Vena Cava Occlusion Research Articles

Vena cava occlusion with balloon to control blood pressure during deployment of transluminally placed endovascular graft

Transluminally placed endovascular graft (TPEG) replacement has been applied to treat various aortic diseases. At the moment of deployment, TPEG receives a pressure pulse force to shove it distally, which possibly results in misplacement. Moreover, deploying the TPEG in the aorta increases cardiac afterload, which may damage myocardial function. To avoid these risks, we developed a new technique to control blood pressure by almost complete venous return occlusion. Two occlusion balloon catheters are inserted into the superior and inferior vena cava via the femoral vein. TPEG is deployed at the proper position during inflation of the vena cava balloon to maintain a blood pressure as low as 60 mm Hg by cardiac preload blockage. We, thus far, have not experienced even a trivial sequela with this technique.

Induction of ventricular collapse by an axial flow blood pump.

An important consideration for clinical application of rotary blood pump based ventricular assist is the avoidance of ventricular collapse due to excessive operating speed. Because healthy animals do not typically demonstrate this phenomenon, it is difficult to evaluate control algorithms for avoiding suction in vivo. An acute hemodynamic study was thus conducted to determine the conditions under which suction could be induced. A 70 kg calf was implanted with an axial flow assist device (Nimbus/UoP IVAS; Nimbus Inc., Rancho Cordova, CA) cannulated from the left ventricular apex to ascending aorta. On initiation of pump operation, several vasoactive interventions were performed to alter preload, afterload, and contractility of the left ventricle. Initially, dobutamine increased contractility and heart rate ([HR] = 139; baseline = 70), but ventricular collapse was not achievable, even at the maximal pump speed of 15,000 rpm. Norepinephrine decreased HR (HR = 60), increased contractility, and increased systemic vascular resistance ([SVR] = 24; baseline = 15), resulting in ventricular collapse at a pump speed of 14,000 rpm. Isoproterenol (beta agonist) increased HR (HR = 103) and decreased SVR (SVR = 12), but ventricular collapse was not achieved. Inferior vena cava occlusion reduced preload, and ventricular collapse was achieved at speeds as low as 11,000 rpm. Esmolol (beta1 antagonist) decreased HR (HR = 55) and contractility, and ventricular collapse was achieved at 11,500 rpm. Episodes of ventricular collapse were characterized initially by the pump output exceeding the venous return and the aortic valve remaining closed throughout the cardiac cycle. If continued, the mitral valve would remain open throughout the cardiac cycle. Using these unique states of the mitral and aortic valves, the onset of ventricular collapse could reliably be identified. It is hoped that the ability to detect the onset of ventricular collapse, rather than the event itself, will assist in the development and the evaluation of control algorithms for rotary ventricular assist devices.

The effects of ventricular pacing on left ventricular geometry, function, myocardial oxygen consumption, and efficiency of contraction in conscious dogs.

The effects of ventricular pacing on left ventricular (LV) dynamic geometry, function, and myocardial oxygen consumption (MVO2) were measured in 12 conscious dogs using sonomicrometry, micromanometry, ultrasonic flow probes, and oximetry catheters during right atrial (A-) and right ventricular (V-) pacing at 150 beats/min. Systolic function was quantified using slopes (MW) and volume-intercepts (VW) of linear relationships between end-diastolic volume (EDV) and stroke work (SW) for data obtained during vena caval occlusion. V-pacing shifted SW-EDV relationships downward (MW decreased from 97 +/- 21 to 81 +/- 21 Kerg/mL) and to the right (VW increased from 14 +/- 11 to 20 +/- 12 mL) in comparison with A-pacing (P < 0.02). These functional changes correlated with altered contractile geometry manifest as early shortening in the septal free wall relative to anterior-posterior dimension (increased minor axis mid-wall eccentricity at end-diastole and begin-ejection). Steady-state LV power output decreased from 802 +/- 213 mW during A-pacing to 514 +/- 170 mW during V-pacing (P < 0.05), while MVO2 remained relatively unchanged during V-pacing (10 +/- 3 mL O2/min vs 11 +/- 3 mL O2/min during A-pacing, P = NS). As a result, overall LV efficiency decreased from 0.24 +/- 0.08 during A-pacing to 0.16 +/- 0.06 during V-pacing (P < 0.05). These data illustrate the impact of V-pacing on dynamic LV geometry and function, including impaired LV work output at all physiological levels of preload. Most importantly, the relationship between LV work output and MVO2 is depressed during V-pacing, emphasizing the interaction between LV mechanics and pump efficiency in intact subjects. As a result, measures taken to restore normal contractile geometry might improve LV efficiency and performance when V-pacing is necessary.

Retrograde cerebral perfusion enhances cerebral protection during prolonged hypothermic circulatory arrest: a study in a chronic porcine model

Background. This study was undertaken to confirm earlier findings that retrograde cerebral perfusion (RCP) can improve cerebral outcome after prolonged hypothermic circulatory arrest (HCA), and to determine whether RCP with inferior vena caval occlusion, which is more effective in removing particulate emboli, is superior to conventional RCP in enhancing cerebral protection. Methods. Sixty-two pigs (27 to 30 kg) were randomly assigned to undergo one of the following for 90 minutes at 20°C: antegrade cerebral perfusion (ACP); conventional RCP (RCP); RCP with occlusion of the inferior vena cava (RCP-O), or HCA with the head packed in ice. RCP flow was regulated to a sagittal sinus pressure of 20 mm Hg. Hemodynamic, electrophysiologic, and metabolic monitoring were carried out until 4 hours after rewarming, daily behavioral and neurologic assessments until elective sacrifice on day 7, and histologic analysis of the brain after death. Results. Complete behavioral recovery was seen in all surviving animals by day 5 after ACP or RCP, but in only 83% after RCP-O and 50% after HCA ( p = 0.001). A histopathologic score of 2 or more, indicating more than mild injury, was not found in any animal after ACP, in 27% after RCP, in 47% after HCA, and in 68% after RCP-O ( p = 0.002). The median oxygen consumption was 6.66 mL/min after ACP, 1.37 mL/min with RCP, and 1.02 mL/min with RCP-O ( p < 0.0001). The median amount of fluid sequestered was 2,450 mL after RCP-O, 760 mL after RCP, and −200 mL after ACP ( p < 0.0001). Conclusions. Conventional RCP without inferior vena caval occlusion results in a significantly better outcome than RCP-O after prolonged HCA, despite more efficient cerebral perfusion during RCP-O, and also provides cerebral protection superior to prolonged HCA alone, but care must be taken during its implementation to minimize cerebral edema and other possible causes of retroperfusion-related cerebral injury.

Improved efficiency of energy transfer to external work in chronic cardiomyoplasty based on the pressure-volume relationship

Objective: Cardiomyoplasty is a surgical procedure to support the failing heart, in which a burst-stimulated latissimus dorsi muscle flap is transposed and wrapped around the ventricles. The effect of dynamic cardiac compression, implemented as cardiomyoplasty, on left ventricular performance remains controversial; the mechanism by which clinical symptoms are improved remains unclear. To investigate the mechanism for improvement of patients' symptoms, it is important to evaluate the effects of cardiomyoplasty on left ventricular energetics and on left ventricular systolic and diastolic function. We therefore evaluated the efficiency of energy transfer from the native pressure-volume area to external work under conditions of 1:3 skeletal muscle burst pacing in an animal model with chronic heart failure. Methods: In seven Merino-Wether sheep, cardiomyoplasty was performed after stable heart failure was induced by staged coronary embolizations (ejection fraction < 35%). Hemodynamic assessment including the assessment of the pressure-volume relationship was performed 8 weeks after cardiomyoplasty when the latissimus dorsi muscle was fully trained. Instantaneous left ventricular pressure and volume were measured with a catheter-tipped manometer and a conductance catheter during steady-state conditions and after a transient inferior vena cava occlusion. The effect of dynamic cardiac compression on left ventricular systolic function was assessed by comparing pre-assisted and assisted beats and on diastolic function by comparing assisted and post-assisted beats. Result: The slope of the end-systolic pressure-volume relationship decreased by 30.5% ± 27.8% ( p = 0.02) during assisted beats. However, left ventricular pump performance improved by increasing stroke volume and external work by 35.9% ± 36.0% ( p = 0.03) and 9.7% ± 6.8% ( p = 0.03), respectively, resulting in a reduction of the volume intercept. As a result, the end-systolic pressure-volume relationship shifted to the left. The efficiency of energy transfer from the native pressure-volume area to the overall external work improved by 7.6% ± 8.2% ( p = 0.04). Cardiomyoplasty did not affect the time constant of left ventricular isovolumic pressure decline or the maximal rate of pressure decay, which suggested that cardiomyoplasty did not affect left ventricular relaxation. Conclusions: Dynamic cardiac compression in the form of cardiomyoplasty enhanced left ventricular pump performance without interrupting left ventricular filling. The ratio of energy transfer from the native pressure-volume area to the overall external work suggests a myocardial oxygen-sparing effect of cardiomyoplasty. (J Thorac Cardiovasc Surg 1998;115:1358-66)

Can retrograde perfusion mitigate cerebal injury after particulate embolization? A study in a chronic porcine model

Objective: We assessed the impact on histologic and behavioral outcome of an interval of retrograde cerebral perfusion after arterial embolization, comparing retrograde cerebral perfusion with and without inferior vena caval occlusion with continued antegrade perfusion. Methods: Sixty Yorkshire pigs (27 to 30 kg) were randomly assigned to the following groups: antegrade cerebral perfusion control; antegrade cerebral perfusion after embolization; retrograde cerebral perfusion control; retrograde cerebral perfusion after embolization; retrograde cerebral perfusion with inferior vena cava occlusion, retrograde cerebral perfusion with inferior vena cava occlusion control, and retrograde cerebral perfusion with inferior vena cava occlusion after embolization. After cooling to 20° C, a bolus of 200 mg of polystyrene microspheres 250 to 750 (μm diameter (or saline solution) was injected into the isolated aortic arch. After 5 minutes of antegrade cerebral perfusion, 25 minutes of antegrade cerebral perfusion, retrograde cerebral perfusion, or retrograde cerebral perfusion with inferior vena cava occlusion was instituted. After the operation, all animals underwent daily assessment of neurologic status until the time of death on day 7. Results: Aortic arch return, cerebral vascular resistance, and oxygen extraction data during retrograde cerebral perfusion showed differences, suggesting that more effective flow occurs during retrograde cerebral perfusion with inferior vena cava occlusion, which also resulted in more pronounced fluid sequestration. Microsphere recovery from the brain revealed significantly fewer emboli after retrograde cerebral perfusion with inferior vena cava occlusion. Behavioral scores showed full recovery in all but one control animal (after retrograde cerebral perfusion with inferior vena cava occlusion) by day 7 but were considerably lower after embolization, with no significant differences between groups. The extent of histopathologic injury was not significantly different among embolized groups. Although no histopathologic lesions were present in either the antegrade cerebral perfusion control group or the retrograde cerebral perfusion control group, mild significant ischemic damage occurred after retrograde cerebral perfusion with inferior vena cava occlusion even in control animals. Conclusions: Although effective washout of particulate emboli from the brain can be achieved with retrograde cerebral perfusion with inferior vena cava occlusion, no advantage of retrograde cerebral perfusion with inferior vena cava occlusion after embolization is seen from behavioral scores, electro- encephalographic recovery, or histopathologic examination; retrograde cerebral perfusion with inferior vena cava occlusion results in greater fluid sequestration and mild histopathologic injury even in control animals. Retrograde cerebral perfusion with inferior vena cava occlusion shows clear promise in the management of embolization, but further refinements must be sought to address its still worrisome potential for harm.(J Thorac Cardiovasc Surg 1998;115:1142-59) J Thorac Cardiovasc Surg 1998;115:1142-59

Protective effect of N-acetyl-L-cysteine on the renal failure induced by inferior vena cava occlusion.

Renal ischemia is produced during orthotopic liver transplantation when the inferior vena cava is clamped above the renal veins (inferior vena cava occlusion [IVCO]), and it often leads to postoperative renal failure. Although free radicals and nitric oxide (NO) have been implicated in the pathogenesis of ischemic renal failure, the effect of free radical scavengers in this model is unknown. The effects of N-acetyl-L-cysteine (NAC), a free radical scavenger, on the acute renal failure that follows IVCO were evaluated in pentobarbital-anesthetized dogs. The effect of NO synthesis inhibition with NG-nitro-L-arginine methyl ester (NAME) was also studied. Renal vascular endothelial function was tested by infusing acetylcholine (Ach) into the renal artery before the ischemia and during reperfusion. Renal failure developed during IVCO and persisted during reperfusion in all groups. However, in NAC-pretreated dogs, the glomerular filtration rate recovered progressively, reaching 31% of basal preischemic values 150 min after reperfusion. During reperfusion, fractional excretion of sodium increased above preischemic values only in the control group, which indicates a beneficial effect of NAC and NAME on the tubular dysfunction observed during reperfusion. The renal response to Ach was abolished in control dogs and in animals given NAME during reperfusion, which indicates endothelial dysfunction. However, in NAC-pretreated dogs, the renal response to Ach was preserved during reperfusion. These results demonstrate that NAC ameliorates the renal failure and renal endothelial dysfunction induced by IVCO. This protective effect was abolished by NAME, which suggests that NO is involved in the beneficial effects of NAC. These data also suggest that the use of NAC could be beneficial in ameliorating the acute renal failure observed after orthotopic liver transplantation.

In vivo murine left ventricular pressure-volume relations by miniaturized conductance micromanometry.

The mouse is the species of choice for creating genetically engineered models of human disease. To study detailed systolic and diastolic left ventricular (LV) chamber mechanics in mice in vivo, we developed a miniaturized conductance-manometer system. alpha-Chloralose-urethan-anesthetized animals were instrumented with a two-electrode pressure-volume catheter advanced via the LV apex to the aortic root. Custom electronics provided time-varying conductances related to cavity volume. Baseline hemodynamics were similar to values in conscious animals: 634 +/- 14 beats/min, 112 +/- 4 mmHg, 5.3 +/- 0.8 mmHg, and 11,777 +/- 732 mmHg/s for heart rate, end-systolic and end-diastolic pressures, and maximum first derivative of ventricular pressure with respect to time (dP/dtmax), respectively. Catheter stroke volume during preload reduction by inferior vena caval occlusion correlated with that by ultrasound aortic flow probe (r2 = 0.98). This maneuver yielded end-systolic elastances of 79 +/- 21 mmHg/microliter, preload-recruitable stroke work of 82 +/- 5.6 mmHg, and slope of dP/dtmax-end-diastolic volume relation of 699 +/- 100 mmHg.s-1.microliter-1, and these relations varied predictably with acute inotropic interventions. The control normalized time-varying elastance curve was similar to human data, further supporting comparable chamber mechanics between species. This novel approach should greatly help assess cardiovascular function in the blood-perfused murine heart.

Assessment of Left Ventricular Contractile State by Preload-Adjusted Maximal Power Using Echocardiographic Automated Border Detection

Objectives. We sought to assess the ability of preload-adjusted maximal power measured by echocardiographic automated border detection (ABD) to quantify left ventricular (LV) contractility by determining the effects of alterations in preload, afterload and contractile state.Background. Preload-adjusted maximal power can reflect LV contractile state relatively independent of changes in loading conditions.Methods. Eight anesthetized dogs had placement of aortic electromagnetic flow probes, LV and arterial pressure catheters and inferior vena caval (IVC) occluders; four had placement of thoracic aortic balloon occluders. Echocardiographic ABD measures of cross-sectional area were used as a surrogate for LV volume, and flow was estimated as the first derivative of area with respect to time. Power was calculated as the product of flow and pressure.Results. Preload independence during vena caval occlusions was achieved by preload adjustment (÷[end-diastolic area]3/2). Afterload independence was demonstrated by preload-adjusted maximal power being unaffected by acute increases in LV systolic pressure induced by aortic occlusion. ABD preload-adjusted maximal power reflected changes in contractile state: increasing with dobutamine infusion from 36 ± 14 to 70 ± 15 mW/cm4(p < 0.05 vs. control) and decreasing with propranolol infusion from 35 ± 13 to 17 ± 7 mW/cm4(p < 0.05 vs. control). These changes were significantly correlated with calculations of preload-adjusted maximal power using aortic flow (r = 0.90, SEE 10.5 mW/cm4) and load-independent measures of end-systolic elastance from pressure–area loops (r = 0.90, SEE 10.6 mW/cm4). Calculations of normalized preload-adjusted maximal power using arterial pressure were also closely correlated with similar calculations using LV pressure (r = 0.99, SEE 3%).Conclusions. Preload-adjusted maximal power using echocardiographic ABD can predict LV contractile state relatively independent of loading conditions and has potential for clinical application.

Load-sensitive diastolic relaxation in hypertrophied left ventricles.

We studied effects of enalaprilat and L-158,809, an angiotensin II type-1 receptor antagonist, on left ventricular (LV) diastolic relaxation in 11 normal control dogs and 16 LV hypertrophied (LVH) dogs with perinephritic hypertension. At baseline, LV systolic and end-diastolic pressures and end-systolic elastance were increased in the LVH group (all P < 0.01 vs. the control group). LV relaxation time constant was also prolonged (P < 0.01), suggesting impaired LV diastolic relaxation in this model of LVH. Before and after the administration of enalaprilat (0.25 mg/kg) and L-158,809 (0.30 mg/kg), LV relaxation was assessed over a wide range of LV loading conditions during vena caval occlusion. LV relaxation time constant was insensitive to load reduction in the control group, which was not affected by enalaprilat or L-158,809. In contrast, LV unloading caused a significant prolongation of the relaxation time constant in the LVH group. This load-sensitive LV relaxation abnormality was significantly improved by enalaprilat or L-158,809. These results support the concept that angiotensin II is involved in the pathogenesis of diastolic dysfunction in pressure-overloaded LVH and also suggest that angiotensin-converting enzyme inhibitors and angiotensin II type-1 receptor antagonists are potentially beneficial in the treatment of the hypertrophied heart.

Modified Ultrafiltration Improves Left Ventricular Systolic Function In Infants After Cardiopulmonary Bypass

Objective: Our objective was to test the hypothesis that use of modified ultrafiltration after cardiopulmonary bypass improves intrinsic left ventricular systolic function in children. Methods: Twenty-one infants undergoing cardiopulmonary bypass were instrumented with ultrasonic dimension transducers, to measure the anteroposterior minor axis diameter, and a left ventricular micromanometer. Patients were randomized to modified ultrafiltration ( n = 11, age 226 ± 355 days, weight 6.7 ± 3.1 kg) or control ( n = 10, age 300 ± 240 days, weight 7.0 ± 2.5 kg) (all differences p > 0.05 between groups). Left ventricular systolic function was assessed by means of the slope of the preload-recruitable stroke work index. Myocardial cross-sectional area was measured by echocardiography. Data were acquired immediately after separation from bypass, at steady state, and during transient vena caval occlusion. Data acquisition was repeated after 13 ± 5 minutes of modified ultrafiltration or after 12 ± 5 minutes without modified ultrafiltration in the control group. Inotropic drug support was the same at both study points. Results: In the modified ultrafiltration group, the filtrate volume was 363 ± 262 ml. The hematocrit value increased from 26.0% ± 2.7% to 36.7% ± 9.5% ( p = 0.018), myocardial cross-sectional area decreased from 3.72 ± 0.35 cm 2 to 3.63 ± 0.36 cm 2 ( p = 0.04), end-diastolic length increased from 25.6 ± 9.0 mm to 28.8 ± 9.9 mm ( p = 0.01), and end-diastolic pressure fell from 5.6 ± 0.8 mm Hg to 4.2 ± 0.8 mm Hg ( p = 0.005), suggesting an improved diastolic compliance. In the control group, the hematocrit value, myocardial cross-sectional area, end-diastolic length, and pressure did not change (all p > 0.05). Mean ejection pressure increased in the ultrafiltration group ( p = 0.001) but did not change in the control group ( p = 0.22). The slope of the preload-recruitable stroke work index increased after ultrafiltration from 52.3 ± 52.0 to 74.2 ± 66.0 (10 3 erg/cm 3) ( p = 0.02) but did not change in the control group ( p = 0.07). One patient from each group died in the postoperative period. Patients in the ultrafiltration group received less inotropic drug support in the first 24 hours after the operation (156.62 ± 92.31 μg/kg in 24 hours) than patients in the control group (865.33 ± 1772.26 μg/kg in 24 hours, p = 0.03). Conclusions: Use of modified ultrafiltration after cardiopulmonary bypass improves intrinsic left ventricular systolic function, improves diastolic compliance, increases blood pressure, and decreases inotropic drug use in the early postoperative period. (J Thorac Cardiovasc Surg 1998;115:361-70)

Measuring regularity by means of a corrected conditional entropy in sympathetic outflow.

A new method for measuring the regularity of a process over short data sequences is reported. This method is based on the definition of a new function (the corrected conditional entropy) and on the extraction of its minimum. This value is taken as an index in the information domain quantifying the regularity of the process. The corrected conditional entropy is designed to decrease in relation to the regularity of the process (like other estimates of the entropy rate), but it is able to increase when no robust statistic can be performed as a result of a limited amount of available samples. As a consequence of the minimisation procedure, the proposed index is obtained without an a-priori definition of the pattern length (i.e. of the embedding dimension of the reconstructed phase space). The method is validated on simulations and applied to beat-to-beat sequences of the sympathetic discharge obtained from decerebrate artificially ventilated cats. At control, regular, both quasiperiodic and periodic (locked to ventilation) dynamics are observed. During the sympathetic activation induced by inferior vena cava occlusion, the presence of phase-locked patterns and the increase in regularity of the sympathetic discharge evidence an augmented coupling between the sympathetic discharge and ventilation. The reduction of complexity of the neural control obtained by spinalization decreases the regularity in the sympathetic outflow, thus pointing to a weaker coupling between the sympathetic discharge and ventilation.

Arterial baroreflex modulation of heat-induced vasodilation in the rabbit ear.

The purpose of this study was to determine whether nonthermal baroreflexes arising from cardiopulmonary and/or arterial baroreceptors modulate rabbit ear blood flow (EBF) during hyperthermia. Intact and sinoaortic-denervated (SAD) rabbits were chronically instrumented with a Doppler ultrasonic flow probe for measurement of EBF velocity (kHz). During whole body heating in conscious rabbits, EBF and ear vascular conductance (EVC) increased as core temperature increased until maximal plateau levels of EBF and EVC were reached. The maximal plateau level of EVC attained during heat stress was lower in SAD than in intact rabbits. Subsequent intrapericardial administration of procaine at maximal EBF blocked cardiac afferents but did not alter EVC in either animal group. In a second experiment, ramp decreases in mean arterial pressure were produced by vena caval occlusion at maximal EBF. In intact rabbits, EBF and EVC decreased linearly as mean arterial pressure fell, but EBF and EVC did not decrease during vena caval occlusion in SAD rabbits. Thus neither pharmacological nor mechanical unloading of cardiac baroreceptors results in reflex vasoconstriction in the heat-stressed rabbit ear. However, baroreflexes arising from arterial baroreceptors may modulate EBF in heat-stressed rabbits.

The effect of sarcoplasmic reticulum blockade on the force/frequency relationship and systolic contraction patterns in the newborn pig heart.

We investigated the relationship between heart rate and contractility in seven anaesthetized young piglets by measuring contractility at different atrial pacing rates. To study the origin of this relationship we repeated the measurements after blocking the sarcoplasmic reticulum calcium release channel with ryanodine. We assessed contractility using indices derived from instantaneous left ventricular pressure and volume measured by micromanometric and conductance catheters during rapid inferior vena cava occlusion, thus generating the end-systolic pressure-volume relationship, which was characterized by its slope Ees, and the maximum rate of change of ventricular pressure (dP/dtmax)/end-diastolic volume relationship, also characterized by its slope. All animals showed an increase in contractility with increasing heart rate (intact force/frequency relationship) which was abolished after ryanodine. The most striking effect of ryanodine on baseline haemodynamics was the dramatic decrease of dP/dtmax to about 50% of its original value, while peak developed pressure and Ees did not change. We conclude that the young piglet, despite its immaturity, has a functional sarcoplasmic reticulum, illustrated by an intact force/frequency relationship. In addition, blockade of the sarcoplasmic reticulum in vivo has profoundly different effects during early and late systole, indicating that indices of contractility derived during different parts of the cardiac cycle represent different aspects of systole.

Isoflurane and halothane do not alter the enhanced afterload sensitivity of left ventricular relaxation in dogs with pacing-induced cardiomyopathy.

The afterload dependence of left ventricular (LV) relaxation is accentuated in the failing heart. The authors tested the hypothesis that isoflurane and halothane alter the afterload sensitivity of LV relaxation in dogs with pacing-induced cardiomyopathy. Dogs (n = 6) were chronically instrumented for measurement of LV and aortic pressures and subendocardial segment length. Hemodynamics were recorded, and LV relaxation was evaluated with a time constant of isovolumic relaxation (tau) under control conditions and during decreases and increases in LV load produced by abrupt inferior vena caval (IVC) occlusion and phenylephrine (intravenous infusion), respectively, in the conscious state and during isoflurane and halothane anesthesia (1.5 MAC) on separate days before and after the development of pacing-induced cardiomyopathy. The slope (R) of the tau versus LV end-systolic pressure (P[es]) relation was also used to determine the afterload sensitivity of LV relaxation. IVC occlusion and phenylephrine produced similar or less profound changes in P(es), regional end-systolic force (an index of LV afterload), and end-systolic segment length in cardiomyopathic compared with healthy dogs. However, IVC occlusion and phenylephrine caused more pronounced alterations in tau in conscious and isoflurane- and halothane-anesthetized dogs after the development of cardiomyopathy. R was also greater in cardiomyopathic compared with healthy dogs (e.g., 0.32 +/- 0.03 before pacing to 1.00 +/- 0.13 ms/mmHg in conscious dogs). No differences in the load dependence of LV relaxation were observed between the conscious and anesthetized states before and after production of LV dysfunction. The results indicate that isoflurane and halothane do not alter the afterload dependence of LV relaxation in the normal and cardiomyopathic heart. The lack of effect of the volatile anesthetics is probably related to anesthetic-induced reductions in the resistance to LV ejection concomitant with simultaneous negative inotropic effects.

Total vascular exclusion of the liver during hepatic surgery. Selective use, extensive use, or abuse?

To review our experience with total vascular exclusion of the liver and to assess its role in hepatic resections. Retrospective survey. University hospital, a tertiary referring center for surgical liver diseases. A total of 722 patients who underwent liver resections from November 1, 1981, to March 31, 1996, of whom 19 (2.6%) required total vascular exclusion because of hepatic lesions closely adherent to or infiltrating the retrohepatic vena cava or centrally located in the liver, strictly in contact with the hepatic vein convergence. chi 2 Test for qualitative data and Student t test for categorical data. Of the 19 resections carried out under total vascular exclusion, 6 had tumoral infiltration of the retrohepatic vena cava: in 4 cases the venous wall was partially resected, while in the remaining 2 it was completely removed and replaced with a prosthetic graft. There were no operative deaths. Of the 722 resections, 227 were major hepatectomies: 74 (32.6%) were performed after ligation of the glissonian elements for the hemiliver to be removed, without clamping of the hepatic pedicle, and a further 36 (15.8%) were performed without any preliminary vascular control. A significant reduction in intraoperative blood transfusions was achieved despite the performance of more extended operations, regardless of the technique used. Total vascular exclusion is a useful tool in controlling blood inflow to the liver, but true need for it during liver resection is limited. Its performance requires a well-trained team familiar with problems regarding surgical access to the inferior vena cava and prolonged occlusion of the hepatic pedicle and the inferior vena cava.

P6 Systematic use of right gastroepiploic artery (rGEA) graft do not increase cardiac postoperative complications

To define the effects of altered left ventricular (LV) geometry on regional myocardial function during ischemia and recovery, regional and global LV geometry and transmural pressure (P) were measured in seven conscious dogs with sonomicrometry and micromanometry. Data were obtained at steady state and during rapid vena caval occlusion (VCO) under control conditions, after 15 min of left anterior descending occlusion, and after 1, 4, and 24 hr of reperfusion. Regional midwall minor axis (MA) Lagrangian strain (ϵ) and stress (σ) were calculated from measured MA segment length (L), MA midwall radius, and wall thickness. Unstressed regional geometry was quantified using Lo, the value of L at P = 0 during maximal VCO. Conventional (SWL) and normalized (SWσϵ) regional MA stroke work were calculated for each cardiac cycle as the area of P vs L and σ vs ϵ relationships, respectively. Regional Frank-Starling mechanisms corrected for changes in unstressed LV geometry were quantified as the slope (Mσϵ) of the linear end diastolic ϵ vs SWσϵ relationship for data obtained during VCO (mean r = 0.98). Mσϵ returned to baseline levels within 1 h of reperfusion (P = 0.314 vs control). In contrast, 15 min of ischemia increased Lo by 15.2 ± 2.5% (P < 0.05), which remained increased 5.7 ± 1.7% above control values after 1 hr of reperfusion (P < 0.05). Both steady-state SWL and SWσϵ decreased with ischemia and slowly returned towards baseline, remaining 28.7 ± 7.5% and 26.4 ± 6.3% below control values after 1 hr of reperfusion (both P < 0.05). Therefore, late functional recovery from reversible ischemic injury is primarily correlated with reversal of changes in regional geometry, specifically the reversal of diastolic creep. As a result, adequate quantification of postischemic regional myocardial performance requires characterization of changes in regional geometry as well as indicators of Frank-Starling mechanisms.

β-Adrenergic Receptor Signalling in Stunned Myocardium of Conscious Pigs

The primary goal of this study was to compare the effects of isoproterenol which stimulatesβ-adrenergic receptors and forskolin, and NKH 477, a water soluble derivative of forskolin, which stimulate adenylyl cyclase in stunned myocardium of conscious pigs, previously instrumented for measurements of left ventricular pressure and dP/dt, arterial pressure, and wall thickening. Ten min of coronary artery occlusion induced transmural reductions in blood flow (radioactive microspheres) in subepicardium (−98±2%) and subendocardium (−99±1%). Wall thickening (piezoelectric crystals) fell from 2.50±0.26 mm to −0.26±0.26 mm and remained depressed at 1.37±0.19 mm after 20–30 min coronary artery reperfusion, reflecting myocardial stunning. At that time, isoproterenol (0.2μg/kg) increased wall thickening in stunned myocardium (+1.40±0.16 mm,P<0.05) more than in control (+0.71±0.22 mm), while forskolin elicited the opposite effects. NKH 477 (30μg/kg), which does not penetrate the blood–brain barrier, increased systolic wall thickening similarly before (+0.95±0.25 mm) and during (+1.01±0.24 mm) myocardial stunning. The reflex inotropic responses to inferior vena caval occlusion on wall thickening were diminished,P<0.05, in the stunned myocardium (+0.53±0.05 mm) compared with control (+0.95±0.07 mm).β-adrenergic receptor density, which was quantitated with125I-cyanopindolol binding, was increased transmurally in stunned myocardium compared with non-ischemic myocardium (subepicardium: +23±5%, subendocardium: +34±13%,P<0.05). Basal and forskolin-stimulated adenylyl cyclase activities were decreased slightly, but significantly, in the stunned subendocardium but not in the subepicardium, while isoproterenol stimulation of adenylyl cyclase activity showed no differences. In summary, paradoxical responses toβ-adrenergic receptor stimulation were observed in stunned myocardium, with pharmacological stimulation with isoproterenol evoking enhanced responses, and neural stimulation with inferior vena caval occlusion eliciting depressed responses. The diminished responses to forskolinin vivo, in stunned myocardium were out of proportion to the biochemical measurements, and may be attributed to neurally mediated cardiac effects of forskolin, since the responses to direct stimulation of adenylyl cyclase by NKH 477 were preserved.

Induction of paradoxic bradycardia in rats by inferior vena cava occlusion during the administration of isoproterenol: the essential role of augmented sympathetic tone.

Testing human susceptibility for vasodepressor reactions involves combining venous return restriction by passive upright tilting and administering isoproterenol. While sympathetic tone is usually increased by the stimuli that incite a vasodepressor reaction, it is not known if the increased sympathetic tone is an essential or passive component of the mechanism that triggers the reaction. Given that paradoxic bradycardia is a major manifestation of vasodepressor reactions and allowing for the possible extrapolation between paradoxic bradycardia in rats and vasodepressor reactions, we examined the role of sympathetic tone in the paradoxic bradycardia reaction. Paradoxic bradycardia was induced in rats by inferior vena cava occlusion during an isoproterenol infusion. To examine the role of increased sympathetic tone on this reaction, we studied whether carotid artery perfusion (80 to 100 mmHg) during inferior vena cava occlusion, a maneuver that blunts the rise in sympathetic tone, inhibits paradoxic bradycardia. The maximum changes in R-R were measured during 60 seconds of inferior vena cava occlusion as follows: (a) in control the heart rate accelerated (delta R-R - 10.2 +/- 2.3 msec, P < 0.001); (b) during an infusion of isoproterenol, paradoxic bradycardia occurred (delta R-R + 140.6 +/- 18.2 msec, P < 0.001), and this was inhibited by common carotid artery perfusion (delta R-R - 6.6 +/- 1.5 msec, P < 0.001); and (c) following carotid sinus denervation and during an infusion of isoproterenol, paradoxic bradycardia was induced without and with carotid artery perfusion (delta R-R + 122.6 +/- 12.0 msec, P < 0.001; delta R-R + 151.8 +/- 12.7 msec, P < 0.001, respectively). Since carotid artery perfusion during inferior vena cava occlusion inhibits paradoxic bradycardia only when the carotid sinus is innervated, we conclude that carotid artery perfusion blocks the reaction by increasing carotid sinus afferents, thereby limiting the increased sympathetic tone during inferior vena cava occlusion, and not as a result of cerebral perfusion. Thus, the paradoxic bradycardia resulting from inferior vena cava occlusion requires activation of sympathetic tone as a result of carotid sinus hypotension.

Right Ventricular Performance and Left Ventricular Assist Device Filling

Background. Right ventricular (RV) function is believed to be an important determinant of left ventricular assist device (LVAD) filling. This study was designed to demonstrate this relation in patients.Methods. To demonstrate the interaction between RV ejection and LVAD filling, 10 patients (mean age, 49 ± 13 years) supported with an LVAD were studied. Right ventricular pressure–area loops from cross-sectional area using transesophageal echocardiographic automated border detection and high-fidelity RV pressure were recorded simultaneously with LVAD volume during intraoperative inferior vena cava occlusion. Beat-by-beat RV ejection phase indices were calculated: stroke area, peak ejection rate, and stroke work. The LVAD filling rate was calculated as the first derivative of the volume, and the peak filling rate and the mean filling rate during RV systole were determined for each cardiac cycle.Results. Right ventricular stroke area, peak ejection rate, and stroke work were closely correlated with LVAD peak filling rate (r = 0.87 ± 0.09, r = 0.83 ± 0.09, and r = 0.85 ± 0.10, respectively). Also, baseline LVAD mean filling rate correlated with RV stroke work (r = 0.77) and LVAD peak filling rate with RV peak ejection rate for the group (r = 0.75).Conclusions. These correlations demonstrate predictable associations of RV ejection with LVAD filling.(Ann Thorac Surg 1997;63:1044–9)