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PubMed1979

[Hemodynamics of the liver. II. Hemodynamics of the dog liver after resection of 70% of the liver and ligation of the left branch of the portal vein].

Blood supply to the liver was determined by help of the direct method after 70 per cent hepatic resection and after ligation of the left branch of portal vein in dogs. The total blood supply remains unchanged after both surgical procedures, while the circulation in the remaining lobes, resp. in those patent for portal blood stream, considerably increases. After the resection portal hypertension develops. This elevated portal pressure was not observed after ligation of the left portal branch.

Animals↗
PubMed2001

Clinical evaluation of St Jude Medical Hemodynamic Plus versus standard aortic valve prostheses: The Italian multicenter, prospective, randomized study.

OBJECTIVE: Hemodynamic and clinical performances of 21-mm and 23-mm St Jude Medical Hemodynamic Plus aortic valves (St Jude Medical, Inc, St Paul, Minn) were compared with those of 21-mm and 23-mm St Jude Medical standard cuff aortic valves in the first such multicenter, prospective, randomized study. Hemodynamic Plus valves are mechanical, bileaflet prostheses suitable for the small aortic anulus. METHODS: Patients with 21-mm and 23-mm anulus diameters were randomized to receive either a Hemodynamic Plus or a standard cuff valve. Postoperatively and at 6 months after the operation, patients underwent 2-dimensional Doppler echocardiography. Ejection fraction, cardiac output, peak gradient, mean gradient, effective orifice area, effective area index, and performance index were calculated. Postoperative and 6-month echocardiographic measurements and their variations across observation times were analyzed statistically. RESULTS: Of the 140 patients enrolled, 5 died at operation and 1 died of aortic dissection during the follow-up period. Eight patients were lost to follow-up. A total of 125 patients completed the study. In 1 patient a sewing cuff escaped intraoperatively. At 6 months the 21-mm and 23-mm Hemodynamic Plus valves showed significantly lower peak gradients and mean gradients than those of the 21-mm and 23-mm standard cuff valves. The 21-mm Hemodynamic Plus valves had gradients similar to those of the 23-mm Hemodynamic Plus valves. The effective orifice area did not differ significantly between the Hemodynamic Plus and standard cuff valves at either measurement. No valve mismatch was found in the 4 groups of patients. A more enhanced decrease of peak gradients and mean gradients and a more enhanced increase of effective orifice areas, effective area indices, and performance indices were found across observation times for patients with Hemodynamic Plus valves compared with those with standard cuff valves. CONCLUSIONS: Clinical hemodynamic performances of 21-mm and 23-mm St Jude Medical Hemodynamic Plus valves correspond closely with those of standard cuff valves, and gradients are substantially better than those of standard cuff valves of the same diameter. Therefore, use of this valve may minimize the need for aortic anulus enlargement. Early follow-up results with the Hemodynamic Plus valves were excellent, although more time is required to confirm this outcome.

Aortic Valve↗
PubMed2002

Mechanisms of hemodynamic changes during off-pump coronary artery bypass surgery.

PURPOSE: To describe the mechanisms of hemodynamic changes during off-pump coronary artery bypass graft surgery (OP-CABG). SOURCE: Pertinent medical literature in the English and French languages was identified through a Medline computerized literature search and a manual search of selected articles, using off-pump coronary artery surgery, beating heart surgery, hemodynamic, and transesophageal echocardiography as key words. Human and animal studies were included. PRINCIPAL FINDING: Hemodynamic variations in OP-CABG may be due to mobilization and stabilization of the heart, or myocardial ischemia occurring during coronary occlusion. Suction type and compression type stabilizers produce hemodynamic effects through different mechanisms. Heart dislocation (90 degrees anterior displacement) and compression of the right ventricle to a greater extent than the left ventricle are responsible for hemodynamic alterations when using suction type stabilizers. Compression of the left ventricular outflow tract and abnormal diastolic expansion secondary to direct deformation of the left ventricular geometry are proposed mechanisms for hemodynamic derangements with compression type stabilizer. Coronary occlusion during the anastomosis can have additional effects on left ventricular function, depending on the status of collateral flow. The value and limitations of electrocardiographic (ECG), hemodynamic and echocardiographic monitoring modalities during OP-CABG are reviewed. CONCLUSIONS: In summary, hemodynamic changes which can either be secondary to the stabilization technique or to transient ischemia represent an important diagnostic challenge during off-bypass procedures. The mechanism can vary according to the stabilization system. Current monitoring such as ECG and hemodynamic monitoring are used but remain limited in establishing the cause of hemodynamic instability. Transesophageal echocardiography is used in selected patients to diagnose the etiology of hemodynamic instability and can direct therapy, particularly in those with severe myocardial systolic and diastolic dysfunction, mild to moderate mitral regurgitation, or for patients who are unstable during the procedure.

Animals↗
PubMed1996

Structure-activity analysis for the effects of gamma-MSH/ACTH-like peptides on cerebral hemodynamics in rats.

In a previous structure-activity analysis we have shown that the gamma-melanocyte-stimulating hormones (gamma-MSHs) and structurally related adrenocorticotropic hormone (ACTH) fragments share an amino-acid sequence which is determinant for the effects of these peptides on peripheral hemodynamics, viz. a pressor and a tachycardiac response, in conscious rats. We now investigated whether these structural features are also important for the effects of these peptides on cerebral hemodynamics in urethane-anesthetized rats. After intracarotid and intravenous administration, the 'mother' peptides, Lys-gamma2-MSH and gamma2-MSH, and, with a 10-fold lower potency, ACTH-(4-10), caused a dose-dependent pressor and tachycardiac response, as well as an increase in extra- and intracranial blood flow and microcirculatory cerebrocortical blood flow. Removal of C-terminal amino acids resulted in gamma-MSH-fragments which were devoid of effects on peripheral and central hemodynamics. Fragments of gamma2-MSH which were shortened at the N-terminal side (gamma-MSH-(4-12) and gamma-MSH-(5-12)) were less potent than gamma2-MSH, but had an intrinsic activity similar to that of gamma2-MSH with respect to the pressor and tachycardiac effect. However, the potency and intrinsic activity of these shortened fragments on intracerebral hemodynamic parameters were the same as those of gamma2-MSH. This suggests that different mechanisms (e.g., site of action and/or melanocortin receptor subtype) are involved in the cerebral hemodynamic effects of the melanocortins and in their peripheral hemodynamic effects. Surprisingly, removal of an additional residue, His5, resulting in the fragment gamma-MSH-(6-12), led to full restoration of potency with respect to extracranial blood flow, blood pressure and heart rate. Neither the structurally related analog, [Nle4,D-Phe7]alpha-MSH (NDP-MSH), nor ACTH-(1-24) was able to induce a pressor effect or cerebral hemodynamic effects. In contrast, both compounds had a depressor effect. It is concluded that the C-terminal amino acids in the structure of gamma-MSH/ACTH-like peptides are essential for efficacy for the central hemodynamic effects, i.e., the increase in intracerebral (microcirculatory) blood flow. However, in contrast to what holds for the peripheral hemodynamic features, the N-terminal sequence has hardly any influence on potency or efficacy. The results with NDP-MSH and ACTH-(1-24) and the other fragments lead us to postulate that it is not one of the five known subtypes of melanocortin receptors which mediates the hemodynamic effects of the melanocortins, but an additional, still unidentified subtype. A clue for the elucidation of such a receptor might be found in the structural features of gamma-MSH-(6-12) that appear to be very important determinants for the effectiveness to alter peripheral and central hemodynamics.

Adrenocorticotropic Hormone↗
PubMed1998

Preoperative intensive care unit admission and hemodynamic monitoring in patients scheduled for major elective noncardiac surgery: a retrospective review of 95 patients.

OBJECTIVE: To review experience with preoperative intensive care unit (ICU) admission and hemodynamic monitoring to determine which patients benefited and how. DESIGN: Retrospective review over 32-month period (1991 to 1994). SETTING: Surgical ICU of a university teaching hospital. PARTICIPANTS: Ninety-five patients admitted to the surgical ICU before a major elective noncardiac, nonthoracic surgical procedure. INTERVENTIONS: All patients underwent hemodynamic monitoring with a pulmonary artery catheter (PAC). Interventions were made at the discretion of the ICU attending and attending surgeon, based on a general algorithm. Patients were categorized based on history or hemodynamics. The historic classification was as follows: group I, patients with cardiac disease documented by history and cardiac imaging, n = 37; group II, patients with cardiac disease documented by history, but not cardiac imaging, n = 24; group III, patients without documented cardiac disease, but with other significant medical problems, n = 34. Hemodynamic classification considered patients to have subnormal parameters if the cardiac index was < 2.5 L/min/m2, the mixed venous oxygen saturation was < 65%, or the oxygen delivery index was < 350 mL/min/m2 (n = 45), and normal parameters if greater than these (n = 50). MAIN RESULTS: There were no differences in APACHE II scores. Group I patients had greater Goldman Cardiac Risk Indices than group III patients (7.4 +/- 4.8 v 5.0 +/- 3.0). Patients in group I had a significantly greater incidence of subnormal initial hemodynamic values (63%) than patients in group II (47%) or group III (32%). The incidence of postoperative cardiovascular complications among groups was not different. Fifty patients (52%) had normal hemodynamics initially; two (4%) developed postoperative cardiovascular complications compared with 10 patients (22%) of the 45 with subnormal initial hemodynamic values. Of these 45 patients, 24 (52%) had their hemodynamic parameters corrected preoperatively with crystalloids, packed red blood cells, inotropes, and/or afterload reduction. Two of these 24 patients (8%) experienced postoperative cardiovascular complications, compared with 8 of the remaining 21 patients who had no attempt to normalize their hemodynamic values preoperatively other than maintaining a normal pulmonary artery occlusion pressure. CONCLUSIONS: Patients who had normal initial preoperative hemodynamic parameters or abnormal initial parameters that were normalized preoperatively experienced significantly fewer perioperative cardiovascular complications than those with abnormal initial values that were not normalized preoperatively. These results suggest that there may be benefit to the practice of preoperative ICU admission, hemodynamic monitoring with a PAC, and "optimization" of cardiac function in selected patients undergoing major elective noncardiac surgery. Further studies are needed to better delineate the most appropriate patient populations and effective therapeutic protocol.

Adult↗
PubMed1997

Acute increase of myocardial workload, hemodynamic instability, and myocardial histological changes induced by brain death in the cat.

Brain death-related hemodynamic instability may preclude donor heart procurement. The relationships between the initial changes of myocardial workload, hemodynamic deterioration, and myocardial histological changes caused by acute induction of brain death are unclear. Cats (n = 15) were submitted to brain death by rapid inflation of an intracranial balloon. A further 12 cats served as a sham-operated control group. The changes in heart rate, mean arterial blood pressure, systolic and diastolic arterial blood pressure, left ventricular developed pressure, LV dP/dtmax, rate-pressure product (RPP), and circulating noradrenaline and adrenaline were studied during 240 min after the induction of brain death. Central venous pressure was kept constant. The hearts were histologically examined afterward. Electrocerebral activity disappeared within 30 sec after balloon inflation. At 3 min, noradrenaline and adrenaline levels had increased 75- and 40-fold, respectively, compared to pre-induction levels. The hemodynamic response was characterized by an early and rapid increase of hemodynamic variables at 2.9 +/- 0.2 min. This was followed by a second phase of normalization or deterioration. Two distinct subgroups (n = 9) became hemodynamically unstable (HDU), characterized by a systolic arterial blood pressure < 90 mm Hg, at 108 +/- 29 min, and progressively deteriorated to 67 +/- 8 mm Hg at 240 min after inflation of the balloon. The hemodynamic variables of the other, hemodynamically stable (HDS), subgroup (n = 6) normalized at 60 min after inflation. Hemodynamic deterioration of the HDU subgroup compared to the HDS subgroup was significant at 10 min after induction of brain death. The maximum values of RPP were similar in the two subgroups. Respiratory and metabolic variables at the end of the experiment were not different in both subgroups. Histological evidence of myocardial damage was present in 73% (11/15) of the brain dead cats and absent in the control group. The histological changes were identified both in hearts of HDU (6/9) and HDS (5/6) cats. In the cat, no relationships were demonstrated between the acute increase of myocardial workload, the occurrence of hemodynamic deterioration, and myocardial histological changes after rapid induction of brain death. These results may contribute to the discussion whether hemodynamic instability of the donor is an appropriate exclusion criterion for heart transplantation.

Animals↗
PubMed1997

Usefulness of gastric intramucosal pH for monitoring hemodynamic complications in critically ill children.

OBJECTIVE: To assess the efficacy of gastric intramucosal pH for the evaluation of tissue perfusion and prediction of hemodynamic complications in critically ill children. DESIGN: Open prospective study without controls. SETTING: Pediatric intensive care unit (ICU) of a tertiary care university pediatric hospital. PATIENTS: Thirty critically ill children (16 boys and 14 girls), age range: 3 months-12 years. MEASUREMENTS AND RESULTS: A tonometry catheter was placed in the stomach of all patients on admission to the pediatric ICU. Simultaneous tonometry and arterial gas measurements were made on admittance and every 6-12 h throughout the study; a total of 202 measurements were made. The catheter was removed after extubation and/or when the patient was hemodynamically stable. Intramucosal pH was calculated using the Henderson-Hasselbalch equation based on the pCO2 of the tonometer and arterial bicarbonate. Intramucosal pH values between 7.30 and 7.45 were considered to be normal. The patient's condition was analyzed using the Pediatric Risk Mortality Score (PRISM). The relations between intramucosal pH and the presence of major hemodynamic complications (cardiopulmonary arrest, shock), minor hemodynamic complications (hypotension, hypovolemia or arrhythmia), death, PRISM score and the duration of the stay in the pediatric ICU were analyzed. Intramucosal pH on admission was 7.48 +/- 0.15 on average (range 7.04-7.68). Five patients (16%) had an intramucosal pH lower than 7.30 on admission; these patients did not have a higher incidence of hemodynamic complications. The 16 patients (53%) who had an intramucosal pH of less than 7.30 at some time during the course of their disease had more hemodynamic complications than the patients who did not have pH lower than 7.30 (p < 0.0001). Every case of cardiopulmonary arrest and shock was related to intramucosal pH of less than 7.30. Patients with major complications (cardiopulmonary arrest and shock) had lower intramucosal pHs than those with minor hemodynamic complications (p = 0.03); similarly, they had low intramucosal pH readings more often than those with minor complications (p = 0.0032). Intramucosal pH values less than 7.30 had a sensitivity of 90% and a specificity of 98% as a predictor of hemodynamic complications. There was no relation between intramucosal pH lower than 7.30 and either PRISM or the duration of the stay in the pediatric ICU. Patients with intramucosal pH less than 7.20 had a higher PRISM than the patients who did not have pH lower than 7.20 (p < 0.05). A patient who died during the study due to cardiopulmonary arrest had prior intramucosal pH measurements of 7.23 and 7.10, and three patients died of late complications after the end of the study. Hemodynamic complications were not detected with arterial pH. Gap pH (arterial pH-intramucosal pH) and standard pH measurements yielded the same results as gastric intramucosal pH. CONCLUSION: Intramucosal pH could provide a useful early indication of hemodynamic complications in critically ill children.

Acid-Base Equilibrium↗
PubMed1995

Dissociation between peak exercise oxygen consumption and hemodynamic dysfunction in potential heart transplant candidates.

OBJECTIVES: The purpose of this study was to determine how often peak exercise oxygen consumption (VO2) misclassifies the severity of cardiac dysfunction in potential heart transplant candidates. BACKGROUND: Cardiopulmonary exercise testing is being used to help select heart transplant candidates on the basis of the assumption that a low peak exercise VO2 indicates severe hemodynamic dysfunction and a poor prognosis. However, noncardiac factors, such as muscle deconditioning, can also influence exercise capacity. Therefore, peak exercise VO2 may overestimate the severity of cardiac dysfunction in some patients. METHODS: Hemodynamic and respiratory responses to maximal treadmill exercise were measured in 64 sequential patients undergoing evaluation for heart transplantation, all of whom had an ejection fraction < 35% and reduced peak exercise VO2 levels (mean [+/- SD] 13.3 +/- 2.7 ml/min per kg). RESULTS: Twenty-eight (44%) of 64 patients exhibited a reduced cardiac output response to exercise and pulmonary wedge pressure > 20 mm Hg at peak exercise, consistent with severe hemodynamic dysfunction. Twenty-three patients (36%) exhibited a normal cardiac output response to exercise but a wedge pressure > 20 mm Hg at peak exercise, suggesting moderate hemodynamic dysfunction. Thirteen patients (20%) exhibited a normal cardiac output and wedge pressure < 20 mm Hg at peak exercise, suggesting mild hemodynamic dysfunction. Despite these markedly different hemodynamic responses, all three groups exhibited similar peak exercise VO2 levels (mild dysfunction 14.2 +/- 3.5 ml/min per kg, moderate dysfunction 13.9 +/- 2.7 ml/min per kg, severe dysfunction 12.4 +/- 2.1 ml/min per kg). A peak exercise VO2 level < 14 ml/min per kg, considered to reflect severe hemodynamic dysfunction, was observed in 18 of the patients with a normal cardiac output response to exercise, whereas 7 patients with severe hemodynamic dysfunction had a peak VO2 level > 14 ml/min per kg. CONCLUSIONS: More than 50% of potential heart transplant candidates with a reduced peak exercise VO2 level exhibit only mild or moderate hemodynamic dysfunction during exercise. Hemodynamic responses to exercise should be directly measured in potential transplant candidates to confirm severe circulatory dysfunction.

Adult↗
PubMed2005

Delayed hemodynamic responses in schizophrenia.

While there are many reports of reduced amplitude of hemodynamic responses in schizophrenia, there are no reports of delayed hemodynamic responses, in spite of event-related brain potential (ERP) evidence of slowed neural responses. Recently, Henson et al. (2002) [Henson, R., Price, C., Rugg, M., Turner, R., Friston, K., 2002. Detecting latency differences in event-related BOLD responses: application to words versus nonwords and initial versus repeated face presentations. NeuroImage, 15:83-97] proposed a new method for testing small latency effects (<2 s) in hemodynamic responses. fMRI data were collected during a visual oddball task with infrequent (12%) targets (K) and frequent (88%) standards (X), presented every 1-3 s pseudorandomly, with 7-24 s between targets. SPM99 yielded parameter estimates for the hemodynamic response and its temporal derivative (TD). Beta images reflecting hemodynamic response magnitude to target stimuli were minimally thresholded (P < 0.05, uncorrected), and latencies were estimated for surviving voxels using TD and hemodynamic response beta values. DSM-IV schizophrenia patients (n = 12) and sex- and age-matched healthy control subjects (n = 12) were recruited from the community. Although groups differed only minimally in activation height, hemodynamic responses were significantly delayed in basal ganglia, thalamus, and anterior cingulate in patients with schizophrenia. Psychomotor slowing reflected in reaction times to targets recorded outside the magnet was related to hemodynamic slowing in basal ganglia, anterior cingulate, thalamus, as well as left cerebellum in controls. Delays in the hemodynamic response have far-reaching implications for understanding the pathophysiology of schizophrenia from slowed neural responses to slowed substrate delivery, and depending of the degree of delay, may raise methodological issues regarding modeling hemodynamic responses in patients and controls.

Adult↗
PubMed2005

Coupling of the cortical hemodynamic response to cortical and thalamic neuronal activity.

Accurate interpretation of functional MRI (fMRI) signals requires knowledge of the relationship between the hemodynamic response and the neuronal activity that underlies it. Here we address the question of coupling between pre- and postsynaptic neuronal activity and the hemodynamic response in rodent somatosensory (Barrel) cortex in response to single-whisker deflection. Using full-field multiwavelength optical imaging of hemoglobin oxygenation and electrophysiological recordings of spiking activity and local field potentials, we demonstrate that a point hemodynamic measure is influenced by neuronal activity across multiple cortical columns. We demonstrate that the hemodynamic response is a spatiotemporal convolution of the neuronal activation. Therefore, positive hemodynamic response in one cortical column might be explained by neuronal activity not only in that column but also in the neighboring columns. Thus, attempts at characterizing the neurovascular relationship based on point measurements of electrophysiology and hemodynamics may yield inconsistent results, depending on the spatial extent of neuronal activation. The finding that the hemodynamic signal observed at a given location is a function of electrophysiological activity over a broad spatial region helps explain a previously observed increase of local vascular response beyond the saturation of local neuronal activity. We also demonstrate that the oxy- and total-hemoglobin hemodynamic responses can be well approximated by space-time separable functions with an antagonistic center-surround spatial pattern extending over several millimeters. The surround "negative" hemodynamic activity did not correspond to observable changes in neuronal activity. The complex spatial integration of the hemodynamic response should be considered when interpreting fMRI data.

Animals↗
PubMed2006

Nitric oxide scavenging by hydroxocobalamin may account for its hemodynamic profile.

BACKGROUND: Antidotal doses of hydroxocobalamin are associated with transient increases in blood pressure in some animals and humans. These studies in anesthetized rabbits were undertaken to explore the possible mechanisms underlying the hemodynamic effects of hydroxocobalamin by investigating 1) possible hemodynamic effects of cyanocobalamin, which is formed on a molar-to-molar basis when hydroxocobalamin binds cyanide, and 2) the interference of hydroxocobalamin with the endothelial nitric oxide system. METHODS: Study 1 investigated the hemodynamic effects of cyanocobalamin. This study included two treatment arms: 1) cyanocobalamin (75 mg/kg, IV) followed by saline (n = 7) and 2) saline followed by cyanocobalamin (n = 7). Study 2 assessed the hemodynamic effects of hydroxocobalamin (75 mg/kg, IV) in the presence and absence of the nitric oxide synthase inhibitor L-Nomega-nitro-L-arginine methyl ester (L-NAME; 30 mg/kg, IV). Nitric oxide synthase inhibition itself increases blood pressure. Thus, as part of Study 2, the hemodynamic effects of hydroxocobalamin were also investigated in the presence of an equipressor dose of angiotensin II (ANGII; 0.05 microg/kg/min, IV) in order to determine whether elevated blood pressure per se could interfere with hydroxocobalamin's hemodynamic effects. This study included six treatment arms (designated as first treatment + second treatment): saline + saline (n = 5), L-NAME + saline (n = 7), saline + hydroxocobalamin (n = 7), L-NAME + hydroxocobalamin (n = 7), ANGII + hydroxocobalamin (n = 7), and ANGII + saline (n = 7). RESULTS: In Study 1, the effects of cyanocobalamin on hemodynamic parameters were indistinguishable from those of saline. In Study 2, hydroxocobalamin infusion was associated with moderate hemodynamic effects, including an increase in systemic vascular resistance, an increase in blood pressure, and a decrease in cardiac output. Administration of L-NAME abolished the effects of hydroxocobalamin on all hemodynamic parameters. ANGII at a dose producing a pressor response comparable to that of L-NAME did not influence the hydroxocobalamin-associated hemodynamic changes. CONCLUSION: These studies in anesthetized rabbits demonstrate that the moderate pressor effect of hydroxocobalamin is not related to the formation of cyanocobalamin but is very likely related to the scavenging of nitric oxide by hydroxocobalamin.

Animals↗
PubMed1992

Right ventricular wall motion disturbance and determinants of the appearance of hemodynamic right ventricular infarction.

In order to elucidate the mechanisms of the appearance of hemodynamic right ventricular infarction (RVI), we studied right and left ventriculograms and hemodynamic findings in 52 patients with acute inferior myocardial infarction. Right ventricular wall motion disturbance (RVWMD) was detected in 69% of patient but hemodynamic RVI was observed only in 16%. Among patients with RVWMD, there was no significant difference in right ventricular ejection fraction between those with (group III) and without (group II) hemodynamic RVI, suggesting that right ventricular (RV) systolic dysfunction does not independently produce hemodynamic RVI. Right ventricular end-diastolic volume index was similar in groups II and III in spite of higher mRA in group III. The result suggested that the RV compliance of group III was decreased. Heart rate (HR) was significantly lower in group III than in group II. Not only physiologic pacing but also VVI pacing significantly improved hemodynamics in patients with hemodynamic RVI. A positive correlation between HR and cardiac index was observed (r = 0.56, p < 0.001) in patients with RVWMD. Decreased RV compliance and bradycardia were considered to be determinants of the appearance of hemodynamic RVI. Volume loading did not improve hemodynamics significantly in patients with hemodynamic RVI.

Angiography, Digital Subtraction↗
PubMed1992

Acute hemodynamic effects of digoxin alone or in combination with other vasoactive agents in patients with congestive heart failure.

Although digitalis preparations have been in use for greater than 200 years, it is only within the last 2 decades that the central hemodynamic and neurohumoral effects occurring over several hours following intravenous administration of digoxin have been investigated in patients with congestive heart failure (CHF). Although digoxin has been shown to stimulate myocardial contractility in tissue preparations, its positive inotropic activity does not consistently translate into improvements in hemodynamic measurements in humans. Digoxin given intravenously results in increased cardiac index and decreased heart rate, left ventricular filling pressure, and right atrial pressure, as well as in acute attenuation of neurohumoral abnormalities, in patients with chronic CHF who have abnormal baseline hemodynamic measurements. Unlike other drugs with positive inotropic activity, however, digoxin does not influence hemodynamics in normal volunteers or in CHF patients in whom hemodynamics have been normalized with other therapies. These differing effects may be related to the drug's diverse peripheral vascular effects in CHF patients in whom vasodilation may occur in comparison with those that occur in normal subjects in whom the peripheral vasoconstrictor effects may prevent the inotropic effects of the drug from being translated into an increase in cardiac output. The hemodynamic effects of digoxin in patients with chronic CHF due primarily to diastolic dysfunction have not been fully investigated. Intravenous digoxin produces hemodynamic effects in patients with CHF associated with acute myocardial infarction, but these changes are small compared with those resulting from the administration of dobutamine. Digoxin does not appear to influence hemodynamic measurements in patients with right ventricular dysfunction unless concomitant left ventricular failure is present. In patients with chronic left ventricular dysfunction, the hemodynamic effects of intravenous digoxin and vasodilators are enhanced when these agents are given in combination.

Cardiotonic Agents↗