Cardiac performances were analyzed in intact turtle heart(Amyda japonica), perfusing with turtle Ringer-Locke's solution containing various hydrogen ion concentration, at several levels of arterial and venous pressure. 1. Ventricular work increased when venous pressure, or venous filling pressure increased, and also increased when arterial pressure increased. 2. The higher the arterial pressure, the lower the cardiac to output, for arterial pressure is the resistance to the ventricular blood flow. On the other hand, in specific arterial pressure, cardiac output was proportional to the venous filling pressure. 3. Heart rates did not change significantly during the perfusion with Ringel· solution of various pH. 4. In the heart Perfused with Ringer solution of various pH, ventricular work was the highest at PH 7.6 (at 6 $cmH_2O$ arterial pressure and 8 $cmH_2O$ venous pressure, the ventricular work was 63.09m$\cdot$cm). However, within the range of pH $7.1{\sim}7.6$, there were no significant changes in cardiac output and ventricular work. Below the level of pH 7.0, ventricular work decreased to less than 56% of maximium value (at $6cmH_2O$ arterial pressure and $8cmH_2O$ venous Pressure, ventricular work was 36.0$gm{\cdot}$ at pH 7.0). At pH 7.7 ventricular work decreased to less than 48% of maximum value (ventricular work: 30.0 $gm{\cdot}$). The nature of the cardiac performance at the various arterial and venous pressures was similar to that of normal heart. 5. Turtle heart seemed to be relatively insensitive to acid-base disturbances. The mechanism of negative inotropic effect of hydrogen ion was discussed.
There have been few reports documenting the outcome of arterial swich operations(ASO) in selected patients with transposition of great arteries(TGA) and with left ventricular outflow tract obstruction(LVOTO). In the case of TGA with LVOTO, if the atrial septal defect(ASD) is large and the ventricular septal defect(VSD) is restricive, this deprives the left ventricle(LV) of approporiate preload and could lead to underdevelopment of the ventircular mass and lead poor LV performance after the arterial switch operation, dspite a high pressure in the LV preoperatively. Because an increase in the systolic ventricular pressure is not necessarily paralleled by an increase in ventricular mass, which is also essential for optimal ventricular performance after the operation. We report here a case of rapid LV training after ASO in TGA with unprepared LV (because of large ASD and restrictive VSD) despite a high pressure in the LV(due to LVOTO) preoperatively.
To predict the postoperative hemodynamic status of right ventricle preoperatively, a retrospective analysis was undertaken to determine the influence of pulmonary artery size on postoperative right ventricular pressure in 32 consecutive patients with tetralogy of Fallot who underwent total correction between July, 1987 to June, 1988 at the Department of Thoracic and Cardiovascular Surgery, Seoul National University Hospital. We have related the ratio of the postrepair peak systolic pressure in the right ventricle and the systemic systolic arterial pressure[PRV/Ao] to the preoperative cineangiographic measurement of pulmonary arterial tree, expressed as pulmonary artery index[PAI], the ratio of diameter of the right pulmonary artery to diameter of ascending aorta[r.PA/A.Ao], the ratio of right and left pulmonary artery to diameter of descending aorta[r.I.PA/D.Ao] There was tendency that the postrepair PRV/Ao seems to be related to the preoperative diameter of right and left pulmonary artery, but there were no statistically significant correlation with PAI, r.PA/A.Ao, r.l.PA/D. Ao to the ratio of the postoperative peak systolic right ventricular pressure and systemic systolic arterial pressure[PRV/Ao]. There was tendency to decrease the postoperative right ventricular pressure[PRV/Ao] about 11.2%[P < 0.025] within several hours than immediately after repair, but after then, there was no change of right ventricular pressure[PRV/Ao] significantly. There was good correlation of pressure change between the immediate and late postrepair right ventricular pressure[48 hour], and the derived linear regression line was; y=0.68534 0.1994[r=0.57294, P < 0.001]. There was no operative death due to residual high right ventricular pressure[PRV/Ao >0.75] related to hypoplastic pulmonary arterial development, thus we expect, for symptomatic patients even infants, that complete repair can be attempted when the pulmonary artery index[PAI] is over 108mm2/BSA, RPA/AAo is over 0.35, RPA LPA/D. Ao is over 1.36.
We investigated differences in ventricular and hippocampal volumes between CSF tap test (CSFTT) responders and non-responders in idiopathic normal-pressure hydrocephalus (INPH) patients and compared these parameters in INPH patients with that of age- and gender-matched healthy controls. We also evaluated relationships between ventricular and hippocampal volumes and clinical profiles in INPH patients. We enrolled 48 patients with INPH and 29 healthy controls. Ventricular and hippocampal volumes were measured on MRI, including 3-dimensional volumetric images. INPH patients, when compared to healthy controls, had significantly larger ventricular and smaller hippocampal volumes. No difference in ventricular and hippocampal volumes was found between CSFTT responders and non-responders in INPH patients. And hippocampal volumes showed significant negative correlations with Clinical Dementia Rating Scale scores, INPH grading scale cognitive scores, Timed Up and Go Test scores, and Unified Parkinson's Disease Rating Scale motor scores in INPH patients. Volumetric assessment of ventricular and hippocampal regions may have no predictive value in differentiating between CSFTT responders and non-responders in INPH patients. Our findings may help us understand the potential pathophysiology of unique symptoms associated with INPH.
Objectives : The management of massive brain swelling remains an unsolved problem in neurosurgical field. Despite newly developed medical and pharmacological therapy, the mortality and morbidity due to massive brain swelling remains high. According to many recent reports, surgical decompression with dura expansion is superior to medical management in patients with massive brain swelling. We performed surgical treatment on the first line of treatment, and followed medical management in case with refractory increased intracranial pressure(ICP). To show the quantitative effect of decompressive surgery on the intracranial pressure, we performed ventricular puncture and checked the ventricular ICP continuously during the decompressive surgery and postoperative period. Materials and Methods : Fifty-one patients with massive brain swelling, undergoing bilateral decompressive craniectomy with dura expansion, were studied in this study. In all patients, ventricular puncture was performed at Kocher's point on the opposite side of massive brain swelling. The ventricular pressure was monitored continuously, during the bilateral decompression procedures and postoperative period. Results : The initial ventricular ICP were varied from 13mmHg to 112mmHg. Immediately after the bilateral craniectomy, mean ventricular ICP decreased to $53.1{\pm}15.8%$ of the initial ICP(ranges from 5mmHg to 87mmHg). Dura opening decreased mean ICP by additional 36.7% and made the ventricular pressure $16.4{\pm}10.5%$ of the initial pressure (ranges from 0mmHg to 28mmHg). Postoperatively, ventricular pressure was lowered to $20.2{\pm}22.6%$(ranged from 0mmHg to 62.3mmHg) of the initial ICP. The ventricular ICP value during the first 24 hours after decompressive surgery was found to be an important prognostic factor. If ICP was over 35mmHg, the mortality was 100% instead of additional medical(barbiturate coma therapy and hypothermia) treatments. Conclusion : Bilateral decompression with dura expansion is considered an effective therapeutic modality in ICP control. To obtain favorable clinical outcome in patients with massive brain swelling, early decision making on surgical management and proper patient selection are mandatory.
Journal of the Korean Society of Manufacturing Process Engineers
/
v.12
no.4
/
pp.22-28
/
2013
It is important to begin left ventricular assist device (LVAD) treatment at appropriate time for heart failure patients who expect cardiac recovery after the therapy. In order to predict the optimal timing of LVAD implantation, we predicted pumping efficacy of LVAD according to the severity of heart failure theoretically. We used LVAD-implanted cardiovascular system model which consist of 8 Windkessel compartments for the simulation study. The time-varying compliance theory was used to simulate ventricular pumping function in the model. The ventricular systolic dysfunction was implemented by increasing the end-systolic ventricular compliance. Using the mathematical model, we predicted cardiac responses such as left ventricular peak pressure, cardiac output, ejection fraction, and stroke work according to the severity of ventricular systolic dysfunction under the treatments of continuous and pulsatile LVAD. Left ventricular peak pressure, which indicates the ventricular loading condition, decreased maximally at the 1st level heart-failure under pulsatile LVAD therapy and 2nd level heart-failure under continuous LVAD therapy. We conclude that optimal timing for pulsatile LVAD treatment is 1st level heart-failure and for continuous LVAD treatment is 2nd level heart-failure when considering LVAD treatment as "bridge to recovery".
Objectives: Sanjointang has been clinically used much for treating sleeplessness. However, the effects of Sanjointang in artificial sleep deprivation situations are not known. The purpose of this study is to evaluate the heart rate, left ventricular systolic pressure, left ventricular diastolic pressure, +dp/dt maximum, -dp/dt maximum, and -dp/dt / +dp/dt ratio which are related to the hemodynamic functions of the heart by using sleep-deprived Sparague-Dawley rats, in order to clarify the impact of Sanjointang on hemodynamic functions of the heart of sleep deprived rats. Methods: Eighteen hearts were removed from the male Sparague-Dawley rats weighting about 180g were perfused by the Langendorff technique with modified 37 Krebs-Henseleit's buffer solution at a constant perfusion pressure (60mmHg). They were randomly assigned to one of the following three groups, 1) Normal group (those which did not have sleep deprivation and received normal saline administration), 2) Control group (sleep deprived and normal saline administered), 3) Sample group (sleep deprived and Sanjointang was administered). Control and sample groups rats were deprived 96 hours of sleep by using the modified multiple platform technique. Heart rate, left ventricular systolic pressure, left ventricular diastolic pressure, +dp/dt maximum, -dp/dt maximum, -dp/dt / +dp/dt ratio were evaluated at baseline after the administration of either normal saline or Sanjointang. Results: The heart rate and -dp/dt / +dp/dt ratio was significantly decreased in rats with 96 hours of sleep deprived significantly decreased. The change in the heart rate after administering Sanjointang did not show any significant difference. The left ventricular systolic pressure of the removed heart significantly decreased due to Sanjointang administration, while the left ventricular diastolic pressure significantly increased (p<0.05). The +dp/dt maximum and -dp/dt maximum both significantly decreased in the removed heart after administering Sanjointang. (p<0.05). There was no significant difference observed in the -dp/dt / +dp/dt ratio after administering Sanjointang. Conclusions: According to the results above, sleep deprivation significantly decreases heart rate and -dp/dt / +dp/dt ratio. This is considered as a result of exhaustion due to accumulation of fatigue. Meanwhile, Sanjointang reduced left ventricular systolic pressure and raised left ventricular diastolic pressure, and relieved the contractility and relaxation of the myocardium. Consequently, this reduces the burden of the heart and creates a relatively stabilized heart condition similar to a sleeping condition.
Congenital aortic stenosis in children is characterized by "excessive" left ventricular hypertrophy with reduced left ventricular systolic wall stress that allows for supernormal ejection performance. We hypothesized that left ventricular wall stress was decreased immediately after surgical correction of pure congenital aortic stenosis. Also measuring postoperative left ventricular wall stress was a useful noninvasive measurement that allowed direct assessment for oxygen consumption of myocardium than measuring the peak systolic pressure gradient between ascending aorta and left ventricle for the assessment of surgical results. Material and Method: Between September 1993 and August 1999, 8 patients with isolated congenital aortic stenosis who underwent surgical correction at Yonsei cardiovascular center were evaluated. There were 6 male and 2 female patients ranging in age from 2 to 11 years(mean age, 10 years). Combined Hemodynamic-Ultrasonic method was used for studying left ventricular wall stress. We compared the wall stress peak systolic pressure gradient and ejection fraction preoperatively and postoperatively. Result: After surgical correction peak aortic gradient fell from 58.4${\pm}$17.6, to 23.7${\pm}$17.7 mmHg(p=0.018) and left ventricular ejection fraction decreased but it is not statistically significant. In the consideration of some factors that influence left ventricular end-systolic wall stress excluding one patient who underwent reoperation for restenosis of left ventricular outflow tract left ventricular end-systolic pressure and left ventricular end-systolic dimension were fell from 170.6${\pm}$24.3 to 143.7${\pm}$27.1 mmHg and from 1.78${\pm}$0.4 to 1.76${\pm}$0.4 cm respectively and left ventricular posterior wall thickness was increased from 1.10${\pm}$0.2, to 1.27${\pm}$0.3cm but it was not statistically singificant whereas left ventricular end-systolic wall stress fell from 79.2${\pm}$24.9 to 57.1${\pm}$27.6 kdynes/cm2(p=0.018) in 7 patients. For one patient who underwent reoperation peak aortic gradient fell from 83.0 to 59.7 mmHg whereas left ventricular end-systolic wall stress increased from 67.2 to 97.0 kdynes/cm2 The intervals did not change significnatly. Conclusion ; We believe that probably some factors that are related to left ventricular geometry influenced the decreased left ventricular wall stress immediately after surgical correction of isolated congenital aortic stenosis. Left ventricular wall stress is a noninvasive measurement and can allow for more direct assesment than measuring peak aortic gradient particularly in consideration of the stress and oxygen consumption of the myocardium therefore we can conclude it is a useful measurement for postoperative assessment of congenital aortic stenosis.
Not a few patients in children and adolescents are suffering from right ventricular (RV) dysfunction resulting from various conditions such as chronic lung disease, left ventricular dysfunction, pulmonary hypertension, or congenital heart defect. The RV is different from the left ventricle in terms of ventricular morphology, myocardial contractile pattern and special vulnerability to the pressure overload. Right ventricular failure (RVF) can be evaluated in terms of decreased RV contractility, RV volume overload, and/or RV pressure overload. The management for RVF starts from clear understanding of the pathophysiology of RVF. In addition to correction of the underlying disease, management of RVF per se is very important. Meticulous control of volume status, inotropic agents, vasopressors, and pulmonary selective vasodilators are the main tools in the management of RVF. The relative importance of each tool depends on the individual clinical status. Medical assist device and surgery can be considered selectively in case of refractory RVF to optimal medical treatment.
Pulmonary atresia with VSD is uncommon congenital anomaly with high mortality in neonatal period.Recently we experienced surgical correction of pulmonary atresia with VSD. The case was 2 month old male patient diagnosed as pulmonary atresia with VSD and PDA. Atretic pulmonary artery segment from Rt ventricular infundibulum to pulmonary artery was lcm in length. The pulmonary trunk tapered toward Right ventricular infundibulum and resulted in blind pouch with diameter of lmm. The left pulmonary artery was stenosed at just proximal and distal part to which PDA was connected. Total correction was undertaken which consisted of PDA ligation, dacron patch closure of VSD, establishment of continuity between right ventricle and pulmonary artery with autogenous pericardium. Postoperative systolic fight ventricular pressure and left ventricular pressure ratio was 0.7. In patient with pulmonary atresia with VSD it is advisable to perform a corrective operation, whenever the size and anatomy of pulmonary artery are acceptable for it.
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