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PubMed1995

Arginase release following liver reperfusion. Evidence of hemodynamic action of arginase infusions.

Immediately after hepatic reperfusion in human orthotopic liver transplantation, high amounts of arginase are released from the graft, thereby influencing nitric oxide metabolism. This metabolic alteration may be one component of the ischemia-reperfusion syndrome in OLT with its hemodynamic disturbances (e.g., systemic hypotension, pulmonary hypertension). The aim of this study was to compare hemodynamic and metabolic changes following OLT in the pigs with those obtained under arginase infusions in catheterized, anesthetized pigs. Following liver revascularization in the pigs, plasma arginase concentrations increased from 48 +/- 19 IU/L to 2613 +/- 944 IU/L, resulting in a drop in plasma levels of L-arginine (-87%) and in a drop in nitrite (-82%) and nitrate (-53%) concentrations. Of the measured organ-specific hemodynamic alterations, the mean pulmonary arterial pressure increased from 17 +/- 2 mmHg to 30 +/- 5 mmHg, whereas the flow/pressure index of the portal vein decreased about 60%. A primed continuous infusion of arginase (25,000 IU) increased plasma arginase levels to a maximum of 3,690 +/- 962 IU and evoked a decrease of L-arginine, but did not alter plasma nitrite or nitrate levels. The administration of arginase in healthy pigs did not influence cardiac output, mean arterial pressure, heart rate, or total peripheral resistance, but led to an increase of mean pulmonary arterial pressure from 19 +/- 3 to 48 +/- 5 mmHg and to a reduction of arterial hepatic blood flow from 229 +/- 65 ml/min to 154 +/- 41 ml/min. From this we conclude that high levels of liver arginase cause hemodynamic alterations in the lung and the liver. We hypothesize that the pulmonary hypertension and the reduced hepatic blood flow found during the immediate reperfusion period after OLT are possibly related to the increased arginase release due to the hepatic damage of the graft.

Animals↗
PubMed1994

[The behavior of central and peripheral hemodynamics in isometric and dynamic stress in hypertensive patients treatment with regular sauna therapy].

Effective treatment of hypertension includes decrease of blood pressure at rest, dynamic and isometric exercise. Therefore, we investigated the hemodynamic changes by radiocardiography (central hemodynamic) and Xenon-133-muscle clearance (peripheral hemodynamic) before and after a sauna treatment during a period of 3 months. 46 hypertensive men (WHO I-II, aged 41 +/- 11 years) participated in the study. Systolic and diastolic blood pressure at rest and during dynamic exercise were decreased significantly (p < or = 0.01) by sauna therapy. Change of blood pressure at isometric exercise was not significant (from 157.5 +/- 16.5 mmHg to 155.0 +/- 15.4 mmHg). The changes of cardiac output and total peripheral resistance were also not significant. Half-time of muscle clearance decreased significantly (from 4.4 +/- 1.9 min to 3.2 +/- 1.2 min, p < or = 0.01) and functional cross-section A increased significantly (from 3.8 +/- 0.9 mm2.c to 4.4 +/- 0.9 mm2.c, p < or = 0.01) after the sauna therapy at dynamic exercise, but not at isometric exercise. These results show the changes between isometric and dynamic exercise, which can only be explained well by a study of peripheral hemodynamic. Contrary to dynamic exercise, sauna therapy did not significantly decrease blood pressure at isometric exercise.

Adult↗
PubMed1994

[Pulmonary hemodynamics during oxygen non-inhalation in patients with home oxygen therapy].

We examined the effects of the stopping of oxygen inhalation on pulmonary hemodynamics in 19 patients with stable chronic cor pulmonary with 1 year of Home Oxygen Therapy (HOT). All patients were classified into two groups in which hemodynamic examination was performed under oxygen inhalation (Group A; 10) or under air breathing from 4 hours before examination (Group B; 9). The hemodynamic examination was repeated after 2 hours of stopping oxygen inhalation in Group A, and was repeated 2 hours after restarting oxygen in Group B. The mean pulmonary arterial pressure (mPAP) decreased significantly from 25.2 +/- 7.2 Torr before HOT to 20.4 +/- 3.2 Torr after 1 year of HOT, and then increased to 27.6 +/- 5.6 Torr after stopping oxygen. In contrast, mPAP in Group B did not change: 32.9 +/- 9.4 Torr before HOT, 29.4 +/- 8.2 Torr during stopping of oxygen and 27.6 +/- 5.6 Torr 2 hours after restarting oxygen after 1 year of HOT. These findings suggest that stopping oxygen inhalation in patients with long-term HOT can markedly affect pulmonary hemodynamics as well as the prognosis.

Aged↗
PubMed1995

[Comparative studies of hemodynamics under prostacyclin and nifedipine in patients with Eisenmenger syndrome].

In 10 patients 4-20 years of age with obstructive pulmonary vascular disease after Eisenmenger reaction pulmonary arterial and aortic pressure, pulmonary and systemic flow (Qp, Qs), and pulmonary and systemic vascular resistance (Rp, Rs) were determined before and during stepwise increasing doses of prostacyclin and nifedipine. Prostacyclin caused a significant decrease of pulmonary and systemic vascular resistance and a significant decrease of pressures in the aorta and the pulmonary artery, whereas no significant changes of hemodynamics were realized following nifedipine. The individual hemodynamic changes during prostacyclin were favorable in only two patients who demonstrated a marked decrease of Rp with no substantial change of Rs resulting in an increase in arterial oxygen saturation. In the other patients prostacyclin resulted in an adverse effect with a decrease of Rs exceeding that of Rp in 5 patients, a paradoxical increase of Rp in 1 patient, and a critical decrease of Qs with respective low central venous blood oxygen saturation and consequently low arterial oxygen saturation caused by a small right-to-left shunt in 2 patients. Nifedipine did not bring about a significant general change of hemodynamic parameters. The individual control showed no effect in 5 patients, an unfavorable effect by a decrease of Rs exceeding that of Rp in 2 patients, and a favorable net effect in only 3 patients, induced in 1 patient only after a very high dosage of nifedipine and leading to a certain increase of arterial oxygen saturation in only 1 other patient. From our results a beneficial effect of nifedipine in an average dosage on the hemodynamics of patients with Eisenmenger syndrome cannot be recognized.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1995

Systemic hemodynamic, forearm vascular, renal, and humoral responses to sustained cardiopulmonary baroreceptor deactivation in well-compensated cirrhosis.

The aim of this study was to assess baroreceptor function in well-compensated cirrhosis by determining the forearm vascular, renal, and humoral responses to sustained baroreceptor deactivation. The effect of sodium status on baroreceptor function was also assessed. Eight cirrhotic patients and 10 age- and sex-matched controls were studied twice after a 20 mmol and 200 mmol of sodium/d diet for 7 days. Systemic and renal hemodynamics, renal sodium handling, forearm blood flow, and neurohumoral factors were assessed before, during, and after the application of lower body negative pressure (LBNP) for 1 hour. Controls and cirrhotic patients had similar baseline mean arterial pressure, heart rate, forearm and renal hemodynamics. High-sodium intake resulted in suppression of sympathetic nervous activity in the controls (plasma norepinephrine, 1.06 +/- 0.11 nmol/L on low vs. 0.76 +/- 0.08 nmol/L on high sodium; P = 0.01) but not in the cirrhotic patients (1.35 +/- 0.22 nmol/L on low vs. 1.26 +/- 0.11 nmol/L on high sodium; P > 0.05). Both groups responded to LBNP with significant further increases in plasma norepinephrine, resulting in significant decreases in forearm blood flow on both sodium diets. Controls also responded with a significant worsening of renal hemodynamics on low-sodium diet only, but this was not observed in the cirrhotic patients on either diet. Therefore, in well-compensated cirrhotic patients: (1) sympathetic activation occurs despite an adequate, effective arterial filling, and this may contribute to sodium retention; and (2) baroreceptor function is normal. Apparent end organ unresponsiveness within the renal circulation may account for the lack of renal hemodynamic changes to reflex sympathetic stimulation.

Adult↗
PubMed1994

Hemodynamic effects of different modes of mechanical ventilation in acute cardiac and pulmonary failure: an experimental study.

OBJECTIVE: To determine the hemodynamic effects of four different modes of mechanical ventilation in an animal model of acute cardiac and pulmonary failure. DESIGN: Prospective, randomized, crossover design. SETTING: University research laboratory. SUBJECTS: Twelve piglets weighing 10 to 16 kg. INTERVENTIONS: The experimental protocol consisted of three stable 30-min periods: when ventricular and pulmonary functions were normal (control), after the induction of acute cardiac failure by the administration of a beta-adrenergic receptor blocker, and after pulmonary failure induced by repeated lung lavage. Modes of mechanical ventilation included controlled mechanical ventilation, high-frequency oscillation, synchronized high-frequency jet ventilation, and external negative pressure oscillation combined with pressure support ventilation. Each mode of respiratory support was randomly and sequentially applied to each animal with the assessment of cardiopulmonary function at the end of each period. MEASUREMENTS AND MAIN RESULTS: Continuous monitoring included electrocardiogram, right atrial, left ventricular end-diastolic, pulmonary arterial, intrathoracic aortic, arterial, esophageal, and transpulmonary pressures and arterial and mixed venous oxygen saturation measurements. In addition, cardiac output using the thermodilution technique was measured intermittently. Whereas in the control period cardiac index was significantly (p < .05) higher during synchronized high-frequency jet ventilation (193 +/- 19.3 mL/kg/min) than during controlled mechanical ventilation (151 +/- 12.1 mL/kg/min) and high-frequency oscillation (151 +/- 18.1 mL/kg/min), there was no significant hemodynamic difference between the four modes of mechanical ventilation in the cardiac and pulmonary failure periods. In the pulmonary failure period, transpulmonary pressure was significantly higher during high-frequency oscillation (7.1 +/- 1.6 mm Hg) than during controlled mechanical ventilation (5.6 +/- 0.6 mm Hg), high-frequency ventilation (4.1 +/- 0.4 mm Hg), and external negative pressure oscillation combined with pressure support ventilation (5.3 +/- 0.5 mm Hg). CONCLUSIONS: Synchronized high-frequency ventilation improves cardiac performance in control conditions. No hemodynamic difference is present between the four modes of mechanical ventilation in the cardiac and pulmonary failure periods. External negative pressure oscillation combined with pressure support ventilation has moderate hemodynamic advantages over controlled mechanical ventilation and high-frequency oscillation in different clinical settings, but it also results in a deterioration of pulmonary gas exchange during the pulmonary failure period.

Animals↗
PubMed1994

Diurnal fluctuations of portal and systemic hemodynamic parameters in patients with cirrhosis.

A close temporal relationship between higher levels of portal pressure during the night and the peak incidence of acute variceal bleeding has recently been demonstrated in patients with cirrhosis. Because hemodynamic changes may have a role in triggering this hemorrhagic episode, we measured systemic and portal hemodynamic parameters at 4-hr intervals for 24 hr in 12 cirrhotic patients. These results were compared with those obtained in eight healthy subjects. Cardiac output, femoral and portal blood flows were measured by Doppler technique. In cirrhotic patients, heart rate and mean arterial pressure remained constant throughout the whole study period. A marked and significant increase in portal blood flow (917 +/- 248 ml/min) (mean +/- S.D.) as compared with mesor values (649 +/- 114 ml/min, p < 0.001) was observed at midnight. This effect was accompanied by a mild but significant rise of cardiac output (from 6.5 +/- 0.7 to 6.8 +/- 0.7 l/min, p < 0.01) at 2400 hr. A significant correlation between both hemodynamic parameters was found (r = 0.78, p < 0.01). Cosinor analysis showed a significant (p < 0.05) circadian rhythm for both portal blood flow and cardiac output with an acrophase at 0050 hr. In the healthy subjects group, a significant decrease of mean arterial pressure and heart rate was observed at 2400 hr. Cosinor analysis confirmed the presence of significant rhythm for both hemodynamic parameters. In contrast with cirrhotic patients, no significant changes were observed in portal blood flow and cardiac output in healthy subjects. Our results show that in patients with cirrhosis, maximal increases in portal blood flow occur at night.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

[Computer monitoring of hemodynamics during assisted circulation and extracorporeal detoxication in abdominal surgery].

Basic central and regional hemodynamic parameters have been studied using a computer monitoring system in 57 patients with acute abdominal surgical diseases during special extracorporeal procedures. Indications for regional assisted circulation (RAC) as well as regularities in hemodynamic changes during and after procedures have been established. The data of monitoring have shown that RAC and RAC in combination with hemosorption have in most cases a marked favourable effect on abdominal hemodynamics: mesenteric and portal blood flow is increased and consequently total hepatic flow is activated. The flow of portal blood leads to an increase in central venous pressure. Unfavourable tendencies have been established in changes of central hemodynamics during the procedures. They are: calculated intervals of the rates of central venous pressure increment and cardiac output decrement. This made it possible to optimize the use of extracorporeal procedures in patients with such diseases.

Abdomen↗
PubMed1994

Making the relationships visible: testing alternative display design strategies for teaching principles of hemodynamic monitoring and treatment.

A hemodynamic monitoring and control task was used to explore the utility of perceptually based displays to teach basic hemodynamic principles. The baseline display showed discrete values of key hemodynamic data elements. Alternative displays showed (a) anatomical relationships between those elements, and (b) causal constraints. Critical care nurses and student nurses used simulated "drugs" to correct simple hemodynamic disturbances using the three displays. Showing the anatomic constraints on pressure and flow improved treatment coordination by novices. Showing how etiological factors related to symptoms shortened the time required to reach a criterion level of performance and improved treatment coordination for both novices and experts.

Computer Graphics↗
PubMed1994

Relationship between hemodynamic changes and blood hormone concentrations after cardiac surgery in children with congenital heart disease.

OBJECTIVES: To evaluate changes in atrial natriuretic factor in relation to modifications in hemodynamic variables, and to evaluate hormones determining salt and water metabolism after heart surgery in children with congenital heart disease. DESIGN: Prospective study. SETTING: Medical-surgical pediatric intensive care unit (ICU) in a tertiary referral center. PATIENTS: Sixty-five infants and children admitted to the pediatric ICU with congenital heart disease who underwent cardiac surgery with extracorporeal circulation. The control group consisted of 48 children undergoing noncardiac surgical interventions, without a history of cardiac disease and with normal hemodynamic variables. MEASUREMENTS AND MAIN RESULTS: Patients with congenital heart disease were distributed into two groups, according to hemodynamic variables. Group 1 consisted of patients with normal pulmonary blood flow (pulmonary/systemic blood flow ratio of < 2, pulmonary arterial systolic pressure of < 35 mm Hg, pulmonary arterial systolic pressure/aortic systolic pressure ratio of < 0.35). Group 2 consisted of patients with relatively increased pulmonary blood flow (pulmonary/systemic blood flow ratio of > 2.5, pulmonary arterial systolic pressure of > 65 mm Hg, pulmonary arterial systolic pressure/aortic systolic pressure ratio of > 0.75). Blood samples were obtained 24 hrs before, and 24 and 48 hrs after surgery. Hormone determinations included plasma concentrations of atrial natriuretic factor, vasopressin, plasma renin activity, corticotropin, cortisol, and aldosterone. Hemodynamic measurements were recorded simultaneously with blood sampling. Twenty-four hours before surgery, plasma concentrations of atrial natriuretic factor were higher in congenital heart disease patients than in the control group (67.36 +/- 93.44 vs. 15.11 +/- 8.29 pmol/L) (p < .001). Plasma concentrations of atrial natriuretic factor were 57.12 +/- 82.20 and 74.63 +/- 101.03 pmol/L in groups 1 and 2, respectively. Before surgery, in group 2 patients, there was a significant correlation between mean right atrial pressure and atrial natriuretic factor (r2 = .64; p < .001), vasopressin (r2 = .55; p < .001), cortisol (r2 = .43; p < .01), corticotropin (r2 = .53; p < .01), and aldosterone (r2 = .57, p < .001). None of these correlations were observed in group 1. However, 24 hrs after surgery, we found a significant correlation between diastolic blood pressure and atrial natriuretic factor in group 1. Plasma concentrations of atrial natriuretic factor did not change significantly after surgery. After surgery, the correlation between mean right atrial pressure and the various hormone concentrations persisted at 24 hrs (p < .05), but not at 48 hrs. Twenty-four hours after surgery, patients with a central venous pressure of > 7 mm Hg showed higher concentrations of atrial natriuretic factor than those patients with central venous pressures of < 7 mm Hg (p < .05). However, there was a large overlap of atrial natriuretic factor values between the two groups. CONCLUSIONS: Patients with congenital heart disease have increased plasma concentrations of atrial natriuretic factor. During the early postoperative period, in patients with a more severe degree of congenital heart disease, the increase in central venous pressure correlated with higher plasma concentrations of atrial natriuretic factor. High pulmonary blood flow was associated with an increase in plasma renin activity and serum aldosterone, and an increased secretion of atrial natriuretic factor.

Adolescent↗
PubMed1994

Hemodynamic responses to external counterbalancing of auto-positive end-expiratory pressure in mechanically ventilated patients with chronic obstructive pulmonary disease.

OBJECTIVE: To study the effect of positive end-expiratory pressure (PEEP) on right ventricular hemodynamics and ejection fraction in patients with chronic obstructive pulmonary disease and positive alveolar pressure throughout expiration by dynamic hyperinflation (auto-PEEP). DESIGN: Open, prospective, controlled trial. SETTING: General intensive care unit of a community hospital. PATIENTS: Ten patients sedated and paralyzed with an acute exacerbation of chronic obstructive pulmonary disease undergoing mechanical ventilation. INTERVENTIONS: Insertion of a pulmonary artery catheter modified with a rapid response thermistor and a radial arterial catheter. PEEP was then increased from 0 (PEEP 0) to auto-PEEP level (PEEP = auto-PEEP) and 5 cm H2O above that (PEEP = auto-PEEP +5). MEASUREMENTS: At each level of PEEP, airway pressures, flow and volume, hemodynamic variables (including right ventricular ejection fraction by thermodilution technique), and blood gas analyses were recorded. MAIN RESULTS: The mean auto-PEEP was 6.6 +/- 2.8 cm H2O and the total PEEP reached was 12.2 +/- 2.4 cm H2O. The degree of lung inflation induced by PEEP averaged 145 +/- 87 mL with PEEP = auto-PEEP and 495 +/- 133 mL with PEEP = auto-PEEP + 5. The PEEP = auto-PEEP caused a right ventricular end-diastolic pressure increase, but there was no other significant hemodynamic change. With PEEP = auto-PEEP + 5, there was a significant increase in intravascular pressures; this amount of PEEP reduced cardiac output (from 4.40 +/- 1.38 L/min at PEEP 0 to 4.13 +/- 1.48 L/min; p < .05). The cardiac output reduction induced by PEEP = auto-PEEP + 5 was > 10% in only five cases and this group of patients had significantly lower right ventricular volumes than the group with less cardiac output variation (right ventricular end-diastolic volume: 64 +/- 9 vs. 96 +/- 26 mL/m2; right ventricular end-systolic volume: 38 +/- 6 vs. 65 +/- 21 mL/m2; p < .05) without significant difference in the other variables that were measured. Neither right ventricular ejection fraction nor right ventricle volumes changed as PEEP increased, but there were marked interpatient differences and also pronounced changes in volume between stages in individual patients. CONCLUSIONS: In the study conditions, PEEP application up to values approaching auto-PEEP did not result in the impairment of right ventricular hemodynamics, while higher levels reduced cardiac output in selected patients.

APACHE↗
PubMed1994

Hemodynamics of mitral stenosis: a review.

This review discusses the latest developments in the hemodynamics of mitral stenosis. English-language journal articles, reviews, and textbooks from the clinical, physiology, and engineering literature related to mitral valve stenosis were identified and reviewed. The main conclusions are: (1) the hemodynamics of mitral stenosis are determined by the complex anatomical and pathophysiologic features of the valve apparatus, (2) the properties of the left ventricle, atrium, and pulmonary vasculature also have a major impact on the hemodynamic significance and the clinical syndrome of mitral stenosis, (3) the valve and the cardiac chambers have a functional reserve that become exhausted as the stenosis worsens and/or the compensatory mechanisms of the chambers fail, and (4) a careful approach to data acquisition and analysis will lead to an accurate assessment of the hemodynamics of mitral stenosis before and after therapeutic interventions.

Atrial Function↗
PubMed1994

Characterization of the hemodynamic and metabolic alterations in the large colon of horses during low-flow ischemia and reperfusion.

Effects of low-flow ischemia and reperfusion of the large colon on systemic and colonic hemodynamic and metabolic variables were determined in horses. Twenty-four adult horses were randomly allocated to 3 groups: sham-operated (n = 6), 6 hours of ischemia (n = 9), and 3 hours of ischemia and 3 hours of reperfusion (n = 9). Low-flow ischemia was induced in groups 2 and 3 by reducing colonic arterial blood flow to 20% of baseline. Heart rate, arterial blood pressures, cardiac index, pulmonary artery pressure, right atrial pressure, and colonic blood flow were monitored. Arterial, mixed-venous, and colonic venous blood gas and oximetry analyses; PCV; and blood lactate and pyruvate and plasma total protein concentrations were measured. Data were recorded, and blood samples were collected at baseline and at 30-minute intervals for 6 hours; additionally, data were collected at 185, 190, and 195 minutes (corresponding to 5, 10, and 15 minutes of reperfusion in group-3 horses). There were no differences among groups at baseline or across time for any systemic hemodynamic or metabolic variable. Colonic blood flow did not change across time in group-1 horses. Colonic blood flow significantly (P < 0.05) decreased to 20% of baseline at induction of ischemia in horses of groups 2 and 3 and remained significantly decreased throughout the ischemic period in horses of groups 2 (6 hours) and 3 (3 hours). Colonic blood flow significantly (P < 0.05) increased above baseline by 5 minutes of reperfusion in group-3 horses. Colonic oxygen delivery and oxygen consumption, and colonic venous pH, PO2, percentage saturation of hemoglobin, and oxygen content were significantly (P < 0.05) decreased within 30 minutes after induction of ischemia in horses of groups 2 and 3; colonic venous PCO2, colonic oxygen extraction ratio, and lactate and pyruvate concentrations were significantly (P < 0.05) increased by 30 minutes of ischemia. These alterations continued throughout ischemia, but within 5 minutes of reperfusion in group-3 horses, these variables either returned to baseline (pH, PCO2, lactate, pyruvate), significantly (P < 0.05) increased above baseline (PO2, oxygen content, % saturation of hemoglobin), or significantly (P < 0.05) decreased below baseline (colonic oxygen extraction ratio). Colonic oxygen consumption remained decreased during reperfusion in group-3 horses. Colonic mucosal ischemia-reperfusion injury observed in this model of ischemia was associated with local colonic hemodynamic and metabolic alterations in the presence of systemic hemodynamic and metabolic stability.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1993

[Changes on hemodynamics and oxygen delivery in patients with septic shock].

Since there are still some confusions in hemodynamics and changes of oxygen delivery (DO2) in septic shock which has a high mortality, the 40 septic shock patients were observed in hemodynamics and DO2 in general ICU of Peking Union Medical College Hospital. Both surviving group and nonsurviving group had their hyperdynaminc state in hemodynamics at the beginning of septic shock. In survivors, hemodynamics were back to normal range at the 4th day of septic shock. But nonsurvivors were still in the hyperdynamic state all way to the end stage. A critical level of DO2, which was found only in survivors, was 670 ml/min.m2. The oxygen supply dependency of oxygen consumption (VO2) was found in nonsurvivors even DO2 was highly increased. The oxygen extraction (O2 ext) in nonsurvivors was lower than in survivors when DO2 was lower than critical level. We think that maintaining hyperdynamic state in septic shock does not certainly improve survival rate. In the septic shock patients with pathologic oxygen supply dependency, DO2 is not able to be increased to meet tissue oxygen demand. The changes of O2 ext have a significance in prediction of outcome of septic shock. The current therapies for septic shock have remarkable limitation. So the new treatment methods of septic shock, not only to increases DO2, should be found out for improving the survival rate further.

Adult↗
PubMed1994

The hemodynamic effects of continuous intravenous infusion of propofol at higher rates.

The new formula of propofol was introduced in 1985. Because of its characteristics of rapid onset and elimination, it was often used as a drug of induction and maintenance of total intravenous anesthesia. However, the hemodynamic effects of propofol was still controversial. The present study was to observe its hemodynamic reactions at higher infusion rate. Hemodynamic studies were performed in 11 female patients, 17 to 54 years old, ASA class I-II, presenting for major lower abdominal operation. Patients with heart, lung, liver, or endocrine disease were excluded. No premedication was given before anesthesia. A radial arterial line and a swan-ganz catheter were inserted under local anesthesia. Cardiac output (CO), arterial blood pressure (ABP), central venous pressure (CVP), pulmonary arterial pressure (PAP), and pulmonary capillary wedge pressure (PCWP) were obtained before induction to foster systemic vascular resistance index (SVRI), left ventricular systolic work index (LVSWI), right ventricular systolic work index (RVSWI), and pulmonary vascular resistance index (PVRI), cardiac index (CI) by an H/p computer analyzer. Propofol (2 mg/kg) was combined with succinylcholine (1.5 mg/kg) for induction. Anesthesia was maintained with propofol and norcuron. The infusion rates of propofol were 10 mg/kg/hr during the first 30 minutes and 8 mg/kg/hr during the following 30 minutes, norcuron, 0.1 mg/kg initially and 1 mg for maintenance after 30 minutes. Normal saline was infused 1000 to 1500 ml in study period to maintain higher preload. Post induction hemodynamic data were collected at the 5th, 15th, 30th, 60th min after induction.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

[The relationship between pulmonary hemodynamics and chest X-ray findings in patients with sequelae of pulmonary tuberculosis].

For better understanding of pathophysiological aspects of tuberculosis sequelae, we investigated the relationship between pulmonary hemodynamics and chest X-ray findings. One hundred and seven patients with sequelae of pulmonary tuberculosis were examined by the right cardiac catheterization, and pulmonary hemodynamic values were measured and calculated. Chest X-ray findings were defined and classified into the following five items. The items were emphysematous change; fibrosis, bronchiectasis and/or cavity (hereafter abbreviated as "fibrosis"); pulmonary resection and/or atelectasis; pleural thickening; and thoracoplasty. The extent of each finding was defined. We tried to describe chest X-ray findings by applying and categorizing these classifications and the extent to each case. First, we tried to estimate the grade of pulmonary hypertension by categorized X-ray findings. Further, we analyzed what kinds of findings were most influential on the increase of pulmonary artery mean pressure (PPA) and pulmonary arteriolar resistance (PAR). Secondly, we investigated whether PPA, cardiac index (CI) and PAR changed before and after oxygen administration. Thirdly, we analyzed what kind of X-ray findings most affected pulmonary hemodynamics under 100% oxygen administration for 10 minutes. The results were as follows: (1) Out of 107 cases, it was possible to predict PPA by categorized chest X-ray findings in 75 cases by Hayashi's first method of quantification, one of multivariative analyses. "Pleural thickening" was the most influential finding on the increase of PPA. "Fibrosis" was the most influential on the increase of PAR. (2) The values of PPA, CI and PAR decreased more after 100% oxygen administration than under room air breathing. Therefore, PAR was used as the index to estimate pulmonary hemodynamics under the condition of oxygen administration. (3) It was possible to measure PAR under oxygen administration (PARO2) in 72 cases. "Emphysematous change" was the most influential X-ray finding on the increase of PARO2. From these results, it was thought that pulmonary circulatory disorder in patients with tuberculosis sequelae was caused by the combination of various chest X-ray findings with the different extent. It was possible to predict pulmonary hypertension to a certain degree from categorized chest X-ray findings. It was suggested that "emphysematous change" less related to hypoxic pulmonary vasoconstriction than "fibrosis" and "pleural thickening" from the results of comparison among the partial correlation coefficients, which were associated with the increase of PAR under room air breathing and oxygen administration.(ABSTRACT TRUNCATED AT 400 WORDS)

Aged↗
PubMed1993

[Cerebral, central and intracardiac hemodynamics in patients with progressive arterial hypertension following the surgical suppression of adrenal hyperfunction].

Forty-eight patients with progressive (malignant) arterial hypertension resistant to conservative therapy were subjected to surgical portalization of the adrenal blood stream in order to metabolize excessively produced aldosterone in the liver of the patients. Cerebral hemodynamics was studied before by tetra- and bipolar rheoencephalography, central hemodynamics was studied by tetrapolar transthoracic rheography, and intracardiac hemodynamics by echocardiography before and after surgery; blood plasma aldosterone and hydrocortisone concentrations and plasma renin activity were measured. A significant reduction of arterial pressure, elimination or alleviation of subjective and objective manifestations of chronic hypertensive encephalopathy were seen in the majority of patients after surgery. Cerebral blood flow improved, blood plasma aldosterone and renin activity reduced, myocardial hypertrophy decreased, and a trend to normalization of intracardiac hemodynamics was observed.

Adrenocortical Hyperfunction↗
PubMed1994

A hemodynamic excitatory response to veratridine in the in utero lamb.

The inhibitory hemodynamic effects of the Bezold-Jarisch reflex in the adult animal, which play a role in the response to disease states, are elicited by veratridine and are mediated by vagal afferents. We tested whether the reported excitatory response to veratridine in the fetal animal may be caused by a maturational phase in the Bezold-Jarisch response. The effects of proprananol and atropine on the hemodynamic response to veratridine were examined at 124-141 d (mean, 133 d) of gestation in 11 fetal lambs instrumented long-term (instrumentation, 111-129 d of gestation). Seven lambs had intact vagal nerves, and four had bilateral cervical vagotomies. Veratridine injected into the superior vena cava (0.3 to 2.8 micrograms/kg) and the left atrium (0.2 to 0.8 microgram/kg) increased heart rate, arterial pressure, and left ventricular output, with the responses to left atrial injections occurring more rapidly. Propranolol markedly inhibited the increase in arterial pressure; atropine had no effect. Neither carbocaine, perfused around the cervical vagi, nor bilateral transection of the vagal nerves altered the hemodynamic excitatory response to veratridine. These findings demonstrate that the fetal excitatory response to veratridine is not mediated by vagal afferents, indicating the Bezold-Jarisch reflex does not undergo a maturational change from an excitatory reflex to an inhibitory one and suggesting the maturational loss of a sympathetically mediated hemodynamic reflex.

Afferent Pathways↗