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MLAB 2401: C LINICAL C HEMISTRY K ERI B ROPHY -M ARTINEZ Disorders of Acid-Base Imbalance.

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Presentation on theme: "MLAB 2401: C LINICAL C HEMISTRY K ERI B ROPHY -M ARTINEZ Disorders of Acid-Base Imbalance."— Presentation transcript:

1 MLAB 2401: C LINICAL C HEMISTRY K ERI B ROPHY -M ARTINEZ Disorders of Acid-Base Imbalance

2 A CID -B ASE I MBALANCES pH< 7.35 = acidosis/acidemia pH> 7.45 = alkalosis/alkalemia The body responds to imbalances by compensation If balance is fully restored to 20:1, it is termed complete If balance is still outside of normal limits it is termed partial

3 C OMPENSATION Respiratory compensation Occurs when underlying problem is metabolic See changes in pCO 2 Body responds by hyper or hypoventilation Metabolic Compensation Occurs when underlying problem is respiratory See changes in bicarbonate concentration Body responds by activating renal mechanisms

4 A CID -B ASE I MBALANCE Four categories Metabolic Acidosis Metabolic Alkalosis Respiratory Acidosis Respiratory Alkalosis

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6 M ETABOLIC VS R ESPIRATORY Metabolic KIDNEY Effects base= bicarbonate Respiratory LUNGS Effects acid= carbonic acid

7 M ETABOLIC A CIDOSIS Bicarbonate deficit : blood concentrations of bicarb drop below 22mEq/L Results in : pH drop Decrease in 20:1 ratio Causes of : Loss of bicarbonate through diarrhea or renal dysfunction Accumulation of acids (lactic acid or ketones) that exceed rate of elimination Failure of kidneys to excrete H + 7

8 S YMPTOMS OF M ETABOLIC A CIDOSIS Headache, Rapid and deep breathing Lethargy Nausea, vomiting, diarrhea Coma Death 8

9 C OMPENSATION FOR M ETABOLIC A CIDOSIS Respiratory Primary mechanism Increased ventilation CO 2 blown off Renal Excretion of hydrogen ions if possible Reabsorption of bicarbonate 9

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11 M ETABOLIC A LKALOSIS Bicarbonate excess - concentration in blood is greater than 26 mEq/L Results in: pH increase Causes of : Loss of acid-rich fluids Excess vomiting = loss of stomach acid Certain diuretics Addition of base to the body Excessive use of alkaline drugs Heavy ingestion of antacids Decrease of base elimination Endocrine disorders ( Cushing’s syndrome) 11

12 C OMPENSATION FOR M ETABOLIC A LKALOSIS Respiratory Primary mechanism Hypoventilation Increased retention of CO 2 Limited by hypoxia ( no oxygen) Alkalosis most commonly occurs with renal dysfunction, so can’t count on kidneys to excrete excess bicarbonate 12

13 S YMPTOMS OF M ETABOLIC A LKALOSIS Respiration slow and shallow Hyperactive reflexes ; tetany Often related to depletion of electrolytes Atrial tachycardia Dysrhythmias 13

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15 R ESPIRATORY A CIDOSIS Increased carbonic acid as indicated by increased pCO 2 Results in : decreased pH Causes of: – Problems within the respiratory system – Organs- lungs – Obstruction in the airway or restriction of gas exchange – Obstructive emphysema – Pulmonary edema/ pulmonary disease – Depression of respiratory center in brain that controls the breathing rate – Drugs – Stroke, Coma

16 C OMPENSATION FOR RESPIRATORY ACIDOSIS Kidneys Primary mechanism Eliminate hydrogen ions Retain bicarbonate ions

17 S IGNS AND S YMPTOMS OF R ESPIRATORY A CIDOSIS Breathlessness Restlessness Lethargy and disorientation Tremors, convulsions, coma Respiratory rate rapid, then gradually depressed Skin warm and flushed due to vasodilation caused by excess CO 2 17

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19 R ESPIRATORY A LKALOSIS Decrease carbonic acid indicated by decreased pCO 2 Most common acid-base imbalance Results in : increased pH Causes of: Hypoxemia Stimulation of the Respiratory Center:

20 R ESPIRATORY A LKALOSIS Hypoxemia Pulmonary disease Congestive heart disease Severe anemia High-altitude exposure Conditions that stimulate respiratory center: Acute anxiety Salicylate intoxication Cirrhosis Gram-negative sepsis Hyperventilation syndrome 20

21 C OMPENSATION FOR RESPIRATORY A LKALOSIS Kidneys Primary mechanism Conserve hydrogen ion Excretion of bicarbonate ion

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23 S UMMARY OF ACID - BASE DISORDERS

24 P RIMARY A CID /B ASE D ISORDERS pCO 2 pHHCO 3 Base Excess Uncompensated acidosis NDDD Uncompensated alkalosis NIII Partially compensated acidosis DDDD Partially compensated alkalosis IIII Compensated Acidosis/alkalosis I/DN

25 DisturbancePrimary AbnormalityCompensationCause Metabolic Acidosis Excess endogenous acid depletes bicarbonate Hyperventilation lowers pCO 2, Kidney excretes excess H + and forms more HCO 3 - Renal failure Ketosis Increased lactic acid Diarrhea Respiratory Acidosis Inefficient excretion of CO 2 by the lungs Formation of excess HCO 3 - by kidney Chronic pulmonary Diseases (COPD), such as emphysema Acute problems, such as pneumonia, airway obstruction, drugs such as opiates, congestive heart failure Metabolic Alkalosis Excess plasma bicarbonate Kidneys excrete excess HCO 3 - and form less HCO 3 - and NH 4, Lungs hypoventilate Loss of gastric juice Chloride depletion Hypokalemia Increased corticosteroid Increased ingestion of antacids Respiratory Alkalosis Hyperventilation lowers pCO 2 Increased excretion of bicarbonate by kidney Hyperventilation, such as with severe anxiety, fever, head injuries Stimulation of resp. center by drugs Central nervous system diseases

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27 R EFERENCES Bishop, M., Fody, E., & Schoeff, l. (2010). Clinical Chemistry: Techniques, principles, Correlations. Baltimore: Wolters Kluwer Lippincott Williams & Wilkins. Carreiro-Lewandowski, E. (2008). Blood Gas Analysis and Interpretation. Denver, Colorado: Colorado Association for Continuing Medical Laboratory Education, Inc. Jarreau, P. (2005). Clinical Laboratory Science Review (3rd ed.). New Orleans, LA: LSU Health Science Center. Sunheimer, R., & Graves, L. (2010). Clinical Laboratory Chemistry. Upper Saddle River: Pearson. 27


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