Acid-base Balance Understanding Is Critical To Treat Patients
Acid-Base Balance Understanding is Critical to Treat Patients By James Tanis, MD, NRP dvxxtrvscafftzcatwdtzeytyyc , Joseph E. DiCorpo, BSC, MMSc, PA , Daniel Friedman, DO, EMT-P , Mark Merlin, DO, EMT-P, FACEP Every critically ill patient we encounter in the field will have an acid-base derangement; therefore, an understanding of acid-base balance is critical to properly treat patients. First, its important you appreciate that every chemical reaction that occurs in the human body is regulated or substantially influenced by the hydrogen ion (H+) concentration in the surrounding tissue, from the way hemoglobin picks up and delivers oxygen to the tissues to the way that sugar, protein and fat are metabolized by the body. The regulation of hydrogen ions, which we measure as pH, is what acid-base balance refers to. The bodys concentration of hydrogen ions must be maintained within a strict range for optimal cellular function, and even a small deviation can significantly affect a patient.1Its a complex balancing act that you can affect based upon your assessment of the patients vital signs. An acid has a pH below 7.0 and an increased concentration of hydrogen ions, while an alkaline has a pH above 7.0 and a decreased concentration of hydrogen ions. The body maintains a slightly alkaline pH range of 7.35 to 7.45. Therefore, a pH higher than this range is in a state of alkalosis and a pH below this range is considered to be acidosis. A pH of 6.9 on the acid side and 7.8 on the alkaline side are considered non-compatible with life.1(See Table 1, above) An excess of acid is usually produced during the normal process of metabolism, so the body must rid itself of this excess acid to maintain the acid-base balance and keep a normal hydrogen ion concentration. Three defense mechanis Continue reading >>
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Sepsis And Septic Shock
(Video) How to do Cardiopulmonary Resuscitation (CPR) in Adults By Paul M. Maggio, MD, MBA, Associate Professor of Surgery, Associate Chief Medical Officer, and Co-Director, Critical Care Medicine, Stanford University Medical Center Sepsis is a clinical syndrome of life-threatening organ dysfunction caused by a dysregulated response to infection. In septic shock, there is critical reduction in tissue perfusion; acute failure of multiple organs, including the lungs, kidneys, and liver, can occur. Common causes in immunocompetent patients include many different species of gram-positive and gram-negative bacteria. Immunocompromised patients may have uncommon bacterial or fungal species as a cause. Signs include fever, hypotension, oliguria, and confusion. Diagnosis is primarily clinical combined with culture results showing infection; early recognition and treatment is critical. Treatment is aggressive fluid resuscitation, antibiotics, surgical excision of infected or necrotic tissue and drainage of pus, and supportive care. Sepsis represents a spectrum of disease with mortality risk ranging from moderate (eg, 10%) to substantial (eg, > 40%) depending on various pathogen and host factors along with the timeliness of recognition and provision of appropriate treatment. Septic shock is a subset of sepsis with significantly increased mortality due to severe abnormalities of circulation and/or cellular metabolism. Septic shock involves persistent hypotension (defined as the need for vasopressors to maintain mean arterial pressure 65 mm Hg, and a serum lactate level > 18 mg/dL [2 mmol/L] despite adequate volume resuscitation [1] ). The concept of the systemic inflammatory response syndrome (SIRS), defined by certain abnormalities of vital signs and laboratory results, has long Continue reading >>
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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 >>
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Metabolic 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. See also separate Lactic Acidosis and Arterial Blood Gases - Indications and Interpretations articles. Description Metabolic acidosis is defined as an arterial blood pH <7.35 with plasma bicarbonate <22 mmol/L. Respiratory compensation occurs normally immediately, unless there is respiratory pathology. Pure metabolic acidosis is a term used to describe when there is not another primary acid-base derangement - ie there is not a mixed acid-base disorder. Compensation may be partial (very early in time course, limited by other acid-base derangements, or the acidosis exceeds the maximum compensation possible) or full. The Winter formula can be helpful here - the formula allows calculation of the expected compensating pCO2: If the measured pCO2 is >expected pCO2 then additional respiratory acidosis may also be present. It is important to remember that metabolic acidosis is not a diagnosis; rather, it is a metabolic derangement that indicates underlying disease(s) as a cause. Determination of the underlying cause is the key to correcting the acidosis and administering appropriate therapy[1]. Epidemiology It is relatively common, particularly among acutely unwell/critical care patients. There are no reliable figures for its overall incidence or prevalence in the population at large. Causes of metabolic acidosis There are many causes. They can be classified according to their pathophysiological origin, as below. The table is not exhaustive but lists those that are most common or clinically important to detect. Increased acid Continue reading >>
Phenotyping Community-acquired Pneumonia According To The Presence Of Acute Respiratory Failure And Severe Sepsis
Phenotyping community-acquired pneumonia according to the presence of acute respiratory failure and severe sepsis Aliberti et al.; licensee BioMed Central Ltd.2014 Acute respiratory failure (ARF) and severe sepsis (SS) are possible complications in patients with community-acquired pneumonia (CAP). The aim of the study was to evaluate prevalence, characteristics, risk factors and impact on mortality of hospitalized patients with CAP according to the presence of ARF and SS on admission. This was a multicenter, observational, prospective study of consecutive CAP patients admitted to three hospitals in Italy, Spain, and Scotland between 2008 and 2010. Three groups of patients were identified: those with neither ARF nor SS (Group A), those with only ARF (Group B) and those with both ARF and SS (Group C) on admission. Among the 2,145 patients enrolled, 45% belonged to Group A, 36% to Group B and 20% to Group C. Patients in Group C were more severe than patients in Group B. Isolated ARF was correlated with age (p < 0.001), COPD (p < 0.001) and multilobar infiltrates (p < 0.001). The contemporary occurrence of ARF and SS was associated with age (p = 0.002), residency in nursing home (p = 0.007), COPD (p < 0.001), multilobar involvement (p < 0.001) and renal disease (p < 0.001). 4.2% of patients in Group A died, 9.3% in Group B and 26% in Group C, p < 0.001. After adjustment, the presence of only ARF had an OR for in-hospital mortality of 1.85 (p = 0.011) and the presence of both ARF and SS had an OR of 6.32 (p < 0.001). The identification of ARF and SS on hospital admission can help physicians in classifying CAP patients into three different clinical phenotypes. PneumoniaSepsisSevere sepsisAcute respiratory failureARDSCAPCommunity-acquired pneumoniaMortalityOxygenation Communi Continue reading >>
Hypercapnia And Acidosis In Sepsis:a Double-edged Sword? | Anesthesiology | Asa Publications
The effects of hypercapnia in sepsis may be a function of the hypercapnia or the acidosis per se . As discussed, the effects of HCA on the immune response seem to be predominantly a function of the acidosis, rather than the hypercapnia per se , but the fact that the acidosis is hypercapnic rather than metabolic is of importance. The potential exists for hypercapnia to exert direct effects, independent of pH changes. A specific example is the binding of carbon dioxide to free amine groups on proteins to form carbamates, which can alter certain protein behavior or activity. The classic example is hemoglobin in which carbamino formation alters HbO2affinity. In addition, the potential for buffering of a HCA to modulate its effects in sepsis is also of importance. Buffered hypercapnia, that is, hypercapnia in the presence of normal pH, seems to worsen lung injury induced by intrapulmonary bacterial instillation. 36 To avoid the confounding effects of the administration of exogenous acid and/or alkali, animals were first exposed to environmental hypercapnia until renal buffering had restored pH to the normal range. These animals were then subjected to intrapulmonary inoculation of E. coli , and the severity of lung injury produced during a 6-h period was compared with that seen in similarly inoculated animals exposed to normocapnia. Buffered hypercapnia significantly increased E. coli -induced lung injury when compared with normocapnic controls, as assessed by arterial oxygenation, lung compliance, proinflammatory pulmonary cytokine concentrations, and measurements of structural lung damage. Of interest, buffered hypercapnia did not reduce the phagocytic capacity of neutrophils and did not increase lung bacterial load. These findings contrast markedly with the protective eff Continue reading >>
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Metabolic Acidosis: Pathophysiology, Diagnosis And Management: Management Of Metabolic Acidosis
Recommendations for the treatment of acute metabolic acidosis Gunnerson, K. J., Saul, M., He, S. & Kellum, J. Lactate versus non-lactate metabolic acidosis: a retrospective outcome evaluation of critically ill patients. Crit. Care Med. 10, R22-R32 (2006). Eustace, J. A., Astor, B., Muntner, P M., Ikizler, T. A. & Coresh, J. Prevalence of acidosis and inflammation and their association with low serum albumin in chronic kidney disease. Kidney Int. 65, 1031-1040 (2004). Kraut, J. A. & Kurtz, I. Metabolic acidosis of CKD: diagnosis, clinical characteristics, and treatment. Am. J. Kidney Dis. 45, 978-993 (2005). Kalantar-Zadeh, K., Mehrotra, R., Fouque, D. & Kopple, J. D. Metabolic acidosis and malnutrition-inflammation complex syndrome in chronic renal failure. Semin. Dial. 17, 455-465 (2004). Kraut, J. A. & Kurtz, I. Controversies in the treatment of acute metabolic acidosis. NephSAP 5, 1-9 (2006). Cohen, R. M., Feldman, G. M. & Fernandez, P C. The balance of acid base and charge in health and disease. Kidney Int. 52, 287-293 (1997). Rodriguez-Soriano, J. & Vallo, A. Renal tubular acidosis. Pediatr. Nephrol. 4, 268-275 (1990). Wagner, C. A., Devuyst, O., Bourgeois, S. & Mohebbi, N. Regulated acid-base transport in the collecting duct. Pflugers Arch. 458, 137-156 (2009). Boron, W. F. Acid base transport by the renal proximal tubule. J. Am. Soc. Nephrol. 17, 2368-2382 (2006). Igarashi, T., Sekine, T. & Watanabe, H. Molecular basis of proximal renal tubular acidosis. J. Nephrol. 15, S135-S141 (2002). Sly, W. S., Sato, S. & Zhu, X. L. Evaluation of carbonic anhydrase isozymes in disorders involving osteopetrosis and/or renal tubular acidosis. Clin. Biochem. 24, 311-318 (1991). Dinour, D. et al. A novel missense mutation in the sodium bicarbonate cotransporter (NBCe1/ SLC4A4) Continue reading >>
Sepsis - Wikipedia
For the genus of flies of this name, see Sepsis (genus) . Blood culture bottles: orange label for anaerobes , green label for aerobes , and yellow label for blood samples from children Sepsis is a life-threatening condition that arises when the body's response to infection causes injury to its own tissues and organs. [8] Common signs and symptoms include fever , increased heart rate , increased breathing rate , and confusion . [1] There also may be symptoms related to a specific infection, such as a cough with pneumonia , or painful urination with a kidney infection . [2] In the very young, old, and people with a weakened immune system , there may be no symptoms of a specific infection and the body temperature may be low or normal, rather than high . [2] Severe sepsis is sepsis causing poor organ function or insufficient blood flow. [9] Insufficient blood flow may be evident by low blood pressure , high blood lactate , or low urine output . [9] Septic shock is low blood pressure due to sepsis that does not improve after reasonable amounts of intravenous fluids are given. [9] Sepsis is caused by an immune response triggered by an infection. [2] [3] Most commonly, the infection is bacterial , but it may also be from fungi , viruses , or parasites . [2] Common locations for the primary infection include lungs, brain, urinary tract , skin, and abdominal organs . [2] Risk factors include young or old age, a weakened immune system from conditions such as cancer or diabetes , major trauma , or burns . [1] An older method of diagnosis was based on meeting at least two systemic inflammatory response syndrome (SIRS) criteria due to a presumed infection. [2] In 2016, SIRS was replaced with qSOFA which is two of the following three: increased breathing rate, change in level of con Continue reading >>
Causes Of Lactic Acidosis
INTRODUCTION AND DEFINITION Lactate levels greater than 2 mmol/L represent hyperlactatemia, whereas lactic acidosis is generally defined as a serum lactate concentration above 4 mmol/L. Lactic acidosis is the most common cause of metabolic acidosis in hospitalized patients. Although the acidosis is usually associated with an elevated anion gap, moderately increased lactate levels can be observed with a normal anion gap (especially if hypoalbuminemia exists and the anion gap is not appropriately corrected). When lactic acidosis exists as an isolated acid-base disturbance, the arterial pH is reduced. However, other coexisting disorders can raise the pH into the normal range or even generate an elevated pH. (See "Approach to the adult with metabolic acidosis", section on 'Assessment of the serum anion gap' and "Simple and mixed acid-base disorders".) Lactic acidosis occurs when lactic acid production exceeds lactic acid clearance. The increase in lactate production is usually caused by impaired tissue oxygenation, either from decreased oxygen delivery or a defect in mitochondrial oxygen utilization. (See "Approach to the adult with metabolic acidosis".) The pathophysiology and causes of lactic acidosis will be reviewed here. The possible role of bicarbonate therapy in such patients is discussed separately. (See "Bicarbonate therapy in lactic acidosis".) PATHOPHYSIOLOGY A review of the biochemistry of lactate generation and metabolism is important in understanding the pathogenesis of lactic acidosis [1]. Both overproduction and reduced metabolism of lactate appear to be operative in most patients. Cellular lactate generation is influenced by the "redox state" of the cell. The redox state in the cellular cytoplasm is reflected by the ratio of oxidized and reduced nicotine ad Continue reading >>
Lactic Acidosis
Background 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 Presentation and Differentials.) The causes of lactic acidosis are listed in the chart below. Go to Acute Lactic Ac Continue reading >>
The Use Of Sodium Bicarbonate In The Treatment Of Acidosis In Sepsis: A Literature Update On A Long Term Debate
Volume2015(2015), Article ID605830, 7 pages The Use of Sodium Bicarbonate in the Treatment of Acidosis in Sepsis: A Literature Update on a Long Term Debate 1Internal Medicine Department, University Hospital of Patras, 26500 Rion, Greece 2University of Patras School of Medicine, 26500 Rion, Greece 3Intensive Care Department, Brugmann University Hospital, 1030 Brussels, Belgium 4Department of Anesthesiology, Washington University School of Medicine, St. Louis, MO 63110, USA Received 22 March 2015; Revised 29 June 2015; Accepted 1 July 2015 Copyright 2015 Dimitrios Velissaris et al. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Introduction. Sepsis and its consequences such as metabolic acidosis are resulting in increased mortality. Although correction of metabolic acidosis with sodium bicarbonate seems a reasonable approach, there is ongoing debate regarding the role of bicarbonates as a therapeutic option. Methods. We conducted a PubMed literature search in order to identify published literature related to the effects of sodium bicarbonate treatment on metabolic acidosis due to sepsis. The search included all articles published in English in the last 35 years. Results. There is ongoing debate regarding the use of bicarbonates for the treatment of acidosis in sepsis, but there is a trend towards not using bicarbonate in sepsis patients with arterial blood gas . Conclusions. Routine use of bicarbonate for treatment of severe acidemia and lactic acidosis due to sepsis is subject of controversy, and current opinion does not favor routine use of bicarbonates. However, available evidence is inconclusive, and Continue reading >>
Acidbase Disturbances In Intensive Care Patients: Etiology, Pathophysiology And Treatment
Acidbase disturbances in intensive care patients: etiology, pathophysiology and treatment Center for Critical Care Nephrology, CRISMA Center, Department of Critical Care Medicine Correspondence and offprint requests to: John A. Kellum; E-mail: [email protected] Search for other works by this author on: Center for Critical Care Nephrology, CRISMA Center, Department of Critical Care Medicine Nephrology Dialysis Transplantation, Volume 30, Issue 7, 1 July 2015, Pages 11041111, Mohammed Al-Jaghbeer, John A. Kellum; Acidbase disturbances in intensive care patients: etiology, pathophysiology and treatment, Nephrology Dialysis Transplantation, Volume 30, Issue 7, 1 July 2015, Pages 11041111, Acidbase disturbances are very common in critically ill and injured patients as well as contribute significantly to morbidity and mortality. An understanding of the pathophysiology of these disorders is vital to their proper management. This review will discuss the etiology, pathophysiology and treatment of acidbase disturbances in intensive care patientswith particular attention to evidence from recent studies examining the effects of fluid resuscitation on acidbase and its consequences. acidbase physiology , acidosis , alkalosis , anion gap , strong ion difference The modern intensive care unit is a place where complex acidbase and electrolyte disorders are common, with one study, showing that 64% of critically ill patients have acute metabolic acidosis [ 1 ]. Although it is generally believed that most cases of acidbase derangement are mild and self-limiting, extremes of blood pH in either direction, especially when happening quickly, can have significant multiorgan consequences. Advances in evaluating acidbase balance have helped in understanding the impact of fluids in the critic Continue reading >>
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4.2 Respiratory Acidosis - Causes
Acid-Base Physiology The arterial pCO2 is normally maintained at a level of about 40 mmHg by a balance between production of CO2 by the body and its removal by alveolar ventilation. If the inspired gas contains no CO2 then this relationship can be expressed by: paCO2 is proportional to VCO2 / VA where: VCO2 is CO2 production by the body VA is Alveolar ventilation An increase in arterial pCO2 can occur by one of three possible mechanisms: Presence of excess CO2 in the inspired gas Decreased alveolar ventilation Increased production of CO2 by the body CO2 gas can be added to the inspired gas or it may be present because of rebreathing : Anaesthetists are familiar with both these mechanisms. In these situations, hypercapnia can be induced even in the presence of normal alveolar ventilation and normal carbon dioxide production by the body. An adult at rest produces about 200mls of CO2 per minute: this is excreted via the lungs and the arterial pCO2 remains constant. An increased production of CO2 would lead to a respiratory acidosis if ventilation remained constant. The system controlling arterial pCO2 is very efficient (ie rapid and effective) and any increase in pCO2 very promptly results in a large increase in ventilation. The result is that increased CO2 production almost never results in respiratory acidosis. It is only in situations where ventilation is fixed that increased production will cause respiratory acidosis. Examples of this would be a ventilated patient who develops acute malignant hyperthermia: the arterial pCO2 will rise unless the alveolar ventilation is substantially increased. Most cases of respiratory acidosis are due to decreased alveolar ventilation. The defect leading to this can occur at any level in the respiratory control mechanism. This provides Continue reading >>
2018 Icd-10-cm Diagnosis Code
A condition in which the blood is too acidic. It may be caused by severe illness or sepsis (bacteria in the bloodstream). A disorder characterized by abnormally high acidity (high hydrogen-ion concentration) of the blood and other body tissues. A pathologic condition of acid accumulation or depletion of base in the body. The two main types are respiratory acidosis and metabolic acidosis, due to metabolic acid build up. A state due to excess retention of carbon dioxide in the body. Acid base imbalance resulting from an accumulation of carbon dioxide secondary to hypoventilation. Acidosis caused by accumulation of lactic acid more rapidly than it can be metabolized. It may occur spontaneously or in association with diseases such as diabetes mellitus, leukemia, or liver failure. Acidosis caused by accumulation of lactic acid more rapidly than it can be metabolized; may occur spontaneously or in association with diseases such as diabetes mellitus, leukemia, or liver failure. An abnormal increase in the acidity of the body's fluids An abnormally high acidity (excess hydrogen-ion concentration) of the blood and other body tissues. An abnormally high acidity of the blood and other body tissues. Acidosis can be either respiratory or metabolic. Excess retention of carbon dioxide in the body resulting from ventilatory impairment. Increased acidity in the blood secondary to acid base imbalance. Causes include diabetes, kidney failure and shock. Metabolic acidosis characterized by the accumulation of lactate in the body. It is caused by tissue hypoxia. Pathologic condition resulting from accumulation of acid or depletion of the alkaline reserve (bicarbonate) content of the blood and body tissues, and characterized by an increase in hydrogen ion concentration (decrease in ph). Respi Continue reading >>
Lactic Acidosis, Hyperlactatemia And Sepsis | Montagnani | Italian Journal Of Medicine
Montagnani and Nardi: Lactic Acidosis, Hyperlactatemia and Sepsis Lactic Acidosis, Hyperlactatemia and Sepsis [1] Division of Internal Medicine, Misericordia Hospital, Grosseto [2] Division of Internal Medicine, Maggiore Hospital, Bologna, Italy Correspondence to: Ospedale Misericordia di Grosseto, via Senese, 58100 Grosseto, Italy. +39.0564.485330. [email protected] Among hospitalized patients, lactic acidosis represents the most common cause of metabolic acidosis. Lactate is not just a metabolic product of anaerobic glycolysis but is triggered by a variety of metabolites even before the onset of anaerobic metabolism as part of an adaptive response to a hypermetabolic state. On the basis of such considerations, lactic acidosis is divided into two classes: inadequate tissue oxygenation (type A) and absence of tissue hypoxia (type B). Lactic acidosis is characterized by non-specific symptoms but it should be suspected in all critical patients who show hypovolemic, hypoxic, in septic or cardiogenic shock or if in the presence of an unexplained high anion gap metabolic acidosis. Lactic acidosis in sepsis and septic shock has traditionally been explained as a result of tissue hypoxia when whole-body oxygen delivery fails to meet whole body oxygen requirements. In sepsis lactate levels correlate with increased mortality with a poor prognostic threshold of 4 mmol/L. In hemodynamically stable patients with sepsis, hyperlactatemia might be the result of impaired lactate clearance rather than overproduction. In critically ill patients the speed at which hyperlactatemia resolves with appropriate therapy may be considered a useful prognostic indicator. The measure of blood lactate should be performed within 3 h of presentation in acute care setting. The presence of lactic a Continue reading >>
