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Vascular Resistance Index (vascular + resistance_index)
Kinds of Vascular Resistance Index Selected AbstractsUnderlying mechanism of portal hypertensive gastropathy in cirrhosis: A hemodynamic and morphological approachJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 9 2009Lílian Amorim Curvęlo Abstract Background and Aim:, Portal hypertensive gastropathy (PHG) is an important cause of bleeding in patients with cirrhosis associated with portal hypertension. Histologically, the condition is characterized by dilation of the mucosal and submucosal vessels of the stomach; however, its mechanisms remain unclear. The aim of the present cross-sectional study was to evaluate the role of portal and systemic hemodynamic features, humoral factors and hepatocellular function in the development and severity of PHG in patients with cirrhosis. Methods:, Forty-six patients with cirrhosis of different etiologies underwent endoscopy. Portal hypertension was evaluated by hepatic venous pressure gradient (HVPG). The gastric mucosa was analyzed using two diagnostic methods: endoscopy according to the McCormack criteria and histological by histomorphometric analysis. Results:, The prevalence of PHG according to the endoscopic and histomorphometric methods was 93.4% and 76.1%, respectively. There were no statistically significant differences in HVPG measurements between the patients with mild (16.0 ± 5.9 mmHg) and severe PHG (16.9 ± 6.5 mmHg; P = 0.80) or between patients who did not have (15.2 ± 8.0 mmHg) and those who had PHG (16.3 ± 5.7 mmHg). No correlation was found between the presence or severity of PHG and systemic vascular resistance index (P = 0.53 and 0.34, respectively), Child,Pugh classification (P = 0.73 and 0.78, respectively) or glucagon levels (P = 0.59 and 0.62, respectively). Conclusions:, The present data show no correlation between the presence or the severity of PHG and portal pressure, Child,Pugh classification or systemic hemodynamics, suggesting that other factors may be involved in the physiopathology of PHG, such as local gastric mucosal factors or other underlying factors. [source] Thrombin generation during reperfusion after coronary artery bypass surgery associates with postoperative myocardial damageJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 7 2006P. RAIVIO Summary.,Background: Cardiopulmonary bypass and coronary artery bypass grafting (CABG) result in significant thrombin generation and activation of fibrinolysis. Thrombin contributes to myocardial ischemia,reperfusion injury in animal studies, but the role of thrombin in myocardial damage after CABG is unknown. Objectives: We measured thrombin generation and fibrin turnover during reperfusion after CABG to evaluate their associations with postoperative hemodynamic changes and myocardial damage. Methods: One hundred patients undergoing primary, elective, on-pump CABG were prospectively enrolled. Plasma prothrombin fragment F1+2 and D-dimer were measured preoperatively and at seven time points thereafter. Mass of the Mb fraction of creatine kinase (Ck-Mbm) and troponin T (TnT) were measured on the first postoperative day. Results: Reperfusion induced an escalation of thrombin generation and fibrin turnover despite full heparinization. F1+2 during early reperfusion associated with postoperative pulmonary vascular resistance index. F1+2 at 6 h after protamine administration correlated with Ck-Mbm (r = 0.40, P < 0.001) and TnT (r = 0.44, P < 0.001) at 18 h postoperatively. Patients with evidence of myocardial damage (highest quintiles of plasma Ck-Mbm and TnT) had significantly higher F1+2 during reperfusion than others (P < 0.002). Logistic regression models identified F1+2 during reperfusion to independently associate with postoperative myocardial damage (odds ratios 2.5,4.4, 95% confidence intervals 1.04,15.7). Conclusions: Reperfusion caused a burst in thrombin generation and fibrin turnover despite generous heparinization. Thrombin generation during reperfusion after CABG associated with pulmonary vascular resistance and postoperative myocardial damage. [source] Comparison of calibrated and uncalibrated arterial pressure,based cardiac output monitors during orthotopic liver transplantation,LIVER TRANSPLANTATION, Issue 6 2010Vladimir Krejci Arterial pressure,based cardiac output monitors (APCOs) are increasingly used as alternatives to thermodilution. Validation of these evolving technologies in high-risk surgery is still ongoing. In liver transplantation, FloTrac-Vigileo (Edwards Lifesciences) has limited correlation with thermodilution, whereas LiDCO Plus (LiDCO Ltd.) has not been tested intraoperatively. Our goal was to directly compare the 2 proprietary APCO algorithms as alternatives to pulmonary artery catheter thermodilution in orthotopic liver transplantation (OLT). The cardiac index (CI) was measured simultaneously in 20 OLT patients at prospectively defined surgical landmarks with the LiDCO Plus monitor (CIL) and the FloTrac-Vigileo monitor (CIV). LiDCO Plus was calibrated according to the manufacturer's instructions. FloTrac-Vigileo did not require calibration. The reference CI was derived from pulmonary artery catheter intermittent thermodilution (CITD). CIV -CITD bias ranged from ,1.38 (95% confidence interval = ,2.02 to ,0.75 L/minute/m2, P = 0.02) to ,2.51 L/minute/m2 (95% confidence interval = ,3.36 to ,1.65 L/minute/m2, P < 0.001), and CIL -CITD bias ranged from ,0.65 (95% confidence interval = ,1.29 to ,0.01 L/minute/m2, P = 0.047) to ,1.48 L/minute/m2 (95% confidence interval = ,2.37 to ,0.60 L/minute/m2, P < 0.01). For both APCOs, bias to CITD was correlated with the systemic vascular resistance index, with a stronger dependence for FloTrac-Vigileo. The capability of the APCOs for tracking changes in CITD was assessed with a 4-quadrant plot for directional changes and with receiver operating characteristic curves for specificity and sensitivity. The performance of both APCOs was poor in detecting increases and fair in detecting decreases in CITD. In conclusion, the calibrated and uncalibrated APCOs perform differently during OLT. Although the calibrated APCO is less influenced by changes in the systemic vascular resistance, neither device can be used interchangeably with thermodilution to monitor cardiac output during liver transplantation. Liver Transpl 16:773-782, 2010. © 2010 AASLD. [source] Myocardial Contractility and Cardiac Filling Measured by Impedance Cardiography in Patients with Nitroglycerine-Induced Vasovagal SyncopePACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 1 2006PETER MITRO Objective: Increased myocardial contractility and inadequate cardiac filling leading to activation of the Bezold-Jarisch reflex were proposed as possible triggering mechanisms of vasovagal syncope (VVS). In the present study noninvasive hemodynamic measurements were performed in order to examine the role of myocardial contractility and cardiac filling in pathogenesis of VVS. Methods: Hemodynamic parameters were measured during head-up tilt test (HUT) by impedance cardiography in 46 patients with unexplained syncope. Myocardial contractility was measured as index of contractility (IC), acceleration index (ACI), and ejection fraction (EF). Afterload was measured as systemic vascular resistance index (SVRI) and preload was expressed as end-diastolic index (EDI). Serial measurements were done 1 minute before HUT, during HUT at 1-minute intervals, and 1 minute after completion of HUT. Results: HUT was positive in 30 patients (10 men, 20 women, mean age 36 ± 16 years) and negative in 16 patients (8 men, 8 women, mean age 31 ± 14 years). No significant differences were observed between HUT(+) and HUT(,) groups in hemodynamic parameters at supine rest and during HUT until the development of syncope. SVRI was lower in HUT(+) than in HUT(,) group at syncope (122.7 + 66.3 vs 185.6 + 51.4 dyn sec cm,5/m2, P = 0.002) and after syncope (117.0 + 61.1 vs 198.0 + 95.7 dyn sec cm,5/m2, P = 0.007). ACI, IC, EF, and EDI did not differ between groups at syncope. After syncope EF was higher in HUT(+) group compared to HUT(,) group (59.2 + 6.1 vs 52.7 + 9.4%, P = 0.02). Conclusion: The role of increased myocardial contractility and decreased cardiac filling is not confirmed in the present study. [source] Hypercapnic acidosis and compensated hypercapnia in control and pulmonary hypertensive piglets,PEDIATRIC PULMONOLOGY, Issue 2 2003K. Jane Lee MD Abstract Low tidal volume/inspiratory pressure ventilator strategies result in hypercapnia, which has been shown to increase pulmonary vasomotor tone. This may be particularly detrimental in infants and children with preexistent pulmonary hypertension. In this study, a piglet model of chronic hypoxia-induced pulmonary hypertension was used to test the hypotheses that: 1) the effects of hypercapnic acidosis are exaggerated by preexistent pulmonary hypertension; and 2) the pulmonary hemodynamic effects of hypercapnic acidosis are attenuated by normalizing pH. Pulmonary hypertension was induced by 2 weeks of hypoxia. Hemodynamic responses were measured in control and pulmonary hypertensive piglets during both normoxia and hypoxia under normocapnic, hypercapnic acidotic, and compensated hypercapnic conditions. We found that: 1) hypercapnic acidosis increased both normoxic and hypoxic pulmonary vascular resistance index (PVRI) in control piglets; 2) the pressor effects of hypercapnia were not attenuated by infusing bicarbonate to normalize the pH; and 3) piglets with chronic hypoxia-induced pulmonary hypertension had elevated baseline normoxic and hypoxic PVRI, but responded to hypercapnic acidosis and compensated hypercapnia in a similar way to control piglets. These data suggest that acute hypercapnic acidosis may have deleterious effects on the pulmonary hemodynamics of normal and pulmonary hypertensive subjects which may not be acutely reversed by buffering the pH. Pediatr Pulmonol. 2003; 36:94,101. © 2003 Wiley-Liss, Inc. [source] The cardiovascular effects of normobaric hyperoxia in patients with heart rate fixed by permanent pacemakerANAESTHESIA, Issue 2 2010K. J. Anderson Summary To investigate whether the established reductions in heart rate and cardiac output with hyperoxia in humans are primary effects or secondary to increases in systemic vascular resistance, we paced the hearts of nine patients with permanent pacemakers at a fixed rate when breathing either medical air (inspired O2 fraction 0.21) or oxygen (inspired O2 fraction 0.80) in a randomised, double-blind fashion. A thoracic bio-impedance machine was used to measure heart rate, stroke volume and blood pressure and calculate cardiac index and systemic vascular resistance index. Oxygen caused no change in cardiac index (p = 0.18), stroke index (p = 0.44) or blood pressure (p = 0.52) but caused a small (5.5%) increase in systemic vascular resistance index (p = 0.03). This suggests that hyperoxia has no direct myocardial depressant effects, but that the changes in cardiac output reported in previous studies are secondary to changes in systemic vascular resistance. [source] Survival in pulmonary hypertension associated with the scleroderma spectrum of diseases: Impact of interstitial lung diseaseARTHRITIS & RHEUMATISM, Issue 2 2009Stephen C. Mathai Objective Pulmonary hypertension (PH) is an important cause of mortality in systemic sclerosis (SSc), where it can be isolated (pulmonary arterial hypertension [PAH]) or associated with interstitial lung disease (ILD). This study was undertaken to characterize determinants of survival among SSc patients with either type of PH who received PAH-specific therapy. Methods Consecutive SSc patients with PAH or ILD-associated PH confirmed by right heart catheterization were included in the study. Kaplan-Meier and Cox proportional hazards models were used to compare survival between SSc patients with PAH and those with ILD-associated PH and to identify predictors of survival. Results Fifty-nine patients (39 with PAH and 20 with ILD-associated PH) were identified. The majority (15 of 20 with ILD-associated PH and 27 of 39 with PAH) received an endothelin receptor antagonist as initial therapy. Median followup time was 4.4 years (range 2.7,7.4 years). Survival was significantly worse in SSc patients with ILD-associated PH than in those with PAH (1-, 2-, and 3-year survival rates 82%, 46%, and 39% versus 87%, 79%, and 64%, respectively; P < 0.01 by log rank test). In a multivariable analysis, ILD-associated PH was associated with a 5-fold increase in risk of death compared with PAH. Pulmonary vascular resistance index was also an independent predictor of mortality in the overall cohort (hazard ratio 1.05, P < 0.01) and was a significant univariable risk factor in each group separately. Type of initial PAH therapy and the use of warfarin were not related to survival. Conclusion Survival in SSc complicated by PH remains poor despite currently available treatment options. While therapy may be associated with improved survival in PAH compared with historical controls, the prognosis for patients with ILD-associated PH is particularly grim. Early diagnosis and treatment may improve outcomes since worsening hemodynamic factors were associated with reduced survival. [source] Effect of a Miniaturized Cardiopulmonary Bypass System on the Inflammatory Response and Cardiac Function in Neonatal PigletsARTIFICIAL ORGANS, Issue 11 2009Ko Yoshizumi Abstract The cognitive impairment and hemodynamic instability after neonatal cardiac surgery with cardiopulmonary bypass (CPB) might be exacerbated by hemodilution. Therefore, this study investigated the impact of different bloodless prime volumes on the hemodynamics and the inflammatory response by a miniaturized CPB system in neonatal piglets. The bypass circuit consisted of a Capiox RX05 (Capiox Baby RX, Terumo Corp., Tokyo, Japan) oxygenator and 3/16 internal diameter arterial and venous polyvinyl chloride tubing lines, with a minimum 75 mL prime volume. Twelve 1-week-old piglets were placed on a mild hypothermic CPB (32°C) at 120 mL/kg/min for 2 h. The animals were divided into two groups, based on the volume of the prime solution. The priming volume was 75 mL in Group I and 175 mL in Group II. No blood transfusions were performed, and no inotropic or vasoactive drugs were used. The interleukin-6 (IL-6) and thrombin-antithrombin (TAT) complex levels, as well as right ventricular and pulmonary functions, were measured before and after CPB. Group I had low levels of IL-6 and TAT immediately after CPB (4370 ± 2346 vs. 9058 ± 2307 pg/mL, P < 0.01 and 9.9 ± 7.7 vs. 25.1 ± 8.8 ng/mL, P < 0.01, respectively). Group I had significantly improved cardiopulmonary function, cardiac index (0.22 ± 0.03 vs. 0.11 ± 0.05 L/kg/min, P < 0.001), and pulmonary vascular resistance index (7366 ± 2860 vs. 28 620 ± 15 552 dynes/cm5/kg, P < 0.01) compared with Group II. The miniaturized bloodless prime circuit for neonatal CPB demonstrated that the influence of hemodilution can reduce the subsequent inflammatory response. In addition, a low prime volume could therefore be particularly effective for attenuating pulmonary vascular resistance and right ventricular dysfunction in neonates. [source] Sildenafil Improves the Beneficial Haemodynamic Effects of Intravenous Nitrite Infusion during Acute Pulmonary EmbolismBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 4 2008Carlos A. Dias-Junior While previous studies have shown that sildenafil (an inhibitor of cGMP-specific phosphodiesterase type 5) or nitrite (a storage molecule for nitric oxide) produces beneficial effects during acute pulmonary embolism, no previous study has examined whether the combination of these drugs can produce additive effects. Here, we expand previous findings and examine whether sildenafil enhances the beneficial haemodynamic effects produced by a low-dose infusion of nitrite in a dog model of acute pulmonary embolism. Haemodynamic and arterial blood gas evaluations were performed in non-embolized dogs treated with saline (n = 4), and in embolized dogs (intravenous injections of microspheres) that received nitrite (6.75 µmol/kg intravenously over 15 min. followed by 0.28 µmol/kg/min.) and sildenafil (0.25 mg/kg over 30 min.; n = 8), or nitrite followed by saline (n = 8), or saline followed by sildenafil (n = 7), or only saline (n = 8). Plasma thiobarbituric acid-reactive substances (TBARS) concentrations were determined using a fluorometric method. Acute pulmonary embolism increased pulmonary artery pressure by ,24 mmHg. While the infusion of nitrite or sildenafil infusions reversed this increase by ,42% (both P < 0.05), the combined infusion of both drugs reversed this increase by ,58% (P < 0.05). Similar effects were seen on the pulmonary vascular resistance index. Nitrite or sildenafil alone produced no significant hypotension. However, the combined infusion of both drugs caused transient hypotension (P < 0.05). Both dugs, either alone or combined, blunted the increase in TBARS concentrations caused by acute pulmonary embolism (all P < 0.05). These results suggest that sildenafil improves the beneficial haemodynamic effects of nitrite during acute pulmonary embolism. [source] Hemodynamic significance of heart rate in neurally mediated syncopeCLINICAL CARDIOLOGY, Issue 11 2004Wan Leong Chan M.D. Abstract Background: Vasovagal and vasodepressor syncope are used interchangeably in the literature to describe the common faint syndrome, now collectively named neurally mediated syncope. The significance of heart rate (HR) in these reflex-induced reactions remains unclear. Hypothesis: The study was undertaken to investigate the hemodynamic significance of HR in tilt-induced neurally mediated syncope. Methods: In all, 113 patients with syncope of unknown etiology were studied by head-up tilt test with invasive hemodynamic monitoring. Thirty-five patients (15 women, 20 men, age range 21 to 72 years) developed syncope and were enrolled for analysis. The hemodynamic data were compared between patients who developed bradycardia (vasovagal group, n = 15) and those without bradycardia (vasodepressor group, n = 20). Results: The baseline hemodynamic data (mean ± standard deviation) and the hemodynamic responses after 10-min head-up tilt were similar between patients in the vasovagal and vasodepressor groups. During syncope, patients with vasovagal reaction developed hypotension and paradoxical bradycardia (HR = 52.4 ± 5.9 beats/min), while patients with vasodepressor reaction developed a precipitous drop in arterial blood pressure with inappropriate HR (105 ± 21 beats/min) compensation. Patients with vasovagal syncope manifested a significantly lower cardiac index and a significantly higher systemic vascular resistance index than patients with vasodepressor syncope (1.47 ±0.29 vs. 1.97 ±0.41 l/min/m2, p< 0.001 and 2098 ± 615 vs. 1573 ± 353 dynes·s·cm,5·m2, p<0.003, respectively). A positive correlation existed between HR and cardiac index (r = 0.44, p = 0.008) during syncope in the patients studied. Conclusions: These findings suggest that the hemodynamic characteristics of vasovagal and vasodepressor reactions are different, and that HR plays a significant role in neurally mediated syncope. [source] Twenty-Year Experience With Heart Transplantation for Infants and Children With Restrictive Cardiomyopathy: 1986,2006AMERICAN JOURNAL OF TRANSPLANTATION, Issue 1 2008A. J. Bograd Idiopathic restrictive cardiomyopathy (RCM) is a rare cardiomyopathy in children notable for severe diastolic dysfunction and progressive elevation of pulmonary vascular resistance (PVR). Traditionally, those with pulmonary vascular resistance indices (PVRI) >6 W.U. × m2 have been precluded from heart transplantation (HTX). The clinical course of all patients transplanted for RCM between 1986 and 2006 were reviewed. Preoperative, intraoperative and postoperative variables were evaluated. A total of 23 patients underwent HTX for RCM, with a mean age of 8.8 ± 5.6 years and a mean time from listing to HTX of 43 ± 60 days. Preoperative and postoperative (114 ± 40 days) PVRI were 5.9 ± 4.4 and 2.9 ± 1.5 W.U. × m2, respectively. At time of most recent follow-up (mean = 5.7 ± 4.6 years), the mean PVRI was 2.0 ± 1.0 W.U. × m2. Increasing preoperative mean pulmonary artery pressure (PA) pressure (p = 0.04) and PVRI > 6 W.U. × m2 (,2= 7.4, p < 0.01) were associated with the requirement of ECMO postoperatively. Neither PVRI nor mean PA pressure was associated with posttransplant mortality; 30-day and 1-year actuarial survivals were 96% and 86%, respectively. Five of the seven patients with preoperative PVRI > 6 W.U. × m2 survived the first postoperative year. We report excellent survival for patients undergoing HTX for RCM despite the high proportion of high-risk patients. [source] | |||||||||||||||||||