scholarly journals Specificity of Compensatory Reserve vs SMO 2 , Lactate and ETCO 2 as Early Predictors of Tolerance to Progressive Reductions in Central Blood Volume

2017 ◽  
Vol 31 (S1) ◽  
Author(s):  
Victor A Convertino ◽  
Jeff T Howard ◽  
Alicia M Schiller
Keyword(s):  
Blood Volume ◽  
Central Blood Volume ◽  
Early Predictors ◽  
Compensatory Reserve

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

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.

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

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.

Manipulation of central blood volume and implications for respiratory control function

2014 ◽  
Vol 306 (12) ◽  
pp. H1669-H1678 ◽  
Author(s):  
Tadayoshi Miyamoto ◽  
Damian Miles Bailey ◽  
Hidehiro Nakahara ◽  
Shinya Ueda ◽  
Masashi Inagaki ◽  
...  
Keyword(s):  
Blood Volume ◽  
Lower Body Negative Pressure ◽  
Control Function ◽  
Minute Ventilation ◽  
Water Immersion ◽  
Respiratory Control ◽  
Intersection Point ◽  
Operating Point ◽  
Central Blood Volume ◽  
End Tidal

The respiratory operating point (ventilatory or arterial Pco2 response) is determined by the intersection point between the controller and plant subsystem elements within the respiratory control system. However, to what extent changes in central blood volume (CBV) influence these two elements and the corresponding implications for the respiratory operating point remain unclear. To examine this, 17 apparently healthy male participants were exposed to water immersion (WI) or lower body negative pressure (LBNP) challenges to manipulate CBV and determine the corresponding changes. The respiratory controller was characterized by determining the linear relationship between end-tidal Pco2 (PetCO2) and minute ventilation (V̇e) [V̇e = S × (PetCO2 − B)], whereas the plant was determined by the hyperbolic relationship between V̇e and PetCO2 (PetCO2 = A/V̇e + C). Changes in V̇e at the operating point were not observed under either WI or LBNP conditions despite altered PetCO2 ( P < 0.01), indicating a moving respiratory operating point. An increase (WI) and a decrease (LBNP) in CBV were shown to reset the controller element (PetCO2 intercept B) rightward and leftward, respectively ( P < 0.05), without any change in S, whereas the plant curve remained unaltered at the operating point. Collectively, these findings indicate that modification of the controller element rather than the plant element is the major factor that contributes toward an alteration of the respiratory operating point during CBV shifts.

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