Harnessing Cardiopulmonary Interactions to Improve Circulation and Outcomes After Cardiac Arrest and Other States of Low Blood Pressure

Author(s):  
Anja Metzger ◽  
Keith Lurie
Shock ◽  
2017 ◽  
Vol 47 (6) ◽  
pp. 759-764 ◽  
Author(s):  
Caroline Fritz ◽  
Antoine Kimmoun ◽  
Fabrice Vanhuyse ◽  
Bogdan Florin Trifan ◽  
Sophie Orlowski ◽  
...  

2009 ◽  
Vol 23 (3) ◽  
pp. 104-112 ◽  
Author(s):  
Stefan Duschek ◽  
Heike Heiss ◽  
Boriana Buechner ◽  
Rainer Schandry

Recent studies have revealed evidence for increased pain sensitivity in individuals with chronically low blood pressure. The present trial explored whether pain sensitivity can be reduced by pharmacological elevation of blood pressure. Effects of the sympathomimetic midodrine on threshold and tolerance to heat pain were examined in 52 hypotensive persons (mean blood pressure 96/61 mmHg) based on a randomized, placebo-controlled, double-blind design. Heat stimuli were applied to the forearm via a contact thermode. Confounding of drug effects on pain perception with changes in skin temperature, temperature sensitivity, and mood were statistically controlled for. Compared to placebo, higher pain threshold and tolerance, increased blood pressure, as well as reduced heart rate were observed under the sympathomimetic condition. Increases in systolic blood pressure between points of measurement correlated positively with increases in pain threshold and tolerance, and decreases in heart rate were associated with increases in pain threshold. The findings underline the causal role of hypotension in the augmented pain sensitivity related to this condition. Pain reduction as a function of heart rate decrease suggests involvement of a baroreceptor-related mechanism in the pain attrition. The increased proneness of persons with chronic hypotension toward clinical pain is discussed.


MedPharmRes ◽  
2018 ◽  
Vol 2 (3) ◽  
pp. 27-32
Author(s):  
Bien Le ◽  
Dai Huynh ◽  
Mai Tuan ◽  
Minh Phan ◽  
Thao Pham ◽  
...  

Objectives: to evaluate the fluid responsiveness according to fluid bolus triggers and their combination in severe sepsis and septic shock. Design: observational study. Patients and Methods: patients with severe sepsis and septic shock who already received fluid after rescue phase of resuscitation. Fluid bolus (FB) was prescribed upon perceived hypovolemic manifestations: low central venous pressure (CVP), low blood pressure, tachycardia, low urine output (UOP), hyperlactatemia. FB was performed by Ringer lactate 500 ml/30 min and responsiveness was defined by increasing in stroke volume (SV) ≥15%. Results: 84 patients were enrolled, among them 30 responded to FB (35.7%). Demographic and hemodynamic profile before fluid bolus were similar between responders and non-responders, except CVP was lower in responders (7.3 ± 3.4 mmHg vs 9.2 ± 3.6 mmHg) (p 0.018). Fluid response in low CVP, low blood pressure, tachycardia, low UOP, hyperlactatemia were 48.6%, 47.4%, 38.5%, 37.0%, 36.8% making the odd ratio (OR) of these triggers were 2.81 (1.09-7.27), 1.60 (0.54-4.78), 1.89 (0.58-6.18), 1.15 (0.41-3.27) and 1.27 (0.46-3.53) respectively. Although CVP < 8 mmHg had a higher response rate, the association was not consistent at lower cut-offs. The combination of these triggers appeared to raise fluid response but did not reach statistical significance: 26.7% (1 trigger), 31.0% (2 triggers), 35.7% (3 triggers), 55.6% (4 triggers), 100% (5 triggers). Conclusions: fluid responsiveness was low in optimization phase of resuscitation. No fluid bolus trigger was superior to the others in term of providing a higher responsiveness, their combination did not improve fluid responsiveness as well.


Hypertension ◽  
1996 ◽  
Vol 28 (4) ◽  
pp. 569-575 ◽  
Author(s):  
Rhona A. Morrison ◽  
Alice McGrath ◽  
Gillian Davidson ◽  
Jehoiada J. Brown ◽  
Gordon D. Murray ◽  
...  

1989 ◽  
Vol 257 (2) ◽  
pp. H506-H510 ◽  
Author(s):  
M. Vincent ◽  
C. E. Gomez-Sanchez ◽  
A. Bataillard ◽  
J. Sassard

The urinary excretion and the plasma concentration of deoxycorticosterone (DOC), corticosterone, 18-hydroxy-DOC (18-OH-DOC), aldosterone, and 19-nor-DOC were measured by specific radioimmunoassays in genetically hypertensive (LH), normotensive (LN), and low blood pressure (LL) male rats of the Lyon strains at two ages that characterize the development of their systolic blood pressure (SBP). When compared with both LN and LL controls, 5-wk-old LH rats exhibited an increased urinary DOC and decreased urinary corticosterone excretions, which were significantly related to the SBP level (r' = 0.618 and -0.520; n = 23; P less than 0.01 for DOC and corticosterone, respectively). In addition, the adrenal synthesis of LH rats was found to rely on an increased 18-hydroxylase activity as indicated by elevated urinary 18-OH-DOC/corticosterone and aldosterone/corticosterone associated with a lower 11-beta-hydroxylase activity shown by the decreased urinary corticosterone/DOC. Twenty-wk-old LH rats with fully developed hypertension exhibited normal urinary excretion of steroids and a decrease in plasma DOC concentration, which negatively correlated with the SBP level (r' = -0.574; n = 25; P less than 0.01). In conclusion, the present study demonstrates that in the Lyon model of genetically hypertensive rats, compared with two genetically different control strains and maintained under physiological unstressed conditions, the development of hypertension is associated with an increased urinary excretion of DOC. After the full development of their hypertension, the mineralocorticoid synthesis in LH rats returns to normal or low levels which could, however, remain inappropriately high for their sodium body content.


1988 ◽  
Vol 255 (4) ◽  
pp. H729-H735 ◽  
Author(s):  
M. Sautel ◽  
J. Sacquet ◽  
M. Vincent ◽  
J. Sassard

Several indirect evidences of alterations in the central catecholaminergic structures were obtained in genetically hypertensive rats. Because they could be of pathogenetic value, we measured, in the present work, the in vivo turnover (TO) of norepinephrine (NE) in brain areas of 5- and 22-wk-old genetically hypertensive (LH) rats of the Lyon strain, and their simultaneously selected normotensive (LN) and low blood pressure (LL) controls. Among the changes observed, the increased TO of NE in the A2 and A6 regions of 5-wk-old LH rats and its decrease in the posteroventral hypothalamic nucleus of 22-wk-old LH animals appeared likely to compensate for hypertension. On the contrary, the decreased TO of NE in the anterior hypothalamic nucleus observed at 5 wk and in the A6 and A1 areas at 22 wk of age in LH rats could participate in the development or the maintenance of hypertension. Above all, it was postulated that the increased TO of NE found in the A7 region of 5-wk-old LH rats could play a primary role in the pathogenesis of hypertension in the Lyon model.


2006 ◽  
Vol 21 (5) ◽  
pp. 1257-1262 ◽  
Author(s):  
Csaba P. Kovesdy ◽  
Bhairvi K. Trivedi ◽  
Kamyar Kalantar-Zadeh ◽  
John E. Anderson

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Wen Wang ◽  
Hongwei Cai ◽  
Huiping Ding ◽  
Xiaoping Xu

Abstract Background Trigeminal-cardiac reflex (TCR) is a brainstem vagus reflex that occurs when any center or peripheral branch of the trigeminal nerve was stimulated or operated on. The typical clinical manifestation is sudden bradycardia with or without blood pressure decline. The rhino-cardiac reflex which is one type of TCR is rare in clinical practice. As the rhino-cardiac reflex caused by disinfection of the nasal cavity is very rare, we report these two cases to remind other anesthesiologists to be vigilant to this situation. Case presentation This case report describes two cases of cardiac arrest caused by rhino-cardiac reflex while disinfecting nasal cavity before endoscopic transsphenoidal removal of pituitary adenomas. Their heart rate all dropped suddenly at the very moment of nasal stimulation and recovered quickly after stimulation was stopped and the administration of drugs or cardiac support. Conclusion Although the occurrence of rhino-cardiac reflex is rare, we should pay attention to it in clinical anesthesia. It is necessary to know the risk factors for preventing it. Once it occurs, we should take active and effective rescue measures to avoid serious complications.


Sign in / Sign up

Export Citation Format

Share Document