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Epinephrine And Metabolic Acidosis

Risk Factors Of Post-operative Severe Hyperlactatemia And Lactic Acidosis Following Laparoscopic Resection For Pheochromocytoma

Risk Factors Of Post-operative Severe Hyperlactatemia And Lactic Acidosis Following Laparoscopic Resection For Pheochromocytoma

Risk factors of post-operative severe hyperlactatemia and lactic acidosis following laparoscopic resection for pheochromocytoma Scientific Reportsvolume7, Articlenumber:403 (2017) Severe hyperlactatemia (SH)/lactic acidosis (LA) after laparoscopic resection of pheochromocytoma is an infrequently reported complication. The study aims to investigate the incidence of this complication and to determine the clinical risk factors. Patients who underwent laparoscopic resection for pheochromocytoma between 2011 and 2014 at Peking Union Medical College Hospital were enrolled. LA was defined as pH < 7.35, bicarbonate <20 mmol/L, and serum lactate 5 mmol/L; SH as lactate 5 mmol/L; and moderate hyperlactatemia (MH) as lactate 2.55.0 mmol/L without evidence of acidosis (pH > 7.35 and/or bicarbonate >20 mmol/L). Data concerning patient demographics, clinical history, and laboratory results were collected and statistical analyses were performed. Out of 145 patients, 59 (40.7%) developed post-operative hyperlactatemia. The incidences of MH and SH/LA were 25.5% and 15.2%, respectively. Multivariate analysis demonstrated that body mass index (BMI) (odds ratio [OR], 1.204; 95% confidence interval [CI], 1.0161.426), 24-hour urine epinephrine concentration (OR, 1.012; 95% CI, 1.0021.022), and tumor size (OR, 1.571; 95% CI, 1.1022.240) were independent predictors of post-operative SH/LA. The data show that post-operative SH/LA is not a rare complication after pheochromocytoma resection and may be closely associated with higher BMI, larger tumor size, and higher levels of urine epinephrine. Pheochromocytoma is a rare, catecholamine-producing neuroendocrine tumor originating from chromaffin cells of the adrenal medulla 1 . Cardinal manifestations of pheochromocytoma include episodic hypertens Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

Metabolic acidosis is a condition that occurs when the body produces excessive quantities of acid or when the kidneys are not removing enough acid from the body. If unchecked, metabolic acidosis leads to acidemia, i.e., blood pH is low (less than 7.35) due to increased production of hydrogen ions by the body or the inability of the body to form bicarbonate (HCO3−) in the kidney. Its causes are diverse, and its consequences can be serious, including coma and death. Together with respiratory acidosis, it is one of the two general causes of acidemia. Terminology : Acidosis refers to a process that causes a low pH in blood and tissues. Acidemia refers specifically to a low pH in the blood. In most cases, acidosis occurs first for reasons explained below. Free hydrogen ions then diffuse into the blood, lowering the pH. Arterial blood gas analysis detects acidemia (pH lower than 7.35). When acidemia is present, acidosis is presumed. Signs and symptoms[edit] Symptoms are not specific, and diagnosis can be difficult unless the patient presents with clear indications for arterial blood gas sampling. Symptoms may include chest pain, palpitations, headache, altered mental status such as severe anxiety due to hypoxia, decreased visual acuity, nausea, vomiting, abdominal pain, altered appetite and weight gain, muscle weakness, bone pain, and joint pain. Those in metabolic acidosis may exhibit deep, rapid breathing called Kussmaul respirations which is classically associated with diabetic ketoacidosis. Rapid deep breaths increase the amount of carbon dioxide exhaled, thus lowering the serum carbon dioxide levels, resulting in some degree of compensation. Overcompensation via respiratory alkalosis to form an alkalemia does not occur. Extreme acidemia leads to neurological and cardia Continue reading >>

Influence Of Respiratory And Metabolic Acidosis On Epinephrine-inotropic Effect In Isolated Guinea Pig Atria

Influence Of Respiratory And Metabolic Acidosis On Epinephrine-inotropic Effect In Isolated Guinea Pig Atria

, Volume 347, Issue4 , pp 297307 | Cite as Influence of respiratory and metabolic acidosis on epinephrine-inotropic effect in isolated guinea pig atria The inotropic effect of calcium and of epinephrine was examined in an isolated guinea pig atrial preparation during a simulated respiratory and metabolic acidosis. Special care was taken to avoid alterations in ionized calcium which usually accompany most forms of acidosis. In acidosis the inotropic response to epinephrine is depressed to a greater extent than the response to calcium, independent of respiratory or metabolic origin. It is concluded that the overall depression of the inotropic response to epinephrine is produced by two mechanisms: firstly, by an unspecific depression of contractility caused by a direct action of hydrogen ions on the heart, and secondly, by a specific depression of the inotropic epinephrine-effector mechanism. The dose-ratios for production of identical epinephrine-specific responses as compared with those at pH 7.5 were calculated. At a pH of 6.9, the doseratio was 1.5 to 2.5; at a pH of 6.6, it was in the range of 4 to 4.6. In conclusion these observations are in accordance with a concept that acute acidosis affects myocardial function in intact animals bydirect andindirect effects in at least four ways: by a depression of contractility, by a diminished responsiveness of the epinephrineinotropic response mechanism, by an increase in the concentration of ionized calcium, and by a release of catecholamines. AcidosispHCardiac ContractilityEpinephrineCalcium This is a preview of subscription content, log in to check access Unable to display preview. Download preview PDF. Andersen, M. N., Border, J. R., Mouritzen, Ch. V.: Acidosis, catecholamines and cardiovascular dynamics: When does acidosi Continue reading >>

Lactate And Lactic Acidosis

Lactate And Lactic Acidosis

The integrity and function of all cells depend on an adequate supply of oxygen. Severe acute illness is frequently associated with inadequate tissue perfusion and/or reduced amount of oxygen in blood (hypoxemia) leading to tissue hypoxia. If not reversed, tissue hypoxia can rapidly progress to multiorgan failure and death. For this reason a major imperative of critical care is to monitor tissue oxygenation so that timely intervention directed at restoring an adequate supply of oxygen can be implemented. Measurement of blood lactate concentration has traditionally been used to monitor tissue oxygenation, a utility based on the wisdom gleaned over 50 years ago that cells deprived of adequate oxygen produce excessive quantities of lactate. The real-time monitoring of blood lactate concentration necessary in a critical care setting was only made possible by the development of electrode-based lactate biosensors around a decade ago. These biosensors are now incorporated into modern blood gas analyzers and other point-of-care analytical instruments, allowing lactate measurement by non-laboratory staff on a drop (100 L) of blood within a minute or two. Whilst blood lactate concentration is invariably raised in those with significant tissue hypoxia, it can also be raised in a number of conditions not associated with tissue hypoxia. Very often patients with raised blood lactate concentration (hyperlactatemia) also have a reduced blood pH (acidosis). The combination of hyperlactatemia and acidosis is called lactic acidosis. This is the most common cause of metabolic acidosis. The focus of this article is the causes and clinical significance of hyperlactatemia and lactic acidosis. The article begins with a brief overview of normal lactate metabolism. Normal lactate production and Continue reading >>

Prime Pubmed | Influence Of Respiratory Acidosis On Ecg And Pressor Responses To Epinephrine, Norepinephrine And Metaramino

Prime Pubmed | Influence Of Respiratory Acidosis On Ecg And Pressor Responses To Epinephrine, Norepinephrine And Metaramino

HOULE, D B., et al. "Influence of Respiratory Acidosis On ECG and Pressor Responses to Epinephrine, Norepinephrine and Metaraminol." Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.), vol. 94, no. 3, 1957, pp. 561-4. HOULE DB, WEIL MH, BROWN EB, et al. Influence of respiratory acidosis on ECG and pressor responses to epinephrine, norepinephrine and metaraminol. Proc Soc Exp Biol Med. 1957;94(3):561-4. HOULE, D. B., WEIL, M. H., BROWN, E. B., & CAMPBELL, G. S. (1957). Influence of respiratory acidosis on ECG and pressor responses to epinephrine, norepinephrine and metaraminol. Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.), 94(3), pp. 561-4. HOULE DB, et al. Influence of Respiratory Acidosis On ECG and Pressor Responses to Epinephrine, Norepinephrine and Metaraminol. Proc Soc Exp Biol Med. 1957;94(3):561-4. PubMed PMID: 13408326. * Article titles in AMA citation format should be in sentence-case TY - JOURT1 - Influence of respiratory acidosis on ECG and pressor responses to epinephrine, norepinephrine and metaraminol.AU - HOULE,D B,AU - WEIL,M H,AU - BROWN,E B,JrAU - CAMPBELL,G S,PY - 1957/3/1/pubmedPY - 1957/3/1/medlinePY - 1957/3/1/entrezKW - ACIDOSIS/experimentalKW - ARTERENOL/effectsKW - ELECTROCARDIOGRAPHY/effect of drugs onKW - EPINEPHRINE/effectsKW - SYMPATHOMIMETICS/effectsSP - 561EP - 4JF - Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.)JO - Proc. Soc. Exp. Biol. Med.VL - 94IS - 3SN - 0037-9727UR - - PRIMEDP - Unbound MedicineER - Continue reading >>

Lactic Acidosis

Lactic Acidosis

Patient professional reference Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use. You may find one of our health articles more useful. Description Lactic acidosis is a form of metabolic acidosis due to the inadequate clearance of lactic acid from the blood. Lactate is a byproduct of anaerobic respiration and is normally cleared from the blood by the liver, kidney and skeletal muscle. Lactic acidosis occurs when the body's buffering systems are overloaded and tends to cause a pH of ≤7.25 with plasma lactate ≥5 mmol/L. It is usually caused by a state of tissue hypoperfusion and/or hypoxia. This causes pyruvic acid to be preferentially converted to lactate during anaerobic respiration. Hyperlactataemia is defined as plasma lactate >2 mmol/L. Classification Cohen and Woods devised the following system in 1976 and it is still widely used:[1] Type A: lactic acidosis occurs with clinical evidence of tissue hypoperfusion or hypoxia. Type B: lactic acidosis occurs without clinical evidence of tissue hypoperfusion or hypoxia. It is further subdivided into: Type B1: due to underlying disease. Type B2: due to effects of drugs or toxins. Type B3: due to inborn or acquired errors of metabolism. Epidemiology The prevalence is very difficult to estimate, as it occurs in critically ill patients, who are not often suitable subjects for research. It is certainly a common occurrence in patients in high-dependency areas of hospitals.[2] The incidence of symptomatic hyperlactataemia appears to be rising as a consequence of the use of antiretroviral therapy to treat HIV infection. It appears to increase in those taking stavudine (d4T) regimens.[3] Causes of lactic acid Continue reading >>

Lactic Acidosis: Background, Etiology, Epidemiology

Lactic Acidosis: Background, Etiology, Epidemiology

Author: Kyle J Gunnerson, MD; Chief Editor: Michael R Pinsky, MD, CM, Dr(HC), FCCP, MCCM more... In basic terms, lactic acid is the normal endpoint of the anaerobic breakdown of glucose in the tissues. The lactate exits the cells and is transported to the liver, where it is oxidized back to pyruvate and ultimately converted to glucose via the Cori cycle. In the setting of decreased tissue oxygenation, lactic acid is produced as the anaerobic cycle is utilized for energy production. With a persistent oxygen debt and overwhelming of the body's buffering abilities (whether from chronic dysfunction or excessive production), lactic acidosis ensues. [ 1 , 2 ] (See Etiology.) Lactic acid exists in 2 optical isomeric forms, L-lactate and D-lactate. L-lactate is the most commonly measured level, as it is the only form produced in human metabolism. Its excess represents increased anaerobic metabolism due to tissue hypoperfusion. (See Workup.) D-lactate is a byproduct of bacterial metabolism and may accumulate in patients with short-gut syndrome or in those with a history of gastric bypass or small-bowel resection. [ 3 ] By the turn of the 20th century, many physicians recognized that patients who are critically ill could exhibit metabolic acidosis unaccompanied by elevation of ketones or other measurable anions. In 1925, Clausen identified the accumulation of lactic acid in blood as a cause of acid-base disorder. Several decades later, Huckabee's seminal work firmly established that lactic acidosis frequently accompanies severe illnesses and that tissue hypoperfusion underlies the pathogenesis. In their classic 1976 monograph, Cohen and Woods classified the causes of lactic acidosis according to the presence or absence of adequate tissue oxygenation. (See Presentationand Differe Continue reading >>

Lactic Acidosis In Pheochromocytoma

Lactic Acidosis In Pheochromocytoma

MICHAEL BORNEMANN, M.D.; SUSAN C. HILL, M.D.; GERALD S. KIDD II, M.D. Article, Author, and Disclosure Information Author, Article, and Disclosure Information Requests for reprints should be addressed to COL Michael Bornemann, MC; Box 700, Tripler Army Medical Center; Honolulu, HI 96859-5000. Lactic acidosis is not generally recognized as a complication of pheochromocytoma. We review three prior case reports of lactic acidosis in patients with pheochromocytoma and one report of lactic acidosis following epinephrine poisoning and describe an additional case report of a patient with lactic acidosis in whom an unsuspected pheochromocytoma was discovered at autopsy. The pathophysiology of lactic acidosis in pheochromocytoma is related to the effect of catecholamines on intermediary metabolism and the peripheral circulation. Although the possible development of lactic acidosis in persons with pheochromocytoma is underappreciated, the differential diagnosis of lactic acidosis should include this tumor. Continue reading >>

Understanding Lactate In Sepsis & Using It To Our Advantage

Understanding Lactate In Sepsis & Using It To Our Advantage

You are here: Home / PULMCrit / Understanding lactate in sepsis & Using it to our advantage Understanding lactate in sepsis & Using it to our advantage Once upon a time a 60-year-old man was transferred from the oncology ward to the ICU for treatment of neutropenic septic shock. Over the course of the morning he started rigoring and dropped his blood pressure from 140/70 to 70/40 within a few hours, refractory to four liters of crystalloid. In the ICU his blood pressure didn't improve with vasopressin and norepinephrine titrated to 40 mcg/min. His MAP remained in the high 40s, he was mottled up to the knees, and he wasn't making any urine. Echocardiography suggested a moderately reduced left ventricle ejection fraction, not terrible but perhaps inadequate for his current condition. Dobutamine has usually been our choice of inotrope in septic shock. However, this patient was so unstable that we chose epinephrine instead. On an epinephrine infusion titrated to 10 mcg/min his blood pressure improved immediately, his mottling disappeared, and he started having excellent urine output. However, his lactate level began to rise. He was improving clinically, so we suspected that the lactate was due to the epinephrine infusion. We continued the epinephrine, he continued to improve, and his lactate continued to rise. His lactate level increased as high as 15 mM, at which point the epinephrine infusion was being titrated off anyway. Once the epinephrine was stopped his lactate rapidly normalized. He continued to improve briskly. By the next morning he was off vasopressors and ready for transfer back to the ward. This was eye-opening. It seemed that the epinephrine infusion was the pivotal intervention which helped him stabilize. However, while clinically improving him, the epineph Continue reading >>

Bench-to-bedside Review: Is There A Place For Epinephrine In Septic Shock?

Bench-to-bedside Review: Is There A Place For Epinephrine In Septic Shock?

Bench-to-bedside review: Is there a place for epinephrine in septic shock? The use of epinephrine in septic shock remains controversial. Nevertheless, epinephrine is widely used around the world and the reported morbidity and mortality rates with it are no different from those observed with other vasopressors. In volunteers, epinephrine increases heart rate, mean arterial pressure and cardiac output. Epinephrine also induces hyperglycemia and hyperlactatemia. In hyperkinetic septic shock, epinephrine consistently increases arterial pressure and cardiac output in a dose dependent manner. Epinephrine transiently increases lactate levels through an increase in aerobic glycolysis. Epinephrine has no effect on splanchnic circulation in dopamine-sensitive septic shock. On the other hand, in dopamine-resistant septic shock, epinephrine has no effect on tonometric parameters but decreases fractional splanchnic blood flow with an increase in the gradient of mixed venous oxygen saturation (SVO2) and hepatic venous oxygen saturation (SHO2). In conclusion, epinephrine has predictable effects on systemic hemodynamics and is as efficient as norepinephrine in correcting hemodynamic disturbances of septic shock. Moreover, epinephrine is cheaper than other commonly used catecholamine regimens in septic shock. The clinical impact of the transient hyperlactatemia and of the splanchnic effects are not established. EpinephrineSeptic ShockMean Arterial PressureDobutamineAerobic Glycolysis Early goal directed therapy [ 1 ] is now considered as a gold standard in the early phase of septic shock. Fluid therapy and vasoactive therapy may be immediately required in order to maintain acceptable blood pressure levels. Invasive or non-invasive assessment of hemodynamic status, although essential to Continue reading >>

Effect Of Severe Acidosis On Vasoactive Effects Of Epinephrine And Norepinephrine In Human Distal Mammary Artery - Sciencedirect

Effect Of Severe Acidosis On Vasoactive Effects Of Epinephrine And Norepinephrine In Human Distal Mammary Artery - Sciencedirect

Volume 147, Issue 5 , May 2014, Pages 1698-1705 Acidosis is a very common pathologic process in perioperative management. However, how to correct severe acidosis to improve the efficacy of vasoconstrictors in hemodynamically unstable patients is still debated. The present study investigated whether severe extracellular acidosis influences the vasoactive properties of vasoconstrictors on human isolated arteries. Segments of intact distal internal mammary arteries were removed from 41 patients undergoing artery bypass grafting. The arterial rings were washed in Krebs-Henseleit solution and suspended in an organ bath. The rings were set at a pretension equivalent of 100 mm Hg, and the relaxation response to 10 M acetylcholine was verified. Concentrationresponse curves for epinephrine, norepinephrine, methoxamine (1A/D-adrenoceptor agonist), phenylephrine (equipotent agonist of 1A/B-adrenoceptors), and clonidine (2-adrenoceptor agonist) were achieved under control conditions (pH 7.40) and under acidic conditions by substitution of the Krebs-Henseleit solution with a modified solution. Decreasing the pH from 7.40 to 7.20, 7.0, or 6.80 did not significantly alter the potency and efficacy of epinephrine and norepinephrine, although the standardized effect size was sometimes large. Severe acidosis (pH6.80) did not significantly change the potency and efficacy of phenylephrine and clonidine, although it increased the efficacy and potency of methoxamine (P<.001 and P=.04 vs paired control conditions, respectively). Extracellular acidosis did not impair the vasoactive properties of epinephrine and norepinephrine in human medium-size arteries until pH 6.80. The results of the present study also suggest that acidosis might potentiate arterial responsiveness to vasoconstrictors, mos Continue reading >>

Lactic Acidosis And Insulin Resistance Associated With Epinephrine Administration In A Patient With Noninsulin-dependent Diabetes Mellitus

Lactic Acidosis And Insulin Resistance Associated With Epinephrine Administration In A Patient With Noninsulin-dependent Diabetes Mellitus

Lactic Acidosis and Insulin Resistance Associated With Epinephrine Administration in a Patient With NonInsulin-Dependent Diabetes Mellitus Epinephrine raises plasma lactate concentrations when infused intravenously in normal subjects. We studied a patient with noninsulin-dependent diabetes mellitus who developed lactic acidosis and marked insulin resistance when treated with epinephrine after open heart surgery. Caruso M, Orszulak TA, Miles JM. Lactic Acidosis and Insulin Resistance Associated With Epinephrine Administration in a Patient With NonInsulin-Dependent Diabetes Mellitus. Arch Intern Med. 1987;147(8):14221424. doi:10.1001/archinte.1987.00370080058013 New! JAMA Network Open is now accepting submissions. Learn more. Customize your JAMA Network experience by selecting one or more topics from the list below. Challenges in Clinical Electrocardiography Clinical Implications of Basic Neuroscience Health Care Economics, Insurance, Payment Scientific Discovery and the Future of Medicine United States Preventive Services Task Force JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Facial Plastic Surgery JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA OtolaryngologyHead & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) AMA Manual of Style Art and Images in Psychiatry Breast Cancer Screening Guidelines Colorectal Screening Guidelines Declaration of Helsinki Depression Screening Guidelines Evidence-Based Medicine: An Oral History Fishbein Fellowship Genomics and Precision Health Health Disparities Hypertension Guidelines JAMA Network Audio JAMA Network Conferences Med Men Medical Education Opioid Management Guidelines Peer Review Congress Research Ethics Sepsis and Septic Shock Continue reading >>

Lactic Acidosis

Lactic Acidosis

hyperlactaemia: a level from 2 to 5 mmol/L normal production is 20 mmols/kg/day, enters the circulation and undergoes hepatic and renal metabolism (Cori cycle) all tissues can produce lactate under anaerobic conditions lactic acid has a pK value of about 4 so it is fully dissociated into lactate and H+ at body pH (i.e. it is a strong ion) during heavy exercise, the skeletal muscles contribute most of the much increased circulating lactate during pregnancy, the placenta is an important producer of lactate (can pass to fetus as well) major source in sepsis and ARDS is the lung lactate is metabolised predominantly in the liver (60%) and kidney (30%) the heart can also use lactate for ATP production 50% is converted into glucose (gluconeogenesis) and 50% into CO2 and water (citric acid cycle) this results in no net acid accumulation but requires aerobic metabolism the small amount of lactate that is renally filtered (180mmol/day) is fully reabsorbed (ii) impaired hepatic metabolism of lactate (large capacity to clear) clinically there is often a combination of the above to produce a persistent lactic acidosis anaerobic muscular activity (sprinting, generalised convulsions) tissue hypoperfusion (shock, cardiac arrest, regional hypoperfusion -> mesenteric ischaemia) reduced tissue oxygen delivery (hypoxaemia, anaemia) or utilisation (CO poisoning) Type B No Evidence of Inadequate Tissue Oxygen Delivery once documented the cause must be found and treated appropriately D lactate is isomer of lactate produced by intestinal bacterial and not by humans it is not detected on standard lactate assays a bed side test may be able to be developed to help with diagnosis of mesenteric ischaemia venous samples are equivalent to arterial in clinical practice do not need to take off tourniq Continue reading >>

Comparison Of Equipressor Doses Of Norepinephrine, Epinephrine, And Phenylephrine On Septic Myocardial Dysfunction | Anesthesiology | Asa Publications

Comparison Of Equipressor Doses Of Norepinephrine, Epinephrine, And Phenylephrine On Septic Myocardial Dysfunction | Anesthesiology | Asa Publications

Comparison of Equipressor Doses of Norepinephrine, Epinephrine, and Phenylephrine on Septic Myocardial Dysfunction *Doctoral Student, Groupe Choc Contrat Avenir Inserm, U961, Faculte de Medecine, Nancy Universite, Nancy, France; Service Ranimation Mdicale, CHU Nancy-Brabois, Vandoeuvre-les-Nancy, France. Masters Degree Student, Groupe Choc Contrat Avenir Inserm, U961, Faculte de Medecine, Nancy Universite. Researcher, Service Mdecine Nuclaire et Nancyclotep, CHU Nancy-Brabois. Professor, Service Mdecine Nuclaire et Nancyclotep, CHU Nancy-Brabois. Professor, Groupe Choc Contrat Avenir Inserm, U961, Faculte de Medecine, Nancy Universite; Service Ranimation Mdicale, CHU Nancy-Brabois. Critical Care Medicine / Cardiovascular Anesthesia / Critical Care / Gastrointestinal and Hepatic Systems / Technology / Equipment / Monitoring Comparison of Equipressor Doses of Norepinephrine, Epinephrine, and Phenylephrine on Septic Myocardial Dysfunction Anesthesiology 5 2012, Vol.116, 1083-1091. doi: Anesthesiology 5 2012, Vol.116, 1083-1091. doi: Comparison of Equipressor Doses of Norepinephrine, Epinephrine, and Phenylephrine on Septic Myocardial Dysfunction You will receive an email whenever this article is corrected, updated, or cited in the literature. You can manage this and all other alerts in My Account Myocardial dysfunction occurs during septic shock Norepinephrine and epinephrine improved global hemodynamics and myocardial function during experimental septic shock but epinephrine increased myocardial oxygen consumption, whereas phenylephrine decreased ventricular performance CARDIOVASCULAR dysfunction is a major contributor in septic shock-induced mortality. 1 Septic shock is characterized by both an alteration in vascular tone 2 and a systolic and diastolic biventricular dys Continue reading >>

Lactic Acidosis | Md Nexus

Lactic Acidosis | Md Nexus

Cohen-Woods Classification of Lactic Acidosis Type A: due to decreased perfusion or oxygenation However, these may cause type A lactic acidosis in some cases Type B2: due to medication or intoxication Type B3: due to inborn error of metabolism Mitochondrial Encephalomyopathy + Lactic Acidosis + Stroke-Like Episodes (MELAS) Tumors May Benefit from Acidosis: acidic microenvironment is critical for tumorigenesis, angiogenesis, and metastasis Physiology: decreased lactate clearance (with severe liver metastases)+ increased glycolytic activity of tumor (Warburg Effect) + tissue tumor hypoxia Treatment: bicarbonate administration may increase lactic acid production Tumor Lysis Syndrome (see Tumor Lysis Syndrome , [[Tumor Lysis Syndrome]]) Anaphylaxis (see Anaphylaxis , [[Anaphylaxis]]) Physiology: decreased oxygen delivery to tissues + epinephrine-induced 2-adrenergic receptor stimulation Congestive Heart Failure (CHF)/Cardiogenic Shock (see Congestive Heart Failure , [[Congestive Heart Failure]] and Cardiogenic Shock , [[Cardiogenic Shock]]): common etiology of lactic acidosis Physiology: decreased oxygen delivery to tissues + epinephrine-induced 2-adrenergic receptor stimulation Hemorrhagic Shock (see Hemorrhagic Shock , [[Hemorrhagic Shock]]): common etiology of lactic acidosis Physiology: decreased oxygen delivery to tissues + epinephrine-induced 2-adrenergic receptor stimulation Hypovolemic Shock (see Hypovolemic Shock , [[Hypovolemic Shock]]): common etiology of lactic acidosis Physiology: decreased oxygen delivery to tissues + epinephrine-induced 2-adrenergic receptor stimulation Sepsis (see Sepsis , [[Sepsis]]): common etiology of lactic acidosis Physiology: decreased lactate clearance (likely due to inhibition of pyruvate dehydrogenase + epinephrine-induced 2-adrene Continue reading >>

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