1. Fluid and Electrolyte Disorders

2. Functions of Body Fluids
Transports gases, nutrients, and wastes
Help to generate the electrical activity needed to power body functions
Takes part in the transforming of food into energy
Maintains the overall function of the body

3. Distribution of Body Fluids
Intracellular compartment (ICF)
Consists of fluid contained within all of the billions of cells in the body
Larger of the two compartments, with approximately two thirds of the body water in healthy adults
High concentration of K+
Extracellular compartment (ECF)
Contains the remaining one third of body water
Contains all the fluids outside the cells, including that in the interstitial or tissue spaces and blood vessels
High concentration of Na+

5. Composition of the ECF, Plasma, and Interstitial Fluids
Large amounts of sodium and chloride
Moderate amounts of bicarbonate
Small quantities of potassium, magnesium, calcium, and phosphorus

6. Composition of the ICF Almost no calcium
Small amounts of sodium, chloride, bicarbonate, and phosphorus
Moderate amounts of magnesium
Large amounts of potassium

7. INTRACELLULAR EXTRACELLULAR POTASSIUM (K+) SODIUM (Na+)
MAGNESIUM (Mg2+)
CHLORIDE (Cl-)
PHOSPHOROUS (P)
BICARBONATE (HCO3-)

8. Question Which ion is in the highest concentration in the ICF? Na+ K+
Cl-
Ca2+

9. Answer
Na+
K+: Potassium is the most abundant ion of the ICF and is responsible for the membrane potential.
Cl-
Ca2+

10. Diffusion and Osmosis Concentration gradient Diffusion Osmosis
Difference in concentration over a distance
Diffusion
The movement of charged or uncharged particles along a concentration gradient from an area of higher concentration to one of lower concentration
Osmosis
The movement of water across a semi-permeable membrane from the side of the membrane with the lesser number of particles and greater concentration of water to the side with the greater number of particles and lesser concentration of water

11. Tonicity
The osmotic pressure gradient of two solutions separated by a semipermeable membrane
Solutions can be classified according to whether or not they cause cells to shrink.
Isotonic: neither shrink nor swell
Hypotonic: swell
Hypertonic: shrink

12. Physiology of water balance
Na+ retention causes this volume to expand
Na+ loss causes this volume to decrease
Water moves freely within intracellular and extracellular compartments, keeping osmolality equal

13. Edema Edema = Accumulation of water in interstitial space
Collections of fluid in body cavities
Hydrothorax – serous fluid in the thoracic cavity
Hydroperitoneum (ascites)
Hydropericardium fluid in the pericardial sac
Anasarca = severe, generalized edema with profound subcutaneous edema

14. Pathophysiology of Edema
The normal flow of fluid through the interstitial space depends on four factors:
Capillary hydrostatic pressure that filters fluid from the blood through the capillary wall
Oncotic pressure exerted by the proteins in the blood plasma
Permeability of the capillaries
Presence of open lymphatic channels that collect some fluid forced out of the capillaries by the hydrostatic pressure of the blood and return the fluid to the circulation

16. Mechanism of Edema Formation
Increased hydrostatic pressure
Reduced plasma oncotic pressure
Decreased lymph outflow (lymphatic channel obstruction
Increased capillary membrane permeability
Retention of water and salts

17. Hydrostatic pressure increases due to:
Venous obstruction:
thrombophlebitis (inflammation of veins)
hepatic obstruction
tight clothing on extremities
prolonged standing
Salt or water retention
congestive heart failure
renal failure

18. Increased Hydrostatic Pressure

19. Decreased plasma oncotic pressure:
↓ plasma albumin • liver disease • protein malnutrition
plasma proteins lost in: • glomerular diseases of kidney • hemorrhage, burns, open wounds
idiopathic edema
protein leakage from capillaries

20. Nephrotic Syndrome
Ascites is the build up of fluid in the space between the lining of the abdomen and abdominal organs (the peritoneal cavity). Ascites results from high pressure in the blood vessels of the liver (portal hypertension) and low levels of a protein called albumin. Usually due to severe liver damage.
Nephrotic syndrome is caused by different disorders that damage the kidneys. This damage leads to the release of too much protein in the urine.
Cancer, diabetes, lupus, genetic disorders can all cause this syndrome.

21. Lymphatic channels blocked
Surgery
Breast carcinoma with lymph node removal
Blocked lymphatics
Hematologic conditions
Parasitoses

22. Lymphatic obstruction
Caused by thread-like parasitic worm
– filaria (filariasis) transmitted by
mosquitoes

23. Effects of Edema Swelling Pitting Increased body weight
Functional impairment
Pain
Impairment of arteriole circulation
Other complications

24. Clinical Consequences of Edema
In skin edema may cause poor wound healing or poor clearance of infection
Edema in a closed space such as the calvarium can cause increased pressure, which may cause herniation of the brain

25. Acute pulmonary edema
Definition: An increase in pulmonary extravascular water, which occurs when transudation or exudation exceeds the capacity of lymphatic drainage.
Transudation - the passage of a substance through a membrane as a result of a difference in hydrostatic pressure; same as exudation
Exudation – oozing out; the slow escape of liquids from blood vessels through pores or breaks in the cell membranes

26. Stages of pulmonary edema
Interstitial pulmonary edema
Cresentic alveolar filling
Alveolar flooding
Airway flooding
With gradual onset these may be identifiable clinically, however with fulminant disease progression may be obscured
There is usually prodromal stage in which lymphatic drainage is increase, though there is no detectable increase in lung water
Crescentic – Interstitial edema increases and there is passage of fluid into the alveoli. However, the center of the alveoli and the most of the alveoli walls remain clear
Alveolar Flooding - Fluid enters the alveoli in a crescentic fashion until the surface tension rises sharply and further fluid is drawn into the alveolus as the pressure gradient rises exponentially.
Clearly no gas exchange can occur in flooded alveoli.
Fulminante - is any event or process that occurs suddenly and quickly, and is intense and severe to the point of lethality
Prodromal - An early symptom indicating the onset of an attack or a disease.

27. Cardioigenic pulmonary edema
Increased hydrostatic pressure secondary to elevated pulmonary venous pressure
Interstitial edema
Alveolar edema

28. Stages of Cardioigenic Pulmonary Edema
Elevated LA pressure causes distention and opening of small pulmonary vessels
Stage 2
Fluid and colloid shift into the lung interstitium from the pulmonary capillaries, but an initial increase in lymphatic outflow efficiently removes the fluid.

29. Stages of Cardioigenic Pulmonary Edema
As fluid filtration continues to increase and the filling of interstitial space occurs, fluid accumulates in the relatively noncompliant interstitial space.
At this stage, abnormalities in gas exchange are noticeable, vital capacity and other respiratory volumes are substantially reduced, and hypoxemia becomes more severe.

30. Toxic pulmonary edema
Increased vascular permeability due to toxic damage of
pulmonary capillaries.

31. High Altitude Pulmonary Edema (HAPE)
Hypoxic vasoconstriction
Blood vessel leakage
Fluid builds up in the lungs
HAPE is a noncardiogenic form of pulmonary edema resulting from a leak in the alveolar capillary membrane.
Autopsy studies performed on patients who died of HAPE have shown a proteinaceous exudate with hyaline membranes. Most reports mention capillary and arteriolar thrombi with deposits of fibrin, hemorrhage, and infarcts. The findings suggest a protein-rich edema with a possibility that clotting abnormalities may be partially responsible for this illness.
The person usually notices fatigue, weakness, and dyspnea on exertion. The condition typically worsens at night, and tachycardia and tachypnea occur at rest. Periodic breathing during sleep is almost universal in sojourners at high altitude. Cough, frothy sputum, cyanosis, rales, and dyspnea progressing to severe respiratory distress are symptoms of the disease. A low-grade fever, respiratory alkalosis, and leukocytosis are other common features. In severe cases, an altered mental status, hypotension, and death may result.

32. Methods for Assessing Edema
Daily weight
Visual assessment
Measurement of the affected part
Application of finger pressure to assess for pitting edema

33. Water and Na+ Balance Gain Water
Oral intake and metabolism of nutrients
Na+
Loss
Kidneys
Skin
Lungs
Gastrointestinal tract
Baroreceptors regulate effective volume
Modulating sympathetic nervous system outflow and ADH secretion
Atrial natriuretic peptide
Renin-angiotensin-aldosterone system
Angiotensin II
Aldosterone

34. Regulators of Sodium The kidney is the main regulator of sodium.
Monitors arterial pressure; retains sodium when arterial pressure is decreased, and eliminates it when arterial pressure is increased
The rate is coordinated by the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS).
Atrial natriuretic peptide (ANP) may also regulate sodium excretion by the kidney.

35. Physiologic Mechanisms Assisting in Regulating Body Water
Thirst
Primarily a regulator of water intake
ADH
A regulator of water output
Both mechanisms respond to changes in extracellular osmolality and volume.

36. Question
Which ion will have the greatest effect on the membrane potential?
Bicarbonate K+
Cl-
Mg2+

37. Answer
Bicarbonate
K+: Slight deviations in potassium concentration will directly change the membrane potential.
Cl-
Mg2+

38. Disorders of ADH Expression
Diabetes insipidus
Deficiency of or a decreased response to ADH
Unable to concentrate urine during periods of water restriction, leading to excretion of large volumes of urine
Neurogenic diabetes insipidus
Central diabetes insipidus
Syndrome of inappropriate antidiuretic hormone (SIAH)
Failure of the negative feedback system that regulates the release and inhibition of ADH

39. Types of Diabetes Insipidus
Central or neurogenic diabetes insipidus
Occurs because of a defect in the synthesis or release of ADH by the Hypothalamus
Usually Idiopathic but may be due to autoimmune disease such as Sarcoidosis, head trauma, or tumor
Nephrogenic diabetes insipidus
Occurs because the kidneys do not respond normally to ADH

40. Diabetes Insipidus Excessive Urination Extreme Thirst
Urine does NOT contain Glucose

41. The End

42. Mechanisms Protecting Extracellular Fluid Volume
Alterations in hemodynamic variables
Vasoconstriction and an increase in heart rate
Alterations in sodium and water balance
Isotonic contraction or expansion of ECF volume
Hypotonic dilution or hypertonic concentration of extracellular sodium brought about by changes in extracellular water

43. Causes of Fluid Volume Excess
Inadequate sodium and water elimination
Excessive sodium intake in relation to output
Excessive fluid intake in relation to output

44. Vitamin D, Calcitonin, and Parathyroid Hormone
Vitamin D acts to sustain normal plasma levels of calcium and phosphorus by increasing their absorption from the intestine.
Calcitonin acts on the kidney and bone to remove calcium from the extracellular circulation.

45. Mechanisms Regulating Calcium, Phosphorus, and Magnesium Balance
Calcium, phosphorus, and magnesium are the major divalent cations in the body.
They are:
Ingested in the diet
Absorbed from the intestine
Filtered in the glomerulus of the kidney
Reabsorbed in the renal tubules
Eliminated in the urine

46. Physiologic Calcium ECF calcium exists in three forms Protein bound
40% of ECF calcium is bound to albumin.
Complexed
10% is chelated with citrate, phosphate, and sulfate.
Ionized
50% of ECF calcium is present in the ionized form.

47. Calcium Gain and Loss Gains Dietary dairy foods
Parathyroid hormone and vitamin D stimulate calcium reabsorption in the nephron.
Losses
Occur when dietary intake and calcium absorption are less than intestinal secretion

48. Causes and Symptoms of Hypercalcemia
Increased intestinal absorption
Excessive vitamin D and calcium
Milk-alkali syndrome
Increased bone resorption
Increased parathyroid hormone
Malignant neoplasms
Prolonged immobilization
Decreased elimination
Thiazide, lithium therapy
Symptoms
Changes in neural excitability
Alterations in smooth and cardiac muscle function
Exposure of the kidneys to high concentrations of calcium

49. Causes and Symptoms of Hypocalcemia
Impaired ability to mobilize calcium from bone stores
Abnormal losses of calcium from the kidney
Increased protein binding or chelation such that greater proportions of calcium are in the nonionized form
Soft tissue sequestration
Symptoms
Increased neuromuscular excitability
Cardiovascular effects
Nerve cells less sensitive to stimuli

50. Role of Phosphorus in the Body
Plays a major role in bone formation
Essential to certain metabolic processes
The formation of ATP and the enzymes needed for metabolism of glucose, fat, and protein
Necessary component of several vital parts of the cell
Incorporated into the nucleic acids of DNA and RNA and the phospholipids of the cell membrane

51. Role of Phosphorus in the Body (cont.)
Serves as an acid–base buffer in the extracellular fluid and in the renal excretion of hydrogen ions
Necessary for delivery of oxygen by the red blood cells
Needed for normal function of other blood cells
White blood cells and platelets

52. Common Causes of Hypophosphatemia and Hyperphosphatemia
Depletion of phosphorus due to insufficient intestinal absorption
Transcompartmental shifts
Increased renal losses
Hyperphosphatemia
Failure of the kidneys to excrete excess phosphate
Rapid redistribution of intracellular phosphate to the ECF compartment
Excessive intake of phosphorus

53. Magnesium Balance Essential to all reactions that require ATP
Regulation at kidney level
Magnesium absorption in the thick ascending loop of Henle is the positive voltage gradient created in the tubular lumen by the Na+-K+-2Cl– cotransport system
Ingested in the diet
Absorbed from the intestine
Excreted by the kidneys

54. Manifestations of Hypomagnesemia
Laboratory values
Serum magnesium level less than l.8 mg/dL
Neuromuscular manifestations
Personality changes, athetoid or choreiform movements, nystagmus, tetany, positive Babinski Chvostek, and Trousseau signs
Cardiovascular manifestations
Tachycardia, hypertension, cardiac dysrhythmias

55. Causes of Hypermagnesemia
Excessive intake
Intravenous administration of magnesium for treatment of preeclampsia
Excessive use of oral magnesium-containing medications
Decreased excretion
Kidney disease
Acute renal failure

56. Question Alterations in ________________ may result in hypercalcemia.
ADH
Na+
Vitamin D K+

57. Answer Alterations in ________________ may result in hypercalcemia.
ADH
Na+
Vitamin D: When increased, vitamin D will result in higher retention of calcium. K+

58. Assessment of Body Fluid Loss
History of conditions that predispose to sodium and water losses, weight loss, and observations of altered physiologic function indicative of decreased fluid volume
Heart rate
Blood pressure
Venous volume/filling
Capillary refill rate

59. Psychogenic Polydipsia
Compulsive water drinking
Psychiatric disorders
Schizophrenia
Drink large amounts of water and excrete large amounts of urine.
Cigarette smoking
ADH
Interferes with water excretion by the kidneys
Antipsychotic medications increase ADH levels

60. Isotonic Fluid Volume Excess
Isotonic expansion of the ECF compartment with increases in both interstitial and vascular volumes
Increase in total body sodium that is accompanied by a proportionate increase in body water
Causes of decreased sodium and water elimination
Renal function
Heart failure
Liver failure
Corticosteroid excess

61. Potassium Distribution and Regulation
Intracellular concentration of 140 to 150 mEq/L
The extracellular concentration of 3.5 to 5.0 mEq/L
Body stores of potassium are related to body size and muscle mass.
Normally derived from dietary sources
Plasma potassium is regulated through two mechanisms:
Renal mechanisms that conserve or eliminate potassium
A transcellular shift between the ICF and ICF compartments

62. Abnormal Potassium
Hypokalemia refers to a decrease in plasma potassium levels below mEq/L.
Inadequate intake
Excessive gastrointestinal, renal, and skin losses
Redistribution between the ICF and ECF compartments
Hyperkalemia refers to an increase in plasma levels of potassium in excess of 5.0 mEq/L.
Decreased renal elimination
Excessively rapid administration
Movement of potassium from the ICF to ECF compartment

63. Diagnosis and Treatment of Potassium Disorders
Diagnosis is based on complete history, physical examination to detect muscle weakness and signs of volume depletion, plasma potassium levels, and ECG findings.
Treatment
Calcium antagonizes the potassium-induced decrease in membrane excitability.
Sodium bicarbonate will cause K+ to move into the ICF.
Insulin will decrease ECF K+ concentration
Curtail intake or absorption, increase renal excretion, and increase cellular uptake

64. ADH and Aquaporin-2 Channels
V1 receptors
Vasoconstriction
V2 receptors
Control water reabsorption
Aquaporins