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[Repercussion on the hemodynamic measurements across a Swan-Ganz catheter with the postural changes].

AIM: Usually hemodynamic measures are done with the patient in dorsal decubitus and the bedside at 0 degrees. Our aim has been to evaluate the influence that postural changes has in the hemodynamic measures which were carried out with a pulmonary artery catheter, so as called Swan-Ganz. MATERIAL AND METHOD: It's a prospective study. The same patient is control group and study group. There were done tree consecutive measures in each patient. Firstly in dorsal decubitus, then right lateral decubitus and finally in left lateral decubitus. Before doing the measures after change of posture a thirty minutes period was left in order to stabilise the hemodynamical flow. The items of study were, a part of demographic ones, cardiac index, pulmonary artery systolic pressure, pulmonary artery diastolic pressure, pulmonary artery mean pressure, pulmonary artery occlusion pressure, right atrial pressure, systolic arterial pressure, diastolic arterial pressure, mean arterial pressure and heart rate. 28 patients were included in the study. RESULTS: The age average was 62.5 years (27.05-67.05); a 78.6% were male. Who had a NEMS average of 42.4 (39.9-44.9). No difference was found between hemodynamic measures in the different postures. CONCLUSIONS: Postural changes in stable patients have no influence in pressures and other hemodynamic variables measures.

Adult↗
PubMed2002

Acute and chronic adaptation to hemodynamic overload and ischemia in the aged heart.

Congestive heart failure occurs more frequently in older individuals. This higher incidence of heart failure may be caused by the diminished capacity of aged hearts to adapt to increased hemodynamic overload and ischemia which are the most important triggers for heart failure in the aged. In the immediate early phase after the imposition of ascending aortic banding, the mRNA expression of proto-oncogenes (c-fos, c-jun and c-myc) was diminished in aged rat hearts compared with young adult hearts. In the later phase, the pattern of expression of contractile protein genes in aged hearts differed quantitatively from that in adult hearts. The hypertrophic responses to the imposition of not only pressure-overload but also volume-overload were also diminished at the organ and cellular levels. In addition, this diminution was observed both in the left and right ventricles. Against ischemic insults, aged hearts responded with a diminished expression of proto-oncogenes and heat shock proteins. Thus, aged hearts are characterized by poor adaptation to hemodynamic overload and by a poor self-protective mechanism against cell death through necrosis and apoptosis. Of interest, more severe hemodynamic overload elevated the diminished responses to a level similar to that in adult hearts, suggesting that the threshold for the heart to respond to hemodynamic overload or ischemia is elevated in aged hearts. In addition, even in aged hearts ischemic preconditioning upregulated the diminished gene expression in a gene-dependent manner. Thus, the capacity for adaptation to hemodynamic overload and ischemia is diminished in aged hearts, but aged hearts preserve the ability to respond to these under some conditions.

Adaptation, Physiological↗
PubMed1993

Plasma cyclic guanosine monophosphate in chronic heart failure: hemodynamic and neurohormonal correlations and response to nitrate therapy.

This study evaluated the relation between plasma cyclic guanosine monophosphate (cGMP) and hemodynamic and neurohormonal parameters in patients with chronic congestive heart failure and assessed the effect of organic nitrate on plasma cGMP levels. Plasma cGMP was fourfold higher in 18 patients with congestive heart failure compared with 15 control subjects (16.7 +/- 9.7 versus 4.0 +/- 1.0 pmol/ml; p < 0.0001) but did not correlate with plasma levels of catecholamines, renin, atrial natriuretic peptide, or with baseline hemodynamic values. The administration of a hemodynamically effective dose of oral isosorbide dinitrate (40 mg) resulted in a transient reduction in plasma cGMP from 16.7 +/- 9.7 pmol/ml at baseline to 13.0 +/- 6.6 pmol/ml at 1 hour (p < 0.05). This change was associated with small and statistically insignificant changes in neurohormonal values and had no relation to any of the hemodynamic changes. We concluded that (1) elevated plasma cGMP in congestive heart failure does not correlate with other neurohormonal or hemodynamic parameters and may be an independent parameter of heart failure, (2) in contrast to previously documented nitrate-mediated increases in intracellular cGMP, nitrate therapy results in a reduction in plasma cGMP, and (3) changes in plasma cGMP cannot serve as a surrogate measurement of changes in intracellular cGMP.

Administration, Oral↗
PubMed1993

Dissociation between the course of the hemodynamic and antiproteinuric effects of angiotensin I converting enzyme inhibition.

Angiotensin I converting enzyme inhibition (ACEi) has been shown to lower urinary protein excretion in human renal disease. The mechanism of this antiproteinuric effect is hypothesized to be mediated by changes in renal hemodynamics. However, clinical studies suggest that the effect on renal hemodynamics is fully established immediately after the start of treatment, whereas others show the antiproteinuric effect to reach maximum only after several weeks. To clarify this issue we studied the course of renal hemodynamics, blood pressure and proteinuria during 28 days of ACEi (enalapril 10 mg oid) in nine patients with proteinuria due to non-diabetic renal disease. The effect of ACEi on blood pressure and renal hemodynamics was already maximal within few hours after start of treatment, and remained stable thereafter: MAP was lowered with 8.6 +/- 1.9%, 10.6 +/- 2.1%, 12.8 +/- 2.3% and 12.9 +/- 2.5%, while FF fell 23.0 +/- 2.0%, 17.0 +/- 2.6%, 16.8 +/- 2.8% and 15.9 +/- 4.0% on days 1, 7, 14 and 28 of ACEi, respectively. However, the antiproteinuric effect only gradually reached its maximum on day 28. Urinary protein excretion decreased with 10.9 +/- 6.1%, 32.7 +/- 6.2%, 46.3 +/- 2.5% and 54.0 +/- 2.5% on days 1, 7, 14 and 28 of ACEi, respectively. After drug withdrawal all parameters returned towards baseline. We conclude that a dissociation occurs in the course of the ACEi induced effects on hemodynamics and urinary protein excretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2005

Spatiotemporal evolution of functional hemodynamic changes and their relationship to neuronal activity.

Brain imaging techniques such as functional magnetic resonance imaging (fMRI) have provided a wealth of information about brain organization, but their ability to investigate fine-scale functional architecture is limited by the spatial specificity of the hemodynamic responses upon which they are based. We investigated the spatiotemporal evolution of hemodynamic responses in rat somatosensory cortex to electrical hindpaw stimulation. We combined the advantages of optical intrinsic signal imaging and spectroscopy to produce high-resolution two-dimensional maps of functional changes in tissue oxygenation and blood volume. Cerebral blood flow changes were measured with laser-Doppler flowmetry, and simultaneously recorded field potentials allowed comparison between hemodynamic changes and underlying neuronal activity. For the first 2 to 3 secs of activation, hemodynamic responses overlapped in a central parenchymal focus. Over the next several seconds, cerebral blood volume changes propagated retrograde into feeding arterioles, and oxygenation changes anterograde into draining veins. By 5 to 6 secs, responses localized primarily in vascular structures distant from the central focus. The peak spatial extent of the hemodynamic response increased linearly with synaptic activity. This spatial spread might be because of lateral subthreshold activation or passive vascular overspill. These results imply early microvascular changes in volume and oxygenation localize to activated neural columns, and that spatial specificity will be optimal within a 2- to 3-sec window after neuronal activation.

Animals↗
PubMed2003

Hemodynamic effects of a continuous infusion of levosimendan in critically ill patients with cardiogenic shock requiring catecholamines.

BACKGROUND: Levosimendan, a novel inodilator, has been shown to improve hemodynamic function in patients with decompensated heart failure with preserved arterial blood pressure. Data on its use in patients with cardiogenic shock are rare. The present series describes the 24-h hemodynamic effects of levosimendan as add-on therapy in desperately ill patients with cardiogenic shock requiring catecholamines. METHODS: Ten patients with cardiogenic shock received levosimendan as continuous infusion of 0.1 microg kg(-1) min(-1) for 24 h. The patients were otherwise unselected. Hemodynamic measurements were routinely performed at baseline (time 0) and at 1, 8, 16 and 24 h after start of levosimendan (LS) using a Swan-Ganz thermodilution catheter. RESULTS: During the levosimendan infusion there was a significant increase in cardiac index from 1.8 +/- 0.4 to 2.4 +/- 0.6 L*min-1*m-2 (P = 0.023) and a significant decrease in systemic vascular resistance from 1559 +/- 430 to 1109 +/- 202 dyn*s*cm-5 (P = 0.001), respectively. Changes in catecholamine dose, and in systolic and diastolic blood pressure were not significant. Given the individual response to LS, 8/10 patients showed an increase in left ventricular stroke work index under reduced or roughly unchanged preload conditions after 8 h. CONCLUSION: This series shows that a LS infusion is feasible and able to improve hemodynamics in severely compromized, critically ill patients with cardiogenic shock requiring catecholamine therapy. Its potential advantages when compared with other inotropes are unclear. To clarify the potential role of LS in this clinical setting randomized controlled trials on hemodynamic and mortality endpoints are needed.

Aged↗
PubMed1999

Altered hemodynamics in chick embryos after extraembryonic venous obstruction.

OBJECTIVE: To obtain insight into hemodynamics during abnormal cardiac development, a chick model was developed recently in which a spectrum of conotruncal anomalies, in combination with abnormal semilunar valves and/or pharyngeal arch artery malformations, was induced through extraembryonic venous obstruction (venous clip) at stage 17 (70-h incubation). METHODS: In chick embryos of stage 24 and stage 34 control (n = 8; n = 21) and with venous clip (n = 11; n = 18), we simultaneously measured dorsal flow velocities with a 20-MHz pulsed Doppler velocity meter and dorsal aortic (stage 24) and vitelline artery (stage 34) blood pressures with a servo-null system. After the hemodynamic recordings were collected, all 58 embryos were subjected to morphological examination. The hemodynamic data were correlated with the morphology. Statistical comparison was performed between control and experimental values. RESULTS: At stage 24, venous clip embryos showed impaired looping. Physiologically, only a decrease in peak acceleration was found in these embryos (p < 0.05). At stage 34, a spectrum of conotruncal malformations was seen, that consisted of a ventricular septal defect in combination with abnormal semilunar valves and/or pharyngeal arch malformations. A dextroposed aorta in combination with a ventricular septal defect was diagnosed as double-outlet right ventricle. Hemodynamically, peak systolic and mean velocities, peak systolic and mean blood flows and stroke volume were increased while the heart rate was reduced after placement of the venous clip (p < 0.05). In both stages, pressure readings showed no statistically significant differences between control and experimental embryos. CONCLUSION: Our findings suggest that the hemodynamic changes seen in venous clip embryos reflect the presence of a compensatory mechanism.

Animals↗
PubMed2005

Enhancing electrical cardioversion and preventing immediate reinitiation of hemodynamically deleterious atrial fibrillation with class III drug pretreatment.

UNLABELLED: Nifekalant for shock-resistant atrial fibrillation. INTRODUCTION: In severely ill patients, the development of atrial fibrillation (AF) may provoke lethal hemodynamic instability requiring immediate electrical defibrillation, which often is unsuccessful. Using the novel potassium channel blocking agent nifekalant, we prospectively assessed the hypothesis that class III antiarrhythmic drugs facilitate electrical cardioversion and suppress the immediate recurrence of hemodynamically deleterious AF. METHODS AND RESULTS: Among 1896 adults admitted to the intensive care unit for cardiovascular diseases, hemodynamically destabilizing new-onset AF (systolic blood pressure<90 mm Hg) resistant to conventional electrical cardioversion occurred in 27 patients, and of these, 24 patients (70+/-12 years) were enrolled. Twenty-one patients had congestive heart failure and 11 patients had been mechanically ventilated. After three failed transthoracic cardioversions due to failure of conversion to SR (11 patients) or immediate reinitiation (13 patients), nifekalant (0.25+/-0.04 mg/kg) was administered intravenously, and electrical defibrillation was reattempted. In 18 patients (75%), sinus rhythm was restored and maintained after nifekalant infusion (6 patients) or subsequent transthoracic cardioversion (12 patients). Nifekalant administration significantly decreased the heart rate and increased systolic blood pressure during AF (P<0.001), and successful cardioversion rapidly further ameliorated these parameters (P<0.001). Logistic regression analysis showed that atrial defibrillation failure (relative risk [RR] 19.34, P=0.05) and age of >75 years (RR 15.25, P=0.03) were independent predictors of in-hospital death. CONCLUSION: Nifekalant renders electrical defibrillation and the prevention of the early recurrence of hemodynamically unstable AF more successful without deteriorating hemodynamics, and successful defibrillation is associated with a more favorable patient outcome. Pretreatment with other class III drugs, e.g., ibutilide or dofetilide, would also be efficacious in patients with failed urgent electrical cardioversion.

Aged↗
PubMed1998

Late fenestration closure in the hypoplastic left heart syndrome: comparison of hemodynamic changes.

BACKGROUND AND OBJECTIVES: Although survival of patients with the hypoplastic left heart syndrome treated by staged surgical palliation has improved, hemodynamic data after fenestrated Fontan operation and after fenestration closure have not been reported in this patient population. We sought to describe the hemodynamic status of these patients at cardiac catheterization performed for the purpose of fenestration closure and to compare these data with data from contemporary patients with other forms of univentricular heart. METHODS AND RESULTS: Hemodynamic responses to fenestration closure during cardiac catheterization were reviewed in 40 consecutive patients, including 20 with the hypoplastic left heart syndrome and 20 with other forms of univentricular heart defects. Hemodynamics before fenestration closure (arterial saturation and pressure, Fontan baffle saturation and pressure, pulmonary capillary wedge pressure, systemic arteriovenous oxygen content difference, and right-to-left shunt fraction) were nearly identical between the two groups. Significant (p < 0.05) changes after fenestration closure included increases in arterial saturation (9%), mean arterial pressure (3 mm Hg), and baffle pressure (1 mm Hg) and arteriovenous oxygen content difference (18 ml/L), with near elimination of right-to-left shunting. Cardiac output decreased by 21% and systemic oxygen transport by 13%, with no differences between the two patient groups. Mean baffle pressures were <17 mm Hg in 32 patients (80%). CONCLUSIONS: Hemodynamics after fenestrated Fontan operation and responses to fenestration closure in patients with the hypoplastic left heart syndrome were remarkably similar to that in patients with other univentricular heart defects.

Adolescent↗
PubMed2000

The hemodynamic response to medical treatment of portal hypertension as a predictor of clinical effectiveness in the primary prophylaxis of variceal bleeding in cirrhosis.

In the prevention of variceal rebleeding, it is already established that hemodynamic response to drug treatment (decrease in hepatic venous pressure gradient [HVPG] to 12 mm Hg or by >20%) is predictive of clinical effectiveness. In primary prophylaxis very few clinical data are available. We assessed the role of the hemodynamic response to beta-blockers or beta-blockers plus nitrates in predicting clinical efficacy of prophylaxis. A total of 49 cirrhotic patients with varices at risk of bleeding, without prior variceal bleeding, were investigated by hepatic vein catheterization before and after 1 to 3 months of chronic treatment with nadolol or nadolol plus isosorbide mononitrate, and were followed during treatment for up to 5 years. A total of 30 patients (61%) were good hemodynamic responders, and among them in 12 (24%) HVPG was </=12 mm Hg during treatment. During treatment 9 patients had variceal bleeding: 7 were poor responders and 2 were good responders. The probability of bleeding at 3 years of follow-up was significantly higher in poor responders (41%) than in good responders (7%; P =.0008). No patient reaching an HVPG of 12 mm Hg or less during treatment had variceal bleeding during follow-up. Cox's regression analysis showed that poor hemodynamic response was the main factor predicting bleeding (beta = 1.91; SE(beta) = 0.80; P =.01). During follow-up 11 patients died of hepatic causes. Survival was related to Child-Pugh class and to initial value of HVPG, according to Cox's analysis. In conclusion, the assessment of hemodynamic response to drugs in terms of HVPG is the best predictor of efficacy of prophylaxis of variceal bleeding in patients treated with beta-blockers or beta-blockers plus nitrates.

Adrenergic beta-Antagonists↗
PubMed2001

Hemodynamic profiles of advanced heart failure: association with clinical characteristics and long-term outcomes.

BACKGROUND: Classifying patients with advanced congestive heart failure (CHF) by baseline measures of congestion and perfusion has been used to estimate hemodynamic status and to select and titrate therapy. We describe clinical characteristics of 4 hemodynamic profiles-wet/cold, wet/warm, dry/cold, and dry/warm-in patients with advanced CHF and assess relations between symptoms, physical signs, and outcomes with each profile. METHODS AND RESULTS: We retrospectively assessed baseline symptoms, physical-examination variables, and 1-year outcomes of 440 patients in a randomized trial. With univariable and multivariable logistic regression, we examined relations of physical-examination variables to hemodynamic profiles. We also assessed the rates of death and death or readmission by profile. Severity of CHF symptoms did not predict the wet-versus-dry profile or cold-versus-warm status, despite significant differences in hemodynamics among groups. Of the physical-examination variables, only a lower proportional pulse pressure was a significant multivariable predictor of the wet category. Among wet patients (n = 348), this same variable was the only significant multivariable predictor of the cold category. For dry patients (n = 92), the cold category was predicted in multivariable analysis by supine heart rate and hepatomegaly. Survival was similar among profiles: wet/cold, 54.2% (n = 91); wet/warm, 58.3% (n = 105); dry/cold, 78.9% (n = 15); and dry/warm, 67.1%, P =.13 (n = 49). Event-free survival also was similar among profiles: wet/cold, 22.0% (n = 37); wet/warm, 29.4% (n = 53); dry/cold, 42.1% (n = 8); and dry/warm, 31.5%, P =.44 (n = 23). CONCLUSIONS: The patient's history and physical examination alone may lead to inaccurate estimation of hemodynamic status and thus suboptimal management for patients with advanced CHF.

Aged↗
PubMed2000

[S-(+)-ketamine versus ketamine racemic mixture: hemodynamic studies].

OBJECTIVE: Evaluation of hemodynamic effects of S-(+)-ketamine versus ketamine-racemic mixture during induction of anesthesia, during steady-state of a fentanyl-midazolam-anesthesia and in the period of aortic cross-clamping during extracorporeal circulation. METHODS PATIENTS: 80 patients scheduled for coronary revascularization. STUDY DESIGN: double-blind, randomized. STUDY 1: Induction of anesthesia with ketamine-racemic mixture (3 mg/kg) or S-(+)-ketamine (1.5 mg/kg) plus midazolam 0.15 mg/kg. PARAMETERS: invasive hemodynamic monitoring including right ventricular volumes and pressure. STUDY 2: Bolus of ketamine-racemic mixture (3 mg/kg), S-(+)-ketamine (1.5 mg/kg) or placebo during steady-state anesthesia with fentanyl and midazolam. PARAMETERS: see study 1, additionally left ventricular systolic and end-diastolic pressure and maximum speed of left ventricular pressure increase (dp/dt). STUDY 3: Bolus of ketamine-racemic mixture (3 mg/kg), S-(+)-ketamine (1.5 mg/kg) or placebo in the period of aortic cross clamping during ECC. PARAMETERS: mean systemic pressure, central venous pressure, reservoir volume. RESULTS STUDY 1: Heart rate and systemic blond pressure remained unchanged until intubation, which caused significant increases of these parameters. Stroke volume Index and cardiac index decreased in the S-(+)-group compared with racemic mixture, right- and left ventricular filling parameters remained unchanged throughout the study. STUDY 2: There were no significant hemodynamic changes with time or between the groups. STUDY 3: Significant arterial vasodilation was observed in the racemic mixture group, venous parameters remained unchanged. CONCLUSION: There were no major differences in the hemodynamic profiles of S-(+)-ketamine and the racemic mixture. S(+)-ketamine did not provide hemodynamic advantages. The use of both preparations should be limited to selected clinical situations in patients with reduced coronary reserve.

Aged↗
PubMed2005

Effect of different operative techniques for myocardial revascularisation on hemodynamics and myocardial perfusion in a porcine model.

BACKGROUND: During surgical coronary revascularisation hemodynamics and myocardial contractility can be affected. This in vivo study aimed to determine the effects of different operative techniques on hemodynamics and regional myocardial perfusion. METHODS: In 24 pigs IMA to LAD bypass was constructed using ECC (n = 8) and cardioplegic arrest, OPCAB techniques (n = 8), or the Impella elect 100 support device (n = 8). 8 animals received a sham operation. Mean arterial pressure (MAP), cardiac output (CO), and left ventricular pressure (LVP, LVdp/dt) were recorded. Regional myocardial perfusion (RMP) of both ventricles was assessed by fluorescent microspheres. RESULTS: MAP significantly decreased during revascularisation in all groups ( p < 0.05), staying below preoperative values thereafter ( p < 0.05). After ECC norepinephrine was administered to maintain MAP. CO and LVdp/dt were impaired more distinctly during OPCAB than with Impella ( p < 0.05) during subsequent recovery. RMP showed global reactive hyperemia during early reperfusion after ECC, remained unchanged in OPCAB, and showed low flow during and after Impella pump run ( p < 0.05). CONCLUSIONS: ECC led to hemodynamic impairment with post-ischemic reactive hyperemia. OPCAB created hemodynamic depression but left RMP unchanged. Hemodynamic depression can be reduced by the Impella pump, however regional myocardial blood flow is decreased.

Animals↗
PubMed2001

The dual endothelin receptor antagonist tezosentan acutely improves hemodynamic parameters in patients with advanced heart failure.

BACKGROUND: Endothelin-1, a potent vasoconstrictor, is elevated in congestive heart failure and is postulated to play a major role in the pathogenesis of the disease. Endothelin receptor antagonism may be a specific therapeutic approach. This study was designed to determine the effective dosage range, hemodynamic effects, and tolerability of tezosentan, an intravenous dual endothelin receptor antagonist, in patients with advanced heart failure. METHODS: This randomized, double-blind, placebo-controlled multicenter trial enrolled 38 patients with symptomatic stable heart failure (New York Heart Association class III, left ventricular ejection fraction <35%) undergoing right heart catheterization. Patients were equally randomized to a 4-hour intravenous infusion of placebo or tezosentan in ascending doses (5, 20, 50, and 100 mg over 1 hour each). Angiotensin-converting enzyme inhibitors and diuretics were withheld 24hours before the study. Hemodynamics were measured during and for 4 hours after the infusion. RESULTS: Compared with placebo, tezosentan treatment produced a significant increase in cardiac index (treatment difference 0.59 L/min/m(2), P =.0001) and decreases in pulmonary and systemic vascular resistances (P </=.01) without changes in heart rate. Consistently greater decreases in pulmonary capillary wedge pressure, mean right atrial pressure, and pulmonary and arterial pressures with tezosentan did not reach statistical significance. Hemodynamic changes were dose dependent with maximal effects at 20 and 50 mg per hour. Tezosentan was well tolerated. Despite increased endothelin-1 concentrations, hemodynamic rebound was not observed. CONCLUSION: Tezosentan rapidly and dose dependently improved hemodynamics. The favorable effects on cardiac index and pulmonary and systemic vascular resistances without changes in heart rate may be beneficial in the treatment of acute heart failure.

Adult↗
PubMed2002

Hemodynamic stability of valve area, valve resistance, and stroke work loss in aortic stenosis: a comparative analysis.

BACKGROUND: Although aortic valve area (AVA) has provided the standard index for assessing aortic stenosis severity, valve resistance and percent left ventricular stroke work (%LVSW) loss have been proposed as alternative flow independent indices of stenosis severity that may provide a more stable measure under diverse hemodynamic conditions. In 30 patients with moderate or severe aortic stenosis (AVA < or = 1.2 cm(2)), Doppler echocardiography indices of AVA, valve resistance, and %LVSW loss were measured at multiple transvalvular flow rates during dobutamine infusions (0-10 microg/kg/min) to compare their hemodynamic stability. RESULTS: From baseline to maximum dobutamine dose in the 30 patients, transvalvular flow rate increased 43% and resulted in a 42% increase in mean transvalvular pressure gradient, a 15% increase in Doppler AVA, and a 26% increase in %LVSW loss. Group mean valve resistance did not change for the total cohort. For individual patients, AVA and %LVSW loss demonstrated a linear relationship with transvalvular flow (median r = 0.74 and 0.84, respectively). In contrast, both flow-mediated increases and decreases in valve resistance were observed in individual patients, resulting in the apparent stability of the group mean valve resistance in the total cohort. For individual patients, Doppler AVA and valve resistance demonstrated comparable stability in response to changes in hemodynamic conditions and were significantly more stable than mean transvalvular pressure gradient and %LVSW loss. CONCLUSION: Doppler AVA and valve resistance provide stenotic indices of equivalent hemodynamic stability. However, transvalvular flow has a predictable directional effect on AVA and an unpredictable directional effect on valve resistance, potentially limiting valve resistance as a measure of hemodynamic severity.

Adult↗
PubMed2003

Contrast-enhanced Doppler hemodynamics for noninvasive assessment of patients with chronic heart failure and left ventricular systolic dysfunction.

We sought to evaluate whether contrast-enhanced Doppler echocardiography can improve the noninvasive estimation of hemodynamic variables in left ventricular (LV) dysfunction. Right-heart catheterization and Doppler echocardiography were simultaneously performed in 45 patients with LV dysfunction (ejection fraction: 29 +/- 7%) in sinus rhythm. Noninvasive variables were estimated as follows: cardiac output by pulsed Doppler of LV outflow tract; pulmonary capillary wedge pressure by a regression equation including mitral and pulmonary venous flow variables; pulmonary artery mean pressure from the calculated systolic and diastolic pulmonary artery pressures; and pulmonary vascular resistance from the previous measurements according to hemodynamic definition. Contrast enhancement increased the feasibility of pulmonary capillary wedge pressure estimation from 60% to 100%; of pulmonary artery mean pressure from 42% to 91%; and of pulmonary vascular resistance from 42% to 91%. Strong correlations between invasive and noninvasive hemodynamic variables were found: r = 0.90, standard error of the estimate (SEE) 0.45 L/min for cardiac output; r = 0.90, SEE 3.1 mm Hg for pulmonary capillary wedge pressure; r = 0.93, SEE 3.7 mm Hg for pulmonary artery mean pressure; and r = 0.85 SEE 1.0 Wood units for pulmonary vascular resistance. Weaker correlations for PAMP (r = 0.82, SEE 5.6 mm Hg) and PVR (r = 0.66, SEE 1.7 Wood units) were apparent prior to contrast enhancement. When patients were separated according to PVR threshold values, the contrast allowed the correct placement of 88% of patients, whereas only 57% were correctly assigned without it. The contrast increased accuracy and reduced interobserver variability in the evaluation of hemodynamic variables. The contrast-enhanced study is capable of increasing the value of noninvasive hemodynamic assessment in LV dysfunction.

Adult↗
PubMed1998

Hemodynamic effects of 8-day DL-028 and octreotide administration in rats with portal hypertension.

BACKGROUND: DL-028 (chemical name: 3-[[4-(2-methoxyphenyl)piperazin-1-yl]methyl]-2,3-dihydroimidaz o[1,2-c]quinazolin-5(6H)-one (27b)) is a synthetic alpha1-adrenoceptor antagonist. The present study was undertaken to investigate the hemodynamic effects of chronic DL-028 administration, alone or in combination with octreotide, in rats with portal hypertension. METHODS: Portal hypertension was induced by partial portal-vein ligation. Portal-hypertensive rats were allocated to one of the four groups: vehicle group (saline, 0.5 ml/12 h), octreotide group (30 microg/kg/12 h), DL-028 group (0.4 mg/kg/12 h), and octreotide (30 mg/kg/l2 h) plus DL-028 (0.4 mg/kg/12 h) group, with eight rats in each group. DL-028 or saline was administered by gavage and octreotide by subcutaneous injection. Drugs were given immediately after ligation and for 8 consecutive days thereafter. Systemic and splanchnic hemodynamic variables were measured thereafter. RESULTS: Portal-vein-ligated rats showed a typical hyperdynamic state as compared with sham-operated rats. The portal venous pressure, portal tributary blood flow, and cardiac index were significantly reduced by treatment with octreotide, DL-028, or octreotide plus DL-028 in portal-hypertensive rats. Hyperdynamic variables of systemic, renal, hepatocollateral, and portal territory vascular resistances and renal and hepatic arterial blood flow were ameliorated by treatment with octreotide or octreotide plus DL-028 in portal-hypertensive rats. Octreotide plus DL-028 treatment exerted better hemodynamic effects on the cardiac index but worse effects on systemic and hepatocollateral vascular resistance than octreotide treatment alone. CONCLUSION: Although either DL-028 or octreotide ameliorated portal hypertension and splanchnic hyperemia in portal-hypertensive rats, octreotide treatment exerted more beneficial hemodynamic effects than DL-028 treatment. The combination of octreotide and DL-028 conferred no better hemodynamic benefits than octreotide alone, except on the cardiac index.

Adrenergic alpha-Antagonists↗
PubMed2002

Flow-induced wall shear stress in abdominal aortic aneurysms: Part I--steady flow hemodynamics.

Numerical predictions of blood flow patterns and hemodynamic stresses in Abdominal Aortic Aneurysms (AAAs) are performed in a two-aneurysm, axisymmetric, rigid wall model using the spectral element method. Homogeneous, Newtonian blood flow is simulated under steady conditions for the range of Reynolds numbers 10 < or =Re < or =2265. Flow hemodynamics are quantified by calculating the distributions of wall pressure (p(w)), wall shear stress (tau(w)), Wall Shear Stress Gradient (WSSG). A correlation between maximum values of hemodynamic stresses and Reynolds number is established, and the spatial distribution of WSSG is considered as a hemodynamic force that may cause damage to the arterial wall at an intermediate stage of AAA growth. The temporal distribution of hemodynamic stresses in pulsatile flow and their physical implications in AAA rupture are discussed in Part II of this paper.

Aorta, Abdominal↗