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PubMed1997

Enalapril and losartan reduced cardiac mass and improved coronary hemodynamics in SHR.

Among the multiple mechanisms postulated for the increased risk of hypertensive left ventricular hypertrophy (LVH), coronary hemodynamic alterations remain a strong possibility. This study was designed to compare the effects of treatment with an ACE inhibitor (enalapril) and an angiotensin AT1 receptor antagonist (losartan) on systemic and coronary hemodynamics and to determine whether the combination of these two renin-angiotensin system (RAS) inhibitor would be as or more effective in reducing mean arterial pressure (MAP), left ventricular (LV) mass, and improving coronary hemodynamics than either regimen alone. Thus, 23 week old spontaneously hypertensive rats (SHR) were treated (12 weeks) with tap water (C), enalapril (30 mg.kg-1.d-1), losartan (30 mg.kg-1.d-1), or their combination (15 mg.kg-1.d-1). Age-matched Wistar-Kyoto (WKY) rats served as normotensive controls. After 12 weeks, systemic and coronary hemodynamics were determined (15 microns radiolabeled microspheres) at baseline, during maximal treadmill exercise, and during maximal dilation (dipyridamole). Enalapril and losartan equally reduced MAP and LV mass in association with a decreased total peripheral resistance. The RAS combination reduced MAP and LV mass more than either drug alone. Resting cardiac index and coronary blood flow (CBF) per unit of LV mass did not differ among the groups. Although enalapril did not improve coronary flow reserve (CFR), it diminished minimal coronary vascular resistance (MCVR); losartan improved both. However, the combination was more effective than either agent alone, reaching values close to normotensive WKY controls. In conclusion, these data demonstrated significantly impaired maximal CBF, CFR, and MCVR in untreated SHR, but losartan alone and in combination with enalapril improved systemic and coronary hemodynamics more than enalapril alone.

Angiotensin Receptor Antagonists↗
PubMed1998

Endogenous interleukin-10 regulates hemodynamic parameters, leukocyte-endothelial cell interactions, and microvascular permeability during endotoxemia.

The objective of this study was to determine whether endogenous IL-10 is capable of regulating hemodynamic parameters, leukocyte recruitment, and microvascular permeability in response to endotoxin. Intravital microscopy was used to examine hemodynamic parameters, leukocyte rolling and adhesion, and microvascular permeability in cremasteric postcapillary venules in wild-type mice and in IL-10-deficient (IL-10(-/-)) mice exposed to lipopolysaccharide (LPS). Doses of LPS (3 or 30 microg/kg, IV), which did not reduce blood pressure and minimally altered microvascular hemodynamic factors in wild-type mice, caused significant reductions in these parameters in IL-10(-/-) mice, demonstrating at least a 10-fold increased sensitivity in IL-10(-/-) mice to LPS-induced hemodynamic alterations. Furthermore, in response to LPS (30 microg/kg, IV), leukocyte rolling, adhesion, and fluorescein isothiocyanate-albumin extravasation were increased in the IL-10(-/-) mice. Antibody blockade experiments showed that in both types of mice, leukocyte rolling was mediated by E-selectin and P-selectin. Leukocyte accumulation into other tissues, such as lung, also was enhanced greatly in IL-10(-/-) mice. This was specific to endotoxin, because acute chemotactic stimuli including N-formyl-methionyl-leucyl-phenylalanine elicited similar responses in IL-10(-/-) and wild-type mice. These results suggest that endogenous IL-10 may be a homeostatic regulator of hemodynamic parameters, leukocyte-endothelial cell interactions, and microvascular dysfunction in response to endotoxin and provide potential mechanisms to explain the protective effect of IL-10 against LPS-induced mortality.

Animals↗
PubMed1994

Frequency and pathogenesis of hemodynamic stroke.

BACKGROUND AND PURPOSE: Hemodynamic stroke is a recognized but poorly described entity. The aim of this study was to define the frequency and pathogenic mechanisms of hemodynamic stroke. METHODS: We prospectively studied 300 consecutive patients with acute ischemic stroke for evidence of a hemodynamic mechanism. All patients with a probable or possible thromboembolic source were excluded. RESULTS: Twenty-nine patients (9.6%) had documented or presumed hypotension at stroke onset, with 27 of 29 (93%) having watershed infarction on computed tomography (CT). Most (21/29) patients had a slow (hours to days) progressive onset to stroke. Myocardial infarction, cardiac arrhythmias, and orthostatic changes in blood pressure related to diabetic dysautonomia and antihypertensive therapy were the predominant causes of hypotension. Ten patients had moderate or severe carotid stenosis (frequently bilateral); 9 had carotid occlusion (19/29 [66%]). Patients with normal carotid arteries (10/29 [34%]) had hypotension with a stuttering onset to stroke and watershed infarction on CT. Many patients continued to have progressive neurological deterioration, often with ongoing hemodynamic instability. Three of 7 patients who underwent carotid endarterectomy had further perioperative ischemic events. Five patients had myocardial infarction, and overall 4 died during 18.4 months of follow-up (mortality, 9%/y). CONCLUSIONS: Recognition of the clinical and CT features of hemodynamic stroke allows early identification and management of cardiac and carotid disease and correction of iatrogenic causes of hypotension, which may reduce the risk of further events.

Aged↗
PubMed1996

Hemodynamic parameter assessment with dynamic susceptibility contrast magnetic resonance imaging in unilateral symptomatic internal carotid artery occlusion.

BACKGROUND AND PURPOSE: Hemodynamic parameters such as regional cerebral blood volume (rCBV), mean transit time (MTT), and regional cerebral blood flow (rCBF) can be assessed by dynamic susceptibility contrast MRI. The aim of the present study was to apply this method in patients who had symptomatic unilateral internal carotid artery occlusion. METHODS: Relative hemodynamic parameters (rCBV, MTT, and rCBF) were evaluated on the occluded side and thus compared with contralateral hemispheric values. We also attempted to detect any relationship between collateral flow and the hemodynamic parameters. RESULTS: Although rCBV was clearly increased in five patients over the whole hemisphere, we did not observe a statistically significant difference regarding the whole sample between sides (mean rCBV, 14.1 +/- 4.58 on the occluded side versus 11.8 +/- 2.99 on the contralateral side, P>.10). MTT was clearly increased on the occluded side (mean MTT, 4.29 +/- 0.83 on the lesion side versus 3.14 +/- 0.81 on the contralateral side, P<.010). A statistically significant decrease of rCBF on the occluded side was observed (mean rCBF, 3.27 +/- 0.73 versus 3.93 +/- 1.03 on the contralateral side; P<.01). CONCLUSIONS: A significant hemodynamic compromise in patients who had unilateral symptomatic carotid occlusion was observed according to CBF and MTT values. This approach might be promising in the understanding of cerebral hemodynamics in patients with vascular disorders.

Aged↗
PubMed2002

Renal hemodynamic control by endothelin and nitric oxide under angiotensin II blockade in man.

To investigate whether endothelin-A receptors and nitric oxide modulate renal hemodynamics in man under angiotensin II receptor-1 blockade, 6 healthy volunteers, on a 240 mmol Na diet, underwent 4 separate renal hemodynamic measurements, in 3 of which endothelin-A blocker BQ-123 0.2 nmol.kg.min(-1) was infused for 90 minutes after pretreatment with either placebo, telmisartan 1 mg.kg center dot day(-1) for 3 days, or telmisartan as well, but with co-infusion of both BQ-123 and N(G)-nitro-L-arginine methylester 0.5 microg.kg center dot min(-1). A fourth infusion was made with N(G)-nitro-L-arginine methylester alone. No change followed infusion of either N(G)-nitro-L-arginine methylester alone or BQ-123 alone. With BQ-123 after telmisartan, renal blood flow rose from 916 +/- 56 mL center dot min(-1) center dot 1.73 m(2) to 1047 +/- 51.2 (P<0.001), and renal vascular resistances fell from 89 +/- 7 mm Hg center dot min center dot L(-1) to 74 +/-4 (P<0.001). These changes were fully abolished by the co-infused N(G)-nitro-L-arginine methylester. Infusion of BQ-123, devoid of renal hemodynamic effects at baseline, produces significant renal vasodilation when angiotensin II receptors are blocked, indicating an increasing renal hemodynamic role of endothelin-A--receptor activity. Because such a vasodilation is prevented by nonvasoconstricting microdoses of N(G)-nitro-L-arginine methylester, nitric oxide--endothelin balance controls substantially renal hemodynamics under angiotensin II blockade. These findings are consistent with a rationale of the association of endothelin-A blockers with angiotensin II blockers or angiotensin-converting enzyme inhibitors in treating nitric oxide--deficient conditions such as arterial hypertension, heart failure, and chronic renal diseases.

Angiotensin II↗
PubMed1978

Role of hemodynamic changes in the increased cation excretion after acute unilateral nephrectomy in the anesthetized dog.

Studies were carried out in anesthetized dogs to characterize the increase in cation excretion which occurs after acute unilateral nephrectomy (AUN). 60 min after AUN, cation excretion had increased from 31.5+/-2.7 to 66.3+/-12.0 mueq/min (P < 0.005) and fractional cation excretion had increased from 0.56+/-0.05 to 1.03+/-0.14% (P < 0.005), as the glomerular filtration rate was unchanged and renal blood flow fell. The increased cation excretion was accompanied by an increase in fractional phosphate excretion, no change in chloride excretion, and a fall in renin secretion. These alterations in renal function were associated with marked changes in systemic hemodynamics: cardiac output fell from 2.52+/-0.24 to 1.85+/-0.16 liters/min (P < 0.001), as diastolic pressure rose without an overall increase in mean arterial pressure, and heart rate fell. To assess the importance of these hemodynamic changes in the renal response, AUN in a separate group of dogs was accompanied by the simultaneous opening of a surgically created femoral artery-to-vein fistula at flow matching the blood flow to the removed kidney. When this was done, no alterations in systemic or renal hemodynamics were observed, and cation excretion did not differ from control. Subsequent closure of the fistula then caused a fall in cardiac output from 2.15+/-0.25 to 1.77+/-0.20 liters/min (P < 0.05), and an increase in cation excretion from 34.6+/-9.5 to 52.3+/-13.7 mueq/min (P < 0.01), thus mimicking the findings with AUN alone.These results demonstrate that AUN causes hemodynamic changes resembling those seen on closure of a chronic arteriovenous fistula. Prevention of these hemodynamic changes after AUN also prevents the functional adjustment of the remaining kidney, suggesting that they may be important in initiating the renal response. The increased electrolyte excretion after AUN may occur through mechanisms similar to that seen on closure of an arteriovenous fistula.

Animals↗
PubMed1998

Effects of chronic hypoxia and altered hemodynamics on endothelial nitric oxide synthase expression in the adult rat lung.

Mechanisms that regulate endothelial nitric oxide synthase (eNOS) expression in normal and hypoxic pulmonary circulation are poorly understood. Lung eNOS expression is increased after chronic hypoxic pulmonary hypertension in rats, but whether this increase is due to altered hemodynamics or to hypoxia is unknown. Therefore, to determine the effect of blood flow changes on eNOS expression in the normal pulmonary circulation, and to determine whether the increase in eNOS expression after chronic hypoxia is caused by hemodynamic changes or low oxygen tension, we compared eNOS expression in the left and right lungs of normoxic and chronically hypoxic rats with surgical stenosis of the left pulmonary artery (LPA). LPA stenosis in normoxic rats reduced blood flow to the left lung from 9.8+/-0.9 to 0.8+/-0.4 ml/100 mg/min (sham surgery controls vs. LPA stenosis, P < 0.05), but there was not a significant increase in right lung blood flow. When compared with the right lung, eNOS protein and mRNA content in the left lung was decreased by 32+/-7 and 54+/-13%, respectively (P < 0.05), and right lung eNOS protein content was unchanged. After 3 wk of hypoxia, LPA stenosis reduced blood flow to the left lung from 5.8+/-0.6 to 1.5+/-0.4 ml/100 mg/min, and increased blood flow to the right lung from 5.8+/-0.5 to 10.0+/-1.4 ml/ 100 mg/min (sham surgery controls vs. LPA stenosis, P < 0.05). Despite reduced flow and pressure to the left lung and increased flow and pressure to the right lung, left and right lung eNOS protein and mRNA contents were not different. There were also no differences in lung eNOS protein levels when compared with chronically hypoxic sham surgery controls (P > 0.05). We conclude that reduction of pulmonary blood flow decreases eNOS mRNA and protein expression in normoxic adult rat lungs, and that hypoxia increases eNOS expression independently of changes in hemodynamics. These findings demonstrate that hemodynamic forces maintain eNOS content in the normoxic pulmonary circulation of the adult rat, and suggest that chronic hypoxia increases eNOS expression independently of changes in hemodynamics.

Animals↗
PubMed2005

Meta-analysis of hemodynamic optimization: relationship to methodological quality.

INTRODUCTION: To review systematically the effect of interventions aimed at hemodynamic optimization and to relate this to the quality of individual published trials. METHODS: A systematic, computerized bibliographic search of published studies and citation reviews of relevant studies was performed. All randomized clinical trials in which adult patients were included in a trial deliberately aiming at an optimized or maximized hemodynamic condition of the patients (with oxygen delivery, cardiac index, oxygen consumption, mixed venous oxygen saturation and/or stroke volume as end-points) were selected. A total of 30 studies were selected for independent review. Two reviewers extracted data on population, intervention, outcome and methodological quality. Agreement between reviewers was high: differences were eventually resolved by third-party decision. The methodological quality of the studies was moderate (mean 9.0, SD 1.7), and the outcomes of the randomized clinical trials were not related to their quality. RESULTS: Efforts to achieve an optimized hemodynamic condition resulted in a decreased mortality rate (relative risk ratio (RR) 0.75 (95% confidence interval (CI) 0.62 to 0.90) in all studies combined. This was due to a significantly decreased mortality in peri-operative intervention studies (RR 0.66 (95% CI 0.54 to 0.81). Overall, patients with sepsis and overt organ failure do not benefit from this method (RR 0.92 (95% CI 0.75 to 1.11)). CONCLUSION: This systematic review showed that interventions aimed at hemodynamic optimization reduced mortality. In particular, trials including peri-operative interventions aimed at the hemodynamic optimization of high-risk surgical patients reduce mortality. Overall, this effect was not related to the trial quality.

Critical Care↗
PubMed1993

Three different strains of heat-killed group B beta-hemolytic streptococcus cause different pulmonary and systemic hemodynamic responses in conscious neonatal lambs.

Although group B beta-hemolytic streptococcus (GBS) causes pathologic hemodynamic alterations in both human neonates and neonatal animal models of sepsis, little is known about strain-dependent differences in hemodynamic responses to GBS. This study compared pulmonary and systemic hemodynamic dose-response profiles in conscious neonatal lambs with three different strains of heat-killed GBS originally isolated from infected human neonates (group 1: serotype Ib, early-onset sepsis; group 2: serotype Ib, necrotizing enterocolitis; and group 3: serotype III, meningitis). Regression models of hemodynamic responses were characterized after lambs were injected with heat-killed GBS (dose range 0.1-6.0 x 10(9) colony-forming units, i.v.). All three GBS strains caused dose-dependent increases in mean pulmonary arterial pressure and pulmonary and systemic vascular resistances and decreases in cardiac output and heart rate. The GBS strain used in group 1 caused a greater effect on mean pulmonary arterial pressure and systemic vascular resistance than those used in groups 2 and 3 and was the only strain to cause an increase in mean systemic arterial pressure. The GBS strains used in groups 1 and 2 had a greater effect on pulmonary vascular resistance than that used in group 3. No group differences were observed in cardiac output and heart rate responses, which were, however, influenced by age, gender, and duration of postoperative recovery of the lambs. No attenuation or augmentation of hemodynamic effect was observed after sequential doses of 10(9) colony-forming units of GBS given in a single day. This study demonstrates strain-dependent quantitative differences in pulmonary vascular response and qualitative differences in systemic vascular response to heat-killed GBS.

Animals↗
PubMed1999

Cerebral hemodynamic impairment: methods of measurement and association with stroke risk.

Stenosis or occlusion of the major arteries of the head and neck may cause hemodynamic impairment of the distal cerebral circulation. Hemodynamic factors may play an important role in the pathogenesis of ischemic stroke for patients with cerebrovascular disease. Several neuroimaging methods are currently available for the indirect assessment of the hemodynamic effect of atherosclerotic stenosis or occlusion on the distal cerebrovasculature. Because these methods rely on different underlying physiologic mechanisms, they are not interchangeable. Two basic categories of hemodynamic impairment can be assessed with these techniques: Stage 1, in which autoregulatory vasodilation secondary to reduced perfusion pressure is inferred by the measurement of either increased blood volume or an impaired blood flow response to a vasodilatory stimulus; and Stage 2, in which increased oxygen extraction fraction (OEF) is noninvasively but directly measured. The correlation of different Stage 1 methods with each other and with Stage 2 techniques is quite variable. Clinical studies associating different manifestations of hemodynamic impairment with stroke risk often suffer from methodologic problems. The best evidence to date for such an association is for increased OEF measured in patients with symptomatic carotid occlusion. In the absence of data demonstrating improvement in patient outcome, there is currently no role for the routine use of these tools to guide clinical management in patients with cerebrovascular disease.

Cerebrovascular Circulation↗
PubMed1999

Brain arteriolosclerosis and hemodynamic disturbance may induce leukoaraiosis.

OBJECTIVE: To investigate whether internal carotid artery (ICA) occlusive disease-induced hemodynamic disturbance is associated with extensive white matter high-intensity lesions (WMLs) on T2-weighted MR images in the hemisphere with lacunar infarct in the basal ganglia. BACKGROUND: Hemodynamic disturbance in the brain with arteriolosclerosis may be one of the mechanisms by which ischemic injury induces extensive WMLs. METHODS: The authors used MRI and PET to study 21 patients with unilateral ICA occlusion or stenosis and lacunar infarct in the bilateral basal ganglia. In hemispheres with ICA disease, the association of WMLs with the mean hemispheric values of oxygen extraction fraction (OEF)-an index of hemodynamic compromise-measured with the 15O-labeled gas steady-state technique was analyzed. Twenty-five patients with ICA occlusive disease without lacunar infarct were studied as control subjects. RESULTS: In the hemispheres with ICA disease, patients with lacunar infarct had a significantly greater severity of WMLs than control subjects, although the mean hemispheric values of the OEF showed no significant difference. The severity of WMLs correlated significantly with the mean hemispheric values of the OEF in patients with lacunar infarct, but not in control subjects. Multivariate analysis revealed that lacunar infarcts and increased OEF were independent predictors of extensive WMLs, with lacunar infarcts the most heavily weighted factor. CONCLUSION: Internal carotid artery occlusive disease-induced hemodynamic disturbance is associated with extensive WMLs in hemispheres with lacunar infarct. Hemodynamic disturbance may contribute to the development of extensive WMLs, although brain arteriolosclerosis may be a major contributing factor.

Aged↗
PubMed1993

Hemodynamic changes during laparoscopic cholecystectomy.

Hemodynamics during laparoscopic cholecystectomy under general anesthesia (isoflurane in N2O/O2 (50%)) were investigated in 15 nonobese ASA Class I patients by using invasive hemodynamic monitoring including a flow-directed pulmonary artery catheter. During surgery, intraabdominal pressure was maintained automatically at 14 mm Hg by a CO2 insufflator, and minute ventilation was controlled and adjusted to avoid hypercapnia. Hemodynamics were measured before anesthesia, after the induction of anesthesia, after tilting into 10 degrees head-up position, 5 min, 15 min, and 30 min after peritoneal insufflation, and 30 min after exsufflation. Induction of anesthesia decreased significantly mean arterial pressure and cardiac index (CI). Tilting the patient to the head-up position reduced cardiac preload and caused further reduction of CI. Peritoneal insufflation resulted in a significant increase (+/- 35%) of mean arterial pressure, a significant reduction (+/- 20%) of CI, and a significant increase of systemic (+/- 65%) and pulmonary (+/- 90%) vascular resistances. The combined effect of anesthesia, head-up tilt, and peritoneal insufflation produced a 50% decrease in CI. Administration of increasing concentrations of isoflurane, via its vasodilatory activity, may have partially blunted these hemodynamic changes. These results demonstrate that laparoscopy for cholecystectomy in head-up position results in significant hemodynamic changes in healthy patients, particularly at the induction of pneumoperitoneum.

Adult↗
PubMed2006

Normothermic beating heart surgery with assistance of miniaturized bypass systems: the effects on intraoperative hemodynamics and inflammatory response.

The use of miniaturized cardiopulmonary bypass (CPB) circuits and avoidance of cardioplegic arrest are attempts to reduce the inflammatory response to cardiac surgery. We studied the effects of beating heart surgery (BHS) with assistance of simplified bypass systems (SBS) on global hemodynamics, myocardial function and the inflammatory response to CPB. We hypothesized that the use of SBS was associated with less hemodynamic instability after CPB resulting from attenuation of the inflammatory response when compared with surgery performed with a conventional CPB (cCPB) circuit. Forty-five patients undergoing coronary artery bypass grafting were prospectively studied. Fifteen patients were randomized to the use of a cCPB circuit, cold crystalloid cardioplegia, and moderate hypothermia. Two groups of 15 patients underwent BHS during normothermia with assistance of two different SBS consisting of only blood pump and oxygenator. Hemodynamic variables were assessed with transpulmonary thermodilution and transesophageal echocardiography. Plasma levels of proinflammatory and antiinflammatory mediators were measured perioperatively. After CPB, variables of global hemodynamics and systolic ventricular function did not differ among groups. Left ventricular diastolic function was impaired after CPB equally in all groups (P < 0.01 versus pre-CPB). At the end of surgery, there was more need for vasopressor (norepinephrine) support in both SBS groups than in the cCPB group (P < 0.01). After CPB, the release of interleukin (IL)-6 did not differ significantly among groups, whereas plasma levels of IL-10 were higher in the cCPB group (P < 0.01 versus SBS). The extent of myocardial necrosis (Troponin T) was comparable in all groups. We conclude that in our study, miniaturizing bypass systems and avoidance of cardioplegic arrest were not effective in improving hemodynamic performance and in attenuating the proinflammatory immune response after CPB.

Anesthesia↗
PubMed1992

Paroxysmal atrial fibrillation and flutter associated with acute myocardial infarction: hemodynamic evaluation in relation to the development of arrhythmias and prognosis.

The hemodynamic background associated with the occurrence of paroxysmal atrial fibrillation and flutter (PAF), in patient with acute myocardial infarction (AMI) were evaluated. Sixty-seven of 381 consecutive AMI patients (17.6%) were noted to have PAF in the acute phase of infarction. These 67 patients with PAF (group 1) were compared with 60 randomly selected patients without PAF (group 2). The hospital mortality rate was 25.4% in group 1, and 11.7% in group 2 (p less than 0.01). The hemodynamic variables measured before the onset of PAF in group 1, showed significantly more unfavorable values than those in group 2, which were measured at the time of admission. The 67 patients in group 1 were divided into 50 patients who survived (group S) and 17 patients who died in the hospital (group D). The hemodynamic status in group D demonstrated significantly larger deterioration before the onset of PAF than in group S. Hemodynamic variables were compared before and during PAF in groups D and S, cardiac index (CI) decreased significantly, and stroke index (SI) decreased by 46% in group D, with no decrease in CI and less decrease in SI (28. p less than 0.05) in group S. In conclusion, not only the occurrence of PAF, but the prognosis of patients with PAF is dependent on the severity of hemodynamic disturbance imposed by AMI. Atrial contribution to ventricular filling has great importance in the maintenance of the cardiac output in this patient population.

Aged↗
PubMed2004

Hemodynamic response to sildenafil, nitric oxide, and iloprost in primary pulmonary hypertension.

STUDY OBJECTIVES: Different vasodilators and different routes of application are used for the treatment of primary pulmonary hypertension (PPH). Recently, sildenafil, a phosphodiesterase-V inhibitor, has been shown to have beneficial hemodynamic effects in PPH. However, the hemodynamic effects of sildenafil have not been characterized and compared to other vasodilators such as inhaled nitric oxide (iNO) or iloprost in PPH in the same group of patients. STUDY DESIGN: We investigated prospectively 10 consecutive patients with PPH using iNO, iloprost aerosol, and oral sildenafil to test acute hemodynamic response during right-heart catheterization. RESULTS: iNO, iloprost aerosol, and sildenafil caused a significant fall of mean pulmonary artery pressure and pulmonary vascular resistance (PVR) [p < 0.05]. Correspondingly, cardiac output and mixed venous saturation increased slightly in all groups. Systemic arterial pressure and vascular resistance were mainly unaltered. Using a PVR reduction of > or =20% to define a significant response, 7 of 10 patients were responders to iloprost aerosol, whereas 4 of 10 patients responded to iNO and oral sildenafil. Improvement of oxygenation as indicated by an increase of arterial oxygen tension was observed with iloprost aerosol (p < 0.01). CONCLUSION: All of the three substances, iNO, iloprost aerosol, and oral sildenafil, significantly improved pulmonary hemodynamics in patients with PPH. The most prominent hemodynamic effects and improvement of oxygenation were observed with iloprost aerosol.

Administration, Inhalation↗
PubMed2005

CT scan findings in chronic thromboembolic pulmonary hypertension: predictors of hemodynamic improvement after pulmonary thromboendarterectomy.

STUDY OBJECTIVES: The aim was to correlate CT scan findings with hemodynamic measurements in patients who had undergone pulmonary thromboendarterectomy (PTE) and to evaluate whether CT scan findings can help to predict surgical outcome. PATIENTS AND METHOD: Sixty patients who underwent PTE and preoperative helical CT scanning were included. Preoperative and postoperative hemodynamics were correlated with preoperative CT imaging features. RESULTS: The diameter of the main pulmonary artery (PA) and the ratio of the PA and the diameter of the ascending aorta correlated with preoperative mean pulmonary artery pressure (PAP) [r = 0.42; p < 0.001; and r = 0.48; p < 0.0001, respectively]. There was a significant correlation of subpleural densities with preoperative pulmonary vascular resistance (PVR) [r = 0.44; p < 0.001] and of the number of abnormal perfused lobes with preoperative PAP (r = 0.66; p < 0.0001) and PVR (r = 0.76; p < 0.0001). Postoperative PVR correlated negatively with the presence and extent of central thrombi (r = -0.36; p = 0.007) and dilated bronchial arteries (p = 0.03) seen on preoperative CT scans. Sixty percent of patients (3 of 5 patients) without visible central thromboembolic material on CT scans had an inadequate hemodynamic improvement in contrast to 4% of patients (2 of 51 patients) with central thrombi (p = 0.003). Preoperative PVR (r = 0.31; p = 0.018) and the extent of abnormal lung perfusion (r = 0.37; p = 0.007) and of subpleural densities (r = 0.32; p = 0.017) were positively correlated with postoperative PVR. CONCLUSIONS: In patients with thromboembolic pulmonary hypertension, CT scan findings can help to predict hemodynamic improvement after PTE. The absence of central thrombi is a significant risk factor for inadequate hemodynamic improvement.

Adolescent↗
PubMed1987

Hemodynamic effects of intravenous isosorbide dinitrate and nitroglycerine in acute myocardial infarction and elevated pulmonary artery wedge pressure.

We compared in a randomized fashion the hemodynamic effects of intravenous (IV) isosorbide dinitrate (ISDN) and nitroglycerine (NTG) in 45 patients with acute myocardial infarction and elevated pulmonary artery wedge pressure (Paw). Titration of ISDN dose to lower Paw greater than or equal to 25 percent resulted in a fall of this parameter from 32 +/- 8 to 24 +/- 5 mm Hg and was associated with a fall in mean blood pressure (96 +/- 15 to 90 +/- 14 mm Hg, p less than 0.05), systemic vascular resistance (1715 +/- 572 to 1548 +/- 414 dynes X s X cm-5, (p less than 0.05), pulmonary vascular resistance (182 +/- 106 to 154 +/- 78 dynes X s X cm-5, p less than 0.05) and mean right atrial pressure (11 +/- 4 to 7 +/- 4 mm Hg, p less than 0.05). In addition, ISDN significantly (p less than 0.05) increased cardiac index from 2.37 +/- 0.54 to 2.54 +/- 0.59 L/min/m2, stroke volume index from 28 +/- 8 to 31 +/- 8 ml/m2, and stroke work index from 28 +/- 11 to 31 +/- 12 g X m/m2. The ISDN dose ranged from 50 to 533 micrograms/min (mean +/- SD 326 +/- 176 micrograms/min) and could not be predicted from baseline hemodynamic values. A comparison between the effect of ISDN and NTG in doses producing comparable reduction in Paw showed similar hemodynamic changes. It was concluded that IV ISDN in patients with elevated mean pulmonary artery wedge pressure due to acute myocardial infarction results in a decrease in right and left ventricular preload and afterload and improvement of cardiac output and cardiac work. The effective dose ranges from 50 to 533 micrograms/min and cannot be predicted from baseline hemodynamic values. In doses producing comparable reduction in Paw, ISDN and NTG had similar hemodynamic effects.

Aged↗
PubMed1991

Evaluation of the hemodynamic and respiratory effects of inverse ratio ventilation with a right ventricular ejection fraction catheter.

Pc-IRV has been shown to have respiratory advantages, compared with CPPV. However, the hemodynamic effects of this ventilation mode have not yet been fully elucidated. We used a REF catheter to monitor the hemodynamic changes in the RV. Fifteen ARDS patients were included in the study. The respiratory data showed a 35 percent decrease of PIP and a 32 percent decrease of VTi and VTe with Pc-IRV 4:1 compared with CPPV. Hemodynamic parameters showed a significant incrase in CI (17 percent) in Pc-IRV 4:1, without change in REF. Observing in retrospect the pressure-volume relationship of the RV, we could differentiate a preload (group 1) and an afterload dependent group of patients (group 2), CI was significantly different in the two groups as it rose only in the preload-dependent patients. RVEDVI showed a significant change in group 1, whereas this was absent in the second group. REF was maintained in switching ventilation from CPPV to Pc-IRV with increasing I:E ratio. Pc-IRV appears to be a good alternative ventilatory mode in comparison with CPPV in a selected group of patients with preload dependency (responders); in these patients with respiratory insufficiency, close hemodynamic monitoring is required to optimize ventilation, especially in relation to the hemodynamic effects.

Adolescent↗