Acute plasma expansion: left ventricular hemodynamics and endocrine function during exercise

1992 ◽  
Vol 73 (5) ◽  
pp. 1791-1796 ◽  
Author(s):  
I. L. Kanstrup ◽  
J. Marving ◽  
P. F. Hoilund-Carlsen
Keyword(s):  
Cardiac Output ◽  
Stroke Volume ◽  
Healthy Subjects ◽  
Venous Pressure ◽  
Left Ventricular ◽  
Endocrine Function ◽  
Plasma Expansion ◽  
Central Venous ◽  
Mean Pressure ◽  
Dextran Solution

In 11 healthy subjects (8 males and 3 females, age 21–59 yr) left ventricular end-diastolic (LVEDV) and end-systolic (LVESV) volumes were measured in the supine position by isotope cardiography at rest and during two submaximal one-legged exercise loads before and 1 h after acute plasma expansion (PE) by use of a 6% dextran solution (500–750 ml). After PE, blood volume increased from 5.22 +/- 0.92 to 5.71 +/- 1.02 (SD) liters (P < 0.01). At rest, cardiac output increased 30% (5.3 +/- 1.0 to 6.9 +/- 1.6 l/min; P < 0.01), stroke volume increased from 90 +/- 20 to 100 +/- 28 ml (P < 0.05), and LVEDV increased from 134 +/- 29 to 142 +/- 40 ml (NS). LVESV was unchanged (44 +/- 11 and 42 +/- 14 ml). Heart rate rose from 60 +/- 7 to 71 +/- 10 beats/min (P < 0.01). The cardiac preload [central venous pressure (CVP)] was insignificantly elevated (4.9 +/- 2.1 and 5.3 +/- 3.0 mmHg); systemic vascular resistance and arterial pressures were significantly reduced (mean pressure fell from 91 +/- 11 to 85 +/- 11 mmHg, P < 0.01). Left ventricular peak filling and peak ejection rates both increased (19 and 14%, respectively; P < 0.05). During exercise, cardiac output remained elevated after PE compared with the control situation, predominantly due to a 10- to 14-ml rise in stroke volume caused by an increased LVEDV, whereas LVESV was unchanged. CVP increased after PE by 2.1 and 3.0 mmHg, respectively (P < 0.05).2+ remained unchanged during exercise compared with rest after PE in

scholarly journals Central venous pressure and cardiac function during spaceflight

1998 ◽  
Vol 85 (2) ◽  
pp. 738-746 ◽  
Author(s):  
Ronald J. White ◽  
C. Gunnar Blomqvist
Keyword(s):  
Cardiac Output ◽  
Stroke Volume ◽  
Central Venous Pressure ◽  
Shape Change ◽  
Venous Pressure ◽  
Left Ventricular ◽  
Filling Pressure ◽  
Central Venous ◽  
End Diastolic Volume ◽  
Reference Measurements

Early in spaceflight, an apparently paradoxical condition occurs in which, despite an externally visible headward fluid shift, measured central venous pressure is lower but stroke volume and cardiac output are higher, and heart rate is unchanged from reference measurements made before flight. This paper presents a set of studies in which a simple three-compartment, steady-state model of cardiovascular function is used, providing insight into the contributions made by the major mechanisms that could be responsible for these events. On the basis of these studies, we conclude that, during weightless spaceflight, the chest relaxes with a concomitant shape change that increases the volume of the closed chest cavity. This leads to a decrease in intrapleural pressure, ultimately causing a shift of blood into the vessels of the chest, increasing the transmural filling pressure of the heart, and decreasing the central venous pressure. The increase in the transmural filling pressure of the heart is responsible, through a Starling-type mechanism, for the observed increases in heart size, left ventricular end-diastolic volume, stroke volume, and cardiac output.

Stroke Volume Optimization: The New Hemodynamic Algorithm

2015 ◽  
Vol 35 (1) ◽  
pp. 11-27 ◽  
Author(s):  
Alexander Johnson ◽  
Thomas Ahrens
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Venous Pressure ◽  
Optimization Strategy ◽  
Central Venous ◽  
Hemodynamic Optimization ◽  
Level Of Consciousness ◽  
Cardiac Output Monitor ◽  
Care Practices

Critical care practices have evolved to rely more on physical assessments for monitoring cardiac output and evaluating fluid volume status because these assessments are less invasive and more convenient to use than is a pulmonary artery catheter. Despite this trend, level of consciousness, central venous pressure, urine output, heart rate, and blood pressure remain assessments that are slow to be changed, potentially misleading, and often manifested as late indications of decreased cardiac output. The hemodynamic optimization strategy called stroke volume optimization might provide a proactive guide for clinicians to optimize a patient’s status before late indications of a worsening condition occur. The evidence supporting use of the stroke volume optimization algorithm to treat hypovolemia is increasing. Many of the cardiac output monitor technologies today measure stroke volume, as well as the parameters that comprise stroke volume: preload, afterload, and contractility.

scholarly journals Haemodynamic Effects of Pericardial Closure after Cardiac Surgery

2020 ◽  
Vol 8 (1) ◽  
pp. 81-85
Author(s):  
Saurabh KS ◽  
AK Padhy ◽  
Madhur Kumar ◽  
R Munjal ◽  
A. Gupta
Keyword(s):  
Cardiac Output ◽  
Cardiac Surgery ◽  
Valve Replacement ◽  
Artery Bypass ◽  
Venous Pressure ◽  
Left Ventricular ◽  
Haemodynamic Effects ◽  
Bypass Grafting ◽  
Central Venous ◽  
Double Valve Replacement

Introduction: Whether pericardial closure should be done or not is still a debated topic. While many studies favour pericardial closure after cardiac surgery, many are still not in favour of the same. Objective : Objective of this study was to analyse the changes induced by pericardial closure on the haemodynamic of the patient using easily measurable variables. Methods : Data of 30 patients were analysed of which 14 underwent mitral valve replacement, 10 underwent coronary artery bypass grafting and 6 underwent double valve replacement. Results: There was statistically significant change in cardiac output (p<0.01), central venous pressure (p<0.05) and left ventricular end diastolic diameter (p<0.01) after pericardial closure. Clinically the pericardial closure was well tolerated. Conclusion: Despite exhaustive experience, the topic of closing pericardium is still debated. Our study shows that clinically pericardial closure is well tolerated and in return it also safeguards the risks associated with re-do operations

Evidence for increased cardiac compliance during exposure to simulated microgravity

1998 ◽  
Vol 275 (4) ◽  
pp. R1343-R1352 ◽  
Author(s):  
Steven C. Koenig ◽  
Victor A. Convertino ◽  
John W. Fanton ◽  
Craig A. Reister ◽  
F. Andrew Gaffney ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Stroke Volume ◽  
Simulated Microgravity ◽  
Lower Body Negative Pressure ◽  
Venous Pressure ◽  
Left Ventricular ◽  
Continuous Exposure ◽  
Orthostatic Tolerance ◽  
Experimental Conditions ◽  
Ventricular Compliance

We measured hemodynamic responses during 4 days of head-down tilt (HDT) and during graded lower body negative pressure (LBNP) in invasively instrumented rhesus monkeys to test the hypotheses that exposure to simulated microgravity increases cardiac compliance and that decreased stroke volume, cardiac output, and orthostatic tolerance are associated with reduced left ventricular peak dP/d t. Six monkeys underwent two 4-day (96 h) experimental conditions separated by 9 days of ambulatory activities in a crossover counterbalance design: 1) continuous exposure to 10° HDT and 2) ∼12–14 h per day of 80° head-up tilt and 10–12 h supine (control condition). Each animal underwent measurements of central venous pressure (CVP), left ventricular and aortic pressures, stroke volume, esophageal pressure (EsP), plasma volume, α1- and β1-adrenergic responsiveness, and tolerance to LBNP. HDT induced a hypovolemic and hypoadrenergic state with reduced LBNP tolerance compared with the control condition. Decreased LBNP tolerance with HDT was associated with reduced stroke volume, cardiac output, and peak dP/d t. Compared with the control condition, a 34% reduction in CVP ( P= 0.010) and no change in left ventricular end-diastolic area during HDT was associated with increased ventricular compliance ( P = 0.0053). Increased cardiac compliance could not be explained by reduced intrathoracic pressure since EsP was unaltered by HDT. Our data provide the first direct evidence that increased cardiac compliance was associated with headward fluid shifts similar to those induced by exposure to spaceflight and that reduced orthostatic tolerance was associated with lower cardiac contractility.

Effects of the Third (Aqueous) Extract of Ginseng on the Cardiovascular Dynamics of Dogs During Halothane Anesthesia

1978 ◽  
Vol 06 (03) ◽  
pp. 253-259
Author(s):  
DONALD H. CLIFFORD ◽  
DO CHIL LEE ◽  
CHONG YUL KIM ◽  
MYUNG O. LEE
Keyword(s):  
Cardiac Output ◽  
Stroke Volume ◽  
Central Venous Pressure ◽  
Aqueous Extract ◽  
Total Peripheral Resistance ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Electromagnetic Flowmeter ◽  
Central Venous ◽  
Cardiovascular Variables

An electromagnetic flowmeter probe was chronically implanted around the ascending aorta in a group of dogs. Subsequently, ten dogs were lightly anesthetized with halothane (0.75%), and a third (aqueous) extract of ginseng (40 mg/kg) was administered intravenously. Five dogs were anesthesized without the administration of ginseng. Eleven cardiovascular variables including cardiac output, stroke volume, heart rate, mean arterial pressure, pulse pressure, central venous pressure, total peripheral resistance, pH, PaCO2, PaO2, and base deficit were compared. The cardiac output, stroke volume, and central venous pressure were decreased significantly, while total peripheral resistance was increased significantly following ginseng.

Changes in cardiac output, stroke volume, and central venous pressure induced by atropine in man

1959 ◽  
Vol 58 (2) ◽  
pp. 204-213 ◽  
Author(s):  
J.Norman Berry ◽  
Howard K. Thompson ◽  
D.Edmond Miller ◽  
Henry D. McIntosh
Keyword(s):  
Cardiac Output ◽  
Stroke Volume ◽  
Central Venous Pressure ◽  
Venous Pressure ◽  
Central Venous

Exercise training prevents decline in stroke volume during exercise in young healthy subjects

1992 ◽  
Vol 72 (6) ◽  
pp. 2458-2462 ◽  
Author(s):  
R. J. Spina ◽  
T. Ogawa ◽  
W. H. Martin ◽  
A. R. Coggan ◽  
J. O. Holloszy ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Stroke Volume ◽  
Endurance Training ◽  
Healthy Subjects ◽  
Maximal Exercise ◽  
Interval Training ◽  
Left Ventricular ◽  
Maximal Heart Rate ◽  
Before And After ◽  
Dimensional Echocardiography

Stroke volume (SV) increases above the resting level during exercise and then declines at higher intensities of exercise in sedentary subjects. The purpose of this study was to determine whether an attenuation of the decline in SV at higher exercise intensities contributes to the increase in maximal cardiac output (Qmax) that occurs in response to endurance training. We studied six men and six women, 25 +/- 1 (SE) yr old, before and after 12 wk of endurance training (3 days/wk running for 40 min, 3 days/wk interval training). Cardiac output was measured at rest and during exercise at 50 and 100% of maximal O2 uptake (Vo2max) by the C2H2-rebreathing method. VO2max was increased by 19% (from 2.7 +/- 0.2 to 3.2 +/- 0.3 l/min, P less than 0.001) in response to the training program. Qmax was increased by 12% (from 18.1 +/- 1 to 20.2 +/- 1 l/min, P less than 0.01), SV at maximal exercise was increased by 16% (from 97 +/- 6 to 113 +/- 8 ml/beat, P less than 0.001) and maximal heart rate was decreased by 3% (from 185 +/- 2 to 180 +/- 2 beats/min, P less than 0.01) after training. The calculated arteriovenous O2 content difference at maximal exercise was increased by 7% (14.4 +/- 0.4 to 15.4 +/- 0.4 ml O2/100 ml blood) after training. Before training, SV at VO2max was 9% lower than during exercise at 50% VO2max (P less than 0.05). In contrast, after training, the decline in SV between 50 and 100% VO2max was only 2% (P = NS). Furthermore, SV was significantly higher (P less than 0.01) at 50% VO2max after training than it was before. Left ventricular hypertrophy was evident, as determined by two-dimensional echocardiography at the completion of training. The results indicate that in young healthy subjects the training-induced increase in Qmax is due in part to attenuation of the decrease in SV as exercise intensity is increased.

Peripheral circulatory control of cardiac output in diabetic rats

1991 ◽  
Vol 261 (3) ◽  
pp. H836-H842 ◽  
Author(s):  
S. E. Litwin ◽  
T. E. Raya ◽  
S. Daugherty ◽  
S. Goldman
Keyword(s):  
Cardiac Output ◽  
Cardiac Index ◽  
Stroke Volume ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Stroke Volume Index ◽  
Diabetic Rats ◽  
Left Ventricular ◽  
Volume Index ◽  
Venous Compliance

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.

Cardiac remodeling and increased central venous pressure underlie elevated stroke volume and cardiac output of seawater-acclimated rainbow trout

2017 ◽  
Vol 312 (1) ◽  
pp. R31-R39 ◽  
Author(s):  
Jeroen Brijs ◽  
Erik Sandblom ◽  
Esmée Dekens ◽  
Joacim Näslund ◽  
Andreas Ekström ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Rainbow Trout ◽  
Stroke Volume ◽  
Central Venous Pressure ◽  
Venous Pressure ◽  
Cardiovascular Responses ◽  
Central Venous ◽  
End Diastolic Volume ◽  
Gastrointestinal Blood Flow ◽  
Cardiac Filling

Substantial increases in cardiac output (CO), stroke volume (SV), and gastrointestinal blood flow are essential for euryhaline rainbow trout ( Oncorhyncus mykiss) osmoregulation in seawater. However, the underlying hemodynamic mechanisms responsible for these changes are unknown. By examining a range of circulatory and cardiac morphological variables of seawater- and freshwater-acclimated rainbow trout, the present study revealed a significantly higher central venous pressure (CVP) in seawater-acclimated trout (~0.09 vs. −0.02 kPa). This serves to increase cardiac end-diastolic volume in seawater and explains the elevations in SV (~0.41 vs. 0.27 ml/kg) and CO (~21.5 vs. 14.2 ml·min−1·kg−1) when compared with trout in freshwater. Furthermore, these hemodynamic modifications coincided with a significant increase in the proportion of compact myocardium, which may be necessary to compensate for the increased wall tension associated with a larger stroke volume. Following a temperature increase from 10 to 16.5°C, both acclimation groups exhibited similar increases in heart rate (Q10 of ~2), but SV tended to decrease in seawater-acclimated trout despite the fact that CVP was maintained in both groups. This resulted in CO of seawater- and freshwater-acclimated trout stabilizing at a similar level after warming (~26 ml·min−1·kg−1). The consistently higher CVP of seawater-acclimated trout suggests that factors other than compromised cardiac filling constrained the SV and CO of these individuals at high temperatures. The present study highlights, for the first time, the complex interacting effects of temperature and water salinity on cardiovascular responses in a euryhaline fish species.

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