Paediatric Acid-base Disorders: A Case-based Review Of Procedures And Pitfalls
Paediatric acid-base disorders: A case-based review of procedures and pitfalls J Bryan Carmody , MD and Victoria F Norwood , MD Department of Pediatrics, Division of Pediatric Nephrology, University of Virginia, Charlottesville, Virginia, USA Correspondence: Dr J Bryan Carmody, Department of Pediatrics, Division of Pediatric Neprhology, University of Virginia, PO Box 800386, Charlottesville, Virginia 22903, USA. Telephone 434-924-2096, e-mail [email protected] , [email protected] Copyright 2013 Pulsus Group Inc. All rights reserved Acid-base disorders occur frequently in paediatric patients. Despite the perception that their analysis is complex and difficult, a straightforward set of rules is sufficient to interpret even the most complex disorders provided certain pitfalls are avoided. Using a case-based approach, the present article reviews the fundamental concepts of acid-base analysis and highlights common mistakes and oversights. Specific topics include the proper identification of the primary disorder; distinguishing compensatory changes from additional primary disorders; use of the albumin-corrected anion gap to generate a differential diagnosis for patients with metabolic acidosis; screening for mixed disorders with the delta-delta formula; recognizing the limits of compensation; use of the anion gap to identify hidden acidosis; and the importance of using information from the history and physical examination to identify the specific cause of a patients acid-base disturbance. Keywords: Acid-base equilibrium, Acid-base imbalances, Acidosis, Alkolosis, Blood Les troubles de lquilibre acido-basique sont frquents chez les patients dge pdiatrique. Mme si on les croit difficiles et complexes analyser, des rgles simples suffsent pour interprter mme les Continue reading >>
Chapter 47. Acidosis And Alkalosis
DuBose TD, Jr.. DuBose T.D., Jr. DuBose, Thomas D., Jr.Chapter 47. Acidosis and Alkalosis. In: Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson J, Loscalzo J. Longo D.L., Fauci A.S., Kasper D.L., Hauser S.L., Jameson J, Loscalzo J Eds. Dan L. Longo, et al.eds. Harrison's Principles of Internal Medicine, 18e New York, NY: McGraw-Hill; 2012. Accessed April 24, 2018. DuBose TD, Jr.. DuBose T.D., Jr. DuBose, Thomas D., Jr.. "Chapter 47. Acidosis and Alkalosis." Harrison's Principles of Internal Medicine, 18e Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson J, Loscalzo J. Longo D.L., Fauci A.S., Kasper D.L., Hauser S.L., Jameson J, Loscalzo J Eds. Dan L. Longo, et al. New York, NY: McGraw-Hill, 2012, Systemic arterial pH is maintained between 7.35 and 7.45 by extracellular and intracellular chemical buffering together with respiratory and renal regulatory mechanisms. The control of arterial CO2 tension (Paco2) by the central nervous system (CNS) and respiratory systems and the control of the plasma bicarbonate by the kidneys stabilize the arterial pH by excretion or retention of acid or alkali. The metabolic and respiratory components that regulate systemic pH are described by the Henderson-Hasselbalch equation: Under most circumstances, CO2 production and excretion are matched, and the usual steady-state Paco2 is maintained at 40 mmHg. Underexcretion of CO2 produces hypercapnia, and overexcretion causes hypocapnia. Nevertheless, production and excretion are again matched at a new steady-state Paco2. Therefore, the Paco2 is regulated primarily by neural respiratory factors and is not subject to regulation by the rate of CO2 production. Hypercapnia is usually the result of hypoventilation rather than of increased CO2 production. Increases or decreases in Paco2 represent de Continue reading >>
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Metabolic Acidosis | Washington Manual Of Medical Therapeutics
Washington Manual of Medical Therapeutics Type your tag names separated by a space and hit enter To view the entire topic, please sign in or purchase a subscription . The Washington Manual of Medical Therapeutics helps you diagnose and treat hundreds of medical conditions. Consult clinical recommendations from a resource that has been trusted on the wards for 50+ years. Explore these free sample topics: -- The first section of this topic is shown below -- The causes of a metabolic acidosis can be divided into those that cause an elevated AG and those with a normal AG. Many of the causes seen in clinical practice can be found in Table 12-3 . AG acidosis results from exposure to acids, which contribute an UA to the ECF. Common causes are DKA, lactic acidosis, and toxic alcohol ingestions. NonAG acidosis can result from the loss of from the GI tract. Renal causes due to renal excretion of or disorders of renal acid handling are referred to collectively as RTAs. loss occurs most commonly in the setting of severe diarrhea. The three forms of RTA correlate with the three mechanisms that facilitate renal acid handling: proximal bicarbonate reabsorption, distal H+ secretion, and generation of NH3, the principle urinary buffer. Urinary buffers reduce the concentration of free H+ in the filtrate, thus attenuating the back leak of H+, which occurs at low urinary pH. Proximal (type 2) RTA is caused by impaired proximal tubular reabsorption. Causes include inherited mutations (cystinosis), heavy metals, drugs (tenofovir, ifosfamide, carbonic anhydrase inhibitors), and multiple myeloma and other monoclonal gammopathies. Distal (type 1) RTA results from impaired distal H+ secretion. This may occur because of impairment in H+ secretion, as seen with a variety of autoimmune (Sjgren syn Continue reading >>
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 >>
Acid-base Disturbances In Gastrointestinal Disease
Acid-Base Disturbances in Gastrointestinal Disease Department of Medicine, University of Vermont College of Medicine, Burlington, Vermont Dr. F. John Gennari, 2319 Rehab, UHC Campus, Fletcher Allen Health Care, Burlington, VT 05401. Phone: 802-847-2534; Fax: 802-847-8736; E-mail: fgennari{at}uvm.edu Disruption of normal gastrointestinal function as a result of infection, hereditary or acquired diseases, or complications of surgical procedures uncovers its important role in acid-base homeostasis. Metabolic acidosis or alkalosis may occur, depending on the nature and volume of the unregulated losses that occur. Investigation into the specific pathophysiology of gastrointestinal disorders has provided important new insights into the normal physiology of ion transport along the gut and has also provided new avenues for treatment. This review provides a brief overview of normal ion transport along the gut and then discusses the pathophysiology and treatment of the metabolic acid-base disorders that occur when normal gut function is disrupted. The gastrointestinal tract is a slumbering giant with regard to acid-base homeostasis. Large amounts of H+ and HCO3 traverse the specialized epithelia of the various components of the gut every day, but under normal conditions, only a small amount of alkali (approximately 30 to 40 mmol) is lost in the stool ( 1 , 2 ). In contrast to the kidney, acid and alkali transport in the gut is adjusted for efficient absorption of dietary constituents rather than for acid-base homeostasis. The small amount of alkali lost as a byproduct of these transport events is easily regenerated by renal net acid excretion, which is regulated by the kidney to maintain body alkali stores. Disruption of normal gut function, however, uncovers its power to overwh Continue reading >>
Metabolic Acidosis And Hyperventilation Induced By Acetazolamide In Patients With Central Nervous System Pathology
ACETAZOLAMIDE, a carbonic anhydrase inhibitor, is used in patients with meningeal inflammation, mild intracranial hypertension, and basal skull fractures to decrease the formation of cerebrospinal fluid (CSF). It causes mild metabolic acidosis by inhibiting the reabsorption of bicarbonate (HCO−3) ions from renal tubules. This effect has been used successfully in the treatment of patients with chronic respiratory acidosis with superimposed metabolic alkalosis 1 and central sleep apnea syndrome. 2 Life-threatening metabolic acidosis during acetazolamide therapy has been observed only in patients with renal impairment or 3 diabetes 4 and in elderly patients. 5 Severe metabolic acidosis, associated with acetazolamide, in the absence of other predisposing factors has not been reported in patients with central nervous system disease. We report three cases of severe metabolic acidosis and hyperventilation during acetazolamide therapy in normal doses in adult patients without renal impairment. A 35-yr-old man with a head injury underwent craniotomy for evacuation of a traumatic left temporal extradural hematoma. Postoperatively, the patient underwent mechanical ventilation to maintain a partial pressure of arterial carbon dioxide (Paco2) of 30–35 mmHg. On the third postoperative day, 250 mg acetazolamide administered every 8 h through a nasogastric tube was started to treat a CSF leak from the operative wound. A T-piece trial of weaning was started on the fourth postoperative day. On the fifth postoperative day, patient respiratory rate increased to 40–44 breaths/min. Arterial blood gas analysis showed metabolic acidosis resulting in compensatory hypocapnia and a normal pH (table 1). The patient was sedated and underwent artificial ventilation for the next 6 days. Attempt Continue reading >>
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 >>
Acid Base Disorders - Learnpicu
Acidemia: Arterial blood pH below the normal range (<7.36) Alkalemia: Arterial bloodpH above the normal range (>7.44) Acidosis: a processthat tends to lower the pH (can be caused by fall in serum bicarbonate or a rise in PCO2 Alkalosis: a processthat tends to raise the pH (can be caused by increase in serum bicarbonate or a decrease in PCO2 Base Excess: the amount of strong acid needed to bring a solution back to a pH of 7.4 while keeping PCO2 at 40 mmHg Anion gap: A calculated value that indicates the presence of typically unmeasured anions (AG= Na -Cl -HCO3) with normal values ~8-12 mEq/L, primarily reflecting the presence of unmeasured organic acids Corrected anion gap: Albumin is negatively charged, effectively an "anion." In cases of hypoalbuminemia, Cl and HCO3 must increase to maintain electroneutrality. Hence, the AG will be falsely low as a result of hypoalbuminemia. Thus, you can correct for this: AGcorr=AG + 2.5 (normal albumin of 4 g/dl - measured albumin g/dl) 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 Continue reading >>
Metabolic Acidosis & Metabolic Alkalosis
Published by Lambert Morgan Modified over 2 years ago Presentation on theme: "Metabolic acidosis & Metabolic alkalosis" Presentation transcript: 1 Metabolic acidosis & Metabolic alkalosis 3 Primary Change Secondary change Net effect Hco3 Pco2 pH ( H+) Pco2 should by 1.2 mmHg for each mEq plasma Hco3 Inability to excrete dietary acid load Renal failure Renal tubular acidosis type 1 &4 Increased H+ load Lactic acidosis Ketoacidosis Toxin ingestions Increased HCO3 loss diarrhoea 5 Normal anion gap or hyper chloremic acidosis AG = Na+ (Hco3 + Cl ) Normal = 12 4 ( 8 16 ) Measure of unmeasured anion (protiens) Normal anion gap or hyper chloremic acidosis High anion gap 6 Metabolic acidosis Lactic acidosis Ketoacidosis Diarrhoea High anion gap Normal anion gap Lactic acidosis Ketoacidosis Renal failure Toxin ingestions Salicylate Methanol Ethylene glycol Diarrhoea Renal tubular acidosis 7 Clinical features Kussmals respiration (increased depth than rate) Neurologic symptoms: lethargy to coma In severe acidosis (pH< 7.1): Cardiac arrhythmia Reduced cardiac contractility Decreased inotropic response to catecholamines. Chronic acidosis Impaired growth in children Osteomalacia/osteopenia 8 Treatment Treat the underlying cause NaHCO3 therapy: Severe metabolic acidosis (pH<7.1) Chronic acidosis (sodium or potassium citrate) To alkalanise urine in salicylate poisoning 9 NaHCO3 therapy in severe acidosis: pH <7.1 Always treat the pH and not the HCO3 Only one half of bicarbonate deficit to be corrected in initial 12 hrs NaHCO3 dose= desired HCO3 observed HCO3 * 50%of body wt desired HCO3 =12 meq/L in HAG acidosis and meq/L in NAG 10 Example A 24 yr old type 1 diabetic male, weighing aroud 50 Kg presenting with fever, tachypnoea and abd pain to the EMU pH HCO pCo Urine ketones + BP 100 Continue reading >>
Metabolic Alkalosis - Endocrine And Metabolic Disorders - Merck Manuals Professional Edition
(Video) Overview of Buffering and the Henderson-Hasselbalch Equation By James L. Lewis, III, MD, Attending Physician, Brookwood Baptist Health and Saint Vincents Ascension Health, Birmingham Metabolic alkalosis is primary increase in bicarbonate (HCO3) with or without compensatory increase in carbon dioxide partial pressure (Pco2); pH may be high or nearly normal. Common causes include prolonged vomiting, hypovolemia, diuretic use, and hypokalemia. Renal impairment of HCO3 excretion must be present to sustain alkalosis. Symptoms and signs in severe cases include headache, lethargy, and tetany. Diagnosis is clinical and with arterial blood gas and serum electrolyte measurement. The underlying condition is treated; oral or IV acetazolamide or hydrochloric acid is sometimes indicated. Metabolic alkalosis is bicarbonate (HCO3) accumulation due to Intracellular shift of hydrogen ion (H+as occurs in hypokalemia ) Regardless of initial cause, persistence of metabolic alkalosis indicates that the kidneys have increased their HCO3 reabsorption, because HCO3 is normally freely filtered by the kidneys and hence excreted. Volume depletion and hypokalemia are the most common stimuli for increased HCO3 reabsorption, but any condition that elevates aldosterone or mineralocorticoids (which enhance sodium [Na] reabsorption and potassium [K] and hydrogen ion [H+] excretion) can elevate HCO3. Thus, hypokalemia is both a cause and a frequent consequence of metabolic alkalosis. The most common causes of metabolic alkalosis are Volume depletion (particularly when involving loss of gastric acid and chloride [Cl] due to recurrent vomiting or nasogastric suction) Among other causes (see Table: Causes of Metabolic Alkalosis ) are disorders that cause Continue reading >>
Surgical Procedures/acid Base Disorder
(Usually in clinical practice, H+ concentration is expressed as pH.) PaCO2 (Arterial CO2 concentration normal = 3545 mm Hg). HCO3 (Serum electrolytes normal = 2231 mmol/liter). Acidosis is a process that causes the accumulation of acid. Alkalosis is a process that causes the accumulation of alkali. The most common causes in the surgical practice include: Diuretic therapy (e.g., contraction alkalosis). Acid loss through GI secretions (e.g., nasogastric suctioning, vomiting). Exogenous administration of HCO3 or HCO3 precursors (e.g., citrate in blood). Chloride-unresponsive metabolic alkalosis is comparatively less common and includes: Renal tubular Cl wasting (Bartters syndrome) Measurement of urinary chloride concentration. Suggestive causes of the metabolic alkalosis if Urine Cl concentration is <15 mmol/liter: Sughgestive causes of the metabolic alkalosis if Urine Cl concentration is > 20 mmol/liter: Treatment principles in metabolic alkalosis:[ edit ] Removing and identifying underlying causes, Discontinuing exogenous alkali, repairing Cl, K+, and volume deficits. Correction of volume deficits (can be used 0.9% NaCl) and hypokalemia. H2-receptor antagonists or other acid-suppressing medications can be used after vomiting or nasogastric suctioning. Acetazolamide (5 mg/kg/day IV or PO) can be used. Eases fluid mobilization while decreasing renal HCO3 reabsorption. Tolerance to this diuretic may develop after 23 days. Ammonium chloride (NH4Cl) can be used in severe alkalemia (HCO3 >40 mmol/liter; rate not exceeding 5 ml/minute). Approximately one-half of the calculated volume of NH4Cl is usually administered and the acid-base status and Cl concentration is usually rechecked to determine the need of further treatment. Hepatic failure is contraindication for NH4Cl. HCl m Continue reading >>
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 >>
Metabolic Acidosis: Practice Essentials, Background, Etiology
Metabolic acidosis is a clinical disturbance characterized by an increase in plasma acidity. Metabolic acidosis should be considered a sign of an underlying disease process. Identification of this underlying condition is essential to initiate appropriate therapy. (See Etiology, DDx, Workup, and Treatment.) Understanding the regulation of acid-base balance requires appreciation of the fundamental definitions and principles underlying this complex physiologic process. Go to Pediatric Metabolic Acidosis and Emergent Management of Metabolic Acidosis for complete information on those topics. An acid is a substance that can donate hydrogen ions (H+). A base is a substance that can accept H+ ions. The ion exchange occurs regardless of the substance's charge. Strong acids are those that are completely ionized in body fluids, and weak acids are those that are incompletely ionized in body fluids. Hydrochloric acid (HCl) is considered a strong acid because it is present only in a completely ionized form in the body, whereas carbonic acid (H2 CO3) is a weak acid because it is ionized incompletely, and, at equilibrium, all three reactants are present in body fluids. See the reactions below. The law of mass action states that the velocity of a reaction is proportional to the product of the reactant concentrations. On the basis of this law, the addition of H+ or bicarbonate (HCO3-) drives the reaction shown below to the left. In body fluids, the concentration of hydrogen ions ([H+]) is maintained within very narrow limits, with the normal physiologic concentration being 40 nEq/L. The concentration of HCO3- (24 mEq/L) is 600,000 times that of [H+]. The tight regulation of [H+] at this low concentration is crucial for normal cellular activities because H+ at higher concentrations can b Continue reading >>
Pediatric Metabolic Alkalosis
Author: Lennox H Huang, MD, FAAP; Chief Editor: Timothy E Corden, MD more... Metabolic alkalosis is an acid-base disturbance caused by an elevation in the plasma bicarbonate (HCO3) concentration. This condition is not a disease; it is a sign or state encountered in certain disease processes. Although metabolic alkalosis may not be referred to as often as metabolic acidosis , it is the most common acid-base abnormality in hospitalized adults, [ 1 ] particularly those in the intensive care unit (ICU). [ 2 ] Alkalosis refers to a loss of acid or gain of base in the extracellular fluid (ECF); alkalemia refers to a change in blood pH. Alkalosis is not necessarily accompanied by alkalemia. The two types of metabolic alkalosis (ie, chloride-responsive, chloride-resistant) are classified based on the amount of chloride in the urine. Chloride-responsive metabolic alkalosis involves urine chloride levels of less than 20 mEq/L, is typically found to be below 10 mEq/L, and is characterized by decreased ECF volume and low serum chloride levels, such as occurs with vomiting. This type responds to administration of chloride salt. Chloride-resistant metabolic alkalosis involves urine chloride levels above 20 mEq/L and is characterized by increased ECF volume. As the name implies, this type resists administration of chloride salt. Primary aldosteronism is an example of chloride-resistant metabolic alkalosis. For a review of metabolic alkalosis in patients of all ages, see Metabolic Alkalosis . Singh AK. Metabolic alkalosis. In: Mushlin SB, Greene HL II, eds. Decision Making in Medicine: An Algorithmic Approach. 3rd ed. Philadelphia, PA: Mosby Elsevier; 2010. 374-5. Mhle K, Haug B, Flaatten H, Nielsen E. Metabolic alkalosis is the most common acid-base disorder in ICU patients. Crit Car Continue reading >>
Metabolic Acidosis Nclex Review Notes
Are you studying metabolic acidosis and need to know a mnemonic on how to remember the causes? This article will give you a clever mnemonic and simplify the signs and symptoms and nursing interventions on how to remember metabolic acidosis for nursing lecture exams and NCLEX. In addition, you will learn how to differentiate metabolic acidosis from metabolic alkalosis. Don’t forget to take the metabolic acidosis and metabolic alkalosis quiz. This article will cover: Metabolic acidosis simplified Lab values expected with metabolic acidosis Causes of metabolic acidosis Signs and symptoms of metabolic acidosis Nursing interventions for metabolic acidosis Lecture on Metabolic Acidosis Metabolic Acidosis Metabolic Acidosis in Simple Terms: a metabolic problem due to the buildup of acid in the body fluids which affects the bicarbonate (HCO3 levels) either from: increased acid production (ex: DKA where ketones (acids) increase in the body which decreases bicarbonate) decreased acid excretion (ex: renal failure where there is high amount of waste left in the body which causes the acids to increase and bicarb can’t control imbalance) loss of too much bicarb (diarrhea) When this acidic phenomena is taking place in the body other systems will try to compensate to increase the bicarb back to normal. One system that tries to compensate is the respiratory system. In order to compensate, the respiratory system will cause the body to hyperventilate by increasing breathing through Kussmaul’s respirations. Kussmaul respirations are deep, rapid breathes. The body hopes this will help expel CO2 (an acid) which will “hopefully” increase the pH back to normal. Lab values expected in Metabolic Acidosis: HCO3: decreased <22 Blood pH: decreased <7.35 CO2: <35 or normal (may be normal b Continue reading >>
