scholarly journals Evidence for misleading decision support in characterizing differences in tolerance to reduced central blood volume using measurements of tissue oxygenation

Transfusion ◽  
2020 ◽  
Vol 60 (S3) ◽  
Author(s):  
Taylor E. Schlotman ◽  
Kevin S. Akers ◽  
Sylvain Cardin ◽  
Michael J. Morris ◽  
Tuan Le ◽  
...  
Keyword(s):  
Decision Support ◽  
Blood Volume ◽  
Tissue Oxygenation ◽  
Central Blood Volume

Specificity of Compensatory Reserve and Tissue Oxygenation as Early Predictors of Tolerance to Progressive Reductions in Central Blood Volume

Shock ◽  
2016 ◽  
Vol 46 (3S) ◽  
pp. 68-73 ◽  
Author(s):  
Jeffrey T. Howard ◽  
Jud C. Janak ◽  
Carmen Hinojosa-Laborde ◽  
Victor A. Convertino
Keyword(s):  
Blood Volume ◽  
Tissue Oxygenation ◽  
Central Blood Volume ◽  
Early Predictors ◽  
Compensatory Reserve

scholarly journals The physiology of blood loss and shock: New insights from a human laboratory model of hemorrhage

2017 ◽  
Vol 242 (8) ◽  
pp. 874-883 ◽  
Author(s):  
Alicia M Schiller ◽  
Jeffrey T Howard ◽  
Victor A Convertino
Keyword(s):  
Blood Loss ◽  
Blood Volume ◽  
Negative Pressure ◽  
Time Course ◽  
Tissue Oxygenation ◽  
Lower Body Negative Pressure ◽  
Lower Body ◽  
Central Blood Volume ◽  
Volume Loss ◽  
Physiological Mechanisms

The ability to quickly diagnose hemorrhagic shock is critical for favorable patient outcomes. Therefore, it is important to understand the time course and involvement of the various physiological mechanisms that are active during volume loss and that have the ability to stave off hemodynamic collapse. This review provides new insights about the physiology that underlies blood loss and shock in humans through the development of a simulated model of hemorrhage using lower body negative pressure. In this review, we present controlled experimental results through utilization of the lower body negative pressure human hemorrhage model that provide novel insights on the integration of physiological mechanisms critical to the compensation for volume loss. We provide data obtained from more than 250 human experiments to classify human subjects into two distinct groups: those who have a high tolerance and can compensate well for reduced central blood volume (e.g. hemorrhage) and those with low tolerance with poor capacity to compensate.We include the conceptual introduction of arterial pressure and cerebral blood flow oscillations, reflex-mediated autonomic and neuroendocrine responses, and respiration that function to protect adequate tissue oxygenation through adjustments in cardiac output and peripheral vascular resistance. Finally, unique time course data are presented that describe mechanistic events associated with the rapid onset of hemodynamic failure (i.e. decompensatory shock). Impact Statement Hemorrhage is the leading cause of death in both civilian and military trauma. The work submitted in this review is important because it advances the understanding of mechanisms that contribute to the total integrated physiological compensations for inadequate tissue oxygenation (i.e. shock) that arise from hemorrhage. Unlike an animal model, we introduce the utilization of lower body negative pressure as a noninvasive model that allows for the study of progressive reductions in central blood volume similar to those reported during actual hemorrhage in conscious humans to the onset of hemodynamic decompensation (i.e. early phase of decompensatory shock), and is repeatable in the same subject. Understanding the fundamental underlying physiology of human hemorrhage helps to test paradigms of critical care medicine, and identify and develop novel clinical practices and technologies for advanced diagnostics and therapeutics in patients with life-threatening blood loss.

Impulse discharges from the low pressure side varying with the central blood volume

1974 ◽  
Vol 352 (2) ◽  
pp. 105-114 ◽  
Author(s):  
Evert Knutsson ◽  
Torgny Sj�strand
Keyword(s):  
Blood Volume ◽  
Low Pressure ◽  
Pressure Side ◽  
Central Blood Volume

Resonance in a mathematical model of baroreflex control: arterial blood pressure waves accompanying postural stress

2005 ◽  
Vol 288 (6) ◽  
pp. R1637-R1648 ◽  
Author(s):  
Peter E. Hammer ◽  
J. Philip Saul
Keyword(s):  
Blood Pressure ◽  
Mathematical Model ◽  
Blood Volume ◽  
Low Frequency ◽  
Pressure Waves ◽  
Central Blood Volume ◽  
Arterial Baroreflex ◽  
Arterial Blood ◽  
Gain Margin ◽  
The Stability

A mathematical model of the arterial baroreflex was developed and used to assess the stability of the reflex and its potential role in producing the low-frequency arterial blood pressure oscillations called Mayer waves that are commonly seen in humans and animals in response to decreased central blood volume. The model consists of an arrangement of discrete-time filters derived from published physiological studies, which is reduced to a numerical expression for the baroreflex open-loop frequency response. Model stability was assessed for two states: normal and decreased central blood volume. The state of decreased central blood volume was simulated by decreasing baroreflex parasympathetic heart rate gain and by increasing baroreflex sympathetic vaso/venomotor gains as occurs with the unloading of cardiopulmonary baroreceptors. For the normal state, the feedback system was stable by the Nyquist criterion (gain margin = 0.6), but in the hypovolemic state, the gain margin was small (0.07), and the closed-loop frequency response exhibited a sharp peak (gain of 11) at 0.07 Hz, the same frequency as that observed for arterial pressure fluctuations in a group of healthy standing subjects. These findings support the theory that stresses affecting central blood volume, including upright posture, can reduce the stability of the normally stable arterial baroreflex feedback, leading to resonance and low-frequency blood pressure waves.

Is oxygen supply a limiting factor for survival during rewarming from profound hypothermia?

2006 ◽  
Vol 291 (1) ◽  
pp. H441-H450 ◽  
Author(s):  
Timofei V. Kondratiev ◽  
Kristina Flemming ◽  
Eivind S. P. Myhre ◽  
Mikhail A. Sovershaev ◽  
Torkjel Tveita
Keyword(s):  
Blood Volume ◽  
Tissue Oxygenation ◽  
Limiting Factor ◽  
Myocardial Tissue ◽  
Circulating Blood Volume ◽  
Profound Hypothermia ◽  
Group 3 ◽  
Vascular Beds ◽  
Group 2 ◽  
Group 1

It has been postulated that unsuccessful resuscitation of victims of accidental hypothermia is caused by insufficient tissue oxygenation. The aim of this study was to test whether inadequate O2supply and/or malfunctioning O2extraction occur during rewarming from deep/profound hypothermia of different duration. Three groups of rats ( n = 7 each) were used: group 1 served as normothermic control for 5 h; groups 2 and 3 were core cooled to 15°C, kept at 15°C for 1 and 5 h, respectively, and then rewarmed. In both hypothermic groups, cardiac output (CO) decreased spontaneously by >50% in response to cooling. O2consumption fell to less than one-third during cooling but recovered completely in both groups during rewarming. During hypothermia, circulating blood volume in both groups was reduced to approximately one-third of baseline, indicating that some vascular beds were critically perfused during hypothermia. CO recovered completely in animals rewarmed after 1 h ( group 2) but recovered to only 60% in those rewarmed after 5 h ( group 3), whereas blood volume increased to approximately three-fourths of baseline in both groups. Metabolic acidosis was observed only after 5 h of hypothermia (15°C). A significant increase in myocardial tissue heat shock protein 70 after rewarming in group 3, but not in group 2, indicates an association with the duration of hypothermia. Thus mechanisms facilitating O2extraction function well during deep/profound hypothermia, and, despite low CO, O2supply was not a limiting factor for survival in the present experiments.

scholarly journals Components of the "Central" Blood Volume in the Dog

1960 ◽  
Vol 8 (1) ◽  
pp. 93-99 ◽  
Author(s):  
ROBERT J. MARSHALL ◽  
YANG WANG ◽  
JOHN T. SHEPHERD
Keyword(s):  
Blood Volume ◽  
Central Blood Volume

scholarly journals Reductions in cardiac output, central blood volume, and stroke volume with thermal stress in normal men during exercise.

1966 ◽  
Vol 45 (11) ◽  
pp. 1801-1816 ◽  
Author(s):  
L B Rowell ◽  
H J Marx ◽  
R A Bruce ◽  
R D Conn ◽  
F Kusumi
Keyword(s):  
Cardiac Output ◽  
Thermal Stress ◽  
Stroke Volume ◽  
Blood Volume ◽  
Central Blood Volume ◽  
Normal Men

Contribution of abdomen and legs to central blood volume expansion in humans during immersion

1997 ◽  
Vol 83 (3) ◽  
pp. 695-699 ◽  
Author(s):  
Lars Bo Johansen ◽  
Thomas Ulrik Skram Jensen ◽  
Bettina Pump ◽  
Peter Norsk
Keyword(s):  
Blood Volume ◽  
Volume Expansion ◽  
Protein Concentration ◽  
Water Immersion ◽  
Venous Pressure ◽  
Cuff Inflation ◽  
Central Blood Volume ◽  
Central Venous ◽  
Plasma Protein Concentration ◽  
Blood Volume Expansion

Johansen, Lars Bo, Thomas Ulrik Skram Jensen, Bettina Pump, and Peter Norsk. Contribution of abdomen and legs to central blood volume expansion in humans during immersion. J. Appl. Physiol. 83(3): 695–699, 1997.—The hypothesis was tested that the abdominal area constitutes an important reservoir for central blood volume expansion (CBVE) during water immersion in humans. Six men underwent 1) water immersion for 30 min (WI), 2) water immersion for 30 min with thigh cuff inflation (250 mmHg) during initial 15 min to exclude legs from contributing to CBVE (WI+Occl), and 3) a seated nonimmersed control with 15 min of thigh cuff inflation (Occl). Plasma protein concentration and hematocrit decreased from 68 ± 1 to 64 ± 1 g/l and from 46.7 ± 0.3 to 45.5 ± 0.4% ( P < 0.05), respectively, during WI but were unchanged during WI+Occl. Left atrial diameter increased from 27 ± 2 to 36 ± 1 mm ( P < 0.05) during WI and increased similarly during WI+Occl from 27 ± 2 to 35 ± 1 mm ( P < 0.05). Central venous pressure increased from −3.7 ± 1.0 to 10.4 ± 0.8 mmHg during WI ( P < 0.05) but only increased to 7.0 ± 0.8 mmHg during WI+Occl ( P < 0.05). In conclusion, the dilution of blood induced by WI to the neck is caused by fluid from the legs, whereas the CBVE is caused mainly by blood from the abdomen.

scholarly journals Can a central blood volume deficit be detected by systolic pressure variation during spontaneous breathing?

2015 ◽  
Vol 16 (1) ◽  
Author(s):  
Michael Dahl ◽  
Chris Hayes ◽  
Bodil Steen Rasmussen ◽  
Anders Larsson ◽  
Niels H. Secher
Keyword(s):  
Blood Volume ◽  
Spontaneous Breathing ◽  
Systolic Pressure ◽  
Pressure Variation ◽  
Central Blood Volume ◽  
Systolic Pressure Variation ◽  
Volume Deficit

scholarly journals Increased tissue oxygenation explains the attenuation of hyperemia upon repetitive pneumatic compression of the lower leg

2017 ◽  
Vol 123 (6) ◽  
pp. 1451-1460 ◽  
Author(s):  
Alessandro Messere ◽  
Gianluca Ceravolo ◽  
Walter Franco ◽  
Daniela Maffiodo ◽  
Carlo Ferraresi ◽  
...  
Keyword(s):  
Blood Flow ◽  
Blood Volume ◽  
Near Infrared ◽  
Tissue Oxygenation ◽  
Femoral Vein ◽  
Lower Leg ◽  
Local Circulation ◽  
Doppler Measurement ◽  
Key Factor ◽  
Interstimulus Intervals

The rapid hyperemia evoked by muscle compression is short lived and was recently shown to undergo a rapid decrease even in spite of continuing mechanical stimulation. The present study aims at investigating the mechanisms underlying this attenuation, which include local metabolic mechanisms, desensitization of mechanosensitive pathways, and reduced efficacy of the muscle pump. In 10 healthy subjects, short sequences of mechanical compressions ( n = 3–6; 150 mmHg) of the lower leg were delivered at different interstimulus intervals (ranging from 20 to 160 s) through a customized pneumatic device. Hemodynamic monitoring included near-infrared spectroscopy, detecting tissue oxygenation and blood volume in calf muscles, and simultaneous echo-Doppler measurement of arterial (superficial femoral artery) and venous (femoral vein) blood flow. The results indicate that 1) a long-lasting (>100 s) increase in local tissue oxygenation follows compression-induced hyperemia, 2) compression-induced hyperemia exhibits different patterns of attenuation depending on the interstimulus interval, 3) the amplitude of the hyperemia is not correlated with the amount of blood volume displaced by the compression, and 4) the extent of attenuation negatively correlates with tissue oxygenation ( r = −0,78, P < 0.05). Increased tissue oxygenation appears to be the key factor for the attenuation of hyperemia upon repetitive compressive stimulation. Tissue oxygenation monitoring is suggested as a useful integration in medical treatments aimed at improving local circulation by repetitive tissue compression. NEW & NOTEWORTHY This study shows that 1) the hyperemia induced by muscle compression produces a long-lasting increase in tissue oxygenation, 2) the hyperemia produced by subsequent muscle compressions exhibits different patterns of attenuation at different interstimulus intervals, and 3) the extent of attenuation of the compression-induced hyperemia is proportional to the level of oxygenation achieved in the tissue. The results support the concept that tissue oxygenation is a key variable in blood flow regulation.

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