Acid-Base Balance and Arterial Blood Gases

Acid-Base Balance and Arterial Blood Gases
Chapter 17 Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Introduction Maintain a steady balance between acids and bases to achieve homeostasis Health problems lead to imbalance Diabetes mellitus Chronic obstructive pulmonary disease (COPD) Kidney disease The body normally maintains a steady balance between the acids produced during normal metabolism and the bases that neutralize and promote the excretion of the acids. Because these acids alter the internal environment of the body, their regulation is necessary to maintain homeostasis and acid-base balance. Many health problems may lead to acid-base imbalances. Patients with diabetes mellitus, COPD, and kidney disease frequently develop acid-base imbalances. It is important to remember that an acid-base imbalance is not a disease but a manifestation of an underlying health problem. Always consider the possibility of acid-base imbalance in patients with serious illnesses. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

pH Measure of H+ ion concentration
Blood is slightly alkaline at pH 7.35 to 7.45 <7.35 is acidosis >7.45 is alkalosis The acidity or alkalinity of a solution depends on its hydrogen ion (H+) concentration. An increase in H+ concentration leads to acidity; a decrease leads to alkalinity. Despite the fact that acids are produced by the body daily, the H+ concentration of body fluids is small and maintained within a narrow range to ensure optimal cell function. Hydrogen ion concentration is usually expressed as a negative logarithm (symbolized as pH) rather than in milliequivalents. The use of the negative logarithm means that the lower the pH, the higher the H+ concentration. The pH of a chemical solution may range from 1 to 14. A solution with a pH of 7 is considered neutral. An acid solution has a pH less than 7, and an alkaline solution has a pH greater than 7. Blood is slightly alkaline (pH 7.35 to 7.45); yet if it drops below 7.35, the person has acidosis, even though the blood may never become truly acidic. If the blood pH is greater than 7.45, the person has alkalosis. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Copyright © 2014 by Mosby, an imprint of Elsevier Inc.
Range of pH In the healthy state, a ratio of 1 part carbonic acid to 20 parts bicarbonate provides a normal serum pH between 7.35 and 7.45. Any deviation to the left of 7.35 results in an acidotic state. Any deviation to the right of 7.45 results in an alkalotic state. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Acid-Base Regulation Metabolic processes produce acids that must be neutralized and excreted Regulatory mechanisms Buffers : react immediately Respiratory system : responds within minutes and reaches maximum effectiveness in hours Renal system :response takes 2-3 days maximum response, but kidneys can maintain balance indefinitely in chronic imbalances Because normal metabolic processes produce acids, the body must neutralize and excrete them to maintain a normal balance between acids and bases. The body has three mechanisms by which it regulates the acid-base balance to maintain the arterial pH between 7.35 and These mechanisms are the buffer systems, the respiratory system, and the renal system. The regulatory mechanisms react at different speeds. Buffers react immediately. The respiratory system responds in minutes and reaches maximum effectiveness in hours. The renal response takes 2 to 3 days to respond maximally, but the kidneys can maintain balance indefinitely in chronic imbalances. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Buffer System Act chemically to change strong acids to weak acids or bind acids Carbonic acid–bicarbonate, phosphate, protein, and hemoglobin buffers Also shifting of hydrogen in and out of cell The buffer system is the fastest-acting system and the primary regulator of acid-base balance. Buffers act chemically to change strong acids into weaker acids or to bind acids to neutralize their effect. This minimizes the effect of acids on blood pH until their excretion from the body. The buffers in the body include carbonic acid–bicarbonate, monohydrogen-dihydrogen phosphate, intracellular and plasma protein, and hemoglobin buffers. The cell can also act as a buffer by shifting hydrogen in and out of the cell. With an accumulation of H+ in the ECF, the cells can accept H+ in exchange for another cation (e.g., K+). The body buffers an acid load better than it neutralizes base excess. Buffers cannot maintain pH without the adequate functioning of the respiratory and renal systems. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Carbonic acid (H2CO3)/Bicarbonate (HCO3–) Buffer
HCl + NaH2CO  NaCl + H2CO3 Strong acid + strong base is buffered into salt and weak acid In this way, combining a strong acid with a strong base prevents the acid from making a large change in the blood’s pH. The carbonic acid is broken down to H2O and CO2. The lungs excrete CO2, either combined with insensible H2O as carbonic acid, or alone as CO2. In this process, the buffer system maintains a 20:1 ratio between bicarbonate and carbonic acid and the normal pH. The other buffers systems (phosphate, proteins, hemoglobin) work in the same manner. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Respiratory System Regulation
CO2 + H2O  H2CO3  H++ HCO3– Respiratory center in medulla controls breathing Increased respirations lead to increased CO2 elimination and decreased CO2 in blood Decreased respirations lead to CO2 retention When released into circulation, CO2 enters RBCs and combines with H2O to form H2CO3. This carbonic acid dissociates into hydrogen ions and bicarbonate. The free hydrogen is buffered by hemoglobin molecules, and the bicarbonate diffuses into the plasma. In the pulmonary capillaries, this process is reversed, and CO2 is formed and excreted by the lungs. The respiratory center in the medulla in the brainstem controls the rate of excretion of CO2. If increased amounts of CO2 or H+ are present, the respiratory center stimulates an increased rate and depth of breathing. If the center senses low H+ or CO2 levels, respirations are inhibited. As a compensatory mechanism, the respiratory system acts on the CO2 + H2O side of the reaction by altering the rate and depth of breathing to “blow off” (through hyperventilation) or “retain” (through hypoventilation) CO2. If a respiratory problem is the cause of an acid-base imbalance (e.g., respiratory failure), the respiratory system loses its ability to correct a pH alteration. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Renal System Regulation
Conserves bicarbonate and excretes acid Three mechanisms for acid elimination Secrete free hydrogen Combine H+ with ammonia (NH3) Excrete weak acids Under normal conditions, the body depends on the kidneys to reabsorb and conserve all of the bicarbonate they filter and excrete a portion of the acid produced by cellular metabolism. The three mechanisms of acid elimination are (1) secretion of small amounts of free hydrogen into the renal tubule, (2) combination of H+ with ammonia (NH3) to form ammonium (NH4+), and (3) excretion of weak acids. To compensate for acidosis, the kidneys can generate additional bicarbonate and eliminate excess H+, lowering the pH of the urine. If the renal system is the cause of an acid-base imbalance (e.g., renal failure), it loses its ability to correct a pH alteration. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Acid-Base Regulation This figure demonstrates the interrelationship between the lungs, kidneys, and buffer system (in this case, erythrocytes) in the maintenance of acid-base balance. The lungs control gas exchange to blow off or retain carbon dioxide (CO2) CO2 generated in tissues is transported in plasma as bicarbonate; the erythrocyte hemoglobin (Hb) also contributes to CO2 transport. Hemoglobin buffers hydrogen ion derived from carbonic acid. The kidneys reabsorb filtered bicarbonate in the proximal tubules and generate new bicarbonate in the distal tubules, where there is a net secretion of hydrogen ion. Ultimate balance between bicarbonate and carbonic acid to maintain pH within normal limits. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Alterations in Acid-Base Balance
Imbalances occur when compensatory mechanisms fail Classification of imbalances : acid-base imbalance seen when ratio is 1:20 between acid-base content is altered Compensatory process may be inadequate because either the pathophysiologic process is overwhelming or there is insufficient time for compensation process to function Imbalances include: Respiratory (CO2) or metabolic (HCO3) Acidosis or alkalosis Acute or chronic An acid-base imbalance results when there is an alteration in the ratio of 20:1 between base and acid content. This occurs when a primary disease or process alters one side of the ratio (e.g., CO2 retention in pulmonary disease) and the compensatory processes that maintain the other side of the ratio (e.g., increased renal bicarbonate reabsorption) either fail or are inadequate. The compensatory process may be inadequate because either the pathophysiologic process is overwhelming or there is insufficient time for the compensatory process to function. Acid-base imbalances are classified as respiratory or metabolic. Respiratory imbalances result from the retention or an excess of carbon dioxide altering carbonic acid concentrations Metabolic imbalances affect the base bicarbonate. Acidosis is caused by an increase in carbonic acid (respiratory acidosis) or a decrease in bicarbonate (metabolic acidosis). Alkalosis is caused by a decrease in carbonic acid (respiratory alkalosis) or an increase in bicarbonate (metabolic alkalosis). Imbalances may be further classified as acute or chronic. Chronic imbalances allow greater time for compensatory changes. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Types of Acid-Base Imbalances
Resp imbalances affect carbonic acid concentration leading to respiratory acidosis (or increased carbonic acid) and decreased carbonic acid leading to respiratory alkalosis Metabolic imbalances affect base bicarbonate , so decreased bicarb leads to metabolic acidosis and increased bicarb leads to metabolic alkalosis Acidosis can be caused by an excess of carbonic acid (respiratory) or a decrease in bicarbonate (metabolic). Alkalosis can be caused by a decrease in carbonic acid (respiratory) or an increase in bicarbonate (metabolic). Respiratory imbalances caused by carbonic acid excess (acidosis) and carbonic acid deficit (alkalosis). Metabolic imbalances caused by bicarbonate deficit (acidosis) and bicarbonate excess (alkalosis). Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Clinical Manifestations of Acid-Base Imbalances
Based on pH, not source of imbalance Acidosis Central nervous system (CNS) depression Kussmaul respirations Alkalosis CNS irritability Hypocalcemia In both respiratory and metabolic acidosis, the CNS is depressed. Headache, lethargy, weakness, and confusion develop, leading eventually to coma and death. In both types of alkalosis, irritability of the CNS occurs causing tingling and numbness of the fingers, restlessness, and tetany. If the degree of alkalosis increases in severity, convulsions and coma may occur.7 The compensatory mechanisms also produce specific clinical manifestations. For example, the deep, rapid respirations of a patient with metabolic acidosis are an example of respiratory compensation. In alkalosis, hypocalcemia occurs because of increased calcium binding with albumin, lowering the amount of ionized, biologically active calcium. The hypocalcemia accounts for many of the clinical manifestations of alkalosis. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Blood Gas Values Arterial blood gas (ABG) values provide information about Acid-base status Underlying cause of imbalance Body's ability to regulate pH Overall oxygen status ABG values provide objective information about a patient’s acid-base status, the underlying cause of an imbalance, the body’s ability to regulate pH, and the patient’s overall oxygen status. Knowledge of the patient’s clinical situation and the physiologic extent of renal and respiratory compensation enables you to identify acid-base disorders, as well as the patient’s ability to compensate. Blood gas analysis also shows the partial pressure of arterial oxygen (PaO2) and oxygen saturation. These values are used to identify hypoxemia. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Interpretation of ABGs
Diagnosis in six steps Evaluate pH : ; pH is a measure of H+ ion concentration. pH less than 6.8 or greater than 7.8 equals death Analyze PaCO Analyze HCO3– Determine if CO2 or HCO3– matches the alteration Decide if the body is attempting to compensate : when compensatory mechanism fail we see imbalances which include resp-carbonic acid concentration and metabolic which affect bicarb To interpret the results of an ABG, perform the following six steps: 1. Determine if the pH is acidotic or alkalotic. Label values less than 7.35 as acidotic and values greater than 7.45 as alkalotic. 2. Analyze the PaCO2 to determine if the patient has respiratory acidosis or alkalosis. Because the lungs control PaCO2, it is the respiratory component of the ABG. Because CO2 forms carbonic acid when dissolved in blood, high PaCO2 levels indicate acidosis and low PaCO2 levels indicate alkalosis. 3. Analyze the HCO3– to determine if the patient has metabolic acidosis or alkalosis. Because the kidneys primarily control HCO3–, it is the metabolic component of the ABG. Because HCO3– is a base, high levels of HCO3– result in alkalosis and low levels result in acidosis. 4. At this point, if the pH is between 7.35 and 7.45, and the CO2 and the HCO3– are within normal limits, the ABGs are normal. 5. Determine if the CO2 or the HCO3– matches the acid or base alteration of the pH. For example, if the pH is acidotic (less than 7.35) and the CO2 is high (respiratory acidosis) but the HCO3– is high (metabolic alkalosis), the CO2 is the parameter that matches the pH alteration of acidosis. The patient’s acid-base imbalance is diagnosed as respiratory acidosis. 6. Determine if the body is attempting to compensate for the pH change. If the parameter that does not match the pH is moving in the opposite direction, the body is attempting to compensate. In the example in step 5, the HCO3– level is alkalotic; this is in the opposite direction of respiratory acidosis and considered compensation. If compensatory mechanisms are functioning, the pH will return toward When the pH is within normal limits, the patient has full compensation. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Normal Blood Gas Values
Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Acid-Base Mnemonic—ROME
Respiratory Opposite Alkalosis ↑ pH ↓ PaCO2 Acidosis ↓ pH ↑ PaCO2 Metabolic Equal Acidosis ↓ pH ↓ HCO3 Alkalosis ↑ pH ↑ HCO3 For acid-base imbalances, a quick memory device (mnemonic) can be used. In Respiratory conditions, the pH and the PaCO2 go in Opposite directions. In respiratory alkalosis, the pH is ↑ and the PaCO2 is ↓. In respiratory acidosis, the pH is ↓ and the PaCO2 is ↑. In Metabolic conditions, the pH and the HCO3− go in the same direction (equal or Equivalent). The PaCO2 may also go in the same direction if compensation is occurring. In metabolic alkalosis, pH and HCO3− are ↑ and the PaCO2 is ↑ or normal. In metabolic acidosis, pH and HCO3− are ↓ and the PaCO2 is ↓ or normal. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Sample ABG Interpretation
Interpret the results of this ABG using the six steps previously discussed: 1. Determine whether the pH is acidotic or alkalotic: The pH is less than 7.35, thus the patient has acidosis. 2. Analyze the PaCO2 to determine if the patient has respiratory acidosis or alkalosis: The PaCO2 is low, indicating respiratory alkalosis. 3. Analyze the HCO3– to determine if the patient has metabolic acidosis or alkalosis: The HCO3– is low, indicating metabolic acidosis. 4. At this point, if the pH, CO2, and HCO3– are all low, therefore the ABGs are abnormal. 5. Determine if the CO2 or the HCO3– matches the acid or base alteration of the pH: The pH is acidotic (less than 7.35), the CO2 is low (respiratory alkalosis), and the HCO3– is low (metabolic acidosis). Because the HCO3 is the parameter that matches the pH alteration of acidosis, the patient’s acid-base imbalance is diagnosed as metabolic acidosis. 6. Determine if the body is attempting to compensate for the pH change. The CO2 is the parameter that does not match the pH and it is moving in the opposite direction (alkalosis). Thus the body is attempting to compensate. Because the pH is still acidotic, the patient has partial compensation. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Case Study 1: Jeri iStockphoto/Thinkstockk Jeri is a 22-year-old female who has been on a 3-day party binge. Her friends bring her to the ED after being unable to awaken her. Assessment reveals shallow respirations with a rate of 8/min, diminished breath sounds, and decreased level of consciousness. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Case Study 1: Jeri What type of acid-base imbalance would you expect Jeri to have? What is causing it? What type of compensation would you expect or not expect? Explain. What type of acid-base imbalance would you expect Jeri to have? Respiratory acidosis. What is causing it? Hypoventilation secondary to alcohol ingestion What type of compensation would you expect? Explain. Compensation might be noted if the respiratory depression has been present for 24 hours or more: The HCO3 may be elevated as the result of renal compensation. If her respiratory depression has lasted less than 24 hours, there will not yet be any renal compensation. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Case Study 1: Jeri iStockphoto/Thinkstock What would Jeri's ABGs look like? What is the treatment? See next slide 1. What would Jeri’s ABGs look like? Respiratory acidosis reflected by pH <7.35 and PCO2 >45 mm Hg. The HCO3 will be normal (20–30 mEq/L) if her respiratory depression has lasted less than 24 hours; if longer than 24 hours, the HCO3 may be elevated as the result of compensation. The PaO2 may be <80 mm Hg because of respiratory depression leading to hypoxemia. 2. What is the treatment? Determine the cause of the respiratory depression. If induced by opioids or benzodiazepines, treat with appropriate antagonists. If induced by alcohol or other CNS depressants, breathing must be stimulated until the effects of drugs have worn off. Mechanical ventilation may be necessary to increase respiratory rate and depth, increasing oxygenation and promoting excretion of carbon dioxide. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Respiratory Acidosis Carbonic acid excess caused by Hypoventilation : increased CO2 Respiratory failure Compensation Kidneys conserve HCO3– and secrete H+ into urine Respiratory acidosis (carbonic acid excess) occurs whenever there is hypoventilation. Hypoventilation results in a buildup of carbon dioxide, resulting in an accumulation of carbonic acid in the blood. Carbonic acid dissociates, liberating hydrogen ions, and there is a decrease in pH. If carbon dioxide is not eliminated from the blood, acidosis results from the accumulation of carbonic acid. To compensate, the kidneys conserve bicarbonate and secrete increased concentrations of hydrogen ion into the urine. During acute respiratory acidosis, the renal compensatory mechanisms begin to operate within 24 hours. Until the renal mechanisms have an effect, the serum bicarbonate level will usually be normal. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Case Study 2: Mayna Mayna is an 18-year-old female who presents to the ED after a sexual assault. She is hysterical and in severe emotional distress. Her blood pressure is 140/96, heart rate 104, respiratory rate 38, and oxygen saturation 96%. Lung sounds are clear. Brand X Pictures/Thinkstock Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Case Study 2: Mayna Brand X Pictures/Thinkstock What type of acid-base imbalance would you expect Mayna to have? What is causing it? What type of compensation would you expect or not expect? Explain. 1. What type of acid-base imbalance would you expect Mayna to have? Respiratory alkalosis 2. What is causing it? Hyperventilation secondary to anxiety and hysteria 3. What type of compensation would you expect or not expect? Explain. None at this point—compensation would not be occurring yet in this acute event. However, buffering of acute respiratory alkalosis may occur with shifting of bicarbonate (HCO3–) into cells in exchange for Cl–. It would take several days for renal compensation to occur. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Case Study 2: Mayna What do Mayna's ABGs look like? What is the treatment? See next slide Brand X Pictures/Thinkstock 1. What ABGs do you expect? Respiratory alkalosis indicated by pH >7.45 and PCO2 <35 mm Hg. The HCO3 will be normal (20–30 mEq/L) because compensation will not occur in this acute event. 2. What is the treatment? Relieve her anxiety and coax her to take slow breaths. Carbon dioxide may be administered by mask, or she may be asked to breathe into a paper bag placed over her nose and mouth. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Respiratory Alkalosis
Carbonic acid deficit caused by Hypoxemia from acute pulmonary disorders Hyperventilation Primary cause is hypoxemia from acute pulmonary disorders; anxiety, CNS disorders and mechanical overventilation; also increase vent rate and decreased PaCO2 Compensation Rarely occurs when acute : renal excretion of HCO3 but not enough time to compensate Can buffer with bicarbonate shift Renal compensation if chronic Respiratory alkalosis is carbonic acid deficit that occurs with hyperventilation. The primary cause of respiratory alkalosis is hypoxemia from acute pulmonary disorders. Anxiety, CNS disorders, and mechanical overventilation also increase the ventilation rate. Hyperventilation “blows off” CO2, leading to a decreased carbonic acid concentration and alkalosis. Compensated respiratory alkalosis is rare. In acute respiratory alkalosis, aggressive treatment of the causes of hypoxemia is essential and usually does not allow time for compensation to occur. However, buffering of acute respiratory alkalosis may occur with shifting of bicarbonate (HCO3–) into cells in exchange for Cl–. In chronic respiratory alkalosis that occurs with pulmonary fibrosis or CNS disorders, compensation may include renal excretion of bicarbonate. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Case Study 3: Alan Alan is a 17-year-old male who comes to the clinic with c/o feeling “bad,” fatigue, constant thirst, and frequent urination. Focused assessment reveals rapid deep respirations (rate 28) with a fruity breath odor. A capillary blood glucose is 484 mg/dL. iStockphoto/Thinkstock Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Case Study 3: Alan What type of acid-base imbalance would you expect Alan to have? What is causing it? What type of compensation would you expect or not expect? Explain. iStockphoto/Thinkstock 1. What type of acid-base imbalance would you expect Alan to have? Metabolic acidosis 2. What is causing it? Breakdown of fats for energy secondary to lack of insulin and subsequent inability to utilize glucose for energy. Ketones are an acid byproduct of fat breakdown. 3. What type of compensation would you expect or not expect? Explain. The deep, rapid respiratory rate (Kussmaul respirations) demonstrate respiratory compensation—may be partial or full, depending on longevity of the hyperglycemia. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Case Study 3: Alan What will Alan's ABGs look like? What is the treatment? See next slide iStockphoto/Thinkstock 1. What ABGs do you expect? A diabetic ketoacidosis is a metabolic acidosis indicated by a pH <7.35 and a HCO3 <20 mEq/L. The PCO2 will be within the normal range if the acidosis is uncompensated but will be <35 mm Hg if compensation has occurred. The PaO2 will not be affected. 2. What is the treatment? Administration of insulin to promote normal glucose metabolism and administration of fluids and electrolytes to replace those lost because of the hyperglycemia. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Metabolic Acidosis Excess carbonic acid or base bicarbonate deficit caused by : Ketoacidosis Lactic acid accumulation (shock) Severe diarrhea : loss of bicarb Kidney disease : inability to reabsorb bicarb and secrete H+ Compensatory metabolic acidosis –body attempts to rid acid by Kussmauls breathing and blowing off CO2 and kidneys excrete extra H+ Metabolic acidosis occurs when an acid other than carbonic acid accumulates in the body or when bicarbonate is lost from body fluids. Ketoacid accumulation in diabetic ketoacidosis and lactic acid accumulation with shock are examples of accumulation of acids. Severe diarrhea results in loss of bicarbonate. In renal disease, the kidneys lose their ability to reabsorb bicarbonate and secrete hydrogen ions. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Metabolic Acidosis Compensatory mechanisms Increased CO2 excretion by lungs Kussmaul respirations (deep and rapid) Kidneys excrete acid Anion gap Na+ – (Cl – + HCO3–) Normal: 10–14 mmol/L Increased with acid gain The compensatory response to metabolic acidosis is to increase CO2 excretion by the lungs. The patient often develops Kussmaul respiration (deep, rapid breathing). In addition, the kidneys attempt to excrete additional acid. If metabolic acidosis is present, calculating the anion gap can help determine the source of metabolic acidosis. The anion gap is the difference between the cations and the anions in the ECF that are routinely measured. You calculate an anion gap by summing the chloride and bicarbonate levels and subtracting this number from the plasma sodium concentration. Ordinarily, the sum of the measured cations is greater than the sum of the measured anions. The anion gap is normally 10 to 14 mmol/L. The anion gap is increased in metabolic acidosis associated with acid gain (e.g., lactic acidosis, diabetic ketoacidosis) but remains normal in metabolic acidosis caused by bicarbonate loss (e.g., diarrhea). Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Case Study 4: Anthony BananaStock/Thinkstock Anthony is a 54-year-old male with a history of nausea and vomiting for the past week. He has been self-medicating himself with baking soda to control his abdominal discomfort. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Case Study 4: Anthony What type of acid-base imbalance would you expect Anthony to have? What is causing it? What type of compensation would you expect or not expect? Explain. BananaStock/Thinkstock 1. What type of acid-base imbalance would you expect Anthony to have? Metabolic alkalosis 2. What is causing it? Loss of gastric acid and excess bicarbonate with baking soda ingestion 3. What type of compensation would you expect or not expect? Explain. There is limited compensation for metabolic alkalosis. The kidneys can respond by increasing excretion of bicarbonate. The respiratory system can respond by decreasing respirations, but once the carbon dioxide level increases, stimulation of chemoreceptors results in increased ventilation. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Case Study 4: Anthony BananaStock/Thinkstock What will Anthony's ABGs look like? What is the treatment? See next slide 1. What ABGs do you expect? The metabolic alkalosis in this case would be reflected by a pH >7.45 and a HCO3 >30 mEq/L. Because of the duration of this condition, compensation may be indicated by a PCO2 >45 mm Hg. 2. What is the treatment? Determine the underlying cause of the vomiting if possible, and stop the use of baking soda (sodium bicarbonate). Antiemetic drugs and nasogastric intubation may help relieve the vomiting, and IV replacement of fluids and electrolytes may be necessary. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Metabolic Alkalosis Base bicarbonate excess caused by Prolonged vomiting or gastric suction Gain of HCO3– : ingestion of baking soda Compensatory mechanisms Renal excretion of HCO3– Decreased respiratory rate to increase plasma CO2 (limited) Metabolic alkalosis (base bicarbonate excess) occurs when a loss of acid (prolonged vomiting or gastric suction) or a gain in bicarbonate (ingestion of baking soda) occurs. Renal excretion of bicarbonate occurs in response to metabolic alkalosis. The compensatory response to metabolic alkalosis is limited. There is a decreased respiratory rate to increase plasma CO2. However, once plasma CO2 reaches a certain level, stimulation of chemoreceptors results in ventilation. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Practice ABG Interpretation Case 1
What imbalance is this? pH 7.33 PaCO2 67 mm Hg PaO2 47 mm Hg HCO3 37 mEq/L Respiratory acidosis, partially compensated pH is low. PaCO2 is high. HCO3 is high. By using the ROME (Respiratory Opposite Metabolic Equal) mnemonic, the respiratory component (PaCO2) is going in the opposite direction as the pH—thus, the patient has respiratory acidosis. Because the HCO3 is elevated, the patient is partially compensating. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

What imbalance is this? pH 7.18 PaCO2 38 mm Hg PaO2 70 mm Hg HCO3– 15 mEq/L Metabolic acidosis pH is low. PaCO2 is normal. HCO3 is low. By using the ROME mnemonic, the metabolic component (HCO3) is going in the same direction as the pH—thus the patient has metabolic acidosis. Because the CO2 is normal, there is no compensation. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

What imbalance is this? pH 7.60 PaCO2 30 mm Hg PaO2 60 mm Hg HCO3– 22 mEq/L Respiratory alkalosis pH is high. PaCO2 is low. HCO3 is normal. By using the ROME mnemonic, the respiratory component (PaCO2) is going in the opposite direction as the pH—thus the patient has respiratory alkalosis. Because the HCO3 is normal, there is no compensation. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Practice ABG interpretation Case 4
What imbalance is this? pH 7.58 PaCO2 35 mm Hg PaO2 75 mm Hg HCO3– 50 mEq/L Metabolic alkalosis pH is high. PaCO2 is normal. HCO3 is high. By using the ROME mnemonic, the metabolic component (HCO2) is going in the same direction as the pH—thus the patient has metabolic alkalosis. Because the PaCO2 is normal, there is no compensation. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

What imbalance is this? pH 7.28 PaCO2 28 mm Hg PaO2 70 mm Hg HCO3– 18 mEq/L Metabolic acidosis, partially compensated pH is low. PaCO2 is low. HCO3 is low. By using the ROME mnemonic, the metabolic component (HCO2) is going in the same direction as the pH—thus the patient has metabolic acidosis. Because the PaCO2 is also low but the pH is not yet back to normal, there is partial compensation. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

ABG Analysis Case 6 ABG results are as follows: pH 7.20 PaCO2 58 mm Hg PaO2 59 mm Hg HCO3– 24 mEq/L Describe a patient who would have these ABGs, including history, assessment, and treatment. These ABGs reflect an uncompensated respiratory acidosis with hypoxemia. This could occur with a respiratory infection causing an exacerbation in a patient with COPD. The hypoxemia may be reflected by restlessness, confusion, or stupor. Respiratory and cardiac findings could include rapid, shallow breathing, rhonchi, crackles, diminished breath sounds, increased work of breathing with use of accessory muscles, orthopnea, tachycardia, and arrhythmias. Treatment includes treatment of any underlying respiratory infections, bronchodilator therapy, corticosteroids, hydration therapy, chest PT and postural drainage, breathing exercises, low-flow oxygen therapy, and mechanical ventilation if the patient continues to deteriorate. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

ABG Analysis Case 7 ABG results are as follows: pH PaCO mm Hg PaO mm Hg HCO3– 24 mEq/L Describe a patient who would have these ABGs, including history, assessment, and treatment. These ABGs indicate a hypoxemic respiratory failure because all ABGs are within normal range except for the PaO2. Patients experiencing hypoxemic respiratory failure may include those with pneumonia, shock, pulmonary embolism, acute respiratory distress syndrome, or pulmonary edema. The patient’s history would include an underlying organ damage or assault. Respiratory symptoms include dyspnea, tachypnea, accessory muscle use, and late cyanosis. The patient may experience decreased level of consciousness, restlessness, tachycardia, and late arrhythmias and hypotension. In addition to treating the underlying cause, oxygen therapy and mobilization of secretions are used to correct the hypoxemia. Positive-pressure ventilation via endotracheal intubation may be necessary. Maintaining adequate cardiac output with IV fluids and medications is also necessary. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

ABG Case Analysis Case 6 ABG results are as follows: pH 7.36 PaCO2 58 mm Hg PaO2 50 mm Hg HCO3 – 33 mEq/L Describe a patient who would have these ABGs, including history, assessment, and treatment. Copyright © 2014 by Mosby, an imprint of Elsevier Inc. These ABGs indicate a hypercapnic respiratory failure indicated by decreased PaO2 and increased PaCO2. Elevated HCO3 and (low) normal pH indicate compensation of a respiratory acidosis. Common causes of hypercapnic respiratory failure include any of the obstructive respiratory diseases (asthma, cystic fibrosis, COPD), CNS–induced respiratory depression such as head injury, spinal cord injury, brainstem infarction, sedative and narcotic overdose, and neuromuscular diseases such as myasthenia gravis, ALS, Guillain-Barré syndrome, and multiple sclerosis. Assessment findings include dyspnea, decreased respiratory rate or increased shallow respirations, and decreased tidal volume. Cerebral symptoms include disorientation and progressive somnolence. The patient may also have tachycardia, bounding pulse, arrhythmias, and hypertension. Treatment of the underlying condition is necessary. In addition, oxygen therapy, mobilization of secretions, positive-pressure ventilation, and drug therapy are used. Commonly used drugs include bronchodilators, corticosteroids, diuretics, antibiotics, sedatives, and analgesics.

ABG Analysis Case 7 ABG results are as follows: pH 7.50 PaCO2 28 mm Hg PaO2 85 mm Hg HCO3 – 24 mEq/L Describe a patient who would have these ABGs, including history, assessment, and treatment. In this case, the increased pH and decreased PaCO2 indicate a respiratory alkalosis. The normal HCO3 reflects no compensation for the alkalosis. Respiratory alkalosis most commonly occurs with hypoxemia from acute pulmonary disorders. Anxiety, CNS disorders, and mechanical over-ventilation also increase the ventilation rate, leading to respiratory alkalosis. Assessment findings may include tingling and numbness of the fingers, restlessness, hyperreflexia, tetany, headache, dizziness, confusion, tachycardia, dysrhythmias, nausea, vomiting, and epigastric pain. Determination of the underlying cause is necessary to treat the alkalosis. Having the patient rebreathe into a paper bag can increase CO2 retention and thus decrease the pH. Correction of hypoxemia with oxygen therapy and bronchodilators can also be useful. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

ABG Case Analysis Case 8 ABG results are as follows: pH 7.20 PaCO2 28 mm Hg PaO2 81 mm Hg HCO3– 18 mEq/L Describe a patient who would have these ABGs, including history, assessment, and treatment. In this case, the decreased pH and decreased HCO3 indicate a metabolic acidosis. The decreased PaCO2 reflects compensation for the acidosis. Metabolic acidosis most commonly occurs in uncontrolled diabetes, but may also be caused by lactic acidosis, starvation, severe diarrhea, renal failure, or shock. Assessment findings may include drowsiness and confusion leading to coma; deep, rapid respirations (compensation); hypotension and arrhythmias; warm, dry, flushed skin; and nausea, vomiting, and abdominal pain. Determination of the underlying cause is necessary to treat the acidosis. Diabetic acidosis is treated with insulin to normalize glucose metabolism, and carbohydrate (glucose) is provided in the case of starvation. Dialysis may be used to treat renal failure, and other underlying causes are treated as appropriate. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

ABG Analysis Case 9 ABG results are as follows: pH 7.57 PaCO2 46 mm Hg PaO2 87 mm Hg HCO3– 38 mEq/L Describe a patient who would have these ABGs, including history, assessment, and treatment. These ABG results indicate a metabolic alkalosis: the pH and HCO3 are elevated. The slightly elevated PaCO2 indicates some compensation for the alkalosis. The history of a patient with metabolic alkalosis may include severe vomiting or excessive gastric suctioning, diuretic therapy, potassium deficit, excessive intake of sodium bicarbonate (baking soda), or excessive mineralocorticoid therapy. Assessment findings may include nervousness and confusion, tachycardia and dysrhythmias, nausea and vomiting, tremors, hypertonic muscles, tetany, and tingling of the fingers and toes. As in all acid-base imbalances, determination and treatment of the underlying cause is necessary. The potassium that is lost in an alkalosis must be replaced to prevent dysrhythmias, and contributing drugs must be discontinued. Vomiting with bicarbonate is treated as in previous case analysis. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Audience Response Question
A patient with an acid-base imbalance has an altered potassium level. The nurse recognizes that the potassium level is altered because Potassium is returned to extracellular fluid when metabolic acidosis is corrected. Hyperkalemia causes an alkalosis that results in potassium being shifted into the cells. Acidosis causes hydrogen ions in the blood to be exchanged for potassium from the cells. In alkalosis, potassium is shifted into extracellular fluid to bind excessive bicarbonate. Answer: c Rationale: Changes in pH (hydrogen ion concentration) will affect potassium balance. In acidosis, hydrogen ions accumulate in the intracellular fluid (ICF), and potassium shifts out of the cell to the extracellular fluid to maintain a balance of cations across the cell membrane. In alkalosis, ICF levels of hydrogen diminish, and potassium shifts into the cell. If a deficit of H+ occurs in the extracellular fluid, potassium will shift into the cell. Acidosis is associated with hyperkalemia, and alkalosis is associated with hypokalemia. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Audience Response Question
A patient has the following ABG results: pH 7.48, PaO mm Hg, PaCO2 44 mm Hg, HCO3 29 mEq/L. When assessing the patient, the nurse would expect the patient to have Muscle cramping Warm, flushed skin Respiratory rate of 36 Blood pressure of 94/52 Answer: a Rationale: The patient is experiencing metabolic alkalosis (elevated pH and elevated HCO3). Clinical manifestations of metabolic alkalosis include hypertonic muscles and cramping and reduced respiratory rate. Hypotension and warm, flushed skin may occur with respiratory acidosis. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Acid-Base Balance and Arterial Blood Gases

Similar presentations

Presentation on theme: "Acid-Base Balance and Arterial Blood Gases"— Presentation transcript:

Similar presentations

About project

Feedback

Log in

Auth with social network:

Acid-Base Balance and Arterial Blood Gases

Similar presentations

Presentation on theme: "Acid-Base Balance and Arterial Blood Gases"— Presentation transcript:

Similar presentations

About project

Feedback