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Hypovolemia

About: Hypovolemia is a research topic. Over the lifetime, 2420 publications have been published within this topic receiving 57912 citations.


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Journal Article
TL;DR: In this review a comprehensive synopsis of pathogenic processes is outlined, showing how positive homeostatic regulation amplifies deterioration of arteriovenous blood pressure gradient, which reversely intensifies the degree of energy depletion in the tissues.
Abstract: Hemodynamic shock syndrome represents an acute circulatory failure leading to a multiple organ failure. Such circulatory failure develops due to a decrease of arteriovenous blood pressure gradient as a consequence of three independent groups of pathogenic mechanisms (cardiogenic, vasohypotonic and hypovolemic), all of which lead to the common pathogenic pathways. A decrease of arteriovenous pressure gradient induces vasomotoric responses, reactive body fluids redistribution, endocrine, metabolic as well as tissue energy adjustments. In this review a comprehensive synopsis of pathogenic processes is outlined. The cardiogenic mechanisms include the acute systolic and/or diastolic heart failure. Vasohypotonic mechanisms (neurogenic, septic and anaphylactic) are due to vascular tonus missadjustment. Hypovolemia caused by blood, plasma, water and electrolytes losses and/or sequestration, leads to decrease of pressure gradient as soon as the extent of hypovolemia overcomes the compensatory vascular capacity. The decrease of tissue perfusion is direct consequence of the arteriovenous pressure gradient loss. Tissue hypoperfusion causes a progressive depletion of cellular ATP concentration (cellular hypoenergosis), which very often falls lower than 0,1 mmol/L. Cellular hypoenergosis plays the critical role in conversion of negative homeostatic regulation into a positive feedback mode. Positive homeostatic regulation (circuli vitiosi) amplifies deterioration of arteriovenous blood pressure gradient, which reversely intensifies the degree of energy depletion in the tissues. Such homeostatic conversion plays a critical role in the development of progressive phase (systemic failure, decompensation) of the shock.

1 citations

Journal Article
TL;DR: These cases demonstrate that ACE inhibitors should not be instituted during extracellular volume depletion and their initial dosage should be low and the dangerous combination of ACE inhibitors with spironolactone and potassium supplements should be avoided wherever possible.
Abstract: In 3 patients with severe cardiac failure high dose therapy with the ACE inhibitor enalapril was instituted during a state of extracellular volume depletion. Severe arterial hypotension with reversible renal insufficiency developed in all the patients. In two the hypovolemia was induced by diuretic treatment and in one by an acute infection with diarrhea. The latter patient also developed life-threatening hyperkalemia with cardiac arrest since he was also receiving spironolactone and potassium supplements. These cases demonstrate that ACE inhibitors should not be instituted during extracellular volume depletion and their initial dosage should be low. The dangerous combination of ACE inhibitors with spironolactone and potassium supplements should be avoided wherever possible.

1 citations

Proceedings ArticleDOI
01 Jul 2020
TL;DR: To mitigate hypovolemia-induced miscalibration of pulse transit time, this work defines a template-based signal quality index (SQI) and shows that the subject-specific calibration of SQI to BP is more robust to changes in blood volume than PTT.
Abstract: Pulse transit time (PTT) is a hemodynamic indicator that may be obtained non-invasively using photoplethysmogram (PPG) signals for continuous blood pressure (BP) monitoring. Among the most promising applications of this technology are military and civilian trauma cases, where reduced blood volume due to hemorrhage, or absolute hypovolemia, is the leading preventable cause of death. However, the drawback of this method is that it requires calibration for each patient; additionally, changes in physiological state may affect PTT calibration. In this work, a porcine model (n = 6) was used to demonstrate that changes in blood volume lead to miscalibration of PTT for BP estimation. To mitigate hypovolemia-induced miscalibration, this work first defines a template-based signal quality index (SQI) for characterizing the morphology of PPG signals; it is then shown that the subject-specific calibration of SQI to BP is more robust to changes in blood volume than PTT. Though changes in PPG signal quality are not necessarily specific to changes in BP, these results suggest that PPG-based monitoring systems may benefit from incorporating morphological information for cuffless BP estimation in trauma settings.

1 citations

Book ChapterDOI
01 Jan 2018

1 citations

Journal Article
TL;DR: It is thought epidural anesthesia is a useful anesthesia method for patients with pure autonomic failure and was considered to cause less hypotension than in patients with normal autonomic function.
Abstract: Pure autonomic failure is characterized by orthostatic hypotension, sweating disorder, urinary incontinence, and syncope. A 64 year-old man with pure autonomia failure was scheduled for suprapubic prostatectomy. We monitoring direct arterial pressure and inserted pulmonary artery catheter prior to the induction of anesthesia. General anesthesia was induced with diazepam 10 mg, fentanyl 0.3 mg, and vecuronium 8 mg for tracheal intubation. Anesthesia was maintained with sevoflurane (0.2-1.5%), 60% nitrous oxide in oxygen supplemented with intermittent epidural anesthesia. During anesthesia, blood loss was immediately replaced with banked blood because autonomic failure could not compensate hypovolemia well. Epidural anesthesia in this patient was considered to cause less hypotension than in patients with normal autonomic function. Therefore, we think epidural anesthesia is a useful anesthesia method for patients with pure autonomic failure. The emergence from anesthesia was smooth and no complications were seen during the perioperative period.

1 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
202373
2022147
202143
202058
201967
201850