1. The Cellular Environment: Fluids and Electrolytes, Acids and Bases
Chapter 3

2. Distribution of Body Fluids
Total body water (TBW) 60% of total body weight
Intracellular fluid – inside the cells
Extracellular fluid – not encased in cells
Interstitial fluid – found in between cells and tissues
Intravascular fluid- plasma found in circulatory system
Lymph, synovial, intestinal, biliary, hepatic, pancreatic, CSF, sweat, urine, pleural, peritoneal, pericardial, and intraocular fluids are extracellular

3. Water Movement Between the ICF and ECF
Osmolality – the concentrations of solutes in water
Osmotic forces – solutes will influence the movement of water across membranes
Aquaporins- water channel proteins in membranes
Starling hypothesis
Net filtration = forces favoring filtration – forces opposing filtration
As fluid flows through capillary it looses water and create greater osmotic return of water as it flows toward veinule end of capillary

4. Water Movement Between the ICF and ECF

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

6. Osmotic Equilibrium

7. Edema Accumulation of fluid within the interstitial spaces Causes:
Increase in hydrostatic pressure
Losses or diminished production of plasma albumin
Increases in capillary permeability
Lymph obstruction – elephantitus, flibitus

8. Edema

9. Water Balance Thirst perception
Osmolality receptors in medula respond to osmotic pressue of ECF
Hyperosmolality and plasma volume depletion
ADH secretion from posterior pituitary – conserves water in kidney to maintain water balance

10. Sodium and Chloride Balance
Primary ECF cation
Regulates osmotic forces
Roles
Neuromuscular irritability, acid-base balance, and cellular reactions
Chloride
Primary ECF anion
Provides electroneutrality

11. Sodium and Chloride Balance
Renin-angiotensin system – substanced produced in both liver and kidney
Angiotensin produced by liver and coverted by enzymes activated by renin from Kidney Juxta Glomerular Aparatus to a powerful vasoconstrictor.
Aldosterone – hormone from adrenal gland to regulate Na and K
Natriuretic peptides
Atrial natriuretic peptide - hormone from heart
Brain natriuretic peptide – hormone from brain
Urodilantin (kidney) – Kidney hormone

12. Alterations in Na+, Cl–, and Water Balance
Isotonic alterations
Total body water change with proportional electrolyte and water change
Isotonic volume depletion
Isotonic volume excess

13. 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.

14. Water Deficit Dehydration Pure water deficits
Renal free water clearance
Manifestations
Tachycardia, weak pulses, and postural hypotension
Elevated hematocrit and serum sodium level

15. Hypochloremia Occurs with hypernatremia or a bicarbonate deficit
Usually secondary to pathophysiologic processes
Managed by treating underlying disorders

16. Hypotonic Alterations
Decreased osmolality
Hyponatremia or free water excess
Hyponatremia decreases the ECF osmotic pressure, and water moves into the cell
Water movement causes symptoms related to hypovolemia

17. Hyponatremia Serum sodium level <135 mEq/L
Sodium deficits cause plasma hypoosmolality and cellular swelling
Pure sodium deficits
Low intake
Dilutional hyponatremia
Hypoosmolar hyponatremia
Hypertonic hyponatremia

18. 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
Manifestations: cerebral edema, muscle twitching, headache, and weight gain

19. Hypochloremia
Usually the result of hyponatremia or elevated bicarbonate concentration
Develops due to vomiting and the loss of HCl
Occurs in cystic fibrosis

20. Potassium Major intracellular cation
Concentration maintained by the 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

21. 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.
Aldosterone, insulin, and catecholamines influence serum potassium levels

22. Hypokalemia Potassium level <3.5 mEq/L
Potassium balance is described by changes in plasma potassium levels
Causes can be reduced intake of potassium, increased entry of potassium, and increased loss of potassium
Manifestations
Membrane hyperpolarization causes a decrease in neuromuscular excitability, skeletal muscle weakness, smooth muscle atony, and cardiac dysrhythmias

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

24. Hyperkalemia Mild attacks Severe attacks
Hypopolarized membrane, causing 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 or muscle tone, and flaccid paralysis

25. Calcium Most calcium is located in the bone as hydroxyapatite
Necessary for structure of bones and teeth, blood clotting, hormone secretion, and cell receptor function

26. Phosphate
Like calcium, most phosphate (85%) is also located in the bone
Necessary for high-energy bonds located in creatine phosphate and ATP and acts as an anion buffer
Calcium and phosphate concentrations are rigidly controlled
Ca++ x HPO4– – = K+ (constant)
If the concentration of one increases, that of the other decreases

27. Calcium and Phosphate Regulated by three hormones
Parathyroid hormone (PTH)
Increases plasma calcium levels
Vitamin D
Fat-soluble steroid; increases calcium absorption from the GI tract
Calcitonin
Decreases plasma calcium levels

28. Hypocalcemia and Hypercalcemia
Decreases the block of Na+ into the cell
Increased neuromuscular excitability (partial depolarization)
Muscle cramps
Hypercalcemia
Increases the block of Na+ into the cell
Decreased neuromuscular excitability
Muscle weakness
Increased bone fractures
Kidney stones
Constipation

29. Hypophosphatemia and Hyperphosphatemia
Osteomalacia (soft bones)
Muscle weakness
Bleeding disorders (platelet impairment)
Anemia
Leukocyte alterations
Antacids bind phosphate
Hyperphosphatemia
See Hypocalcemia
High phosphate levels are related to the low calcium levels

30. Magnesium Intracellular cation
Plasma concentration is 1.8 to 2.4 mEq/L
Acts as a cofactor in protein and nucleic acid synthesis reactions
Required for ATPase activity
Decreases acetylcholine release at the neuromuscular junction

31. Hypomagnesemia and Hypermagnesemia
Associated with hypocalcemia and hypokalemia
Neuromuscular irritability
Tetany
Convulsions
Hyperactive reflexes
Hypermagnesemia
Skeletal muscle depression
Muscle weakness
Hypotension
Respiratory depression
Lethargy, drowsiness
Bradycardia

32. 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).
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.

33. pH
Acids are formed as end products of protein, carbohydrate, and fat metabolism
To maintain the body’s normal pH ( ) 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

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

35. 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 system and hemoglobin

36. Carbonic Acid–Bicarbonate Pair
Operates in both 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

37. Carbonic Acid–Bicarbonate Pair
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
The respiratory system compensates by increasing or decreasing ventilation
The renal system compensates by producing acidic or alkaline urine

38. Carbonic Acid–Bicarbonate Pair

39. Other Buffering Systems
Protein buffering
Proteins have negative charges, so they can serve as buffers for H+
Renal buffering
Secretion of H+ in the urine and reabsorption of HCO3–
Cellular ion exchange
Exchange of K+ for H+ in acidosis and alkalosis

40. Buffering Systems

41. Acid-Base Imbalances Normal arterial blood pH Acidosis Alkalosis
7.35 to 7.45
Obtained by arterial blood gas (ABG) sampling
Acidosis
Systemic increase in H+ concentration
Alkalosis
Systemic decrease in H+ concentration

42. Acidosis and Alkalosis
Four categories of acid-base imbalances:
Respiratory acidosis—elevation of pCO2 due to ventilation depression
Respiratory alkalosis—depression of pCO2 due to alveolar hyperventilation
Metabolic acidosis—depression of HCO3– or an increase in non-carbonic acids
Metabolic alkalosis—elevation of HCO3– usually due to an excessive loss of metabolic acids

43. Metabolic Acidosis

44. Anion Gap
Used cautiously to distinguish different types of metabolic acidosis
By rule, the concentration of anions (–) should equal the concentration of cations (+). Not all normal anions are routinely measured.
Normal anion gap = Na+ + K+ = Cl– + HCO3– + 10 to 12 mEq/L (other misc. anions [the ones we don’t measure]—phosphates, sulfates, organic acids, etc.)

45. Anion Gap
An abnormal anion gap occurs due to an increased level of an abnormal unmeasured anion
Examples: DKA—ketones, salicylate poisoning, lactic acidosis—increased lactic acid, renal failure, etc.
As these abnormal anions accumulate, the measured anions have to decrease to maintain electroneutrality

46. Metabolic Alkalosis

47. Respiratory Acidosis

48. Respiratory Alkalosis