Fluids and Electrolytes, Acids and Bases

1. Fluids and Electrolytes, Acids and Bases Chapter 4

2. Distribution of Body Fluids Total body water (TBW) Intracellular fluid Extracellular fluid: Interstitial fluid Intravascular fluid Lymph, synovial, intestinal, CSF, sweat, urine, pleural, peritoneal, pericardial, and intraocular fluids

3. Distribution of Body Fluids (cont’d) Pediatrics 75% to 80% of body weight Susceptible to significant changes in body fluids Dehydration in newborns Aging Decreased percent of total body water Increase adipose and decrease muscle mass Renal decline Diminished thirst perception

4. Water Movement Between Fluid Compartments Osmolality Osmotic forces Aquaporins Starling hypothesis Net filtration = forces favoring filtration minus forces opposing filtration

5. Fluid Movement Between Plasma and Interstitial Space

6. Net Filtration Forces favoring filtration: Capillary hydrostatic pressure (blood pressure) Interstitial oncotic pressure (water-pulling) Forces favoring reabsorption: Plasma oncotic pressure (water-pulling) Interstitial hydrostatic pressure

7. Edema Accumulation of fluid within the interstitial spaces Causes: Increase in capillary hydrostatic pressure Decrease in plasma oncotic pressure Increases in capillary permeability Lymph obstruction (lymphedema) Localized vs. generalized Pitting edema

8. Edema (cont’d)

9. Sodium and Chloride Balance Sodium Primary ECF cation Regulates osmotic forces, thus water Roles Neuromuscular irritability, acid-base balance, and cellular chemical reactions and membrane transport Chloride Primary ECF anion Provides electroneutrality

10. Sodium and Chloride Balance (cont’d) Renin-angiotensin-aldosterone system Aldosterone—leads to sodium and water reabsorption back into the circulation and potassium and hydrogen secretion to be lost in urine Natriuretic peptides

11. Renin-Angiotensin-Aldosterone System

12. Water Balance ADH secretion Thirst perception Osmolality receptors Hyperosmolality and plasma volume depletion Volume receptors Baroreceptors

13. Antidiuretic Hormone (ADH) System

14. Alterations in Na+, Cl–, and Water Balance Isotonic alterations Total body water change with proportional electrolyte and water change (no change in concentration) Isotonic fluid loss Isotonic fluid excess

15. Alterations in Na+, Cl–, and Water Balance (cont’d) Hypertonic alterations Hypernatremia Serum sodium >147 mEq/L Related to sodium gain or water loss Water movement from the ICF to the ECF Intracellular dehydration Manifestations Intracellular dehydration, convulsions, pulmonary edema, hypotension, tachycardia, etc.

16. Alterations in Na+, Cl–, and Water Balance (cont’d) Hypertonic alterations (cont’d) Water deficit Dehydration Pure water deficits Rena-l free water clearance Manifestations: Hypovolemia Tachycardia, weak pulses, and postural hypotension Marked water deficit Headache, thirst, dry skin and mucous membranes, fever, weight loss, concentrated urine Elevated hematocrit and serum sodium level

17. Alterations in Na+, Cl–, and Water Balance (cont’d) Hypertonic alterations (cont’d) Hyperchloremia Occurs with hypernatremia or a bicarbonate deficit Usually secondary to pathophysiologic processes Managed by treating underlying disorders

18. Alterations in Na+, Cl–, and Water Balance (cont’d) Hypotonic alterations Decreased osmolality Hyponatremia or free water excess Hyponatremia decreases the ECF osmotic pressure, and water moves into the cell via osmosis Cells expand

19. Hyponatremia Serum sodium level <135 mEq/L Sodium deficits cause plasma hypo-osmolality and cellular swelling Causes: Pure sodium loss Low intake Dilutional hyponatremia Hypo-osmolar hyponatremia Hypertonic hyponatremia

20. Hyponatremia (cont’d) Manifestations: Lethargy, confusion, decreased reflexes, seizures, and coma If leads to loss of ECF and hypovolemia, see hypotension, tachycardia, decreased urine output If dilutional from excess water, see weight gain, edema, ascites, jugular vein distention

21. Water Excess Compulsive water drinking Decreased urine formation Syndrome of inappropriate ADH (SIADH) ADH secretion in the absence of hypovolemia or hyperosmolality Hyponatremia with hypervolemia

22. Water Excess (cont’d) Manifestations: cerebral edema (with confusion and convulsions), weakness, muscle twitching, nausea, headache, and weight gain

23. Hypochloremia Usually the result of hyponatremia or elevated bicarbonate concentration Develops as a result of vomiting and the loss of HCl Occurs in cystic fibrosis Alters acid-base balance

24. Potassium Major intracellular cation Concentration maintained by Na+/K+pump Regulates intracellular electrical neutrality in relation to Na+ and H+ Essential for transmission and conduction of nerve impulses, normal cardiac rhythms, and skeletal and smooth muscle contraction

25. Potassium Levels Changes in pH affect K+ balance Hydrogen ions accumulate in the ICF during states of acidosis; K+ shifts out to maintain a balance of cations across the membrane; result is hyperkalemia Aldosterone, insulin, and catecholamines influence serum potassium levels Potassium adaptation Slow changes tolerated better than acute

26. Hypokalemia Potassium level <3.5 mEq/L Potassium balance is described by changes in plasma potassium levels Causes: reduced intake of potassium, increased entry of potassium into cells, and increased loss of potassium

27. Hypokalemia (cont’d) Manifestations (depend on rate and severity) Membrane hyperpolarization causes a decrease in neuromuscular excitability, skeletal muscle weakness, smooth muscle atony, and cardiac dysrhythmias

28. Hyperkalemia Potassium level >5.5 mEq/L Hyperkalemia is rare because of efficient renal excretion Caused by increased intake, shift of K+ from ICF into ECF, decreased renal excretion, insulin deficiency, or cell trauma

29. Hyperkalemia (cont’d) Mild attacks Increased neuromuscular irritability Tingling of lips and fingers, restlessness, intestinal cramping, and diarrhea Severe attacks The cell is not able to repolarize, resulting in muscle weakness, loss of muscle tone and flaccid paralysis, bradycardia to cardiac arrest

30. ECG Changes with Potassium Changes

31. Calcium and Phosphate Calcium and phosphate concentrations are rigidly controlled Ca++ x HPO4– – = K+ (constant) If the concentration of one increases, that of the other decreases; if phosphate increases, calcium absorption from gut decreases-hypocalcemia Serum concentration 2.5 to 4.5 mg/dL

32. Calcium 99% of calcium is located in the bone as hydroxyapatite Necessary for structure of bones and teeth, blood clotting, hormone secretion, cell receptor function, plasma membrane stability, transmission of nerve impulses, muscle contraction Serum concentration 8.8 to 10.5 mg/dL

33. Hypocalcemia Causes: Inadequate intestinal absorption, deposition of ionized calcium into bone or soft tissue, blood administration Decreases in PTH and vitamin D Nutritional deficiencies occur with inadequate sources of dairy products or green leafy vegetables Effects: Increased neuromuscular excitability Tingling, muscle spasm (particularly in hands, feet, and facial muscles), intestinal cramping, hyperactive bowel sounds Severe cases show convulsions and tetany Prolonged QT interval, cardiac arrest

34. Hypercalcemia Causes: (cont’d) Hyperparathyroidism Bone metastases with calcium resorption from breast, prostate, renal, and cervical cancer Sarcoidosis Excess vitamin D Many tumors that produce PTH Effects: Many nonspecific: fatigue, weakness, lethargy, anorexia, nausea, constipation Impaired renal function, kidney stones Dysrhythmias, bradycardia, cardiac arrest Bone pain, osteoporosis

35. Phosphate Like calcium, most phosphate is also located in the bone Necessary for high-energy bonds located in creatine phosphate and ATP and acts as an anion buffer

36. Hypophosphatemia Causes: Intestinal malabsorption (vitamin D deficiency, use of magnesium- and aluminum-containing antacids, long-term alcohol abuse); Malabsorption syndromes Respiratory alkalosis Increased renal excretion of phosphate associated with hyperparathyroidism • Effects: • Reduced capacity for oxygen transport by red blood cells thus disturbed energy metabolism • Leukocyte and platelet dysfunction • Deranged nerve and muscle function • In severe cases, irritability, confusion, numbness, coma, convulsions, possibly respiratory failure, cardiomyopathies, bone resorption

37. Hyperphosphatemia (cont’d) Causes: Acute or chronic renal failure with significant loss of glomerular filtration Treatment of metastatic tumors with chemotherapy that releases large amounts of phosphate into serum Long-term use of laxatives or enemas containing phosphates Hypoparathyroidism • Effects: • Symptoms primarily related to low serum calcium levels (caused by high phosphate levels) similar to the results of hypocalcemia • When prolonged, calcification of soft tissues in lungs, kidneys, joints

38. Magnesium Intracellular cation Serum concentration 1.8 to 3.0 mEq/L Acts as a cofactor in intracellular enzymatic reactions Increases neuromuscular excitability

39. Hypomagnesemia Causes: Malnutrition, Malabsorption syndromes Alcoholism Urinary losses (renal tubular dysfunction, loop diuretics) • Effects: • Behavioral changes • Irritability • Increased reflexes • Muscle cramps • Ataxia • Nystagmus • Tetany • Convulsions • Tachycardia • Hypotension

40. Hypermagnesemia Causes: Usually renal insufficiency or failure Also excessive intake of magnesium-containing antacids Adrenal insufficiency Effects: Skeletal smooth muscle contraction Excess nerve function Loss of deep tendon reflexes Nausea and vomiting Muscle weakness Hypotension Bradycardia Respiratory distress

41. Acid-Base Balance Acid-base balance is carefully regulated to maintain a normal PH via multiple mechanisms

42. pH Inverse logarithm of the H+ concentration If the H+ are high in number, the pH is low (acidic); If the H+are low in number, the pH is high (alkaline)

43. pH (cont’d) The pH scale ranges from 0 to 14: 0 is very acidic, 14 is very alkaline Each number represents a factor of 10 If a solution moves from a pH of 6 to a pH of 5, the H+ have increased 10 times

44. pH (cont’d) Acids are formed as end products of protein, carbohydrate, and fat metabolism To maintain the body’s normal pH (7.35-7.45), the H+ must be neutralized or excreted The bones, lungs, and kidneys are the major organs involved in the regulation of acid and base balance

45. pH (cont’d) Body acids exist in two forms: Volatile H2CO3 (can be eliminated as CO2 gas) Nonvolatile Sulfuric, phosphoric, and other organic acids Eliminated by the renal tubules with the regulation of HCO3–

46. Buffering Systems A buffer is a chemical that can bind excessive H+ or OH– without a significant change in pH A buffering pair consists of a weak acid and its conjugate base The most important plasma buffering systems are the carbonic acid-bicarbonate pair CO2+ H2O <>H2CO3<>H + HCO3

47. Carbonic Acid-Bicarbonate Pair Operates in the lung and the kidney The greater the partial pressure of carbon dioxide, the more carbonic acid is formed At a pH of 7.4, the ratio of bicarbonate to carbonic acid is 20:1 Bicarbonate and carbonic acid can increase or decrease, but the ratio must be maintained

48. Carbonic Acid–Bicarbonate Pair (cont’d) If the amount of bicarbonate decreases, the pH decreases, causing a state of acidosis The pH can be returned to normal if the amount of carbonic acid also decreases This type of pH adjustment is referred to as compensation

49. Carbonic Acid–Bicarbonate Pair (cont’d) The respiratory system compensates by increasing ventilation to expire carbon dioxide or by decreasing ventilation to retain carbon dioxide The renal system compensates by producing acidic or alkaline urine

50. Other Buffering Systems Protein buffering (hemoglobin) Proteins have negative charges, so they can serve as buffers for H+ Renal buffering Secretion of H+ in the urine and reabsorption of HCO3– Ion exchange (between ICF and ECF) Exchange of K+ for H+ in acidosis and alkalosis