimization for biventricular pacing.

Aged↗

PubMed2006

Load dependence of cardiac output in biventricular pacing: left ventricular volume overload in pigs.

OBJECTIVE: Previous work from our laboratory has demonstrated that optimization of biventricular pacing is load dependent. Cardiac output was maximized with a ventricular-ventricular delay of +40 milliseconds (right ventricle-first pacing) during right ventricular pressure overload and with a ventricular-ventricular delay of -40 milliseconds (left ventricle-first pacing) during right ventricular volume overload. We hypothesized that a model of left ventricular volume overload would also have specific timing requirements during biventricular pacing for optimization of cardiac output. METHODS: After median sternotomy in 6 anesthetized pigs, complete heart block was induced by ethanol ablation. A conduit was grafted from the left ventricle to the left atrium to produce left ventricular volume overload. An ultrasonic flow probe was placed around the conduit to measure retrograde flow that averaged 50% of cardiac output. During epicardial atrial tracking DDD biventricular pacing, atrioventricular delay was varied between 60 and 270 milliseconds in 30-millisescond increments for 20-second intervals. After determination of optimum atrioventricular delay, ventricular-ventricular delay was varied in 20-millisecond increments from +80 to -80 milliseconds for 20-second intervals. RESULTS: Ventricular-ventricular delays had no significant effect on cardiac output with the graft clamped (control). With the graft unclamped, however, there was a statistically significant (P = .0001 by repeated-measures analysis of variance) trend toward higher cardiac output with right ventricle-first pacing. CONCLUSIONS: Right ventricle-first pacing in swine significantly increased cardiac output during acute left ventricular volume overload, but not during the control state. Understanding load-specific pacing requirements will facilitate the development of perioperative temporary biventricular pacing for acute heart failure.

Animals↗

PubMed2005

Ethanol induction of complete heart block in swine.

OBJECTIVES: A method for the induction of complete heart block (CHB) by ethanol injection and its success rate in a pig model of acute right ventricular failure is reported. Additionally, a review of the literature for the induction of CHB in laboratory animals is detailed. The literature review was undertaken to both compare our rate of success with other methods and provide insight into our technique and refine its implementation. BACKGROUND: Animal models of CHB have facilitated the understanding of therapeutics for various cardiac pathologies in humans. In our laboratory, CHB in pigs is used for complete control of heart rhythm in studies of biventricular pacing. MATERIALS AND METHODS: Experiments carried out on pigs in our laboratory that required the induction of CHB were reviewed retrospectively. In addition, review of the literature for creating CHB in animals was undertaken. Our success rate was compared to that of other groups. RESULTS: Our success rate (93%) is similar to other models of CHB, in general, and to those models that used the injection of caustic substances with thoracotomy. CONCLUSIONS: Review of the literature indicates that our success rate is comparable to other groups and that, although many approaches have been described in both open- and closed-chest models, success is likely dependent on the practice and skill of the experimenter. In addition, review of the literature has afforded us new perspectives on the experimental induction of CHB.

Animals↗

PubMed2005

Optimized biventricular pacing in atrioventricular block after cardiac surgery.

BACKGROUND: Temporary pacing is required after open-heart surgery for treatment of heart block. Atrioventricular delay and ventricular pacing site might be manipulated to increase cardiac output. We hypothesized that by optimizing both atrioventricular delay and ventricular pacing site a 10% improvement in cardiac output would be observed compared with a standard pacing protocol. METHODS: Seven patients in first or third degree heart block after valve replacement surgery had temporary wires sewn to the right atrium, right ventricle, and left ventricle. Cardiac output was measured by integrating flow velocity from an ultrasonic aortic flow probe. After optimization of atrioventricular delays during atrial synchronous right ventricular pacing, the effects of ventricular pacing site were tested at the optimum atrioventricular delay for 10-second intervals. RESULTS: Biventricular pacing was beneficial in all patients with a mean increase of 22% in cardiac index over right ventricular pacing (1.95 L/min/m2 +/- 0.27 standard error of the mean (SEM) to 2.38 L/min/m2 +/- 0.27 SEM, p = 0.0012) and 14% over left ventricular pacing (2.08 L/min/m2 +/- 0.22 SEM to 2.38 L/min/m2 +/- 0.27 SEM, p = 0.0133). Comparing optimized with standard pacing for 30-second intervals yielded a mean increase of 10% in cardiac index over three respiratory cycles (2.87 L/min/m2 +/- 0.33 SEM to 2.60 L/min/m2 +/- 0.37 SEM, p = 0.009) and 17% at the corresponding end-expiratory beats (2.76 L/min/m2 +/- 0.33 SEM to 2.36 L/min/m2 +/- 0.36 SEM, p = 0.011). CONCLUSIONS: Biventricular pacing at optimum atrioventricular delay improves cardiac output in patients with postoperative heart block by at least 10% compared with standard pacing.

Blood Pressure↗

PubMed2004

Regional functional depression immediately after ventricular septal defect closure.

Left ventricular ejection is depressed immediately after repair of ventricular septal defect (VSD). Postrepair functional depression seen after VSD closure could result from a reduction in preload. However, other mechanisms could be at work. Functional depression could also be caused by closure of a low-impedance path for left ventricular ejection, the introduction of a stiff akinetic patch, or the operation itself. We reasoned that functional depression mediated by changes in preload or afterload should symmetrically affect end-diastole and end-systole, whereas depression resulting from changes in septal mechanics should be localized. We, therefore, performed segmental wall-motion analysis on intraoperative echocardiograms from patients undergoing VSD and atrial septal defect repair. After VSD closure, there was an asymmetric change in left ventricular end-systolic segment length and a decrease in fractional segment shortening localized to the septal and lateral walls, whereas patients with atrial septal defect had a symmetric increase in fractional shortening. These results suggest that acute functional depression after VSD repair is a result of localized impairment of septal function.

Cardiac Surgical Procedures↗

PubMed2004

Load dependence of cardiac output in biventricular pacing: right ventricular volume overload in pigs.

BACKGROUND: Previous work from our laboratory has demonstrated that optimization of biventricular pacing is load dependent. During acute pulmonary stenosis and right ventricular pressure overload in swine, cardiac output was maximized by pacing the right ventricle 40 ms before the left ventricle. To extend those studies, this experiment examined biventricular pacing optimization during right ventricular volume overload. METHODS: After median sternotomy in 6 anesthetized domestic pigs, complete heart block was induced by ethanol ablation. A conduit was grafted from the right ventricle to the right atrium to simulate tricuspid insufficiency. During epicardial, atrial tracking DDD biventricular pacing, atrioventricular delay was varied between 60 and 180 ms in 30-ms increments. Right ventricular-left ventricular delay was varied at each atrioventricular delay from +80 ms (right ventricle first) to -80 ms (left ventricle first) in 20-ms increments. Aortic flow, right ventricular pressure, and electrocardiogram were measured at each pacemaker setting with the graft clamped and unclamped. RESULTS: Atrioventricular and right ventricular-left ventricular delays had no significant effect on cardiac output with the graft clamped. With the graft unclamped, however, there was a statistically significant (P =.003 by mixed modeling repeated measures analysis of variance) trend toward higher cardiac output with left ventricle-first pacing. CONCLUSION: Left ventricle-first biventricular pacing in swine significantly increased cardiac output during acute tricuspid insufficiency but not during the control state. Trials are warranted to develop clinical biventricular pacing for treatment of perioperative right ventricular dysfunction.

Animals↗

PubMed2004

Echocardiographic analysis of ventricular geometry and function during repair of congenital septal defects.

BACKGROUND: This study investigated changes in left ventricular (LV) geometry and systolic function after corrective surgery for atrial (ASD) and ventricular septal defects (VSD). METHODS: Transesophageal LV short-axis echocardiograms were recorded before and after operative repair of ASD (n = 11) and VSD (n = 7). Preload was measured using LV end-diastolic area indexed for body surface area. Measurements of septal-freewall (D1) and anterior-posterior (D2) endocardial diameters were used to assess LV symmetry from D1/D2. Systolic indices included stroke area, area ejection fraction, and fractional shortening. RESULTS: Preload, stroke area, area ejection fraction, and fractional shortening of D1 increased after ASD repair but decreased after VSD repair (p < 0.05). End-diastolic symmetry increased after ASD closure and decreased after VSD closure (p < 0.05). Increases in stroke area and ejection fraction after ASD correction primarily reflected increased shortening of D1. A positive correlation was found overall between percent change in end-diastolic area (EDA) and percent change in area ejection fraction (r(2) = 0.80, p < 0.0001, n = 18). CONCLUSIONS: Preload was the primary determinant of changes in LV function in this series of ASD and VSD repairs. Intraoperative changes in position of the interventricular septum affected systolic and diastolic LV symmetry and septal free wall shortening. Additional studies are needed to define changes in afterload and contractility as well as diastolic compliance and systolic mechanics.

Child↗

PubMed2004

Load dependence of cardiac output in biventricular pacing: right ventricular pressure overload in pigs.

BACKGROUND: The effect of biventricular pacing on stroke volume is believed to be dependent on right ventricular/left ventricular delay, but effects in individual patients are unpredictable. This variability may reflect relative right and left ventricular volume and/or pressure overloads. Accordingly, we tested the hypothesis that the relation of cardiac output to right ventricular/left ventricular delay is load dependent in a pig model of pulmonary stenosis. METHODS: After median sternotomy in 6 anesthetized, domestic pigs, complete heart block was induced by ethanol ablation. During epicardial, atrial tracking DDD biventricular pacing, atrioventricular delay was varied between 60 and 180 ms in 30-ms increments. Right ventricular/left ventricular delay was varied at each atrioventricular delay from +80 ms (right ventricle first) to -80 ms (left ventricle first) in 20-ms increments. Aortic flow, right ventricular pressure, peripheral arterial pressure, and electrocardiogram were measured in the control state and during pulmonary stenosis, created by tightening a snare around the pulmonary artery until cardiac output decreased by 50%. RESULTS: Atrioventricular and right ventricular/left ventricular delay had no effect on cardiac output during the control state, but during pulmonary stenosis there was a statistically significant (P =.0001, repeated-measures analysis of variance) right ventricular/left ventricular delay-related trend toward higher cardiac output with right ventricular pacing first. This effect was more pronounced when the optimal atrioventricular delay was determined first, resulting in a 20% increase in cardiac output when the optimal right ventricular/left ventricular delay was compared with simultaneous biventricular pacing. CONCLUSIONS: Optimized biventricular pacing in swine is associated with increased cardiac output during acute pulmonary stenosis, but not during the control state. Further studies are needed to determine whether specific types of right ventricular and left ventricular overload predictably affect the relation between right ventricular/left ventricular delay and cardiac output.

Animals↗

PubMed2004

Mechanisms of optimized biventricular pacing in pulmonary stenosis: effects on left ventricular geometry in swine.

We tested the hypothesis that optimized biventricular pacing (BiVP) enhances cardiac output (CO) during critical pulmonary stenosis (PS) by attenuating distortions in left ventricular (LV) geometry. Following median sternotomy in six anesthetized pigs, heart block was induced by ethanol ablation. During epicardial, DDD BiVP, atrioventricular delay (AVD) was varied from 60 ms to 180 ms in 30 ms increments. At the AVD with the highest CO right-left delay (RLD) was varied from (+) 80 ms (RV first) to (-) 80 ms (LV first) in 20 ms increments. At each pacing setting, aortic flow, ECG, and LV diameter were measured in the control state (CON) and during PS, created by snaring the pulmonary artery until CO decreased 50%. Short axis LV echocardiograms were obtained at (+) and (-) 80 ms. In CON, RLD had no effect on function or geometry. During PS optimum BiVP resulted in significant increases in CO (1.12 L/min +/- 0.13 SEM at RLD =+ 40 ms versus 0.92 +/- 0.12 at RLD = 0 and 0.73 +/- 0.08 at RLD =-80), and LV fractional shortening (8.97%+/- 0.51% at RLD =+ 40 ms versus 7.34%+/- 0.58% at RLD = 0 and 6.21%+/- 0.66% at RLD =-80). In addition, LV eccentricity with (-) RLD was significantly different versus CON at both end-diastole (0.79 +/- 0.07 vs 1.02 +/- 0.03, P = 0.011 Student's t-test) and end-systole (0.83 +/- 0.05 vs 1.00 +/- 0.02, P = 0.017). However, with (+) RLD differences versus CON were not significant at either end-diastole (0.88 +/- 0.06 vs 0.99 +/- 0.03) or end-systole (0.92 +/- 0.03 vs 1.01 +/- 0.03). In swine hearts with PS, optimized BiVP increases CO, fractional shortening, and LV symmetry. BiVP warrants further study as treatment for acute postoperative heart failure.

Animals↗

PubMed2003

Cariporide is cardioprotective after iatrogenic ventricular fibrillation in the intact swine heart.

BACKGROUND: We sought to introduce sodium-hydrogen exchange inhibition as prophylaxis against the development of ventricular dysfunction in the setting of implantable cardioverter defibrillator insertion in high-risk patients. Cariporide, shown to be safe in humans, was used to reproduce previous results in our laboratory that demonstrated that sodium-hydrogen exchange inhibition preserves left ventricular (LV) function after ventricular fibrillation (VF) and reperfusion. METHODS: Twelve pigs (weight, 35 to 55 kg) were divided into two groups of six. Baseline ventricular function studies were based on echocardiography, conductance, aortic flow, and LV pressure. Animals were given vehicle (control) or cariporide (3 mg/kg intravenously). Ten minutes later, hearts underwent 80 seconds of VF. After reperfusion for 40 minutes, function studies were repeated. RESULTS: Postmortem examination included measuring passive pressure-volume curves and myocardial water content. Systolic indices, including preload recruitable stroke work and ejection fraction, were significantly depressed from baseline after VF and reperfusion for control animals (preload recruitable stroke work, 30.13 +/- 0.59 [standard error of the mean] versus 43.85 +/- 2.60 mm Hg; ejection fraction, 25.7% +/- 2.4% versus 33.5% +/- 3.0%) but not for those in the cariporide group (preload recruitable stroke work, 38.36 +/- 1.87 versus 40.86 +/- 1.45 mm Hg; ejection fraction, 33.9% +/- 3.5% versus 32.8% +/- 3.9%). In vivo diastolic indices demonstrated trends toward diminished ventricular compliance in control animals but not in the cariporide group after VF and reperfusion. Control animals had significantly increased postmortem LV stiffness, myocardial water content, and normalized LV mass. CONCLUSIONS: Cariporide preserves LV function after 80 seconds of VF and 40 minutes of reperfusion. Cariporide may prove useful in patients with severe LV dysfunction undergoing VF for implantable cardioverter defibrillator testing.

Animals↗

PubMed2003

Sodium-hydrogen exchange inhibition preserves ventricular function after ventricular fibrillation in the intact swine heart.

BACKGROUND: We tested the hypothesis that sodium-hydrogen exchange inhibition attenuates ventricular dysfunction after ischemia-reperfusion injury in the intact porcine heart. METHODS: Twelve pigs (weight, 30-45 kg) were evenly divided into 2 groups. Baseline ventricular function studies were based on echocardiography, conductance, aortic flow, and left ventricular pressure. Animals were given vehicle (control) or benzamide-N-(aminoiminomethl)-4-(4-[2-furanylcarbonyl]-1-piperazinyl)-3-(methylsulfonyl)methanesulfonate (BIIB 513; 3 mg/kg administered intravenously). Ten minutes later, hearts were subjected to 75 seconds of ventricular fibrillation. After reperfusion for 40 minutes, function studies were repeated. Hearts were arrested and excised. Postmortem data included passive pressure-volume curves and myocardial water content. RESULTS: Preload recruitable stroke work was significantly decreased from baseline after ischemia and reperfusion in the control group (27.7 +/- 2.5 vs 48.0 +/- 5.6 mm Hg [+/- SEM], P =.001) but not in the BIIB 513 group (43.0 +/- 5.8 vs 45.5 +/- 4.1 mm Hg, P = not significant). In vivo diastolic and postmortem passive left ventricular compliance were reduced after ischemia and reperfusion for control animals but remained unchanged for animals receiving BIIB 513. Time required to recover baseline blood pressure after ventricular fibrillation was significantly longer for control animals (159 +/- 15 vs 88 +/- 14 seconds [+/- SEM], P =.008). Myocardial water content (78.97% +/- 0.94% vs 77.86% +/- 0.46% [+/- SEM]) and normalized left ventricular mass (137.24 +/- 6.17 vs 128.41 +/- 1.96 g [+/- SEM]) were insignificantly increased in control animals. CONCLUSIONS: Sodium-hydrogen exchange inhibition attenuates ventricular dysfunction after 75 seconds of ventricular fibrillation and 40 minutes of reperfusion. This family of agents might prove useful in patients with severe left ventricular dysfunction undergoing ventricular fibrillation for implantable cardioverter defibrillator testing.

Animals↗

PubMed2003

Correlation of the Tei index with invasive measurements of ventricular function in a porcine model.

BACKGROUND: The Doppler myocardial performance (Tei) index has been reported to be clinically useful in assessing left ventricular systolic and diastolic function in both adults and children. However, there are limited data to compare the Tei index with invasive measurements of ventricular function. We used a porcine model to directly correlate the Tei index with invasive indices of systolic and diastolic function. METHODS: Pressure volume loops were obtained from 10 pigs (32-45 kg). A micromanometer and a conductance catheter were placed in the left ventricle to record pressure and volume, respectively. A flow probe was placed around the ascending aorta to record cardiac output. Baseline pressure volume loops were generated during preload reduction through caval occlusion. Epicardial echocardiograms were performed just before the caval occlusion. Invasive indices including preload recruitable stroke work, ventricular stiffness constant, and cardiac output were assessed, as were noninvasive echocardiographic indices including Tei index and ejection fraction. An ischemic insult, ventricular fibrillation, was induced to alter ventricular function. After cardioversion and 40 minutes of reperfusion, echocardiographic and invasive measurements were repeated. RESULTS: There was a statistically significant inverse relationship between the percent change in Tei and the percent change in preload recruitable stroke work after ventricular fibrillation (r = -0.70, P =.02), although the correlation between the actual values of Tei and preload recruitable stroke work were not statistically significant. There was a statistically significant inverse relationship between the percent change in Tei and the percent change in cardiac output (r = -0.65, P =.03). There was a direct correlation between the value of Tei and the ventricular stiffness constant at baseline (r = 0.63, P <.05). As anticipated, the value of Tei was inversely related to ejection fraction by epicardial echocardiogram at baseline (r = -0.85, P <.001). The percent change in Tei was inversely related to the percent change in ejection fraction as well (r = -0.69, P <.05). CONCLUSIONS: This animal model is one of the first studies to demonstrate a direct correlation between the Tei index and systolic and diastolic invasive measurements of ventricular function. This supports the clinical use of this index as a measure of global ventricular function.

Animals↗

PubMed2003

Aortic regurgitation in the heterotopic rat heart transplant: effect on ventricular remodeling and diastolic function.

OBJECTIVES: Use of the heterotopic rat cardiac isograft model is limited by ventricular atrophy attributable to the left ventricle's non-working state. Previous studies indicate that increased left ventricular pressure-volume work minimizes atrophy. We used a simpler approach to increase ventricular work, imposing aortic regurgitation on the transplant. We hypothesized that this would prevent atrophy and preserve left ventricular compliance. METHODS: We analyzed heterotopic transplants with aortic valvotomy and without aortic valvotomy (controls). Recipient native hearts served as separate controls. After 15 to 25 days, we measured cardiac wet weight, dry weight, and water content of all groups and measured echocardiographic left ventricular wall thickness and end-diastolic and end-systolic diameters in both transplant groups. Left ventricular volume infusions yielded pressure-volume data that we analyzed using regression methods. RESULTS: Aortic regurgitant transplants weighed more than control transplants (dry weight, 0.109 +/- 0.013 g vs 0.097 +/- 0.016 g; p = 0.020, 2-way analysis of variance), but all transplants weighed less than native hearts weighed (p = 0.001). Control transplants were less compliant than regurgitant transplants (p = 0.002), but the latter were similar to their own native hearts (p = 0.34). Wall thickness decreased in regurgitant vs control transplants (p = 0.020, Student's t-test), but end-diastolic and end-systolic diameters increased (p < or = 0.001). CONCLUSIONS: Aortic regurgitation in heterotopic transplants improves left ventricular compliance through chamber dilatation without preventing atrophy. Moderate acute aortic regurgitation affects ventricular remodeling more than it stimulates myocardial hypertrophy. Smaller end-diastolic diameter, greater wall thickness, and myocardial edema may explain decreased compliance in non-working transplants.

Animals↗

PubMed2002

Left ventricular end-diastolic volume from ejection fraction and stroke volume in pigs during IVC occlusion.

BACKGROUND: Real-time measurement of left ventricular end-diastolic volume (LVEDV), combined with left ventricular end-diastolic pressure (LVEDP), would allow continuous measurement of intraoperative diastolic function. In pursuit of this goal, we examined stroke volume divided by ejection fraction for calculation of LVEDV(sv/ef). METHODS: Five anesthetized pigs underwent median sternotomy and pericardiotomy. A transit-time ultrasonic flow probe on the ascending aorta provided cardiac output. A micromanometer provided LV end-diastolic pressure. End-diastolic and end-systolic areas were measured from LV short-axis cross sections to obtain ejection fraction. LVEDV(sv/ef) was calculated during IVC occlusion. Steady-state LVEDV(echo) was determined using a three-plane echocardiography model. LVEDV(echo) was used to validate steady-state LVEDA in each experiment. RESULTS: Correlation coefficients for linear and pressure-volume relation analyses ranged from 0.46 to 0.99. The two methods for measuring LVEDV generated compliance curves with an overall reliability coefficient of 0.84. CONCLUSIONS: The LVEDV(sv/ef) method may facilitate real-time determination of LV compliance.

Animals↗

PubMedDate not supplied

Validation of left ventricular end-diastolic volume from stroke volume and ejection fraction.

The present study examines an innovative approach to measurement of left ventricular (LV) end-diastolic volume (LVEDV). Measurement of LVEDV is fundamental to the assessment of intraoperative systolic and diastolic LV function. We compared steady state LVEDV values obtained from stroke volume (SV) and ejection fraction (EF) with echocardiographic and postmortem LVEDV measurements. Five anesthetized pigs (40-45 kg) underwent median sternotomy and pericardiotomy. A transit time ultrasonic flow probe was placed on the ascending aorta to provide cardiac output. A micromanometer provided LV end-diastolic pressure. LV short axis cross sectional echocardiograms and electrocardiograms were also obtained. LV end-diastolic area (LVEDA) and end-systolic area (LVESA) were measured to obtain EF. LVEDVsv/ef was calculated from cardiac output, heart rate, and EF. LVEDVecho was determined using a three-plane echocardiography model. Postmortem (LVEDVpm/vv) volumes were also measured. LVEDVsv/ef correlated well with volumes obtained by echocardiography (r2 = 0.92) and postmortem (r2 = 0.73) measurements. Values of p < 0.05 indicated significant linearity of LVEDA-LVEDVsv/ef (r2 =0.93), LVEDA-LVEDVecho (r2 = 0.96), and LVEDA-LVEDVpm/vv (r2 = 0.81) relationships. Determination of LVEDV from SV and EF is valid and may facilitate real-time determination of LV mechanics.

Animals↗

PubMedDate not supplied

Validation study of PulseCO system for continuous cardiac output measurement.

Ultrasonic flow probes have been used to optimize biventricular pacing immediately after cardiopulmonary bypass, improving cardiac output (CO) by 10%; however, flow probes must be removed with chest closure. The PulseCO system (LiDCO Limited, Cambridge, UK) may extend optimization into the postoperative period, but controlled validations have not been reported. Six anesthetized pigs were instrumented for right heart bypass. Flow was varied from 3 to 1 L/min and then back to 3 in 0.5 L/min increments for 60 second intervals. CO was measured by ultrasonic flow probe on the aorta and by PulseCO using a femoral arterial line. PulseCO and flow probe accurately measured CO (PulseCO R2: 0.79-0.95; flow probe R2: 0.96-0.99). At flow of 2 L/min, when the heart was paced 30 bpm over the sinus rate, PulseCO falsely indicated an increase in CO (2.13 vs. 2.30 L/min, p = 0.014). When mean arterial pressure was increased by 20% using a phenylephrine infusion, PulseCO falsely indicated an increase in CO (2.13 vs. 2.47 L/min, p = 0.014). When mean arterial pressure was decreased by 20% using a nitroprusside infusion, PulseCO falsely indicated a decrease in CO (2.13 vs. 1.79 L/min, p = 0.003). PulseCO appears to be useful for assessing acute changes in CO if its limitations are recognized.

Animals↗