Blood withdrawal acutely impairs cardiac filling, output and aerobic capacity in proportion to induced hypovolemia in middle-aged and older women

2021 ◽  
pp. 1-8
Author(s):  
Candela Diaz-Canestro ◽  
Brandon Pentz ◽  
Arshia Sehgal ◽  
David Montero
Keyword(s):  
Cardiac Output ◽  
Aerobic Capacity ◽  
Blood Donation ◽  
Left Ventricular ◽  
Incremental Exercise ◽  
Mature Adult ◽  
Adult Lifespan ◽  
Blood Withdrawal ◽  
End Diastolic Volume ◽  
Cardiac Filling

Blood donation entails acute reductions of cardiorespiratory fitness in healthy men. Whether these effects can be extrapolated to blood donor populations comprising women remains uncertain. The purpose of this study was to comprehensively assess the acute impact of blood withdrawal on cardiac function, central hemodynamics and aerobic capacity in women throughout the mature adult lifespan. Transthoracic echocardiography and O2 uptake were assessed at rest and throughout incremental exercise (cycle ergometry) in healthy women (n = 30, age: 47–77 yr). Left ventricular end-diastolic volume (LVEDV), stroke volume (SV), cardiac output (Q̇) and peak O2 uptake (V̇O2peak), and blood volume (BV) were determined with established methods. Measurements were repeated following a 10% reduction of BV within a week period. Individuals were non-smokers, non-obese and moderately fit (V̇O2peak = 31.4 ± 7.3 mL·min–1·kg–1). Hematocrit and BV ranged from 38.0 to 44.8% and from 3.8 to 6.6 L, respectively. The standard 10% reduction in BV resulted in 0.5 ± 0.1 L withdrawal of blood, which did not alter hematocrit (P = 0.953). Blood withdrawal substantially reduced cardiac LVEDV and SV at rest as well as during incremental exercise (≥10% decrements, P ≤ 0.009). Peak Q̇ was proportionally decreased after blood withdrawal (P < 0.001). Blood withdrawal induced a 10% decrement in V̇O2peak (P < 0.001). In conclusion, blood withdrawal impairs cardiac filling, Q̇ and aerobic capacity in proportion to the magnitude of hypovolemia in healthy mature women. Novelty: The filling of the heart and therefore cardiac output are impaired by blood withdrawal in women. Oxygen delivery and aerobic capacity are reduced in proportion to blood withdrawal.

Left ventricular mechanical limitations to stroke volume in healthy humans during incremental exercise

2011 ◽  
Vol 301 (2) ◽  
pp. H478-H487 ◽  
Author(s):  
Eric J. Stöhr ◽  
José González-Alonso ◽  
Rob Shave
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Left Ventricular ◽  
Incremental Exercise ◽  
Diastolic Filling ◽  
Systolic Volume ◽  
Young Males ◽  
Healthy Humans ◽  
End Diastolic Volume

During incremental exercise, stroke volume (SV) plateaus at 40–50% of maximal exercise capacity. In healthy individuals, left ventricular (LV) twist and untwisting (“LV twist mechanics”) contribute to the generation of SV at rest, but whether the plateau in SV during incremental exercise is related to a blunting in LV twist mechanics remains unknown. To test this hypothesis, nine healthy young males performed continuous and discontinuous incremental supine cycling exercise up to 90% peak power in a randomized order. During both exercise protocols, end-diastolic volume (EDV), end-systolic volume (ESV), and SV reached a plateau at submaximal exercise intensities while heart rate increased continuously. Similar to LV volumes, two-dimensional speckle tracking-derived LV twist and untwisting velocity increased gradually from rest (all P < 0.001) and then leveled off at submaximal intensities. During continuous exercise, LV twist mechanics were linearly related to ESV, SV, heart rate, and cardiac output (all P < 0.01) while the relationship with EDV was exponential. In diastole, the increase in apical untwisting was significantly larger than that of basal untwisting ( P < 0.01), emphasizing the importance of dynamic apical function. In conclusion, during incremental exercise, the plateau in LV twist mechanics and their close relationship with SV and cardiac output indicate a mechanical limitation in maximizing LV output during high exercise intensities. However, LV twist mechanics do not appear to be the sole factor limiting LV output, since EDV reaches its maximum before the plateau in LV twist mechanics, suggesting additional limitations in diastolic filling to the heart.

Does fitness level modulate the cardiovascular hemodynamic response to exercise?

2006 ◽  
Vol 100 (6) ◽  
pp. 1895-1901 ◽  
Author(s):  
Michael K. Stickland ◽  
Robert C. Welsh ◽  
Stewart R. Petersen ◽  
John V. Tyberg ◽  
William D. Anderson ◽  
...  
Keyword(s):  
Aerobic Fitness ◽  
Maximal Oxygen Consumption ◽  
Left Ventricular ◽  
Right Atrial ◽  
Peak Exercise ◽  
Fitness Level ◽  
End Diastolic Volume ◽  
Diastolic Compliance ◽  
Cardiac Filling ◽  
Response To Exercise

Subjects with greater aerobic fitness demonstrate better diastolic compliance at rest, but whether fitness modulates exercise cardiac compliance and cardiac filling pressures remains to be determined. On the basis of maximal oxygen consumption (V̇o2max), healthy male subjects were categorized into either low (LO: V̇o2max = 43 ± 6 ml·kg−1·min−1; n = 3) or high (HI: V̇o2max = 60 ± 3 ml·kg−1·min−1; n = 5) aerobic power. Subjects performed incremental cycle exercise to 90% V̇o2max. Right atrial (RAP) and pulmonary artery wedge (PAWP) pressures were measured, and left ventricular (LV) transmural filling pressure (TMFP = PAWP − RAP) was calculated. Cardiac output (CO) and stroke volume (SV) were determined by direct Fick, and LV end-diastolic volume (EDV) was estimated from echocardiographic fractional area change and Fick SV. There were no between-group differences for any measure at rest. At a submaximal workload of 150 W, PAWP and TMFP were higher ( P < 0.05) in LO compared with HI (12 vs. 8 mmHg, and 9 vs. 4 mmHg, respectively). At peak exercise, CO, SV, and EDV were lower in LO ( P < 0.05). RAP was not different at peak exercise, but PAWP (23 vs. 15 mmHg) and TMFP (12 vs. 6 mmHg) were higher in LO ( P < 0.05). Compared with less fit subjects, subjects with greater aerobic fitness demonstrated lower LV filling pressures during exercise, whereas SV and EDV were either similar (submaximal exercise) or higher (peak exercise), suggesting superior diastolic function and compliance.

Generalized Transformed Hough: Segmentation of Contours in Angiographic Images

2017 ◽  
Vol 5 (2) ◽  
pp. 345
Author(s):  
Oscar Eduardo Gualdron
Keyword(s):  
Cardiac Output ◽  
Left Ventricular ◽  
Functional Study ◽  
Severe Damage ◽  
Systolic Volume ◽  
Generalized Hough Transform ◽  
End Diastolic Volume ◽  
The World ◽  
End Systolic Volume ◽  
Causes Of Mortality

<span lang="EN-US">The morphologic and functional study of cardiovascular system is of vital importance because problems related to this system are one of the main causes of   mortality in the world. It is important to mention that the left ventricle (VI) is the most susceptible to suffer severe damage, in diseases, such as arterial hypertension, mellitus diabetes or arteriosclerosis. This article presents a new methodology directed to segmentation of left ventricular contours, in angiographic images by using Generalized Hough Transform (TGH). It is important to obtain the ventricular edge, because analyzing processes of systole and diastole end, it is possible to calculate parameters of the cardiac functionality as the end-diastolic volume, end systolic volume, ejection fraction, cardiac output, Hyperkinéticos, Hypokinéticos segments, and normal; in this work we focus only on the removal of the same. </span>

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.

Volume overload hypertrophy in a closed-chest model of mitral regurgitation

1988 ◽  
Vol 254 (6) ◽  
pp. H1034-H1041 ◽  
Author(s):  
J. P. Kleaveland ◽  
W. G. Kussmaul ◽  
T. Vinciguerra ◽  
R. Diters ◽  
B. A. Carabello
Keyword(s):  
Cardiac Output ◽  
Mitral Regurgitation ◽  
Diastolic Pressure ◽  
Volume Ratio ◽  
Volume Overload ◽  
Canine Model ◽  
Left Ventricular ◽  
Closed Chest ◽  
Cardiac Decompensation ◽  
End Diastolic Volume

Chronic volume overload hypertrophy as seen in mitral regurgitation in humans eventually may cause left ventricular dysfunction. Longitudinal study of the mechanisms leading to such dysfunction is difficult in humans and more easily performed in an animal model. In this study, we describe a canine model of volume overload hypertrophy produced by mitral regurgitation. An arterially placed grasping forceps was used to disrupt mitral chordae or leaflets; thus mitral regurgitation was produced without the need for thoracotomy. Eleven of 22 dogs had severe mitral regurgitation (regurgitant fraction greater than 0.50) and survived for greater than or equal to 3 mo (average 9.2 +/- 6 mo) after the production of mitral regurgitation. At 3 mo, end-diastolic volume increased from 48 +/- 9 to 85 +/- 19 ml, P less than 0.01. Left ventricular mass increased from 71 +/- 13 to 90 +/- 10 g, P less than 0.01. Left ventricular end-diastolic pressure increased from 9 +/- 3 to 19 +/- 6 mmHg, P less than 0.01. Cardiac output decreased from 2.3 +/- 0.61 to 1.80 +/- 0.64 l/min, P less than 0.05. The mass-to-volume ratio decreased from 1.44 +/- 0.17 to 1.09 +/- 0.13, P less than 0.01. We conclude that this closed-chest model of chronic mitral regurgitation produces significant eccentric cardiac hypertrophy. Despite a doubling of end-diastolic volume, there was a fall in cardiac output and a rise in left ventricular end-diastolic pressure, suggesting cardiac decompensation.

Hemodynamic heterogeneity of inadequate cardiac output increase identified by 2-dimensional volumetric exercise echocardiography: slow, stiff or weak heart?

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
T Bombardini ◽  
A Zagatina ◽  
Q Ciampi ◽  
L Cortigiani ◽  
A D'Andrea ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Peak Stress ◽  
Suspected Coronary Artery Disease ◽  
Left Ventricular ◽  
Exercise Stress ◽  
Contractile Reserve ◽  
Systolic Volume ◽  
End Diastolic Volume ◽  
End Systolic Volume ◽  
Artery Disease

Abstract Background Two-dimensional (2-D) volumetric exercise stress echocardiography (ESE) provides an integrated view of preload reserve through end-diastolic volume (EDV) and left ventricular contractile reserve (LVCR) through end-systolic volume (ESV) changes. Purpose To assess the dependence of stroke volume (SV) and cardiac output (CO) upon LVCR EDV changes and heart rate (HR) during ESE. Methods We prospectively performed semi-supine bicycle or treadmill ESE in 1,344 patients (age 59.8±11.4 years; 550 female; ejection fraction = 62.5±8%) referred for known or suspected coronary artery disease in 20 quality controlled laboratories of 16 countries from 2016 to 2019. SV was calculated at rest and peak stress from raw measurement of LV EDV and ESV by biplane Simpson rule, 2-D echo. LVCR was the stress-rest ratio of force (systolic blood pressure by cuff sphygmomanometer/ESV, abnormal values &lt;2.0 identify a “weak” heart). Preload reserve was defined by an increase in LV EDV. Abnormal values (lack of EDV increase, peak EDV ≤ rest EDV) identify a “stiff” heart. Cardiac output was calculated as SV * HR (measured with standard EKG). HR reserve (stress/rest ratio) &lt;1.85 identifies a “slow” heart with chronotropic incompetence. Results By selection, all patients had negative SE by wall motion criteria. Of the 1,344 patients included in the study, 448 belonged to the lowest tertile of CO increase. Of them 326 (73%) achieved HR reserve &lt;1.85; 220 (49%) had a blunted LVCR and 374 (83%) a reduction of preload reserve, with 348 patients (78%) showing ≥2 abnormalities. The more the abnormal criteria, the worse the CO response, which was lowest in slow, stiff and weak hearts: see figure. Conclusion Patients with normal CO reserve during exercise usually have a fast, compliant and strong heart. Abnormal CO reserve is associated with heterogeneous hemodynamic responses, with slow, stiff and/or weak hearts. The clarification of underlying hemodynamic heterogeneity is the prerequisite for a personalized treatment, and can be easily extracted from a standard 2-D volumetric SE. Hearts with normal CO are all alike; every heart with abnormal CO is abnormal in its own way. CO % changes in subsets (*p&lt;0.001) Funding Acknowledgement Type of funding source: None

Heart size and maximal cardiac output are limited by the pericardium

1992 ◽  
Vol 263 (6) ◽  
pp. H1675-H1681 ◽  
Author(s):  
H. K. Hammond ◽  
F. C. White ◽  
V. Bhargava ◽  
R. Shabetai
Keyword(s):  
Cardiac Output ◽  
Oxygen Consumption ◽  
Diastolic Pressure ◽  
Maximal Oxygen Consumption ◽  
Left Ventricular ◽  
Treadmill Running ◽  
Oxygen Utilization ◽  
End Diastolic Volume ◽  
Maximal Cardiac Output ◽  
Heart Size

We tested the hypothesis that the pericardium, by restricting heart size, limits maximal cardiac output and oxygen consumption. We studied 15 pigs. Five underwent maximal treadmill running before and 14–21 days after thoracotomy and pericardiectomy; these pigs also received sequential volume infusions to determine end-diastolic pressure-dimension relationships. Five underwent maximal treadmill running before and 14–21 days after thoracotomy (pericardium undisturbed) to determine the effect of thoracotomy on exercise performance. Finally, five underwent thoracotomy, instrumentation, loose closure of the pericardium, and sequential volume infusions to determine the effect of thoracotomy without pericardiectomy on end-diastolic pressure-dimension relationships. Pericardiectomy caused similar increases in maximal cardiac output (29% increase; P = 0.007) and maximal oxygen consumption (31% increase; P = 0.02). These results were associated with increased left ventricular end-diastolic dimension (10% increase; P = 0.01) and an estimated 33% increase in end-diastolic volume. In addition, left ventricular mass was increased by pericardiectomy (18% increase; P < 0.04). Thus the pericardium, by limiting utilization of the Starling mechanism, limits maximal cardiac output, and the limit to cardiorespiratory performance lies not in oxygen utilization, but in oxygen delivery. Furthermore, removal of pericardium is associated with myocardial hypertrophy.

scholarly journals Sex and age interaction in fundamental circulatory volumetric variables at peak working capacity

2022 ◽  
Vol 13 (1) ◽  
Author(s):  
Candela Diaz-Canestro ◽  
David Montero
Keyword(s):  
Physical Activity ◽  
Older Women ◽  
Vigorous Physical Activity ◽  
Age Groups ◽  
Left Ventricular ◽  
Older Age ◽  
Peak Exercise ◽  
Lower Heart Rate ◽  
End Diastolic Volume ◽  
Cardiac Filling

Abstract Background Whether the fundamental hematological and cardiac variables determining cardiorespiratory fitness and their intrinsic relationships are modulated by major constitutional factors, such as sex and age remains unresolved. Methods Transthoracic echocardiography, central hemodynamics and pulmonary oxygen (O2) uptake were assessed in controlled conditions during submaximal and peak exercise (cycle ergometry) in 85 healthy young (20–44 year) and older (50–77) women and men matched by age-status and moderate-to-vigorous physical activity (MVPA) levels. Main outcomes such as peak left ventricular end-diastolic volume (LVEDVpeak), stroke volume (SVpeak), cardiac output (Qpeak) and O2 uptake (VO2peak), as well as blood volume (BV), BV–LVEDVpeak and LVEDVpeak–SVpeak relationships were determined with established methods. Results All individuals were non-smokers and non-obese, and MVPA levels were similar between sex and age groups (P ≥ 0.140). BV per kg of body weight did not differ between sexes (P ≥ 0.118), but was reduced with older age in men (P = 0.018). Key cardiac parameters normalized by body size (LVEDVpeak, SVpeak, Qpeak) were decreased in women compared with men irrespective of age (P ≤ 0.046). Older age per se curtailed Qpeak (P ≤ 0.022) due to lower heart rate (P < 0.001). In parallel, VO2peak was reduced with older age in both sexes (P < 0.001). The analysis of fundamental circulatory relationships revealed that older women require a higher BV for a given LVEDVpeak than older men (P = 0.024). Conclusions Sex and age interact on the crucial circulatory relationship between total circulating BV and peak cardiac filling, with older women necessitating more BV to fill the exercising heart than age- and physical activity-matched men.

Hypertonic saline is a negative inotropic agent in normovolumic dogs

1994 ◽  
Vol 267 (2) ◽  
pp. H667-H677 ◽  
Author(s):  
P. D. Constable ◽  
W. W. Muir ◽  
P. F. Binkley
Keyword(s):  
Cardiac Output ◽  
Hypertonic Saline ◽  
Diastolic Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Rate Of Change ◽  
Inotropic Agent ◽  
Inotropic Effects ◽  
End Diastolic Volume

The inotropic effects of hypertonic saline (HS) and hyperosmotic dextrose (HD; 2,400 mosmol/l, 4 ml/kg) were determined in normovolumic, chloralose-anesthetized, intact (n = 14) and autonomically blocked (n = 8) dogs. Solutions were infused intravenously over 3 min. HS and HD rapidly increased preload in both intact and autonomically blocked dogs, as assessed by significant (P < 0.05) increases in plasma volume, end-diastolic volume, and end-diastolic pressure. In intact dogs, HS produced a nonsignificant decrease in end-systolic elastance (Ees) and a nonsignificant increase in the maximal rate of change of left ventricular pressure (dP/dtmax) and cardiac output, whereas HD produced a significant increase in Ees, dP/dtmax, and cardiac output. In autonomically blocked dogs, HS significantly decreased Ees and significantly increased dP/dtmax but did not alter cardiac output, whereas HD significantly increased Ees, dP/dtmax, and cardiac output. We conclude that in normovolumic animals, HS is a negative inotropic agent, HD is a positive inotropic agent, and the in vivo effect of an ionic hyperosmotic agent (HS) differs from that of a nonionic hyperosmotic agent (HD).

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