Cardiac Filling (cardiac + filling)

Distribution by Scientific Domains


Selected Abstracts


Myocardial Contractility and Cardiac Filling Measured by Impedance Cardiography in Patients with Nitroglycerine-Induced Vasovagal Syncope

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 1 2006
PETER MITRO
Objective: Increased myocardial contractility and inadequate cardiac filling leading to activation of the Bezold-Jarisch reflex were proposed as possible triggering mechanisms of vasovagal syncope (VVS). In the present study noninvasive hemodynamic measurements were performed in order to examine the role of myocardial contractility and cardiac filling in pathogenesis of VVS. Methods: Hemodynamic parameters were measured during head-up tilt test (HUT) by impedance cardiography in 46 patients with unexplained syncope. Myocardial contractility was measured as index of contractility (IC), acceleration index (ACI), and ejection fraction (EF). Afterload was measured as systemic vascular resistance index (SVRI) and preload was expressed as end-diastolic index (EDI). Serial measurements were done 1 minute before HUT, during HUT at 1-minute intervals, and 1 minute after completion of HUT. Results: HUT was positive in 30 patients (10 men, 20 women, mean age 36 ± 16 years) and negative in 16 patients (8 men, 8 women, mean age 31 ± 14 years). No significant differences were observed between HUT(+) and HUT(,) groups in hemodynamic parameters at supine rest and during HUT until the development of syncope. SVRI was lower in HUT(+) than in HUT(,) group at syncope (122.7 + 66.3 vs 185.6 + 51.4 dyn sec cm,5/m2, P = 0.002) and after syncope (117.0 + 61.1 vs 198.0 + 95.7 dyn sec cm,5/m2, P = 0.007). ACI, IC, EF, and EDI did not differ between groups at syncope. After syncope EF was higher in HUT(+) group compared to HUT(,) group (59.2 + 6.1 vs 52.7 + 9.4%, P = 0.02). Conclusion: The role of increased myocardial contractility and decreased cardiac filling is not confirmed in the present study. [source]


Central and peripheral cardiovascular adaptations to exercise in endurance-trained children

ACTA PHYSIOLOGICA, Issue 2 2002
S. NOTTIN
ABSTRACT Stroke volume (SV) response to exercise depends on changes in cardiac filling, intrinsic myocardial contractility and left ventricular afterload. The aim of the present study was to identify whether these variables are influenced by endurance training in pre-pubertal children during a maximal cycle test. SV, cardiac output (Doppler echocardiography), left ventricular dimensions (time,movement echocardiography) as well as arterial pressure and systemic vascular resistances were assessed in 10 child cyclists (VO2max: 58.5 ± 4.4 mL min,1 kg,1) and 13 untrained children (UTC) (VO2max: 45.9 ± 6.7 mL min,1 kg,1). All variables were measured at the end of the resting period, during the final minute of each workload and during the last minute of the progressive maximal aerobic test. At rest and during exercise, stroke index was significantly higher in the child cyclists than in UTC. However, the SV patterns were strictly similar for both groups. Moreover, the patterns of diastolic and systolic left ventricular dimensions, and the pattern of systemic vascular resistance of the child cyclists mimicked those of the UTC. SV patterns, as well as their underlying mechanisms, were not altered by endurance training in children. This result implied that the higher maximal SV obtained in child cyclists depended on factors influencing resting SV, such as cardiac hypertrophy, augmented myocardium relaxation properties or expanded blood volume. [source]


Relationship between stroke volume, cardiac output and filling of the heart during tilt

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 10 2009
M. BUNDGAARD-NIELSEN
Background: Cardiac function curves are widely accepted to apply to humans but are not established for the entire range of filling of the heart that can be elicited during head-up (HUT) and head-down tilt (HDT), taken to represent minimal and maximal physiological filling of the heart, respectively. With the supine resting position as a reference, we assessed stroke volume (SV), cardiac output (CO) and filling of the heart during graded tilt to evaluate whether SV and CO are maintained during an assumed maximal physiological filling of the heart elicited by 90° HDT in healthy resting humans. Methods: In 26 subjects, central blood volume was manipulated with graded tilt from 60° HUT to 90° HDT. We measured SV, CO (Finometer®) and cardiac filling by echocardiography of the left ventricular end-diastolic volume (LVEDV; n=12). Results: From supine rest to 60° HUT, SV and CO decreased 23 ml [confidence intervals (CI): 16,30; P<0.001; 23%] and 0.9 l/min (0.4,1.4; P<0.0001; 14%), respectively, but neither SV nor CO changed during HDT up to 70°. However, during 90° HDT, SV decreased 12 ml (CI: 6,19; P<0.0001; 12%), with an increase of 21 ml (9,33; P=0.002; 16%) in LVEDV because HR increased 3 bpm and CO decreased 0.5 l/min (ns). Conclusion: This study confirmed that SV and CO are maximal in resting, supine, healthy humans and decrease during HUT. However, 90° HDT was associated with increased LVEDV and induced a reduction in SV. [source]


Myocardial Contractility and Cardiac Filling Measured by Impedance Cardiography in Patients with Nitroglycerine-Induced Vasovagal Syncope

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 1 2006
PETER MITRO
Objective: Increased myocardial contractility and inadequate cardiac filling leading to activation of the Bezold-Jarisch reflex were proposed as possible triggering mechanisms of vasovagal syncope (VVS). In the present study noninvasive hemodynamic measurements were performed in order to examine the role of myocardial contractility and cardiac filling in pathogenesis of VVS. Methods: Hemodynamic parameters were measured during head-up tilt test (HUT) by impedance cardiography in 46 patients with unexplained syncope. Myocardial contractility was measured as index of contractility (IC), acceleration index (ACI), and ejection fraction (EF). Afterload was measured as systemic vascular resistance index (SVRI) and preload was expressed as end-diastolic index (EDI). Serial measurements were done 1 minute before HUT, during HUT at 1-minute intervals, and 1 minute after completion of HUT. Results: HUT was positive in 30 patients (10 men, 20 women, mean age 36 ± 16 years) and negative in 16 patients (8 men, 8 women, mean age 31 ± 14 years). No significant differences were observed between HUT(+) and HUT(,) groups in hemodynamic parameters at supine rest and during HUT until the development of syncope. SVRI was lower in HUT(+) than in HUT(,) group at syncope (122.7 + 66.3 vs 185.6 + 51.4 dyn sec cm,5/m2, P = 0.002) and after syncope (117.0 + 61.1 vs 198.0 + 95.7 dyn sec cm,5/m2, P = 0.007). ACI, IC, EF, and EDI did not differ between groups at syncope. After syncope EF was higher in HUT(+) group compared to HUT(,) group (59.2 + 6.1 vs 52.7 + 9.4%, P = 0.02). Conclusion: The role of increased myocardial contractility and decreased cardiac filling is not confirmed in the present study. [source]


Circadian systemic haemodynamics in borderline and mild hypertension

CLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 6 2000
R. Takalo
Circadian variations in blood pressure (BP), stroke volume (SV), heart rate (HR), cardiac output (CO) and total peripheral resistance (TPR) were determined by a pulse contour method from the intra-arterial pulse wave in 32 normotensive (NT), 32 borderline hypertensive (BHT) and 31 hypertensive (HT) middle-aged men. Daytime averages were used as the reference levels. The nocturnal decrease in BP and HR were similar in the three groups. In the night, SV did not change in the NT group, but was increased in the BHT and HT groups. The nocturnal increase in SV may reflect reduced venous capacity causing increased cardiac filling. As a consequence of the difference in SV, the nocturnal CO fall was diminished in the HT group as compared with the NT group. Moreover, TPR had a tendency to decrease in the HT group, which may be considered as a baroreflex response to buffer the expected rise in BP. Five years later, 25 NT, 24 BHT and 19 HT subjects were reassessed using casual BP measurements. In the NT and BHT groups, six and 17 subjects, respectively, had progressed to hypertension. In a logistic regression model for those who became HT, the nocturnal increase in SV was a significant predictor for future hypertension. In conclusion, the results suggest that circadian systemic haemodynamics may be altered before BP is markedly elevated, and that haemodynamic studies might be useful in predicting the development of sustained hypertension. [source]