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562842 research-article2014 NCPXXX10.1177/0884533614562842Nutrition in Clinical PracticeAyers et al Invited Review Nutrition in Clinical Practice Volume XX Number X Month 201X 1–7 © 2014 American Society for Parenteral and Enteral Nutrition DOI: 10.1177/0884533614562842 ncp.sagepub.com hosted at online.sagepub.com Acid-Base Disorders: Learning the Basics Phil Ayers, PharmD, BCNSP, FASHP1; Carman Dixon, PharmD1; and Andrew Mays, PharmD1 Abstract Nutrition support practitioners should be confident in their ability to recognize and treat various metabolic and respiratory disorders encountered in daily practice. A clinician’s comprehension of the underlying physiologic processes and/or exogenous causes that occur during acid-base disorders is essential when making therapeutic decisions regarding fluids, parenteral nutrition, and electrolyte management. This invited review will discuss basic metabolic and respiratory disorders while briefly addressing mixed acid-base disorders. (Nutr Clin Pract. XXXX;xx:xx-xx) Keywords acid-base imbalance; acid-base equilibrium; acidosis; alkalosis; nutritional support; parenteral nutrition Introduction Acid-base disorders are often present in patients requiring nutrition support. The body maintains acid-base homeostasis through a complex system that involves the lungs, the kidneys, and endogenous buffers. Therefore, the interpretation of acidbase disorders should be done with a patient’s overall clinical condition in mind. Clinician uncertainty can be caused from a lack of experience, a misunderstanding of the significance of arterial blood gas results, or a lack of understanding the physiologic and pathophysiologic issues that accompany acid-base disorders. The purpose of this tutorial is to enhance the nutrition support clinician’s ability to recognize these disorders, identify precipitating causes, and provide specialized nutrition support to these patients. Definition of an Acid and a Base An acid is a substance that can donate a proton (H+). HCl ( hydrochloric acid ) → H + + Cl− A base is a substance that can accept a proton (H+). NH3 + H + → NH + 4 ( base ) Some common acid-base pairs include carbonic acid/bicarbonate, monobasic/dibasic phosphate, and lactic acid/lactate.1-3 The acidity of body fluids is expressed in terms of the hydrogen ion concentration. The degree of acidity is expressed as pH. The pH varies inversely with the H+ concentration; thus, an increase in H+ reduces the pH and a decrease elevates the pH. The normal pH of the body is maintained within a range of 7.35-7.45. Hydrogen regulation involves 3 steps: (1) extracellular and intracellular chemical buffering mechanisms, (2) partial pressure of carbon dioxide control by alterations in the rate of ventilation, and (3) plasma bicarbonate concentration control by renal H+ excretion. A pH of < 6.7 or > 7.7 is considered incompatible with life. Buffers Buffering is defined as the ability of a weak acid and its corresponding base to resist change in the pH upon the addition of a strong acid or base.1,3,4 The principal buffer in the body is the carbonic acid/bicarbonate system. Carbonic acid (H2CO3−), a weak acid, and its conjugate base (HCO3−) exist in equilibrium with H+. HCO3− + H + ↔ H 2CO3− Essentially all carbonic acid in the body exists as carbon dioxide gas; thus, carbon dioxide is the acid form of the carbonic acid/bicarbonate buffer system. When hydrogen ions are released, the concentration of bicarbonate will fall and the concentration of carbon dioxide gas will rise as the acid is buffered. From 1Mississippi Baptist Medical Center, Jackson, Mississippi. Financial disclosure: None declared. Corresponding Author: Phil Ayers, PharmD, BCNSP, FASHP, Mississippi Baptist Medical Center, 1225 N. State Street, Jackson, MS 39202, USA. Email: [email protected] Downloaded from ncp.sagepub.com at PENNSYLVANIA STATE UNIV on May 11, 2016 2 Nutrition in Clinical Practice XX(X) The Henderson-Hasselbalch equation for the carbonic acid/ bicarbonate buffer system describes the mathematical relationship of pH, bicarbonate concentration in milliequivalents per liter, and partial pressure of carbon dioxide (pCO2) in millimeters of mercury. ( pH = 6.1 + log HCO3− / 0.03 x pCO 2 ) The Henderson-Hasselbalch equation demonstrates that the ratio alone and not the absolute values of bicarbonate and carbon dioxide determines pH. The normal range for the anion gap is 3-11 mEq/L. Unmeasured serum anions such as proteins, phosphate, sulfate, and organic ions make the normal range for the anion gap a positive number. Serum albumin levels account for a significant portion of the unmeasured serum anions. A 1 g/dl drop in albumin will lower the anion gap by 2.5 mEq/L. Application of the anion gap allows the clinician to differentiate between Normal anion gap acidosis (hyperchloremic acidosis) Elevated anion gap acidosis Common causes of normal and elevated anion gap metabolic acidosis are listed in Tables 1 and 2. Role of the Kidneys in Acid-Base Regulating the concentration of bicarbonate is the principal role of the kidneys in acid-base balance.3-5 Approximately 90% of bicarbonate reabsorption occurs in the proximal tubule. This process is catalyzed by carbonic anhydrase. Filtered bicarbonate combines with hydrogen ions to form carbonic acid. Carbonic anhydrase, located in the brush border of the tubule, catalyzes carbonic acid to carbon dioxide (CO2). The unchanged CO2 crosses the cell membrane and passively diffuses into the renal tubule. Inside the cell, bicarbonate and carbonic acid are reformed. This process is also catalyzed by carbonic anhydrase. Bicarbonate is then reabsorbed into the capillary blood. Sodium and bicarbonate reabsorption are the net result of this process. Carbonic anhydrase inhibitors (eg, acetazolamide) cause excessive amounts of bicarbonate to be lost in the urine, which may lead to a metabolic acidosis. The kidneys also excrete 50-100 mEq/day of nonvolatile acids produced by the body. This process requires carbonic anhydrase. The distal tubule is the primary site of occurrence. The hydrogen ions secreted into the tubule lumen are buffered by phosphates and ammonia. The urine is normally acidic but usually not < 4.5. Case #1 A 21-year-old female presented to the emergency department (ED) with complaints of nausea, vomiting, and confusion.4,7,8 She is a type 1 diabetic with a continuous subcutaneous insulin infusion (CSII). Her last fingerstick blood glucose read “High” on her glucometer, and she realized that her insulin pump was disconnected from her body right before coming to the ED. Labs and ABGs are shown in Table 3. Disorder: Elevated Anion Gap Metabolic Acidosis Anion gap is elevated at 25 mEq/L. Hypovolemia should be addressed with expansion of the extracellular volume. Intravenous insulin infusion should be initiated to stop production of ketoacids. Potassium should be replaced once volume is replenished and insulin is administered. The patient should be transitioned off of insulin infusion back to CSII when deemed appropriate. Metabolic Alkalosis Metabolic Acidosis A metabolic acidosis is defined as an arterial pH < 7.35 (acidemia) and/or a low serum bicarbonate concentration.1-4,6 The bicarbonate concentration can be determined by the arterial blood gases (ABGs) (calculated) or as the total carbon dioxide concentration on the serum chemistry panel (measured). In most circumstances, the body compensates by hyperventilating to increase carbon dioxide excretion. This is seen by a low PaCO2 on arterial blood gas measurement. Once a metabolic acidosis is diagnosed, the next step is calculation of the anion gap. The most commonly used equation for the anion gap is noted below: ( Anion Gap = Na + - Cl− + HCO3 _ ) An elevated pH on ABGs and an elevated serum bicarbonate concentration are hallmark signs of a metabolic alkalosis.1,2,4,6,9 Respiratory compensation is minor in patients presenting with a metabolic alkalosis. The most common causes are loss of gastric acid secondary to vomiting or nasogastric suctioning and/or loss of intravascular volume and chloride as a result of diuretic use. Patients receiving parenteral nutrition may develop a metabolic alkalosis from excessive acetate and inadequate chloride in the formulation. Acetate is metabolized to bicarbonate, which leads to the alkalosis. A metabolic alkalosis can be classified into volume mediated (saline responsive) and volume independent (saline resistant). Obtaining a urine chloride concentration is useful in the diagnosis of patients who may respond to volume replacement. Table 4 lists the most common causes of saline responsive and saline resistant metabolic alkalosis. Downloaded from ncp.sagepub.com at PENNSYLVANIA STATE UNIV on May 11, 2016 Ayers et al 3 Table 1. Causes of Normal Anion Gap Metabolic Acidosis.1-4,6 Gastrointestinal Bicarbonate Loss •• •• •• •• •• •• •• Diarrhea Pancreatic fistula Small bowel fistula Obstructed ileal conduit Ureterosigmoidostomy Calcium Magnesium Drug-Induced Hyperkalemia with Renal Insufficiency Renal Acidosis Hypokalemic RTA type II (proximal) Drug induced: •• Acetazolamide •• Topiramate RTA type I (distal) Drug induced: •• Amphotericin B •• Ifosfamide Hyperkalemic •• RTA type IV (distal nephron dysfunction) •• Mineralocorticoid deficiency •• Hypoaldosteronism •• Tubulointerstitial disease •• Potassium sparing diuretics •• Angiotensin converting enzyme inhibitors •• Angiotensin receptor blockers •• Nonsteroidal antiinflammatory drugs •• Trimethoprim •• Pentamidine Other •• •• •• •• •• Acid loads Ammonium chloride Parenteral nutrition Rapid saline administration Cation exchange resins RTA, renal tubular acidosis. Table 2. Causes of Elevated Anion Gap Metabolic Acidosis.1-4,6 Renal Failure Failure to excrete acid Ketoacidosis Lactic Acidosis •• Diabetes •• Starvation •• Ethanol ingestion •• Shock (septic, cardiogenic, hypovolemic) •• Carbon monoxide poisoning •• Tonic-clonic seizures •• Hepatic disease Drugs Intoxications Linezolid Lorazepam (intravenous) Metformin Nitroprusside (cyanide accumulation) •• Nucleoside reverse transcriptase inhibitors •• Methanol •• Ethylene glycol •• •• •• •• Table 3. Case #1. Laboratory Laboratory Value (normal range) Laboratory Sodium Potassium Chloride CO2 BUN Creatinine Phosphorus Glucose 136 (135–145 mEq/L) 4.8 (3.5–5 mEq/L) 101 (98–107 mEq/L) 10 (22–31 mEq/L) 23 (7–20 mg/dL) 1.4 (0.7–1.5 mg/dL) 2.7 (2.5–4.5 mg/dL) 540 (70–110 mg/dL) pH pCO2 pO2 HCO3− WBC Hgb Hct UA Laboratory Value (normal range) 7.25 (7.35–7.45) 20 (35–45 mmHg) 130 (80–100 mmHg) 8.5 (24–30 mEq/L) 16 × 103/mm3 (4.8–10.8 × 103/mm3) 14.1 (13.5–17.5 g/dL) 52% (41%–53%) (+) ketones, glucose BUN, blood urea nitrogen; Hct, hematocrit; Hgb, hemoglobin; UA, urinalysis; WBC, white blood cell count. Case #2 A 60-year-old male postoperative day 4 of exploratory laparoscopy with lysis of adhesions had a positive kidney ureter bladder (KUB) for postoperative ileus.4,8 He currently has a nasogastric tube to suction with > 1000 mL output per 24 hours. He is receiving lactated ringers at 60 mL/hour and parenteral nutrition at 60 mL/hour with maximized acetate load. He also has furosemide 40 mg intravenous push (IVP) scheduled every 12 hours. Labs and ABGs are shown in Table 5. Disorder: Metabolic Alkalosis The patient has metabolic alkalosis secondary to maximized acetate load in PN, lactate from lactated ringers, nasogastric Downloaded from ncp.sagepub.com at PENNSYLVANIA STATE UNIV on May 11, 2016 4 Nutrition in Clinical Practice XX(X) Table 4. Causes of Metabolic Alkalosis.1,2,4,6,9 Saline Responsive (Urine Chloride < 10 mEq/L) •• •• •• •• •• •• Saline Resistant (Urine Chloride > 10 mEq/L) •• •• •• •• Vomiting Nasogastric suction Diuretic therapy Excessive bicarbonate administration Acetate salt in parenteral nutrition Rapid correction of hypocapnia Excessive mineralocorticoids Cushing’s syndrome Hyperaldosteronism Profound potassium and magnesium depletion •• Excessive licorice ingestion Sodium Potassium Chloride CO2 Creatinine Laboratory Value (normal range) •• •• •• •• Bartter syndrome Gitelman syndrome Renin secreting tumor Renal artery stenosis Table 6. Causes of Respiratory Acidosis.1,4,6,10 Table 5. Case #2. Laboratory Other Laboratory 145 (135–145 mEq/L) pH 3 (3.5–5 mEq/L) pCO2 96 (98–107 mEq/L) pO2 40 (22–31 mEq/L) HCO3− 1.2 (0.7–1.5 mg/dL) Base excess Laboratory Value (normal range) 7.52 (7.35–7.45) 48 (35–45 mmHg) 70 (80–100 mmHg) 39 (24–30 mEq/L) 14 (± 2) tube to suction, and furosemide diuresis. PN acetate load should be changed to maximize chloride load. Base intravenous fluids (IVF) should be changed to a non-lactate containing fluid and to maintain fluid balance. The PN and base IVF are exogenous sources of bicarbonate as acetate and lactate are both metabolized to bicarbonate. The nasogastric tube to suction is causing a loss of gastric acid. Thiazide or loop diuretics can cause a contraction metabolic alkalosis secondary to extracellular volume loss and stimulation of aldosterone secretion. Respiratory Acidosis Respiratory acidosis can be a chronic or acute condition that is due to hypoventilation secondary to a disruption in the respiratory system.1,2,4,6,10 Common causes of acute respiratory acidosis include central nervous system depression, acute exacerbations of chronic pulmonary diseases, and neuromuscular disorders. Chronic respiratory acidosis is commonly associated with chronic obstructive pulmonary disease, Pickwickian syndrome (obesity hypoventilation syndrome), and interstitial pulmonary disease. Patients have complications of altered mental status, motor disturbances, and dyspnea. Both chronic and acute respiratory acidosis will present in patients with a decreased pH and elevated PaCO2 on ABGs. However, patients who are in a state of chronic respiratory acidosis will have adequate time for renal compensation and have a smaller alteration of pH compared to those with acute respiratory acidosis. Patients with severely impaired CO2 excretion and/or life-threatening hypoxemia should have adequate oxygenation Acute CNS depression •• Opiates, benzodiazepines, propofol •• Head trauma Muscle weakness •• Guillain-Barre syndrome •• Myasthenia gravis crisis •• Severe hypokalemia or hypophosphatemia Diseases affecting gas exchange in pulmonary capillary •• Status asthmaticus •• COPD exacerbation •• Pneumothorax Chronic Extreme obesity Pickwickian syndrome Amyotropic lateral sclerosis Multiple sclerosis Poliomyelitis Muscular dystrophy Myasthenia gravis Kyphoscoliosis COPD Chronic ILD CNS, central nervous system; COPD, chronic obstructive pulmonary disease; ILD, interstitial lung disease. provided. This may require mechanical ventilation. The underlying cause of the acidosis should be treated accordingly (eg, reversal of narcotics or benzodiazepines with naloxone and flumazenil, bronchodilators and steroids for bronchospasm, adjustment of mechanical ventilation). Sodium bicarbonate (NaHCO3) should be reserved for the severely acidotic patient (pH < 7.15) to assist with ventilation and possibly restore responsiveness to bronchodilators. NaHCO3 should be used with caution because of the following potential complications: increased pulmonary congestion, no central nervous system protection, increased CO2 generation, and metabolic alkalosis. Table 6 lists some of the most common causes of respiratory acidosis. Case #3 A 28-year-old male was brought to the ED with unknown medical history.4,8 Medication bottles of alprazolam and hydrocodone were found empty. He arrived at the ED with laboratory and ABGs as shown in Table 7. After questioning of girlfriend, it was found that the patient recently returned from deployment in Afghanistan, and he has been dealing with chronic pain and anxiety. Downloaded from ncp.sagepub.com at PENNSYLVANIA STATE UNIV on May 11, 2016 Ayers et al 5 Table 8. Causes of Respiratory Alkalosis.1,4,6,11 Table 7. Case #3. Laboratory Sodium Potassium Chloride CO2 Creatinine Laboratory Value (normal range) Laboratory Laboratory Value (normal range) 137 (135–145 mEq/L) pH 7.25 (7.35–7.45) 60 (35–45 mmHg) 4.5 (3.5–5 mEq/L) pCO2 55 (80–100 mmHg) 100 (98–107 mEq/L) pO2 25 (22–31 mEq/L) HCO3− 26 (24–30 mEq/L) 0.7 (0.7–1.5 mg/dL) Glucose 89 (70–110 mg/dL) Disorder: Respiratory Acidosis Secondary to Opiate and Benzodiazepine Overdose The patient’s airway should be protected and adequate oxygen delivered. Naloxone and flumazenil should be administered for reversal of causative agents. Hypoxemia •• Pneumonia •• Pulmonary emboli •• Pulmonary edema •• Diffuse interstitial fibrosis •• Congestive heart failure Medications •• Salicylates •• Nicotine •• Xanthine CNS disorders •• CVA •• Pontine tumors •• Meningitis, encephalitis •• Head trauma •• Anxiety CNS, central nervous system; CVA, cerebral vascular accident. Respiratory Alkalosis Respiratory alkalosis is characterized by a decrease in PaCO2 and elevation in pH secondary to hyperventilation, as the lungs are excreting more CO2 than is being produced metabolically.1,4-6,11 Common causes of respiratory alkalosis are increased central stimulation of respiration, hypoxemia, and pulmonary disease. Patients can present with light-headedness, confusion, muscle cramps, and tetany. Respiratory alkalosis is found in many pulmonary diseases such as pneumonia, interstitial lung disease, and pulmonary emboli. This hyperventilation can be caused from hypoxemia, anemia, pain, or anxiety. Chemoreceptors in the brainstem and in the carotid and aortic bodies regulate ventilation, and these receptors sense increases in PaCO2 or decreases in serum bicarbonate, triggering hyperventilation. The correction of respiratory alkalosis should be geared toward correcting the underlying disorder. Respiratory depressants or the administration of acid has no place in the treatment of respiratory alkalosis. Many cases can be corrected by breathing into a paper bag to increase inspired CO2 and relieve symptoms. Table 8 shows causes of respiratory alkalosis. Case #4 A 65-year-old obese male s/p total knee arthroplasty 2 weeks ago presented to the ED after developing chest pain, shortness of breath, and tachypnea.4,8 Oxygen administered via nasal cannula at 2 L/minute did not increase oxygen saturation. After questioning, it was determined that he had not taken his enoxaparin as directed. He arrived to the ED with laboratory and ABGs as shown in Table 9. Disorder: Respiratory Alkalosis Computed tomography angiogram of the chest confirms pulmonary embolus. Appropriate treatment dose anticoagulation should be initiated after oxygenation and hemodynamic Table 9. Case #4. Laboratory Laboratory Value (normal range) Sodium 135 (135–145 mEq/L) Potassium 4 (3.5–5 mEq/L) Chloride 100 (98–107 mEq/L) 25 (22–31 mEq/L) CO2 Creatinine 0.8 (0.7–1.5 mg/dL) Laboratory Laboratory Value (normal range) pH pCO2 pO2 HCO3− O2 Sat 7.5 (7.35–7.45) 25 (35–45 mmHg) 52 (80–100 mmHg) 24 (24–30 mEq/L) 92% (97%–99%) O2 Sat, oxygen saturation. Table 10. Reference Blood Gas Values.1,4,6 Laboratory pH PaCO2, mmHg PaO2, mmHg HCO3−, mEq/L Base excess, mEq/L Arterial Blood Value 7.40 (7.35–7.45) 35–45 > 70 24–30 –2.4 to +2.3 support is addressed. Venous dopplers and further cardiac workup may be indicated. Arterial Blood Gases A key in the assessment of acid-base disorders is the interpretation of arterial blood gases to determine a patient’s oxygenation and acid-base status.1,4,6,12 The results from the ABGs will consist of the following: pH, partial pressure of carbon dioxide (PaCO2), partial pressure of oxygen (PaO2), calculated bicarbonate (HCO3−), and base excess. The reference values for ABGs are listed in Table 10. Downloaded from ncp.sagepub.com at PENNSYLVANIA STATE UNIV on May 11, 2016 6 Nutrition in Clinical Practice XX(X) The pH should be the first value assessed when diagnosing acid-base disorders. A pH < 7.35 represents an acidemia, and a pH > 7.45 represents an alkalemia. However, the pH can be within the normal range (7.35–7.45) when mixed acid-base disorders are present. Once it is determined whether the patient is acidemic or alkalemic based on pH, the PaCO2, commonly reported as pCO2 on ABG reports, should be evaluated to determine the lungs’ ability to excrete carbon dioxide (CO2). An elevated PaCO2 shows that the body is abnormally retaining CO2, and a decreased PaCO2 shows that the body is increasing the excretion of CO2. Once the pH and PaCO2 are measured, the bicarbonate concentration is then calculated using the Henderson-Hasselbalch equation. The calculated bicarbonate and serum bicarbonate can then be used to determine a patient’s metabolic component of acid-base disorder. Base excess/deficit is a calculated value that estimates the metabolic component of a patient’s acid-base status. This is calculated by determining the amount of H+ ions required to return the blood to a pH of 7.4 if the PaCO2 were adjusted to normal. Base excess could represent a patient with metabolic alkalosis, and base deficit could represent a patient with metabolic acidosis. tubule, leading to an increase of serum HCO3−. After 3–5 days, a new steady state is obtained solely due to the increase in renal H+ secretion. The opposite occurs during periods of respiratory alkalosis. A decrease in hydrogen ion secretion causes a loss of bicarbonate secondary to a rise in renal tubular cell pH. Therefore, the increased renal loss of bicarbonate produces a drop in serum HCO3−. This compensatory mechanism begins in about 2 hours but is not complete for 2–3 days. This compensatory mechanism typically occurs in 2 phases. The change in HCO3− is approximately equal to 0.1 times the variation in PaCO2 in acute respiratory acidosis and equal to 0.2 times the variation in PaCO2 in acute respiratory alkalosis. A more dramatic change in HCO3− is seen with respiratory conditions that persist for several hours. The increase or decrease in HCO3− is approximately equal to 0.4 times the variation in PaCO2 in respiratory acidosis or alkalosis, respectively. These calculations are estimates of normal compensation and are dependent on multiple factors. A > 10% variation in the predicted correction of PaCO2 or HCO3− in response to an alkalosis or acidosis could indicate a mixed acid-base disorder. Compensation Most of the discussion to this point has focused on singular acid-base disturbances and subsequent compensatory mechanisms. In practice, however, patients often experience a combination of more than 1 of these 4 primary disorders. Both metabolic acidosis and alkalosis can occur in tandem or in combination with respiratory acidosis or alkalosis as a double acid-base disorder. A triple acid-base disorder can occur if metabolic acidosis, metabolic alkalosis, and either respiratory acidosis or alkalosis are present. Respiratory acidosis and alkalosis are not seen in combination, though patients on a respirator can quickly change between hyperventilation and hypoventilation. Compensation via renal and respiratory systems will move the pH toward normal, but they will rarely correct pH to normal. Therefore, patients who present with a normal pH and alterations in PaCO2 and plasma HCO3− should be expected to have a mixed acid-base disorder.1-3,6,9-11,13 The body naturally corrects for simple acid-base disturbances via respiratory and renal mechanisms.1,3,9-12 The compensatory response to each of the previously listed disorders is predictable and occurs over varying lengths of time. Respiratory compensation begins within minutes and continues over a period of hours. However, it may take several days for renal mechanisms to fully compensate for acid-base abnormalities. The degree to which the body responds to a simple variance in pH may also be affected by the acute or chronic nature of the causative disorder, lung capacity, and normal renal function. In metabolic acidosis, the normal physiologic mechanism to compensate is to expel available carbon dioxide through hyperventilation. This action will decrease PaCO2 by approximately 1.2 times the decrease in HCO3−. If the change in PaCO2 is greater than this calculated value, a respiratory alkalosis could be present, and if the calculated change is less than expected, respiratory acidosis may be suspected. Hypoventilation and subsequent increase in PaCO2 is the body’s respiratory response to metabolic alkalosis. The expected increase in PaCO2 is equal to 0.6 times the measured increase in HCO3−. A minimal increase in PaCO2 could indicate the presence of respiratory alkalosis, a common disorder in critically ill patients. A higher than expected compensation would suggest an underlying respiratory acidosis. Compensatory mechanisms in the kidney are primarily responsible for the correction of respiratory acid-base disorders. In respiratory acidosis, the kidneys increase secretion of hydrogen ions and reabsorption of bicarbonate in the proximal Mixed Acid-Base Disorders Summary Interpreting acid-base disorders begins by understanding normal physiologic function. The body uses buffering processes, rate of ventilation, and renal mechanisms to maintain acid-base status. The relationship of carbonic acid and bicarbonate as described by the Henderson-Hasselbalch equation in addition to the partial pressure of gases, calculated bicarbonate, and base excess are used to help identify a potential variation in acid-base homeostasis. Each of these values is assessed by evaluating the patient’s arterial blood gases and aids in the identification of metabolic and respiratory acidosis or alkalosis. Metabolic acidosis may be further classified as having a normal or elevated anion gap. Knowledge of the typical causes Downloaded from ncp.sagepub.com at PENNSYLVANIA STATE UNIV on May 11, 2016 Ayers et al 7 of these disorders in combination with a thorough history and physical can aid the clinical practitioner to accurately assess the patient’s condition. Several tutorials and tools are available to further enhance a clinician’s understanding of acid-base disturbances. Nomograms using pH, pCO2, and HCO3 as coordinates can facilitate the recognition of compensation and mixed acid-base disorders. With the appropriate practice and understanding, they may be useful in the differentiation of acid-base conditions. These tools can be complex and are not necessary to diagnosis the patient’s status. An understanding of the principles outlined in this article will give the nutrition support clinician confidence in his or her ability to recognize metabolic and respiratory acid-base disorders in daily practice. References 1. Devlin JW, Matzke GR. Acid–base disorders. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey L, eds. Pharmacotherapy: A Pathophysiologic Approach. 9th ed. New York, NY: McGraw-Hill; 2014:797-814. 2. Langley G, Tajchman S. Fluid, electrolytes, and acid–base disorders. In: Mueller CM, ed. A.S.P.E.N. Adult Nutrition Support Core Curriculum. 2nd ed. Silver Spring, MD: 2012;98-120. 3. Rose B, Post T. Metabolic acidosis. In: Clinical Physiology of AcidBase and Electrolyte Disorders. 5th ed. New York, NY: McGraw-Hill; 2001:578-646. 4. Roberts AR. Arterial blood gases and acid–base balance. In: Lee M, ed. Basic Skills in Interpreting Laboratory Data. 5th ed. Bethesda, MD: American Society of Health-System Pharmacists; 2014:193-205. 5. Atherton JC. Role of the kidney in acid–base balance. Anaesthesia & Intensive Care Medicine. 2009;10(6):276-278. 6. DuBose TD Jr. Acidosis and alkalosis. In: Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson J, Loscalzo J, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York, NY: McGraw-Hill; 2012. http:// accesspharmacy.mhmedical.com/content.aspx?bookid=331&Sectio nid=40726770. Accessed August 9, 2014. 7. Vivian E, Blackorbay B. Endocrine disorders. In: Lee M, ed. Basic Skills in Interpreting Laboratory Data. 5th ed. Bethesda, MD: American Society of Health-System Pharmacists; 2014:283-330. 8. Langley G, Canada T, Day L. Acid-base disorders and nutrition support treatment. Nutr Clin Pract. 2003;18(3):259-261. 9. Rose B, Post T. Metabolic alkalosis. In: Clinical Physiology of AcidBase and Electrolyte Disorders. 5th ed. New York, NY: McGraw-Hill; 2001:551-577. 10. Rose B, Post T. Respiratory acidosis. In: Clinical Physiology of AcidBase and Electrolyte Disorders. 5th ed. New York, NY: McGraw-Hill; 2001:647-672. 11. Rose B, Post T. Respiratory alkalosis. In: Clinical Physiology of AcidBase and Electrolyte Disorders. 5th ed. New York, NY: McGraw-Hill; 2001:673-681. 12. Fulop M. Flow diagrams for the diagnosis of acid-base disorders. J Emerg Med. 1998;16(1):97-109. 13.Moviat M, van Haren F, van der Hoeven H. Conventional or Physicochemical Approach in Intensive Care Unit Patients with Metabolic Acidosis. Crit Care. 2003;7:R41-R45. http://ccforum.com/content/7/3/ R41. Accessed August 8, 2014. 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