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PubMed1976

[Influence of dopamine on the pulmonary pressure and shunt volume after cardiac surgery (author's transl)].

After the administration of Dopamine to 20 patients after cardiac surgery pulmonary shunt volume was determined with regard to the cardiac output and pulmonary pressure. It was shown that the infusion of Dopamine leads to decrease of the arterio-venous oxygen difference (AVDO2) as well as to the decrease of the PO2 in the arterial blood. On the contrary, in venous bood, PO2, Oxygen saturation, content and pulmonary pressure increased. The increase of the pulmonary right-to-left shunt observed (Qs Qt form 14.9 to 19.2%) is in proportion with the increase in cardiac output. Hence we do not suppose a specific shunting effect of Dopamine. Our findings suggest, that in the case of an already reduced blood oxygen level a further fall of the arterial oxygen saturation caused by a shunt must be avoided by additional enrichment of oxygen content of the inspired air.

Adolescent↗
PubMed2002

Stroke volume variations for assessment of cardiac responsiveness to volume loading in mechanically ventilated patients after cardiac surgery.

OBJECTIVE: We hypothesized that measuring stroke volume variation (SVV) during mechanical ventilation by continuous arterial pulse contour analysis allows the accurate prediction and monitoring of changes in cardiac index (CI) in response to volume administration. DESIGN AND SETTING: Prospective study in an university hospital. PATIENTS: Twenty mechanically ventilated patients following cardiac surgery. INTERVENTIONS: Volume loading with oxypolygelatin (3.5%) 20 ml x body mass index over 10 min. MEASUREMENTS AND RESULTS: SVV, central venous pressure (CVP), pulmonary artery occlusion pressure (PAOP), left ventricular end-diastolic area index (LVEDAI) by transesophageal echocardiography, intrathoracic blood volume index (ITBVI) by transpulmonary thermodilution and CI were determined immediately before and after volume loading. SVV decreased, while CI, CVP, PAOP, ITBVI, and LVEDAI increased significantly. Percentage changes in CI were significantly correlated to percentage changes in SVV (r(2)=-0.59, p<0.001), ITBVI (r(2)=0.79, p<0.001), and PAOP (r(2)=0.33, p<0.05) and to baseline values of SVV (r(2)=0.55, p<0.05) and LVEDAI (r(2)=-0.68, p<0.001). CONCLUSIONS: SVV may help to determine the preload condition of ventilated patients following cardiac surgery and to predict and continuously monitor effects of volume administered as part of their hemodynamic management.

Aged↗
PubMed2005

Quantification of left ventricular volumes from cardiac cine MRI using active contour model combined with gradient vector flow.

We investigated the feasibility of combining the active contour model with gradient vector flow (Snakes-GVF) to estimate left ventricular (LV) volumes from cardiac cine magnetic resonance imaging (MRI). MRI data were acquired from 27 patients, including 14 adults (9 men, 5 women, 55.0+/-23.3 years) and 13 children (10 boys, 3 girls, 2.7+/-2.1 years) using Gyroscan Intera (1.5 Tesla, Philips Medical Systems). LV volumes were calculated by adding the areas surrounded by the contour extracted by Snakes-GVF and compared with volumes estimated by manual tracing. Those estimated by Snakes-GVF [y (mL)] correlated well with those estimated by manual tracing [x (mL)]. In adult cases, the regression equation and correlation coefficient were y=1.008x - 0.517 and 0.996, respectively. In pediatric cases, they were y=1.174x - 2.542 and 0.992, respectively. In conclusion, Snakes-GVF is a powerful and useful tool for quantifying LV volumes using cardiac MRI.

Cardiac Volume↗
PubMed1981

Continuous stroke volume and cardiac output from intra-ventricular dimensions obtained with impedance catheter.

To improve assessment of ventricular function during cardiac catheterisation there should be available a continuous registration of stroke volume and cardiac output in addition to ventricular pressure. To obtain the desired volumetric quantities a catheter has been developed which measures changes in intraventricular dimensions by electrical impedance. For this purpose, the catheter is equipped with eight electrodes spaced over a distance equal to the long axis of the left ventricle into which it is introduced. A constant current is imposed between the outermost electrodes while the inner six are used to measure resistance of volume segments of the blood contained within the ventricular cavity. The difference in resistance at the beginning and end of ejection is proportional to the contribution of each segment to stroke volume, which follows from addition to the segmental terms. Calibration is obtained by measuring electrical conductivity of a blood sample. The catheter was tested over a tenfold range of cardiac output, both in vitro, using an artificial heart model, while performance in vivo was evaluated in 12 dogs. In the animals study, stroke volume and cardiac output from the catheter were compared with flows obtained with an electromagnetic flowmeter. In both studies, linear regression analysis showed excellent correlation of cardiac output (r = 0.99, n = 10 in vitro, r = 0.95, n = 126 in vivo) while the regression equations were close to those of identity. Very good correlation (r = 0.98, n = 28) was also obtained for stroke volumes on a beat to beat basis during arrhythmia. It is concluded that the catheter, which has great potential for application in man, fulfills its primary aim of continuously recording stroke volume and cardiac output.

Animals↗
PubMed2003

Variation and significance of microtubules in rat volume overload cardiac hypertrophy.

OBJECTIVE: To investigate the function of microtubules in volume overload cardiac hypertrophy of rat. METHODS: The structure of microtubules was observed using an immunofluorescent microscope, while the pixel intensity and distribution of microtubule imaging was estimated from laser scanning confocal images of left ventricular cardiocytes immuno-labeled with an antibody to beta-tubulin. RESULTS: The pixels of the microtubule image taken just after volume overload were not evenly distributed. At 6 hours after overload, the pixel intensity of the microtubule image was decreased to less than 150 (arbitrary units), which was the same as the pixel intensity and distribution of the colchicine depolymerized microtubule image. The changes were partially recovered to 200 (arbitrary units) after 4 more days. The pixel intensity of the control microtubule image was 250 (arbitrary units) and had an even distribution. The structuring of the microtubules was more disordered as volume overload hypertrophy developed. CONCLUSIONS: There are disorders in the signal transduction pathways governing the hypertrophic response of cardiomyocytes in the hypertrophic myocardium and microtubule is one of the members of the signal transduction pathways governing the hypertrophic response of cardiomyocytes in the hypertrophic myocardium. The disordered microtubule array may be targeted during heart failure treatment.

Animals↗
PubMed2004

Regulation of protein kinase C isozymes in volume overload cardiac hypertrophy.

Protein kinase C (PKC) is a family of at least 11 isozymes and known to play a crucial role in myocardial growth. The present study was performed to investigate whether PKC-isozymes are differentially regulated during the development of volume-overload cardiac hypertrophy. After 2, 7 and 30 days of sham or aortocaval shunt operation in male Wistar rats, PKC-activity and the expression of cardiac PKC-isozymes (PKC-alpha, delta and epsilon) were determined at the protein and at the mRNA-level in the left and the right ventricle separately. Myocardial hypertrophy after 2, 7 and 30 days of aortocaval shunt was more pronounced in the right than in the left ventricle. Right ventricular hypertrophy was associated with an increased PKC-enzyme activity, a selectively enhanced protein expression of cytosolic PKC-delta (day 7: +83 +/- 12%, day 30: +94 +/- 14%) and PKC-alpha (day 7: +48 +/- 11%, day 30: +62 +/- 16%) and a transcriptional upregulation of the absolute mRNA-levels of these PKC-isozymes in the aortocaval shunt group as compared to controls. In contrast, the expression of PKC-epsilon was unchanged. A significant upregulation of PKC-delta both on the protein and on the mRNA-level was also noted in volume-overload induced left ventricular hypertrophy, whereas the expression of PKC-alpha and PKC-epsilon were not altered. Furthermore, the expression of calcineurin in both ventricles was not significantly changed in response to volume-overload. This study characterizes in the left and right ventricle a differential regulation of the dominant PKC-isozymes in volume-overload cardiac hypertrophy both at the protein and at the mRNA-level.

Animals↗
PubMed1996

Application of the flow convergence region method to the determination of stroke volume and cardiac output in patients with mitral stenosis.

OBJECTIVE: This study was undertaken to investigate the feasibility and accuracy of determination of stroke volume and cardiac output by calculating transmitral flow volume using the flow convergence region method in patients with mitral stenosis. PATIENTS AND INTERVENTIONS: Fifty-six patients with rheumatic mitral stenosis were studied using imaging and Doppler echocardiography. Aliasing velocities of 20 to 23 cm/s were used to record the flow vonvergence region proximal to the stenotic mitral orifice. The stroke volume (mL) was calculated by multiplying peak transmitral flow rate which was obtained using an angle-corrected hemispheric flow convergence equation, by transmitral velocity time integral (cm) divided by peak transmitral velocity (cm/s) recorded using continuous wave Doppler method. MAIN RESULTS: Stroke volume calculated using the flow convergence region method was not significantly different from that calculated using aortic Doppler two-dimensional echocardiographic method in 39 patients with pure mitral stenosis (75+/-19 [mean+/-1SD] versus 73+/-19 mL, P=0.12), and from that calculated using pulmonic Doppler two-dimensional echocardiographic method in nine patients with mitral stenosis with associated>2+ aortic regurgitation (77+/-12 versus 75+/-14 mL, P=0.49). No significant difference existed between the cardiac output obtained using the flow convergence region method and that obtained using Fick method in 12 patients with pure mitral stenosis. The stroke volume was overestimated by the flow convergence region method when compared with those obtained using aortic Doppler two-dimensional echocardiographic method in patients with mitral stenosis with associated >2+ mitral regurgitation (123+/-40 versus 67+/-15 mL, P=0.001). CONCLUSIONS: The present study provided an alternative way to calculate the stroke volume and cardiac output in patients with mitral stenosis.

Adult↗
PubMed1997

Blood volume and cardiac index in rats after exchange transfusion with hemoglobin-based oxygen carriers.

We have measured plasma volume and cardiac index in rats after 50% isovolemic exchange transfusion with human hemoglobin cross-linked between the alpha-chains with bis(3,5-dibromosalicyl)fumarate (alpha alpha Hb) and with bovine hemoglobin modified with polyethylene glycol (PEGHb). alpha alpha Hb and PEGHb differ in colloid osmotic pressure (23.4 and 118.0 Torr, respectively), oxygen affinity (oxygen half-saturation pressure of hemoglobin = 30.0 and 10.2 Torr, respectively), viscosity (1.00 and 3.39 cP, respectively), and molecular weight (64,400 and 105,000, respectively). Plasma volume was measured by Evans blue dye dilution modified for interference by plasma hemoglobin. Blood volumes in PEGHb-treated animals were significantly elevated (74.0 +/- 3.5 ml/kg) compared with animals treated with alpha alpha Hb (49.0 +/- 1.2 ml/kg) or Ringer lactate (48.0 +/- 2.0 ml/kg) or with controls (58.2 +/- 1.9 ml/kg). Heart rate reduction after alpha alpha Hb exchange is opposite to that expected with blood volume contraction, suggesting that alpha alpha Hb may have a direct myocardial depressant action. The apparently slow elimination of PEGHb during the 2 h after its injection is a consequence of plasma volume expansion: when absolute hemoglobin (concentration x plasma volume) is compared for PEGHb and alpha alpha Hb, no difference in their elimination rates is found. These studies emphasize the need to understand blood volume regulation when the effects of cell-free hemoglobin on hemodynamic measurements are evaluated.

Animals↗
PubMed1988

Noninvasive maternal stroke volume and cardiac output determinations by pulsed Doppler echocardiography.

Sixteen obstetric patients with pulmonary artery catheters were studied by two-dimensional and pulsed Doppler echocardiography to compare prospectively pulsed Doppler-and thermodilution-derived estimations of left ventricular stroke volume and cardiac output. Systolic aortic flow velocity waveforms were obtained by pulsed Doppler ultrasound from the apical five-chamber echocardiographic window. Aortic diameters were obtained by two-dimensional echocardiography from the left parasternal long axis view. The mean (+/- SEM) aortic diameter averaged 2.1 +/- 0.1 cm, with a mean calculated aortic valve area of 3.6 +/- 0.2 cm2. The mean aortic flow velocity integral was 21.8 +/- 0.8 cm. This information was used to calculate aortic stroke volume and cardiac output. Thermodilution- and Doppler-derived estimations for maternal stroke volume (r = 0.86) and cardiac output (r = 0.94) were significantly correlated when aortic diameter measurements based on a leading vessel edge method were used. Our findings verify the accuracy of an important noninvasive technique for quantitating maternal stroke volume and cardiac output by pulsed Doppler echocardiography. This methodology should provide an alternative approach to invasive monitoring in the study of normal and abnormal maternal circulatory hemodynamics.

Aorta↗
PubMed1984

Pulsed Doppler echocardiographic determination of stroke volume and cardiac output: clinical validation of two new methods using the apical window.

Two methods of measuring stroke volume and cardiac output with pulsed Doppler two-dimensional echocardiography were developed and validated against the thermodilution technique in 39 patients, 33 of which were in an intensive care unit. With the use of the apical four-chamber view, a mitral inflow method combined the velocity of left ventricular inflow at the mitral anulus with the cross-sectional area of the anulus calculated from its diameter at middiastole (area = pi r2). From the apical five-chamber view a left ventricular outflow method combined the velocity of left ventricular outflow with the cross-sectional area of the aortic anulus calculated from its diameter during early systole (parasternal long-axis view). Measurements with the mitral inflow and left ventricular outflow methods were obtained in 35 of 39 (90%) and 39 of 39 (100%) patients, respectively. Validation of the mitral method excluded patients with mitral regurgitation (n = 11) and validation of the left ventricular outflow method excluded those with aortic regurgitation (n = 4). Good correlations were observed between thermodilution and Doppler measurements of stroke volume and cardiac output for both the mitral anulus method (R = .96 and .87, respectively) and the left ventricular outflow method (R = .95 and .91, respectively). The results of the two methods correlated well with each other in patients without regurgitant valve lesions. A greater interobserver variability was observed with the mitral anulus method, which was related solely to greater variability in measuring the annular diameter.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2006

Parametric EIT for monitoring cardiac stroke volume.

The bio-impedance technique appears appropriate for non-invasive cardiac stroke volume (SV) measurement, as the thoracic conductivity distribution is altered during the cardiac cycle due to the heart contraction and blood perfusion. In the present work, the feasibility of a parametric electrical impedance tomography (EIT) for assessing the cardiac SV was studied. An impedance model of the thorax was constructed from segmented axial MRI images along 19 phases of the cardiac cycle. The heart was simulated as an ellipsoid, with its axes' lengths set as the reconstruction parameters, while all other tissues' geometry and conductivity values were kept fixed. A Newton-Raphson parametric optimization scheme was utilized, yielding a correlation between the reconstructed and anatomical left ventricular volumes of 0.97 (p = 2 x 10(-11)). An analysis of noise sensitivity showed that the proposed algorithm requires an SNR greater than 65 dB. The simulation results were compared to physical data, collected with a portable EIT system (PulmoTrace, CardioInspect). The validation study was employed for a group of N = 28 healthy patients, and a comparison with impedance cardiography measurements (BioZ, Cardiodynamics) was made, showing a correlation of r = 0.86 (p = 4 x10(-9)). The preliminary results demonstrate that parametric EIT has the potential to measure SV, and may be applicable for both clinical and home environment usage.

Algorithms↗
PubMed2001

Enhanced cardiac thermal dilution measurement of cardiac output, volumes, regurgitation, valve effective diameters, ventricular power and efficiency -- Feasibility analysis using digital simulation.

Cardiac output is measured by the thermal dilution method which uses a quadruple lumen catheter, with a thermistor on the tip, through the right atrium, right ventricle and into the pulmonary artery. Cold saline is injected into the right atrium and the resulting pulmonary artery temperature profile is integrated. The same procedure performed with three thermistors and three pressure sensors located on the catheter to measure temperature and pressure in the atrium, ventricle and artery respectively will produce a set of temperature and pressure curves with shapes determined by injectate temperature, injectate volume, heart rate, systolic time interval, body temperature, cardiac output, volumes, flow rates and valve openings. A digital computer program has been developed to optimize the fit of a lumped parameter model to the thermodilution curves in order to determine heart rate, systolic time as a fraction of cardiac cycle, right atrial systolic and diastolic volumes, ventricular systolic and diastolic volumes, cardiac output, inflow valve forward and reverse flow rates and effective diameters, outflow valve forward and reverse flow rates and effective diameters, ventricular power and efficiency. The program has been tested over a range of operating conditions including noise in the temperature and pressure signals, randomly varying heart rate and cardiac cycle. All of the data for the tests were produced by a digital computer simulation of a pulsatile artificial heart. The results of these tests indicate that the enhanced thermal dilution analysis method is feasible.

Cardiac Output↗
PubMed1975

Heart volume determination with phase synchronization in normal subjects and postinfarct patients.

The authors investigated the influence of the systole-and-dyastole cycle upon the cardiac volume measured radiologically with ECG phase synchronization in prone subjects. Measurements were made in 30 healthy subjects and 27 patients with a history of myocardial infarction, all of them ambulatory. As expected, the mean cardiac volume relative to body surface was greater in postinfarct patients than in normal subjects to a high degree of statistical significance. Conversely, the differences between end-systolic and end-diastolic cardiac volumes fell short of statistical significance both in healthy subjects and in postinfarct patients. Accordingly, radiological measurements of cardiac volume without phase synchronization seem justified in the functional evaluation of postinfarct patients.

Adult↗
PubMedDate not supplied

[Clinical and physiological studies of flight personnel with 1st stage hypertensive disease].

An examination of the functional state of the cardiovascular system of 30 pilots with hypertension of the I stage showed that the parameters expressing an increase of the blood ejected to the vascular bed were the most informative hemodynamic and polycardiographic values. It was found that the stroke volume, cardiac output, volume velocity of the ejection, power of the left ventricle, energy expenditure per I 1 of cardiac output and time of the isometric contraction phase increased. The interactions of the cardiac output and peripheral resistance made it possible to distinguish hemodynamic modifications of the hypertensive disease: cardiac-increased cardiac output (15 pilots), vascular--increased peripheral resitance (11 pilots) and mixed--simultaneous increase of both parameters (4 pilots). The identification of the modification is important for proper treatment and expertise.

Aerospace Medicine↗
PubMed1991

Effects of beta-adrenergic agonists on splanchnic vascular volume and cardiac output.

The effect of beta-adrenergic agonists on splanchnic intravascular volume (SIV), measured with radionuclide imaging, and the subsequent influence of such volume changes on cardiac output (CO) were examined in 40 anesthetized dogs. Isoproterenol (6 micrograms/min) caused a decrease in total SIV of 12 +/- 1% (P less than 0.001). The decrease was due entirely to a decrease in splenic volume of 24 +/- 3% (P less than 0.001), since volume increased in the remainder of the splanchnic vasculature [hepatic and mesenteric volume increased 12 +/- 2% (P less than 0.001) and 11 +/- 3% (P less than 0.02), respectively]. CO increased from 1,724 +/- 187 to 3,138 +/- 321 ml/min (P less than 0.001); after subsequent splenectomy, isoproterenol caused a similar increment. Isoproterenol-associated SIV changes were not altered by carotid denervation and vagotomy or by beta 1-adrenergic inhibition with metoprolol but were abolished by nonselective beta-adrenergic inhibition with propranolol. With a larger dose of metoprolol and smaller dose of isoproterenol to minimize beta 1-adrenergic effects, the isoproterenol-associated CO increment was attenuated (P less than 0.01) by splenectomy. With the beta 2-agonist terbutaline (41 micrograms/min) after metoprolol, total SIV decreased 15 +/- 4% (P less than 0.001). After subsequent alpha-adrenergic inhibition with phenoxybenzamine, terbutaline caused no change in SIV and an attenuated (P less than 0.05) increase in CO. Thus beta-adrenergic agonist administration causes a decrease in total SIV due entirely to a decrease in splenic volume. The SIV decrement is dependent on beta 2- and alpha-adrenoceptor stimulation and appears to enhance CO only if beta 1-adrenergic effects are minimized.

Adrenergic beta-Agonists↗
PubMed1995

Effects of ACE inhibitors on circulating versus cardiac angiotensin II in volume overload-induced cardiac hypertrophy in rats.

BACKGROUND: Cardiac volume overload by an aortocaval shunt increases left ventricular end-diastolic pressure (LVEDP) and plasma and cardiac renin activity and results in LV hypertrophy. To a similar extent, the angiotensin-converting enzyme (ACE) inhibitors enalapril and quinapril prevent the increase in LVEDP. However, only quinapril attenuates the development of LV hypertrophy. We hypothesize that a low affinity of enalapril for cardiac ACE results in continuing generation of cardiac angiotensin II and thus hypertrophic growth of cardiomyocytes. METHODS AND RESULTS: In the present study, we assessed plasma and cardiac angiotensins I and II 1 and 7 days after aortocaval shunt and the effects of enalapril and quinapril started 3 days before surgery on plasma and cardiac angiotensin I and II at the same time points. Aortocaval shunt increased plasma angiotensin II at 1 day by 180%, but only a small increase (by 40%) persisted at 7 days. Aortocaval shunt increased LV angiotensin II by 100% and 65% at 1 and 7 days, respectively. Both blockers similarly prevented the increase in plasma angiotensin II by aortocaval shunt at both time points. In contrast, only quinapril prevented the rise in LV angiotensin II induced by shunt at 1 and 7 days. CONCLUSIONS: Aortocaval shunt increases LVEDP and plasma and cardiac angiotensin II and results in LV hypertrophy. Only prevention of the increase in LVEDP and in plasma and cardiac angiotensin II attenuates the development of LV hypertrophy, consistent with the concept that angiotensin II is involved in the development of cardiac hypertrophy by aortocaval shunt by both hemodynamic and cardiac trophic effects. This study is the first to show that differences in affinity for cardiac ACE may determine the effect of ACE inhibitors on cardiac angiotensin II and therefore cardiac hypertrophy.

Angiotensin I↗