1. Basics of Acid-Base Balance Naveed Aslam, MD Consultant & clinical tutor Department of Nephrology Prince Sultan Military Medical City

2. Key concepts Introduction Overview of pH Buffering systems Metabolic imbalances Respiratory imbalances Illustrative Cases

3. Acid-base balance refers to the mechanisms the body uses to keep its fluids close to neutral pH (that is, neither basic nor acidic) so that the body can function normally. Arterial blood pH is normally closely regulated to between 7.35 and 7.45. Acid Base balance

4. acids ？ acids ？ bases ？ Any ionic or molecular substance that can act as a proton donor. Strong acid ： HCl, H 2 SO 4, H 3 PO 4. Weak acid ： H 2 CO 3, CH 3 COOH. Any ionic or molecular substance that can act as a proton acceptor. Strong alkali ： NaOH, KOH. Weak alkali ： NaHCO 3, NH 3, CH 3 COONa.

5. Lactic acid Ketone bodies Sulfuric acid Phosphoric acid Intracellular metabolism Volatile acids 300~400L CO (15mol H + ) 300~400L CO 2 (15mol H + ) Fixed acids 50~100 mmol H +  NH 3  NH 3, sodium citrate, sodium lactate Origin of acids Much more Origin of bases less CO 2 +H 2 O=H 2 CO 3

6. pH Overview

7. pH overview pH is a measure of hydrogen (H+) concentration in a solution H+ changes occur tenfold on the pH scale Body pH = 7.35 – 7.45 - pH is variable in certain areas (stomach, CSF, etc)

8. pH - pH of ECF is between 7.35 and 7.45. Deviations, outside this range affect membrane function, alter protein function, etc. - You cannot survive with a pH 7.7 - Acidosis- below 7.35 Alkalosis- above 7.45 Alkalosis- above 7.45 CNS function deteriorates, coma, cardiac CNS function deteriorates, coma, cardiac irregularities, heart failure, peripheral irregularities, heart failure, peripheral vasodilation, drop in Bp. vasodilation, drop in Bp.

9. Given that normal body pH is slightly alkaline and that normal metabolism produces acidic waste products such as carbonic acid (carbon dioxide reacted with water) and lactic acid, body pH is constantly threatened with shifts toward acidity. In normal individuals, pH is controlled by two major and related processes; - pH regulation is a function of the buffer systems of the body in combination with the respiratory and renal systems. - pH compensation requires further intervention of the respiratory and/or renal systems to restore normalcy.

10. ABB disorders Acidemia7,40 Alkalemia Normal arterial blood pH 7.35 – 7.45 acidosisalkalosis Normal range 7.35 7.45

11. Definitions Normal pH is 7.35 - 7.45  If this value is normal, but one of the below values is abnormal, the patient has compensated. Normal C02 is 35 -45 mmHg  If this value is abnormal, the patient has respiratory acidosis or alkalosis. Normal HC03 is 22-26 mEq/L If this value is abnormal, the patient has metabolic acidosis or alkalosis Normal O2 Saturation is 80-100 ml/dl  If this value is normal in a respiratory pH problem, patient is compensating.

12. Acid-base balance is maintained by  normal pulmonary excretion of carbon dioxide,  metabolic utilization of organic acids,  and renal excretion of nonvolatile acids

13. Buffers “Buffers are solutions which can resist changes in pH when acid or alkali is added.”

14. Buffering Capacity in Body 52% of the buffering capacity is in cells 5% is in RBCs 43% of the buffering capacity is in the extracellular space  of which 40% by bicarbonate buffer, 1% by proteins and 1% by phosphate buffer system

15. 15

16. Buffering Systems The three different buffering systems are: 1) Respiratory buffering system Uses bicarbonate 2) Blood buffering system Uses bicarbonate, phosphate, and protein 3) Renal buffering system Uses bicarbonate, phosphate, and ammonia

17. Respiratory Buffering System Lungs (only if not a respiratory problem)  If too much acid (low pH)— respiratory system will ventilate more (remove CO 2 ) and this will raise pH back toward set point  If too little acid (high pH)—respiratory will ventilate less (trap CO 2 in body) and this will lower pH back toward set point Peripheral receptors detect CO2 concentration changes and send the appropriate signal to the respiratory system. Low pH = Hyperventilation High pH = Hypoventilation

18. Blood Buffering System The blood buffering system uses three different chemical buffers: phosphate, bicarbonate and proteins. The phosphate buffer is not abundant in blood. Blood contains a high concentration of proteins.

19. Renal Buffering System The renal buffer system uses; - bicarbonate, - phosphate - ammonium. In the kidneys, the bicarbonate buffer may increase plasma pH in three ways; - secreton of H+ -- occurs mostly in proximal tubule - reabsorbtion of bicarbonate -- PCT - producing new bicarbonate -- intercalated cells

20. How can the kidneys control acids and bases? Bicarbonate is filtered and enters nephron at Bowman’s capsule Proximal convoluted tubule  Can reabsorb all bicarbonate (say, when you need it to neutralize excessive acids in body) OR  Can reabsorb some or NONE of the bicarbonate (maybe you have too much base in body and it needs to be eliminated)

21. How can the kidneys control acids and bases? Acidosis Intercalated cells  Secrete excessive hydrogen  Secreted hydrogen binds to buffers in the lumen (ammonia and phosphate bases)  Secretion of hydrogen leads to formation of bicarbonate HPO 4 - NH 3 Phosphate: important renal tubular buffer HPO4- + H+ H2PO4 Ammonia: important renal tubular buffer NH3 + H+ NH4+

22. Acids must be buffered, transported away from cells, and eliminated from the body. These are the most important buffers. Phosphate: important renal tubular buffer HPO 4 - + H + H 2 PO 4 Ammonia: important renal tubular buffer NH 3 + H + NH 4 + Proteins: important intracellular and plasma buffers H + + HbHHb Bicarbonate: most important Extracellular buffer and is also another important renal tubular buffer. H 2 O + CO 2 H 2 CO 3 H + + HCO 3 -

23. Buffering is good, but it is a temporary solution. Excess acids and bases must be eliminated from the body H 2 O + CO 2 H 2 CO 3 H + + HCO 3 - Lungs eliminate carbon dioxide Kidneys can remove excess non- gas acids and bases gasaqueous

24. Simple acid base disorder

25. a change in the normal value of extracellular pH An acid base disorder is a change in the normal value of extracellular pH that may result when renal or respiratory function is abnormal or when an acid or base load overwhelms excretory capacity. Definition of acid-base disorders

26. Excessive Acids and Bases can cause pH changes---denature proteins Normal pH of body fluids is 7.40 Alkalosis (alkalemia) – arterial blood pH rises above 7.45 Acidosis (acidemia) – arterial pH drops below 7.35 Acidosis: – Too much acid – Too little base Alkalosis – Too much base – Too little acid

27. Acidosis: pH < 7.4 - Metabolic: HCO 3 - - respiratory: pCO 2 Alkalosis: pH > 7.4 - Metabolic: HCO 3 - - respiratory: pCO 2 How can you detect if the acid-base imbalance is from a kidney disorder or a lung disorder?

28. REASONS FOR METABOLIC ACIDOSIS AND ALKALOSIS

29. What would happen if the respiratory system had a problem with ventilation? Respiratory Acidosis and Alkalosis Normal P CO2 fluctuates between 35 and 45 mmHg Respiratory Acidosis (elevated CO 2 greater than 45mmHg) Depression of respiratory centers via narcotic, drugs, anesthetics CNS disease and depression, trauma (brain damage) Interference with respiratory muscles by disease, drugs, toxins Restrictive, obstructive lung disease (pneumonia, emphysema) Respiratory Alkalosis (less than 35mmHg- lowered CO 2 ) Hyperventilation syndrome/ psychological (fear, pain) Overventilation on mechanical respirator Ascent to high altitudes Fever

30. What if your metabolism changed? Metabolic acidosis Bicarbonate levels below normal (22 mEq/L) Metabolic alkalosis bicarbonate ion levels higher (greater than 26mEq/L) Ingestion, infusion or production of more acids (alcohol) Salicylate overdose (aspirin) Diarrhea (loss of intestinal bicarbonate) Accumulation of lactic acid in severe Diabetic ketoacidosis starvation Excessive loss of acids due to loss of gastric juice during vomiting Excessive bases due to ingestion, infusion, or renal reabsorption of bases Intake of stomach antacids Diuretic abuse (loss of H+ ions) Severe potassium depletion Steroid therapy

31. Acid-Base Balance How would your ventilation change if you had excessive acid?  You would hyperventilate How would your ventilation change if you had excessive alkalosis?  Your breathing would become shallow Low pH = acidosis = HyperventilationHigh pH = alkalosis = Hypoventilation

32. Acidosis Metabolic acidosis Respiratory acidosis Excessive blood acidity caused by an overabundance of acid in the blood or a loss of bicarbonate from the blood Excessive amount of carbon dioxide in the blood that results from poor lung function or slow breathing

33. Metabolic acidosis Metabolic acidosis Causes: Causes: 1) lose of bases (bicarbonate decreased) Gastrointestinal losses: diarrhea Renal losses: proximal renal tubular acidosis and distal renal tubular acidosis Gastrointestinal losses: diarrhea Renal losses: proximal renal tubular acidosis and distal renal tubular acidosis Lactic acidosis: tissue hypoxia, impaired oxygen utilization, severe liver dysfunction, and shock Ketoacidosis: diabetic,hepatic cirrhosis, alcoholic poisoning, or starvation Renal failure: conservation of acids 2) Gaining acids (bicarbonate consumed in buffering) Lactic acidosis: tissue hypoxia, impaired oxygen utilization, severe liver dysfunction, and shock Ketoacidosis: diabetic,hepatic cirrhosis, alcoholic poisoning, or starvation Renal failure: conservation of acids Exogenous acid intake: ammonium chloride, salicylate, ethylene glycol (commonly used in antifreeze), or methanol intoxication Exogenous acid intake: ammonium chloride, salicylate, ethylene glycol (commonly used in antifreeze), or methanol intoxication

34. Metabolic acidosis Compensation The body will compensate with hyperventilation and increased bicarbonate reabsorption in the kidney. Since the primary abnormality is a decrease in HCO3, the compensatory response includes extracellular buffering (by bicarbonate), intracellular buffering (by phosphate and proteins), respiratory compensation and renal hydrogen excretion. Metabolic acidosis stimulates an increase in ventilation (reducing pCO2). This hyperventilation is called Kussmaul's respiration.

35. The Response to Metabolic Acidosis

36. Metabolic acidosis Symptoms Most symptoms are caused by the underlying disease or condition that is causing the metabolic acidosis. Metabolic acidosis itself usually causes rapid breathing. Confusion or lethargy may also occur. Severe metabolic acidosis can lead to shock or death. In some situations, metabolic acidosis can be a mild, chronic (ongoing) condition.

37. Respiratory acidosis Respiratory acidosis is due to an accumulation of CO2 in the blood stream. This pushes the carbonic anhydrase reaction to the right, generating H + : carbonic anhydrase CO 2 H 2 CO 3 HCO 3 (-) + H +

38. Respiratory acidosis Cause The increase in CO2 in the blood is often caused by hypoventilation. This can be caused by asthma, COPD, and overuse of sedatives, barbiturates, or narcotics such as valium, heroin, or other drugs which make you sleepy. Any trauma where the breathing muscles are damaged (causing decreased ventilation), airway obstruction, or lung disease (pneumonia, cystic fibrosis, emphysema, etc.).

39. Respiratory acidosis Compensation The kidneys will compensate by secreting H+. If H+ excretion cannot restore the balance, the kidneys will also generate bicarbonate. Since the primary abnormality is an increase in pCO2, the compensatory response is intracellular buffering of hydrogen (by hemoglobin) and renal retention of bicarbonate, which takes several days to occur.

40. Respiratory acidosis Figure 27.12a

41. Respiratory acidosis Symptoms May have no symptoms but usually experience headache, nausea, vomiting, and fatigue. Breathing becomes deeper and slightly faster (as the body tries to correct the acidosis by expelling more carbon dioxide). As the acidosis worsens, people begin to feel extremely weak and drowsy and may feel confused and increasingly nauseated. Eventually, blood pressure can fall, leading to shock, coma, and death.

42. Respiratory acidosis Treatment Treatment is aimed at the underlying disease, and may include: Bronchodilator drugs to reverse some types of airway obstruction Noninvasive positive-pressure ventilation (sometimes called CPAP or BiPAP) or a breathing machine, if needed Oxygen if the blood oxygen level is low

43. Alkalosis Metabolic alkalosis Respiratory alkalosis Excessive blood alkalinity caused by an overabundance of bicarbonate in the blood or a loss of acid from the blood Loss of carbon dioxide in the blood that results from rapid or deep breathing

44. Metabolic alkalosis Cause An increase in bicarbonate in the blood because of ingestion of excess bicarbonate in the form of an antacid (Tums), eating excess fruits (vegetarian diets and fad diets*), Excessive loss of hydrogen ions, chloride or potassium ions Gastrointestinal H+ loss: vomiting, gastric suction Renal H+ loss: Aldosteronism, cushing’s syndrome thiazide Volume contraction Dehydration Diuretic therapy

45. Metabolic alkalosis Compensation This is initially buffered by hydrogen buffers (such as plasma proteins and lactate). Chemoreceptors in the respiratory center sense the alkalosis and trigger hypoventilation, resulting in increased pCO2. The respiratory system will hypoventilate but this will not be effective because CO2 will accumulate and the CO2 receptors will override the pH receptors. In addition to respiratory compensation, the kidneys excrete the excess bicarbonate. However, this takes several days to occur.

46. Metabolic Alkalosis

47. Metabolic alkalosis Symptoms Confusion (can progress to stupor or coma) Hand tremor Light-headness Muscle twitching Nausea, vomiting Numbness or tingling in the face, hands, or feet Prolonged muscle spasms (tetany)

48. Respiratory alkalosis Respiratory alkalosis is generally caused by hyperventilation, usually due to anxiety. The primary abnormality is a decreased pCO2. Cause Caused from a decrease in CO2 in the blood because the lungs are hyperventilating (anxiety, but not panting). Fever or aspirin toxicity may also cause respiratory alkalosis.

49. Respiratory alkalosis Compensation The body will reduce the breathing rate, and the kidney will excrete bicarbonate.

50. Respiratory alkalosis Compensation The compensatory response to a respiratory alkalosis is initially a release of hydrogen from extracellular and intracellular buffers. This is followed by reduced hydrogen excretion by the kidneys. This results in decreased plasma bicarbonates. In chronic respiratory alkalosis, compensation can lead to pH returning to normal.

51. Respiratory alkalosis Figure 27.12b

52. Summary DISTURBANCEpHPRIMARY CHANGE RATIOSECONDARY CHANGE Metabolic Acidosis DecreasedDeficit of bi- carbonate <20Decrease in PaCO2 Metabolic Alkalosis IncreasedExcess of bicarbonate >20Increase in PaCO2 Respiratory acidosis DecreasedExcess of carbonic acid <20Increase in bicarbonate Respiratory alkalosis IncreasedDeficit of carbonic acid >20Decrease in bicarbonate

53. Summary CO 2 = Acid   CO 2 =  pH (acidemia)   CO 2 =  pH (alkalemia) HCO 3 = Base   HCO 3 =  pH (alkalemia)   HCO 3 =  pH (acidemia) Respiratory Metabolic

54. Reference ranges and points ParameterReference rangeReference point pH7.35-7.457.40 P CO 2 33-44 mm Hg40 mm Hg P O 2 75-105 mm Hg80mm Hg HCO 3 - 22-28 mEq/L24mEq/L Anion gap8-16 mEq/L12 mEq/L Osmolar gap <10 mOsm/L

55. Interpreting Arterial Blood Gases (ABG) This blood test is from arterial blood, usually from the radial artery. There are three critical questions to keep in mind when attempting to interpret arterial blood gases (ABGs). First Question: Does the patient exhibit acidosis or alkalosis? Second Question: What is the primary problem? Metabolic? or Respiratory? Third Question: Is the patient exhibiting a compensatory state?

56. Assessment Step 1 Step One: Determine the acid/base status of the arterial blood. If the blood's pH is less than 7.35 this is an acidosis, and if it is greater than 7.45 this is an alkalosis. You may hear nurses or doctors say: "The patient is 'acidotic' or 'alkalotic'

57. Assessment Step 1 If the pH is low, it is acidosis. If it is high, it is alkalosis. pH

58. Assessment Step 2 Once you have determined the pH, you can move on to determine which system is the 'primary' problem: respiratory or metabolic. To do this, examine the pCO2 and HCO3 levels.

59. Assessment Step 2 If the pCO2 is the only one that is abnormal, it is respiratory. If the HCO3 is the only one that is abnormal, it is metabolic. If they are both abnormal, we need to evaluate it further. Go to step 3.

60. Assessment Step 3 Determine if the body is attempting to compensate for the imbalance or not. If they are both high or both low, the patient is compensating. You will never have a case where one is high and one is low.

61. If both the pCO2 and HCO3 are high, what does it mean? If the pH is low, it is compensated respiratory acidosis. If the pH is high, it is compensated metabolic acidosis.

62. Look at dirrection of arrows RESPIRATORY arrow dirrection oposite to PH pH HC03 PC02= RESPIRATORY ALKALOSIS pH HC03 PC02= RESPIRATORY ACIDOSIS

63. Look at dirrection of arrows Metabolic all arrow same dirrection  pH HC03 PC02 = METABOLIC ACIDOSIS  pH HC03 PC02 = METABOLIC ALKALOSIS

64. If both the pCO2 and HCO3 are high, and the pH is low, how do you know it is compensated respiratory acidosis instead of compensated metabolic acidosis? In respiratory acidosis, the first thing to go wrong is the pCO2 will become high. To compensate, the HCO3 will become elevated. If it was metabolic acidosis, the first thing to go wrong would be the HCO3 levels would be too low. To compensate, the pCO2 levels would start dropping to raise the pH.

65. Review the three essential steps of ABG analysis Number One: Determine if the patient is demonstrating an acidotic (remember: pH less than 7.35) or alkalotic (pH greater than 7.45) condition. Number Two: What is the 'primary problem? If the patient is acidotic with a pC02 greater than 45 mmHg it is RESPIRATORY If the patient is alkalotic with a pC02 less than 35 mmHg it is RESPIRATORY! If the patient is acidotic with a HC03 less than 22 mEq/L it is METABOLIC! If the patient is alkalotic with a HC03 greater than 26 mEq/L it is METABOLIC!

66. Review the three essential steps of ABG analysis Number Three: Is the patient compensating? Are both components (HCO3 and pCO2) shifting in the same direction? Both going up or both going down? If so, the patient is compensating. Their buffering systems are functioning and are trying to bring the acid-base balance back to normal.

67. ACID BASE PARAMETERS (The problem chemical is in yellow) Respiratory Acidosis PHPCO2HCO3 If compensating Respiratory Alkalosis PHPCO2HCO3 If compensating Metabolic Acidosis PHPCO2 If compensating HCO3 Metabolic Alkalosis PHPCO2 If compensating HCO3 Or normal if not compensating

68. Four Primary Disorders: PCO 2 < 35 = respiratory alkalosis PCO 2 > 45 = respiratory acidosis HCO 3 < 22 = metabolic acidosis HCO 3 > 26 = metabolic alkalosis  Can have mixed pictures with compensation  Can have up to 3 abnormality simultaneously (1 respiratory + 2 metabolic)  The direction of the pH will tell you which is primary!

69. Compensation Primary DisturbancepHHCO 3 - P CO 2 Compensation Respiratory acidosis<7.35Compensatory increase Primary increaseAcute: 1-2 mEq/L increase in HCO 3 - for every 10 mm Hg increase in P CO 2 Chronic: 3-4 mEq/L increase in HCO 3 - for every 10 mm Hg increase in P CO 2 Respiratory alkalosis>7.45Compensatory decrease Primary decrease Acute: 1-2 mEq/L decrease in HCO 3 - for every 10 mm Hg decrease in P CO 2 Chronic: 4-5 mEq/L decrease in HCO 3 - for every 10 mm Hg decrease in P CO 2 Metabolic acidosis<7.35Primary decreaseCompensatory decrease 1.2 mm Hg decrease in P CO 2 for every 1 mEq/L decrease in HCO 3 - Metabolic alkalosis>7.45Primary increaseCompensatory increase 0.6-0.75 mm Hg increase in P CO 2 for every 1 mEq/L increase in HCO 3 -, P CO 2 should not rise above 55 mm Hg in compensation

70. Find the patient’s CO2 and Bicarb pattern on this table. Only look at the row with the patient’s pH That will tell you the patient’s condition and compensation ConditionpHRespCO2BicarbCompensating? Resp acidosisLowHypoventilatingHigh Yes Resp acidosisLowHypoventilatingHighNormNo Resp alkalosisHighHyperventilatingLow Yes Resp alkalosisHighHyperventilatingLowNormNo Metab acidosisLowNormalLow Yes Metab acidosisLowNormalHighNormNo Metab AlkalosisHighNormalHigh Yes Metab AlkalosisHighNormalLowNormNo

71. Acute Respiratory Alkalosis

72. Acute Respiratory Acidosis

73. Chronic Respiratory Acidosis with Metabolic Compensation

74. Metabolic Alkalosis with Respiratory Compensation

76. ABG: 7.40 / 40 / 80 / 24  pH  PaCO 2  PaO 2  HCO 3

77. Example # 1: Blood gas: 7.50 / 29 / 23 Alkalemic  pH 7.50  PaCO 2 29  HCO 3 23

78. Acute respirstory alkalosis Low PCO 2 is the primary (respiratory alkalosis) No metabolic compensation = acute process Acute Respiratory Alkalosis Acute: 1-2 mEq/L decrease in HCO 3 - for every 10 mm Hg decrease in PCO 2

79. Example 2 A 65-year-old man with a history of emphysema comes to the physician with a 3-hour history of shortness of breath. pH7.18 P CO 2 58 mm Hg P O 2 61 mm Hg HCO 3 - 25 mEq/L Acute respiratory acidosis

80. Acute Respiratory acidosis R acid acute-History suggests hypoventilation, supported by increased P CO 2 and lower than anticipated P O 2. Acute: 1-2 mEq/L increase in HCO 3 - for every 10 mm Hg increase in P CO 2 Chronic: 3-4 mEq/L increase in HCO 3 - for every 10 mm Hg increase in P CO 2 Respiratory acidosis (acute) incomplete/no renal compensation.

81. Example # 3: Blood gas: 7.34 / 60 / 31 Acidemic Elevated CO 2 is primary (respiratory acidosis) Metabolic compensation has occurred = chronic process Chronic Respiratory Acidosis with Metabolic Compensation* * true metabolic compensation takes 3 days (72hrs)

82. Example # 4: Blood gas: 7.50 / 48 / 36 Alkalemic Elevated HCO 3 is primary (metabolic alkalosis) Respiratory compensation has occurred = acute /chronic ? Metabolic Alkalosis with Respiratory Compensation*-incomplete *Respiratory compensation takes only minutes

83. Example # 5: Blood gas: 7.20 / 21 / 8 Acidemic Low HCO 3 Is primary (metabolic acidosis) Respiratory compensation is present Metabolic Acidosis with Respiratory Compensation

84. Case Study 1 A patient recovering from surgery in the post-anesthesia care unit is difficult to arouse two hours following surgery. The nurse in the PACU has been administering Morphine Sulfate intravenously to the patient for complaints of post-surgical pain. The patient’s respiratory rate is 7 per minute and demonstrates shallow breathing. The patient does not respond to any stimuli! The nurse assesses the ABCs (remember Airway, Breathing, Circulation!) and obtains ABGs STAT! The STAT results come back from the laboratory and show: pH = 7.15 (low) C02 = 68 mmHg (high) HC03 = 22 mEq/L (normal) 1. Compensated Respiratory Acidosis 2. Uncompensated Metabolic Acidosis 3. Compensated Metabolic Alkalosis 4.Uncompensated Respiratory Acidosis

85. Answer The answer is #4 Uncompensated respiratory acidosis

86. Case Study 2 An infant, three weeks old, is admitted to the Emergency Room. The mother reports that the infant has been irritable, difficult to breastfeed and has had diarrhea for the past 4 days. The infant’s respiratory rate is elevated and the fontanels are sunken. The Emergency Room physician orders ABGs after assessing the ABCs. The results from the ABGs come back from the laboratory and show: pH = 7.37 (normal) C02 = 29 mmHg (low) HC03 = 17 mEq/L (low) 1.Compensated Respiratory Alkalosis 2. Uncompensated Metabolic Acidosis 3 Compensated Metabolic Acidosis 4Uncompensated Respiratory Acidosis

87. Answer Answer is #3 Compensated Metabolic Acidosis

88. Case Study 3 A patient, 5 days post-abdominal surgery, has a nasogastric tube. The nurse notes that the nasogastric tube (NGT) is draining a large amount (900 cc in 2 hours) of coffee ground secretions. The patient is not oriented to person, place, or time. The nurse contacts the attending physician and STAT ABGs are ordered. The results from the ABGs come back from the laboratory and show: pH = 7.52 (high) C02 = 35 mmHg (normal) HC03 = 29 mEq/L (high) 1. Compensated Respiratory Alkalosis 2. Uncompensated Metabolic Acidosis 3. Compensated Metabolic Acidosis 4. Uncompensated Metabolic Alkalosis

89. Answer Answer is #4 Uncompensated Metabolic Alkalosis

90. Case Study 4 A patient is admitted to the hospital and is being prepared for a craniotomy (brain surgery). The patient is very anxious and scared of the impending surgery. He begins to hyperventilate and becomes very dizzy. The patient looses consciousness and the STAT ABGs reveal: The results from the ABGs come back from the laboratory and show: pH = 7.57 (high) C02 = 26 mmHg (low) HC03 = 24 mEq/L (normal) 1. Compensated Metabolic Acidosis 2. Uncompensated Metabolic Acidosis 3. Uncompensated Respiratory Alkalosis 4. Uncompensated Respiratory Acidosis

91. Answer The answer is #3 Uncompensated Respiratory Alkalosis

92. Case Study 5 A two-year-old is admitted to the hospital with a diagnosis of asthma and respiratory distress syndrome. The father of the infant reports to the nurse that he has observed slight tremors and behavioral changes in his child over the past three days. The attending physician orders routine ABGs following an assessment of the ABCs. The ABG results are: pH = 7.36 (normal) C02 = 69 mmHg (high) HC03 = 36 mEq/L (high) 1. Compensated Respiratory Alkalosis 2. Uncompensated Metabolic Acidosis 3. Compensated Respiratory Acidosis 4. Uncompensated Respiratory Alkalosis

93. Answer Answer is #3 Compensated Respiratory Acidosis

94. Anion Gap (AG): The calculated difference between the positively charged (cations) and negatively charged (anions) electrolytes in the body: AG= Na + - (Cl - + HCO 3 - ) Normal AG = 12 ± 2 (10 – 14)

95. Rule Calculate the anion gap. If the anion gap is  20, there is a primary metabolic acidosis regardless of pH or serum bicarbonate concentration Principle: The body does not generate a large anion gap to compensate for a primary disorder (anion gap must be primary)

96. High anion metabolic acidosis Renal failure DKA ETHANOL OR METHANOL POISONING

97. Rule Calculate the excess anion gap (total anion gap – normal anion gap) and add this value to the measured bicarbonate concentration:  if the sum is > than normal bicarbonate (> 30) there is an underlying metabolic alkalosis  if the sum is less than normal bicarbonate (< 23) there is an underlying non anion gap metabolic acidosis 1. Excess AG = Total AG – Normal AG (12) 2. Excess AG + measured HCO 3 = > 30 or < 23?

98. Mixed Acid-Base Disorders

99. M acid high AG A 20-year-old man with a history of diabetes is brought to the emergency department with a 3-day history of feeling ill. He is non-adherent with his insulin. Urine ketones are 2+ and glucose is 4+. pH7.26 Na + 136 mEq/L P O 2 110 mm HgK + 4.8 mEq/L P CO 2 19 mm HgCl - 101 mEq/L HCO 3 - 8 mEq/LCO 2, total10 mEq/L Glucose343 mg/dLUrea49 mg/dL Creatinine1 mg/dL.

100. Example 1 pH7.26Na + 136 mEq/L P O 2 110 mm HgK + 4.8 mEq/L P CO 2 19 mm HgCl - 101 mEq/L HCO 3 - 8 mEq/LGlucose343 mg/dL Urea49 mg/dL Creatinine1 mg/dL 1.2 mm Hg decrease in P CO 2 for every 1 mEq/L decrease in HCO 3 -. HCO 3 - decrease = 24-8 = 16 mEq/L P CO 2 decrease predicted = 1.2 x 16 = 19 mm Hg. subtract from 40 mm Hg (reference point) = 21 mm Hg

101. History suggests diabetic ketoacidosis. AG = 136-101-8=27 mEq/L Metabolic acidosis with appropriate respiratory compensation

102. A 43-year-old man comes to the physician with a 3-day history of diarrhea. He has decreased skin turgor. pH7.31 Na + 134 mEq/L P O 2 -- mm HgK + 2.9 mEq/L P CO 2 31 mm HgCl - 113 mEq/L HCO 3 - 16 mEq/LUrea74 mgl/dL Creatinine3.4 mmol/L History is limited. Metabolic acidosis with respiratory compensation.

103. Description pH7.31Na + 134 mEq/L P O 2 -- mm HgK + 2.9 mEq/L P CO 2 31 mm HgCl - 113 mEq/L HCO 3 - 16 mEq/LUrea74 mg/dL Creatinine3.4 mg/dL AG = 134-113-16=5 mEq/L 1.2 mm Hg decrease in P CO 2 for every 1 mEq/L decrease in HCO 3 -. HCO 3 - decrease = 24-16 = 8 mEq/L P CO 2 decrease predicted = 1.2 x 8 = 10 mm Hg. subtract from 40 mm Hg (reference point) = 30 mm Hg

104. Remember the Rules 1. Look at the Ph: 2. Calculate the anion gap: if AG  20 there is a primary metabolic acidosis (regardless of pH or HCO 3 ) 3. Calculate the excess anion gap, add it to HCO 3 : Excess AG = Total AG – Normal AG (12) Excess AG + HCO 3 = ? If sum > 30 there is an underlying metabolic alkalosis If sum < 23 there is an underlying nonanion gap metabolic acidosis

105. Example # 1 Blood gas: 7.50 / 20 / 15 Na= 140, Cl = 103 Alkalemic Low CO 2 is primary (respiratory alkalosis) Partial metabolic compensation for chronic condition? AG = 22 (primary metabolic acidosis) Excess AG (AG – 12) + HCO 3 = 25 (no other primary abnormalities) Respiratory Alkalosis and Metabolic Acidosis The patient ingested a large quantity of ASA and had both centrally mediated resp. alkalosis and anion gap met. Acidosis associated with salicylate overdose

106. Example # 2 Blood gas: 7.40 / 40 / 24 Na= 145, Cl= 100 pH normal AG = 21 (primary metabolic acidosis) Excess AG (AG – 12) + HCO 3 = 33 ( underlying metabolic alkalosis) Metabolic Acidosis and Metabolic Alkalosis This patient had chronic renal failure (met. acidosis) and began vomiting (met. alkalosis) as his uremia worsened. The acute alkalosis of vomiting offset the chronic acidosis of renal failure = normal pH

107. Example # 3 Blood gas 7.50 / 20 / 15 Na= 145, Cl = 100 Alkalemic Low CO 2 is primary (respiratory alkalosis) AG = 30 (primary metabolic acidosis) Excess AG (AG – 12) + HCO 3 = 33 (underlying metabolic alkalosis) Respiratory alkalosis, Metabolic Acidosis and Metabolic Alkalosis This patient had a history of vomiting (met. alkalosis), poor oral intake (met. acidosis) and tachypnea secondary to bacterial pneumonia (resp. alkalosis)

108. How Many Primary Abnormalities Can Exist in One Patient? Three primary abnormalities is the max because a person cannot simultaneously hyper and hypoventilate One patient can have both a metabolic acidosis and a metabolic alkalosis – usually one chronic and one acute

109. Example # 5 Blood gas: 7.15 / 15 / 5 Na= 140, Cl= 110 Acidemic Low HCO 3 - primary (metabolic acidosis) AG= 25 (metabolic acidosis is anion gap type) Excess AG + HCO 3 = 18 (underlying nonanion gap metabolic acidosis) Anion Gap and Nonanion gap Metabolic Acidosis Diabetic ketoacidosis was present (anion gap met. acidosis). Patient also had a hyperchloremic nonanion gap met. acidosis secondary to failure to regenerate bicarbonate from ketoacids lost in the urine.

110. 40 year male admitted to surgical unit due to infected diabetic foot, other co-morbidities hypertension and dyslipidemia were reasonabally controlled. He was febrile with temperature 38.5c and blood pressure 130/80. His laboratory investigations showed. WBC 12, Hb 9.6, Platelets 822 while renal profile showed. Serum Urea 8mmol/L,Serum creatinine 76 umol/L, Serum Na 142 mmol/L serum K 6.5 mmol/L. ABGs PH.7.4, Hco3 24, K 4.9 mmol/L. What is most likely diagnosis. A.Type IV Renal tubular acidosis B.Pseudohperkalemia C.Type II renal tubular acidosis D.Type I renal tubular acidosis E.Addison’s disease.

111. Answer:B Type IV renal tubular acidosis is common in diabetic patients with acidosis and hyperkalemia, While others two types I &II have hypokalemia and acidosis.Patient did not have acidosis or features of Addisons disease.Postassium in ABGs was within normal limits which suggested patient had pseudohyperkalemia secondary to thrombocytosis.

112. A 20 years female known to have type 1 diabetes mellitus,she missed her insulin dose presented to emergency room complaining of recurrent vomiting,on examination she is tachypnic with repiratory rate of 22, blood pressure 100/60mmHg. Pulse 95/min and afebrile. Other systemic review unremarkable. Laboratory investigations showed; Urine ketone 3,+ Glucose 2+. ABG’s.PH 7.2, HCO3 26, PCO2 30. Renal profile; urea 5mmol/L, creatinin 65 umol/L Na140mmol/L, K 3.5mmol/L Cl.95, Random blood sugar 20 mmol/L. What is acid base abnormality in this patient. A. Metabolic acidosis B. Respirtaory acidosis C. Mixed metabolic and respiratory acidosis D. High anion gap metabolic acidosis,metablolic and respiratory alkalosis E. Normal anion gap metabolic acidosis, metabolic and respiratory alkalosis.

113. Answer: D.This young female developed High anion gap metabolic acidosis secondary to ketones in the blood, Repiratory alkalosis due to tachypnia secondary to anxiety and metabolic alkalosis due to recurrent vomiting. Her Calculated Anion gap is 140-(95+26)=19

114. A 16 years female was referred for further investigations for short stature and stone disease. She was behind her milestones.Laboratory investigations showed.MSU, PH 7 otherwise bland sediment.Renal profile.Na 135mmol/L K 2.9 mmol/L Chloride 115 mmolL, Serum urea and Creatinine normal.Serum HCO3 10.what is the diagnosis. A.Type 1 renal tubular acidosis B.Type 2 renal tubular acidosis C.Type 4 renal tubulare acidosis D.High anion gap metabolic acidosis E.Metabolic alkalosis.

115. Answer: A.Anion gap for this patient is 10 while the patient having low bicarbonate suggesting metabolic acidosis.It is normal anion gap metabolic acidosis.As there is history of nephrolithiasis and patient is hypokalemia which favours the diagnosis of type 1 renal tubular acidosis.Urinary PH is 7 which is high and these patient can not acidify urine and maintain urinary PH always above 5.5 due to defect in the secretion of H ion in the distal convoluted tubules.

116. 60 years old male was treated ifosfamide based chemotherapy for soft tissue sarcoma.He was found persistant hypokalemia with low serum bicarbonate level on laboratory investigations.His current laboratory investigations are as following.Renal profile.Serum Urea 7 mmol/L, Serum creatinine 95 umol/L, Serum Na 140mmol/L and Serum K 3 mmol/L, Serum chloride 113mmol/L.ABG’s.PH.7.4,HCO3,18 and PCO2.47.What kind of acid base disorder happened. A..Metabolic alkalosis B..Type 1 renal tubular acidosis C..Type 2 renal tubular acidosis D..Type 4 renal tubular acidosis E..Respiratory acidosis.

117. Answer: C.Ifosfamide chemotherapy is effective in treating soft tissue cancer and it causes proximal renal tubular defect leading to proximal renal tubular acidosis with hyperchloremic,hypokalemic,normal anion gap metabolic acidosis.Here anion gap is 9.

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