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Respiratory Acidosis Compensation Formula

Have A Question - Step 2 Ck - Uworld Forums For Usmle, Abim, Abfm, And Nclex Forums

Have A Question - Step 2 Ck - Uworld Forums For Usmle, Abim, Abfm, And Nclex Forums

c.mixed respiratory and metabolic acidosis d.mixed metabolic acidosis and respiratory alkalosis my first impresion: acidic pH with low bicarbonate makes metabolic acidosis; normal Pco2 makes NO respiratory compensation....i choose answer a.; on explinations they said is c. why? because co2 should be 32 mmHG(after Winter formula); well...here is my question: if we are taking this explination as granted, then ALL the acid base disturbances should have compensation and my concern is how will look the noncompensated acid base disturbances???? that means we should not choose that answer where says 'compansation'; if anybody can give me a real and strong explanation, i will really apreciate it....thanks! Pco2 increase .7mmHg for every 1 mEq/L bicarbonate increase. In this case, Pco2 should be in range of 30 and 34mmHg. 40mmHg is normal Pco2 in individual but in acidosis, it should decrease if there is respiratory compensation. So the answer is mixed respiratory and metabolic acidosis. fantastic explanation and thank you for that....very similar to what offer uworld....still i got 1 more question: we ALWAYS have to see which is the respiratory compensation based on Winter formula....how it will look this scenario if we don't have respiratory compansation???? how i am supose to know WHEN we have and IF we have compensation???? you said in your comment that Pco2 should be 30 to 34 IF WE HAVE COMPENSATION!!!! my frustation is not with the explanation which i agree with it....my opinion: both answers are good...why? if you have compensation, Pco2 should be arround 32(jusy like you explain) but we don't have that; so we remain with 2 options: pure metabolic acidosis WITHOUT compensation or mixed metabolic and respiratory acidosis; if we don't have compensation, Pco2 should be norm Continue reading >>

Perfecting Your Acid-base Balancing Act

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 >>

Simple Method Of Acid Base Balance Interpretation

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 >>

Additional Step In Abg Analysis

Additional Step In Abg Analysis

Michelle Kirschner , RN, MSN, APRN, CNP, CCRN The article Assessing Tissue Oxygenation (June 2002:2240) contains a comprehensive overview of arterial blood gas analysis, which will prove to be a valuable resource for nurses and other healthcare professionals in the intensive care environment. The steps outlined are useful in determining an acid-base imbalance involving either the metabolic or respiratory systems and the effectiveness of attempted compensation. However, severely ill patients who develop multiple organ failure frequently present with several acid-base abnormalities occurring simultaneously. Therefore, I routinely add an additional step in the analysis of arterial blood gases to determine if another primary acid-base process is present. The purpose of the additional step is to determine the expected compensation for the primary disorder. If the actual compensation falls within the calculated range, then a second disorder does not coexist. If the calculated value does not match the measured value, then a mixed disorder is present or compensation has not had time to occur. The expected compensation is calculated by using one of 4 formulas based on the primary process: metabolic acidosis, metabolic alkalosis, respiratory acidosis, or respiratory alkalosis. Metabolic conditions are generally compensated fairly quickly by the respiratory system by eliciting an alteration in the Pco2 level. The Winters formula predicts the expected degrees of compensation in a stable, steady-state metabolic disorder: If the actual Pco2 is higher than calculated with Winters formula, then a respiratory acidosis is mostly likely present in addition to the metabolic acid-base disorder. If the Pco2 is greater than 50 to 55 mm Hg, then respiratory acidosis is almost certainly presen Continue reading >>

Abg Interpreter

Abg Interpreter

pH CO2 HCO3 Result appears in here. Normal Arterial Blood Gas Values pH 7.35-7.45 PaCO2 35-45 mm Hg PaO2 80-95 mm Hg HCO3 22-26 mEq/L O2 Saturation 95-99% BE +/- 1 Four-Step Guide to ABG Analysis Is the pH normal, acidotic or alkalotic? Are the pCO2 or HCO3 abnormal? Which one appears to influence the pH? If both the pCO2 and HCO3 are abnormal, the one which deviates most from the norm is most likely causing an abnormal pH. Check the pO2. Is the patient hypoxic? I used Swearingen's handbook (1990) to base the results of this calculator. The book makes the distinction between acute and chronic disorders based on symptoms from identical ABGs. This calculator only differentiates between acute (pH abnormal) and compensated (pH normal). Compensation can be seen when both the PCO2 and HCO3 rise or fall together to maintain a normal pH. Part compensation occurs when the PCO2 and HCO3 rise or fall together but the pH remains abnormal. This indicates a compensatory mechanism attempted to restore a normal pH. I have not put exact limits into the calculator. For example, it will perceive respiratory acidosis as any pH < 7.35 and any CO2 > 45 (i.e. a pH of 1 and CO2 of 1000). These results do not naturally occur. pH PaCO2 HCO3 Respiratory Acidosis Acute < 7.35 > 45 Normal Partly Compensated < 7.35 > 45 > 26 Compensated Normal > 45 > 26 Respiratory Alkalosis Acute > 7.45 < 35 Normal Partly Compensated > 7.45 < 35 < 22 Compensated Normal < 35 < 22 Metabolic Acidosis Acute < 7.35 Normal < 22 Partly Compensated < 7.35 < 35 < 22 Compensated Normal < 35 < 22 Metabolic Alkalosis Acute > 7.45 Normal > 26 Partly Compensated > 7.45 > 45 > 26 Compensated Normal > 45 > 26 Mixed Disorders It's possible to have more than one disorder influencing blood gas values. For example ABG's with an alkale Continue reading >>

9.3 Bedside Rules For Assessment Of Compensation

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 >>

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 >>

Acid-base

Acid-base

Normal anion gap = 3-11 mEq/L. (8-16 if K is included in equation). Made upof unmeasured anions. Consist of proteins, mainly albumin. As a result areduction of albumin can reduce the baseline anion gap so that ahypoalbuminaemic patient may not have a high anion gap even in the presence of adisorder which usually produces an increased anion gap. Anion gap is reduced byapprox 2.5 mEq/L for every 10g/L fall in albumin. Alternatively a correctedvalue for a a normal anion gap (assuming K is included in calculation of aniongap) can be otained from: Corrected normal anion gap = 0.2[albumin] x 1.5[phosphate] where albumin is in g/L and phosphate in mmol/L - with hypokalaemia: classic distal (type 1) RTA - with hyperkalaemia: hyperkalaemic distal RTA , hypoaldosteronism (type 4) RTA Metabolic acidosis and respiratory alkalosis stimulation of respiratory centre by acidaemia causes a fall in PCO2 that in uncomplicated metabolic acidosis can be estimated from: lower than expected PCO2 indicates a superimposed respiratory alkalosis whereas a higher PCO2 indicates a respiratory acidosis. Equation only useful if plasma bicarbonate <20 mmol/L alternatively: a decrease in PCO2 of 0.16 kPa can be expected for a decrease in bicarbonate of 1 mmol/L. Ideally use nomogram complete respiratory compensation for primary metabolic acidosis does not occur respiratory compensation for acute acidosis tends to be somewhat greater than for chronic metabolic acidosis. Minimum level of PCO2 that can usually be attained is approx 1.3 kPa. Levels <2-2.7 kPa rarely maintained in chronic metabolic acidosis - combined hepatic and renal insufficiency (cirrhosis often associated with chronic respiratory alkalosis) - recent alcohol binge (alcoholic ketoacidosis + hyperventilation due to DTs) Metabolic acidosi Continue reading >>

Metabolic Acidosis

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 >>

Interpretation Of Arterial Blood Gas

Interpretation Of Arterial Blood Gas

Go to: Introduction Arterial blood gas (ABG) analysis is an essential part of diagnosing and managing a patient’s oxygenation status and acid–base balance. The usefulness of this diagnostic tool is dependent on being able to correctly interpret the results. Disorders of acid–base balance can create complications in many disease states, and occasionally the abnormality may be so severe so as to become a life-threatening risk factor. A thorough understanding of acid–base balance is mandatory for any physician, and intensivist, and the anesthesiologist is no exception. The three widely used approaches to acid–base physiology are the HCO3- (in the context of pCO2), standard base excess (SBE), and strong ion difference (SID). It has been more than 20 years since the Stewart’s concept of SID was introduced, which is defined as the absolute difference between completely dissociated anions and cations. According to the principle of electrical neutrality, this difference is balanced by the weak acids and CO2. The SID is defined in terms of weak acids and CO2 subsequently has been re-designated as effective SID (SIDe) which is identical to “buffer base.” Similarly, Stewart’s original term for total weak acid concentration (ATOT) is now defined as the dissociated (A-) plus undissociated (AH) weak acid forms. This is familiarly known as anion gap (AG), when normal concentration is actually caused by A-. Thus all the three methods yield virtually identical results when they are used to quantify acid–base status of a given blood sample.[1] Continue reading >>

Common Laboratory (lab) Values - Abgs

Common Laboratory (lab) Values - Abgs

A B C D E F G H I J K L M N O P Q R S T U V W X Y Z Laboratory VALUES Home Page Arterial Blood Gases Arterial blood gas analysis provides information on the following: 1] Oxygenation of blood through gas exchange in the lungs. 2] Carbon dioxide (CO2) elimination through respiration. 3] Acid-base balance or imbalance in extra-cellular fluid (ECF). Normal Blood Gases Arterial Venous pH 7.35 - 7.45 7.32 - 7.42 Not a gas, but a measurement of acidity or alkalinity, based on the hydrogen (H+) ions present. The pH of a solution is equal to the negative log of the hydrogen ion concentration in that solution: pH = - log [H+]. PaO2 80 to 100 mm Hg. 28 - 48 mm Hg The partial pressure of oxygen that is dissolved in arterial blood. New Born – Acceptable range 40-70 mm Hg. Elderly: Subtract 1 mm Hg from the minimal 80 mm Hg level for every year over 60 years of age: 80 - (age- 60) (Note: up to age 90) HCO3 22 to 26 mEq/liter (21–28 mEq/L) 19 to 25 mEq/liter The calculated value of the amount of bicarbonate in the bloodstream. Not a blood gas but the anion of carbonic acid. PaCO2 35-45 mm Hg 38-52 mm Hg The amount of carbon dioxide dissolved in arterial blood. Measured. Partial pressure of arterial CO2. (Note: Large A= alveolor CO2). CO2 is called a “volatile acid” because it can combine reversibly with H2O to yield a strongly acidic H+ ion and a weak basic bicarbonate ion (HCO3 -) according to the following equation: CO2 + H2O <--- --> H+ + HCO3 B.E. –2 to +2 mEq/liter Other sources: normal reference range is between -5 to +3. The base excess indicates the amount of excess or insufficient level of bicarbonate in the system. (A negative base excess indicates a base deficit in the blood.) A negative base excess is equivalent to an acid excess. A value outside of the normal r Continue reading >>

Acid-base Disorders

Acid-base Disorders

Content currently under development Acid-base disorders are a group of conditions characterized by changes in the concentration of hydrogen ions (H+) or bicarbonate (HCO3-), which lead to changes in the arterial blood pH. These conditions can be categorized as acidoses or alkaloses and have a respiratory or metabolic origin, depending on the cause of the imbalance. Diagnosis is made by arterial blood gas (ABG) interpretation. In the setting of metabolic acidosis, calculation of the anion gap is an important resource to narrow down the possible causes and reach a precise diagnosis. Treatment is based on identifying the underlying cause. Continue reading >>

Response To Disturbances

Response To Disturbances

The body tries to minimize pH changes and responds to acid-base disturbances with body buffers, compensatory responses by the lungs and kidney (to metabolic and respiratory disturbances, respectively) and by the kidney correcting metabolic disturbances. Body buffers: There are intracellular and extracellular buffers for primary respiratory and metabolic acid-base disturbances. Intracellular buffers include hemoglobin in erythrocytes and phosphates in all cells. Extracellular buffers are carbonate (HCO3–) and non-carbonate (e.g. protein, bone) buffers. These immediately buffer the rise or fall in H+. Compensation: This involves responses by the respiratory tract and kidney to primary metabolic and respiratory acid-base disturbances, respectively. Compensation opposes the primary disturbance, although the laboratory changes in the compensatory response parallel those in the primary response. This concept is illustrated in the summary below. Respiratory compensation for a primary metabolic disturbance: Alterations in alveolar ventilation occurs in response to primary metabolic acid-base disturbances. This begins within minutes to hours of an acute primary metabolic disturbance. Note that complete compensation via this mechanism may take up to 24 hours. Renal compensation for a primary respiratory disturbance: Here, the kidney alters excretion of acid (which influences bases as well) in response to primary respiratory disturbances. This begins within hours of an acute respiratory disturbance, but take several days (3-5 days) to take full effect. Correction of acid-base changes: Correction of a primary respiratory acid-base abnormality usually requires medical or surgical intervention of the primary problem causing the acid-base disturbance, e.g. surgical relief of a colla Continue reading >>

Rules For Respiratory Acid-base Disorders

Rules For Respiratory Acid-base Disorders

Rule 1 : The 1 for 10 Rule for Acute Respiratory Acidosis * For every 10 mmHg increase in pCO2 (above 40 mmHg) Comment:The increase in CO2 shifts the equilibrium between CO2 and HCO3 to result in an acute increase in HCO3. This is a simple physicochemical event and occurs almost immediately. Example: A patient with an acute respiratory acidosis (pCO2 60mmHg) has an actual [HCO3] of 31mmol/l. The expected [HCO3] for this acute elevation of pCO2 is 24 + 2 = 26mmol/l. The actual measured value is higher than this indicating that a metabolic alkalosis must also be present. Rule 2 : The 4 for 10 Rule for Chronic Respiratory Acidosis The [HCO3] will increase by 4 mmol/l for every 10 mmHg elevation in pCO2 above 40mmHg. Expected [HCO3] = 24 + 4 { (Actual pCO2 - 40) / 10} Comment: With chronic acidosis, the kidneys respond by retaining HCO3, that is, renal compensation occurs. This takes a few days to reach its maximal value. Example: A patient with a chronic respiratory acidosis (pCO2 60mmHg) has an actual [HCO3] of 31mmol/l. The expected [HCO3] for this chronic elevation of pCO2 is 24 + 8 = 32mmol/l. The actual measured value is extremely close to this so renal compensation is maximal and there is no evidence indicating a second acid-base disorder Rule 3 : The 2 for 10 Rule for Acute Respiratory Alkalosis * For every 10 mmHg decrease in pCO2 (below 40 mmHg) Comment: In practice, this acute physicochemical change rarely results in a [HCO3] of less than about 18 mmol/s. (After all there is a limit to how low pCO2 can fall as negative values are not possible!) So a [HCO3] of less than 18 mmol/l indicates a coexisting metabolic acidosis. The arterial pCO2 at maximal compensation has been measured in many patients with a metabolic acidosis. A consistent relationship between bicar Continue reading >>

Assessment Of Compensation: Boston And Copenhagen Methods - Deranged Physiology

Assessment Of Compensation: Boston And Copenhagen Methods - Deranged Physiology

Assessment of Compensation: Boston and Copenhagen Methods This page acts as a footnote to the "Boston vs. Copenhagen" chapter from Acid-Base Physiology by Kerry Brandis. The aforementioned chapter in my opinion remains the definitive resource on the topic. Brandis' chapter explores the epistemology of acid-base interpretation systems by means of which we might be able to determine whether a patient has a single or mixed acid base disorder; i.e. whether there is a purely metabolic or a purely respiratory disturbance, or some mixture of the two. As it happens, there are two well-accepted systems for doing this, each with its own merits and demerits. These are the Boston and Copenhagen methods of acid-base interpretation. There is also another not-so-well accepted system, the physicochemical method proposed by Peter Stewart - which possess a satisfying explanatory power as an instrument of academic physiology. Unfortunately, it is rather complicated, and difficult to apply at the bedside. Furthermore, there does not seem to be much of a difference in hard outcomes, regardless of which system one uses. Thus, this chapter will focus on the Boston and Copenhagen systems, which have equivalent validity as far as acid-base interpretation is concerned. "Which is the system I need to rote-learn to pass my primaries?" Such a question is expected from the fairweather intensivist, who will flee from the ICU as soon as a position opens in a more cushy training program. For the rest, one might remark that these analytical tools are all in common use, and any sufficiently advanced ICU trainee is expected to be intimately familiar with all of these systems. However, the time-poor exam candidate may need to focus their attention on the area which would yield the greatest number of marks Continue reading >>

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