scholarly journals Prognostic value of base excess as indicator of acid-base balance in acute heart failure

2020 ◽  
Vol 9 (5) ◽  
pp. 399-405 ◽  
Author(s):  
Hiroki Nakano ◽  
Toshiyuki Nagai ◽  
Yasuyuki Honda ◽  
Satoshi Honda ◽  
Naotsugu Iwakami ◽  
...  
Keyword(s):  
Heart Failure ◽  
Confidence Interval ◽  
Acute Heart Failure ◽  
Base Excess ◽  
Acid Base Balance ◽  
Acid Base ◽  
Heart Failure Patients ◽  
Base Balance ◽  
High Base

Background: Acid-base balance can change as a result of pulmonary oedema and low tissue perfusion in acute heart failure patients. However, its long-term prognostic significance remains to be clarified. Methods: We prospectively examined a cohort of 472 consecutive acute heart failure patients who underwent arterial blood gas analysis on admission between January 2013 and May 2016. Acidaemia, alkalaemia and normal range of base excess were defined as pH <7.38, >7.42 and −2 to 2 mEq/L, respectively. The primary outcome was all-cause death. Results: During a median follow-up period of 714 days, 101 patients died. Although there was no difference in mortality among patients with acidaemia, normal pH and alkalaemia ( p = 0.92), patients with high base excess had the highest mortality compared with others. Multivariable Cox proportional hazard models revealed that high base excess was an independent determinant of mortality (hazard ratio 1.83, 95% confidence interval 1.08–3.13 (high versus normal base excess), hazard ratio 0.81, 95% confidence interval 0.47–1.41 (low versus normal base excess)), even after adjustment for significant prognostic covariates. Furthermore, regarding mortality stratified by base excess and carbon dioxide partial pressure (pCO2), patients with high base excess (>2.1 mEq/L) and high pCO2 (>40 mmHg) had the highest mortality compared with others. Conclusions: High base excess, but not low base excess, on admission was associated with long-term mortality in acute heart failure patients, indicating the importance of evaluating acid-base balance on admission by base excess for stratifying the risk of mortality in patients with acute heart failure.

scholarly journals Clinical significance of acid–base balance in an emergency setting in patients with acute heart failure

2012 ◽  
Vol 60 (4) ◽  
pp. 288-294 ◽  
Author(s):  
Akihiro Shirakabe ◽  
Noritake Hata ◽  
Nobuaki Kobayashi ◽  
Takuro Shinada ◽  
Kazunori Tomita ◽  
...  
Keyword(s):  
Heart Failure ◽  
Acute Heart Failure ◽  
Clinical Significance ◽  
Emergency Setting ◽  
Acid Base Balance ◽  
Acid Base ◽  
Base Balance

Prognostic Impact of Clinical Scenarios (CS) and Acid-Base Balance in Patients with Acute Heart Failure

2011 ◽  
Vol 17 (9) ◽  
pp. S174-S175
Author(s):  
Akihiro Shirakabe ◽  
Noritake Hata ◽  
Takuro Shinada ◽  
Nobuaki Kobayashi ◽  
Kazunori Tomita ◽  
...  
Keyword(s):  
Heart Failure ◽  
Acute Heart Failure ◽  
Prognostic Impact ◽  
Acid Base Balance ◽  
Acid Base ◽  
Clinical Scenarios ◽  
Base Balance

The Effect of Long-term Topiramate Treatment on Acid-base Balance in Children with Epilepsy

2016 ◽  
Vol 24 (3) ◽  
pp. 116-121
Author(s):  
김지용 ◽  
남상욱 ◽  
김영미 ◽  
이윤진 ◽  
이훈상 ◽  
...  
Keyword(s):  
Acid Base Balance ◽  
Acid Base ◽  
Base Balance

Long-term regulation of renal Na-dependent cotransporters and ENaC: response to altered acid-base intake

2000 ◽  
Vol 279 (3) ◽  
pp. F459-F467 ◽  
Author(s):  
Gheun-Ho Kim ◽  
Stephen W. Martin ◽  
Patricia Fernández-Llama ◽  
Shyama Masilamani ◽  
Randall K. Packer ◽  
...  
Keyword(s):  
Collecting Duct ◽  
Na Channel ◽  
Thick Ascending Limb ◽  
Acid Base Balance ◽  
Acid Base ◽  
Opposite Pattern ◽  
Α Subunit ◽  
Base Balance ◽  
Acid Loading

Increased systemic acid intake is associated with an increase in apical Na/H exchange in the renal proximal tubule mediated by the type 3 Na/H exchanger (NHE3). Because NHE3 mediates both proton secretion and Na absorption, increased NHE3 activity could inappropriately perturb Na balance unless there are compensatory changes in Na handling. In this study, we use semiquantitative immunoblotting of rat kidneys to investigate whether acid loading is associated with compensatory decreases in the abundance of renal tubule Na transporters other than NHE3. Long-term (i.e., 7-day) acid loading with NH4Cl produced large decreases in the abundances of the thiazide-sensitive Na-Cl cotransporter (TSC/NCC) of the distal convoluted tubule and both the β- and γ-subunits of the amiloride-sensitive epithelial Na channel (ENaC) of the collecting duct. In addition, the renal cortical abundance of the proximal type 2 Na-dependent phosphate transporter (NaPi-2) was markedly decreased. In contrast, abundances of the bumetanide-sensitive Na-K-2Cl cotransporter of the thick ascending limb and the α-subunit of ENaC were unchanged. A similar profile of changes was seen with short-term (16-h) acid loading. Long-term (7-day) base loading with NaHCO3resulted in the opposite pattern of response with marked increases in the abundances of the β- and γ-subunits of ENaC and NaPi-2. These adaptations may play critical roles in the maintenance in Na balance when changes in acid-base balance occur.

Blood lactate and acid-base balance in graded neonatal hypoxia: evidence for oxygen-restricted metabolism

1994 ◽  
Vol 77 (5) ◽  
pp. 2318-2324 ◽  
Author(s):  
S. M. Torrance ◽  
C. Wittnich
Keyword(s):  
Lactic Acidosis ◽  
Oxygen Uptake ◽  
Anaerobic Metabolism ◽  
Base Excess ◽  
Severe Hypoxia ◽  
Oxygen Extraction ◽  
Acid Base Balance ◽  
Acid Base ◽  
Neonatal Response ◽  
Base Balance

This study examines the neonatal response to graded hypoxia and determines the arterial PO2 (PaO2) threshold for oxygen-restricted metabolism as confirmed by the development of lactic acidosis and altered oxygen handling. Anesthetized, intubated, and ventilated 3-day-old pigs (n = 56) were randomly assigned to one of five predetermined acute (120 min) graded hypoxia groups: normoxia (PaO2 = 80 Torr) or mild (60 Torr), moderate (40 Torr), moderately severe (30 Torr), or severe (20 Torr) hypoxia. In moderate hypoxia, lactate and acid-base homeostasis were unaltered due to a significant increase in oxygen extraction (P < 0.05) that was sufficient to maintain the arteriovenous oxygen content difference (oxygen uptake). In moderately severe hypoxia, increased arterial lactate and decreased HCO3- and base excess were evidence of anaerobic metabolism, yet pH was unaltered, indicating adequate buffering. In this group, despite the increase in oxygen extraction, oxygen uptake was reduced, indicating the onset of oxygen-restricted metabolism. The severe hypoxia group had significantly increased lactate (21.7 +/- 3.9 mmol/l), decreased pH (7.01 +/- 0.07) and base excess (-21.5 +/- 3.0 mmol/l), and depletion of HCO3- (9.7 +/- 1.6 mmol/l) (P < 0.0001). Here, increases in oxygen extraction were severely limited by availability, resulting in significantly reduced oxygen uptake, anaerobic metabolism, and profound lactic acidosis.

scholarly journals Creatinine Levels at Admission as Predictors of In-Hospital Major Adverse Cardiovascular Events in Acute Heart Failure Patient

2020 ◽  
Vol 6 (1) ◽  
pp. 16-22
Author(s):  
Farida Hanum Margolang ◽  
Refli Hasan ◽  
Abdul Halim Raynaldo ◽  
Harris Hasan ◽  
Ali Nafiah ◽  
...  
Keyword(s):  
Heart Failure ◽  
Acute Heart Failure ◽  
Roc Curve ◽  
Cardiovascular Events ◽  
Major Adverse Cardiovascular Events ◽  
High Morbidity ◽  
Roc Curve Analysis ◽  
Heart Failure Patients ◽  
Long Term Prognosis

Background: Acute heart failure is a global health problem with high morbidity and mortality. Short term and long term prognosis of these patients is poor. Therefore, early identification of patients at high risk for major adverse cardiovascular events (MACEs) during hospitalization was needed to improve outcome. Creatinine levels at admission could be used as predictors of major adverse cardiovascular events in acute heart failure patients because creatinine is a simple and routine biomarker of renal function examined in patients with acute heart failure. This study aimed to determine whether creatinine can be used as a predictor of major adverse adverse cardiovascular events in patients with acute heart failure.Methods: This study is a prospective cohort study of 108 acute heart failure patients treated at H. Adam Malik Hospital from July 2018 to January 2019. Creatinine cut-off points were determined using the ROC curve, then bivariate and multivariate analyzes were performed to determine predictors of major adverse cardiovascular events during hospitalization.Results: From 108 study subjects, 24 (22.2%) subjects experienced major adverse cardiovascular events during hospitalization. The subjects who died were 20 people (83.4%), subjects with arrhythmia were 2 people (8.3%), and those who had stroke were 2 people (8.3 %). Through the ROC curve analysis, we found creatinine cut-off values of ≥1.7 mg / dl (AUC 0.899, 95% CI 0.840- 0.957, p <0.05). Creatinine ≥1.7 mg/dl could predict major adverse cardiovascular events with a sensitivity of 87.5% and specificity of 79.5%. Multivariate analysis showed that creatinine ≥1.7 mg / dl was an independent factor to predict MACEs during hospitalization in this study (OR 18,310, p 0.001) as well as creatinine clearance and heart rate.Conclusion: Creatinine levels at admission is an independent predictor for major adverse cardiovascular events during hospitalization in acute heart failure patients.

scholarly journals Isoflurane-induced acidosis depresses basal and PGE2-stimulated duodenal bicarbonate secretion in mice

2007 ◽  
Vol 292 (3) ◽  
pp. G899-G904 ◽  
Author(s):  
Markus Sjöblom ◽  
Olof Nylander
Keyword(s):  
Base Excess ◽  
Ringer Solution ◽  
Bicarbonate Secretion ◽  
Acid Base Balance ◽  
Acid Base ◽  
In Vivo Experiments ◽  
Arterial Blood ◽  
Blood Ph ◽  
Base Balance

When running in vivo experiments, it is imperative to keep arterial blood pressure and acid-base parameters within the normal physiological range. The aim of this investigation was to explore the consequences of anesthesia-induced acidosis on basal and PGE2-stimulated duodenal bicarbonate secretion. Mice (strain C57bl/6J) were kept anesthetized by a spontaneous inhalation of isoflurane. Mean arterial blood pressure (MAP), arterial acid-base balance, and duodenal mucosal bicarbonate secretion (DMBS) were studied. Two intra-arterial fluid support strategies were used: a standard Ringer solution and an isotonic Na2CO3 solution. Duodenal single perfusion was used, and DMBS was assessed by back titration of the effluent. PGE2 was used to stimulate DMBS. In Ringer solution-infused mice, isoflurane-induced acidosis became worse with time. The blood pH was 7.15–7.21 and the base excess was about −8 mM at the end of experiments. The continuous infusion of Na2CO3 solution completely compensated for the acidosis. The blood pH was 7.36–7.37 and base excess was about 1 mM at the end of the experiment. Basal and PGE2-stimulated DMBS were markedly greater in animals treated with Na2CO3 solution than in those treated with Ringer solution. MAP was slightly higher after Na2CO3 solution infusion than after Ringer solution infusion. We concluded that isoflurane-induced acidosis markedly depresses basal and PGE2-stimulated DMBS as well as the responsiveness to PGE2, effects prevented by a continuous infusion of Na2CO3. When performing in vivo experiments in isoflurane-anesthetized mice, it is recommended to supplement with a Na2CO3 infusion to maintain a normal acid-base balance.

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