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Results for “Hemodynamics”

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At least 19 recordsLinked to original sources

PubMed1992

Hemodynamic observations following orthotopic cardiac transplantation: hemodynamic responses to upright exercise at 1 year.

Central hemodynamic responses during upright exercise were studied at 1 year in 40 orthotopic cardiac transplant recipients. Hemodynamic responses were characterized by slow rise in heart rate and blunted peak exercise heart rate response, a significant early increase in stroke index followed by a plateau phase, and a steady increase in ventricular filling pressures and pulmonary artery pressure. In spite of exclusive utilization of the Frank-Starling mechanism to augment cardiac output during early exercise, the pressure responses were comparable to those reported in normal subjects. Our observations also indicate that similarly to normal subjects, the heart rate response plays an important role in the cardiac output achieved at maximum exercise. Although patients with younger donor hearts achieved a more favorable maximum heart rate, the other hemodynamic parameters showed no correlation with the donor heart age. Thus, no hemodynamic disadvantage of older donor hearts could be demonstrated. These data provide further enlightenment regarding the mechanisms of the well-preserved functional capacity noted in these patients.

Adult↗

PubMed1991

[Tumor hemodynamics in hepatic nodules associated with liver cirrhosis: relationship between cancer progression and tumor hemodynamic change].

Tumor hemodynamics including arterial vascularity (AV) and portal perfusion (PP) were evaluated in histologically confirmed 55 hepatic nodules associated with cirrhosis using ultrasonographic (US) angiography during intraarterial carbon dioxide microbubbles injection and CT during arterial portography. Tumor hemodynamic patterns were classified into 6 types as follows: Type I (n = 10): PP (+), AV (hypo); Type I' (n = 2): PP (+), AV (iso); Type II (n = 5): PP (-), AV (hypo); Type III (n = 8): PP (-), AV (iso); Type IV (n = 25): PP (-), AV (hyper), Type V (n = 5): PP (partially +), AV (vascular spot in hypovascular). Eight nodules of Type I were diagnosed as benign nodules histologically including adenomatous hyperplasia (AH) (n = 6) and regenerative nodule (n = 2). Hundred percent (5/5) of Type II and 88% (7/8) of Type III nodules were well-differentiated HCC, in contrast to 8% (2/25) of Type IV nodules, typical HCCs. Fatty metamorphosis was observed in 75% (6/8) of Type III nodules, in contrast to 16% (4/25) of typical (classical) HCC nodules (Type IV). We concluded that at the malignant transformation from AH to HCC, reduction of portal blood flow in the nodule precedes the initiation of the increase of the arterial tumor vessel. Moreover, early stage HCC could exhibit hypovascular (Type I, II), isovascular (Type III), or vascular spot in hypovascular pattern (Type V) compared with a typical HCC (Type IV). It was also suggested that the more mature as a neoplasms the HCC becomes, the more the arterial tumor vessel in the nodule increases and fatty metamorphosis of well-differentiated HCC is highly related with tumor hemodynamic condition, i.e., hypoperfusion state from both arterial and portal vessel.

Carcinoma, Hepatocellular↗

PubMed1978

Systemic and pulmonary hemodynamic effects of saralasin infusion in hypertension. Predictability of plasma renin status from hemodynamic changes.

Hemodynamic measurements were obtained before and after 30 minutes of saralasin infusion in 26 fasting adults with hypertension (25 men and 1 woman). Nine showed a depressor response with a decrease in mean intaarterial pressure greater than 20 mm Hg. Ten were nonresponders and seven had an agonistic response with an increase in mean arterial pressure of greater than 10 mm Hg. Heart rate, pulmonary arterial and wedge pressures and pulmonary vascular resistance were nearly identical in the three groups and remained unchanged. Cardiac index decreased from a mean of 2.76 +/- 0.14 (standard error of the mean) to 2.48 +/- 0.1 liters/min per m2 in the nonresponders (P less than 0.02) but remained unchanged in the groups with a depressor or an agonistic response. The mean systemic vascular resistance decreased from 2,406 +/- 303 to 1,839 +/- 265 dynes sec/cm5 in the group with a depressor response (P less than 0.001) and increased in nonresponders (less than 0.02) and those with an agonistic response (P less than 0.01). However, regardless of the response of mean arterial pressure, systemic vascular resistance decreased only in the 10 patients with a plasma renin activity greater than 5 ng/ml per hour (8 from the depressor response group and 1 each from the nonresponse and agonistic response groups). It is concluded that (1) classification based soley on the response of aterial pressure to saralasin ignores important hemodynamic changes; (2) the response of cardiac index--no change in the patients with a depressor response and a reduction in nonresponders--suggests that endogenous angiotension II supports cardiac output in these groups; (3) a decrease in systemic vascular resistance is better than a decrease in mean arteiral pressure as a predictor of the status of the plasma renin activity; and (4) lack of change in pulmonary vascular resistance suggests that endogenous angiotension II plays an insignificant role in maintaining the resistance of the pulmonary vasculature.

Adult↗

PubMed1992

Hemodynamic observations following orthotopic cardiac transplantation: evolution of rest hemodynamics in the first year.

The evolution of resting hemodynamics was studied at 1 week and 1 year in 40 patients following orthotopic cardiac transplantation. Abnormal hemodynamics after transplantation, characterized by elevated ventricular filling pressures (indicating diastolic dysfunction) and also by pulmonary hypertension, showed normalization by 1 year. In the absence of innervation, the resting heart rate of heart transplant recipients should theoretically be close to the intrinsic heart rate predicted by the age of the donor heart. In this study, a high incidence of relative sinus bradycardia (an indicator of sinus node dysfunction) was noted in the first post-operative week, although again there was a tendency to normalization by 1 year. These beneficial changes help to explain the dramatic and sustained improvement in the functional capacity of these patients late after transplantation.

Adult↗

PubMed1979

Hemodynamic patterns in human hepatic cirrhosis: a prospective randomized study of the hemodynamic sequelae of distal splenorenal (Warren) and mesocaval shunts.

Increasingly successful operative management of gastroesophageal variceal hemorrhage has been achieved by newer techniques of portal venous reconstruction. Although it is postulated that the clinical success may be due to more selectivity in portal venous shunting, direct determination of the effect of portasystemic shunt on portal vein blood flow has not been possible. Direct determinations of portal vein blood flow were performed preoperative on unanesthetized, hemodynamically stable cirrhotic patients by observation of radiopaque water-insoluble droplets. Patients were then randomized into elective distal splenorenal (Warren) or mesocaval shunt and determinations were performed postoperatively under similar conditions when clinically possible. Although portal vein blood flow was not significantly different before (929 +/- 147 ml/min) or after 899 +/- 271 ml/min) distal splenorenal shunt, there was a large change in portal vein blood flow after mesocaval shunt, decreasing from 772 +/- 177 ml/min (hepatopetal) to -1021 +/- 310 ml/min (hepatofugal) p < 0.01). After either procedure total hepatic blood flow (as determined by cardiac green clearance) was not significantly changed, nor was renal blood flow; however, cardiac output was significantly increased after mesocaval shunt. Thus the theoretical hemodynamic goals of the selective distal splenorenal shunt, i.e., preservation of the hepatopetal flow within the portal vein, is achieved as determined in the early postoperative period. The correlation between these changes and the eventual clinical outcome remains to be determined.

Cardiac Output↗

PubMed1990

[Hemodynamic correction of patients with acute myocardial infarct in hemodynamic subgroup III by plasma-exchange expansion with low-molecular dextran].

To 20 patients with acute myocardial infarction from the III hemodynamic group catheterized with a microcatheter or a balloon thermodilution catheter 332 (from 100 up to 500) ml of a 10% solution dextran 40 were infused intravenously with mean velocity of 33 ml/min. The cardiac index was measured by the dye or thermodilution methods. The left ventricular filling pressure (LVFP) increased with 47% (from 1.7 +/- 0.4 to 2.5 +/- 0.5 kPa), the cardiac index--15.8% (from 2.02 +/- 0.8 to to 2.34 +/- 0.37 l/min/m2), systolic and diastolic arterial pressure with 7.7%, stroke index--with 10.2% stroke working index--with 10.7%, total pulmonary resistance--with 37.9% (il all, p less than 0.001), cardiac rate--with 4.7% (p less than 0.05) but the systemic arterial resistance did not change (p greater than 0.10). The increase of the cardiac index for an increase of LVFP with I KPa was almost equal in the patients with different initial LVFP but was due mainly to the increase of the stroke index by LVFP below 1.3 kPa and to an increase of the heart rate by LVFP above 2.0 kPa. The cardiac index increased above 2.2 l/min/m2 in 45% of the patients (87% by LVFP below 1.3 kPa, 56% by LVFP 1.4-1.9 kPa and 0% by LVFP above 2 kPa). The cardiac rate remained increased up to the 4th hour after the infusion. The arterial pressure fell below its initial value after 30 min and remained low up to the 12 h. The LVFP decreased progressively according to the dependence: LVFP = -5.06 + 2.09 1g T.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1976