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Pulmonary Vascular Resistance (pulmonary + vascular_resistance)
Terms modified by Pulmonary Vascular Resistance Selected AbstractsPercutaneous Closure of a Large PDA in a 35-Year-Old Man with Elevated Pulmonary Vascular ResistanceCONGENITAL HEART DISEASE, Issue 2 2008John S. Hokanson MD ABSTRACT The presence of a large patent ductus arteriosus (PDA) may result in significant pulmonary hypertension, which may not be reversible. We present the case of a 35-year-old man with pulmonary hypertension who had successful percutaneous closure of a large PDA with an Amplatzer muscular ventricular septal defect occluder and resolution of his pulmonary hypertension. The use of prior balloon test occlusion of the PDA suggested that the procedure would be successful, despite the lack of an immediate fall in the pulmonary artery pressure. [source] Noninvasive Estimation of Pulmonary Vascular Resistance in Pulmonary HypertensionECHOCARDIOGRAPHY, Issue 5 2009Navin Rajagopalan M.D. Background: Determination of pulmonary vascular resistance (PVR) in patients with suspected or known pulmonary hypertension (PH) requires right heart catheterization. Our purpose was to use Doppler echocardiography to estimate PVR in patients with PH. Methods: Patient population consisted of 52 patients (53 ± 12 years; 35 females) who underwent Doppler echocardiography and right heart catheterization within 24 hours of each other. The ratio of peak tricuspid regurgitation velocity (TRV) and right ventricular outflow time-velocity integral (VTIRVOT) was measured via transthoracic echocardiography and correlated to invasively determined PVR. A linear regression equation was generated to determine PVR by echocardiography based upon the TRV/VTIRVOT ratio. PVR by echocardiography was compared to invasive PVR using Bland-Altman analysis. Results: Significant correlation was demonstrated between TRV/VTIRVOT and PVR by catheterization (r = 0.73; P < 0.001). However, Bland-Altman analysis showed that agreement between PVR determined by echocardiography and invasive PVR was poor (bias = 0; standard deviation = 4.3 Wood units). In a subset of patients with invasive PVR < 8 Wood units (26 patients), correlation between TRV/VTIRVOT and invasive PVR was strong (r = 0.94; P < 0.001). In these patients, agreement between PVR by echocardiography and invasive PVR was satisfactory (bias = 0; standard deviation = 0.5 Wood units). There was no correlation between TRV/VTIRVOT and invasive PVR in patients with PVR > 8 Wood units (n = 26; r = 0.17). Conclusion: While TRV/VTIRVOT correlates significantly with PVR, using it to estimate PVR in a PH patient population cannot be recommended. [source] Equine pulmonary and systemic haemodynamic responses to endothelin-1 and a selective ETA receptor antagonistEQUINE VETERINARY JOURNAL, Issue 4 2001A. E. BENAMOU Summary Based on previous in vitro studies, we hypothesised that endothelin (ET) would induce vasoconstriction in the pulmonary circululation of the horse and that this action would be mediated via ETA receptors. Pulmonary and systemic haemodynamic responses to endothelin-1 (ET-1), a potent vasoactive endogenous peptide, were investigated in 6 conscious, nonsedated horses at rest. Bolus i.v. injections of exogenous ET-1 (0.1, 0.2 and 0.4 ,g/kg bwt) caused significant increases in pulmonary (PAP) and carotid (CAP) artery pressures, with peak increases of 79% and 51% for mean PAP and CAP, respectively. The effect of ET-1 on PAP and CAP was rapid and transient for PAP (,10 min) but prolonged for CAP (up to 60 min). ET-1 significantly decreased cardiac output by up to 35% and significantly increased systemic vascular resistance (SVR) by up to 104%. Pulmonary vascular resistance (PVR) showed a trend (P>0.05) to increase with 0.2 and 0.4 ,g/kg bwt ET-1. Infusion of a selective ETA receptor antagonist (TBC11251) completely inhibited the responses to a subsequent bolus of 0.2 ,g/kg bwt ET-1. We conclude that exogenous ET-1 exerts a potent vasoconstrictive action on the pulmonary and systemic circulations of the horse. These effects appear to be mediated largely through ETA receptors in both circulations. Endothelin may play a role in hypertensive conditions in the horse. [source] Rest and exercise hemodynamics before and after valve replacement-A combined doppler/catheter studyCLINICAL CARDIOLOGY, Issue 1 2000G. Inselmann M.D. Abstract Background: Hemodynamic improvement is a common finding following valve replacement. However, despite a normally functioning prosthesis and normal left ventricular ejection fraction, some patients may show an abnormal hemodynamic response to exercise. Methods: In a combined catheter/Doppler study, rest and exercise hemodynamics were evaluated in 23 patients following aortic (n = 12) (Group 1) or mitral valve (n = 11) (Group 2) replacement and compared with preoperative findings. Patient selection was based on absence of coronary artery disease and left ventricular failure as shown by preoperative angiography. Cardiac output, pulmonary artery pressure, pulmonary capillary pressure, and pulmonary resistance were measured by right heart catheterization, whereas the gradient across the valve prosthesis was determined by Doppler echocardiography. Postoperative evaluation was done at rest and during exercise. The mean follow-up was 8.2 ± 2.2 years in Group 1 and 4.2 ± 1 years in Group 2. Results: With exercise, there was a significant rise in cardiac output in both groups. In Group 1, mean pulmonary pressure/capillary pressure decreased from 24 ± 9/18 ± 9 mmHg preoperatively to 18 ± 2/12 ± 4 mmHg postoperatively (p < 0.05), and increased to 43 ± 12/30 ± 8 mmHg with exercise (p < 0.05). The corresponding values for Group 2 were 36 ± 12/24 ± 6 mmHg preoperatively, 24 ± 7/17 ± 6 mmHg postoperatively (p < 0.05), and 51 ± 2/38 ± 4 mmHg with exercise (p < 0.05). Pulmonary vascular resistance was 109 ± 56 dyne·s·cm -5 preoperatively, 70 ± 39 dyne·s·cm -5 postoperatively (p < 0.05), and 70 ± 36 dyne·s·cm -5 with exercise in Group 1. The corresponding values for Group 2 were 241 ± 155 dyne·s·cm -5, 116 ± 39 dyne·s·cm -5 (p < 0.05), and 104 ± 47 dyne·s·cm -5. There was a significant increase in the gradients across the valve prosthesis in both groups, showing a significant correlation between the gradient at rest and exercise. No correlation was found between valve prosthesis gradient and pulmonary pressures. Conclusion: Exercise-induced pulmonary hypertension and abnormal left ventricular filling pressures seem to be a frequent finding following aortic or mitral valve replacement. Both hemodynamic abnormalities seem not to be determined by obstruction to flow across the valve prosthesis and may be concealed, showing nearly normal values at rest but a pathologic response to physical stress. [source] Meconium aspiration syndrome: a role for phospholipase A2 in the pathogenesis?ACTA PAEDIATRICA, Issue 4 2001P KääpäArticle first published online: 2 JAN 200 The pathophysiology of neonatal meconium aspiration syndrome (MAS), often resulting in severe respiratory failure, is complex and still largely unclear. Factors involved in the propagation of acute lung injury after perinatal aspiration of meconium include obstruction of the airways, ventilation/perfusion mismatch, increase of the pulmonary vascular resistance and a rapidly developing parenchymal and alveolar inflammatory reaction with associated surfactant dysfunction. Conclusion: Although the early pulmonary inflammatory response is believed to play a central pathogenetic role in the meconium-induced acute lung damage, its initiating mechanisms are still poorly defined. However, increasing evidence indicates a direct toxic effect of meconium. [source] Identifying Left Ventricular Dysfunction in Pulmonary HypertensionCONGESTIVE HEART FAILURE, Issue 5 2009Navin Rajagopalan MD The significance of left ventricular (LV) dysfunction in patients with pulmonary hypertension (PH) is unknown. Our purpose was to quantify LV function in PH patients by measuring LV myocardial performance index (MPI) and correlating it with invasively determined hemodynamic variables. The authors prospectively measured LV MPI via transthoracic echocardiography in 50 patients with PH (53±11 years; 35 women) who also underwent right heart catheterization within 1 day of echocardiography. For comparative purposes, LV MPI was also measured in 15 healthy volunteers who served as controls. LV MPI was significantly increased in the PH group compared with controls (0.62±0.27 vs 0.36±0.08; P<.001), indicating worse LV dysfunction despite that LV ejection fraction was not significantly different between the groups (58%±4% vs 60%±3%). LV MPI demonstrated significant correlations with invasively determined mean pulmonary artery pressure (r=.50; P<.001), pulmonary vascular resistance (r=.57; P<.001), and cardiac index (r=,.64; P<.001). By receiver operating characteristic analysis, LV MPI >0.75 predicted cardiac index <2 L/min/m2 with 89% sensitivity and 78% specificity (area under the curve, 0.89). In a multivariate model, LV MPI was independently associated with cardiac index (P<.01). Patients with PH demonstrate abnormal LV function as quantified by elevated LV MPI, which correlates significantly with pulmonary vascular resistance and cardiac index. [source] Correlation of Tricuspid Annular Velocities With Invasive Hemodynamics in Pulmonary HypertensionCONGESTIVE HEART FAILURE, Issue 4 2007Navin Rajagopalan The authors performed tissue Doppler imaging of the tricuspid annulus in patients with pulmonary hypertension to assess its correlation with invasive indices of right ventricular function. The study population consisted of 32 patients with suspected pulmonary hypertension who underwent pulsed tissue Doppler imaging of the tricuspid annulus and right heart catheterization. Peak systolic (Sa), early diastolic (Ea), and late diastolic (Aa) velocities of the lateral tricuspid annulus were measured and correlated with hemodynamic variables. Peak Sa demonstrated excellent correlation with hemodynamic variables, including cardiac index (r=0.78; P<.001), pulmonary vascular resistance (r=,0.79; P<.001), and transpulmonary gradient (r=,0.72; P<.001). Peak Sa <10 cm/s predicted cardiac index <2.0 L/min/m2 with 89% sensitivity and 87% specificity. In conclusion, tissue Doppler imaging of the tricuspid annulus is a complementary method to assess right ventricular function in pulmonary hypertensive patients. [source] 5-Hydroxytryptamine-induced microvascular pressure transients in lungs of anaesthetized rabbitsACTA PHYSIOLOGICA, Issue 2 2001N. Sen We determined lung microvascular pressure transients induced by 5-hydroxytryptamine (5HT), by the micropuncture technique. We mechanically ventilated anaesthetized (halothane 0.8%), open-chested rabbits, in which we recorded pulmonary artery (PA), left atrial (LA) and carotid artery pressures and cardiac output. For 4-min periods of stopped ventilation, we constantly inflated the lung with airway pressure of 7 cmH2O, then micropunctured the lung to determine pressures in arterioles and venules of 20,25 ,m diameter. An intravenous bolus infusion of 5HT (100 ,g), increased total pulmonary vascular resistance by 59%. Prior to 5HT infusion, the arterial, microvascular and venous segments comprised 30, 50 and 19% of the total pulmonary vascular pressure drop, respectively. However 14 s after 5HT infusion, the PA-arteriole pressure difference (arterial pressure drop) increased 46%, while the venule-LA pressure difference (venous pressure drop) increased >100%. The arteriole,venule pressure difference (microvascular pressure drop) was abolished. The increase in the arterial pressure drop was maintained for 4.8 min, whereas the increased venous pressure drop reverted to baseline in <1 min. We conclude that in the rabbit lung in situ, a 5HT bolus causes sustained arterial constriction and a strong but transient venous constriction. [source] Noninvasive Estimation of Pulmonary Vascular Resistance in Pulmonary HypertensionECHOCARDIOGRAPHY, Issue 5 2009Navin Rajagopalan M.D. Background: Determination of pulmonary vascular resistance (PVR) in patients with suspected or known pulmonary hypertension (PH) requires right heart catheterization. Our purpose was to use Doppler echocardiography to estimate PVR in patients with PH. Methods: Patient population consisted of 52 patients (53 ± 12 years; 35 females) who underwent Doppler echocardiography and right heart catheterization within 24 hours of each other. The ratio of peak tricuspid regurgitation velocity (TRV) and right ventricular outflow time-velocity integral (VTIRVOT) was measured via transthoracic echocardiography and correlated to invasively determined PVR. A linear regression equation was generated to determine PVR by echocardiography based upon the TRV/VTIRVOT ratio. PVR by echocardiography was compared to invasive PVR using Bland-Altman analysis. Results: Significant correlation was demonstrated between TRV/VTIRVOT and PVR by catheterization (r = 0.73; P < 0.001). However, Bland-Altman analysis showed that agreement between PVR determined by echocardiography and invasive PVR was poor (bias = 0; standard deviation = 4.3 Wood units). In a subset of patients with invasive PVR < 8 Wood units (26 patients), correlation between TRV/VTIRVOT and invasive PVR was strong (r = 0.94; P < 0.001). In these patients, agreement between PVR by echocardiography and invasive PVR was satisfactory (bias = 0; standard deviation = 0.5 Wood units). There was no correlation between TRV/VTIRVOT and invasive PVR in patients with PVR > 8 Wood units (n = 26; r = 0.17). Conclusion: While TRV/VTIRVOT correlates significantly with PVR, using it to estimate PVR in a PH patient population cannot be recommended. [source] Incorporation of Pulmonary Vascular Resistance Measurement into Standard Echocardiography: Implications for Assessment of Pulmonary HypertensionECHOCARDIOGRAPHY, Issue 10 2007Kimberly B. Ulett B.S Doppler estimation of pulmonary artery systolic pressure (PASP) from tricuspid regurgitation velocity is a simple approach to the detection of pulmonary hypertension but may be influenced by right ventricular stroke volume. We sought the clinical utility of incorporating Doppler calculation of pulmonary vascular resistance (PVR) into determination of pulmonary hypertension in 578 consecutive patients with tricuspid regurgitation. Right atrial pressure was estimated from vena caval dimensions and collapsibility. Pulmonary hypertension was classified on the basis of a) PASP >35mmHg, b) age-/gender normalized PASP, c) PVR >2 Wood units. The mean PASP was 40 ± 13 mmHg and PVR was 1.9 ± 0.8 Wood units. Standard PASP identified pulmonary hypertension in 58%, compared with 36% by age-/gender normalized PASP (P < 0.0001), and 31% by PVR (P < 0.0001). Of patients who had pulmonary hypertension by PASP, 33% were reclassified as normal on the basis of PVR and 6% were reclassified from normal to pulmonary hypertension. PVR is easy to incorporate into a standard echo exam, and identifies a small group with normal PASP as having PAH, and a larger group of apparently increased PASP as normal. [source] Hepatopulmonary Syndrome and Right Ventricular Diastolic Functions: An Echocardiographic ExaminationECHOCARDIOGRAPHY, Issue 4 2006Aziz Karabulut M.D. Aim: Liver functions are affected in the course of cardiac diseases, and similarly, liver diseases affect cardiac functions. Many studies in the literature have shown that left ventricular systolic and/or diastolic dysfunction may develop during chronic liver disease. However, there are limited studies investigating right ventricular functions during chronic liver diseases. Methods: A total of 84 patients who had no systolic and/or diastolic dysfunction in the left ventricle (LV) were evaluated; 46 patients with liver cirrhosis; 10 (21.74%) cirrhotic patients with hepatopulmonary syndrome (HPS) (group 1), 36 (78.26) cirrhotic patients without HPS (group 2), and 38 healthy individuals were treated as control. Results: Right ventricular diastolic dysfunction was determined in all patients of group 1 (100%), 26 of group 2 (72.22 %), and 4 of the controls (10.52%) (P < 0.05). Tricuspid deceleration time (dt) was significantly different between the groups (P < 0.05). In addition, right atrium (RA) diameters, right ventricle (RV) diameters, and RV wall thickness were significantly different between the groups (P < 0.05). Pulmonary artery pressure (P < 0.05) and pulmonary vascular resistance (P < 0.05) were also seen to be higher in group 1 than those in group 2 and control group. Conclusions: Right ventricular diastolic dysfunction rate is high in chronic liver diseases. In the presence of HPS, right ventricular diastolic dysfunction is more remarkable in patients than those without HPS. Right ventricular diastolic dysfunction may result in dilatation and hypertrophy in the right heart. [source] Cardiopulmonary, blood and peritoneal fluid alterations associated with abdominal insufflation of carbon dioxide in standing horsesEQUINE VETERINARY JOURNAL, Issue 3 2003F. G. LATIMER Summary Reasons for performing study: Abdominal insufflation is performed routinely during laparoscopy in horses to improve visualisation and facilitate instrument and visceral manipulations during surgery. It has been shown that high-pressure pneumoperitoneum with carbon dioxide (CO2) has deleterious cardiopulmonary effects in dorsally recumbent, mechanically ventilated, halothane-anaesthetised horses. There is no information on the effects of CO2 pneumoperitoneum on cardiopulmonary function and haematology, plasma chemistry and peritoneal fluid (PF) variables in standing sedated horses during laparoscopic surgery. Objectives: To determine the effects of high pressure CO2 pneumoperitoneum in standing sedated horses on cardiopulmonary function, blood gas, haematology, plasma chemistry and PF variables. Methods: Six healthy, mature horses were sedated with an i.v. bolus of detomidine (0.02 mg/kg bwt) and butorphanol (0.02 mg/kg bwt) and instrumented to determine the changes in cardiopulmonary function, haematology, serum chemistry and PF values during and after pneumoperitoneum with CO2 to 15 mmHg pressure for standing laparoscopy. Each horse was assigned at random to either a standing left flank exploratory laparoscopy (LFL) with CO2 pneumoperitoneum or sham procedure (SLFL) without insufflation, and instrumented for measurement of cardiopulmonary variables. Each horse underwent a second procedure in crossover fashion one month later so that all 6 horses had both an LFL and SLFL performed. Cardiopulmonary variables and blood gas analyses were obtained 5 mins after sedation and every 15 mins during 60 mins baseline (BL), insufflation (15 mmHg) and desufflation. Haematology, serum chemistry analysis and PF analysis were performed at BL, insufflation and desufflation, and 24 h after the conclusion of each procedure. Results: Significant decreases in heart rate, cardiac output and cardiac index and significant increases in mean right atrial pressure, systemic vascular resistance and pulmonary vascular resistance were recorded immediately after and during sedation in both groups of horses. Pneumoperitoneum with CO2 at 15 mmHg had no significant effect on cardiopulmonary function during surgery. There were no significant differences in blood gas, haematology or plasma chemistry values within or between groups at any time interval during the study. There was a significant increase in the PF total nucleated cell count 24 h following LFL compared to baseline values for LFL or SLFL at 24 h. There were no differences in PF protein concentrations within or between groups at any time interval. Conclusions: Pneumoperitoneum with CO2 during standing laparoscopy in healthy horses does not cause adverse alterations in cardiopulmonary, haematology or plasma chemistry variables, but does induce a mild inflammatory response within the peritoneal cavity. Potential relevance: High pressure (15 mmHg) pneumoperitoneum in standing sedated mature horses for laparoscopic surgery can be performed safely without any short-term or cumulative adverse effects on haemodynamic or cardiopulmonary function. [source] Effects of phlebotomy on haemodynamic characteristics during exercise in Standardbred trotters with red cell hypervolaemiaEQUINE VETERINARY JOURNAL, Issue 4 2001P. FUNKQUIST Summary Five Standardbred trotters with red cell hypervolaemia (RCHV) were compared before and after removal of approximately 22% (36 ml/kg bwt) of the total blood volume in order to evaluate the haemodynamic responses, haemorheological alterations and oxygen transport during exercise to fatigue. Data were recorded during submaximal exercise at 4 different speeds on a treadmill and then during continued running at the highest speed step until fatigue. Oxygen uptake (V,O2), pulmonary artery pressure (PAP), systemic artery pressure (SAP), heart rate (HR), haematocrit and haemoglobin concentrations (Hb) were measured. Arteriovenous O2 content difference (C(a-v,)O2), pulmonary vascular resistance (PVR) and total systemic resistance (TSR) were calculated. Whole blood and plasma viscosity and erythrocyte aggregation tendency were determined with a rotational viscometer. Endoscopy was performed after exercise. ANOVA was used for statistical analysis. Phlebotomy resulted in a decrease in haematocrit and Hb during the course of exercise. Blood and plasma viscosity were lower and erythrocyte aggregation tendency was higher after phlebotomy. Throughout exercise, including submaximal work and continued running to fatigue, PAP, SAP, PVR, TSR and C(a-v,)O2 were lower after phlebotomy. HR was higher after phlebotomy during submaximal exercise. Oxygen delivery and VO2 were lower after phlebotomy in the period from submaximal exercise to fatigue. Run time to fatigue was shorter after phlebotomy. Four horses showed exercise-induced pulmonary haemorrhage (EIPH) before phlebotomy and the degree of bleeding was diminished but not abolished after phlebotomy. The reductions in PVR, TSR, PAP and SAP after phlebotomy were probably a result of reduced blood viscosity. In conclusion, although a 22% reduction in blood volume improved the haemodynamic and haemorheological parameters and the degree of EIPH, it was found that RCHV trotters have to rely on high oxygen delivery to the working muscles for maintenance of maximal performance. [source] Metalloproteinase-9 in circulating monocytes in pulmonary hypertensionFUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 4 2006Caroline Cantini-Salignac Abstract The role of matrix metalloproteinases (MMPs) in pulmonary hypertension (PH) is complex as MMPs are involved in both the vascular and cardiac remodelling associated with PH. To gain insight into this problem, monocytes were isolated from pulmonary arterial blood in patients suffering from PH, related to chronic obstructive pulmonary disease (n = 6), chronic pulmonary thromboembolism (n = 3) or pulmonary arterial hypertension (n = 8). The severity of PH was associated with decreases in cardiac index (CI) and mixed venous blood oxygen saturation (SO2), and an increase in right atrial pressure (). Monocyte pro-MMP-9 content (zymography) was positively correlated with SO2 (r = 0.73, P < 0.05) and CI (r = 0.66, P < 0.05), and negatively with (r = 0.54, P < 0.05); there was no significant correlation with pulmonary vascular resistance. In conclusion, the pro-MMP-9 content of circulating monocytes was lower in the more severe forms of PH which showed heart failure suggesting that such MMP enzymatic activity reflects heart failure following pulmonary vascular and myocardial remodelling in PH. [source] Clinical risk factors for portopulmonary hypertension,HEPATOLOGY, Issue 1 2008Steven M. Kawut Portopulmonary hypertension affects up to 6% of patients with advanced liver disease, but the predictors and biologic mechanism for the development of this complication are unknown. We sought to determine the clinical risk factors for portopulmonary hypertension in patients with advanced liver disease. We performed a multicenter case-control study nested within a prospective cohort of patients with portal hypertension recruited from tertiary care centers. Cases had a mean pulmonary artery pressure > 25 mm Hg, pulmonary vascular resistance > 240 dynes · second · cm,5, and pulmonary capillary wedge pressure , 15 mm Hg. Controls had a right ventricular systolic pressure < 40 mm Hg (if estimable) and normal right-sided cardiac morphology by transthoracic echocardiography. The study sample included 34 cases and 141 controls. Female sex was associated with a higher risk of portopulmonary hypertension than male sex (adjusted odds ratio = 2.90, 95% confidence interval 1.20-7.01, P = 0.018). Autoimmune hepatitis was associated with an increased risk (adjusted odds ratio = 4.02, 95% confidence interval 1.14-14.23, P = 0.031), and hepatitis C infection was associated with a decreased risk (adjusted odds ratio = 0.24, 95% confidence interval 0.09-0.65, P = 0.005) of portopulmonary hypertension. The severity of liver disease was not related to the risk of portopulmonary hypertension. Conclusion: Female sex and autoimmune hepatitis were associated with an increased risk of portopulmonary hypertension, whereas hepatitis C infection was associated with a decreased risk in patients with advanced liver disease. Hormonal and immunologic factors may therefore be integral to the development of portopulmonary hypertension. (HEPATOLOGY 2008.) [source] Scintigraphic evaluation of intrapulmonary shunt in normoxemic cirrhotic patients and effects of terlipressinHEPATOLOGY RESEARCH, Issue 10 2010George Kalambokis Aim:, The magnitude of intrapulmonary shunt (IPS) in cirrhotic patients without hypoxemia remains undefined. We evaluated the severity and clinical correlations of IPS in normoxemic cirrhotics, and possible IPS alterations after terlipressin treatment. Methods:, Fifteen patients with alcoholic cirrhosis without hypoxemia were studied at baseline and after the administration of 2 mg of terlipressin. The IPS fraction was evaluated by lung perfusion scan after the i.v. injection of technetium-99m -labeled macroaggregated albumin (99mTc-MAA) and calculation of brain uptake (positive value ,6%). Cardiac output (CO), pulmonary artery systolic pressure (PASP) and pulmonary vascular resistance (PVR) were evaluated by Doppler echocardiography. Mean arterial pressure (MAP) was measured and the ratio MAP/CO was calculated as an index of systemic vascular resistance (SVR). Portal vein velocity (PVV) and portal venous flow (PVF) were also assessed by Doppler ultrasonography. Results:, Three patients (20%) had an IPS fraction of more than 6%. A significant inverse correlation with platelet count (P = 0.001) and a direct correlation with Child,Pugh score (P = 0.06), PVV (P = 0.07) and PVF (P = 0.07) were noted. IPS fractions decreased significantly after terlipressin administration (P = 0.00001); the IPS fraction fell below 6% in all three patients with positive baseline values. Terlipressin treatment induced a significant decrease in CO (P = 0.003) and significant increases in MAP (P = 0.0003), SVR (P = 0.0003), SPAP (P = 0.001) and PVR (P = 0.01). Conclusion:, IPS fractions detected by 99mTc-MAA lung scan were inversely correlated with platelet count and directly with liver disease severity, and found abnormal in 20% of normoxemic cirrhotic patients. Terlipressin reduced significantly the magnitude of the shunt. [source] Iron chelation prevents lung injury after major hepatectomyHEPATOLOGY RESEARCH, Issue 8 2010Konstantinos Kalimeris Aim:, Oxidative stress has been implicated in lung injury following ischemia/reperfusion and resection of the liver. We tested whether alleviating oxidative stress with iron chelation could improve lung injury after extended hepatectomy. Methods:, Twelve adult female pigs subjected to liver ischemia for 150 min, 65,70% hepatectomy and reperfusion of the remnant liver for 24 h were randomized to a desferrioxamine (DF) group (n = 6) which received i.v. desferrioxamine to a total dose of 100 mg/kg during both ischemia and reperfusion, and a control (C) group (n = 6). We recorded hemodynamic and respiratory parameters, plasma interleukin-6 and malondialdehyde levels, as well as liver malondialdehyde and protein carbonyls content. Total non-heme iron was measured in lung and liver. Pulmonary tissue was evaluated histologically for its nitrotyrosine and protein carbonyls content and for superoxide dismutase (SOD) and platelet-activating factor acetylhydrolase (PAF-AcH) activities. Results:, Reperfusion of the remnant liver resulted in gradual deterioration of gas-exchange and pulmonary vascular abnormalities. Iron chelation significantly decreased the oxidative markers in plasma, liver and the lung and lowered activities of pulmonary SOD and PAF-AcH. The improved liver function was followed by improved arterial oxygenation and pulmonary vascular resistance. DF also improved alveolar collapse and inflammatory cell infiltration, while serum interleukin-6 increased. Conclusion:, In an experimental pig model that combines liver resection with prolonged ischemia, iron chelation during reperfusion of the remnant liver is associated with improvement of several parameters of oxidative stress, lung injury and arterial oxygenation. [source] Cardiovascular and Metabolic Effects of High-dose Insulin in a Porcine Septic Shock ModelACADEMIC EMERGENCY MEDICINE, Issue 4 2010Joel S. Holger MD Abstract Objectives:, High-dose insulin (HDI) has inotropic and vasodilatory properties in various clinical conditions associated with myocardial depression. The authors hypothesized that HDI will improve the myocardial depression produced by severe septic shock and have beneficial effects on metabolic parameters. In an animal model of severe septic shock, this study compared the effects of HDI treatment to normal saline (NS) resuscitation alone. Methods:, Ten pigs were randomized to an insulin (HDI) or NS group. All were anesthetized and instrumented to monitor cardiovascular function. In both arms, Escherichia coli endotoxin lipopolysaccharide (LPS) and NS infusions were begun. LPS was titrated to 20 ,g/kg/hour over 30 minutes and continued for 5 hours, and saline was infused at 20 mL/kg/hour throughout the protocol. Dextrose (50%) was infused to maintain glucose in the 60,150 mg/dL range, and potassium was infused to maintain a level greater than 2.8 mmol/L. At 60 minutes, the HDI group received an insulin infusion titrated from 2 to 10 units/kg/hour over 40 minutes and continued at that rate throughout the protocol. Survival, heart rate (HR), mean arterial pressure (MAP), pulmonary artery and central venous pressure, cardiac output, central venous oxygen saturation (SVO2), and lactate were monitored for 5 hours (three pigs each arm) or 7 hours (two pigs each arm) or until death. Cardiac index, systemic vascular resistance (SVR), pulmonary vascular resistance (PVR), O2 delivery, and O2 consumption were derived from measured data. Outcomes from the repeated-measures analysis were modeled using a mixed-effects linear model that assumed normally distributed errors and a random effect at the subject level. Results:, No significant baseline differences existed between arms at time 0 or 60 minutes. Survival was 100% in the HDI arm and 60% in the NS arm. Cardiovascular variables were significantly better in the HDI arm: cardiac index (p < 0.001), SVR (p < 0.003), and PVR (p < 0.01). The metabolic parameters were also significantly better in the HDI arm: SVO2 (p < 0.01), O2 delivery (p < 0.001), and O2 consumption (p < 0.001). No differences in MAP, HR, or lactate were found. Conclusions:, In this animal model of endotoxemic-induced septic shock that results in severe myocardial depression, HDI is associated with improved cardiac function compared to NS resuscitation alone. HDI also demonstrated favorable metabolic, pulmonary, and peripheral vascular effects. Further studies may define a potential role for the use of HDI in the resuscitation of septic shock. ACADEMIC EMERGENCY MEDICINE 2010; 17:429,435 © 2010 by the Society for Academic Emergency Medicine [source] Haemodynamic effects of ,75 mmHg negative pressure therapy in a porcine sternotomy wound modelINTERNATIONAL WOUND JOURNAL, Issue 1 2009Arash Mokhtari Abstract Previous research has shown ,125 mmHg to be the optimal negative pressure for creating an environment that promotes wound healing, and this has therefore been adopted as a standard pressure for patients with deep sternal wound infection. However, it has not yet been clearly shown that ,125 mmHg is the optimal pressure from a haemodynamic point of view. Furthermore, there have been reports of cardiac rupture during ,125 mmHg negative pressure therapy. We therefore studied the effects of a lower pressure: ,75 mmHg. Twelve pigs were used. After median sternotomy, sealed negative pressure therapy of ,75 mmHg was applied. Baseline measurements were made and continuous recording of the cardiac output, end-tidal CO2 production, mean arterial pressure, mean pulmonary pressure (pulmonary artery pressure), systemic vascular resistance, pulmonary vascular resistance, left atrial pressure and central venous pressure was started. Six pigs served as controls. No statistically significant difference was observed in any of the haemodynamic parameters studied, compared with the controls. The present study shows that, with a suitable foam application technique, ,75 mmHg can be applied without compromising the central haemodynamics. [source] Twenty-Four Hours Postoperative Results After Orthotopic Cardiac Transplantation in SwineJOURNAL OF CARDIAC SURGERY, Issue 4 2007Matthias Siepe M.D. However, there is no functional data available for a longer time period after transplantation. We have established a pig model to investigate myocardial function 24 hours after orthotopic transplantation.Materials and Methods: Orthotopic cardiac transplantations (HTx) in pigs were performed with a postoperative observation period of 24 hours (n = 6). To analyze myocardial function after transplantation, hemodynamical parameters (Swan-Ganz- and impedance-catheter data) as well as tissue and blood samples were obtained. Regional myocardial blood flow (RMBF) was assessed using fluorescent microspheres. Results: The impedance-catheter parameters demonstrated a preserved contractility in both ventricles 24 hours post-transplantation. In contrast, cardiac output 24 hours after HTx was diminished by 50% as compared to the preoperative value. Conversely, pulmonary vascular resistance increased significantly. The RMBF was increased in both ventricles. Metabolic and histological analyses indicate myocardial recovery 24 hours after HTx with no irreversible damage. Conclusions: For the first time, we were able to establish a porcine model to investigate myocardial function 24 hours after heart transplantation. While the contractility of the transplanted hearts was well-preserved, impaired cardiac output was going along with an increase in pulmonary vascular resistance. Using this clinical relevant model, improvements of human cardiac transplantation and post-transplant contractile dysfunction, especially, could be investigated. [source] Comparison of relaxation responses to multiple vasodilators in TxA2 -analog and endothelin-1-precontracted pulmonary arteriesACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 6 2007C. Piamsomboon Background:, Peri-operative pulmonary hypertension can lead to right ventricular dysfunction and to an increase in morbidity and mortality. Altered function of the pulmonary vascular endothelium and vasoconstriction play a crucial role in the development of elevated pulmonary vascular resistance. Because pulmonary artery vasoreactivity is dependent on many factors including the constricting agent that precipitated the event therefore the aim of the current study was to investigate the effectiveness of different classes of vasodilator agents to reverse endothelin-1 (ET-1) or thromboxane A2 (TxA2)-induced vasoconstriction in porcine pulmonary artery (PA) in vitro. Methods:, Relaxation responses to vasodilatory drugs were studied in PA precontracted with ET-1 (1 × 10,8 M) or TxA2 analog (U46619, 1 × 10,8 M). All vasodilating drugs were added in a cumulative fashion and isometric tension measurements were obtained using an organ chamber technique. Results:, In both groups relaxation responses to the vasodilators were dose dependent. When ET-1 was used as a constrictor nitroglycerin and milrinone caused nearly complete (80,100%) relaxation, whereas other agents were of limited effectiveness (40,50%). On the other hand, in the vessels constricted with U46619, olprinone, indomethacin, prostaglandin E1 (PGE1), nitroglycerin, milrinone and clevidipine induced complete (90,110%) vasodilatation but brain natriuretic peptide (BNP), l -arginine, and isoproterenol relaxed the vessels maximally by 45,60%. Conclusions:, Nitroglycerin and milrinone are very effective in reversing ET-1 and U46619-induced pulmonary vasoconstriction in vitro. The effectiveness of other drugs studied was dependent on the type of constrictor used. BNP, l -arginine and isoproterenol were shown to have minimal vasodilatory effects in porcine PA. [source] The haemodynamic response to propranolol in cirrhosis with arterial hypertension: a comparative analysis with normotensive cirrhotic patientsALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 1 2010P. Sharma Aliment Pharmacol Ther 2010; 32: 105,112 Summary Background, Cirrhosis with arterial hypertension is not uncommon. Haemodynamic alterations in these patients and the effects of beta-blocker on hepatic venous pressure gradient (HVPG) and systemic haemodynamics have not been evaluated. Aims, To compare the systemic haemodynamic alterations in hypertensive and normotensive cirrhotics, and to investigate the effects of propranolol on these parameters. Methods, A retrospective analysis of consecutive hypertensive cirrhotic patients (n = 33) who underwent haemodynamic assessment and paired HVPG measurement was done. Normotensive cirrhotics (n = 50) served as controls. Results, Hypertensive patients had a significantly higher heart rate, systemic (SVRI), and pulmonary vascular resistance. There was a significant reduction in mean arterial pressure (MAP) in the hypertensive cirrhotic group from 112 (107,130) mmHg to 95 (77,114) mmHg (P < 0.01), but no change in the normotensives. SVRI remained the same in the hypertensive cirrhotic group, but it increased in the normotensives. There was no correlation between MAP reduction and HVPG reduction. Conclusions, The frequency of HVPG response with propranolol treatment in hypertensive cirrhotics is similar to normotensive cirrhotics. Propranolol treatment reduces MAP significantly in hypertensive patients with cirrhosis. Treatment with a nonselective beta-blocker is a good strategy for hypertensive cirrhotic patients. [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] Retrospective Evaluation of Sildenafil Citrate as a Therapy for Pulmonary Hypertension in DogsJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 5 2006Jonathan F. Bach DACVIM (SA-IM) Pulmonary arterial hypertension (PH) is a pathologic condition in dogs characterized by abnormally high pressures in the pulmonary circulation and has been associated with a poor outcome. Sildenafil is a type V phosphodiesterase inhibitor that produces nitric oxide-mediated vasodilatation. Sildenafil treatment decreases pulmonary arterial pressure and pulmonary vascular resistance in people with PH. The purpose of this study was to describe the clinical characteristics and outcome of dogs with PH treated with sildenafil. The cardiology database was searched for dogs with PH treated with sildenafil. PH was defined as systolic pulmonary arterial pressure (PAPS) 25 mmHg at rest. Medical records were reviewed for the following information: signalment, duration and type of clinical signs before treatment, underlying disease, estimated or measured PAPS, dosage and dosing interval of sildenafil, and the effect of treatment on clinical signs and pulmonary arterial pressure and survival time. Thirteen affected dogs were identified. Clinical signs included collapse, syncope, respiratory distress, and cough. Duration of clinical signs before presentation ranged from 3 days to 5 months. An underlying cause was identified in 8 dogs. The median sildenafil dosage was 1.9 mg/kg. Ten dogs received concurrent medications. Median PAPS was 90 mmHg; 8 dogs were reevaluated after therapy, and the median decrease in PAPS was 16.5 mmHg. The median survival time of all dogs was 91 days. Sildenafil appeared to be well tolerated in dogs with PH and was associated with decreased PAPS and amelioration of clinical signs in most. Sildenafil represents a reasonable treatment option for dogs with pulmonary hypertension. [source] Liver transplantation in patients with severe portopulmonary hypertension treated with preoperative chronic intravenous epoprostenolLIVER TRANSPLANTATION, Issue 8 2001Henkie P. Tan MD Portopulmonary hypertension (PPHTN) is no longer an absolute contraindication to orthotopic liver transplantation (OLT). The pre-OLT management of patients with PPHTN requires early diagnosis and chronic therapy with intravenous epoprostenol to decrease pulmonary vascular resistance (PVR). Close follow-up is necessary to reassess pulmonary artery pressures (PAPs) and evaluate right ventricular (RV) function. This assists in the optimal timing of OLT. Successful management also necessitates reassessment of pulmonary artery hemodynamics just before OLT, with clearly defined parameters used to determine whether to proceed. Even with the intraoperative and postoperative availability of potent pulmonary vasodilators, clinical management may be suboptimal in reducing PAP. Adequate reduction in PVR and improvement in RV function in response to chronic epoprostenol therapy may facilitate successful OLT. We present a case report and review the limited experience with this treatment. [source] Haemodynamics in leptospirosis: Effects of plasmapheresis and continuous venovenous haemofiltrationNEPHROLOGY, Issue 1 2005TONGPRAKOB SIRIWANIJ SUMMARY: Background: Haemodynamics in leptospirosis may differ from that of sepsis because of frequently obeserved myocarditis and severe cholestatic jaundice. A haemodynamic study was therefore made in 10 patients with severe leptospirosis. Methods and Results: All patients had pulmonary complications with a chest X-ray showing either pulmonary oedema or infiltration. Renal failure was present in nine patients. Three patterns of haemodynamics were revealed. The first pattern was observed in six patients who showed increased cardiac index, decreased systemic vascular resistance, normal pulmonary capillary wedge pressure, normal pulmonary vascular resistance and hypotension. The pattern resembled that of sepsis. The second pattern shown in two patients with haemoptysis consisted of a normal cardiac index, normal systemic vascular resistance, normal blood pressure, normal pulmonary capillary wedge pressure and increased pulmonary vascular resistance. The third pattern was observed in two patients with severe jaundice who had hypotension, a relatively low cardiac index, increased systemic vascular resistance and normal pulmonary capillary wedge pressure, and pulmonary vascular resistance. Plasmapheresis performed in two patients and continuous venovenous haemofiltration performed in two patients improved systemic haemodynamics and normalized blood pressure with a resolution of lung signs. [source] Coronary and systemic hemodynamic effects of clevidipine, an ultra-short-acting calcium antagonist, for treatment of hypertension after coronary artery surgeryACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 2 2000N. Kieler-Jensen Background: The aim was to evaluate the use of clevidipine, a new vascular selective, ultra-short-acting calcium antagonist for blood pressure control after coronary artery bypass grafting (CABG). Methods: The effects of clevidipine on central hemodynamics, myocardial blood flow and metabolism were studied at two different phases after CABG. In phase 1 (n=13), the hypertensive phase, the effects of clevidipine were compared to those of sodium nitroprusside (SNP) when used to control postoperative hypertension. In phase 2 (n=9), the normotensive phase, a clevidipine dose-response relationship was established. Results: At a target mean arterial pressure (MAP) of 75 mmHg, systemic vascular resistance (SVR) and heart rate (HR) were lower, preload, stroke volume (SV) and pulmonary vascular resistance (PVR) were higher, while there were no differences in myocardial lactate metabolism or oxygen extraction with clevidipine compared to SNP. In the normotensive phase, clevidipine induced a dose-dependent decrease in MAP (,19%), SVR (,27%) and PVR (,15%), accompanied by an increase in SV (10%), but no reflex increase in HR or changes in cardiac preload. Clevidipine caused a direct coronary vasodilation, as indicated by a decrease in myocardial oxygen extraction from 54% to 45%. Myocardial lactate metabolism was unaffected by clevidipine. The blood clearance of clevidipine was 0.05 l ,· ,min,1 ,· ,kg,1, the volume of distribution at steady state was 0.08 l ,· ,kg,1 and the initial and terminal half-lives were <1 min and 4 min, respectively. Conclusions: Clevidipine rapidly reduced MAP and induced a systemic, pulmonary and coronary vasodilation with no effect on venous capacitance vessels or HR. Clevidipine caused no adverse effects on myocardial lactate metabolism. Clevidipine thus appears suitable to control blood pressure after CABG. [source] A simple method to reduce the inspiratory oxygen fraction for high pulmonary blood flow patients in an operating roomPEDIATRIC ANESTHESIA, Issue 12 2007AYAKO ASAKURA MD Summary Background:, Low inspired oxygen acutely increases pulmonary vascular resistance and decreases pulmonary-systemic blood flow ratio. We present a simple method to lower inspired oxygen fraction (FIO2 < 0.21) without supplemental nitrogen, during mechanical ventilation by an anesthesia machine. Methods:, After institutional approval, seven healthy adult volunteers and three infants (0,12 month old) scheduled for congenital heart surgery were enrolled in this study. All the infants were diagnosed with congestive heart failure because of high pulmonary blood flow and were thought to benefit from low FIO2. The volunteers performed spontaneous ventilation (fresh air flow rate = 10 l·min,1, tidal volume = 600 ml, frequency = 10 br·min,1). The infants were mechanically ventilated with air (fresh air flow rate = 6 l·min,1, tidal volume = 10 ml·kg,1, 15 < frequency < 30 br·min,1 to adjust PaCO2 between 5.8 kPa and 6.5 kPa (45,50 mmHg), after induction of general anesthesia and tracheal intubation. The fresh gas flow rates were determined by the following formula. Fresh gas flow rate = (FIO2 , FEO2) EVE/(0.21 + FIO2 , FEO2 , target FIO2). We recorded FIO2 every 5 min for 30 min. When arterial oxygen saturation decreased >15%, fresh gas flow rates were increased to adjust FIO2 to 0.21. Results:, In all of the seven volunteers and three infants target FIO2 was achieved in <10 min. FIO2 was kept at 0.18 ± 0.01 (SD) by calculated fresh air flow rates. In one infant, SpO2 decreased >15% 20 min after lowering FIO2, we had to discontinue this study, and increase fresh gas flow to ventilate the infant with FIO2 0.21. In the other two infants, FIO2 was maintained throughout the study. Conclusions:, This simple and convenient method to decrease FIO2, has a utility in clinical situations, in which pulmonary vascular resistance is to be increased to improve systemic oxygen delivery in patients with high pulmonary blood flow during cardiac surgery. [source] Combining low inspired oxygen and carbon dioxide during mechanical ventilation for the Norwood procedurePEDIATRIC ANESTHESIA, Issue 1 2003Ilan Keidan MD Summary Background: Staged reconstruction has become the preferred approach for treating neonates with hypoplastic left heart syndrome (HLHS). The haemodynamic instability of a single ventricle providing blood flow in parallel to the systemic and the pulmonary circulation, combined with the effects of cardiopulmonary bypass (CPB), results in precarious perioperative conditions. The two ventilatory manoeuvres commonly used for increasing pulmonary vascular resistance are (i) decreasing the fraction of inspired oxygen to <,0.21 and (ii) adding carbon dioxide (CO2) to the ventilatory circuit. Whether molecular nitrogen (N2) or CO2 is used in these situations is a matter of physician and institutional preference. The effect of the two modalities in combination has not been studied in depth. Methods: This prospective observational study was designed to look at the effects of adding inhaled CO2 to children with HLHS who were already on a hypoxic mixture during the immediate perioperative period. Results: Twelve suitable neonates were enrolled in the study. Combining the two ventilatory modalities had an additive effect. The effect was more significant in the prebypass (83% of patients) compared with the postbypass period (25% of patients). Conclusions: Low inspired oxygen and CO2 have an additive vasoconstrictive effect on the pulmonary vessels. The use of both of these ventilatory manoeuveres is less effective postoperatively compared with the prebypass period. [source] Neuronal nitric oxide synthase does not contribute to the modulation of pulmonary vascular tone in fetal lambs with congenital diaphragmatic hernia (nNOS in CDH lambs),PEDIATRIC PULMONOLOGY, Issue 4 2008Anthony S. de Buys Roessingh MD Abstract Aim The aim of this study was to determine the presence of the neuronal nitric oxide synthase (nNOS) in near full-term lambs with congenital diaphragmatic hernia (CDH) and its role in the modulation of pulmonary vascular basal tone. Methods We surgically created diaphragmatic hernia on the 85th day of gestation. On the 135th, catheters were used to measure pulmonary pressure and blood flow. We tested the effects of 7-nitroindazole (7-NINA), a specific nNOS antagonist and of N -nitro- l -arginine (l -NNA), a nonspecific nitric oxide synthase antagonist. In vitro, we tested the effects of the same drugs on isolated pulmonary vessels. The presence of nNOS protein in the lungs was detected by Western blot analysis. Results Neither 7-NINA nor l -NNA modified pulmonary vascular basal tone in vivo. After l -NNA injection, acetylcholine (ACh) did not decrease significantly pulmonary vascular resistance (PVR). In vitro, l -NNA increased the cholinergic contractile-response elicited by electric field stimulation (EFS) of vascular rings from lambs with diaphragmatic hernia. Conclusion We conclude that nNOS protein is present in the lungs and pulmonary artery of near full-term lamb fetuses with diaphragmatic hernia, but that it does not contribute to the reduction of pulmonary vascular tone at birth. Pediatr Pulmonol. 2008; 43:313,321. © 2008 Wiley-Liss, Inc. [source] | |||||||||||||||||||||||||||||||