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At least 163 records · Page 9Linked to original sources
PubMed1994

Long-duration +Gz acceleration on cardiac volumes determined by two-dimensional echocardiography.

To enhance protection of humans exposed to long-duration low-gravity environments such as the Space Shuttle and National Aerospace Plane during re-entry or in the short-duration high(-)+Gz environment of fighter aircraft, the effects of +Gz acceleration on cardiovascular hemodynamics must be understood. This study reports the use of two-dimensional echocardiography in normal men during +Gz acceleration. The heart's position in relation to the chest did not change during acceleration up to +7 Gz. The success in maintaining high-quality images during exposures to G-forces of this magnitude may be attributed to the relatively low rate of G onset. End-diastolic volumes (EDV) and stroke volumes (SV) decreased during a +Gz acceleration ramp that increased until the subject experienced peripheral light loss (PLL) (P < .05). An inflated G-suit partially counteracted this effect. By 30 seconds of a +3 Gz acceleration plateau, the protective effects of the inflated G-suit to maintain EDV is lost and the EDV of the inflated G-suit was lower than the EDV of the uninflated G-suit (P < .05).

Acceleration↗
PubMedDate not supplied

[Determination of the ejection fraction and cardiac volumes using magnetic resonance tomography].

The results of NMR-tomography and radiocontrast ventriculography (VG) were compared in 20 CHD patients to determine ejection fraction (EF), and left ventricular (LV) end-diastolic and end-systolic volumes (EDV and ESV). NMR-tomography of the heart was performed at the field power of 0.23 T using the synchronization with ECG. Two methods of orientation of NMP-section on the LV long axis were employed. A sufficiently high correlation of NMR-tomography and VG findings in the determination of EF (r = 0.9) was obtained, low and insignificant--in the determination of EDV and ESV. Possible causes of differences between the results of both methods are under discussion.

Adult↗
PubMed1995

Acute environmental stress overrides cardiac volume receptor reflex in borderline hypertensive rats.

OBJECTIVE: To examine whether acute environmental stress (air-jet stress) modulates the exaggerated natriuresis to volume expansion in conscious borderline hypertensive rats. DESIGN: Intravenous isotonic saline volume expansion was performed with and without superimposed acute air-jet stress in conscious borderline hypertensive rats which had consumed a 1% NaCl diet (normotensive) or an 8% NaCl diet (hypertensive) for 12 weeks. METHODS: Conscious rats were instrumented for measurement of arterial pressure, renal sympathetic nerve activity and collection of bladder urine. RESULTS: Arterial pressure was greater in the 8% NaCl borderline hypertensive rats than in the 1% NaCl borderline hypertensive rats. In the absence of acute air-jet stress the 8% NaCl borderline hypertensive rats exhibited exaggerated natriuresis and exaggerated inhibition of renal sympathetic nerve activity compared with the 1% NaCl borderline hypertensive rats. Acute air-jet stress increased both arterial pressure and renal sympathetic nerve activity reversibly, and attenuated natriuresis in the 8% NaCl but not in the 1% NaCl borderline hypertensive rats. CONCLUSION: Acute environmental stress (air-jet stress) attenuates exaggerated natriuresis in hypertensive but not in normotensive borderline hypertensive rats via increased renal sympathetic nerve activity.

Acute Disease↗
PubMed1983

Echocardiographic formula for computation of left ventricular volume and stroke volume. Comparison with cardiac catheterization and the Teichholz formula.

An elementary computational formula for estimating cardiac volume and stroke volume from either M-mode or bi-dimensional echographic data is developed from an analysis of retrospective catheterization, angiographic and echographic data. The proposed equation has the form, V = 0.01 D12/5, where V is the cardiac volume in ml, 0.01 is a unit conversion constant and D is the ventricular dimension in mm. The new model assumes the validity of the Teichholz correction factor to the volume of an ellipsoid of revolution as an approximation of left ventricular cardiac volume. Application of this model to retrospective echographic data reveals that the new formula enjoys an identical domain of validity as the Teichholz formula, deviating from this model by less than 1% over a range of cardiac volumes from 20 to 180 ml. Comparison of this cardiac volume formula with a series of 37 echographic and catheterization measurements of stroke volume yields a correlation of r = 0.95 with a standard error of S.E. = 14.3 ml in comparison with the Fick principle method for cardiac stroke volume. The results of this study suggest that the present expression offers a computational simplification of the Teichholz formula, facilitating modifications for other configurations while retaining this expressions favorable correlation with invasive measurements of cardiac volume.

Cardiac Catheterization↗
PubMed1994

Role of active changes in venous capacity by the carotid baroreflex: analysis with a mathematical model.

To elucidate the role of venous capacity active changes in short-term cardiovascular homeostasis, a mathematical model of the carotid-sinus baroreflex system has been developed. In the model the cardiovascular system is represented as the series arrangement of six lumped compartments, which synthesize the fundamental hemodynamic properties of the systemic arterial, systemic venous, pulmonary arterial, and pulmonary venous circulations as well as of the left and right cardiac volumes. Cardiac outputs from the left and right ventricles are computed as a function of both downstream arterial pressure (afterload) and upstream atrial pressure (preload). Four distinct feedback regulatory mechanisms, working on systemic arterial resistance, heart rate, systemic venous unstressed volume, and systemic venous compliance, are assumed to operate on the cardiovascular system in response to carotid sinus pressure changes. All model parameters, both in the cardiovascular system and in feedback regulatory mechanisms, have been assigned on the basis of physiological data now available. The model is used here to simulate the pattern of the main hemodynamic quantities in the short time period (1-2 min) after acute carotid sinus activation in vagotomized subjects. Simulation results indicate that the model can reproduce experimental data quite well, with reference both to open-loop experiments and to an acute blood hemorrhage performed in closed-loop conditions. Moreover, computer simulations indicate that active changes in venous unstressed volume are of primary importance in regulating cardiac output and systemic arterial pressure during activation of the carotid sinus baroreflex.

Animals↗
PubMed1981

The use of a computerized algorithm to determine single cardiac cell volumes.

Single cardiac muscles cell volume data have been difficult to obtain, especially because the shape of a cell is quite complex. With the aid of a surface reconstruction method, a cell volume estimation algorithm has been developed that can be used on serial of cells. The cell surface is reconstructed by means of triangular tiles so that the cell is represented as a polyhedron. When this algorithm was tested on computer generated surfaces of a known volume, the difference was less than 1.6%. Serial sections of two phantoms of a known volume were also reconstructed and a comparison of the mathematically derived volumes and the computed volume estimations gave a per cent difference of between 2.8% and 4.1%. Finally cell volumes derived using conventional methods and volumes calculated using the algorithm were compared. The mean atrial muscle cell volume derived using conventional methods was 7752.7 +/- 644.7 micrometers3, while the mean computerized algorithm estimated atrial muscle cell volume was 7110.6 +/- 625.5 micrometers3. For AV bundle cells the mean cell volume obtained by conventional methods was 484.4 +/- 88.8 micrometers3 and the volume derived from the computer algorithm was 506.0 +/- 78.5 micrometers3. The differences between the volumes calculated using conventional methods and the algorithm were not significantly different.

Animals↗
PubMed1983

Effect of blood volume on forearm venous and cardiac stroke volume during exercise.

Five healthy men exercised at 65-70% of maximum O2 uptake (VO2 max) for 30 min in an ambient temperature of 30 degrees C. Duplicate experiments were conducted at three levels of plasma volume:control, hypovolemia, in which blood volume (BV) was reduced an average of 490 ml (9.7%) with diuretics, and hypervolemia, in which BV was increased an average of 440 ml (7.8%) by infusing an isotonic solution containing 5% human serum albumin. Marked venoconstriction occurred during exercise in all conditions and persisted despite large increases in deep body temperature. The degree of venoconstriction was similar during control and hypervolemic conditions, but was potentiated during hypovolemia. The observed venoconstriction appeared to consist of two components: an early one related to autonomic adjustments at the onset of exercise, and a later one possibly related to progressive decreases in cardiac filling. Heart rate, cardiac stroke volume (SV), and cardiac output during exercise were significantly affected by changes in BV. During hypovolemia the average differences from control values were 10 beats X min-1, -14 ml, and -2.2 l X min-1, respectively; during hypervolemia the differences from control were -7 X min-1, 10 ml, and 1.0 l X min-1, respectively. The pattern of SV over the course of exercise indicates that pooling of blood in veins may be quantitatively more important than plasma water loss in reducing cardiac filling pressure in the heat.

Adult↗
PubMed1993

Managing low cardiac output states: maintaining volume after cardiac surgery.

Low cardiac output after cardiac surgery may be caused by hypovolemia, myocardial depression, vasoconstriction, and dysrhythmias. Postoperative hypovolemia occurs because of blood volume loss and decreased diastolic filling. Diuresis, intravascular fluid shift into the interstitium, hormonal influences, and bleeding deplete blood volume. Diastolic filling may be compromised by positive end-expiratory pressure, vasodilation, dysrhythmias, and venous return obstruction. The primary indicator of intravascular volume is ventricular preload, which may be measured indirectly with central venous pressure, left atrial pressure, or pulmonary capillary wedge pressure. Recognition of hypovolemia is aided through the use of cardiac pressure trend monitoring and evaluation of noninvasive indicators of hypovolemia. Nursing goals, in response to hypovolemia, are to increase the circulating volume, optimize oxygen delivery, stabilize hemodynamics, improve tissue perfusion, and prevent shock.

Aged↗