1. Serum Electrolytes & Arterial blood gases Dr. Mohammed K. El-Habil MSC. Pharmacology 2014

2. Electrolytes  Solutes that form ions (electrical charge)  Cation (+)  Anion (-)  Major body electrolytes:  Na+, K+, Ca++, Mg++  Cl-, HCO 3 -, HPO 4 --, SO 4 -

3. Electrolyte Distribution  Major ICF ions  K+  HPO 4 --  Major ECF ions  NA+  CL-, HCO 3 -

4. Electrolyte Normal Values  Sodium 135 – 145 mEq/L  Potassium 3.5 – 5 mEq/L  Phosphrus 1.8-2.3 mEq/L  Chloride 98 – 106 mEq/L  Calcium 9 – 11 mEq/L  Urea 20 – 40 mEq/L  Creatinine 0.7 – 1.2 mEq/L  Magnesium: 1.5 – 3 mEq/L  CO2 22 – 26 mEq/L  Bicarbonate 24-30 mEq/L

5. Hypernatremia  Na + is more than 135 – 145 mEq/L  Manifestations  Thirst, lethargy, agitation, seizures, and coma, shrinking of brain.  Similar to :  Central or nephrogenic diabetes insipidus (DI).  In treatment, reduce Na + levels gradually to avoid cerebral edema

6. Hyponatremia  Results from loss of sodium-containing fluids  Sweat, diarrhea, emesis,..etc.  Or from water excess  Inefficient kidneys  Drowning, excessive intake  Manifestations  Confusion, nausea, vomiting, seizures, Brain edema and coma

7. Hyperkalemia  Serum Potassium greater than 5.5 mEq/L - More dangerous than hypokalemia because cardiac arrest is frequently associated with high serum K+ levels

8. Hyperkalemia  Manifestations  Weak or paralyzed skeletal muscles  Ventricular fibrillation or cardiac block  Abdominal cramping or diarrhea

9. Hypokalemia  Low serum potassium caused by  Abnormal losses of K + via the kidneys or gastrointestinal tract  Drugs: Diuretics  Magnesium deficiency  Metabolic alkalosis enhance H-K pumping & entrance of K intracellular.

10. Hypokalemia  Manifestations  Most serious are cardiac arrhythemias  Skeletal muscle weakness  Weakness of respiratory muscles  Decreased gastrointestinal motility

11. Calcium  Obtained from ingested foods  More than 99% combined with phosphorus and concentrated in skeletal system  Inverse relationship with phosphorus  Otherwise…

12. Calcium  Balance controlled by  Parathyroid hormone  Calcitonin  Vitamin D/Intake  Bone used as reservoir

13. Hypercalcemia  High serum calcium levels more than 9 – 11 mEq/L caused by  Hyperparathyroidism (two thirds of cases)‏  Malignancy (parathyroid tumor)‏  Vitamin D overdose  Prolonged mobilization

14. Hypercalcemia  Manifestations  Decreased memory  Confusion  Disorientation  Fatigue  Constipation

15. Treatment  Excretion of Ca with loop diuretic  Hydration with isotonic saline infusion  Synthetic calcitonin

16. Hypocalcemia  Low serum Ca levels caused by  Decreased production of PTH  Acute pancreatitis  Multiple blood transfusions  Alkalosis  Decreased intake

17. Hypocalcemia  Manifestations  Weakness/Tetany  Positive Trousseau’s or Chvostek’s sign  Laryngeal stridor  Dysphagia  Tingling around the mouth or in the extremities

18. Treatment  Treat cause  Oral or IV calcium supplements  Not IM to avoid local reactions  Treat pain and anxiety to prevent hyperventilation-induced respiratory alkalosis

19. Phosphate  Primary anion in ICF  Essential to function of muscle, red blood cells, and nervous system  Deposited with calcium for bone and tooth structure

20. Hyperphosphatemia  High serum PO 4 3  (more than1.8-2.3 mEq/L) caused by:  Acute or chronic renal failure  Chemotherapy  Excessive ingestion of phosphate or vitamin D  Manifestations  Calcified deposition: joints, arteries, skin, kidneys, and corneas  Neuromuscular irritability and tetany

21. Hypophosphatemia  Low serum PO 4 3  caused by  Malnourishment/malabsorption  Alcohol withdrawal  Use of phosphate-binding antacids  During parenteral nutrition with inadequate replacement

22. Hypophosphatemia  Manifestations  CNS depression  Confusion  Muscle weakness and pain  Dysrhythmias  Cardiomyopathy

23. Magnesium  50% to 60% contained in bone  Coenzyme in metabolism of protein and carbohydrates  Factors that regulate calcium balance appear to influence magnesium balance.  Acts directly on myoneural junction  Important for normal cardiac function

24. Hypermagnesemia  High serum Mg more than 1.5 – 3 mEq/L caused by  When renal insufficiency or failure is present  Manifestations  Lethargy or drowsiness  Nausea/vomiting  Impaired reflexes***  Respiratory and cardiac arrest

25. Hypomagnesemia  Manifestations  Confusion  Hyperactive deep tendon reflexes  Tremors  Seizures  Cardiac dysrhythmias

26. Electrolytes

28. Renal Function

29. Arterial blood gases Arterial blood gases

31. Interpretation of ABGs  Diagnosis in six steps  Evaluate pH  Analyze PaCO 2  Analyze HCO 3   Determine if Balanced or Unbalanced  Determine if CO 2 or HCO 3  matches the alteration  Decide if the body is attempting to compensate

32. Interpretation of ABG 1. pH over balance 2. PaCO2 = “respiratory” balance 3. HC03- = “metabolic” balance 4. If all three normal = balanced 5. Match direction. e.g., if pH and PaCO2 are both acidotic, then primary respiratory acidosis 6. Together, CO2 & HCO3 act as metabolic & respiratory buffer like: 7. H2O + CO2 H2CO3 HCO3 + H

33. Metabolic Acid-base Disorders: Some Clinical Causes METABOLIC ACIDOSIS ↓HCO 3 - & ↓ pH - lactic acidosis; ketoacidosis; drug poisonings (e.g., aspirin, ethylene glycol, methanol) -diarrhea; some kidney problems (e.g., renal tubular acidosis, interstitial nephritis) METABOLIC ALKALOSIS ↑ HCO 3 - & ↑ pH contraction alkalosis, diuretics, corticosteroids, gastric suctioning, vomiting hyperaldosterone state (e.g., Cushing’s syndrome, Bartter’s syndrome, severe K + depletion)

34. RESPIRATORY ACIDOSIS ↑PaCO 2 & ↓ pH Central nervous system depression (e.g., drug overdose) Chest bellows dysfunction (e.g., Guillain-Barré syndrome, myasthenia gravis) Disease of lungs and/or upper airway (e.g., chronic obstructive lung disease, severe asthma attack, severe pulmonary edema) RESPIRATORY ALKALOSIS ↓PaCO 2 & ↑ pH Hypoxemia (includes altitude) AnxietySepsis Any acute pulmonary insult (e.g., pneumonia, mild asthma attack, early pulmonary edema, pulmonary embolism) Respiratory Acid-base Disorders: Some Clinical Causes

35. Acid-Base Disorders

37. Interpretation of ABGs  pH 7.26 Normal (7.35-7.45)  PaCO 2 67 mm Hg (35-45)  PaO 2 47 mm Hg (80-100)  HCO 3 26 mEq/L (22-26)  What is this?

38.  Respiratory acidosis

39. Interpretation of ABGs  pH 7.18  PaCO 2 38 mm Hg  PaO 2 70 mm Hg  HCO 3  15 mEq/L  What is this?

40.  Metabolic acidosi