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 >>
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Acid-base Disorders - Endocrine And Metabolic Disorders - Merck Manuals Professional Edition
(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 Acid-base disorders are pathologic changes in carbon dioxide partial pressure (Pco2) or serum bicarbonate (HCO3) that typically produce abnormal arterial pH values. Acidosis refers to physiologic processes that cause acid accumulation or alkali loss. Alkalosis refers to physiologic processes that cause alkali accumulation or acid loss. Actual changes in pH depend on the degree of physiologic compensation and whether multiple processes are present. Primary acid-base disturbances are defined as metabolic or respiratory based on clinical context and whether the primary change in pH is due to an alteration in serum HCO3 or in Pco2. Metabolic acidosis is serum HCO3< 24 mEq/L. Causes are Metabolic alkalosis is serum HCO3> 24 mEq/L. Causes are Respiratory acidosis is Pco2> 40 mm Hg (hypercapnia). Cause is Decrease in minute ventilation (hypoventilation) Respiratory alkalosis is Pco2< 40 mm Hg (hypocapnia). Cause is Increase in minute ventilation (hyperventilation) Compensatory mechanisms begin to correct the pH (see Table: Primary Changes and Compensations in Simple Acid-Base Disorders ) whenever an acid-base disorder is present. Compensation cannot return pH completely to normal and never overshoots. A simple acid-base disorder is a single acid-base disturbance with its accompanying compensatory response. Mixed acid-base disorders comprise 2 primary disturbances. Compensatory mechanisms for acid-base disturbances cannot return pH completely to normal and never overshoot. Primary Changes and Compensations in Simple Acid-Base Disorders 1.2 mm Hg decrease in Pco2 for every 1 mmol/L decrease in HC Continue reading >>
Recognizing Mixed Acid Base Disturbances - Acvim 2008 - Vin
A proper understanding of the terms acidosis, alkalosis, acidemia, and alkalemia is necessary to differentiate simple from mixed acid base disorders.1 Acidosis and alkalosis refer to the pathophysiologic processes that cause net accumulation of acid or alkali in the body, whereas acidemia and alkalemia refer specifically to the pH of extracellular fluid. In acidemia, the extracellular fluid pH is less than normal and the [H+] is higher than normal. In alkalemia, the extracellular fluid pH is higher than normal and the [H+] is lower than normal. Due to the effectiveness of compensatory mechanisms, animals can have acidosis or alkalosis but not acidemia or alkalemia. For example, a dog with chronic respiratory alkalosis may have a blood pH that is within the normal range. Such a patient has alkalosis, but does not have alkalemia. The primary acid base disorders are divided into metabolic and respiratory disturbances: metabolic acidosis, metabolic alkalosis, respiratory acidosis, and respiratory alkalosis. The Henderson-Hasselbach equation in its clinically relevant form emphasizes the relationship between the metabolic and respiratory systems in determining extracellular fluid pH: Traditionally, the kidneys have been considered responsible for regulation of the metabolic component (blood bicarbonate concentration, [HCO3-]) and the lungs for regulation of the respiratory component (partial pressure of CO2, [pCO2]). In this form, the Henderson-Hasselbach equation makes it clear that the pH of extracellular fluid is determined by the ratio of the bicarbonate concentration and pCO2. Each primary (metabolic or respiratory) acid base disturbance is accompanied by a secondary (opposing) response in the other system (respiratory or metabolic). Blood pH is returned nearly, but no Continue reading >>
Simple Method Of Acid Base Balance Interpretation
A FOUR STEP METHOD FOR INTERPRETATION OF ABGS Usefulness This method is simple, easy and can be used for the majority of ABGs. It only addresses acid-base balance and considers just 3 values. pH, PaCO2 HCO3- Step 1. Use pH to determine Acidosis or Alkalosis. ph < 7.35 7.35-7.45 > 7.45 Acidosis Normal or Compensated Alkalosis Step 2. Use PaCO2 to determine respiratory effect. PaCO2 < 35 35 -45 > 45 Tends toward alkalosis Causes high pH Neutralizes low pH Normal or Compensated Tends toward acidosis Causes low pH Neutralizes high pH Step 3. Assume metabolic cause when respiratory is ruled out. You'll be right most of the time if you remember this simple table: High pH Low pH Alkalosis Acidosis High PaCO2 Low PaCO2 High PaCO2 Low PaCO2 Metabolic Respiratory Respiratory Metabolic If PaCO2 is abnormal and pH is normal, it indicates compensation. pH > 7.4 would be a compensated alkalosis. pH < 7.4 would be a compensated acidosis. These steps will make more sense if we apply them to actual ABG values. Click here to interpret some ABG values using these steps. You may want to refer back to these steps (click on "linked" steps or use "BACK" button on your browser) or print out this page for reference. Step 4. Use HC03 to verify metabolic effect Normal HCO3- is 22-26 Please note: Remember, the first three steps apply to the majority of cases, but do not take into account: the possibility of complete compensation, but those cases are usually less serious, and instances of combined respiratory and metabolic imbalance, but those cases are pretty rare. "Combined" disturbance means HCO3- alters the pH in the same direction as the PaCO2. High PaCO2 and low HCO3- (acidosis) or Low PaCO2 and high HCO3- (alkalosis). Continue reading >>
Acid–base Imbalance
Acid–base imbalance is an abnormality of the human body's normal balance of acids and bases that causes the plasma pH to deviate out of the normal range (7.35 to 7.45). In the fetus, the normal range differs based on which umbilical vessel is sampled (umbilical vein pH is normally 7.25 to 7.45; umbilical artery pH is normally 7.18 to 7.38).[1] It can exist in varying levels of severity, some life-threatening. Classification[edit] A Davenport diagram illustrates acid–base imbalance graphically. An excess of acid is called acidosis or acidemia and an excess in bases is called alkalosis or alkalemia. The process that causes the imbalance is classified based on the cause of the disturbance (respiratory or metabolic) and the direction of change in pH (acidosis or alkalosis). This yields the following four basic processes: process pH carbon dioxide compensation metabolic acidosis down down respiratory respiratory acidosis down up renal metabolic alkalosis up up respiratory respiratory alkalosis up down renal Mixed disorders[edit] The presence of only one of the above derangements is called a simple acid–base disorder. In a mixed disorder more than one is occurring at the same time.[2] Mixed disorders may feature an acidosis and alkosis at the same time that partially counteract each other, or there can be two different conditions affecting the pH in the same direction. The phrase "mixed acidosis", for example, refers to metabolic acidosis in conjunction with respiratory acidosis. Any combination is possible, except concurrent respiratory acidosis and respiratory alkalosis, since a person cannot breathe too fast and too slow at the same time... Calculation of imbalance[edit] The traditional approach to the study of acid–base physiology has been the empirical approach. Continue reading >>
What Is Metabolic Acidosis?
Metabolic acidosis happens when the chemical balance of acids and bases in your blood gets thrown off. Your body: Is making too much acid Isn't getting rid of enough acid Doesn't have enough base to offset a normal amount of acid When any of these happen, chemical reactions and processes in your body don't work right. Although severe episodes can be life-threatening, sometimes metabolic acidosis is a mild condition. You can treat it, but how depends on what's causing it. Causes of Metabolic Acidosis Different things can set up an acid-base imbalance in your blood. Ketoacidosis. When you have diabetes and don't get enough insulin and get dehydrated, your body burns fat instead of carbs as fuel, and that makes ketones. Lots of ketones in your blood turn it acidic. People who drink a lot of alcohol for a long time and don't eat enough also build up ketones. It can happen when you aren't eating at all, too. Lactic acidosis. The cells in your body make lactic acid when they don't have a lot of oxygen to use. This acid can build up, too. It might happen when you're exercising intensely. Big drops in blood pressure, heart failure, cardiac arrest, and an overwhelming infection can also cause it. Renal tubular acidosis. Healthy kidneys take acids out of your blood and get rid of them in your pee. Kidney diseases as well as some immune system and genetic disorders can damage kidneys so they leave too much acid in your blood. Hyperchloremic acidosis. Severe diarrhea, laxative abuse, and kidney problems can cause lower levels of bicarbonate, the base that helps neutralize acids in blood. Respiratory acidosis also results in blood that's too acidic. But it starts in a different way, when your body has too much carbon dioxide because of a problem with your lungs. Continue reading >>
Perfecting Your Acid-base Balancing Act
When it comes to acids and bases, the difference between life and death is balance. The body’s acid-base balance depends on some delicately balanced chemical reactions. The hydrogen ion (H+) affects pH, and pH regulation influences the speed of cellular reactions, cell function, cell permeability, and the very integrity of cell structure. When an imbalance develops, you can detect it quickly by knowing how to assess your patient and interpret arterial blood gas (ABG) values. And you can restore the balance by targeting your interventions to the specific acid-base disorder you find. Basics of acid-base balance Before assessing a patient’s acid-base balance, you need to understand how the H+ affects acids, bases, and pH. An acid is a substance that can donate H+ to a base. Examples include hydrochloric acid, nitric acid, ammonium ion, lactic acid, acetic acid, and carbonic acid (H2CO3). A base is a substance that can accept or bind H+. Examples include ammonia, lactate, acetate, and bicarbonate (HCO3-). pH reflects the overall H+ concentration in body fluids. The higher the number of H+ in the blood, the lower the pH; and the lower the number of H+, the higher the pH. A solution containing more base than acid has fewer H+ and a higher pH. A solution containing more acid than base has more H+ and a lower pH. The pH of water (H2O), 7.4, is considered neutral. The pH of blood is slightly alkaline and has a normal range of 7.35 to 7.45. For normal enzyme and cell function and normal metabolism, the blood’s pH must remain in this narrow range. If the blood is acidic, the force of cardiac contractions diminishes. If the blood is alkaline, neuromuscular function becomes impaired. A blood pH below 6.8 or above 7.8 is usually fatal. pH also reflects the balance between the p Continue reading >>
9.3 Bedside Rules For Assessment Of Compensation
The method of assessing acid-base disorders discussed here uses a set of six rules which are used primarily to assess the magnitude of the patients compensatory response. These rules are now widely known and are soundly based experimentally. These rules are used at Step 4 of the method of Systematic Acid-Base Diagnosis outlined in Section 9.2.- (You should read section 9.1 & 9.2 before this section.) These rules are called 'bedside rules' because that can be used at the patient's bedside to assist in the assessment of the acid-base results. The rules should preferably be committed to memory - with practice this is not difficult. A full assessment of blood-gas results must be based on a clinical knowledge of the individual patient from whom they were obtained and an understanding of the pathophysiology of the clinical conditions underlying the acid-base disorder. Do not interpret the blood-gas results as an intellectual exercise in itself. It is one part of the overall process of assessing and managing the patient. A set of blood-gas and electrolyte results should NOT be interpreted without these initial clinical details. They cannot be understood fully without knowledge of the condition being diagnosed. Diagnosing a metabolic acidosis, for example, is by itself, often of little clinical use. What is really required is a more specific diagnosis of the cause of the metabolic acidosis (eg diabetic ketoacidosis, acute renal failure, lactic acidosis) and to initiate appropriate management. The acid-base analysis must be interpreted and managed in the context of the overall clinical picture. The snapshot problem: Are the results 'current'? Remember also that a set of blood gas results provides a snapshot at a particular point in time and the situation may have changed since Continue reading >>
6.3 Respiratory Alkalosis - Maintenance
The alkalosis persists as long as the initiating disorder is acting The alkalosis persists as long as the initiating disorder persists unless some other disorder or complication causing impairment of the hyperventilation intervenes. For example, a hyperventilating head injury patient may develop acute neurogenic pulmonary oedema and this complication would tend to cause the arterial pCO2 to rise. This is different to the situation with a metabolic alkalosis where maintenance of the disorder requires an abnormality to maintain it as well as the problem which initiated it. Only one respiratory acid-base disorder can be present at one time. A patient cannot have both a respiratory alkalosis and a respiratory acidosis. There may of course be multiple factors acting to alter an individual's alveolar ventilation but each of these various factors are not considered separate respiratory acid-base disorders. Essentially this is because a person cannot be both hyperventilating and hypoventilating at the same time. Using the above hyperventilating head injured patient example: This patient has a neurogenic cause for hyperventilation and if the arterial pCO2 is lowered, then she is said to have a respiratory alkalosis. If neurogenic pulmonary oedema develops subsequently and decreases alveolar ventilation to normal and returns arterial pCO2 to 40mmHg (assuming no metabolic acid-base disorders are present), then she now has no respiratory acid-base disorder. More than one metabolic acid-base disorder can be present at the one time The above respiratory situation is different to that occurring with a metabolic disorder. A patient can have a lactic acidosis and then develop a metabolic alkalosis (eg due to vomiting) and end up with a HCO3 level & pH which are normal. This is possible Continue reading >>
Types Of Disturbances
The different types of acid-base disturbances are differentiated based on: Origin: Respiratory or metabolic Primary or secondary (compensatory) Uncomplicated or mixed: A simple or uncomplicated disturbance is a single or primary acid-base disturbance with or without compensation. A mixed disturbance is more than one primary disturbance (not a primary with an expected compensatory response). Acid-base disturbances have profound effects on the body. Acidemia results in arrythmias, decreased cardiac output, depression, and bone demineralization. Alkalemia results in tetany and convulsions, weakness, polydipsia and polyuria. Thus, the body will immediately respond to changes in pH or H+, which must be kept within strict defined limits. As soon as there is a metabolic or respiratory acid-base disturbance, body buffers immediately soak up the proton (in acidosis) or release protons (alkalosis) to offset the changes in H+ (i.e. the body compensates for the changes in H+). This is very effective so minimal changes in pH occur if the body is keeping up or the acid-base abnormality is mild. However, once buffers are overwhelmed, the pH will change and kick in stronger responses. Remember that the goal of the body is to keep hydrogen (which dictates pH) within strict defined limits. The kidney and lungs are the main organs responsible for maintaining normal acid-base balance. The lungs compensate for a primary metabolic condition and will correct for a primary respiratory disturbance if the disease or condition causing the disturbance is resolved. The kidney is responsible for compensating for a primary respiratory disturbance or correcting for a primary metabolic disturbance. Thus, normal renal function is essential for the body to be able to adequately neutralize acid-base abnor Continue reading >>
Metabolic Alkalosis
Practice Essentials Metabolic alkalosis is a primary increase in serum bicarbonate (HCO3-) concentration. This occurs as a consequence of a loss of H+ from the body or a gain in HCO3-. In its pure form, it manifests as alkalemia (pH >7.40). As a compensatory mechanism, metabolic alkalosis leads to alveolar hypoventilation with a rise in arterial carbon dioxide tension (PaCO2), which diminishes the change in pH that would otherwise occur. Normally, arterial PaCO2 increases by 0.5-0.7 mm Hg for every 1 mEq/L increase in plasma bicarbonate concentration, a compensatory response that is very quick. If the change in PaCO2 is not within this range, then a mixed acid-base disturbance occurs. For example, if the increase in PaCO2 is more than 0.7 times the increase in bicarbonate, then metabolic alkalosis coexists with primary respiratory acidosis. Likewise, if the increase in PaCO2 is less than the expected change, then a primary respiratory alkalosis is also present. The first clue to metabolic alkalosis is often an elevated bicarbonate concentration that is observed when serum electrolyte measurements are obtained. Remember that an elevated serum bicarbonate concentration may also be observed as a compensatory response to primary respiratory acidosis. However, a bicarbonate concentration greater than 35 mEq/L is almost always caused by metabolic alkalosis. Metabolic alkalosis is diagnosed by measuring serum electrolytes and arterial blood gases. If the etiology of metabolic alkalosis is not clear from the clinical history and physical examination, including drug use and the presence of hypertension, then a urine chloride ion concentration can be obtained. Calculation of the serum anion gap may also help to differentiate between primary metabolic alkalosis and metabolic compe Continue reading >>
9.4 Assessment : The Rationale
The rules assess compensation & are therefore a guide to detecting the presence of a second primary acid-base disorder Rules 1 to 4 deal with respiratory acid-base disorders and provide a simple way to calculate the [HCO3-] that would be expected in a person who has a simple respiratory acid-base disorder. That is they predict the maximal amount of compensation that would occur. Question: How were these rules determined? Answer: By direct animal and human experimentation. For example, the pCO2 of the subjects was altered and the blood gases were measured. The data from these whole-body titrations allowed the normal physiological response and its time course to be quantified. Question: What is the principle behind the use of these rules? Answer: The rules allow calculation of the compensatory response that would be 'expected' if the primary respiratory or metabolic acid-base disorder were the only disorder present. That is, we predict the expected compensatory response so that we can separate what is expected (ie compensation) from the unexpected (ie a co-existent second disorder). For example, consider a patient with a primary metabolic acidosis. Using rule 5 , we calculate what we expect the arterial pCO2 will be in that person if this metabolic acidosis was the ONLY acid-base disorder present. We then compare this 'expected' pCO2 with the actual pCO2 (ie the measured value in the patient). If there is a significant difference between these two values, then this 'reveals' the presence of a second primary acid-base disorder (In this case, a discrepancy would reveal a co-existent respiratory acid-base disorder.) Question: Are there limitations in this method? Answer: Yes. Certain combinations of primary acid-base disorders cannot be revealed in this way. In particular, Continue reading >>
Metabolic Acidosis Or Respiratory Alkalosis? Evaluation Of A Low Plasmabicarbonate Using The Urine Anion Gap.
1. Am J Kidney Dis. 2017 Sep;70(3):440-444. doi: 10.1053/j.ajkd.2017.04.017. Epub2017 Jun 7. Metabolic Acidosis or Respiratory Alkalosis? Evaluation of a Low PlasmaBicarbonate Using the Urine Anion Gap. Batlle D(1), Chin-Theodorou J(2), Tucker BM(3). (1)Division of Nephrology & Hypertension, Department of Medicine, The Feinberg School of Medicine, Northwestern University, Chicago, IL. Electronic address: [email protected] (2)Division of Nephrology & Hypertension, Department of Medicine, The Feinberg School of Medicine, Northwestern University, Chicago, IL. (3)Section of Nephrology, Department of Medicine, Yale University School of Medicine, New Haven, CT. Hypobicarbonatemia, or a reduced bicarbonate concentration in plasma, is afinding seen in 3 acid-base disorders: metabolic acidosis, chronic respiratoryalkalosis and mixed metabolic acidosis and chronic respiratory alkalosis.Hypobicarbonatemia due to chronic respiratory alkalosis is often misdiagnosed as a metabolic acidosis and mistreated with the administration of alkali therapy.Proper diagnosis of the cause of hypobicarbonatemia requires integration of thelaboratory values, arterial blood gas, and clinical history. The informationderived from the urinary response to the prevailing acid-base disorder is useful to arrive at the correct diagnosis. We discuss the use of urine anion gap, as asurrogate marker of urine ammonium excretion, in the evaluation of a patient withlow plasma bicarbonate concentration to differentiate between metabolic acidosis and chronic respiratory alkalosis. The interpretation and limitations of urineacid-base indexes at bedside (urine pH, urine bicarbonate, and urine anion gap)to evaluate urine acidification are discussed.Copyright 2017 National Kidney Foundation, Inc. Published by E Continue reading >>
Abg’s—it’s All In The Family
By Cyndi Cramer, BA, RN, OCN, PCRN RealNurseEd.com 3.0 Contact Hour Self Learning Module Objectives: Identify the components of the ABG and their normal ranges Interpret ABG values and determine the acid base abnormality given Identify the major causes of acid base abnormalities Describe symptoms associated with acid base abnormalities Describe interventions to correct acid base abnormalities Identify the acceptable O2 level per ABG and Pulse Oximetry Identify four causes of low PaO2 The Respiratory System (Acid); CO2 is a volatile acid If you increase your respiratory rate (hyperventilation) you "blow off" CO2 (acid) therefore decreasing your CO2 acid—giving you ALKLAOSIS If you decrease your respiratory rate (hypoventilation) you retain CO2 (acid) therefore increasing your CO2 (acid)—giving you ACIDOSIS The Renal System (Base); the kidneys rid the body of the nonvolatile acids H+ (hydrogen ions) and maintain a constant bicarb (HCO3). Bicarbonate is the body’s base You have Acidosis when you have excess H+ and decreased HCO3- causing a decrease in pH. The Kidneys try to adjust for this by excreting H+ and retaining HCO3- base. The Respiratory System will try to compensate by increasing ventilation to blow off CO2 (acid) and therefore decrease the Acidosis. You have Alkalosis when H+ decreases and you have excess (or increased) HCO3- base. The kidneys excrete HCO3- (base) and retain H+ to compensate. The respiratory system tries to compensate with hypoventilation to retain CO2 (acid) To decrease the alkalosis Compensation The respiratory system can effect a change in 15-30 minutes The renal system takes several hours to days to have an effect. RESPIRATORY ACIDOSIS: pH < 7.35 (Normal: 7.35 - 7.45) CO2 > 45 (Normal: 35 – 45) 1. Causes: Hypoventilation a. Depressio Continue reading >>
Abg: Respiratory Acidosis/metabolic Alkalosis
Home / ABA Keyword Categories / A / ABG: Respiratory acidosis/metabolic alkalosis ABG: Respiratory acidosis/metabolic alkalosis A combined respiratory acidosis / metabolic alkalosis will result in elevated PaCO2 and serum bicarbonate. Which process is the primary disorder (e.g. primary respiratory acidosis with metabolic compensation versus primary metabolic alkalosis with respiratory compensation) is dependent on the pH in an acidotic patient, the acidosis is primary (and the alkalosis is compensatory) and vice versa. Compensation behaves in accordance with the following rules: Metabolic Acidosis: As bicarbonate goes from 10 to 5, pCO2 will bottom out at 15. pCO2 = 1.5 x [HCO3-] + 8 (or pCO2 = 1.25 x [HCO3-]) Metabolic Alkalosis: compensation here is less because CO2 is driving force for respiration. pCO2 = 0.7 x [HCO3-] + 21 (or pCO2 = 0.75 x [HCO3-]) Acutely: [HCO3-] = 0.1 x pCO2 or pH = 0.008 x pCO2 Chronically: [HCO3-] = 0.4 x pCO2 or pH = 0.003 x pCO2 Respiratory Alkalosis: Metabolic compensation will automatically be retention of chloride (i.e., hyperchloremic, usually referred to as loss of bicarb although it is the strong ion difference that matters). If you have an anion gap, then youve automatically got a little bit of an acidosis on top of the compensation (because the compensation should be a NON-gap acidotic process. Acutely: [HCO3-] = 0.2 x pCO2 (or pH = 0.008 x pCO2) Chronically: [HCO3-] = 0.4 x pCO2 (or pH = 0.017 x pCO2) Continue reading >>
