			Home About us Contact

Systemic Vascular Resistance (systemic + vascular_resistance)

Distribution by Scientific Domains

Medical Sciences	92%

Distribution within Medical Sciences

Anesthesia & Pain Management	21%
General & Introductory Veterinary Medicine	18%
Cardiovascular Disease	7%
Hepatology	5%
14 Other Subdomains	49%

Terms modified by Systemic Vascular Resistance

systemic vascular resistance index

Selected Abstracts

Low Systemic Vascular Resistance After Cardiopulmonary Bypass: Incidence, Etiology, and Clinical Importance

JOURNAL OF CARDIAC SURGERY, Issue 5 2000
T. Carrel M.D.
The etiology is not completely elucidated and the clinical importance remains speculative. Methods: In this prospective clinical trial, we assessed the incidence of postoperative low systemic vascular resistance in 800 consecutive patients undergoing elective coronary artery bypass grafting and/or valve replacement. We have attempted to identify the predictive factors responsible for the presence of low systemic vascular resistance and we have examined the subsequent postoperative outcome of those patients who developed early postoperative vasoplegia. The severity of vasoplegia was divided into three groups according either to the value of systemic resistance and/or the dose of vasoconstrictive agents necessary to correct the hemodynamic. Results: Six hundred twenty-five patients (78.1%) did not develop vasoplegia, 115 patients (14.4%) developed a mild vasoplegia, and 60 patients (7.5%) suffered from severe vasoplegia. Low systemic vascular resistance did not affect hospital mortality but was the cause for delayed extubation and prolonged stay on the intensive care unit IICU). Logistic regression analysis identified temperature and duration of cardiopulmonary bypass, total cardioplegic volume infused, reduced left ventricular function, and preoperative treatment with angiotensin-converting enzyme (ACE)-inhibitors, out of 25 parameters, as predictive factors for early postoperative vasoplegia. Conclusion. The occurrence of low systemic vascular resistance following cardiopulmonary bypass is as high as 21.8%. The etiology of this clinical condition is most probably multifactorial. Mortality is not affected by vasoplegia, but there is a trend to higher morbidity and prolonged stay in the ICU. [source]

Change in Vasoconstrictive Function During Prolonged Nonpulsatile Left Heart Bypass

ARTIFICIAL ORGANS, Issue 5 2001
Tomohiro Nishinaka
Abstract: We investigated changes in vasoconstrictive function accompanying prolonged nonpulsatile left heart bypass (NLHB). After 2-week pulsatile left heart bypass (PLHB) in 11 goats, NLHB was conducted for another 4 weeks (Group N) in 6 goats. In the other 5 goats, PLHB was continued for another 4 weeks (Group P). Systemic vascular resistance at rest (rSVR) was measured on the last days of the second and sixth postoperative week (W2 and W6, respectively). Subsequently, phenylephrine was injected, and the maximum values (SVRmax) and the maximum increasing change in SVR (,SVR) were measured. No significant difference was observed in rSVR between groups at W2 or W6. The SVRmax and the ,SVR at W2 were consistent in both groups. However, at W6, the SVRmax and the ,SVR of Group N were significantly lower than those of Group P. In conclusion, prolonged NLHB caused a significant decrease in the SVR response to phenylephrine, indicating a dimunition of vasoconstrictive function. [source]

Cardiovascular function in the heat-stressed human

ACTA PHYSIOLOGICA, Issue 4 2010
C. G. Crandall
Abstract Heat stress, whether passive (i.e. exposure to elevated environmental temperatures) or via exercise, results in pronounced cardiovascular adjustments that are necessary for adequate temperature regulation as well as perfusion of the exercising muscle, heart and brain. The available data suggest that generally during passive heat stress baroreflex control of heart rate and sympathetic nerve activity are unchanged, while baroreflex control of systemic vascular resistance may be impaired perhaps due to attenuated vasoconstrictor responsiveness of the cutaneous circulation. Heat stress improves left ventricular systolic function, evidenced by increased cardiac contractility, thereby maintaining stroke volume despite large reductions in ventricular filling pressures. Heat stress-induced reductions in cerebral perfusion likely contribute to the recognized effect of this thermal condition in reducing orthostatic tolerance, although the mechanism(s) by which this occurs is not completely understood. The combination of intense whole-body exercise and environmental heat stress or dehydration-induced hyperthermia results in significant cardiovascular strain prior to exhaustion, which is characterized by reductions in cardiac output, stroke volume, arterial pressure and blood flow to the brain, skin and exercising muscle. These alterations in cardiovascular function and regulation late in heat stress/dehydration exercise might involve the interplay of both local and central reflexes, the contribution of which is presently unresolved. [source]

Blunted Hemodynamic Response and Reduced Oxygen Delivery With Exercise in Anemic Heart Failure Patients With Systolic Dysfunction

CONGESTIVE HEART FAILURE, Issue 2 2007
Jennifer Listerman MD
Anemic heart failure patients with systolic dysfunction are known to have reduced exercise capacity. Whether this is related to poor hemodynamic adaptation to anemia is not known. Peak exercise oxygen consumption (VO2) and hemodynamics at rest and peak exercise were assessed among 209 patients and compared among those who were (n=90) and were not (n=119) anemic. Peak VO2 was significantly lower among anemic patients (11.7±3.3 mL/min/kg vs 13.4±3.1 mL/min/kg; P=.01). At rest, right atrial pressure was higher (10±5 mm Hg vs 8±4 mm Hg; P=.02) and venous oxygen saturation lower (62%±8% vs 58%±10%; P<.01) among anemic patients. At peak exercise, anemic patients had a higher wedge pressure (27±9 mm Hg vs 24±10 mm Hg; P=.04). No significant differences in stroke volume, cardiac index, systemic vascular resistance, or oxygen saturation were noted between the 2 groups. In conclusion, the relative hemodynamic response to exercise among anemic heart failure patients appears blunted and may contribute to worse exercise tolerance. [source]

Central and peripheral cardiovascular adaptations to exercise in endurance-trained children

ACTA PHYSIOLOGICA, Issue 2 2002
S. NOTTIN
ABSTRACT Stroke volume (SV) response to exercise depends on changes in cardiac filling, intrinsic myocardial contractility and left ventricular afterload. The aim of the present study was to identify whether these variables are influenced by endurance training in pre-pubertal children during a maximal cycle test. SV, cardiac output (Doppler echocardiography), left ventricular dimensions (time,movement echocardiography) as well as arterial pressure and systemic vascular resistances were assessed in 10 child cyclists (VO2max: 58.5 ± 4.4 mL min,1 kg,1) and 13 untrained children (UTC) (VO2max: 45.9 ± 6.7 mL min,1 kg,1). All variables were measured at the end of the resting period, during the final minute of each workload and during the last minute of the progressive maximal aerobic test. At rest and during exercise, stroke index was significantly higher in the child cyclists than in UTC. However, the SV patterns were strictly similar for both groups. Moreover, the patterns of diastolic and systolic left ventricular dimensions, and the pattern of systemic vascular resistance of the child cyclists mimicked those of the UTC. SV patterns, as well as their underlying mechanisms, were not altered by endurance training in children. This result implied that the higher maximal SV obtained in child cyclists depended on factors influencing resting SV, such as cardiac hypertrophy, augmented myocardium relaxation properties or expanded blood volume. [source]

Subclinical vascular alterations in young adults with type 1 diabetes detected by arterial tonometry

DIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 8 2009
I. Barchetta
Abstract Background Diabetes mellitus is characterized by a very high prevalence of atherosclerotic disease. Aims of this study were to determine arterial compliance parameters in type 1 diabetes (T1D) patients as an expression of early pre-clinical endothelial dysfunction and to evaluate the impact of glucose exposure parameters such as the duration of diabetes and glycosylated haemoglobin (HbA1c) on the risk of developing alterations in vascular compliance. Methods 23 patients with uncomplicated type 1 diabetes (mean age: 32.78 ± 9.06 years, mean disease duration: 10.78 ± 7.51 years, mean HbA1c levels: 7.7 ± 1.9) and 26 age- and sex-matched healthy subjects (mean age: 32.3 ± 8.51 years) were recruited. In these subjects, we evaluated arterial compliance by calibrated tonometry (HDI/PulsewaveÔ CR-2000). Parameters included the following: large artery elasticity (C1), small artery elasticity (C2), systemic vascular resistance (SVR) and total vascular impedance (TVI). Results Patients with longer duration of T1D (>10 years) showed significant alterations in C2 (4.97 ± 2.7 mL/mmHg × 100) and in SVR (1464.67 ± 169.16 dina × s × cm,5) when compared with both healthy individuals (C2: 8.28 ± 2.67 mL/mmHg × 100, p = 0.001; SVR: 1180.58 ± 151.55 dina × s × cm,5, p = 0.01) and patients with recent-onset disease (,10 years) (C2: 10.02 ± 3.6 mL/mmHg × 100, p < 0.001; SVR: 1124.18 ± 178.5 dina × s × cm,5, p < 0.000). Both disease duration and HbA1c independently predicted impaired arterial compliance. Conclusions Young adult T1D patients with no signs of disease complication have detectable vessel wall abnormalities, particularly of small arteries, suggestive of hyperglycaemia-related early endothelial dysfunction. Copyright © 2009 John Wiley & Sons, Ltd. [source]

Acute Cardiac Effects of Nicotine in Healthy Young Adults

ECHOCARDIOGRAPHY, Issue 6 2002
Catherine D. Jolma M.D.
Background: Nicotine is known to have many physiologic effects. The influence of nicotine delivered in chewing gum upon cardiac hemodynamics and conduction has not been well-characterized. Methods: We studied the effects of nicotine in nonsmoking adults (6 male, 5 female; ages 23,36 years) using a double-blind, randomized, cross-over study. Subjects chewed nicotine gum (4 mg) or placebo. After 20 minutes (approximate time to peak nicotine levels), echocardiograms and signal-averaged electrocardiograms (SAECG) were obtained. After 40 minutes, subjects were again given nicotine gum or placebo in cross-over fashion. Standard echocardiographic measurements were made from two-dimensional images. We then calculated end-systolic wall stress (ESWS), shortening fraction (SF), systemic vascular resistance (SVR), velocity for circumferential fiber shortening corrected for heart rate (Vcfc), stroke volume, and cardiac output. P wave and QRS duration were measured from SAECG. Results: Significant differences (P < 0.05) from control or placebo were found for ESWS, mean blood pressure, cardiac output, SVR, heart rate, and P wave duration. No significant changes were seen in left ventricular ejection time (LVET), LV dimensions, SF, contractility (Vcfc), or QRS duration. Conclusions: These results suggest that nicotine chewing gum increases afterload and cardiac output. Cardiac contractility does not change acutely in response to nicotine gum. Heart rate and P wave duration are increased by chewing nicotine gum. [source]

Cardiopulmonary, blood and peritoneal fluid alterations associated with abdominal insufflation of carbon dioxide in standing horses

EQUINE VETERINARY JOURNAL, Issue 3 2003
F. 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]

Equine pulmonary and systemic haemodynamic responses to endothelin-1 and a selective ETA receptor antagonist

EQUINE VETERINARY JOURNAL, Issue 4 2001
A. 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]

Asymmetric dimethylarginine (ADMA): the silent transition from an ,uraemic toxin' to a global cardiovascular risk molecule

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 2 2005
D. Fliser
Abstract Endothelial dysfunction as a result of reduced bioavailability of nitric oxide (NO) plays a central role in the process of atherosclerotic vascular disease. In endothelial cells NO is synthesized from the amino acid l -arginine by the action of the NO synthase (NOS), which can be blocked by endogenous inhibitors such as asymmetric dimethylarginine (ADMA). Acute systemic administration of ADMA to healthy subjects significantly reduces NO generation, and causes an increase in systemic vascular resistance and blood pressure. Increased plasma ADMA levels as a result of reduced renal excretion have been associated with atherosclerotic complications in patients with terminal renal failure. However, a significant relationship between ADMA and traditional cardiovascular risk factors such as advanced age, high blood pressure and serum LDL-cholesterol, has been documented even in individuals without manifest renal dysfunction. As a consequence, the metabolism of ADMA by the enzyme dimethylarginine dimethylaminohydrolase (DDAH) has come into the focus of cardiovascular research. It has been proposed that dysregulation of DDAH with consecutive increase in plasma ADMA concentration and chronic NOS inhibition is a common pathophysiological pathway in numerous clinical conditions. Thus, ADMA has emerged as a potential mediator of atherosclerotic complications in patients with coronary heart disease, peripheral vascular disease, stroke, etc., being the culprit and not only an innocent biochemical marker of the atherosclerotic disease process. [source]

Increased lipopolysaccharide binding protein in cirrhotic patients with marked immune and hemodynamic derangement

HEPATOLOGY, Issue 1 2003
Agustín Albillos
Intestinal bacterial overgrowth and translocation, both common in cirrhosis with ascites, may lead to the activation of monocytes and lymphocytes, increased levels of proinflammatory cytokines, and enhanced synthesis of nitric oxide present in cirrhosis. Bacterial endotoxin promotes the synthesis of lipopolysaccharide (LPS)-binding protein (LBP), and forms a LPS-LBP complex that binds to CD14. This study was designed to evaluate LBP levels and their correlation to the immune response and the hemodynamic status in cirrhotic patients. Plasma LBP, endotoxin, soluble CD14 (sCD14), cytokines, renin, nitrites, and systemic vascular resistance were determined before and 4 weeks after norfloxacin or placebo in 102 cirrhotic patients and 30 controls. LBP was elevated in 42% of ascitic cirrhotic patients (15.7 ± 0.7 versus 6.06 ± 0.5 ,g/mL, P < .01). In 60% of high LBP patients, endotoxin was within normal range. Among ascitic patients, those with high LBP showed greater (P < .05) levels of sCD14, tumor necrosis factor , (TNF-,), interleukin 6 (IL-6), nitrites + nitrates (NOx)/creatinine, and renin, and lower vascular resistance. In the cirrhotic patients with high LBP, norfloxacin normalized (P < .01) LBP (from 16.6 ± 0.5 to 5.82 ± 0.8 , g/mL) and sCD14; reduced the level of cytokines, NOx/creatinine, and renin; and increased vascular resistance; but lacked effect in patients with normal LBP. Portal pressure was unchanged after norfloxacin in another group of 18 cirrhotic patients with high and 19 with normal LBP. In conclusion, the subset of ascitic cirrhotic patients with marked immune and hemodynamic derangement is identified by increased LBP levels. Amelioration of these abnormalities by norfloxacin suggests the involvement of enteric bacteria or their products in the triggering of the process. [source]

Scintigraphic evaluation of intrapulmonary shunt in normoxemic cirrhotic patients and effects of terlipressin

HEPATOLOGY RESEARCH, Issue 10 2010
George 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]

Cardiovascular and Metabolic Effects of High-dose Insulin in a Porcine Septic Shock Model

ACADEMIC EMERGENCY MEDICINE, Issue 4 2010
Joel 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]

Differential effects of sevoflurane and propofol anesthesia on left ventricular,arterial coupling in dogs

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 8 2010
Y. L. J. M. DERYCK
Background: General anesthetics interfere with arterial and ventricular mechanical properties, often altering left ventricular,arterial (LVA) coupling. We hypothesized that sevoflurane and propofol alter LVA coupling by different effects on arterial and ventricular properties. Methods: Experiments were conducted in six anesthetized open-chest dogs for the measurement of left ventricular pressure and aortic pressure and flow. Measurements were performed during anesthesia with 0.5, 1.0 and 1.5 minimum alveolar concentration sevoflurane and 12, 24 and 36 mg/kg/h propofol. LVA coupling was assessed as the ratio of ventricular end-systolic elastance (Ees, measuring ventricular contractility) to effective arterial elastance (Ea, measuring ventricular afterload). The steady component of afterload, arterial tone, was assessed by systemic vascular resistance and arterial pressure,flow curves. The pulsatile component of afterload was assessed by aortic impedance and compliance. Results: Sevoflurane decreased aortic pressure and cardiac output more than propofol. Sevoflurane reduced arterial tone, increased arterial stiffness and did not affect wave reflections. It increased Ea, decreased Ees and reduced LVA coupling. Propofol reduced arterial tone, did not affect arterial stiffness and decreased wave reflections. It did not affect Ea, Ees or LVA coupling. Conclusions: Sevoflurane increased ventricular afterload and decreased ventricular performance, thereby altering LVA coupling. Propofol did not affect ventricular afterload or ventricular performance, thereby preserving LVA coupling. Thus, propofol preserves LVA coupling in dogs better, and might be a better choice for patients with compromised left ventricular function. [source]

Haemodynamic effects of ,75 mmHg negative pressure therapy in a porcine sternotomy wound model

INTERNATIONAL WOUND JOURNAL, Issue 1 2009
Arash 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]

Low Systemic Vascular Resistance After Cardiopulmonary Bypass: Incidence, Etiology, and Clinical Importance

Hyperthyroidism: A Secondary Cause of Isolated Systolic Hypertension

JOURNAL OF CLINICAL HYPERTENSION, Issue 8 2006
L. Michael Prisant MD
Isolated systolic hypertension is the most common form of hypertension, especially among patients 50 years or older. What is not appreciated is that there are secondary causes of isolated systolic hypertension. Hyperthyroidism increases systolic blood pressure by decreasing systemic vascular resistance, increasing heart rate, and raising cardiac output. Potential cardiovascular consequences of hyperthyroidism include atrial arrhythmias (especially atrial fibrillation), pulmonary hypertension, left ventricular hypertrophy, and heart failure. The prevalence of hypertension is greater among hyperthyroid patients than euthyroid patients. Whether there is a blunted nocturnal decline in ambulatory blood pressure among hyperthyroid patients is more controversial. Treatment is associated with a reduction in systolic blood pressure, heart rate, and cardiac output. [source]

Vasopressin decreases intestinal mucosal perfusion: a clinical study on cardiac surgery patients in vasodilatory shock

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 5 2009
A. NYGREN
Background: Low to moderate doses of vasopressin have been used in the treatment of cathecholamine-dependent vasodilatory shock in sepsis or after cardiac surgery. We evaluated the effects of vasopressin on jejunal mucosal perfusion, gastric-arterial pCO2 gradient and the global splanchnic oxygen demand/supply relationship in patients with vasodilatory shock after cardiac surgery. Methods: Eight mechanically ventilated patients, dependent on norepinephrine to maintain mean arterial pressure (MAP) ,60 mmHg because of septic/post-cardiotomy vasodilatory shock and multiple organ failure after cardiac surgery, were included. Vasopressin was sequentially infused at 1.2, 2.4 and 4.8 U/h for 30-min periods. Norepinephrine was simultaneously decreased to maintain MAP at 75 mmHg. At each infusion rate of vasopressin, data on systemic hemodynamics, jejunal mucosal perfusion, jejunal mucosal hematocrit and red blood cell velocity (laser Doppler flowmetry) as well as gastric-arterial pCO2 gradient (gastric tonometry) and splanchnic oxygen and lactate extraction (hepatic vein catheter) were obtained. Results: The cardiac index, stroke volume index and systemic oxygen delivery decreased and systemic vascular resistance and systemic oxygen extraction increased significantly, while the heart rate or global oxygen consumption did not change with increasing vasopressin dose. Jejunal mucosal perfusion decreased and the arterial-gastric-mucosal pCO2 gradient increased, while splanchnic oxygen or lactate extraction or mixed venous,hepatic venous oxygen saturation gradient were not affected by increasing infusion rates of vasopressin. Conclusions: Infusion of low to moderate doses of vasopressin in patients with norepinephrine-dependent vasodilatory shock after cardiac surgery induces an intestinal and gastric mucosal vasoconstriction. [source]

Trauma: physiology, pathophysiology, and clinical implications

JOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE, Issue 4 2006
DACVA, DACVECC, William Muir DVM
Abstract Objective: To review the physiology, pathophysiology, and consequences of trauma. The therapeutic implications of hypovolemia, hypotension, hypothermia, tissue blood flow, oxygen delivery, and pain will be discussed. Data Sources: Human and veterinary clinical and research studies. Human and veterinary data synthesis: Trauma is defined as tissue injury that occurs more or less suddenly as a result of violence or accident and is responsible for initiating hyothalamic,pituitary,adrenal axis, immunologic and metabolic responses that are designed to restore homeostasis. Tissue injury, hemorrhage, pain, and fear are key components of any traumatic event. Trauma and blood loss result in centrally integrated autonomic-mediated cardiovascular responses that are designed to increase heart rate, systemic vascular resistance, and maintain arterial blood pressure (ABP) to vital organs at the expense of blood flow to the gut and skeletal muscle. Severe trauma elicits exuberant physiologic, immunologic, and metabolic changes predisposing the animal to organ malfunction, a systemic inflammatory response, infection, and multiple organ dysfunctions. The combination of both central and local influences produces regional redistribution of blood flow among and within tissue beds which, when combined with impaired vascular reactivity, leads to maldistribution of blood flow to tissues predisposing to tissue hypoperfusion and impaired oxygen delivery and extraction. Gut blood flow and viability may serve as a sentinel of patient survival. These consequences are magnified in animals suffering from pain or that become hypothermic. Successful treatment of traumatized animals goes beyond the restoration of blood pressure and urine output, is dependent on a fundamental understanding of the pathophysiologic processes responsible for the animals current physical status, and incorporates the reduction of pain, stress, and the systemic inflammatory response and methods that restore microcirculatory blood flow and tissue oxygenation. Conclusions: Severe trauma is a multifaceted event and is exacerbated by hypothermia, pain, and stress. Therapeutic approaches must go beyond the simple restoration of vascular volume and ABP by maintaining tissue blood flow, restoring tissue oxygenation, and preventing systemic inflammation. [source]

Cardiovascular effects of desflurane following acute hemorrhage in dogs

JOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE, Issue 1 2003
Paulo S.P. Santos DVM
Abstract Objective: To determine the cardiovascular effects of desflurane in dogs following acute hemorrhage. Design: Experimental study. Animals: Eight mix breed dogs. Interventions: Hemorrhage was induced by withdrawal of blood until mean arterial pressure (MAP) dropped to 60 mmHg in conscious dogs. Blood pressure was maintained at 60 mmHg for 1 hour by further removal or replacement of blood. Desflurane was delivered by facemask until endotracheal intubation could be performed and a desflurane expiratory end-tidal concentration of 10.5 V% was maintained. Measurements and main results: Systolic, diastolic, and mean arterial blood pressure (SAP, DAP and MAP), central venous pressure (CVP), cardiac output (CO), stroke volume (SV), cardiac index (CI), systemic vascular resistance (SVR), heart rate (HR), respiratory rate (RR), partial pressure of carbon dioxide in arterial blood (PaCO2), and arterial pH were recorded before and 60 minutes after hemorrhage, and 5, 15, 30, 45 and 60 minutes after intubation. Sixty minutes after hemorrhage, SAP, DAP, MAP, CVP, CO, CI, SV, PaCO2, and arterial pH decreased, and HR and RR increased when compared with baselines values. Immediately after intubation, MAP and arterial pH decreased, and PaCO2 increased. Fifteen minutes after intubation SAP, DAP, MAP, arterial pH, and SVR decreased. At 30 and 45 minutes, MAP and DAP remained decreased and PaCO2 increased, compared with values measured after hemorrhage. Arterial pH increased after 30 minutes of desflurane administration compared with values measured 5 minutes after intubation. Conclusions: Desflurane induced significant changes in blood pressure and arterial pH when administered to dogs following acute hemorrhage. [source]

Pressor Therapy in Critically III Patients

JOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE, Issue 1 2000
ACVECC, ACVIM, James S. Wohl DVM Diplomate
Summary Vasopressors are agents that increase systemic vascular resistance by increasing vasoconstriction. Therapy with intravenous vasopressors may be required in critically ill patients when efforts to optimize cardiac output and blood pressure with intravascular fluid therapy fail. Increasing systemic vascular resistance can promote a favorable perfusion pressure gradient to vital organs in critically ill patients with severe, unresponsive vasodilation. Improperly administered, vasopressors may impede cardiac output and reduce oxygen transport to vital tissue sites. The understanding of systemic and regional effects of vasopressors is currently evolving. Recent literature of the commonly used agents is reviewed. Individual drugs, drug combinations, and potential new therapies are discussed. (Vet. Emerg. & Crit. Care, 10:19,33, 2000) [source]

The Effect of Angiotensin-Converting Enzyme Inhibitors of Left Atrial Pressure in Dogs with Mitral Valve Regurgitation

JOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 2 2010
T. Ishikawa
Background: Despite many epidemiological reports concerning the efficacy of angiotensin-converting enzyme (ACE) inhibitors in dogs with mitral regurgitation (MR), the hemodynamic effects of ACE inhibitor administration have not been fully evaluated. Objectives: To document left atrial pressure (LAP) in dogs with MR administered ACE inhibitors, in order to obtain interesting information about daily LAP changes with administration of ACE inhibitors. Animals: Five healthy Beagle dogs weighing 9.8 to 14.2 kg (2 males and 3 females; aged 2 years). Methods: Experimental, crossover, and interventional study. Chordae tendineae rupture was induced, and a radiotelemetry transmitter catheter was inserted into the left atrium. LAP was recorded for 72 consecutive hours during which each of 3 ACE inhibitors,enalapril (0.5 mg/kg/d), temocapril (0.1 mg/kg/d), and alacepril (3.0 mg/kg/d),were administered in a crossover study. Results: Averaged diurnal LAP was significantly, but slightly reduced by alacepril (P= .03, 19.03 ± 3.01,18.24 ± 3.07 mmHg). The nightly drops in LAP caused by alacepril and enalapril were significantly higher than the daily drops (P= .03, ,0.98 ± 0.19 to ,0.07 ± 0.25 mmHg, and P= .03, ,0.54 ± 0.21,0.02 ± 0.17 mmHg, respectively), despite the fact that the oral administrations were given in the morning. Systolic blood pressure (122.7 ± 14.4,117.4 ± 13.1 mmHg, P= .04) and systemic vascular resistance (5800 ± 2685,5144 ± 2077 dyne × s/cm5, P= .03) were decreased by ACE inhibitors. Conclusions and Clinical Importance: ACE inhibitors decrease LAP minimally, despite reductions in left ventricular afterload. ACE inhibitors should not be used to decrease LAP. [source]

Effects of Norepinephrine and Combined Norepinephrine and Fenoldopam Infusion on Systemic Hemodynamics and Indices of Renal Function in Normotensive Neonatal Foals

JOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 5 2008
A.R. Hollis
Background: Norepinephrine increases arterial blood pressure but may have adverse effects on renal blood flow. Fenoldopam, a dopamine-1 receptor agonist, increases urine output in normotensive foals. The combination of norepinephrine and fenoldopam may lead to improved renal perfusion compared with an infusion of norepinephrine alone. The combined effects of these drugs have not been reported in the horse. Hypothesis: Norepinephrine will alter the hemodynamic profile of foals without affecting renal function. Addition of fenoldopam will change the renal profile during the infusions without changing the hemodynamic profile. Animals: Five conscious pony foals. Methods: Each foal received norepinephrine (0.3 ,g/kg/min), combined norepinephrine (0.3 ,g/kg/min) and fenoldopam (0.04 ,g/kg/min), and a control dose of saline in a masked, placebo-controlled study. Heart rate (HR), arterial blood pressure (direct), and cardiac output (lithium dilution) were measured, and systemic vascular resistance (SVR), stroke volume, cardiac index (CI), and stroke volume index were calculated. Urine output, creatinine clearance, and fractional excretion of electrolytes were measured. Results: Norepinephrine and a combined norepinephrine and fenoldopam infusion increased arterial blood pressure, SVR, urine output, and creatinine clearance and decreased HR and CI compared with saline. The combination resulted in higher HR and lower arterial blood pressure than norepinephrine alone. Conclusions and Clinical Importance: Norepinephrine might be useful for hypotensive foals, because in normal foals, this infusion rate increases SVR without negatively affecting renal function (creatinine clearance increased). Fenoldopam does not provide additional benefit to renal function. These findings warrant further investigation. [source]

Cardiovascular and Pulmonary Effects of Hetastarch Plus Hypertonic Saline Solutions during Experimental Endotoxemia in Anesthetized Horses

JOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 6 2006
DACVIM, Lucas G. Pantaleon MV
Background:Small volume resuscitation has been advocated as a beneficial therapy for endotoxemia in horses but this therapy has not been investigated in a prospective manner. The objective of this study was to determine the cardiopulmonary effects of small-volume resuscitation using hypertonic saline solution (HSS) plus Hetastarch (HES) during experimental endotoxemia in anesthetized horses. Hypothesis:Treatment of horses with induced endotoxemia using HES-HSS does not alter the response of various cardiopulmonary indices when compared to treatment with either small-or large-volume isotonic crystalloid solutions. Animals:Eighteen healthy horses were randomly assigned to 1 of 3 groups. Anesthesia was maintained with halothane. Endotoxemia was induced by administering 50 ,g/kg of Escherichia coli endotoxin IV. The horses were treated over 30 minutes with 15 mL/kg of balanced polyionic crystalloid solution (control), 60 mL/kg of balanced polyionic crystalloid solution (ISO), or 5 mL/kg of HSS followed by 10 mL/kg of HES (HSS-HES). Methods:Prospective randomized trial. Results:Cardiac output (CO) after endotoxin infusion increased significantly (P < .05) from baseline in all groups, whereas mean central venous pressure increased significantly (P < .05) in the ISO group only. Mean pulmonary artery pressure increased from baseline (P < .05) in horses treated with isotonic fluids and HSS-HES. There was no effect of treatment with HSS-HES on CO, systemic vascular resistance (SVR), mean arterial pressure, blood lactate concentrations, or arterial oxygenation. Conclusions and Clinical Importance: The use of HSS-HES failed to ameliorate the deleterious hemodynamic responses associated with endotoxemia in horses. The clinical value of this treatment in horses with endotoxemia remains unconfirmed. [source]

Acute systemic, splanchnic and renal haemodynamic changes induced by molecular adsorbent recirculating system (MARS) treatment in patients with end-stage cirrhosis

ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 5 2007
G. DONATI
Summary Aim To evaluate the acute effect of treatment with the molecular adsorbent recirculating system (MARS) on splanchnic, renal and systemic haemodynamics in patients with end-stage cirrhosis. Methods Twelve patients with end-stage cirrhosis, undergoing MARS treatment, were enrolled. The following haemodynamic parameters were measured by means of Doppler ultrasonography and thoracic electrical bioimpedance, before and after each session: portal velocity, renal and splenic resistance indices, cardiac output, cardiac stroke volume, heart rate, mean arterial pressure, systemic vascular resistance. Results Median portal velocity increased significantly after treatment (23.7 vs. 20.3 cm/s, P < 0.05) while renal resistance index (0.72 vs. 0.75, P < 0.05) and splenic resistance index (0.60 vs. 0.65, P < 0.05) decreased significantly. Mean arterial pressure (83 vs. 81 mmHg, P < 0.05) and vascular resistance (899 vs. 749 dyne. s/cm5, P < 0.05) increased significantly, while cardiac output and stroke volume showed no significant changes. Conclusions Data emerging from this investigation suggest that MARS treatment improves significantly various haemodynamic alterations in cirrhotic patients in the short term. The observed decrease in renal vascular resistance and improvement in splenic resistance index, a parameter related to portal resistance, which leads us to hypothesize that these haemodynamic effects are probably mediated by clearance of vasoactive substances during MARS treatment. [source]

Comparison of calibrated and uncalibrated arterial pressure,based cardiac output monitors during orthotopic liver transplantation,

LIVER TRANSPLANTATION, Issue 6 2010
Vladimir 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]

Anesthesia for free vascularized tissue transfer

MICROSURGERY, Issue 2 2009
Natalia Hagau M.D., Ph.D.
Anesthesia may be an important factor in maximizing the success of microsurgery by controlling the hemodynamics and the regional blood flow. The intraanesthetic basic goal is to maintain an optimal blood flow for the vascularized free flap by: increasing the circulatory blood flow, maintaining a normal body temperature to avoid peripheral vasoconstriction, reducing vasoconstriction resulted from pain, anxiety, hyperventilation, or some drugs, treating hypotension caused by extensive sympathetic block and low cardiac output. A hyperdynamic circulation can be obtained by hypervolemic or normovolemic hemodilution and by decrease of systemic vascular resistance. The importance of proper volume replacement has been widely accepted, but the optimal strategy is still open to debate. General anesthesia combined with various types of regional anesthesia is largely preferred for microvascular surgery. Maintenance of homeostasis through avoidance of hyperoxia, hypocapnia, and hypovolemia (all factors that can decrease cardiac output and induce local vasoconstriction) is a well-established perioperative goal. As the ischemia,reperfusion injury could occur, inhalatory anesthetics as sevoflurane (that attenuate the consequences of this process) seem to be the anesthetics of choice. © 2008 Wiley-Liss, Inc. Microsurgery, 2009. [source]

Pneumoperitoneum versus abdominal wall lift: effects on central haemodynamics and intrathoracic pressure during laparoscopic cholecystectomy

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 7 2003
L. Andersson
Background:, It has been shown repeatedly that laparoscopic cholecystectomy using pneumoperitoneum (CO2 insufflation) may be associated with increased cardiac filling pressures and an increase in blood pressure and systemic vascular resistance. In the present study, the effects on the central circulation during abdominal wall lift (a gasless method of laparoscopic cholecystectomy) were compared with those during pneumoperitoneum. The study was also aimed at elucidating the relationships between the central filling pressures and the intrathoracic pressure. Methods:, Twenty patients (ASA I), scheduled for laparoscopic cholecystectomy, were randomised into two groups, pneumoperitoneum or abdominal wall lift. Measurements were made by arterial and pulmonary arterial catheterization before and during pneumoperitoneum or abdominal wall lift with the patient in the horizontal position. Measurements were repeated after head-up tilting the patients as well as after 30 min head-up tilt. The intrathoracic pressure was monitored in the horizontal position before and during intervention using an intraesophageal balloon. Results:, After pneumoperitoneum or abdominal wall lifting there were significant differences between the two groups regarding MAP, SVR, CVP, CI, and SV. Analogous to previous studies, in the pneumoperitoneum group CVP, PCWP, MPAP, and MAP as well as SVR were increased after CO2 insufflation (P < 0.01), while CI and SV were not affected. In contrast, in the abdominal wall lift group, CI and SV were significantly increased (P < 0.01), as was MAP (P < 0.01), while CVP, PCWP, MPAP, and SVR were not significantly affected. There was a significant difference in intraesophageal pressure between the two groups. In the pneumoperitoneum group, the intraesophageal pressure was increased by insufflation (P < 0.01) while, in the abdominal wall lift group, it was unaffected. In the pneumoperitoneum group the mean increases in cardiac filling pressures were of the same magnitude as the mean increase in the intraesophageal pressure. Conclusions:, In healthy patients, abdominal wall lift increased cardiac index while pneumoperitoneum did not. Cardiac filling pressures and systemic vascular resistance were increased by pneumoperitoneum but unaffected by abdominal wall lift. The recorded elevated cardiac filling pressures during pneumoperitoneum may be only a reflection of the increased intra-abdominal pressure. [source]

Haemodynamics in leptospirosis: Effects of plasmapheresis and continuous venovenous haemofiltration

NEPHROLOGY, Issue 1 2005
TONGPRAKOB 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 surgery

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 2 2000
N. 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]