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Is Copd Respiratory Acidosis Or Alkalosis?

Acid-base Disturbance In Copd

Acid-base Disturbance In Copd

Summarized from Bruno M, Valenti M. Acid-base disorders in patients with chronic obstructive pulmonary disease: A pathophysiological review. J Bomedicine and Biotechnology (2012) Article ID 915150 8 pages ( available at :) Arterial blood gases are frequently useful in the clinical management of patients with chronic obstructive pulmonary disease (COPD) to assess both oxygenation and acid-base status. A recent review article focuses on disturbance of acid-base in these patients, which occurs in advanced disease when pulmonary gas exchange is so compromised that the rate of carbon dioxide production in the tissues exceeds the rate of carbon dioxide elimination by the lungs. The article begins with an explanation of how the resulting carbon dioxide accumulation in blood leads to respiratory acidosis, the acid-base disturbance that commonly occurs in advanced COPD. An important distinction is made between acute and chronic respiratory acidosis; compensation is less effective in the former. Then follows a detailed description of the several renal mechanisms involved in the compensatory response to chronic respiratory acidosis. Although this mitigates the acidosis to a considerable extent, it often does not result in normalisation of pH. The deleterious effects of acidosis are enumerated and the authors also briefly review the epidemiological study that links severity of acidosis to poorer outcome among COPD patients. The significance of renal compensatory mechanisms is highlighted again in the discussion of the co-existence of renal failure in patients with COPD who to a greater or lesser extent lack these mechanisms and thereby have worse acidosis and poorer outcome. Many COPD patients with respiratory acidosis are suffering other conditions or prescribed drugs that affect Continue reading >>

Respiratory Acidosis

Respiratory Acidosis

Respiratory acidosis is an abnormal clinical process that causes the arterial Pco2 to increase to greater than 40 mm Hg. Increased CO2 concentration in the blood may be secondary to increased CO2 production or decreased ventilation. Larry R. Engelking, in Textbook of Veterinary Physiological Chemistry (Third Edition) , 2015 Respiratory acidosis can arise from a break in any one of these links. For example, it can be caused from depression of the respiratory center through drugs or metabolic disease, or from limitations in chest wall expansion due to neuromuscular disorders or trauma (Table 90-1). It can also arise from pulmonary disease, card iog en ic pu lmon a ryedema, a spira tion of a foreign body or vomitus, pneumothorax and pleural space disease, or through mechanical hypoventilation. Unless there is a superimposed or secondary metabolic acidosis, the plasma anion gap will usually be normal in respiratory acidosis. Kamel S. Kamel MD, FRCPC, Mitchell L. Halperin MD, FRCPC, in Fluid, Electrolyte and Acid-Base Physiology (Fifth Edition) , 2017 Respiratory acidosis is characterized by an increased arterial blood PCO2 and H+ ion concentration. The major cause of respiratory acidosis is alveolar hypoventilation. The expected physiologic response is an increased . The increase in concentration of bicarbonate ions (HCO3) in plasma ( ) is tiny in patients with acute respiratory acidosis, but is much larger in patients with chronic respiratory acidosis. Respiratory alkalosis is caused by hyperventilation and is characterized by a low arterial blood PCO2 and H+ ion concentration. The expected physiologic response is a decrease in . As in respiratory acidosis, this response is modest in patients with acute respiratory alkalosis and much larger in patients with chronic respir Continue reading >>

Respiratory Acidosis

Respiratory Acidosis

(Video) Overview of Acid-Base Maps and Compensatory Mechanisms By James L. Lewis, III, MD, Attending Physician, Brookwood Baptist Health and Saint Vincents Ascension Health, Birmingham Respiratory acidosis is primary increase in carbon dioxide partial pressure (Pco2) with or without compensatory increase in bicarbonate (HCO3); pH is usually low but may be near normal. Cause is a decrease in respiratory rate and/or volume (hypoventilation), typically due to CNS, pulmonary, or iatrogenic conditions. Respiratory acidosis can be acute or chronic; the chronic form is asymptomatic, but the acute, or worsening, form causes headache, confusion, and drowsiness. Signs include tremor, myoclonic jerks, and asterixis. Diagnosis is clinical and with ABG and serum electrolyte measurements. The cause is treated; oxygen (O2) and mechanical ventilation are often required. Respiratory acidosis is carbon dioxide (CO2) accumulation (hypercapnia) due to a decrease in respiratory rate and/or respiratory volume (hypoventilation). Causes of hypoventilation (discussed under Ventilatory Failure ) include Conditions that impair CNS respiratory drive Conditions that impair neuromuscular transmission and other conditions that cause muscular weakness Obstructive, restrictive, and parenchymal pulmonary disorders Hypoxia typically accompanies hypoventilation. Distinction is based on the degree of metabolic compensation; carbon dioxide is initially buffered inefficiently, but over 3 to 5 days the kidneys increase bicarbonate reabsorption significantly. Symptoms and signs depend on the rate and degree of Pco2 increase. CO2 rapidly diffuses across the blood-brain barrier. Symptoms and signs are a result of high CO2 concentrations and low pH in the CNS and any accompanying hypoxemia. Acute (or acutely wor Continue reading >>

A Primer On Arterial Blood Gas Analysis By Andrew M. Luks, Md(cont.)

A Primer On Arterial Blood Gas Analysis By Andrew M. Luks, Md(cont.)

Step 4: Identify the compensatory process (if one is present) In general, the primary process is followed by a compensatory process, as the body attempts to bring the pH back towards the normal range. If the patient has a primary respiratory acidosis (high PCO2 ) leading to acidemia: the compensatory process is a metabolic alkalosis (rise in the serum bicarbonate). If the patient has a primary respiratory alkalosis (low PCO2 ) leading to alkalemia: the compensatory process is a metabolic acidosis (decrease in the serum bicarbonate) If the patient has a primary metabolic acidosis (low bicarbonate) leading acidemia, the compensatory process is a respiratory alkalosis (low PCO2 ). If the patient has a primary metabolic alkalosis (high bicarbonate) leading to alkalemia, the compensatory process is a respiratory acidosis (high PCO2 ) The compensatory processes are summarized in Figure 2. (opens in a new window) Important Points Regarding Compensatory Processes There are several important points to be aware of regarding these compensatory processes: The body never overcompensates for the primary process. For example, if the patient develops acidemia due to a respiratory acidosis and then subsequently develops a compensatory metabolic alkalosis (a good example of this is the COPD patient with chronic carbon dioxide retention), the pH will move back towards the normal value of 7.4 but will not go to the alkalemic side of normal This might result in a pH of 7.36, for example but should not result in a pH such as 7.44 or another value on the alkalemic side of normal. If the pH appears to "over-compensate" then an additional process is at work and you will have to try and identify it. This can happen with mixed acid-base disorders, which are described further below. The pace of co Continue reading >>

Respiratory Acidosis

Respiratory Acidosis

What is respiratory acidosis? Respiratory acidosis is a condition that occurs when the lungs can’t remove enough of the carbon dioxide (CO2) produced by the body. Excess CO2 causes the pH of blood and other bodily fluids to decrease, making them too acidic. Normally, the body is able to balance the ions that control acidity. This balance is measured on a pH scale from 0 to 14. Acidosis occurs when the pH of the blood falls below 7.35 (normal blood pH is between 7.35 and 7.45). Respiratory acidosis is typically caused by an underlying disease or condition. This is also called respiratory failure or ventilatory failure. Normally, the lungs take in oxygen and exhale CO2. Oxygen passes from the lungs into the blood. CO2 passes from the blood into the lungs. However, sometimes the lungs can’t remove enough CO2. This may be due to a decrease in respiratory rate or decrease in air movement due to an underlying condition such as: There are two forms of respiratory acidosis: acute and chronic. Acute respiratory acidosis occurs quickly. It’s a medical emergency. Left untreated, symptoms will get progressively worse. It can become life-threatening. Chronic respiratory acidosis develops over time. It doesn’t cause symptoms. Instead, the body adapts to the increased acidity. For example, the kidneys produce more bicarbonate to help maintain balance. Chronic respiratory acidosis may not cause symptoms. Developing another illness may cause chronic respiratory acidosis to worsen and become acute respiratory acidosis. Initial signs of acute respiratory acidosis include: headache anxiety blurred vision restlessness confusion Without treatment, other symptoms may occur. These include: sleepiness or fatigue lethargy delirium or confusion shortness of breath coma The chronic form of Continue reading >>

Acid-base Disorders In Patients With Chronic Obstructive Pulmonary Disease: A Pathophysiological Review

Acid-base Disorders In Patients With Chronic Obstructive Pulmonary Disease: A Pathophysiological Review

Acid-Base Disorders in Patients with Chronic Obstructive Pulmonary Disease: A Pathophysiological Review Department of Internal Medicine and Systemic Diseases, University of Catania, 95100 Catania, Italy Received 29 September 2011; Accepted 26 October 2011 Copyright 2012 Cosimo Marcello Bruno and Maria Valenti. 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. The authors describe the pathophysiological mechanisms leading to development of acidosis in patients with chronic obstructive pulmonary disease and its deleterious effects on outcome and mortality rate. Renal compensatory adjustments consequent to acidosis are also described in detail with emphasis on differences between acute and chronic respiratory acidosis. Mixed acid-base disturbances due to comorbidity and side effects of some drugs in these patients are also examined, and practical considerations for a correct diagnosis are provided. Chronic obstructive pulmonary disease (COPD) is a major public health problem. Its prevalence varies according to country, age, and sex. On the basis of epidemiologic data, the projection for 2020 indicates that COPD will be the third leading cause of death worldwide and the fifth leading cause of disability [ 1 ]. About 15% of COPD patients need admission to general hospital or intensive respiratory care unit for acute exacerbation, leading to greater use of medical resources and increased costs [ 2 5 ]. Even though the overall prognosis of COPD patients is lately improved, the mortality rate remains high, and, among others, acid-base disorders occurring in these subjects can affect the outcome. The aim of this pa Continue reading >>

Respiratory Acidosis

Respiratory Acidosis

Respiratory Acidosis Definition Respiratory acidosis is a condition in which a build-up of carbon dioxide in the blood produces a shift in the body's pH balance and causes the body's system to become more acidic. This condition is brought about by a problem either involving the lungs and respiratory system or signals from the brain that control breathing. Description Respiratory acidosis is an acid imbalance in the body caused by a problem related to breathing. In the lungs, oxygen from inhaled air is exchanged for carbon dioxide from the blood. This process takes place between the alveoli (tiny air pockets in the lungs) and the blood vessels that connect to them. When this exchange of oxygen for carbon dioxide is impaired, the excess carbon dioxide forms an acid in the blood. The condition can be acute with a sudden onset, or it can develop gradually as lung function deteriorates. Causes and symptoms Respiratory acidosis can be caused by diseases or conditions that affect the lungs themselves, such as emphysema, chronic bronchitis, asthma, or severe pneumonia. Blockage of the airway due to swelling, a foreign object, or vomit can induce respiratory acidosis. Drugs like anesthetics, sedatives, and narcotics can interfere with breathing by depressing the respiratory center in the brain. Head injuries or brain tumors can also interfere with signals sent by the brain to the lungs. Such neuromuscular diseases as Guillain-Barré syndrome or myasthenia gravis can impair the muscles around the lungs making it more difficult to breathe. Conditions that cause chronic metabolic alkalosis can also trigger respiratory acidosis. The most notable symptom will be slowed or difficult breathing. Headache, drowsiness, restlessness, tremor, and confusion may also occur. A rapid heart rate Continue reading >>

Respiratory Acidosis

Respiratory Acidosis

Respiratory acidosis is an acid-base balance disturbance due to alveolar hypoventilation. Production of carbon dioxide occurs rapidly and failure of ventilation promptly increases the partial pressure of arterial carbon dioxide (PaCO2). [ 1 ] The normal reference range for PaCO2 is 35-45 mm Hg. Alveolar hypoventilation leads to an increased PaCO2 (ie, hypercapnia). The increase in PaCO2, in turn, decreases the bicarbonate (HCO3)/PaCO2 ratio, thereby decreasing the pH. Hypercapnia and respiratory acidosis ensue when impairment in ventilation occurs and the removal of carbon dioxide by the respiratory system is less than the production of carbon dioxide in the tissues. Lung diseases that cause abnormalities in alveolar gas exchange do not typically result in alveolar hypoventilation. Often these diseases stimulate ventilation and hypocapnia due to reflex receptors and hypoxia. Hypercapnia typically occurs late in the disease process with severe pulmonary disease or when respiratory muscles fatigue. (See also Pediatric Respiratory Acidosis , Metabolic Acidosis , and Pediatric Metabolic Acidosis .) Respiratory acidosis can be acute or chronic. In acute respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range (ie, >45 mm Hg) with an accompanying acidemia (ie, pH < 7.35). In chronic respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range, with a normal or near-normal pH secondary to renal compensation and an elevated serum bicarbonate levels (ie, >30 mEq/L). Acute respiratory acidosis is present when an abrupt failure of ventilation occurs. This failure in ventilation may result from depression of the central respiratory center by one or another of the following: Central nervous system disease or drug-induced r Continue reading >>

Respiratory Acidosis

Respiratory Acidosis

Causes of respiratory acidosis include: Diseases of the lung tissue (such as pulmonary fibrosis, which causes scarring and thickening of the lungs) Diseases of the chest (such as scoliosis) Diseases affecting the nerves and muscles that signal the lungs to inflate or deflate Drugs that suppress breathing (including powerful pain medicines, such as narcotics, and "downers," such as benzodiazepines), often when combined with alcohol Severe obesity, which restricts how much the lungs can expand Obstructive sleep apnea Chronic respiratory acidosis occurs over a long time. This leads to a stable situation, because the kidneys increase body chemicals, such as bicarbonate, that help restore the body's acid-base balance. Acute respiratory acidosis is a condition in which carbon dioxide builds up very quickly, before the kidneys can return the body to a state of balance. Some people with chronic respiratory acidosis get acute respiratory acidosis because an illness makes their condition worse. Continue reading >>

Mixed Acid-base Disorders, Hydroelectrolyte Imbalance And Lactate Production In Hypercapnic Respiratory Failure: The Role Of Noninvasive Ventilation

Mixed Acid-base Disorders, Hydroelectrolyte Imbalance And Lactate Production In Hypercapnic Respiratory Failure: The Role Of Noninvasive Ventilation

Mixed Acid-Base Disorders, Hydroelectrolyte Imbalance and Lactate Production in Hypercapnic Respiratory Failure: The Role of Noninvasive Ventilation Affiliation: Fondazione Eleonora Lorillard Spencer Cenci, Sapienza University of Rome, Rome, Italy Affiliation: Fondazione Eleonora Lorillard Spencer Cenci, Sapienza University of Rome, Rome, Italy Affiliation: Fondazione Eleonora Lorillard Spencer Cenci, Sapienza University of Rome, Rome, Italy Affiliation: Laboratory of Biostatistics, Department of Biomedical Science, University G. d'Annunzio of Chieti-Pescara, Chieti, Italy Affiliation: Fondazione Eleonora Lorillard Spencer Cenci, Sapienza University of Rome, Rome, Italy Affiliation: Fondazione Eleonora Lorillard Spencer Cenci, Sapienza University of Rome, Rome, Italy Affiliation: Fondazione Eleonora Lorillard Spencer Cenci, Sapienza University of Rome, Rome, Italy Hypercapnic Chronic Obstructive Pulmonary Disease (COPD) exacerbation in patients with comorbidities and multidrug therapy is complicated by mixed acid-base, hydro-electrolyte and lactate disorders. Aim of this study was to determine the relationships of these disorders with the requirement for and duration of noninvasive ventilation (NIV) when treating hypercapnic respiratory failure. Sixty-seven consecutive patients who were hospitalized for hypercapnic COPD exacerbation had their clinical condition, respiratory function, blood chemistry, arterial blood gases, blood lactate and volemic state assessed. Heart and respiratory rates, pH, PaO2 and PaCO2 and blood lactate were checked at the 1st, 2nd, 6th and 24th hours after starting NIV. Nine patients were transferred to the intensive care unit. NIV was performed in 11/17 (64.7%) mixed respiratory acidosismetabolic alkalosis, 10/36 (27.8%) respiratory acidosis Continue reading >>

Respiratory Acidosis

Respiratory Acidosis

Acid-base balance disturbance from alveolar hypoventilation Rapid production of carbon dioxide Failure of ventilation increases partial pressure of arterial carbon dioxide (PaCO2) Respiratory acidosis can be acute or chronic In acute respiratory acidosis: PaCO2 is > 45 mm Hg with accompanying acidemia (pH < 7.35) In chronic respiratory acidosis: PaCO2 is > 45 mm HG with normal/near-normal pH (renal compensation) and serum bicarbonate levels > 30 mEq/L Treatment directed at underlying disorder/pathophysiologic process Caution: too-rapid correction of hypercapnia can result in metabolic alkalemia CSF alkalization can result in seizures Due to alveolar hypoventilation from any cause CNS depression causing impaired ventilation most common cause Lung diseases causing abnormal alveolar gas exchange usually don't cause hypoventilation Stimulate ventilation and hypocapnia 2 degrees to hypoxia Hypercapnia only occurs if severe disease, respiratory muscle fatigue Accompanying acidemia (can be severe) Only acute compensatory response is intracellular buffering CNS: CVA, infection, trauma, tumor Pulmonary: PNA, COPD, PTX, PE. Pulmonary edema, Smoke inhalation Neuromuscular disease (myasthenia gravis, ALS, Guillain-Barre) Airway Obstruction: Foreign body, edema Increased dead space ventilation (from increased V/Q mismatch) Decreased diaphragm function (from fatigue and hyperinflation) Obesity hypoventilation syndrome (Pickwickian Syndrome) Severe restrictive ventilatory processes (interstitial fibrosis, thoracic deformities) Usually that of underlying disease Depends on rate of hypercapnia development Slowly developing hypercapnia (mild-moderate) - minimal symptoms When PCO2 > 70 [SI: > 9.3 kPa] acutely Confusion, somnolence, obtundation (CO2 narcosis) Mental status may be depresse Continue reading >>

Acid Base Status In Chronic Obstructive Pulmonary Disease Patients

Acid Base Status In Chronic Obstructive Pulmonary Disease Patients

Acid base status in chronic obstructive pulmonary disease patients 348 patients of chronic obstructive pulmonary diseases (COPD) were studied for their acid base profile using ABL-3 blood gas analyser (Radiometer, copenhagan). 185 patients (53.1%) had simple disorders (respiratory acidosis53%, respiratory alkalosis25.4%, metabolic acidosis11.3%, metabolic alkalosis10.2%). Mixed disorders were present in 131 patients (34.9%) (respiratory acidosis and metabolic acidosis75.2%, respiratory acidosis and metabolic acidosis14%, metabolic acidosis and metabolic alkalosis5.7%, metabolic alkalosis and respiratory alkalosis4.9%). Hypoxemia without other acid base abnormalities was observed in early patients of GOPD (42 patients12%). Chronic respiratory acidosis was the most common finding in advanced cases of COPD (98%). An almost equal number of such patients had a mixed disorder of respiratory acidosis with metabolic alkalosis (91%). Salt restriction, prolonged use of steriods and hypokalemia were often related to metabolic alkalosis in such patients. Chronic Obstructive Pulmonary DiseaseChronic Obstructive Pulmonary Disease PatientMetabolic AcidosisHypokalemiaAcid Base These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves. This is a preview of subscription content, log in to check access Unable to display preview. Download preview PDF. Snider GL. Chronic obstructive pulmonay diseases: a definition and implication of structural determinants of airflow obstruction for epidemiology (1989) Am. Rev. Respir. Dis. 140, 5358. Google Scholar Kaehny WO. Respiratory acid base disorders (1983). Med. Clin. North. Am 57, 915928. Google Scholar Nrins RG, Emmett M. Simple and mixed acid base Continue reading >>

Why Does Emphysema Cause Respiratory Alkalosis?

Why Does Emphysema Cause Respiratory Alkalosis?

SDN members see fewer ads and full resolution images. Join our non-profit community! Why does emphysema cause respiratory ALKALOSIS? I get that in chronic bronchitis, the mucus plugs up the bronchioles and makes it hard for CO2 to get out, so PCO2 goes up and pH goes down. Since emphysema is also an obstructive lung disease, why does PCO2 not go up there as well? (Goljan pg 304) Easiest way to remember is that Emphysema, Asthma and COPD are obstructive pulmonary diseases which reduce FEV/FVC and thus you retain CO2 because you can't expire it as quickly. That's why the guys with really bad COPD turn blue. As for emphysema, you could theoretically become alkalotic but only because CO2's diffusion rate is limited only by surface area. But I doubt it. I get that in chronic bronchitis, the mucus plugs up the bronchioles and makes it hard for CO2 to get out, so PCO2 goes up and pH goes down. Since emphysema is also an obstructive lung disease, why does PCO2 not go up there as well? Don't remember ever learning this. I've always thought decrease CO2 expired--> chronic respiratory acidosis. May be wrong, but I don't think I am in this case. I believe, emphysema blows out alveoli (not really obstructive, in the literal sense of the word) so less gas exchange (due to less surface area) so tissues are oxygen starved. you need to increase ventilation rate which blows off co2, elevating blood ph. You might be confusing emphysema with pulmonary fibrosis. In pulmonary fibrosis (pink puffer) you breathe very quickly but shallowly, and you become alkalotic (it's the same reason why babies cry themselves into alkalosis) Emphysema, if anything, would cause a respiratory acidosis. Well that's what I thought too except it says clearly in Goljan that emphysema causes alkalosis. Error perha Continue reading >>

Respiratory Acidosis

Respiratory Acidosis

Respiratory acidosis is a medical emergency in which decreased ventilation (hypoventilation) increases the concentration of carbon dioxide in the blood and decreases the blood's pH (a condition generally called acidosis). Carbon dioxide is produced continuously as the body's cells respire, and this CO2 will accumulate rapidly if the lungs do not adequately expel it through alveolar ventilation. Alveolar hypoventilation thus leads to an increased PaCO2 (a condition called hypercapnia). The increase in PaCO2 in turn decreases the HCO3−/PaCO2 ratio and decreases pH. Terminology[edit] Acidosis refers to disorders that lower cell/tissue pH to < 7.35. Acidemia refers to an arterial pH < 7.36.[1] Types of respiratory acidosis[edit] Respiratory acidosis can be acute or chronic. In acute respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range (over 6.3 kPa or 45 mm Hg) with an accompanying acidemia (pH <7.36). In chronic respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range, with a normal blood pH (7.35 to 7.45) or near-normal pH secondary to renal compensation and an elevated serum bicarbonate (HCO3− >30 mm Hg). Causes[edit] Acute[edit] Acute respiratory acidosis occurs when an abrupt failure of ventilation occurs. This failure in ventilation may be caused by depression of the central respiratory center by cerebral disease or drugs, inability to ventilate adequately due to neuromuscular disease (e.g., myasthenia gravis, amyotrophic lateral sclerosis, Guillain–Barré syndrome, muscular dystrophy), or airway obstruction related to asthma or chronic obstructive pulmonary disease (COPD) exacerbation. Chronic[edit] Chronic respiratory acidosis may be secondary to many disorders, including COPD. Hypoventilation Continue reading >>

The Abcs Of Abgs: Blood Gas Analysis

The Abcs Of Abgs: Blood Gas Analysis

A systematic and step-wise process based upon pH shift is the key to correct interpretation and application of arterial blood gas results In a previous article, “The Pitfalls of Arterial Blood Gases” (RT, April 2013), I described how simple pre-analytical, analytical, and post-analytical errors can produce arterial blood gas test results (ABGs) that are of little or no value, and perhaps even dangerous. In this article, I will assume that we have avoided all of those pitfalls and and will discuss how to interpret valid ABG results. (Some of the foundational information in this article is necessary for those new to interpreting. I encourage more experienced practitioners to bear with me.) This article will not attempt to discuss all of the possible causes or disease states that could relate to the results. Neither will it attempt to go into the interpretation of electrolytes or co-oximetry results. Adequate review of these subjects could require—in fact, have required—whole textbooks, and are beyond the scope of this article. What Is Normal? To interpret ABGs, we first need to know the normal values for the various analytes. Where do these normal values come from? They mostly come from collected results of volunteers or study subjects who appear to have uncompromised lungs and gas exchange. Researchers plotted the results of the various parameters, found the collective center of the bell-shaped curve of data, and declared the results shown in Table 1. Whichever range you and your facility prefer, it is important to think in terms of a normal range, not a single, specific, always “normal” value—except when it comes to pH for interpreting acid-base balance. We will get to why shortly. It is also vital to remember that the aggregate “normal” value is a con Continue reading >>

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