Lingual, splanchnic, and systemic hemodynamic and carbon dioxide tension changes during endotoxic shock and resuscitation

2005 ◽  
Vol 98 (1) ◽  
pp. 108-113 ◽  
Author(s):  
Jorge A. Guzman ◽  
Mathew S. Dikin ◽  
James A. Kruse
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Endotoxic Shock ◽  
Mucosal Blood Flow ◽  
Canine Model ◽  
Endotoxin Shock ◽  
Carbon Dioxide Tension ◽  
Systemic Hemodynamic ◽  
Hemodynamic Variables ◽  
Blood Flow Patterns

Sublingual and intestinal mucosal blood flow and Pco2 were studied in a canine model of endotoxin-induced circulatory shock and resuscitation. Sublingual Pco2 (PsCO2) was measured by using a novel fluorescent optrode-based technique and compared with lingual measurements obtained by using a Stowe-Severinghaus electrode [lingual Pco2 (PlCO2)]. Endotoxin caused parallel changes in cardiac output, and in portal, intestinal mucosal, and sublingual blood flow (Q̇s). Different blood flow patterns were observed during resuscitation: intestinal mucosal blood flow returned to near baseline levels postfluid resuscitation and decreased by 21% after vasopressor resuscitation, whereas Q̇s rose to twice that of the preshock level and was maintained throughout the resuscitation period. Electrochemical and fluorescent Pco2 measurements showed similar changes throughout the experiments. The shock-induced increases in PsCO2 and PlCO2 were nearly reversed after fluid resuscitation, despite persistent systemic arterial hypotension. Vasopressor administration induced a rebound of PsCO2 and PlCO2 to shock levels, despite higher cardiac output and Q̇s, possibly due to blood flow redistribution and shunting. Changes in PlCO2 and PsCO2 paralleled gastric and intestinal Pco2 changes during shock but not during resuscitation. We found that the lingual, splanchnic, and systemic circulations follow a similar pattern of blood flow variations in response to endotoxin shock, although discrepancies were observed during resuscitation. Restoration of systemic, splanchnic, and lingual perfusion can be accompanied by persistent tissue hypercarbia, mainly lingual and intestinal, more so when a vasopressor agent is used to normalize systemic hemodynamic variables.

The following is the abstract of the article discussed in the subsequent letter:

2005 ◽  
Vol 98 (3) ◽  
pp. 1149-1150 ◽  
Author(s):  
Colin L. Verdant ◽  
Daniel De Backer ◽  
Jacques Creteur ◽  
Jean-Louis Vincent
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Mucosal Blood Flow ◽  
Canine Model ◽  
Endotoxin Shock ◽  
Systemic Hemodynamic ◽  
Hemodynamic Variables ◽  
Vasopressor Agent ◽  
Blood Flow Patterns ◽  
Blood Flow Redistribution

Sublingual and intestinal mucosal blood flow and Pco2 were studied in a canine model of endotoxin-induced circulatory shock and resuscitation. Sublingual Pco2 (Ps[Formula: see text]) was measured by using a novel fluorescent optrode-based technique and compared with lingual measurements obtained by using a Stowe-Severinghaus electrode [lingual Pco2 (Pl[Formula: see text])]. Endotoxin caused parallel changes in cardiac output, and in portal, intestinal mucosal, and sublingual blood flow (Q̇s). Different blood flow patterns were observed during resuscitation: intestinal mucosal blood flow returned to near baseline levels postfluid resuscitation and decreased by 21% after vasopressor resuscitation, whereas Q̇s rose to twice that of the preshock level and was maintained throughout the resuscitation period. Electrochemical and fluorescent Pco2 measurements showed similar changes throughout the experiments. The shock-induced increases in Ps[Formula: see text] and Pl[Formula: see text] were nearly reversed after fluid resuscitation, despite persistent systemic arterial hypotension. Vasopressor administration induced a rebound of Ps[Formula: see text] and Pl[Formula: see text] to shock levels, despite higher cardiac output and Q̇s, possibly due to blood flow redistribution and shunting. Changes in Pl[Formula: see text] and Ps[Formula: see text] paralleled gastric and intestinal Pco2 changes during shock but not during resuscitation. We found that the lingual, splanchnic, and systemic circulations follow a similar pattern of blood flow variations in response to endotoxin shock, although discrepancies were observed during resuscitation. Restoration of systemic, splanchnic, and lingual perfusion can be accompanied by persistent tissue hypercarbia, mainly lingual and intestinal, more so when a vasopressor agent is used to normalize systemic hemodynamic variables.

scholarly journals Relative contributions of systemic hemodynamic variables to cerebral autoregulation during orthostatic stress

2018 ◽  
Vol 124 (2) ◽  
pp. 321-329 ◽  
Author(s):  
Hisao Yoshida ◽  
Jason W. Hamner ◽  
Keita Ishibashi ◽  
Can Ozan Tan
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Cerebral Blood Flow ◽  
Pressure Fluctuations ◽  
Dynamic Changes ◽  
Systemic Hemodynamic ◽  
Hemodynamic Variables ◽  
Central Volume ◽  
The Impact

Postural changes impair the ability of the cerebrovasculature to buffer against dynamic pressure fluctuations, but the mechanisms underlying this impairment have not been elucidated. We hypothesized that autoregulatory impairment may reflect the impact of static central volume shifts on hemodynamic factors other than arterial pressure (AP). In 14 young volunteers, we assessed the relation of fluctuations in cerebral blood flow (CBF) to those in AP, cardiac output, and CO2, during oscillatory lower body pressure (LBP) (±20 mmHg at 0.01 and 0.06 Hz) at three static levels (−20, 0, and +20 mmHg). Static and dynamic changes in AP, cardiac output, and CO2 explained over 70% of the variation in CBF fluctuations. However, their contributions were different across frequencies and levels: dynamic AP changes explained a substantial proportion of the variation in faster CBF fluctuations (partial R2 = 0.75, standardized β = 0.83, P < 0.01), whereas those in CO2 explained the largest portion of the variation in slow fluctuations (partial R2 = 0.43, β = 0.51, P < 0.01). There was, however, a major contribution of slow dynamic AP changes during negative (β = 0.43) but not neutral (β = 0.05) or positive (β = −0.07) LBP. This highlights the differences in contributions of systemic variables to dynamic and static autoregulation and has important implications for understanding orthostatic intolerance. NEW & NOTEWORTHY While fluctuations in blood pressure drive faster fluctuations in cerebral blood flow, overall level of CO2 and the magnitude of its fluctuations, along with cardiac output, determine the magnitude of slow ones. The effect of slow blood pressure fluctuations on cerebrovascular responses becomes apparent only during pronounced central volume shifts (such as when standing). This underlines distinct but interacting contributions of static and dynamic changes in systemic hemodynamic variables to the cerebrovascular regulation.

Independent control of mucosal and total airway blood flow during hypoxemia

1991 ◽  
Vol 71 (1) ◽  
pp. 223-228 ◽  
Author(s):  
S. Elsasser ◽  
W. M. Long ◽  
H. J. Baier ◽  
A. D. Chediak ◽  
A. Wanner
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Blood Circulation ◽  
Mucosal Blood Flow ◽  
Systemic Arterial Pressure ◽  
Microvascular Network ◽  
Flow Probe ◽  
Electromagnetic Flow Probe ◽  
6 Hydroxydopamine ◽  
Tracheal Mucosal Blood Flow

In the larger airways, the blood circulation forms a subepithelial (mucosal) and outer (peribronchial) microvascular network. This raises the possibility that blood flow in these two networks is regulated independently. We used hypoxemia as a stimulus to induce changes in tracheal mucosal blood flow normalized for systemic arterial pressure (Qtr n) measured with an inert soluble gas technique and total bronchial blood flow (Qbr) and normalized Qbr (Qbrn) measured with an electromagnetic flow probe in anesthetized sheep. Fifteen minutes of hypoxemia [PO2 40 +/- 7 (SD) Torr] decreased mean Qtr n from 1.1 +/- 0.4 to 0.8 +/- 0.4 ml.min-1.mmHg-1.10(2) (-27%; P less than 0.05; n = 7) and increased mean Qbr n from 12.1 +/- 3.2 to 17.1 +/- 5.4 ml.min-1.mmHg-1.10(2) (+41%; P less than 0.05; n = 6). The rise in Qbr correlated with cardiac output (r = 0.68; P less than 0.05). Phentolamine pretreatment (0.1 mg/kg iv) blunted the hypoxemia-related decrease of mean Qtr n (-8%; P = NS). Tyramine (2.5 mg) applied locally to the trachea decreased mean Qtr n significantly after 30 and 45 min by 31 and 19%, respectively (P less than 0.05). 6-Hydroxydopamine (0.2 mg 4 times for 1 h locally applied) prevented the hypoxemia-induced as well as local tyramine-induced decrease in mean Qtr n (0 and 0%).(ABSTRACT TRUNCATED AT 250 WORDS)

Dobutamine improves gastrointestinal mucosal blood flow in a porcine model of endotoxic shock

1997 ◽  
Vol 25 (8) ◽  
pp. 1371-1377 ◽  
Author(s):  
Remi Neviere ◽  
Jean-Luc Chagnon ◽  
Benoit Vallet ◽  
Nathalie Lebleu ◽  
Xavier Marechal ◽  
...  
Keyword(s):  
Blood Flow ◽  
Porcine Model ◽  
Endotoxic Shock ◽  
Mucosal Blood Flow

Respiratory muscle energetics during endotoxic shock in dogs

1986 ◽  
Vol 60 (2) ◽  
pp. 486-493 ◽  
Author(s):  
S. N. Hussain ◽  
R. Graham ◽  
F. Rutledge ◽  
C. Roussos
Keyword(s):  
Blood Flow ◽  
Respiratory Muscle ◽  
Muscle Blood Flow ◽  
Endotoxic Shock ◽  
Lactate Production ◽  
Respiratory Muscles ◽  
Experimental Period ◽  
Endotoxin Shock ◽  
Glycogen Depletion ◽  
Muscle Energetics

Respiratory muscle O2 consumption, lactate production, and endogenous substrate utilization during endotoxic shock were assessed in two groups of anesthetized spontaneously breathing dogs. In the endotoxin group (Escherichia coli endotoxin 10 mg/kg iv) and the sham group (saline iv), we sampled diaphragm, external intercostal, and gastrocnemius muscle tissue for glycogen and lactate concentrations before and after 3 h of the experimental period. Only in the endotoxin group did blood pressure and cardiac output decline significantly. Arterial O2 content did not change significantly during shock, whereas mixed venous, phrenic venous, and femoral venous O2 contents dropped to 8.0 +/- 1.1, 5.8 +/- 0.8, and 3.6 +/- 0.6 ml/dl at 60 min of shock, respectively, with little change thereafter. At 30 min of shock, femoral venous lactate rose higher than arterial values, whereas at 90 min of shock, onward, phrenic venous lactate was significantly higher than arterial concentrations. All muscle tissues showed significant lactate production and glycogen depletion after shock. In a second set of experiments we measured respiratory muscle blood flow during shock with radioactive microspheres. At 60 min of shock, diaphragmatic and intercostal blood flow rose by six- and twofold, respectively, whereas gastrocnemius blood flow declined significantly. We conclude that during endotoxin shock 1) the increased demands of the respiratory muscles are met by increasing blood flow and O2 extraction; 2) anaerobic metabolism and respiratory muscle substrate depletion, or both, may contribute to the observed fatigue.

Distribution of respiratory muscle and organ blood flow during endotoxic shock in dogs

1985 ◽  
Vol 59 (6) ◽  
pp. 1802-1808 ◽  
Author(s):  
S. N. Hussain ◽  
C. Roussos
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Arterial Blood Pressure ◽  
Respiratory Muscle ◽  
Muscle Blood Flow ◽  
Endotoxic Shock ◽  
Organ Blood Flow ◽  
Similar Reduction ◽  
Arterial Blood

Respiratory muscle blood flow and organ blood flow during endotoxic shock were studied in spontaneously breathing dogs (SB, n = 6) and mechanically ventilated dogs (MV, n = 5) with radiolabeled microspheres. Shock was produced by a 5-min intravenous injection of Escherichia coli endotoxin (0.55:B5, Difco, 10 mg/kg) suspended in saline. Mean arterial blood pressure and cardiac output in the SB group dropped to 59 and 45% of control values, respectively. There was a similar reduction in arterial blood pressure and cardiac output in the MV group. Total respiratory muscle blood flow in the SB group increased significantly from the control value of 51 +/- 4 ml/min (mean +/- SE) to 101 +/- 22 ml/min at 60 min of shock. In the MV group, respiratory muscle perfusion fell from control values of 43 +/- 12 ml/min to 25 +/- 3 ml/min at 60 min of shock. In the SB group, 8.8% of the cardiac output was received by the respiratory muscle during shock in comparison with 1.9% in the MV group. In both groups of dogs, blood flow to most organs was compromised during shock; however, blood flow to the brain, gut, and skeletal muscles was higher in the MV group than in the SB group. Thus by mechanical ventilation a fraction of the cardiac output used by the working respiratory muscles can be made available for perfusion of other organs during endotoxic shock.

scholarly journals The endothelin receptor antagonist bosentan restores gut oxygen delivery and reverses intestinal mucosal acidosis in porcine endotoxin shock

Gut ◽  
1998 ◽  
Vol 42 (5) ◽  
pp. 696-702 ◽  
Author(s):  
A Oldner ◽  
M Wanecek ◽  
M Goiny ◽  
E Weitzberg ◽  
A Rudehill ◽  
...  
Keyword(s):  
Septic Shock ◽  
Blood Flow ◽  
Receptor Antagonist ◽  
Oxygen Delivery ◽  
Endotoxic Shock ◽  
Endotoxin Shock ◽  
Endothelin Receptor Antagonist ◽  
Endothelin Receptor ◽  
Endotoxin Challenge ◽  
Arterial Blood

Background—Endothelin-1, the most potent vasoconstrictor known, is produced in septic states and may be involved in the pathophysiology of the deteriorated splanchnic circulation seen in septic shock.Aims—To elucidate the capability of bosentan, a non-peptide mixed endothelin receptor antagonist, to attenuate splanchnic blood flow disturbances and counteract intestinal mucosal acidosis in endotoxic shock.Methods—In 16 anaesthetised pigs, central and regional haemodynamics were monitored by thermodilution and ultrasonic flow probes, respectively. A tonometer in the ileum was used for measurement of mucosal pH. Onset of endotoxin challenge was followed by bosentan administration (to eight pigs) two hours later.Results—Endotoxin infusion reduced cardiac index and systemic oxygen delivery; bosentan restored these parameters. The reduced mean arterial blood pressure and renal blood flow remained unaffected by bosentan. The profound reduction in gut oxygen delivery in response to endotoxin was completely abolished by bosentan. Bosentan significantly improved the notably deteriorated intestinal mucosal pH and mucosal-arterial Pco2 gap. The mucosal-portal vein Pco2 gap, used to monitor the mucosa in relation to the gut as a whole (including the spleen and pancreas), was also greatly increased by endotoxaemia and significantly reversed by bosentan.Conclusion—Bosentan completely restored the profound endotoxin induced reductions in systemic and gut oxygen delivery with a concomitant reversal of intestinal mucosal acidosis. Results suggest that endothelin is involved in the pronounced perfusion disturbances seen in the gut in endotoxic shock. Bosentan may prove useful in reducing gut ischaemia in septic shock.

Abstract 17363: Cardiac Output and Valve Orientation Affect Blood Flow Patterns Local to Bioprosthetic Pulmonary Valves in Tetralogy of Fallot

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Nicole Schiavone ◽  
Christopher Elkins ◽  
Doff B McElhinney ◽  
John K Eaton ◽  
Alison L Marsden
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Tetralogy Of Fallot ◽  
Flow Patterns ◽  
Velocity Fields ◽  
4D Flow Mri ◽  
4D Flow ◽  
Flow Mri ◽  
Leaflet Motion ◽  
Blood Flow Patterns

Introduction: Tetralogy of Fallot (ToF) typically requires surgical repair of the right ventricular outflow tract (RVOT) and subsequent placement of an artificial pulmonary valve. Bioprosthetic valve longevity is highly variable and there is currently little understanding of what hemodynamic factors may lead to early valve dysfunction. Hypothesis: We hypothesize that cardiac output and valve orientation impact the performance of bioprosthetic valves by affecting blood flow patterns in the RVOT. Methods: We analyzed hemodynamics in a 3D printed ToF anatomy model in a physiological flow loop. A 25mm surgical valve was implanted in the model at two orientations: native and rotated 180 degrees. Full 3D, three-component, phase-averaged velocity fields were obtained over the cardiac cycle using 4D flow MRI at cardiac outputs of 2, 3.5, and 5 L/min. We acquired images of valve leaflet motion at 1500Hz. The 4D flow MRI and high-speed camera experiments were run identically, allowing us to examine the relationship between flow fields and leaflet motion. Results: The full velocity fields from the MRI scans revealed key differences among cases in flow features including location of reverse flow regions, systolic jet shape, and asymmetry local to the valve. At 2 L/min, the forward flow through the jet was more asymmetric compared to the other cases and a strong vortex formed, indicating a region of recirculation. With the rotated valve orientation, the 2 L/min case also produced a unique pattern as flow was washed from the RVOT inner curve back toward the center of the valve (Fig 1). Leaflet behavior during systole varied with cardiac output as well, as higher frequency flutter was observed at 5 L/min and the effective valve orifice area was decreased by 8.5% at 2 L/min compared to 5 L/min. Conclusions: We observed key differences in flow patterns and leaflet motion due to cardiac output and valve orientation that could impact leaflet loading and fatigue and long-term valve function.

Naloxone alters organ perfusion during endotoxin shock in conscious rats

1988 ◽  
Vol 255 (5) ◽  
pp. H1106-H1113 ◽  
Author(s):  
W. R. Law ◽  
J. L. Ferguson
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Survival Time ◽  
Lethal Dose ◽  
Peripheral Resistance ◽  
Endotoxin Shock ◽  
Endogenous Opioids ◽  
Circulatory Effects ◽  
Naloxone Treatment

Antagonism of endogenous opioids has been shown to improve survival time, increase blood pressure, and attenuate acidosis during endotoxin shock. However, some of the most severe problems associated with this condition arise from the circulatory disturbances that occur. We investigated the circulatory effects of naloxone during endotoxin shock as they relate to hemodynamic parameters in conscious, unrestrained rats. Blood flow and hemodynamic variables were measured in male, Sprague-Dawley rats (300-400 g) 24 h after surgical preparation. Rats were challenged with either 10 mg/kg Escherichia coli endotoxin (100% lethal dose) or intravenous saline. Measurements were made at 0, 10, 30, and 60 min postchallenge. Naloxone (2 mg/kg) or saline was given as a treatment (intravenous bolus) at 25 min postchallenge. Cardiac output and blood distribution (%CO) and flow were measured with radiolabeled microspheres. Cardiac output was depressed and total peripheral resistance was elevated 10 min into endotoxin shock. Naloxone treatment improved blood pressure significantly during endotoxin shock, as would be expected with the observed increase in total peripheral vascular resistance and no significant change in cardiac output. Improved perfusion of skeletal muscle is a likely explanation for lower serum lactate levels that have been reported to occur in this model after naloxone administration. Our data also indicate that naloxone may improve cardiac efficiency and does not interfere with maintenance of global cerebral blood flow. Collectively, these effects would contribute to the observed improved survival time after naloxone treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

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