Stroke Volume Dynamics During Progressive Exercise in Healthy Adolescents

2013 ◽  
Vol 25 (2) ◽  
pp. 173-185 ◽  
Author(s):  
Thomas Rowland ◽  
Viswanath Unnithan
Keyword(s):  
Stroke Volume ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Cardiovascular Responses ◽  
Left Ventricular ◽  
Diastolic Filling ◽  
Original Research ◽  
Ventricular Contractility ◽  
Cardiac Responses ◽  
Progressive Exercise

Understanding cardiac responses to exercise in healthy subjects is important in the evaluation of youth with heart disease. This review article incorporates previously published original research from the authors’ laboratory to examine changes in stroke volume during progressive exercise which are consistent with a model in which circulatory responses are controlled by alterations in the systemic vascular resistance. Stroke volume dynamics and cardiovascular responses to a progressive upright cycle test were examined in three groups of healthy, untrained adolescent subjects. These indicated a) a progressive decease in systemic vascular resistance, b) little change in stroke volume after an initial rise related to orthostatic changes in ventricular refilling, c) evidence of a constant or slightly declining left ventricular end diastolic filling pressure, d) and increases in markers of ventricular contractility. These observations are consistent with peripheral (vascular resistance) rather than central (cardiac) control of circulation with exercise. Changes in stroke volume during exercise need to be interpreted in respect to alterations in heart rate and myocardial functional capacity.

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)

scholarly journals Quantitative Analysis of an Intraoperative Digitalized Esophageal Heart Sound Signal to Speculate on Perturbed Cardiovascular Function

2019 ◽  
Vol 8 (5) ◽  
pp. 715 ◽  
Author(s):  
Young-Jin Moon ◽  
Sung-Hoon Kim ◽  
Yong-Seok Park ◽  
Jae-Man Kim ◽  
Gyu-Sam Hwang
Keyword(s):  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Cardiovascular Function ◽  
Tissue Doppler ◽  
Left Ventricular ◽  
Heart Sounds ◽  
Ventricular Contractility ◽  
Hemodynamic Assessment ◽  
Frequency Domains ◽  
Time And Frequency Domains

Although visualization of heart sounds, known as phonocardiography, provides valuable information on cardiovascular hemodynamics, its use has not been widely encouraged due to the scarcity of information on its interpretation. In the present study, using the intraoperative phonocardiogram recorded by an esophageal stethoscope, we quantitatively evaluated the time and frequency domains of modulation of the heart sounds components and their association with left ventricular contractility and systemic vascular resistance under the effects of various cardiovascular drugs. We analyzed 29 pairs of intraoperative digitalized phonocardiographic signals and their corresponding hemodynamic data before and after cardiovascular drug administration (ephedrine, esmolol, phenylephrine, and/or nicardipine) in 17 patients who underwent liver transplantation. The S1 and S2 components of the heart sounds (the first and second heart sounds, respectively) were identified and their modulation in time and frequency domains was analyzed. As an index of cardiovascular function, systolic tissue Doppler wave velocity (TDI S’), maximal dP/dt from the arterial waveform, and systemic vascular resistance were simultaneously evaluated. Ephedrine/esmolol and phenylephrine/nicardipine primarily affected the S1 and S2 components of the heart sounds, respectively. This result implies that the intraoperative phonocardiogram may have the potential to be useful in detecting the changes in contractility and afterload that commonly occur in patients receiving anesthesia. In an era of constant need for noninvasive hemodynamic assessment, phonocardiography has the potential for use as a novel and informative tool for monitoring of hemodynamic function.

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.

Endurance training in older men and women. I. Cardiovascular responses to exercise

1984 ◽  
Vol 57 (4) ◽  
pp. 1024-1029 ◽  
Author(s):  
D. R. Seals ◽  
J. M. Hagberg ◽  
B. F. Hurley ◽  
A. A. Ehsani ◽  
J. O. Holloszy
Keyword(s):  
Stroke Volume ◽  
Endurance Training ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Aerobic Power ◽  
Cardiovascular Responses ◽  
Older Individuals ◽  
Uptake Capacity ◽  
Maximal Cardiac Output ◽  
Older Men And Women

The effects of prolonged endurance training on maximal O2 uptake capacity (VO2max) and its determinants were studied in 11 older individuals (63 +/- 2 yr). The subjects were evaluated before training, after 6 mo of low-intensity (LI) training, and after an additional 6 mo of higher intensity (HI) training. VO2max was 25.4 +/- 4.6 ml X kg-1 X min-1 before training, 28.2 +/- 5.2 ml X kg-1 X min-1 after LI training (P less than 0.05), and 32.9 +/- 7.6 ml X kg-1 X min-1 after HI training (P less than 0.01), with an overall increase of 30%. The increase in VO2max in response to training appeared to be mediated primarily through an increase in maximal arteriovenous O2 difference (P less than 0.01), with little augmentation of maximal cardiac output (Q) (P greater than 0.05). At the same absolute work rates, stroke volume was higher (P less than 0.05); heart rate (HR), blood pressure (BP), and systemic vascular resistance were lower (P less than 0.05); and Q and arteriovenous O2 difference were unchanged after training. At the same relative work rates, arteriovenous O2 difference was higher (P less than 0.01); BP and systemic vascular resistance were lower (P less than 0.05); and HR, Q, and stroke volume did not change significantly. These findings show that older individuals can adapt to prolonged endurance training with a large increase in aerobic power.

Cardiovascular responses to metabolic acidosis

1965 ◽  
Vol 208 (2) ◽  
pp. 237-242 ◽  
Author(s):  
S. Evans Downing ◽  
Norman S. Talner ◽  
Thomas H. Gardner
Keyword(s):  
Heart Rate ◽  
Metabolic Acidosis ◽  
Vascular Resistance ◽  
Diastolic Pressure ◽  
Cardiovascular Responses ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Ventricular Contractility ◽  
Precise Control ◽  
Arterial Ph

The performance of the left ventricle was examined in a feline preparation which allowed precise control of aortic pressure, cardiac output, heart rate, and temperature. The arterial pH, Po2, and Pco2 were continuously measured with a Jewett flow-through electrode assembly. Reduction of arterial pH from 7.45 to 6.80 by HCl or lactic acid infusion was associated with a minimal reduction or no change of left ventricular contractility as measured by the stroke volume or mean ejection rate for a given left ventricular end-diastolic pressure at a constant aortic pressure and heart rate. No evidence for a diminished positive inotropic response to norepinephrine was found. Simultaneous systemic and pulmonary pressure-flow curves demonstrated that metabolic acidosis caused a reduction of systemic vascular resistance and a concurrent increase of pulmonary vascular resistance.

Hemodynamic effects of epinephrine: concentration-effect study in humans

1985 ◽  
Vol 58 (4) ◽  
pp. 1199-1206 ◽  
Author(s):  
J. R. Stratton ◽  
M. A. Pfeifer ◽  
J. L. Ritchie ◽  
J. B. Halter
Keyword(s):  
Heart Rate ◽  
Ejection Fraction ◽  
Stroke Volume ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Hemodynamic Effects ◽  
Plasma Epinephrine ◽  
Ventricular Performance

The hemodynamic effects of three different infusion rates of epinephrine (25, 50, or 100 ng X kg-1 X min-1 for 14 min) were examined in 10 normal human subjects. Ejection fraction and changes in cardiac volumes were assessed by radionuclide ventriculography. Plasma epinephrine was increased to levels that spanned the normal physiological range (178 +/- 15, 259 +/- 24, and 484 +/- 69 pg/ml, respectively). Epinephrine infusions resulted in dose-dependent increases in heart rate (8 +/- 3, 12 +/- 2, and 17 +/- 1 beats/min, mean +/- SE) and systolic pressure (8 +/- 1, 18 +/- 2, and 30 +/- 6 mmHg). Although epinephrine infusions had minimal effects on end-diastolic volume, there were significant increases in stroke volume (+26 +/- 2, 31 +/- 4, and 40 +/- 4%), ejection fraction (+0.10 +/- 0.01, 0.14 +/- 0.02 and 0.16 +/- 0.03 ejection fraction units), and cardiac output (+41 +/- 4, 58 +/- 5, and 74 +/- 1%). These increases in left ventricular performance were associated with a decreased systemic vascular resistance (-31 +/- 3, -42 +/- 2, and -48 +/- 8%). Supine bicycle exercise resulted in similar plasma epinephrine levels (417 +/- 109 pg/ml) and similar changes in stroke volume, ejection fraction, and systemic vascular resistance but greater increases in heart rate and systolic blood pressure. Since infusion-associated hemodynamic changes occurred at plasma epinephrine levels commonly achieved during many types of physical and emotional stress, epinephrine release may have an important role in regulating systemic vascular resistance, stroke volume, and ejection fraction responses to stress in man.

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.

L-propionylcarnitine increases postischemic blood flow but does not affect recovery of energy charge

1991 ◽  
Vol 261 (1) ◽  
pp. H172-H180 ◽  
Author(s):  
L. M. Sassen ◽  
K. Bezstarosti ◽  
W. J. Van der Giessen ◽  
J. M. Lamers ◽  
P. D. Verdouw
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Systemic Vascular Resistance ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Contractile Function ◽  
Energy Charge ◽  
Left Ventricular ◽  
Arterial Blood

Effects of pretreatment with L-propionylcarnitine (50 mg/kg, n = 9) or saline (n = 10) were studied in open-chest anesthetized pigs, in which ischemia was induced by decreasing left anterior descending coronary artery blood flow to 20% of baseline. After 60 min of ischemia, myocardium was reperfused for 2 h. In both groups, flow reduction abolished contractile function of the affected myocardium and caused similar decreases in ATP (by 55%) and energy charge [(ATP + 0.5ADP)/(ATP + ADP + AMP); decrease from 0.91 to 0.60], mean arterial blood pressure (by 10-24%), the maximum rate of rise in left ventricular pressure (by 26-32%), and cardiac output (by 20-30%). During reperfusion, “no-reflow” was attenuated by L-propionylcarnitine, because myocardial blood flow returned to 61 and 82% of baseline in the saline- and L-propionylcarnitine-treated animals, respectively. Cardiac output of the saline-treated animals further decreased (to 52% of baseline), and systemic vascular resistance increased from 46 +/- 3 to 61 +/- 9 mmHg.min.l-1, thereby maintaining arterial blood pressure. In L-propionylcarnitine-treated pigs, cardiac output remained at 75% of baseline, and systemic vascular resistance decreased from 42 +/- 3 to 38 +/- 4 mmHg.min.l-1. In both groups, energy charge but not the ATP level of the ischemic-reperfused myocardium tended to recover, whereas the creatine phosphate level showed significantly more recovery in saline-treated animals. We conclude that L-propionylcarnitine partially preserved vascular patency in ischemic-reperfused porcine myocardium but had no immediate effect on “myocardial stunning.” Potential markers for long-term recovery were not affected by L-propionylcarnitine.

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