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Metabolic Acidosis Pco2

Metabolic Acidosis

Metabolic Acidosis

Metabolic acidosis is a condition that occurs when the body produces excessive quantities of acid or when the kidneys are not removing enough acid from the body. If unchecked, metabolic acidosis leads to acidemia, i.e., blood pH is low (less than 7.35) due to increased production of hydrogen ions by the body or the inability of the body to form bicarbonate (HCO3−) in the kidney. Its causes are diverse, and its consequences can be serious, including coma and death. Together with respiratory acidosis, it is one of the two general causes of acidemia. Terminology : Acidosis refers to a process that causes a low pH in blood and tissues. Acidemia refers specifically to a low pH in the blood. In most cases, acidosis occurs first for reasons explained below. Free hydrogen ions then diffuse into the blood, lowering the pH. Arterial blood gas analysis detects acidemia (pH lower than 7.35). When acidemia is present, acidosis is presumed. Signs and symptoms[edit] Symptoms are not specific, and diagnosis can be difficult unless the patient presents with clear indications for arterial blood gas sampling. Symptoms may include chest pain, palpitations, headache, altered mental status such as severe anxiety due to hypoxia, decreased visual acuity, nausea, vomiting, abdominal pain, altered appetite and weight gain, muscle weakness, bone pain, and joint pain. Those in metabolic acidosis may exhibit deep, rapid breathing called Kussmaul respirations which is classically associated with diabetic ketoacidosis. Rapid deep breaths increase the amount of carbon dioxide exhaled, thus lowering the serum carbon dioxide levels, resulting in some degree of compensation. Overcompensation via respiratory alkalosis to form an alkalemia does not occur. Extreme acidemia leads to neurological and cardia 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 >>

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 >>

Bun, Glucose, Creatinine

Bun, Glucose, Creatinine

Normal Values pH = 7.38 - 7.42 [H+] = 40 nM/L for a pH of 7.4 PaCO2 = 40 mm Hg [HCO3] = 24 meq/L Acid base definitions Acid base disorder is considered present when there is abnormality in HCO3 or PaCO2 or pH. Acidosis and alkalosis refer to in-vivo derangement's and not to any change in pH. Acidemia (pH < 7.38) and Alkalemia (pH >7.42) refer to derangement's of blood pH. Kidney and Respiratory system play a key roles in maintaining the acid base status. Primary Acid base disorders Metabolic acidosis loss of [HCO3] 0r addition of [H+] Metabolic alkalosis loss of [H+] or addition of [HCO3] Respiratory acidosis increase in pCO2 Respiratory alkalosis decrease in pCO2 Recquired lab values/information Arterial blood gases: pH, PaCO2,PaO2,Sat,CO BUN, Glucose, Creatinine FIO2 and Clinical history Anion and Cations ANIONS CATIONS Chloride Sodium Bicarbonate(Total CO2) Potassium Proteins Calcium Organic acids Magnesium Phosphates Sulfates Electrochemical balance means that the total anions are the same as total Cations. For practical purposes anion gap is calculated using only Sodium, Chlorides and Total CO2.((140-(104+24)) = 12. Compensatory measures Buffering---occurs immediately Respiratory regulation of pCO2 is intermediate (12-24 hours) Renal regulation of [H] and [HCO3] occurs more slowly (several days) Extracellular almost entirely through bicarbonate whose concentration highest of all buffers small contribution from phosphate Intracellular Hemoglobin can directly buffer protons H+ entry into RBC matched by exit of Na and K+ Hemoglobin can directly buffer dissolved intracellular conversion of Buffer systems Hemoglobin can directly buffer protons H+ entry into RBC matched by exit of Na and K+ Hemoglobin can directly buffer dissolved intracellular conversion of Bicarbonate Continue reading >>

Basics | Blood Gas Analysis

Basics | Blood Gas Analysis

Introduction Blood gas analysis (BGA) serves the purpose of assessing respiratory function and the acid-base balance. The most important parameters for determining respiratory function are the partial pressures for oxygen (p02) and carbon dioxide (pCO2), as well as oxygen saturation (sO2). Using these parameters it is possible to detect pulmonary or, synonymously, respiratory insufficiency (formerly termed respiratory partial insufficiency) and ventilator insufficiency (formerly termed respiratory global insufficiency). For assessing the acid-base balance, pH value, pCO2 and base excess (BE) are important. By referring to the pH value, either acidosis or alkalosis can be diagnosed. By observing changes in pCO2 and BE it may be determined whether these are due to respiratory or non-respiratory causes (metabolic, renal, intestinal). CO2 indicates acidity and gives us information as to the respiratory system; the regulation of pCO2 takes place via ventilation (pCO2 lowered: hyperventilation; pCO2 elevated: hypoventilation). BE represents the bases and provides information on the non-respiratory system. BGA can be arterial or venous. For those who want to learn more… Indication Disturbances in acid-base balance and respiratory function. Normal findings and normal values The normal values are given in mean values. The width of the normal range should be taken from the responsible laboratory. Original findings Findings: 55-year-old female patient. Arterial BGA. Normal findings. Findings: 56-year-old male patient. Arterial BGA. Compensated respiratory acidosis with normal pO2 values, for example, in association with respiratory insufficiency during oxygen therapy.. Findings: 56-year-old female patient. Arterial BGA. Severe respiratory acidosis without compensation in connect 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 >>

Metabolic Acidosis Flashcards | Quizlet

Metabolic Acidosis Flashcards | Quizlet

pH = pKa(6.10) + log([HCO3-]/(0.03 x PCO2)) Will cause a respiratory compensation that causes the PCO2 to change in the *same direction* as the serum HCO3 to mitigate the change in pH The renal compensation will cause the HCO3 to change in the *same direction* as the PCO2 to lessen the pH change Will compensation return the arterial pH to normal? No. *A normal pH with an abnormal pCO2 and HCO3 indicates the presence of a mixed disorder* How do we know if there is a mixed or single disorder? If the change in HCO3 or PCO2 is less or more than would be expected as compensation then there is a mixed acid/base disorder present. Compensatory responses in chronic states: Compensatory responses can return the pH to a high-normal range with chronic respiratory alkalosis and to a low-normal range with chronic respiratory acidosis. What is the respiratory compensation in Metabolic Acidosis? For every *1 mEq/L* decrease in HCO3, we will get a *1.2 mmHG* decrease in PCO2 *arterial PCO2 should be similar to the decimal digits of the arterial pH. For example, if the serum bicarb is 11 and the arterial pH is 7.25, the arterial pCO2 should be 25. The degree to which the anion gap rises in relation to the fall in bicarb varies with the cause of the acidosis. - Renal losses of anions in ketoacidosis, D-lactic acidosis, and toluene intoxication - CKD when there is increased renal excretion of filtered anions, but hydorgen ion secretion is limited - Mixed disorder: combination of a non-gap and a gap metabolic acidosis - If between *1-2* it can usually be from *lactic acidosis* due to larger space of distribution of hydrogen ions compared to lactate anions and limited lactate excretion in hypoperfusion induced lactic acidosis where there is limited or no renal function - If between *2+* it 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 >>

Acid-base (anesthesia Text)

Acid-base (anesthesia Text)

There are four native buffer systems – bicarbonate, hemoglobin, protein, and phosphate systems. Bicarbonate has a pKa of 6.1, which is not ideal. Hemoglobin has histidine residues with a pKa of 6.8. Chemoreceptors in the carotid bodies, aortic arch, and ventral medulla respond to changes in pH/pCO2 in a matter of minutes. The renal response takes much longer. Arterial vs. Venous Gases Venous blood from the dorsum of the hand is moderately arterialized by general anesthesia, and can be used as a substitute for an ABG. pCO2 will only be off by ~ 5 mm Hg, and pH by 0.03 or 0.04 units [Williamson et. al. Anesth Analg 61: 950, 1982]. Confounding variables include air bubbles, heparin (which is acidic), and leukocytes (aka “leukocyte larceny”). VGB/ABG samples should be cooled to minimize leukocyte activity, however when blood is cooled, CO2 solubility increases (less volatile), and thus pCO2 drops. As an example – a sample taken at 37°C and at 7.4 will actually read as a pH of 7.6 if measured at 25°C. Most VBG/ABGs are actually measured at 37°C. A-aDO2 increases with age, as well as with increased FiO2 and vasodilators (which impair hypoxic pulmonary vasoconstriction). In the setting of a shunt, pulse oximetry can be misleading, thus the A-aDO2 should be calculated. If PaO2 is > 150 mm Hg (i.e., Hg saturation is essentially 100%), every 20 mm Hg of A-aDO2 represents 1% shunting of cardiac output. A/a is even better than A-aDO2 because it is independent of FiO2. PaO2/FiO2 is a reasonable alternative, with hypoxia defined as PaO2/FiO2 < 300 (a PaO2/FiO2 < 200 suggests a shunt fraction of 20% or more). Mixed venous blood should have a pO2 of ~ 40 mm Hg. Values < 30 mm Hg suggest hypoxemia, although one must always keep in mind that peripheral shunting and cyanide tox Continue reading >>

References

References

Arterial samples: pH 7.36-7.44, HCO3 21-27, PCO2 36-44 Venous: pH 0.03 units lower, HCO3 similar, PCO2 3-8 higher Capillary: similar to arterial (assuming no prolonged tourniquet use, ischemia, etc) 1. Look at the pH. What is the primary process occurring? low pH and high PCO2: respiratory acidosis high pH and low PCO2: respiratory alkalosis high pH and high HCO3: metabolic alkalosis if the pH is near normal but PCO2 and HCO3 are significantly abnormal, there is likely a mixed disorder 2. Assess the degree/chronicity of compensation present. Acute respiratory acidosis: HCO3 increases by 1 me/L and pH decreased by 0.08 for every 10 mmHg increase in PCO2 Chronic respiratory acidosis (3-5 days for renal compensation): HCO3 increases by 4me/Lfor and pH decreased by 0.03 for every 10 mmHg increase in PCO2 Metabolic acidosis: Expected PCO2= 1.5 X HCO3 + 8 +/-2 (Winter's Formula) or the decimal digits of pH should be similar to the PCO2 (ie pH 7.25 should have a PCO2 of 25 in a metabolic acidosis). If the patient's PCO2 is higher than expected, there is a concurrent respiratory acidosis. If the patient's PCO2 is lower than expected, there is a concurrent respiratory alkalosis. If it similar to expected, the compensation is appropriate Metabolic alkalosis: PCO2 increases by 0.7 mmHg for every 1 meq/L increase in HCO3 3. If there is a metabolic acidosis, assess the anion gap. Elevated anion gap --> MUDPILES (Methanol, uremia, diabetic ketoacidosis, propylene glycol, INH, lactic acidosis, ethylene glycol, salicylates) If there is an elevated anion gap, consider calculating the / = Anion gap/ [HCO3-]. <0.4 is consistent with hyperchloremic nongap acidosis, <1 with high AG and normal AG acidosis, 1-2 pure AG acidosis, >2 concurrent metabolic alkalosis or preexisting compensated re Continue reading >>

How To Compute Expected Pco2 In Chronic Metabolic Acidosis ?

How To Compute Expected Pco2 In Chronic Metabolic Acidosis ?

How to compute PaCO2 during chronic metabolic acidosis? We dont have to compute for chronic metabolic acidosis (CMA) since the PaCO2 value in mmHg is equal to the two digits of the pH value For instance IF pH = 7.25, PaCO2 should be about 25 mmHg, With this formula, we can immediately focus on the respiratory compensation: If PaCO2 is significantly greater than 25 mmHg, the respiratory compensation is inadequate, thus a respiratory insufficiency is associated; If PaCO2 is largely lower than 25 mmHg, the respiratory is higher than CMA required, therefore a respiratory alkalosis is associated to CMA. Furthermore, according to the alveolar gas equation (Fi02 of 21%): Pa02 + PaCO2= 140 mmHg; in this case, in absence of pulmonary disease, PaO2 should be elevated, near 115 mmHg FG Brivet, FM Jacobs: Anomalies de lEquilibre Acido-basique dOrigine Mtabolique in Ranimation Mdicale ; Collge National des Enseignants de Ranimation Mdicale, Masson Paris 2009 PP 1356-1365. In the same way for ACUTE Metabolic Acidosis, instead of using Narinss formula: It is easier to use Schlichtigs formula: Delta PaCO2 (mmHg) = Standard base excess (2) Thus in case of acute metabolic acidosis, with the same value of pH (7.25) and an SBE of 18, for instance (SBE value being systematically reported by lab but rarely used.), PaC02 should be near 22 mmHg (40- 18). If PaCO2 value is greater than the expected value, respiratory compensation is inadequate, the patient is at risk of respiratory failure, whereas if PaCO2 is lower than 18 we can claim that a respiratory alkalosis is associated. With this approach I can say goodbye Mr. Davenport, you are too sophisticated for me at 5 in the morning 1/ Narins RG, Emmet M. Simple and mixed acid-base disorders: a practical approach. Medicine, 1980, 59: 161-167. 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 >>

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 >>

Arterial Blood Gases (blood Gases), Acidosis And Alkalosis

Arterial Blood Gases (blood Gases), Acidosis And Alkalosis

Sample The better choice is the Radial artery. The sample may be taken from the femoral artery or brachial. The tests are done immediately because oxygen and carbon dioxide are unstable. Arterial blood is better than the venous blood. For arterial blood don't use the tourniquet and no pull on the syringe plunger. For venous blood syringe or tubes are completely filled and apply a tourniquet for few seconds. Arterial VS Venous blood Arterial blood gives good mixture of blood from various areas of the body. Venous blood gives information of the local area from where the blood sample is taken. Metabolism of the extremity varies from area to area. Arterial blood measurement gives the better status of the lung oxygenating the blood. Arterial blood gives information about the ability of the lung to regulate the acid-base balance through retention or release of CO2. Precautions for the collection of blood Avoid pain and anxiety to the patient which will lead to hyperventilation. Hyperventilation due to any cause leads to decreased CO2 and increased pH. Keep blood cool during transit. Don't clench finger or fist. This will leads to lower CO2 and increased acid metabolites. pCO2 values are lower in the sitting or standing position in comparison with the supine position. Don't delay the performance of the test. Avoid air bubbles in the syringe. Excess of heparin decreases the pCO2 may be 40% less. Not proper mixing of the blood before running the test. Purpose of the test This test is done on the mostly hospitalized patient. Mostly the patients are on ventilator or unconscious. For patients in pulmonary distress. To assess the metabolic (renal) acid-base and electrolytes imbalance. Its primary use is to monitor arterial blood gases and pH of blood. Also used to monitor oxygenatio Continue reading >>

Pco2 And [k+]p In Metabolic Acidosis: Certainty For The First And Uncertainty For The Other

Pco2 And [k+]p In Metabolic Acidosis: Certainty For The First And Uncertainty For The Other

PCO2 and [K+]p in Metabolic Acidosis: Certainty for the First and Uncertainty for the Other *Department of Medicine, Renal Section, Baylor College of Medicine, The Methodist Hospital, and Veterans Affairs Medical Center, Houston, Texas; and Department of Medicine, Tufts University School of Medicine, Division of Nephrology, Caritas St. Elizabeths Medical Center, Boston, Massachusetts. Correspondence to Dr. Nicolaos E. Madias, Department of Medicine, Tufts University School of Medicine, Division of Nephrology, Caritas St. Elizabeths Medical Center, 736 Cambridge St., Boston, MA 02135. Phone: 617-562-7502; Fax: 617-562-7797; E-mail: nicolaos_madias{at}cchcs.org Studies by Schwartz and colleagues at Tufts University School of Medicine in the 1960s described the whole-body acid-base response (i.e., secondary changes in plasma [HCO3] to graded degrees of acute respiratory acidosis and acute respiratory alkalosis in humans ( 1,2 ). Corresponding data for acute metabolic acid-base disorders (i.e., secondary changes in PaCO2) are essentially unavailable: meager observations have been made in acute metabolic alkalosis, and no data exist for acute metabolic acidosis. The report by Wiederseiner et al. ( 3 ) in this issue of JASN addresses the secondary physiologic response to acute mineral acid-induced metabolic acidosis in humans. In a carefully conducted study, the slope of the PCO2 (arterialized)/[HCO3] relationship averaged 0.85 mmHg per mmol/L in six healthy male volunteers with acute NH4Cl-induced metabolic acidosis who had attained an operational steady state (by convention, acute corresponds to the interval before any meaningful contribution of changes in renal acidification to plasma [HCO3]). The range of hypobicarbonatemia achieved in this study was limited (nadir of ap Continue reading >>

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