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Metabolic Compensation For Respiratory Acidosis

Compensated Respiratory Acidosis

Compensated Respiratory Acidosis

Definition In a compensated respiratory acidosis, although the PCO2 is high, the pH is within normal range. The kidneys compensate for a respiratory acidosis by tubular cells reabsorbing more HCO3 from the tubular fluid, collecting duct cells secreting more H+ and generating more HCO3, and ammoniagenesis leading to increased formation of the NH3 buffer. Compensated respiratory acidosis is typically the result of a chronic condition, the slow nature of onset giving the kidneys time to compensate. Common causes of respiratory acidosis include hypoventilation due to: Respiratory depression (sedatives, narcotics, CVA, etc.) Respiratory muscle paralysis (spinal cord injury, Guillan-Barre, residual paralytics). Chest wall disorders (flail chest, pneumothorax) Lung parenchyma disorders (ARDS, pneumonia, COPD, CHF, aspiration) Abdominal distension (laporoscopic surgery, ascites, obesity, etc.). Subspecialty Keyword history Similar Keyword: Respiratory acidosis: Compensation Sources Miller’s Anesthesia, 7th ed. Ch. 49. PubMed Continue reading >>

Acute Renal Response To Rapid Onset Respiratory Acidosis

Acute Renal Response To Rapid Onset Respiratory Acidosis

Acute Renal Response to Rapid Onset Respiratory Acidosis Jayanth Ramadoss , Randolph H. Stewart , and Timothy A. Cudd Department of Veterinary Physiology and Pharmacology and Michael E. DeBakey Institute, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, Texas, 77843, USA Send correspondence to: Timothy A. Cudd, DVM, PhD, Department of Veterinary Physiology and Pharmacology, Hwy 60, Building VMA, Rm 332, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX 77843-4466 Fax: 979-845-6544 [email protected] The publisher's final edited version of this article is available at Can J Physiol Pharmacol See other articles in PMC that cite the published article. Renal strong ion compensation to chronic respiratory acidosis has been established but the nature of the response to acute respiratory acidosis is not well defined. We hypothesized that the response to acute respiratory acidosis in sheep is a rapid increase in the difference in renal fractional excretions of chloride and sodium (FeCl-FeNa). Inspired CO2 concentrations were increased for one hour to alter significantly PaCO2 and pHa from 32 1 mm Hg and 7.52 0.02 to 74 2 mm Hg and 7.22 0.02, respectively. FeCl-FeNa increased significantly from 0.372 0.206 to 1.240 0.217 % and returned to baseline at two hours when PaCO2 and pHa were 37 0.6 mm Hg and 7.49 0.01, respectively. Arterial pH and FeCl-FeNa were significantly correlated. We conclude that the kidney responds rapidly to acute respiratory acidosis, within 30 mins of onset, by differential reabsorption of sodium and chloride. Disturbances of acid-base balance are common in patients admitted to intensive care units; causes include acute respiratory failure, diabetic ketoacidosis a 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 >>

4.5 Respiratory Acidosis - Compensation

4.5 Respiratory Acidosis - Compensation

Acid-Base Physiology 4.5.1 The compensatory response is a rise in the bicarbonate level This rise has an immediate component (due to a resetting of the physicochemical equilibrium point) which raises the bicarbonate slightly. Next is a slower component where a further rise in plasma bicarbonate due to enhanced renal retention of bicarbonate. The additional effect on plasma bicarbonate of the renal retention is what converts an "acute" respiratory acidsosis into a "chronic" respiratory acidosis. As can be seen by inspection of the Henderson-Hasselbalch equation (below), an increased [HCO3-] will counteract the effect (on the pH) of an increased pCO2 because it returns the value of the [HCO3]/0.03 pCO2 ratio towards normal. pH = pKa + log([HCO3]/0.03 pCO2) 4.5.2 Buffering in Acute Respiratory Acidosis The compensatory response to an acute respiratory acidosis is limited to buffering. By the law of mass action, the increased arterial pCO2 causes a shift to the right in the following reaction: CO2 + H2O <-> H2CO3 <-> H+ + HCO3- In the blood, this reaction occurs rapidly inside red blood cells because of the presence of carbonic anhydrase. The hydrogen ion produced is buffered by intracellular proteins and by phosphates. Consequently, in the red cell, the buffering is mostly by haemoglobin. This buffering by removal of hydrogen ion, pulls the reaction to the right resulting in an increased bicarbonate production. The bicarbonate exchanges for chloride ion across the erythrocyte membrane and the plasma bicarbonate level rises. In an acute acidosis, there is insufficient time for the kidneys to respond to the increased arterial pCO2 so this is the only cause of the increased plasma bicarbonate in this early phase. The increase in bicarbonate only partially returns the extracel Continue reading >>

Respiratory Acidosis

Respiratory Acidosis

DEFINITION Respiratory acidosis = a primary acid-base disorder in which arterial pCO2 rises to an abnormally high level. PATHOPHYSIOLOGY 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. PaCO2 is proportional to VCO2/VA VCO2 = CO2 production by the body VA = 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 CAUSES Inadequate Alveolar Ventilation central respiratory depression drug depression of respiratory centre (eg by opiates, sedatives, anaesthetics) neuromuscular disorders lung or chest wall defects airway obstruction inadequate mechanical ventilation Over-production of CO2 -> hypercatabolic disorders Malignant hyperthermia Thyroid storm Phaeochromocytoma Early sepsis Liver failure Increased Intake of Carbon Dioxide Rebreathing of CO2-containing expired gas Addition of CO2 to inspired gas Insufflation of CO2 into body cavity (eg for laparoscopic surgery) EFFECTS CO2 is lipid soluble -> depressing effects on intracellular metabolism RESP increased minute ventilation via both central and peripheral chemoreceptors CVS increased sympathetic tone peripheral vasodilation by direct effect on vessels acutely the acidosis will cause a right shift of the oxygen dissociation curve if the acidosis persists, a decrease in red cell 2,3 DPG occurs which shifts the curve back to the left CNS cerebral vasodilation increasing cerebral blood flow and intracranial pressure central depression at very high levels of pCO2 potent stimulation of ventilation this can result in dyspnoea, disorientation, acute confusion, headache, 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 >>

Renal Compensation

Renal Compensation

Chronic Carbon Dioxide Retainer Renal compensation of respiratory acidosis is by increased urinary excretion of hydrogen ions and resorption of HCO3−. This relatively slow process occurs over several days. Slowly, pH reaches low normal values, but HCO3− levels and BE are increased. This is the situation of the patient with chronic respiratory failure. Pulmonary patients usually have chronic obstructive pulmonary disease or restrictive pulmonary disease, or they are morbidly obese. Increased Co2 stores are the rule, and the normal respiratory drive to Paco2 is obtunded. This group of patients is sensitive to O2 supplementation because respiratory drive is predominantly determined by hypoxemia. Patients with a Pao2 in the mid-50s and a Paco2 at the same level usually receive home O2 treatment, initially at night to reduce pulmonary hypertension and to relieve dyspnea. When the chronic Co2 retainer develops an acute respiratory problem and pH levels fall to less than 7.20, noninvasive ventilatory assistance is usually indicated. Fetoplacental Elimination of Metabolic Acid Load Fetal respiratory and renal compensation in response to changes in fetal pH is limited by the level of maturity and the surrounding maternal environment. However, although the placentomaternal unit performs most compensatory functions,3 the fetal kidneys have some, although limited, ability to contribute to the maintenance of fetal acid–base balance. The most frequent cause of fetal metabolic acidosis is fetal hypoxemia owing to abnormalities of uteroplacental function or blood flow (or both). Primary maternal hypoxemia or maternal metabolic acidosis secondary to maternal diabetes mellitus, sepsis, or renal tubular abnormalities is an unusual cause of fetal metabolic acidosis. Pregnant women, a Continue reading >>

Acid Base Disorders

Acid Base Disorders

Arterial blood gas analysis is used to determine the adequacy of oxygenation and ventilation, assess respiratory function and determine the acid–base balance. These data provide information regarding potential primary and compensatory processes that affect the body’s acid–base buffering system. Interpret the ABGs in a stepwise manner: Determine the adequacy of oxygenation (PaO2) Normal range: 80–100 mmHg (10.6–13.3 kPa) Determine pH status Normal pH range: 7.35–7.45 (H+ 35–45 nmol/L) pH <7.35: Acidosis is an abnormal process that increases the serum hydrogen ion concentration, lowers the pH and results in acidaemia. pH >7.45: Alkalosis is an abnormal process that decreases the hydrogen ion concentration and results in alkalaemia. Determine the respiratory component (PaCO2) Primary respiratory acidosis (hypoventilation) if pH <7.35 and HCO3– normal. Normal range: PaCO2 35–45 mmHg (4.7–6.0 kPa) PaCO2 >45 mmHg (> 6.0 kPa): Respiratory compensation for metabolic alkalosis if pH >7.45 and HCO3– (increased). PaCO2 <35 mmHg (4.7 kPa): Primary respiratory alkalosis (hyperventilation) if pH >7.45 and HCO3– normal. Respiratory compensation for metabolic acidosis if pH <7.35 and HCO3– (decreased). Determine the metabolic component (HCO3–) Normal HCO3– range 22–26 mmol/L HCO3 <22 mmol/L: Primary metabolic acidosis if pH <7.35. Renal compensation for respiratory alkalosis if pH >7.45. HCO3 >26 mmol/L: Primary metabolic alkalosis if pH >7.45. Renal compensation for respiratory acidosis if pH <7.35. Additional definitions Osmolar Gap Use: Screening test for detecting abnormal low MW solutes (e.g. ethanol, methanol & ethylene glycol [Reference]) An elevated osmolar gap (>10) provides indirect evidence for the presence of an abnormal solute which is prese Continue reading >>

Disorders Of Acid-base Balance

Disorders Of Acid-base Balance

Module 10: Fluid, Electrolyte, and Acid-Base Balance By the end of this section, you will be able to: Identify the three blood variables considered when making a diagnosis of acidosis or alkalosis Identify the source of compensation for blood pH problems of a respiratory origin Identify the source of compensation for blood pH problems of a metabolic/renal origin Normal arterial blood pH is restricted to a very narrow range of 7.35 to 7.45. A person who has a blood pH below 7.35 is considered to be in acidosis (actually, physiological acidosis, because blood is not truly acidic until its pH drops below 7), and a continuous blood pH below 7.0 can be fatal. Acidosis has several symptoms, including headache and confusion, and the individual can become lethargic and easily fatigued. A person who has a blood pH above 7.45 is considered to be in alkalosis, and a pH above 7.8 is fatal. Some symptoms of alkalosis include cognitive impairment (which can progress to unconsciousness), tingling or numbness in the extremities, muscle twitching and spasm, and nausea and vomiting. Both acidosis and alkalosis can be caused by either metabolic or respiratory disorders. As discussed earlier in this chapter, the concentration of carbonic acid in the blood is dependent on the level of CO2 in the body and the amount of CO2 gas exhaled through the lungs. Thus, the respiratory contribution to acid-base balance is usually discussed in terms of CO2 (rather than of carbonic acid). Remember that a molecule of carbonic acid is lost for every molecule of CO2 exhaled, and a molecule of carbonic acid is formed for every molecule of CO2 retained. Figure 1. Symptoms of acidosis affect several organ systems. Both acidosis and alkalosis can be diagnosed using a blood test. Metabolic Acidosis: Primary Bic Continue reading >>

Intro To Arterial Blood Gases, Part 2

Intro To Arterial Blood Gases, Part 2

Arterial Blood Gas Analysis, Part 2 Introduction Acute vs. Chronic Respiratory Disturbances Primary Metabolic Disturbances Anion Gap Mixed Disorders Compensatory Mechanisms Steps in ABG Analysis, Part II Summary Compensatory Mechanisms Compensation refers to the body's natural mechanisms of counteracting a primary acid-base disorder in an attempt to maintain homeostasis. As you learned in Acute vs. Chronic Respiratory Disturbances, the kidneys can compensate for chronic respiratory disorders by either holding on to or dumping bicarbonate. With Chronic respiratory acidosis: Chronic respiratory alkalosis: the kidneys hold on to bicarbonate the kidneys dump bicarbonate With primary metabolic disturbances, the respiratory system compensates for the acid-base disorder. The lungs can either blow off excess acid (via CO2) to compensate for metabolic acidosis, or to a lesser extent, hold on to acid (via CO2) to compensate for metabolic alkalosis. With Metabolic acidosis: Metabolic alkalosis: ventilation increases to blow off CO2 ventilation decreases to hold on to CO2 The body's response to metabolic acidosis is predictable. With metabolic acidosis, respiration will increase to blow off CO2, thereby decreasing the amount of acid in the blood. Recall that with metabolic acidosis, central chemoreceptors are triggered by the low pH and increase the drive to breathe. For now, it is only important to learn (qualitatively) that there is a predictable compensatory response to metabolic acidosis. Later, during your 3rd or 4th year rotations, you might learn how to (quantitatively) determine if the compensatory response to metabolic acidosis is appropriate by using the Winter's Formula. The body's response to metabolic alkalosis is not as complete. This is because we would need to hypov Continue reading >>

Assessment Of Compensation In Acute Respiratory Acidosis - Deranged Physiology

Assessment Of Compensation In Acute Respiratory Acidosis - Deranged Physiology

Assessment of Compensation in Acute Respiratory Acidosis Mechanisms and classification of metabolic acidosis This chapter is concerned with the changes in pH and serum bicarbonate which result from acute fluctuations in dissolved CO2, as a consequence of acute changes in ventilation. It is a more detailed look at the wayCO2interacts with the human body fluid, and the resulting changes which develop in theserum bicarbonate concentration and pH. The discussion which follows builds upon and benefits from someof thebackground knowledgeoffered in otherchapters: Let us consider the favoured model of acute respiratory acidosis, the patient who has stopped breathing. Conventional wisdom dictates that so long as the oxygen supply continues to mass-transfer its way into the patient, then the patient will continue to produce CO2, and as a result of this metabolic activity the PaCO2will rise at a rate of around 3mmHg every minute. This technique of "apnoeic anaesthesia" is well known to anaesthetists, and has enjoyed a fluctuating level of interest since the sixties. With a high PEEP and a sufficient attention to detail one may go through the entire hour-long case without any breaths being taken by the patient. But, let us consider a situation where the airway isnotpatent, and a constant supply of oxygen is not available. The patient has stopped exhaling CO2. What will happen? Well, the PaCO2will rise by about 12mmHg over the first minute, and by about 3.4 mmHg per minute for every minute after that. How do we know this? Because in 1989, 14 volunteers consented to having their tube clamped during an anaesthetic. The clamps were released after 5 minutes, or if the patients became dangerously hypoxic. Magnitude of pH change due to pCO2increase Knowing the change in PaCO2,one can att Continue reading >>

Respiratory Compensation

Respiratory Compensation

Metabolic Acidosis Respiratory compensation for metabolic disorders is quite fast (within minutes) and reaches maximal values within 24 hours. A decrease in Pco2 of 1 to 1.5 mm Hg should be observed for each mEq/L decrease of in metabolic acidosis.27 A simple rule for deciding whether the fall in Pco2 is appropriate for the degree of metabolic acidosis is that the Pco2 should be equal to the last two digits of the pH. For example, compensation is adequate if the Pco2 decreases to 28 when the pH is 7.28. Alternatively, the Pco2 can be predicted by adding 15 to the observed (down to a value of 12). Although reduction in Pco2 plays an important role in correcting any metabolic acidosis, evidence suggests that it may in some respects be counterproductive because it inhibits renal acid excretion. Fetoplacental Elimination of Metabolic Acid Load Fetal respiratory and renal compensation in response to changes in fetal pH is limited by the level of maturity and the surrounding maternal environment. However, although the placentomaternal unit performs most compensatory functions,3 the fetal kidneys have some, although limited, ability to contribute to the maintenance of fetal acid–base balance. The most frequent cause of fetal metabolic acidosis is fetal hypoxemia owing to abnormalities of uteroplacental function or blood flow (or both). Primary maternal hypoxemia or maternal metabolic acidosis secondary to maternal diabetes mellitus, sepsis, or renal tubular abnormalities is an unusual cause of fetal metabolic acidosis. Pregnant women, at least in late gestation, maintain a somewhat more alkaline plasma environment compared with that of nonpregnant control participants. This pattern of acid–base regulation in pregnant women is present during both resting and after maximal e 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 >>

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 >>

Abg: Respiratory Acidosis/metabolic Alkalosis

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 >>

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