Cardiac performance enhancement from dobutamine in patients refractory to hypervolemic therapy for cerebral vasospasm

1993 ◽  
Vol 79 (4) ◽  
pp. 494-499 ◽  
Author(s):  
Michael L. Levy ◽  
Craig H. Rabb ◽  
Vladimir Zelman ◽  
Steven L. Giannotta

✓ The use of the beta-agonist dobutamine in combination with hypervolemic preload enhancement of cardiac performance was analyzed in 23 patients who failed to respond to traditional preload enhancement following aneurysmal subarachnoid hemorrhage. The patients ranged in age from 13 to 82 years, and three had a history of cardiac disease. Each patient underwent placement of a flow-directed balloon-tipped catheter and the following measurements were obtained during hyperdynamic therapy: pulmonary artery wedge pressure, central venous pressure, cardiac index, stroke volume index, total peripheral resistance, and left ventricular stroke work index (LVSWI). Mean baseline cardiac function was found to be within normal limits (LVSWI = 47.6 ± 4.2 gm/min/sq m and cardiac index = 3.30 ± 0.22 liter/min/sq m). After baseline measurements were recorded, 5% albumin was infused at 300 cc/hr and dobutamine was initiated at a rate of 5 to 10 µg/kg/hr. This hyperdynamic therapy with dobutamine in the presence of volume loading resulted in a 52% increase in cardiac index, a 15% increase in LVSWI, and a 21% decrease in total peripheral resistance. The clinical reversal of ischemic symptoms due to subarachnoid hemorrhage was evident in 18 (78%) of the 23 patients.

1991 ◽  
Vol 75 (1) ◽  
pp. 27-31 ◽  
Author(s):  
Michael L. Levy ◽  
Steven L. Giannotta

✓ The effect of hypervolemic preload enhancement on cardiac performance was systematically analyzed in nine patients following aneurysmal subarachnoid hemorrhage. The patients ranged in age from 34 to 63 years, and none had a history of cardiac disease. Each patient underwent placement of a flow-directed balloon-tipped catheter and the following measurements were taken during hypervolemic therapy: pulmonary artery wedge pressure (PAWP), central venous pressure (CVP), cardiac index (CI), stroke volume index (SVI), and left ventricular stroke work index (LVSWI). After baseline measurements were recorded, hetastarch or plasmanate was infused intravenously at 300 cc/hr. Thermal output determination and pressures were measured every 15 minutes. The PAWP did not correlate in a statistically significant fashion with the CVP in the ranges recorded; however, a statistically significant correlation did exist between PAWP increases and increases in CI, SVI, and LVSWI (p < 0.01). There was no statistical correlation between PAWP increases above 14 mm Hg and improvement in cardiac performance as evidenced by CI, SVI, and LVSWI measurements. It is concluded that CVP is an unreliable index of cardiac performance during hypervolemic therapy and that, in previously healthy individuals, a PAWP of 14 mm Hg is associated with maximum cardiac performance.


1991 ◽  
Vol 261 (3) ◽  
pp. H836-H842 ◽  
Author(s):  
S. E. Litwin ◽  
T. E. Raya ◽  
S. Daugherty ◽  
S. Goldman

Diabetes is believed to be associated with impaired systolic and diastolic function of the heart; however, some investigators have found that diabetic rats have increased cardiac output. We investigated changes in the peripheral circulation that could account for an increased cardiac output in diabetic rats (n = 30), 4 wk after a single tail vein injection of streptozotocin (60 mg/kg), and age-matched control rats (n = 31). Compared with controls, diabetic rats exhibited decreased (P less than 0.05) mean arterial pressure, characteristic aortic impedence, and total peripheral resistance; however, cardiac index and stroke volume index were increased. Aortic compliance, mean circulatory filling pressure, central venous pressure, pressure gradient for venous return, and venous compliance were unchanged in the diabetic rats compared with control. Baseline left ventricular end-diastolic pressure and end-diastolic volume were increased in the diabetic rats. Following a volume load of 30 ml/kg, cardiac index and stroke volume index increased less in the diabetic than in the control rats (35 vs. 102% and 69 vs. 105%, respectively). Thus, even with impaired systolic function, cardiac output is increased or maintained in diabetic rats because of the combination of decreased afterload and maintenance of preload.


1995 ◽  
Vol 268 (2) ◽  
pp. H692-H702 ◽  
Author(s):  
W. Karzai ◽  
J. M. Reilly ◽  
W. D. Hoffman ◽  
R. E. Cunnion ◽  
R. L. Danner ◽  
...  

To study how sepsis affects hemodynamic responses to catecholamines and fluids, either Escherichia coli-infected (septic, n = 8) or sterile (controls, n = 6) fibrin clots were implanted intraperitoneally into 2-yr-old beagles. Hemodynamics were measured at each of four doses of dopamine (0, 5, 10, and 20 micrograms.kg-1.min-1) and norepinephrine (0, 10, 20, and 40 micrograms.min-1), before and after infusion of fluid (Ringer 40 ml.kg-1). Septic animals had lower mean arterial pressure (MAP, P = 0.04), stroke volume index (SVI, P = 0.0001), and left ventricular (LV) ejection fraction (LVEF) (P = 0.0001) than controls. During this time, increasing doses of dopamine and norepinephrine produced corresponding increases (P < 0.001) in LVEF, SVI, and MAP. However, during sepsis, the ability of dopamine to increase MAP diminished, while its ability to increase LVEF and SVI was maintained. Conversely, the ability of norepinephrine to increase LVEF and SVI diminished, but its ability to increase MAP was maintained. During sepsis, fluids alone increased (P < 0.05) MAP, LVEF, SVI, and cardiac index (CI). Fluids with catecholamines also significantly increased (P < 0.05) MAP with only minimal increases in LVEF, SVI, and CI. These data demonstrate that during sepsis without catecholamines, fluids improve cardiac performance and systemic pressures, but with catecholamines, fluids have minimal effects on cardiac performance and augment MAP. Furthermore, during sepsis dopamine is more effective than norepinephrine in increasing LV performance, but norepinephrine is more effective than dopamine in increasing systemic pressures.


1983 ◽  
Vol 244 (3) ◽  
pp. H320-H327 ◽  
Author(s):  
W. E. Kanten ◽  
D. G. Penney ◽  
K. Francisco ◽  
J. E. Thill

The effects of carbon monoxide on the hemodynamics of the adult rat were investigated. A number of parameters were measured using an open-chest, chloralose-urethan anesthetized preparation. Our experiments showed this anesthetic agent to have several advantages over pentobarbital sodium. One group inhaled 150 ppm CO for 0.5-2 h, carboxyhemoglobin (HbCO) reaching 16%. Heart rate, cardiac output, cardiac index, dF/dtmax (aortic), and stroke volume rose significantly; mean arterial pressure, total peripheral resistance, and left ventricular systolic pressure fell, whereas stroke work, left ventricular dP/dtmax, and stroke power changed little. These effects were evident at a HbCO saturation as low as 7.5% (0.5 h). A second group inhaled 500 ppm CO for 5-48 h, HbCO reaching 35-38%. The same parameters changed in the same direction as in the first group, with mean arterial pressure and peripheral resistance remaining depressed, while heart rate, cardiac output, cardiac index, and stroke volume remained elevated. Heart rate and arterial systolic pressure were also monitored in conscious rats; rats in one group inhaled 500 ppm CO for 24 h, and rats in a second group were injected with a bubble of pure CO ip. In both cases heart rate was sharply elevated and blood pressure depressed as HbCO saturation increased. Both parameters recovered on CO washout. There was no significant difference between the response to inhaled vs. injected CO.


1993 ◽  
Vol 265 (5) ◽  
pp. H1727-H1733 ◽  
Author(s):  
D. S. Martin ◽  
J. R. Haywood

The present study was undertaken to determine the hemodynamic responses associated with stimulation of the hypothalamic paraventricular nucleus (PVN). Male Sprague-Dawley rats (n = 21) were instrumented with guide cannulas directed bilaterally at the PVN, with an electromagnetic flow probe placed on the ascending aorta and with femoral venous and arterial catheters. Bicuculline methiodide (BMI, 2 mM) was infused bilaterally (100 nl/20 min) into the PVN region before and after treatment with the beta 1-adrenergic antagonist, metoprolol bitartrate (2 mg/kg iv) or the alpha 1-adrenergic receptor antagonist, prazosin hydrochloride (2 mg/kg iv). Infusion of BMI into the PVN increased mean arterial pressure by 17 +/- 2 mmHg, and heart rate rose by 91 +/- 8 beats/min. Cardiac index increased 17 +/- 3%, whereas total peripheral resistance index was not altered significantly. After metoprolol treatment, the mean arterial pressure response to BMI was similar to control (16 +/- 2 mmHg), but the tachycardia was reduced significantly (10 +/- 4 beats/min). In addition, the blood flow response was changed qualitatively. Total peripheral resistance increased 13 +/- 3%, whereas the cardiac index response was abolished (1 +/- 2%). After prazosin treatment, BMI administration into the PVN failed to increase arterial pressure (-1 +/- 4 mmHg). Nevertheless, the BMI infusion was associated with significant hemodynamic effects. Total peripheral resistance index decreased (-24 +/- 6%), whereas cardiac index and stroke volume index increased 34 +/- 8 and 17 +/- 5%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)


1988 ◽  
Vol 254 (3) ◽  
pp. H558-H569 ◽  
Author(s):  
C. Natanson ◽  
R. L. Danner ◽  
M. P. Fink ◽  
T. J. MacVittie ◽  
R. I. Walker ◽  
...  

We investigated cardiovascular dysfunction by injecting lethal and nonlethal bacterial challenges into conscious dogs. E. coli bacteria of varying numbers were placed in a peritoneal clot. Cardiovascular function was studied with simultaneous radionuclide scans and thermodilution cardiac outputs. In surviving animals, the number of bacteria in the clot increased as the corresponding systolic cardiac function decreased (P = 0.01). Cardiac function was measured by left ventricular (LV) ejection fraction (EF) and LV function curves [LV stroke work index (LVSWI) vs. end-diastolic volume index (EDVI), and peak systolic pressure vs. end-systolic volume index]. Furthermore, the diastolic volume-pressure relationship of survivors shifted progressively to the right [i.e., increasing EDVI (P less than 0.02) with minimal change (P = NS) in LV filling pressure]. This increase in LV size was associated with maintenance of measures of cardiac performance [stroke volume index (SVI) and stroke work index (SWI)] at similar levels. Death occurred only in the group with the highest bacterial dose. Compared with survivors receiving the same number of bacteria, nonsurvivors had a decrease in (P less than 0.05) LV size, a leftward shift (P less than 0.01) in LV diastolic volume-pressure relationship, and a decrease in both LVSWI and SVI (possibly related to volume and/or LV functional status). Data from survivors suggest that increasing the number of bacteria produces changes in myocardial compliance and contractility. These changes increase LV size (preload), a major determinant of cardiac performance that possibly enhances survival.


2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Matthias Rau ◽  
Kirsten Thiele ◽  
Niels-Ulrik Korbinian Hartmann ◽  
Alexander Schuh ◽  
Ertunc Altiok ◽  
...  

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)


2020 ◽  
Author(s):  
Matthias Rau ◽  
Kirsten Thiele ◽  
Niels-Ulrik Korbinian Hartmann ◽  
Alexander Schuh ◽  
Ertunc Altiok ◽  
...  

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.


Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Frederik H Verbrugge ◽  
Endry Willems ◽  
Philippe B Bertrand ◽  
Ellen Gielen ◽  
Wilfried Mullens ◽  
...  

Introduction: Cardiac magnetic resonance (CMR) imaging with quantitative T2-mapping allows identi[[Unable to Display Character: &#64257;]]cation of myocardial edema, improving risk-stratification in acute coronary syndromes and myocarditis. Hypothesis: Global myocardial edema contributes to left ventricular (LV) dysfunction in advanced decompensated heart failure (ADHF). Methods: CMR with quantitative T2-mapping was performed in consecutive ADHF patients (n=17) undergoing right heart catheterization for worsening dyspnea and volume overload. Patients received vasodilators and diuretics to achieve pulmonary capillary wedge pressure (PCWP) ≤18 mmHg and central venous pressure (CVP) ≤10 mmHg, while maintaining mean arterial pressure ≥65 mmHg. After reaching hemodynamic targets, the pulmonary arterial catheter was removed and CMR imaging repeated. Changes in LV T2-values, hemodynamics, and CMR volumetric measurements were compared. Results: Study patients (64±11 years, male 88%, LV ejection fraction 23±8%, ischemic cardiomyopathy 50%) received decongestive treatment during 5±2 days. PCWP and CVP decreased from 25±7 to 17±4 mmHg and 13±6 to 7±3 mmHg, respectively (p<0.001 for both), while cardiac index increased from 2.14±0.60 to 2.58±0.49 L/min/m 2 (p=0.012). LV T2-values dropped consistently from 59.6±4.9 ms to 56.3±5.2 ms after decongestion (p=0.002; Figure). Decreasing LV T2-values correlated well to both decreasing PCWP (r=0.75; p=0.001) and increasing cardiac index (r=0.58; p=0.023). Although LV end-diastolic volume index (142±31 to 135±34 mL/m 2 ; p=0.033) and end-systolic volume index (110±29 to 99±33 mL/m 2 ; p=0.001) both decreased significantly, the extent of these changes were not correlated to changing T2-values (r=0 and 0.11, respectively; p=ns). Conclusions: Global LV myocardial edema is observed in ADHF and reversible with successful decongestive therapy. Relief of myocardial edema strongly correlates with improvements in systolic and diastolic function.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
H Z R McConkey ◽  
M Marber ◽  
J Lee ◽  
H Ellis ◽  
J Joseph ◽  
...  

Abstract Background Low gradient severe aortic stenosis (LGAS) is associated with unfavourable outcomes when compared to high gradient aortic stenosis (HGAS), yet the contributing pathophysiology is poorly understood. Methods Symptomatic LGAS and HGAS patients undergoing trans-catheter aortic valve implantation (TAVI) underwent 3T stress perfusion cardiac magnetic resonance imaging (CMR) pre-(within 24 hours) and post-(4–6 months) TAVI. Left ventricular (LV) contractility and coronary flow/pressure were measured during hyperaemia and rapid pacing, immediately before and after TAVI, using a conductance LV catheter and dual-pressure and Doppler sensor–tipped guidewire in the mid-left anterior descending coronary artery. Results 24 patients were recruited resulting in 19 suitable datasets (LGAS N=9, HGAS N=10, equally matched for comorbidities and B-natriuretic peptide level). LGAS patients had a smaller LV end diastolic volume index (p=0.035) and lower LV mass index (LVMI) (p=0.037). Pre-TAVI stress global endocardium-epicardium gradient was 0.88±0.09 and global myocardial perfusion reserve (MPR) 2.0±0.48 in 14 patients (6 LGAS and 8 HGAS patients, no difference between groups). Pre-TAVI, baseline coronary data demonstrated lower augmentation pressure (AP, p=0.035) and augmentation index (AIx, p=0.02) in the LGAS group. LGAS patients also exhibited a shorter ejection time (p=0.015), larger forward compression waves during rest, hyperaemia and rapid pacing, and smaller backward expansion waves (BEW) (p=0.001). Lower baseline end systolic pressure (p=0.004), inotropy (dP/dt+, p=0.045), lusitropy (dP/dt-, p=0.069), and stroke work (p=0.019) were observed in the LGAS group. Whilst LV size was smaller the LGAS group, rapid pacing induced a more significant drop in end systolic volume (p=0.045) and ejection fraction (p=0.015) in patients with HGAS. Post-TAVI, the hyperaemic BEW fell sharply (p<0.001), along with coronary VTI (p=0.02), and average pulse velocity (p=0.028), and AP and AIx remained lower (p=0.034 and p=0.031, respectively). The forward expansion wave was reduced in LGAS during rapid pacing. The HGAS group displayed a more profound drop in dP/dt+ (p=0.011) and dP/dt- p=0.014) at rest following intervention. Repeat CMR demonstrated statistically significant reduction in LV size and LVMI (p=0.012 and p<0.001, respectively) with significant increase in 3D global peak radial, circumferential and longitudinal strain (p=0.004, p=0.001 and p=0.018, respectively). Post-TAVI stress global endocardium-epicardium gradient was 0.88±0.13 and MPR 2.46±0.59 (improved from pre-TAVI, p=0.05). There was no difference in remodelling patterns or perfusion between the two groups. Conclusion This is the first study detailing the combined invasive and CMR pathophysiological changes in LGAS. Despite invasive parameters indicating a disease of less severe AS, the level of perfusion abnormality is disproportionate which may in part, relate to their adverse prognosis. Acknowledgement/Funding This research is funded by a Clinical Research Training Fellowship grant from the British Heart Foundation (FS/16/51/32365).


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