Acute isovolemic anemia impairs central processing as determined by P300 latency

Weiskopf, Richard B.; Toy, Pearl; Hopf, Harriet W.; Feiner, John; Finlay, Heather E.; Takahashi, Michelle; Bostrom, Alan; Songster, Christopher; Aminoff, Michael J.

doi:10.1016/j.clinph.2004.12.009

Cited by 72 publications

(48 citation statements)

References 26 publications

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“…Th e P300 response was signifi cantly prolonged when unmedi cated healthy volunteers were hemodiluted from hemo globin concentrations of 12.4 ± 1.3 to 5.1 ± 0.2 g/dl [15]. Th e increased P300 latencies could be reversed to values not signifi cantly diff erent from baseline when inspired oxygen concentration was increased from 21 (room air) to 100%.…”

Section: The Concept Of Physiologic Transfusion Triggermentioning

confidence: 64%

Venous Oxygen Saturation as a Physiologic Transfusion Trigger

Vallet¹,

Robin²,

Lebuffe³

2010

Yearbook of Intensive Care and Emergency Medicine

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IntroductionVenous oxygen saturation is a clinical tool which integrates the whole body oxygen uptake-to-delivery (VO 2 -DO 2 ) relationship. In the clinical setting, in the absence of pulmonary artery catheter (PAC)-derived mixed venous oxygen saturation (SvO 2 ), the central venous oxygen saturation (ScvO 2 ) is increasingly being used as a reasonably accurate surrogate [1]. Central venous catheters (CVCs) are simpler to insert, and generally safer and cheaper than PACs. Th e CVC allows sampling of blood for measurement of ScvO 2 or even continuous monitoring if an oximetry catheter is being used. Th e normal range for SvO 2 is 68 to 77% and ScvO 2 is considered to be 5% above these values [2].A decrease in hemoglobin (Hb, g/dl) is likely to be associated with a decrease in DO 2 when cardiac output (CO) remains unchanged, since DO 2 = CO x CaO 2 , where CaO 2 is arterial oxygen content and is ≈ Hb × SaO 2 x 1.34 (where SaO 2 is the arterial oxygen saturation in%; and 1.34 is the oxygen-carrying capacity of Hb in mlO 2 /g Hb), when one ignores the negligible oxygen not bound to Hb [1]. A decrease in Hb is one of the four determinants responsible for a decrease in SvO 2 (or ScvO 2 ), alone or in combination with hypoxemia (decrease in SaO 2 ), an increase in VO 2 without a concomitant increase in DO 2 , or a fall in cardiac output.When Because it integrates Hb, cardiac output, VO 2 and SaO 2 , the venous oxygen saturation therefore helps to assess the VO 2 -DO 2 relationship and tolerance to anemia during blood loss. Venous oxygen saturation as a physiologic transfusion triggerWhen DO 2 decreases beyond a certain threshold, it induces a decrease in VO 2 . Th is point is known as the critical DO 2 (DO 2 crit), below which there is a state of VO 2 -DO 2 dependency also called tissue dysoxia. In humans, dysoxia is usually present when SvO 2 falls below a critical 40-50% (SvO 2 crit); this may, however, also occur at higher levels of SvO 2 when O 2 ER is impaired. Usually eff orts in correcting cardiac output (by fl uids or inotropes), and/or Hb and/or SaO 2 and/or VO 2 must target a return of SvO 2 (ScvO 2 ) from 50 to 65-70% [4]. In sedated critically ill patients in whom life support was discontinued, the DO 2 crit was found to be approximately 3.8 to 4.5 mlO 2 /kg/min for a VO 2 of about 2.4 mlO 2 /g/ min; O 2 ER reached an O 2 ERcrit of 60% [5] with SvO 2 crit being ≈ 40%.In a landmark study by Rivers et al. [6], patients admitted to an emergency department with severe sepsis and septic shock were randomized to standard therapy (aiming for a central venous pressure [CVP] of 8-12 mmHg, mean arterial pressure (MAP) ≥ 65 mmHg, and urine output ≥ 0.5 ml/kg/h) or to early goal-directed therapy where, in addition to the previous parameters, an ScvO 2 of at least 70% was targeted by optimizing fl uid administration, keeping hematocrit ≥ 30%, and/or giving dobutamine to a maximum of 20 μg/kg/min. Th e initial ScvO 2 in both groups was low (49 ± 12%), suggesting a hypodynamic condition before resuscitation was started.

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Section: The Concept Of Physiologic Transfusion Triggermentioning

confidence: 64%

Venous Oxygen Saturation as a Physiologic Transfusion Trigger

Vallet¹,

Robin²,

Lebuffe³

2010

Yearbook of Intensive Care and Emergency Medicine

View full text Add to dashboard Cite

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“…In the final adjusted model, we controlled for baseline depressive symptom scores, age, sex, BMI, menopause status, cigarette smoking, alcohol drinking, marriage status, hypertension, dyslipidemia, diabetes mellitus, medical history of cardiovascular disease, medical history of cancer, and aspirin intake. As hemoglobin concentration depends on age and sex (Weiskopf et al 2005), we included age and sex in the model. In addition, we included smoking status, alcohol drinking, marriage status, chronic underlying diseases, aspirin intake, menopause, and BMI because they could influence hemoglobin and depression.…”

Section: Discussionmentioning

confidence: 99%

“…One possible explanation is related to brain oxygen supply (Weiskopf et al 2005). Because the brain is a major oxygen-and energy-consuming organ, it is sensitive to even mild hemoglobin insufficiency (Umegaki et al 2011).…”

Section: Strengthsmentioning

confidence: 99%

Association between Mean Corpuscular Hemoglobin Concentration and Future Depressive Symptoms in Women

Lee

Nadimpalli²,

Yoon

et al. 2017

Tohoku J. Exp. Med.

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Insufficient hemoglobin and depression share several symptoms and often occur in the same patients. Here, we sought to clarify their relationship by investigating two indices of oxygenation at the tissue level: mean corpuscular hemoglobin concentration (MCHC) and hemoglobin level. We hypothesized that MCHC would be more informative than hemoglobin levels. This prospective, longitudinal, community-based study included 337 participants (108 men and 229 women; age range, 38-87 years) who received evaluations of MCHC, hemoglobin levels and depressive symptom scores (DSS) during baseline and follow-up examinations, which were performed in 2008-2011 and 2010-2012, respectively. MCHC and hemoglobin levels were measured as part of complete blood counts, while DSS was evaluated using the Beck Depression Inventory. Associations were analyzed using linear regression. We found a statistically significant association between baseline MCHC and follow-up DSS (β = −0.69, p = 0.026), which remained statistically significant after controlling for potential confounders (β = −0.71, p = 0.011). Further, when we analyzed the relationship separately for men and women, we observed that it remained stable for women before (β = −1.00, p = 0.014) and after (β = −1.09, p = 0.003) adjusting for confounders. The stable association indicates that MCHC may be superior to hemoglobin level as a prognostic factor for future depressive symptoms in women. MCHC is easy to measure and low MCHC is usually treatable. Therefore, screening and intervention efforts could be targeted at women with low MCHC, who appear to have elevated risks of developing depressive symptoms.

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“…Acute anemia has been associated with cognitive and neurophysiologic dysfunction in healthy volunteers 1,2 and increased neurological injury and mortality in perioperative patients by currently undefined mechanisms. [3][4][5][6] One of the most common causes of acute anemia is acute blood loss and fluid resuscitation (hemodilution).…”

Section: Introductionmentioning

confidence: 99%

L’expression génique dans le cortex cérébral de rats anémiques aigus: une analyse par microarray

Briet

Mazer

Tsui

et al. 2009

Can J Anesth/J Can Anesth

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Purpose Hemodilution in perioperative patients has been associated with neurological morbidity and increased mortality by undefined mechanisms. This study assesses whether hemodilutional anemia up-regulated inflammatory cerebral gene expression (microarray) to help define the mechanism. Methods Hemodilution was performed in anesthetized rats by exchanging 50% of the estimated blood volume (30 mL kg -1 ) with pentastarch. Two groups of control animals were utilized, i.e., a non-anesthetized control (Normal Control) and an anesthetized control group (Anesthesia Control). Blood pressure, hemoglobin concentration, and arterial blood gas analysis were performed before and after hemodilution. Cerebral cortex was harvested from isoflurane-anesthetized rats (n = 6) after 6 and 24 hr of recovery and was used to perform complimentary DNA (cDNA) microarray analyses. Pro-inflammatory chemokine and cytokine protein levels were also measured.Results Microarray analysis demonstrated up-regulation of 72 and 27 genes (6 and 24 hr, respectively) in anemic cerebral cortex. These genes were involved in a number of biological functions, including (1) inflammatory responses; (2) angiogenesis; (3) vascular homeostasis; (4) cellular biology; and (5) apoptosis. Chemokine ribonucleic acid (RNA) expression (CXCL-1, -10, and -11) was highest in anemic brain tissue (P \ 0.0125 for each). Protein measurements demonstrated a significant increase in interleukin-6, tumor necrosis factor a, and monocyte chemoattractant protein-1 (P \ 0.05 for each). Conclusion This study utilizes microarray technology to elucidate changes in cerebral cortical gene expression in response to acute hemodilution. These findings demonstrate an increase in pro-inflammatory chemokines (RNA, protein) and cytokines (protein). An improved understanding of the inflammatory response to anemia may help to minimize associated morbidity and mortality. RésuméObjectif L'he´modilution en pe´riope´ratoire chez les patients a e´te´associe´e à une morbidite´neurologique et une mortalite´accrue en raison de me´canismes inde´termine´s. Cette e´tude examine si l'ane´mie par he´modilution re´gule al a hausse l'expression ge´nique ce´re´brale inflammatoire (microarray) afin d'aider a`de´finir ce me´canisme. Méthode Une he´modilution a e´te´re´alise´e chez des rats anesthe´sie´s en e´changeant 50 % du volume sanguin estime( 30 mLÁkg -1 ) avec du pentastarch. Deux groupes d'animaux te´moins ont e´te´utilise´s, soit un groupe te´moin non anesthe´sie´(te´moin normal) et un groupe te´moin anesthe´sie( te´moin anesthe´sie´). La pression arte´rielle, la concentration d'he´moglobine et une gazome´trie sanguine arte´rielle

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Acute isovolemic anemia impairs central processing as determined by P300 latency

Cited by 72 publications

References 26 publications

Venous Oxygen Saturation as a Physiologic Transfusion Trigger

Venous Oxygen Saturation as a Physiologic Transfusion Trigger

Association between Mean Corpuscular Hemoglobin Concentration and Future Depressive Symptoms in Women

L’expression génique dans le cortex cérébral de rats anémiques aigus: une analyse par microarray

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