diabetestalk.net

Respiratory Acidosis Formula

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 >>

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 >>

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 >>

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 >>

Acid-base Disorders - Endocrine And Metabolic Disorders - Merck Manuals Professional Edition

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 >>

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 >>

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

LABORATORY TESTS The following lab tests can be used to interpret and explain acidosis and alkalosis conditions. All are measured on blood samples. 1. pH: This measures hydrogen ions - Normal pH = 7.35-7.45 2. pCO2= Partial Pressure of Carbon Dioxide: Although this is a pressure measurement, it relates to the concentration of GASEOUS CO2 in the blood. A high pCO2 may indicate acidosis. A low pCO2 may indicate alkalosis. 3. HCO3- = Bicarbonate: This measures the concentration of HCO3- ion only. High values may indicate alkalosis since bicarbonate is a base. Low values may indicate acidosis. 4. CO2 = Carbon Dioxide Content: This is a measure of ALL CO2 liberated on adding acid to blood plasma. This measure both carbon dioxide dissolved and bicarbonate ions and is an older test. Do not confuse with pCO2 Typically, dissolved carbon dioxide = l.2-2.0 mmoles/L and HCO3- = 22-28 mmoles/L Therefore, although it is listed as CO2 content, the lab test really reflects HCO3- concentration. Respiratory Acidosis .ABNORMAL pH IN THE BODY: ACIDOSIS AND ALKALOSIS: INTRODUCTION: Normal blood pH is maintained between 7.35 and 7.45 by the regulatory systems. The lungs regulate the amount of carbon dioxide in the blood and the kidneys regulate the bicarbonate. When the pH decreases to below 7.35 an acidosis condition is present. Acidosis means that the hydrogen ions are increased and that pH and bicarbonate ions are decreased. A greater number of hydrogen ions are present in the blood than can be absorbed by the buffer systems. Alkalosis results when the pH is above 7.45. This condition results when the buffer base (bicarbonate ions) is greater than normal and the concentration of hydrogen ions are decreased. Both acidosis and alkalosis can be of two different types: respiratory and metabol 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 >>

American Thoracic Society - Interpretation Of Arterial Blood Gases (abgs)

American Thoracic Society - Interpretation Of Arterial Blood Gases (abgs)

Interpretation of Arterial Blood Gases (ABGs) Chief, Section of Pulmonary, Critical Care & Sleep Medicine Bridgeport Hospital-Yale New Haven Health Assistant Clinical Professor, Yale University School of Medicine (Section of Pulmonary & Critical Care Medicine) Interpreting an arterial blood gas (ABG) is a crucial skill for physicians, nurses, respiratory therapists, and other health care personnel. ABG interpretation is especially important in critically ill patients. The following six-step process helps ensure a complete interpretation of every ABG. In addition, you will find tables that list commonly encountered acid-base disorders. Many methods exist to guide the interpretation of the ABG. This discussion does not include some methods, such as analysis of base excess or Stewarts strong ion difference. A summary of these techniques can be found in some of the suggested articles. It is unclear whether these alternate methods offer clinically important advantages over the presented approach, which is based on the anion gap. Step 1: Assess the internal consistency of the values using the Henderseon-Hasselbach equation: If the pH and the [H+] are inconsistent, the ABG is probably not valid. Step 2: Is there alkalemia or acidemia present? Remember: an acidosis or alkalosis may be present even if the pH is in the normal range (7.35 7.45) You will need to check the PaCO2, HCO3- and anion gap Step 3: Is the disturbance respiratory or metabolic? What is the relationship between the direction of change in the pH and the direction of change in the PaCO2? In primary respiratory disorders, the pH and PaCO2 change in opposite directions; in metabolic disorders the pH and PaCO2 change in the same direction. Decrease in [HCO3-] = 5( PaCO2/10) to 7( PaCO2/10) If the observed compensa Continue reading >>

Acid Base Evaluation

Acid Base Evaluation

Use the measured total CO2 from venous blood as HCO3 anion gap is an artifact because some anions are not measured gap is mainly due to unmeasured proteins, phosphates and sulfates Normal anion gap is 8-12 meq/L (Varies from Lab to Lab) useful in identifying mixed acidbase disorders in single acidbase disorder the difference between anion gap and the change in total CO2 should be negligible in other words change in total CO2 (Normal total CO2-observed total CO2) should be equal to anion gap. Excess bicarbonate gap suggests metabolic alkalosis Decrease in the gap suggests metabolic acidosis Respiratory compensation for Metabolic acid basedisturbance You can use the following crude formula 0.1 change in pH 10 mm change of PaCO2. If all else is well the PaCO2 should be the same as decimal values of pH i.e. for a pH of 7.28, the CO2 levels would be 28 mm Hg. Acidosis increases respiratory drive, alveolar ventilation and gets rid of Carbonic acid. Respiratory system can never completely compensate for a metabolic defect. Respiratory compensation attempts to maintain pH in a reasonable range. It is unusual to see CO2 retention (I don't agree with Books and others) Compensation is never complete. If the pH is normal there is probablya superimposed second acid base disturbance. Estimation of expected PaCO2for a given acidic pH also enables us to determine whether respiratorycompensation is appropriate. 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 >>

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 >>

Blood Gas Analysis--insight Into The Acid-base Status Of The Patient

Blood Gas Analysis--insight Into The Acid-base Status Of The Patient

Acid-Base Physiology Buffers H+ A- HCO3- CO2 Buffers H+ A- CO2 Cells Blood Kidney Lungs Fluids, Electrolytes, and Acid-Base Status in Critical Illness Blood Gas Analysis--Insight into the Acid-Base status of the Patient The blood gas consists of pH-negative log of the Hydrogen ion concentration: -log[H+]. (also, pH=pK+log [HCO3]/ 0.03 x pCO2). The pH is always a product of two components, respiratory and metabolic, and the metabolic component is judged, calculated, or computed by allowing for the effect of the pCO2, ie, any change in the pH unexplained by the pCO2 indicates a metabolic abnormality. CO +H 0ºº H CO ººHCO + H2 2 2 3 3 - + CO2 and water form carbonic acid or H2CO3, which is in equilibrium with bicarbonate (HCO3-)and hydrogen ions (H+). A change in the concentration of the reactants on either side of the equation affects the subsequent direction of the reaction. For example, an increase in CO2 will result in increased carbonic acid formation (H2CO3) which leads to an increase in both HCO3- and H+ (\pH). Normally, at pH 7.4, a ratio of one part carbonic acid to twenty parts bicarbonate is present in the extracellular fluid [HCO3-/H2CO3]=20. A change in the ratio will affect the pH of the fluid. If both components change (ie, with chronic compensation), the pH may be normal, but the other components will not. pCO -partial pressure of carbon dioxide. Hypoventilation or hyperventilation (ie, minute2 ventilation--tidal volume x respitatory rate--imperfectly matched to physiologic demands) will lead to elevation or depression, respectively, in the pCO2. V/Q (ventilation/perfusion) mismatch does not usually lead to abnormalities in PCO2 because of the linear nature of the CO2 elimination curve (ie, good lung units can make up for bad lung units). Diffus Continue reading >>

More in ketosis