Inhalant Anesthesia and Partial Intravenous Anesthesia
Michele Barletta, Jane Quandt, Rachel Reed in Equine Anesthesia and Pain Management, 2023
Factors that reduce the MAC requirement: Hypothermia.Pregnancy.Age (younger animals require less).Severe hypotension.Severe hypoxemia.Metabolic acidosis.The use of analgesics, tranquilizers, sedatives, injectables or local anesthetics, etc.
Clinical biochemistry at the extremes of age
Martin Andrew Crook in Clinical Biochemistry & Metabolic Medicine, 2013
The causes of metabolic acidosis include the following: renal dysfunction,lactic acidosis due to: – tissue hypoxia resulting from poor tissue perfusion caused by hypotension and the low PO2 accompanying asphyxia or sepsis,– some inborn errors of metabolism, such as glucose-6-phosphatase deficiency,inborn errors of amino acid or organic acid metabolism (see Chapter 27).Also consider: congenital heart disease and patent ductus arteriosus,acute blood loss.
Electrolyte and Acid-Base Disturbances
John K. DiBaise, Carol Rees Parrish, Jon S. Thompson in Short Bowel Syndrome Practical Approach to Management, 2017
Metabolic acidosis generally causes nonspecific symptoms; however, it can also lead to diverse multiorgan effects, such as disturbances in endocrinologic, cardiovascular, musculoskeletal, and neurologic function. Metabolic acidosis is associated with hypercatabolism and inhibition of protein synthesis, thus leading to protein–calorie malnutrition [11]. Endocrinological derangements include insulin resistance, impaired glucose tolerance, and alterations in thyroid and parathyroid hormone secretion (see list below) [10]. Cardiovascular effects of metabolic acidosis include increased catecholamine release and resistance, which could present with perturbations in cardiac contractility, arrhythmias, arterial vasodilation, and hypotension [15]. Tachypnea occurs as the body strives to exhale CO2. Finally, chronic metabolic acidosis leads to progressive bone degradation and metabolic bone disease, manifested as osteopenia or osteoporosis.
Serum anion gap at admission predicts all-cause mortality in critically ill patients with cerebral infarction: evidence from the MIMIC-III database
Published in Biomarkers, 2020
Xuefang Liu, Yanlin Feng, Xinyu Zhu, Ying Shi, Manting Lin, Xiaoyan Song, Jiancheng Tu, Enwu Yuan
The serum anion gap (AG) is a mathematical derivation parameter calculated from the difference between cation and anion concentrations (Glasmacher and Stones 2016, Torrente 2017). The equation, AG = [Na+ (mmol/L) + K+ (mmol/L)] − [Cl− (mmol/L) + HCO3− (mmol/L)], was widely used. AG reflects the unmeasured anion concentration. In clinical practice, it has been regarded as a parameter to evaluate the acid-base status and helps to identify various forms of metabolic acidosis. Recent studies have shown that levels of AG were linked to prognosis for coronary artery disease (CAD) (Yang et al. 2017), sepsis (Mohr et al. 2018), acute kidney injury (AKI) (Cheng et al. 2020) and chronic kidney disease (CKD) (Abramowitz et al. 2012). Disturbances in brain metabolism occur, once there are instabilities in cerebral blood flow (CBF), causing shifts in ion concentrations. Research revealed that acid/base balance in the systemic circulation responded rapidly to the ischaemic event in the brain (Martha et al. 2018), suggesting that AG could be a potential biomarker for cerebral infarction.
Hypoglycemia and lactic acidosis outperform King’s College criteria for predicting death or transplant in acetaminophen toxic patients
Published in Clinical Toxicology, 2018
Michael Levine, Samuel J. Stellpflug, Anthony F. Pizon, David A. Peak, Janna Villano, Timothy Wiegand, Christian Dib, Stephen H. Thomas
Hepatic injury was defined as an aspartate transaminase (AST) or an alanine transaminase (ALT) exceeding 1000 IU/L at any point during the index hospitalization. Length of the stay was defined in calendar days, not 24 h periods. This study utilized a composite endpoint of liver transplant or death. The King’s College criteria include a creatinine of 3.4 mg/dL as one of the endpoints. Patients who were started on continuous renal replacement therapy (CRRT) or hemodialysis prior to reach a creatinine of 3.4 mg/dL were considered to have met these criteria, as we assumed that creatinine would likely rise to that level without intervention in that context of acute renal insufficiency. The King’s College “endpoint” for coagulopathy and acidosis were defined as a prothrombin time (PT) > 100 s and a pH of <7.30, respectively. An “elevated” PT or lactic acid was defined as any laboratory value above the hospital’s reference range. Metabolic acidosis was defined as a pH ≤7.30. Hypoglycemia was defined as a venous or capillary glucose <50 mg/dL. In cases of exogenous insulin administration, the hypoglycemic episode must not have been within 3 h of the administration of regular insulin to be considered. For purposes of calculations, any glucose reading of “low” or “less than 5 mg/dL” was interpreted as 0. Similarly, any laboratory parameter that was recorded as “greater than XX” was interpreted as that result (e.g., an AST >60,000 IU/L was interpreted as 60,000 for purposes of calculations).
Approach to the patient presenting with metabolic acidosis
Published in Acta Clinica Belgica, 2019
Jill Vanmassenhove, Norbert Lameire
This article covers the following topics regarding metabolic acidosis: How to define and diagnose metabolic acidosis.How to differentiate high anion gap metabolic acidosis vs non anion gap metabolic acidosis and how to recognize mixed acid base disturbances.How to be aware of the potential caveats of the several diagnostic tools.