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Hemodynamic attenuation and the nitrate-free interval: alternative dosing strategies for transdermal nitroglycerin.

Various dosing strategies to determine therapeutic effects of nitroglycerin (NTG) preparations are reviewed. The importance of individual patient titration in establishing an effective NTG dosage is emphasized by reviewing a nitroglycerin ointment study and a crossover study. Studies reporting the development of hemodynamic attenuation ("tolerance") with longterm nitrate therapy are also discussed. The results of these and other studies suggest that the magnitude of the hemodynamic response to NTG or isosorbide dinitrate diminishes over time, with acute or first-dose effects far exceeding those obtained during long-term therapy. However, patients on long-term therapy continue to respond to sublingual NTG, which suggests that this phenomenon is not true NTG tolerance. The effect of a nitrate-free interval as a mechanism for avoiding hemodynamic attenuation of NTG therapy is reviewed. The results of 4 studies discussed found that intermittent nitrate protocols were not associated with the attenuated hemodynamic effect observed during chronic therapy. Two possible mechanisms for the vasodilatory effects of nitroglycerin are discussed. The first relates to the production of cyclic guanosine monophosphate in the smooth muscle cells of arteries and veins; the second to the synthesis of prostaglandin I2 by vascular endothelial cells. A mechanism by which nitrate receptors could be manipulated to increase vascular responsiveness is theorized, as well as a means by which a nitrate-free interval might avoid the development of hemodynamic attenuation in terms of cellular mechanisms and receptors.

Acetylcysteine↗

Hemodynamic benefits of synchronized 1:1 atrial pacing during sustained ventricular tachycardia with severely depressed ventricular function in coronary heart disease.

The hemodynamic effects of atrial pacing were studied in 8 patients who had ventricular tachycardia (VT) during electrophysiologic testing. These patients had chronic recurrent VT associated with organic heart disease and depression of left ventricular function (ejection fraction = 0.23 to 0.35). Hemodynamic variables were recorded during sinus rhythm (58 to 103 beats/min), pacing-induced VT (133 to 214 beats/min) and synchronized 1:1 triggered atrial pacing (atrium paced, ventricle sensed and triggered mode) during VT. For the latter, the ventriculoatrial coupling interval was adjusted to produce a maximal blood pressure response; the optimal interval was observed to be between 60% and 73% of the RR interval. Mean arterial blood pressure decreased after the onset of VT (90 +/- 11 to 79 +/- 14 mm Hg, p less than 0.05) but increased again when atrial pacing was added, to 98 +/- 12 mm Hg. Cardiac index decreased during VT (2.2 +/- 0.5 to 1.8 +/- 0.5 liters/min/m2 p less than 0.05), but in each case improved by the addition of atrial pacing, to 1.9 +/- 0.5 liters/min/m2. Evidence from pressure recordings suggested that optimal atrial pacing resulted in atrial contraction in early left ventricular diastole. Thus, appropriately timed atrial pacing during VT can result in significant increases in blood pressure and a consistent increase in cardiac index. In addition to offering insight into the mechanisms of hemodynamic compromise during VT, the clinical use of this technique may be to improve hemodynamic values in patients with hemodynamically unstable VT.

Aged↗

Spectrum of acute hemodynamic effects of nifedipine in severe congestive heart failure.

The acute hemodynamic effects of 20 to 50 mg of orally administered nifedipine were evaluated in 31 patients with severe chronic congestive heart failure (CHF) and the results were analyzed according to the response of the cardiac index (CI). Although the group mean value of CI increased significantly after nifedipine treatment (from 2.1 +/- 0.5 to 2.4 +/- 0.8 liters/min/m2, p less than 0.001), the individual response was variable. Twenty of the patients had 15% or greater increase in CI (group A) and 11 patients had less than a 15% increase or a decrease in CI (group B). Marked differences were also noted in the effects of nifedipine on other hemodynamic variables. Stroke volume increased 29 +/- 14% in group A and decreased 11 +/- 18% in group B (p less than 0.001). Systemic vascular resistance decreased 34 +/- 11% in group A (p less than 0.001) and increased slightly, 2 +/- 28%, in group B. Left ventricular (LV) stroke work index increased 11 +/- 19% in group A (p less than 0.001) and decreased markedly in Group B (21 +/- 20%). Six group B patients had a substantial worsening (20% or more) of one or more hemodynamic measurements, including CI, stroke volume index, LV stroke work index and mean pulmonary artery wedge pressure. A comparison of control hemodynamic values at rest, LV ejection fraction, associated coronary artery disease, nifedipine dose, and concomitant diuretic therapy revealed no significant differences between the 2 groups. This study confirms, in a large group of patients with severe CHF, the variable hemodynamic effects of nifedipine therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗

Assessment of peak oxygen consumption, lactate and ventilatory thresholds and correlation with resting and exercise hemodynamic data in chronic congestive heart failure.

To determine the clinical value of respiratory gas analysis during exercise, oxygen consumption (VO2) at peak exercise and at lactate and ventilatory threshold was assessed in 34 patients with chronic heart failure who underwent maximal exercise testing with expiratory gas monitoring and serial determinations of mixed venous lactate and hemodynamics by Swan-Ganz catheterization. A lactate threshold, defined as the point of abrupt increment of blood lactate, could be identified in every patient; the ventilatory threshold, detected on the basis of the respiratory changes, was found in 26 patients (77%). Lactate and ventilatory thresholds were significantly related to each other (r = 0.94; p less than 0.001) and to peak VO2 (r = 0.89; p less than 0.001 in both). Among the resting hemodynamic measurements, peak VO2 was significantly related only to total pulmonary resistances (r = -0.35). Among the parameters at maximal exercise, it was positively related to cardiac index, stroke work, stroke volume index and mean arterial pressure (r = 0.89, 0.74, 0.74 and 0.56, respectively) and inversely related to systemic vascular and total pulmonary resistances (r = -0.74 and -0.63). Using multivariate stepwise regression analysis only maximal cardiac index and, to a lesser degree, total pulmonary resistance were related to peak VO2. Similar correlations were found between the hemodynamics and the lactate and ventilatory threshold. Thus, peak VO2, lactate and ventilatory thresholds can be detected in most patients with chronic heart failure. These parameters are highly correlated to each other and bear similar relations to the hemodynamic response to exercise. The cardiac index is the main central hemodynamic determinant of exercise capacity.

Adult↗

A dose-finding study of the hemodynamic effect of isosorbide dinitrate spray in congestive heart failure.

A dose-finding study of the hemodynamic effect of a new formulation of isosorbide dinitrate (ISDN) spray was performed in 12 patients with chronic congestive heart failure. Doses of 1.25, 2.5, 5.0 mg and placebo, as 1 squirt, were randomly given to all patients. Hemodynamic measurements were performed by a Swan-Ganz catheter before and at 30 seconds and 1, 5, 10, 20 and 30 minutes after drug administration and every 30 minutes thereafter, until return of hemodynamic variables to baseline. Hemodynamic improvement evident as decreases in right-sided pressures and an increase in cardiac output was observed within 1 minute from administration of ISDN spray, and peaked at 5 minutes. Near maximal effect was achieved by the 2.5-mg dose. Thus, 2.5 mg of ISDN spray (new formulation) dose. Thus, 2.5 mg of ISDN spray (new formulation) produces rapid, near-maximal hemodynamic improvement in patients with congestive heart failure.

Administration, Oral↗

Hemodynamic effects of oral nicorandil in congestive heart failure.

Twenty-five patients with congestive heart failure (CHF) underwent a double-blind randomized study of the acute hemodynamic effects of orally administered nicorandil, a newly developed vasodilator drug. A dose range of 10 to 60 mg was studied. Nicorandil, at a dose of 60 mg, caused statistically significant decreases in systemic systolic and diastolic blood pressure, right atrial pressure, pulmonary capillary wedge pressure, systemic and pulmonary vascular resistance and systolic and diastolic pulmonary arterial pressure. A brief increase in cardiac index attributable to an increase in stroke volume without a change in heart rate was also observed. A dose of 40 mg produced similar results in cardiac index and systemic and pulmonary vascular resistance, but changes in other hemodynamic parameters were much smaller in magnitude and usually not of statistical significance. No significant hemodynamic response was seen to doses of 10 and 20 mg of nicorandil. Duration of action was short with nearly all hemodynamic parameters returning close to baseline within 3 hours. This rapid decrease in activity occurred in concert with a rapid plasma clearance of nicorandil as determined by serial measurements of plasma drug concentration. This study suggests that first-dose orally administered nicorandil elicits favorable, but brief, hemodynamic effects in CHF at doses greater than or equal to 40 mg.

Administration, Oral↗

Prediction of risk for hemodynamic compromise during percutaneous transluminal coronary angioplasty.

The availability of circulatory support devices has increased the importance of accurately identifying patients at risk for hemodynamic compromise during percutaneous transluminal coronary angioplasty (PTCA). Accordingly, prospective evaluation of 3 criteria to predict hemodynamic compromise (defined as a decrease in systolic blood pressure > or = 20 to < 90 mm Hg during balloon inflation) in 157 patients (group A) undergoing PTCA was performed. Left ventricular ejection fraction < 35% had a sensitivity of 13% and a specificity of 95%. Greater than 50% of the myocardium at risk was associated with a sensitivity of 31% and a specificity of 85%. The angiographer's assessment of high risk for hemodynamic compromise had the highest sensitivity of 56% and a specificity of 86%. The clinical and angiographic characteristics of these patients were reviewed to identify risk factors retrospectively. Multivariate analysis of 28 variables identified multivessel disease, diffuse disease, myocardium at risk, and stenosis before PTCA as independent predictors of hemodynamic compromise. With use of this analysis, a 13-point weighted scoring system was created based on the regression of coefficients of the variables. Defining high risk for hemodynamic compromise as a risk score > or = 4, the sensitivity of this criterion in group A patients was 81% and the specificity was 74%. The scoring system was then prospectively applied to 61 consecutive patients (group B) undergoing PTCA. In using a risk score > or = 4 to define high risk, this scoring system had a sensitivity of 92% and a specificity of 92%.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Hemodynamic effects of high-dose sustained-action oral isosorbide dinitrate in stable angina.

Hemodynamic effects of sustained-action oral isosorbide dinitrate (40 or 80 mg) were studied in 10 patients with stable angina for a period of 16 hours. Control hemodynamic parameters monitored for eight hours prior to the administration of isosorbide dinitrate showed no significant change. However significant reduction in mean arterial pressure, cardiac index, pulmonary artery wedge pressure, mean pulmonary artery pressure, double product (systolic pressure multiplied by heart rate), stroke volume index, and stroke work index occurred in the first two hours and persisted for 12 hours following the administration of isosorbide dinitrate. Heart rate did not change significantly for 12 hours. It can be concluded that the hemodynamic effects of sustained-action oral isosorbide dinitrate occur in the first two hours and last up to 12 hours. The predominant hemodynamic effect appears to be on the myocardial preload. The antianginal effect of the drug could be attributed to the reduction of myocardial oxygen demand reflected by a decrease in the double product and stroke work. The duration of the hemodynamic changes observed in this study indicates that high-dose oral isosorbide dinitrate could be administered conveniently two or three times daily.

Administration, Oral↗

Hemodynamic effects of calcium channel blockers at rest and during exercise in essential hypertension.

The main hemodynamic disturbance occurring in patients with essential hypertension is an increase in the total peripheral resistance. In young patients with hypertension, this disturbance is clearly seen during muscular exercise, even though the calculated resistance might be normal during rest. This article reports results of studies on the long-term hemodynamic effects of two calcium channel blockers, verapamil and nifedipine, in patients with mild to moderate hypertension. Twenty-five men, aged 20 to 64 years, with diastolic blood pressures between 100 and 120 mm Hg before treatment were studied at rest and during exercise on ergometer bicycles. Blood pressure was recorded intra-arterially, and cardiac output was measured. After this initial study, 10 patients were treated with verapamil (from 40 to 80 mg, three times daily) and 15 patients with nifedipine (long-acting form, from 40 to 80 mg daily). After one year, the hemodynamic study was repeated. Both drugs induced a reduction in blood pressure and in the total peripheral resistance without any reduction in the cardiac index. Verapamil reduced heart rate, particularly during exercise, but this effect was compensated by an increase in the stroke volume. The hemodynamic profile of these two calcium channel blockers clearly differs from the hemodynamic effects of beta blockers.

Adult↗

Hemodynamic alterations associated with amniotic fluid embolism: a reappraisal.

Experimental amniotic fluid embolism in animals produces profound pulmonary hypertension and acute cor pulmonale without evidence of left ventricular compromise. Authors reporting hemodynamic alterations associated with clinical amniotic fluid embolism have traditionally attempted to explain their findings within this experimental framework. A reanalysis of the five published cases of amniotic fluid embolism, which include hemodynamic data derived from pulmonary artery catheterization as well as a report of a sixth case suggests a hemodynamic interpretation different from the traditional one based on the animal model. Left ventricular failure is the only hemodynamic abnormality consistently observed in humans, and the published data are most readily explained on this basis alone. A theoretical model of hemodynamic changes accompanying amniotic fluid embolism that incorporates both experimental and clinical observations is presented. Therapeutic implications are discussed.

Adult↗

Inadequacy of the noninvasive hemodynamic evaluation of percutaneous transluminal angioplasty.

The role of noninvasive hemodynamic tests in the evaluation of percutaneous transluminal angioplasty success or failure was studied. The ankle-brachial pressure index and pulse volume recording amplitude were measured before and after 37 iliac and 46 femoropopliteal angiographically successful percutaneous transluminal angioplasties. Immediate evidence of hemodynamic improvement was seen in 53 percent of angiographically successful dilatations using the ankle-brachial pressure index and in 60 percent using the pulse volume recording amplitude alone. A better correlation was seen when improvement was noted on either test but was still only 71 percent. Twelve primary iliac percutaneous transluminal angioplasties were considered to be successful immediately by angiography, yet no hemodynamic improvement was recorded. Nine primary iliac percutaneous transluminal angioplasties, however, had continued clinical success and limb viability. Twelve angiographically successful femoropopliteal percutaneous transluminal angioplasties also showed no improvement in hemodynamic values, yet three have continued clinical evidence of patency. Thus, although noninvasive hemodynamic tests are important and must be carried out, they are only one of many ways to assess the effectiveness of angioplasty.

Adult↗

Early in vivo experience with the Hemodynamic Plus St. Jude Medical heart valves in patients with narrowed aortic annulus.

BACKGROUND: Small aortic orifice primarily resulted in heart prosthesis mismatch in a significant number of patients. The Hemodynamic Plus (HP) series of St. Jude Medical heart valves represents an interesting innovation, allowing a larger valve orifice area with an equivalent tissue annulus diameter. METHODS: Hemodynamic characteristics of the 21-mm HP St. Jude Medical valve were prospectively compared with those of the standard 21-mm and 23-mm St. Jude Medical valves in three groups of 22 patients. Patients were selected from a database to be rigorously matched for age, sex, body surface area, functional class, underlying lesion, native valve opening area, left ventricular function, and preoperative peak and mean valve gradients. Postoperative evaluation (follow-up ranging from 3 to 24 months; mean, 11.5 months) included clinical examination and echocardiographic studies. RESULTS: There was no operative mortality or significant perioperative complications. Short-term clinical follow-up was marked by a complete absence of valve-related complications. Presently, all but 1 patient in the 21-mm HP group and 2 in the 21-mm standard group are in New York Heart Association functional class I. Doppler echocardiography-derived mean and maximal pressure gradients were significantly lower in the 21-mm HP group (8.1 +/- 1.9 and 16.4 +/- 3.4 mm Hg) than in the 21-mm standard group (13.4 +/- 3.9 and 21.2 +/- 4.3 mm Hg; p = 0.002 and p = 0.0004, respectively), confirming the better hemodynamic performance already described in in vitro studies. Pressure gradients did not differ significantly between the 21-mm HP and the 23-mm standard groups. The 21-mm HP valve demonstrated the highest performance index; 0.66 +/- 0.08, compared with 0.49 +/- 0.09 for the 21-mm standard valve (p < 0.001) and 0.59 +/- 0.07 for the 23-mm standard valve (p < 0.001). CONCLUSIONS: In vivo hemodynamic performance of the 21-mm HP valve corresponds closely to that of the 23-mm standard valve and is substantially better than that of the 21-mm standard valve. The 21-mm HP St. Jude Medical valve demonstrates excellent hemodynamic characteristics and can be recommended in normal-sized adult patients with narrow aortic root. This valve will minimize the need for aortic annulus enlargement.

Adult↗

Hemodynamic effects of different pacing ratios in chronic dynamic double cardiomyoplasty.

BACKGROUND: Dynamic cardiomyoplasty is being used clinically worldwide, and evaluated by a clinical trial (phase III) in the United States. Some centers stimulate the skeletal muscle wrap with every heart beat (1:1 [muscle:heart]), whereas others use every other heart beat (1:2). Recent concern over the possible deleterious effects of too-frequent stimulation of the muscles motivated the attempt to evaluate, in a canine model of chronic, double cardiomyoplasty, the effects of two different pacing ratios on several hemodynamic parameters of interest. METHODS: Double cardiomyoplasty was performed using both latissimus dorsi muscles in 11 dogs. Fatigue resistance was achieved using the clinical transformation protocol. At a final experiment, acute cardiac failure was induced by administration of propranolol. Hemodynamic measurements of eight physiologic variables were averaged over complete pacing cycles, including the nonpaced beat at a 1:2 pacing ratio. RESULTS: The net effects of latissimus dorsi muscle stimulation at each of two pacing ratios were compared using nonparametric statistics. With the exception of left ventricular pressure (p = 0.0262) and its first derivative, dP/dt (p = 0.0099), there was no significant difference between hemodynamic performance at the two pacing ratios. CONCLUSIONS: In this canine model, pacing every other beat produces hemodynamic results that are statistically similar to pacing every beat. Less frequent stimulation of the latissimus dorsi muscle may preserve its function and improve clinical results without compromising hemodynamic benefit.

Acute Disease↗

Influence of hypothyroidism and the reversal of hypothyroidism on hemodynamics and cell size in the adult rat heart.

Hypothyroid-induced atrophy of cardiac myocytes was examined in adult female rats in an effort to correlate hemodynamic and cellular changes associated with this disorder. Additional rats were studied 6 weeks after discontinuing antithyroid treatment to determine if structural and functional changes were completely reversible. To induce hypothyroidism, rats were injected daily with propylthiouracil (PTU) for 4 weeks. Control animals were injected similarly with Tris buffer. At the end of the treatment period, hemodynamic measurements were made prior to obtaining isolated myocytes. Cell volume, length, and cross-sectional area were obtained from the septum, and left and right ventricles of treated and untreated rats. After four weeks treatment with PTU, body weight was unchanged but heart weight was significantly reduced by 24%. Characteristic hemodynamic changes associated with hypothyroidism in the rat were noted (eg. reduced heart rate, cardiac output, dP/dtmax, and ventricular pressure). Cell volume was significantly smaller in hypothyroid rats primarily due to a reduction in myocyte cross-sectional area. The hemodynamic and cellular response to hypothyroidism was similar in the right and left ventricle. Six weeks after discontinuing PTU treatment, cellular and hemodynamics changes had returned to normal. It was concluded that hypothyroidism caused a true cardiac atrophy which was reversible. Reduced myocyte cross-sectional area was responsible for most of the myocyte atrophy.

Animals↗

Increased prostacyclin and adverse hemodynamic responses to protamine sulfate in an experimental canine model.

Prostanoid activity was correlated with the hemodynamic effects of protamine sulfate reversal of heparin in 24 dogs undergoing three different pretreatment regimens: Group I (n = 8) received saline, Group II (n = 8) received the thromboxane synthetase inhibitor U63,557A (30 mg/kg), and Group III (n = 8) received indomethacin (10 mg/kg). Pretreatment substances were administered as 5-min intravenous infusions 20 min before anticoagulation with intravenous heparin (150 IU/kg). Protamine sulfate (1.5 mg/kg) was subsequently given as a 10-sec intravenous infusion 30 min after heparin had been administered. Hemodynamic data, as well as prostacyclin (PGI2) and thromboxane (TxA2) activity in aortic, venous, and pulmonary artery blood samples, were assessed over a 30-min time period following protamine administration. Group III indomethacin pretreatment provided the most protection from declines in blood pressure, heart rate, cardiac output, venous oxygen saturation, oxygen consumption, and elevations in pulmonary pressures and was accompanied with actual declines in PGI2. Group II U63,557A pretreatment was associated with the most severe hemodynamic changes and the greatest increase in PGI2 (+576%). Elevated PGI2 correlated with hypotension at 1 and 3 min (P less than 0.01), as well as pulmonary artery pressure declines at all times following protamine reversal. TxA2 changes did not correlate with hemodynamic changes. Protamine's adverse hemodynamic responses were attenuated with cyclooxygenase blockade by indomethacin, but were worsened with selective TxA2 blockade with U63,557A. Excess arachadonic acid precursors in the latter setting may increase PGI2 production. This study, for the first time, raises the possibility that PGI2 contributes to the adverse effects accompanying protamine reversal of heparin anticoagulation.

Animals↗

Perinatal results of hemodynamic and conservative temporizing treatment in severe pre-eclampsia.

OBJECTIVE: To evaluate maternal and perinatal outcome of hemodynamic temporizing management in severe pre-eclampsia. DESIGN: Study group of 57 pre-eclamptic women, gestational age 35 weeks or less, treated with plasma volume expansion and vasodilatation under invasive hemodynamic monitoring, retrospectively matched with a control group treated in another center without volume expansion and invasive monitoring. RESULTS: In both groups pregnancy was prolonged with 10-11 days. Maternal morbidity was low in both groups. No complications of hemodynamic monitoring were observed. Perinatal mortality was not significantly different between the study group (7.1%) and the control group (14.3%). SGA-infants were significantly less frequent in the study group (9%) than in controls (33%). CONCLUSION: Temporizing treatment of patients with early severe pre-eclampsia, with or without plasma volume expansion and invasive hemodynamic monitoring, may reduce neonatal mortality and morbidity. The difference in birthweight between study group and control group may be an effect of the therapy or may be caused by selection bias. The perinatal outcome in the study group suggests that there may be a subgroup of patients who might benefit from hemodynamic treatment.

Cerebral Hemorrhage↗

Noninvasive evaluation of cardiac hemodynamics during exercise in patients with chronic heart failure: effects of short-term coenzyme Q10 treatment.

In patients with chronic heart failure (CHF), the addition of coenzyme Q10 to conventional therapy reduces the hospitalization rate for worsening of heart failure and the incidence of serious cardiovascular complications. The present study was planned to assess the hemodynamic mechanisms underlying this phenomenon. Cardiac hemodynamics was evaluated continuously using an ambulatory radionuclide detector (VEST) which allows a noninvasive monitoring of left ventricular function. Six patients wit CHF (mean ejection fraction (EF): 29%) clinically documented were studied. This study was organized as a randomized double-blind, placebo controlled, cross-over trial. The enrolled patients, after a washout period, underwent the first hemodynamic evaluation with VEST. Subsequently they were randomized to receive placebo or coenzyme Q10 for 4 weeks. At the end of this period they underwent the second VEST study. The third VEST study was performed after a further 4-week period with inverted treatment. Cardiac hemodynamics were evaluated during bicycle exercise. The EF in control conditions (CC) changed from 27 +/- 11%, at rest, to 24 +/- 8%, at peak exercise. During coenzyme Q10 treatment EF showed a significant increase both at rest (33 +/- 13%, P < 0.05 vs CC) and at peak exercise (30 +/- 12%, P < 0.05 vs CC). The same trends were recorded for the stroke volume and the cardiac output. Our results demonstrate that coenzyme Q10 improves cardiac hemodynamic response to exercise in patients with CHF and suggest that noninvasive monitoring of left ventricular function allows a more reliable assessment of therapy efficacy.

Adult↗

Hemodynamic and renal effects of ascites apheresis, concentration and reinfusion in advanced cirrhosis.

BACKGROUND/AIMS: We studied the effects of ascites apheresis, concentration and reinfusion, a new form of treatment for tense or refractory ascites, on systemic hemodynamics and renal function. METHODS: Twelve patients with advanced cirrhosis (two belonging to Child-Pugh's class B and the remainder to class C) were monitored. They were evaluated under baseline conditions, just after the treatment, and 24 and 48 h after baseline assessment. In addition to systemic hemodynamics--as evaluated by Doppler echocardiography--and renal function, indirect markers of effective volemia, such as atrial natriuretic factor, plasma renin activity and aldosterone concentration, and plasma norepinephrine were also measured. RESULTS: The technique led to significant changes in systemic hemodynamics, such as an increase in stroke volume and cardiac output. However, due to a striking reduction in peripheral vascular resistance, mean arterial pressure also declined. The hemodynamic changes were associated with a parallel increase in atrial natriuretic factor. Despite the reduction in arterial pressure, plasma renin activity also significantly declined, while plasma norepinephrine did not undergo significant changes. Although an improvement in glomerular filtration rate and renal sodium excretion occurred, neither change reached statistical significance. All the hemodynamic, renal and neuro-humoral changes described above subsided almost entirely after 48 h, when no significant changes with respect to baseline values were any longer detectable with the exception of a slight reduction in mean arterial pressure. CONCLUSIONS: In advanced cirrhosis ascites apheresis, concentration and reinfusion enhance central volemia, but an exaggerated peripheral vasodilation largely wastes the potential favourable effect on arterial volemia. As a result, no significant improvement in renal perfusion and sodium excretion can ensue.

Adult↗