CHANGES IN RADIAL-AORTIC PRESSURE GRADIENTS, SYSTEMIC VASCULAR RESISTANCE AND CARDIAC INDEX FOLLOWING CARDIO-PULMONARY BYPASS

1995 ◽  
Vol 80 (Supplement) ◽  
pp. SCA72 ◽  
Author(s):  
K. R. Ediale ◽  
S. Pothula ◽  
V. Kumar ◽  
M. A. Inchiosa
Keyword(s):  
Cardiac Index ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Aortic Pressure ◽  
Pressure Gradients ◽  
Cardio Pulmonary Bypass ◽  
Pulmonary Bypass

scholarly journals Empagliflozin does not change cardiac index nor systemic vascular resistance but rapidly improves left ventricular filling pressure in patients with type 2 diabetes: a randomized controlled study

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Matthias Rau ◽  
Kirsten Thiele ◽  
Niels-Ulrik Korbinian Hartmann ◽  
Alexander Schuh ◽  
Ertunc Altiok ◽  
...  
Keyword(s):  
Cardiac Index ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Resistance Index ◽  
Stroke Volume Index ◽  
Left Ventricular ◽  
Volume Index ◽  
Hemodynamic Parameters ◽  
Mitral Inflow ◽  
Ventricular Filling Pressure

Abstract Background In the EMPA-REG OUTCOME trial (Empagliflozin Cardiovascular Outcome Event Trial) treatment with the sodium-glucose cotransporter-2 (SGLT2) inhibitor empagliflozin significantly reduced heart failure hospitalization (HHF) in patients with type 2 diabetes mellitus (T2D) and established cardiovascular disease. The early separation of the HHF event curves within the first 3 months of the trial suggest that immediate hemodynamic effects may play a role. However, hitherto no data exist on early effects of SGLT2 inhibitors on hemodynamic parameters and cardiac function. Thus, this study examined early and delayed effects of empagliflozin treatment on hemodynamic parameters including systemic vascular resistance index, cardiac index, and stroke volume index, as well as echocardiographic measures of cardiac function. Methods In this placebo-controlled, randomized, double blind, exploratory study patients with T2D were randomized to empagliflozin 10 mg or placebo for a period of 3 months. Hemodynamic and echocardiographic parameters were assessed after 1 day, 3 days and 3 months of treatment. Results Baseline characteristics were not different in the empagliflozin (n = 22) and placebo (n = 20) group. Empagliflozin led to a significant increase in urinary glucose excretion (baseline: 7.3 ± 22.7 g/24 h; day 1: 48.4 ± 34.7 g/24 h; p < 0.001) as well as urinary volume (1740 ± 601 mL/24 h to 2112 ± 837 mL/24 h; p = 0.011) already after one day compared to placebo. Treatment with empagliflozin had no effect on the primary endpoint of systemic vascular resistance index, nor on cardiac index, stroke volume index or pulse rate at any time point. In addition, echocardiography showed no difference in left ventricular systolic function as assessed by left ventricular ejections fraction and strain analysis. However, empagliflozin significantly improved left ventricular filling pressure as assessed by a reduction of early mitral inflow velocity relative to early diastolic left ventricular relaxation (E/eʹ) which became significant at day 1 of treatment (baseline: 9.2 ± 2.6; day 1: 8.5 ± 2.2; p = 0.005) and remained apparent throughout the study. This was primarily attributable to reduced early mitral inflow velocity E (baseline: 0.8 ± 0.2 m/s; day 1: 0.73 ± 0.2 m/sec; p = 0.003). Conclusions Empagliflozin treatment of patients with T2D has no significant effect on hemodynamic parameters after 1 or 3 days, nor after 3 months, but leads to rapid and sustained significant improvement of diastolic function. Trial registration EudraCT Number: 2016-000172-19; date of registration: 2017-02-20 (clinicaltrialregister.eu)

scholarly journals Empagliflozin does not change cardiac index nor systemic vascular resistance but rapidly improves left ventricular filling pressure in patients with type 2 diabetes: a randomized controlled study 

2020 ◽  
Author(s):  
Matthias Rau ◽  
Kirsten Thiele ◽  
Niels-Ulrik Korbinian Hartmann ◽  
Alexander Schuh ◽  
Ertunc Altiok ◽  
...  
Keyword(s):  
Cardiac Index ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Resistance Index ◽  
Stroke Volume Index ◽  
Left Ventricular ◽  
Volume Index ◽  
Hemodynamic Parameters ◽  
Mitral Inflow ◽  
Ventricular Filling Pressure

Abstract Background: In the EMPA-REG OUTCOME trial (Empagliflozin Cardiovascular Outcome Event Trial) treatment with the sodium-glucose cotransporter-2 (SGLT2) inhibitor empagliflozin significantly reduced heart failure hospitalization (HHF) in patients with type 2 diabetes mellitus (T2D) and established cardiovascular disease. The early separation of the HHF event curves within the first 3 months of the trial suggest that immediate hemodynamic effects may play a role. However, hitherto no data exist on early effects of SGLT2 inhibitors on hemodynamic parameters and cardiac function. Thus, this study examined early and delayed effects of empagliflozin treatment on hemodynamic parameters including systemic vascular resistance index, cardiac index, and stroke volume index, as well as echocardiographic measures of cardiac function.Methods: In this placebo-controlled, randomized, double blind, exploratory study patients with T2D were randomized to empagliflozin 10 mg or placebo for a period of 3 months. Hemodynamic and echocardiographic parameters were assessed after 1 day, 3 days and 3 months of treatment. Results: Baseline characteristics were not different in the empagliflozin (n=22) and placebo (n=20) group. Empagliflozin led to a significant increase in urinary glucose excretion (baseline: 7.3 ± 22.7 g/24 hrs; day 1: 48.4 ± 34.7 g/24 hrs; p<0.001) as well as urinary volume (1740 ± 601 mL/24 hrs to 2112 ± 837 mL/24 hrs; p=0.011) already after one day compared to placebo. Treatment with empagliflozin had no effect on the primary endpoint of systemic vascular resistance index, nor on cardiac index, stroke volume index or pulse rate at any time point. In addition, echocardiography showed no difference in left ventricular systolic function as assessed by left ventricular ejections fraction and strain analysis. However, empagliflozin significantly improved left ventricular filling pressure as assessed by a reduction of early mitral inflow velocity relative to early diastolic left ventricular relaxation (E/e’) which became significant at day 1 of treatment (baseline: 9.2 ± 2.6; day 1: 8.5 ± 2.2; p=0.005) and remained apparent throughout the study. This was primarily attributable to reduced early mitral inflow velocity E (baseline: 0.8 ± 0.2 m/sec; day 1: 0.73 ± 0.2 m/sec; p=0.003). Conclusions: Empagliflozin treatment of patients with T2D has no significant effect on hemodynamic parameters after 1 or 3 days, nor after 3 months, but leads to rapid and sustained significant improvement of diastolic function.

Increased organ blood flow in chronic endotoxemia is reversed by nitric oxide synthase inhibition

1994 ◽  
Vol 76 (6) ◽  
pp. 2785-2793 ◽  
Author(s):  
J. Meyer ◽  
F. Hinder ◽  
J. Stothert ◽  
L. D. Traber ◽  
D. N. Herndon ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cardiac Index ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Resistance Index ◽  
No Synthase ◽  
Organ Blood Flow ◽  
Systemic Vascular Resistance Index ◽  
Blood Flows ◽  
Regional Blood Flows

We evaluated regional blood flows in a hyperdynamic sepsis model and the reversal of increased flows by blockade of nitric oxide (NO) synthase. Seven awake sheep were continuously infused with Escherichia coli endotoxin [lipopolysaccharide (LPS), 10 ng.kg-1.min-1] for 48 h. The NO synthase inhibitor N omega-nitro-L-arginine methyl ester (L-NAME, 25 mg/kg) was injected after 24 h. Blood flows to systemic organs were determined with the radioactive microsphere technique. LPS induced elevation of cardiac index by 36% (P < 0.05) and a fall in systemic vascular resistance index by 37% (P < 0.05) at 0 h [time of L-NAME administration, 24 h after infusion of LPS had begun] L-NAME administration normalized cardiac index [6.1 +/- 0.5 at 4 h posttreatment, 6.1 +/- 0.5 l.min-1.m-2 at -24 h (baseline)] and systemic vascular resistance index (1,333 +/- 105 at 4 h posttreatment, 1,280 +/- 163 dyn.s.cm-5.m2 at -24 h) and reduced all regional blood flows to near-baseline levels for the remainder of the study period (24 h). O2 consumption was unaffected by treatment.

Cardiovascular responses to exhaustive upright cycle exercise in highly trained older men

1994 ◽  
Vol 77 (3) ◽  
pp. 1500-1506 ◽  
Author(s):  
J. L. Fleg ◽  
S. P. Schulman ◽  
F. C. O'Connor ◽  
G. Gerstenblith ◽  
L. C. Becker ◽  
...  
Keyword(s):  
Cardiac Index ◽  
Stroke Volume ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Stroke Volume Index ◽  
Cardiovascular Responses ◽  
Radionuclide Ventriculography ◽  
Volume Index ◽  
Heart Rates ◽  
Peak Vo2

It is unclear whether the markedly enhanced aerobic exercise capacity of older endurance-trained men relative to their sedentary age peers is mediated primarily by central or peripheral cardiovascular mechanisms. To address this question, we performed radionuclide ventriculography with respiratory gas exchange measurements during exhaustive upright cycle ergometry in 16 endurance-trained men aged 63 +/- 7 yr and in 35 untrained men of similar age. As expected, maximal O2 consumption during treadmill exercise was much higher in athletes than in controls. At rest and during fixed submaximal cycle work rates through 100 W, athletes demonstrated lower heart rates and greater stroke volume indexes than controls while maintaining similar cardiac indexes and O2 uptake (VO2). At exhaustion, athletes achieved 53% higher work rates and peak VO2 per kilogram body weight than the sedentary men. The higher peak VO2 in athletes was achieved by a 22.5% larger cardiac index and a 15.6% greater arteriovenous O2 difference. The larger peak cardiac index in the athletes than in sedentary controls was mediated entirely by a greater stroke volume index; peak heart rates were virtually identical. The athletes' greater stroke volume index was achieved through an 11% larger end-diastolic volume index and a 7% higher ejection fraction, both of borderline significance. At exhaustion, athletes demonstrated a lower systemic vascular resistance than controls, despite a higher value at rest. Athletes also showed greater exercise-induced increments in heart rate, stroke volume index, and cardiac index and a greater reduction in systemic vascular resistance from rest to maximal workload.(ABSTRACT TRUNCATED AT 250 WORDS)

Peripheral circulatory control of preload-afterload mismatch with angiotensin in dogs

1987 ◽  
Vol 253 (1) ◽  
pp. H126-H132
Author(s):  
R. W. Lee ◽  
L. D. Lancaster ◽  
D. Buckley ◽  
S. Goldman
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Arterial Compliance ◽  
Peripheral Circulation ◽  
Aortic Pressure ◽  
Venous Compliance ◽  
Mean Aortic Pressure

To determine whether changes in the venous circulation were responsible for preload-afterload mismatch with angiotensin, we examined the changes in the heart and the peripheral circulation in six splenectomized dogs after ganglion blockade during an angiotensin infusion to increase mean aortic pressure 25 and then 50%. The peripheral circulation was evaluated by measuring mean circulatory filling pressure (MCFP), arterial compliance, and venous compliance. A 25% increase in mean aortic pressure increased MCFP from 6.2 +/- 0.3 to 7.6 +/- 0.3 mmHg (P less than 0.001) but did not change cardiac output, heart rate, or stroke volume. Systemic vascular resistance increased (P less than 0.01) from 0.50 +/- 0.02 to 0.59 +/- 0.03 mmHg X min X kg X ml-1. Arterial and venous compliances decreased (P less than 0.01) from 0.08 +/- 0.03 to 0.06 +/- 0.03 ml X mmHg-1 X kg-1 and from 2.1 +/- 0.1 to 1.6 +/- 0.1 ml X mmHg-1 X kg-1, respectively. A 50% elevation in mean aortic pressure increased MCFP from 7.1 +/- 0.4 to 9.5 +/- 0.9 mmHg (P less than 0.001) but did not change heart rate. At this level of aortic pressure, cardiac output and stroke volume decreased (P less than 0.01) 12 and 19%, respectively, whereas systemic vascular resistance increased (P less than 0.001) from 0.48 +/- 0.03 to 0.83 +/- 0.05 mmHg X min X kg X ml-1. Arterial and venous compliances decreased (P less than 0.01) from 0.08 +/- 0.01 to 0.05 +/- 0.01 ml X mmHg-1 X kg-1 and from 2.1 +/- 0.1 to 1.4 +/- 0.1 ml X mmHg-1 X kg-1, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Pathogenetic mechanisms of venous congestion after the Fontan procedure

2001 ◽  
Vol 11 (2) ◽  
pp. 161-168 ◽  
Author(s):  
Reiner Buchhorn ◽  
Dietmar Bartmus ◽  
Wolfgang Buhre ◽  
Joachim Bürsch
Keyword(s):  
Cardiac Index ◽  
Capillary Pressure ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Postoperative Period ◽  
Venous Pressure ◽  
Resistance Index ◽  
Venous Congestion ◽  
Systemic Vascular Resistance Index ◽  
Central Venous

Background: The hemodynamic status after a Fontan type procedure for definitive palliation of functionally univentricular hearts is dominated by a high central venous pressure, which seems to be one of several factors responsible for venous congestion appearing as a frequent complication in the early and late postoperative course. The purpose of our study was to find other hemodynamic parameters correlating with the presence of venous congestion and effusions in these patients. Methods: We compared the hemodynamic data of 18 patients who had an uneventful long-term course after a Fontan type procedure with the respective data of 10 patients who developed symptoms of venous congestion in the immediate postoperative period. Based on a theoretical model, we developed an algorithm to calculate mean hydrostatic capillary pressure from mean arterial pressure, systemic vascular resistance index and central venous pressure. Results: Pulmonary vascular resistance index (2.1 ± 1.0 mmHg L-1 min m2), mean left atrial pressure (9.7 ± 4.0 mmHg) and cardiac index (3.6 ± 0.6 1/min/m2) are mainly normal in patients with venous congestion in the immediate postoperative period, but mean hydrostatic capillary pressure is significantly higher compared to patients without venous congestion (24.3 ± 3.1 vs 18.3 ± 4.0 mmHg). Lower mean hydrostatic capillary pressures in these patients are due to a highly significant increase of systemic vascular resistance index (18.6 ± 4.2 versus 33.6 ± 6.6 mmHg L-1 min m2) and a concomitant decrease of cardiac index to 2.4 ± 0.3 1/min/m2. Conclusions: The increase of mean hydrostatic capillary pressure, caused by high central venous pressures but also by relatively low systemic vascular resistance indexes, seems to be the hemodynamic key parameter responsible for venous congestion and effusions in patients after a Fontan type procedure in the immediate postoperative period.

Effects of priming fluids and oxygenators on arterial pressure and vascular resistance during cardio-pulmonary bypass

1989 ◽  
Vol 3 (5) ◽  
pp. 74 ◽  
Author(s):  
G.F. Karliczek ◽  
A.M. Vd Maas ◽  
U. Brenken ◽  
R. Gallandat-Huet ◽  
N. Borgstein ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Vascular Resistance ◽  
Cardio Pulmonary Bypass ◽  
Pulmonary Bypass

Effects of vasopressin on pulmonary and systemic vascular mechanics

1989 ◽  
Vol 257 (4) ◽  
pp. H1228-H1234 ◽  
Author(s):  
A. W. Wallace ◽  
C. M. Tunin ◽  
A. A. Shoukas
Keyword(s):  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Venous Pressure ◽  
Venous Blood ◽  
Pressure Flow ◽  
Before And After ◽  
Pulmonary Arterial ◽  
High Doses ◽  
Pulmonary Bypass

The direct effects of vasopressin on the resistance and capacitance properties of the pulmonary and systemic vasculature were studied in nine aneural dogs on systemic and pulmonary bypass. The systemic and pulmonary pressure-flow, the systemic and pulmonary arterial pressure-volume, and the systemic and pulmonary venous pressure-volume relationships were determined for five levels of infused vasopressin. Vasopressin levels of approximately 10, 30, 150, 300, and 500 pg/ml were achieved by intravenous infusions. Samples of venous blood were drawn before and after each set of pressure-flow and pressure-volume relationships for the determination of vasopressin level by radioimmunoassay. A linear relationship was found between vasopressin level and systemic vascular resistance. Systemic vascular resistance increased 0.072 +/- 0.011 mmHg.kg.min.ml-1 for a change in vasopressin level of 100 pg/ml. Vasopressin did not affect pulmonary vascular resistance or any vascular compliance. High doses of infused arginine vasopressin were necessary to elicit substantial vasoconstriction.

Effects of enhanced ventricular filling on cardiac pump performance in exercising dogs

1985 ◽  
Vol 59 (6) ◽  
pp. 1886-1890 ◽  
Author(s):  
L. D. Horwitz ◽  
J. Lindenfeld
Keyword(s):  
Heart Rate ◽  
Stroke Volume ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Left Ventricular Pressure ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Increase Stroke Volume ◽  
Normal Increase ◽  
Ventricular Filling

The extent to which the normal increase in stroke volume during exercise can be augmented by increasing preload by dextran infusion was studied in seven dogs. Each dog ran 3 min on a level treadmill at mild (3–4 mph), moderate (6–8 mph), and severe (9–13 mph) loads during the control study and immediately after 10% dextran 14 ml/kg iv. During severe exercise dextran-augmented stroke volume (+5.4 ml or 19% vs. exercise without dextran, P less than 0.01) and left ventricular end-diastolic diameter and pressure did not change heart rate, aortic pressure, or maximum derivative of left ventricular pressure but decreased systemic vascular resistance by 16%. Similar increases in stroke volume and preload after dextran occurred during mild and moderate exercise when arterial pressure and heart rate were unchanged or increased and systemic vascular resistance was decreased. Thus altering preload above those levels normally encountered during exercise is a potential mechanism to increase stroke volume and cardiac output.

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