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Craig G. Crandall - One of the best experts on this subject based on the ideXlab platform.
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hypercoagulability in response to elevated body temperature and Central hypovolemia
Journal of Surgical Research, 2013Co-Authors: Niels H. Secher, Craig G. Crandall, Martin A S Meyer, Sisse R Ostrowski, Anders Overgaard, Matthew S GanioAbstract:Background Coagulation abnormalities contribute to poor outcomes in critically ill patients. In trauma patients exposed to a hot environment, a systemic inflammatory response syndrome, elevated body temperature, and reduced Central Blood Volume occur in parallel with changes in hemostasis and endothelial damage. The objective of this study was to evaluate whether experimentally elevated body temperature and reduced Central Blood Volume (CBV) per se affects hemostasis and endothelial activation.
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Colloid Volume loading does not mitigate decreases in Central Blood Volume during simulated haemorrhage while heat stressed.
The Journal of Physiology, 2012Co-Authors: Craig G. Crandall, Niels H. Secher, Thad E. Wilson, J. Marving, Morten Bundgaard-nielsen, Thomas Seifert, Thomas Levin Klausen, F. Andersen, Birger HesseAbstract:Key points • The capacity for humans to withstand a haemorrhagic challenge is reduced while heat stressed. • Identification of changes in Central Blood Volume during simulated haemorrhage may help identify the mechanisms by which tolerance to haemorrhage is reduced during heat stress. • We found that the magnitude of reduction in Central Blood Volume to a simulated hemorrhagic challenge is approximately three fold greater when individuals are heat stressed. • Volume loading did not change the relative magnitude of the reduction in Central Blood Volume to that simulated haemorrhagic challenge. • These data show that greater reductions in Central Blood Volume during a simulated haemorrhagic challenge while heat stressed may be a primary mechanism for impaired capacity to withstand that challenge in this thermal condition.
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Atrial Natriuretic Peptide and Acute Changes in Central Blood Volume by Hyperthermia in Healthy Humans.
The Open Neuroendocrinology Journal, 2012Co-Authors: Thomas W. Vogelsang, Niels H. Secher, Craig G. Crandall, J. Marving, Birger Hesse, Chad Wilson, Chie C. Yoshiga, Andreas KjaerAbstract:Background: Hyperthermia induces vasodilatation that reduces Central Blood Volume (CBV), Central venous pressure (CVP) and mean arterial pressure (MAP). Inhibition of atrial natriuretic peptide (ANP) could be a relevant homeostatic defense mechanism during hyperthermia with a decrease in CBV. The present study evaluated how changes in plasma ANP reflect the changes in CBV during hyperthermia. Methods: Ten healthy subjects provided with a water perfused body suit increased body core temperature 1 °C. In situ labeled autologous red Blood cells were used to measure the CBV with a gamma camera. Regions of interest were traced manually on the images of the whole body Blood pool scans. Two measures of CBV were used: Heart/whole body ratio and thorax/whole body ratio. CVP and MAP were recorded. Arterial (ANPart) and venous plasma ANP were determined by radioimmunoassay. Results: The ratio thorax/whole body and heart/whole body decreased 7 % and 11 %, respectively (p
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atrial natriuretic peptide and acute changes in Central Blood Volume by hyperthermia in healthy humans
The Open Neuroendocrinology Journal, 2012Co-Authors: Thomas W. Vogelsang, Niels H. Secher, Craig G. Crandall, J. Marving, Birger Hesse, Chad Wilson, Chie C. Yoshiga, Andreas KjaerAbstract:Background: Hyperthermia induces vasodilatation that reduces Central Blood Volume (CBV), Central venous pressure (CVP) and mean arterial pressure (MAP). Inhibition of atrial natriuretic peptide (ANP) could be a relevant homeostatic defense mechanism during hyperthermia with a decrease in CBV. The present study evaluated how changes in plasma ANP reflect the changes in CBV during hyperthermia. Methods: Ten healthy subjects provided with a water perfused body suit increased body core temperature 1 °C. In situ labeled autologous red Blood cells were used to measure the CBV with a gamma camera. Regions of interest were traced manually on the images of the whole body Blood pool scans. Two measures of CBV were used: Heart/whole body ratio and thorax/whole body ratio. CVP and MAP were recorded. Arterial (ANPart) and venous plasma ANP were determined by radioimmunoassay. Results: The ratio thorax/whole body and heart/whole body decreased 7 % and 11 %, respectively (p<0.001). MAP and CVP decreased during hyperthermia by 6.8 and 5.0 mmHg, respectively (p<0.05; p<0.001). Changes in both thorax/whole body (R=0.80; p<0.01) and heart/whole body ratios (R=0.78; p<0.01) were correlated with changes in ANPart. However, there was no correlation between venous ANP and changes in CBV, nor between ANPart and MAP or CVP. Conclusion: Arterial but not venous plasma concentration of ANP, is correlated to changes in CBV, but not to pressures. We suggest that plasma ANPart may be used as a surrogate marker of acute CBV changes.
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effect of Volume loading on the frank starling relation during reductions in Central Blood Volume in heat stressed humans
The Journal of Physiology, 2010Co-Authors: Morten Bundgaardnielsen, Niels H. Secher, Craig G. Crandall, Thad E. Wilson, Thomas SeifertAbstract:During reductions in Central Blood Volume while heat stressed, a greater decrease in stroke Volume (SV) for a similar decrease in ventricular filling pressure, compared to normothermia, suggests that the heart is operating on a steeper portion of a Frank–Starling curve. If so, Volume loading of heat-stressed individuals would shift the operating point to a flatter portion of the heat stress Frank–Starling curve thereby attenuating the reduction in SV during subsequent decreases in Central Blood Volume. To investigate this hypothesis, right heart catheterization was performed in eight males from whom pulmonary capillary wedge pressure (PCWP), Central venous pressure and SV (via thermodilution) were obtained while Central Blood Volume was reduced via lower-body negative pressure (LBNP) during normothermia, whole-body heating (increase in Blood temperature ∼1°C), and during whole-body heating after intravascular Volume expansion. Volume expansion was accomplished by administration of a combination of a synthetic colloid (HES 130/0.4, Voluven) and saline. Before LBNP, SV was not affected by heating (122 ± 30 ml; mean ±s.d.) compared to normothermia (110 ± 20 ml; P= 0.06). However, subsequent Volume loading increased SV to 143 ± 29 ml (P= 0.003). LBNP provoked a larger decrease in SV relative to the decrease in PCWP during heating (8.6 ± 1.9 ml mmHg−1) compared to normothermia (4.5 ± 3.0 ml mmHg−1, P= 0.02). After Volume loading while heat stressed, the reduction in the SV to PCWP ratio during LBNP was comparable to that observed during normothermia (4.8 ± 2.3 ml mmHg−1; P= 0.78). These data support the hypothesis that a Frank–Starling mechanism contributes to compromised Blood pressure control during simulated haemorrhage in heat-stressed individuals, and extend those findings by showing that Volume infusion corrects this deficit by shifting the operating point to a flatter portion of the heat stress Frank–Starling curve.
Niels H. Secher - One of the best experts on this subject based on the ideXlab platform.
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The Central Blood Volume as measured by thoracic electrical impedance and plasma proANP is not compromised by donation of 900 mL of Blood in men.
Transfusion Medicine, 2020Co-Authors: Mikkel Gybel-brask, Niels H. Secher, Jens P. Goetze, Nikolai Baastrup Nordsborg, Pär I. Johansson, Jacob BejderAbstract:OBJECTIVES To evaluate whether the donation of 900 mL of Blood reduces the Central Blood Volume (CBV) assessed by thoracic electrical impedance (TI) and plasma pro-atrial natriuretic peptide (proANP). BACKGROUND Donation of 450 mL of Blood carries a 1% risk of a vasovagal reaction. Withdrawal of 900 mL of Blood decreases cardiac output; however, the effect on CBV remains unknown. METHODS/MATERIALS A randomised, single-blinded, placebo-controlled, crossover design was used, where 21 healthy semi-recumbent men donated 2 × 450 mL Blood or were sham-phlebotomised. Changes in CBV were estimated by proANP and TI at 1.5 (TI1.5 ) and 100 (TI100 ) kHz, reflecting extracellular Volume and (regional) total body water, respectively, and the index value (IDX; 1/T1.5 -1/TI100 ) was used to estimate changes in intracellular (red cell) Volume. Systolic, diastolic and mean arterial Blood pressure; heart rate; stroke Volume; cardiac output; and systemic vascular resistance were monitored. After completion of the study, 1000 mL of isotonic saline was infused. RESULTS Changes (mean% ± SD) in TI1.5 , TI100 and IDX were similar after 450 mL (-0.2 ± 1.6%, 0.0 ± 1.1%, -0.4 ± 10.1%) and 900 mL (0.1 ± 1.6%, 0.2 ± 1.5% and -2.0 ± 15.8%) of Blood donation compared to after a sham donation of 450 mL (-0.9 ± 1.2%, -0.5 ± 1.5% and -0.1 ± 6.1%) and 900 mL (-1.2 ± 1.5%, -0.6 ± 1.3% and 0.5 ± 9.9%). In addition, changes in plasma proANP were similar after 450 and 900 mL of Blood donation (-0.8 ± 6.7% and -7.6 ± 7.9%) as after sham donations (1.3 ± 7.3% and -4.5 ± 5.6%). Monitoring haemodynamic variables revealed that stroke Volume decreased after the donation of 900 mL of Blood (-12 ± 12 mL) compared to sham donations. CONCLUSION During a 900-mL Blood loss in semi-recumbent men, CBV measured by TI and plasma proANP is not affected.
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Effect of hypotensive hypovolemia and thoracic epidural anesthesia on plasma pro-atrial natriuretic peptide to indicate deviations in Central Blood Volume in pigs: a blinded, randomized controlled trial.
Local and regional anesthesia, 2019Co-Authors: Rune B. Strandby, Niels H. Secher, Rikard Ambrus, Michael Patrick Achiam, Amalie Henriksen, Jens P. Goetze, Lars Bo SvendsenAbstract:Purpose Changes in plasma pro-atrial natriuretic peptide (proANP) may indicate deviations in the Central Blood Volume (CBV). We evaluated the plasma proANP response to hypotensive hypovolemia under the influence of thoracic epidural anesthesia (TEA) in pigs. We hypothesized that plasma proANP would decrease in response to hypotensive hypovolemia and that TEA would aggravate the proANP response, reflecting a further decrease in CBV. Design Randomized, blinded, controlled trial. Setting A university-affiliated experimental facility. Participants Twenty pigs randomized to administration of saline (placebo) or bupivacaine with morphine (TEA) in the epidural space at Th8-Th10. Interventions Relative hypovolemia was established by an inflatable Foley catheter positioned in the inferior caval vein just below the heart (caval obstruction), and hemorrhage-induced hypovolemia was by withdrawal of Blood from the femoral artery, both aiming at a mean arterial pressure (MAP) of 50-60 mmHg. Hemodynamic variables and plasma proANP were determined before and after the interventions. Results Caval obstruction and withdrawal of Blood reduced MAP to 50-60 mmHg. Accordingly, cardiac output, Central venous pressure, and mixed venous oxygen saturation decreased (p
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effect of hypotensive hypovolemia and thoracic epidural anesthesia on plasma pro atrial natriuretic peptide to indicate deviations in Central Blood Volume in pigs a blinded randomized controlled trial
Regional anesthesia, 2019Co-Authors: Rune B. Strandby, Niels H. Secher, Rikard Ambrus, Michael Patrick Achiam, Amalie Henriksen, Jens P. Goetze, Lars Bo SvendsenAbstract:Purpose Changes in plasma pro-atrial natriuretic peptide (proANP) may indicate deviations in the Central Blood Volume (CBV). We evaluated the plasma proANP response to hypotensive hypovolemia under the influence of thoracic epidural anesthesia (TEA) in pigs. We hypothesized that plasma proANP would decrease in response to hypotensive hypovolemia and that TEA would aggravate the proANP response, reflecting a further decrease in CBV. Design Randomized, blinded, controlled trial. Setting A university-affiliated experimental facility. Participants Twenty pigs randomized to administration of saline (placebo) or bupivacaine with morphine (TEA) in the epidural space at Th8-Th10. Interventions Relative hypovolemia was established by an inflatable Foley catheter positioned in the inferior caval vein just below the heart (caval obstruction), and hemorrhage-induced hypovolemia was by withdrawal of Blood from the femoral artery, both aiming at a mean arterial pressure (MAP) of 50-60 mmHg. Hemodynamic variables and plasma proANP were determined before and after the interventions. Results Caval obstruction and withdrawal of Blood reduced MAP to 50-60 mmHg. Accordingly, cardiac output, Central venous pressure, and mixed venous oxygen saturation decreased (p<0.05). Yet, plasma proANP was stable after both caval obstruction (TEA: 72 [63-78] to 80 pmol/L [72-85], p=0.09 and placebo: 64 [58-76] to 69 pmol/L [57-81], p=0.06) and withdrawal of Blood (TEA: 74 [73-83] to 79 pmol/L [77-87], p=0.07 and placebo: 64 [56-77] to 67 pmol/L [58-78], p=0.15). Conclusion Plasma proANP was stable in response to relative and hemorrhage-induced hypovolemia to a MAP of 50-60 mmHg, and the response was independent of TEA. The findings suggest that alterations in plasma proANP do not follow deviations in CBV during hypotensive hypovolemia in pigs.
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Effect of early versus delayed activation of thoracic epidural anesthesia on plasma pro-atrial natriuretic peptide to indicate deviations in Central Blood Volume during esophagectomy.
Regional Anesthesia & Pain Medicine, 2019Co-Authors: Rune B. Strandby, Niels H. Secher, Rikard Ambrus, Michael Patrick Achiam, Jens P. Goetze, Lars Bo SvendsenAbstract:Background and Objectives A side effect to thoracic epidural anesthesia (TEA) is hypotension induced by Central hypovolemia. This study addressed whether early activation (EA) versus late activation (LA) of TEA affects plasma pro-atrial natriuretic peptide (proANP) reflecting deviations in the Central Blood Volume (CBV). We hypothesized that EA TEA would reduce plasma proANP, thus reflecting a decrease in CBV. Methods A randomized, controlled, single-blinded trial was conducted. Patients undergoing open esophagectomy were randomized to EA (n=25, after induction of general anesthesia) or LA TEA (n=25, after re-established gastric continuity) with the epidural catheter placed at the interspaces Th7-8 or Th8-9. Plasma proANP was determined repetitively along with hemodynamic variables and administration of fluid/vasopressors as postoperative complications were noted. Results With EA TEA, plasma proANP decreased following induction of anesthesia to the end of surgery (13%; 113±68 to 99±49 pmol/L; p=0.026), but that was not the case in the LA group (3%; 97±44 to 94±49 pmol/L; p=0.565) despite equal fluid balance (+1584±582 vs +1560±563 mL; p=0.888). Accordingly, the EA group required excessive treatment with vasopressors to maintain MAP >60 mm Hg during surgery (2.7±2 vs 1.6±1.4 ephedrine boluses; p=0.033 and infusion of phenylephrine for 216±86 vs 58±91 min; p Conclusions EA TEA reduces plasma proANP indicating that CBV becomes affected. Based on a correlation between plasma proANP and fluid balance, a 2000 mL Volume surplus of lactated Ringer’s solution is required to maintain plasma proANP stable during open esophagectomy. Trial registration number 2014-002036-14 (https://www.clinicaltrialsregister.eu/ctr-search/search?query=2014-002036-14).
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Effect of pulmonary hyperinflation on Central Blood Volume: An MRI study.
Respiratory Physiology & Neurobiology, 2017Co-Authors: Tanja Mijacika, Kasper Kyhl, Daria Frestad, F. Otto Barak, Ivan Drvis, Niels H. Secher, Zeljko Dujic, Per Lav MadsenAbstract:Pulmonary hyperinflation attained by glossopharyngeal insufflation (GPI) challenges the circulation by compressing the heart and pulmonary vasculature. Our aim was to determine the amount of Blood translocated from the Central Blood Volume during GPI. Cardiac output and cardiac chamber Volumes were assessed by magnetic resonance imaging in twelve breath-hold divers at rest and during apnea with GPI. Pulmonary Blood Volume was determined from pulmonary Blood flow and transit times for gadolinium during first-pass perfusion after intravenous injection. During GPI, the lung Volume increased by 0.8±0.6L (11±7%) above the total lung capacity. All cardiac chambers decreased in Volume and despite a heart rate increase of 24±29 bpm (39±50%), pulmonary Blood flow decreased by 2783±1820mL (43±20%). The pulmonary transit time remained unchanged at 7.5±2.2s and pulmonary Blood Volume decreased by 354±176mL (47±15%). In total, Central Blood Volume decreased by 532±248mL (46±14%). Voluntary pulmonary hyperinflation leads to ∼50% decrease in pulmonary and Central Blood Volume.
Victor A Convertino - One of the best experts on this subject based on the ideXlab platform.
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Variability in integration of mechanisms associated with high tolerance to progressive reductions in Central Blood Volume: the compensatory reserve
Physiological Reports, 2016Co-Authors: Robert H Carter, Carmen Hinojosa-laborde, Victor A ConvertinoAbstract:High tolerance to progressive reductions in Central Blood Volume has been associated with higher heart rate (HR), peripheral vascular resistance (PVR), sympathetic nerve activity (SNA), and vagally mediated cardiac baroreflex sensitivity (BRS). Using a database of 116 subjects classified as high tolerance to presyncopal-limited lower body negative pressure (LBNP), we tested the hypothesis that subjects with greater cardiac baroreflex withdrawal (i.e., BRS > 1.0) would demonstrate greater LBNP tolerance associated with higher HR, PVR, and SNA. Subjects underwent LBNP to presyncope. Mean and diastolic arterial pressure (MAP; DAP) was measured by finger photoplethysmography and BRS (down sequence) was autocalculated (WinCPRS) as ∆R-R Interval/∆DAP. DownBRS : ms/mmHg) was used to dichotomize subjects into two groups (Group 1 = DownBRS > 1.0, N = 49, and Group 2 = DownBRS 1.0) had lower HR (107 ± 19 vs. 131 ± 20 bpm), higher stroke Volume (45 ± 15 vs. 36 ± 15 mL), less SNA (45 ± 13 vs. 53 ± 7 bursts/min), and less increase in PVR (4.1 ± 1.3 vs. 4.5 ± 2.6) compared to Group 2 (DownBRS
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variability in integration of mechanisms associated with high tolerance to progressive reductions in Central Blood Volume the compensatory reserve
Physiological Reports, 2016Co-Authors: Robert H Carter, Carmen Hinojosalaborde, Victor A ConvertinoAbstract:High tolerance to progressive reductions in Central Blood Volume has been associated with higher heart rate (HR), peripheral vascular resistance (PVR), sympathetic nerve activity (SNA), and vagally mediated cardiac baroreflex sensitivity (BRS). Using a database of 116 subjects classified as high tolerance to presyncopal-limited lower body negative pressure (LBNP), we tested the hypothesis that subjects with greater cardiac baroreflex withdrawal (i.e., BRS > 1.0) would demonstrate greater LBNP tolerance associated with higher HR, PVR, and SNA. Subjects underwent LBNP to presyncope. Mean and diastolic arterial pressure (MAP; DAP) was measured by finger photoplethysmography and BRS (down sequence) was autocalculated (WinCPRS) as ∆R-R Interval/∆DAP. DownBRS : ms/mmHg) was used to dichotomize subjects into two groups (Group 1 = DownBRS > 1.0, N = 49, and Group 2 = DownBRS 1.0) had lower HR (107 ± 19 vs. 131 ± 20 bpm), higher stroke Volume (45 ± 15 vs. 36 ± 15 mL), less SNA (45 ± 13 vs. 53 ± 7 bursts/min), and less increase in PVR (4.1 ± 1.3 vs. 4.5 ± 2.6) compared to Group 2 (DownBRS < 1.0). Both groups had similar tolerance times (1849 ± 260 vs. 1839 ± 253 sec), MAP (78 ± 11 vs. 79 ± 12 mmHg), compensatory reserve index (CRI) (0.10 ± 0.03 vs. 0.09 ± 0.01), and cardiac output (4.5 ± 1.2 vs. 4.7 ± 1.1 L/min) at presyncope. Contrary to our hypothesis, higher HR, PVR, SNA, and BRS were not associated with greater tolerance to reduced Central Blood Volume. These data are the first to demonstrate the variability and uniqueness of individual human physiological strategies designed to compensate for progressive reductions in Central Blood Volume. The sum total of these integrated strategies is accurately reflected by the measurement of the compensatory reserve.
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Specificity of Compensatory Reserve and Tissue Oxygenation as Early Predictors of Tolerance to Progressive Reductions in Central Blood Volume.
Shock, 2016Co-Authors: Jeffrey T. Howard, Carmen Hinojosa-laborde, Jud C. Janak, Victor A ConvertinoAbstract:We previously reported that measurements of muscle oxygen saturation (SmO2) and the compensatory reserve index (CRI) provided earlier indication of reduced Central Blood Volume than standard vital signs (e.g., Blood pressure, heart rate, arterial oxygen saturation). In the present study, we hypothesized that the CRI would provide greater sensitivity and specificity to detect progressive decrease in Central circulating Blood Volume compared with SmO2. Continuous noninvasive measures of CRI (calculated from feature changes in the photoplethysmographic arterial waveforms) were collected from 55 healthy volunteer subjects before and during stepwise lower body negative pressure (LBNP) to the onset of hemodynamic decompensation. Near infrared spectroscopy was used on the forearm to obtain deep SmO2, hydrogen ion concentration ([H]), and hemoglobin Volume (HbT; decreases reflect vasoconstriction). CRI decreased by 97% in a linear fashion across progressive Blood Volume loss, with no clinically significant alterations in vital signs. The receiver operating characteristic (ROC) area under the curve (AUC) for the CRI was 0.91, with a sensitivity of 0.87 and specificity of 0.80, when predicting decompensation at progressive levels of LBNP. In comparison, SmO2, [H], and HbT had significantly lower ROC AUC, sensitivity and specificity values for detecting the same outcome. Consistent with our hypothesis, CRI detected Central hypovolemia with significantly greater specificity than measures of tissue metabolism. Single measurement of CRI may enable more accurate triage, while CRI monitoring may allow for earlier detection of casualty deterioration.
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respiratory pump contributes to increased physiological reserve for compensation during reductions in Central Blood Volume 707 4
The FASEB Journal, 2014Co-Authors: Paula Poh, Robert H Carter, Carmen Hinojosalaborde, Jane Mulligan, Gregory Z Grudic, Victor A ConvertinoAbstract:The impedance threshold device (ITD) represents a therapy for increasing systemic circulation through creation of negative intrathoracic pressure. PURPOSE: To evaluate the respiratory pump effect on the diminution of compensatory responses during progressive reductions in Central Blood Volume. METHODS: The Compensatory Reserve Index (CRI) algorithm measured compensation capacity to reduced Central Blood Volume. Continuous analog recordings of arterial waveforms were extracted from data files of 7 volunteers. Subjects had previously participated in experiments designed to induce hemodynamic decompensation by application of graded lower body negative pressure (LBNP). The LBNP protocol was completed while spontaneously breathing through a standard medical facemask without (sham ITD) and with (active ITD) a resistance (~-7cmH2O). RESULTS: At the onset of pre-syncope in the sham ITD, CRI (0.08±0.02) was smaller (P=0.05) than CRI at the same time point in the active ITD (0.09±0.01). CRI at pre-syncope in the ac...
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Variability in mechanisms associated with tolerance to progressive reductions in Central Blood Volume (1157.3)
The FASEB Journal, 2014Co-Authors: Victor A Convertino, Robert H Carter, Carmen Hinojosa-labordeAbstract:High tolerance to reductions in Central Blood Volume has been associated with higher heart rate (HR), sympathetic nerve activity (SNA), and cardiac baroreflex sensitivity (BRS). Using subjects classified as high tolerance to lower body negative pressure (LBNP), we tested the hypothesis that subjects with BRS > 1.0 would demonstrate greater LBNPtolerance associated with higher HR, PVR, and SNA than subjects with BRS 1.0, N = 49, and Group 2 = BRS 1.0) had lower HR (107 ± 19 vs. 131 ± 20 beats/min), higher SV (45 ± 15 vs. 36 ...
Thorkild I. A. Sørensen - One of the best experts on this subject based on the ideXlab platform.
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estimated Central Blood Volume in cirrhosis relationship to sympathetic nervous activity β adrenergic blockade and atrial natriuretic factor
Hepatology, 1992Co-Authors: H Jens M D Henriksen, Flemming Bendtsen, Alexander L. Gerbes, Niels Juel Christensen, Helmer Ringlarsen, Thorkild I. A. SørensenAbstract:The estimated Central Blood Volume (i.e., Blood Volume in the heart cavities, lungs and Central arterial tree) was determined by multiplying cardiac output by circulatory mean transit time in 19 patients with cirrhosis and compared with sympathetic nervous activity and circulating level of atrial natriuretic factor. Arterial norepinephrine level, an index of overall sympathetic nervous activity (3.08 nmol/L in patients vs. 1.36 nmol/L in controls; p < 0.01) was negatively correlated (r = -0.54, p < 0.01) with estimated Central Blood Volume (mean = 23 ml/kg in patients vs. 27 ml/kg in controls; p < 0.05). Similarly, renal venous norepinephrine level (an index of renal sympathetic tone; 4.26 nmol/L in patients vs. 1.78 nmol/L in controls; p < 0.01) was inversely correlated with estimated Central Blood Volume (r = -0.53, n = 18, p < 0.02). No significant correlation could be established between arterial atrial natriuretic factor level (8.9 pmol/L in patients vs. 9.6 pmol/L in controls; not significant) and estimated Central Blood Volume. Hemodynamic values were subsequently modified with oral propranolol (80 mg). During -adrenergic blockade, the mean estimated Central Blood Volume was not altered significantly, except in six patients who exhibited decreases in mean arterial Blood pressure (85 to 69 mm Hg; n = 6) and decreases in mean estimated Central Blood Volume (23.2 to 20.6 ml/kg; n = 6, p < 0.05). Slight increases were observed in mean right atrial pressure (2.2 to 3.7 mm Hg; n = 14, p < 0.05); this change was positively correlated with the change in estimated Central Blood Volume (r = 0.44, n = 14, p = 0.06). In conclusion, reduced estimated Central Blood Volume probably unloads Volume receptors and baroreceptors, thus provoking enhanced overall and renal sympathetic nervous activity and thereby contributing to increased water and salt retention in cirrhosis. During -adrenergic blockade estimated Central Blood Volume changes correlated with alterations in preload and afterload. These findings indicate that Central circulatory and arterial underfilling is a key element of the hemodynamic derangement observed in cirrhosis.
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Estimated Central Blood Volume in cirrhosis: Relationship to sympathetic nervous activity, β‐adrenergic blockade and atrial natriuretic factor
Hepatology, 1992Co-Authors: Jens H. Henriksen, Flemming Bendtsen, Helmer Ring-larsen, Alexander L. Gerbes, Niels Juel Christensen, Thorkild I. A. SørensenAbstract:The estimated Central Blood Volume (i.e., Blood Volume in the heart cavities, lungs and Central arterial tree) was determined by multiplying cardiac output by circulatory mean transit time in 19 patients with cirrhosis and compared with sympathetic nervous activity and circulating level of atrial natriuretic factor. Arterial norepinephrine level, an index of overall sympathetic nervous activity (3.08 nmol/L in patients vs. 1.36 nmol/L in controls; p < 0.01) was negatively correlated (r = -0.54, p < 0.01) with estimated Central Blood Volume (mean = 23 ml/kg in patients vs. 27 ml/kg in controls; p < 0.05). Similarly, renal venous norepinephrine level (an index of renal sympathetic tone; 4.26 nmol/L in patients vs. 1.78 nmol/L in controls; p < 0.01) was inversely correlated with estimated Central Blood Volume (r = -0.53, n = 18, p < 0.02). No significant correlation could be established between arterial atrial natriuretic factor level (8.9 pmol/L in patients vs. 9.6 pmol/L in controls; not significant) and estimated Central Blood Volume. Hemodynamic values were subsequently modified with oral propranolol (80 mg). During -adrenergic blockade, the mean estimated Central Blood Volume was not altered significantly, except in six patients who exhibited decreases in mean arterial Blood pressure (85 to 69 mm Hg; n = 6) and decreases in mean estimated Central Blood Volume (23.2 to 20.6 ml/kg; n = 6, p < 0.05). Slight increases were observed in mean right atrial pressure (2.2 to 3.7 mm Hg; n = 14, p < 0.05); this change was positively correlated with the change in estimated Central Blood Volume (r = 0.44, n = 14, p = 0.06). In conclusion, reduced estimated Central Blood Volume probably unloads Volume receptors and baroreceptors, thus provoking enhanced overall and renal sympathetic nervous activity and thereby contributing to increased water and salt retention in cirrhosis. During -adrenergic blockade estimated Central Blood Volume changes correlated with alterations in preload and afterload. These findings indicate that Central circulatory and arterial underfilling is a key element of the hemodynamic derangement observed in cirrhosis.
L M Blendis - One of the best experts on this subject based on the ideXlab platform.
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the effect of posture on Central Blood Volume in patients with preascitic cirrhosis on a sodium restricted diet
Hepatology, 1996Co-Authors: Florence Wong, Peter Liu, Yasmin Allidina, L M BlendisAbstract:Abstract The status of the Central Blood Volume in cirrhosis is controversial. A combination of sodium restriction and upright posture, which redistributes intravascular Volume to dependent parts of the body should further aggravate a contracted Central Blood Volume reduction. The aim of this study was to determine the effect of upright posture and sodium restriction on Central Blood Volume (CBV) in preascitic cirrhotic patients, compared with controls. Eight male, preascitic, alcoholic cirrhotic subjects and eight healthy male controls were studied while on a 20-mmol/d sodium diet. Measurements of CBV by radionuclide angiography, and neurohumoral factors were performed on day 7 in both supine and erect positions and cardiac output and systemic vascular resistance (SVR) was calculated. Sodium restriction resulted in less weight loss in the cirrhotic patients (P = .03), with significantly lower plasma renin activity (P = .001). Similar Central Blood Volumes and systemic hemodynamics were observed in both groups in the supine posture. In contrast to the cirrhotic patients, in the control subjects, upright posture resulted in a significant reduction in cardiac output (P = .002) and increase in SVR (P = .005), associated with a decrease in all Blood Volumes which were significantly less than in the cirrhotic patients. Mean arterial pressure was maintained in both groups in both postures. In conclusion, with sodium restriction, preascitic cirrhotic patients have less intravascular Volume contraction than control patients. Erect posture results in redistribution of this relatively expanded intravascular Volume to the CBV. Therefore, a low-sodium diet can be safely administered in preascitic cirrhotic patients. (Hepatology 1996 May;23(5):1141-7)