Fluid And Electolytes 2

Front 1

What are the Functions of body water?

Back 1

➢ Transportation of nutrients, electrolytes, and oxygen to the cells
➢ Excretion of waste products
➢ Regulation of body temperature
➢ Lubrication of joints and membranes
➢ Medium for digested food

Front 2

What is Body fluid influenced by?

Back 2

1) Age: Infant – 70-80% of body weight- become very sick if electrolytes are inbalances, adult 60%, older adult 45-55%, less body water more at risk for problems.
2) Sex: males have more body water (leaner body mass)
3) Body fat: is essentially free of water, therefore an obese person has less body water than a thin person

Front 3

What is the Distribution of body water?

Back 3

ICF (intracellular) (2/3 of body water in adults) 40%
ECF (extracellular) (1/3 of body water in adults)
Interstitial 15%
Intravascular 5%
-------
60% (40L)

Front 4

What are the Daily body fluid intake and losses?

Back 4

Fluid Intake Fluid Losses

Liquid 1000-1200 mL Urine 1000-1400 mL
Food 800-1000 mL Feces 100 mL
Oxidation 200-300 mL Lungs 400-500 mL
Skin 300-500 mL
---------------- -----------------
2000-2500 mL 1800-2500 mL

Front 5

Electolyte imbalances cause?

Back 5

problems with muscular, and calcium

Front 6

Sodium is?

Back 6

Extracellular

Front 7

Potassium is?

Back 7

Intercellular

Front 8

Colloid is?

Back 8

a protein

Front 9

SIADH does this?

Back 9

Increases ADH Urine output

Front 10

Diabetes Insipudus?

Back 10

Decreases ADH, Increases urine output

Front 11

Ions carry what kind of charges?

Back 11

Weak electrical

Front 12

examples of +ions are?

Back 12

na+,k+,ca++, mg++

Front 13

examples of - ions anions are?

Back 13

cl-,po,hco3

Front 14

Majour ECF

Back 14

Sodium

Front 15

Majour ICF

Back 15

Potassium

Front 16

what is included with the regulation of body fluids?

Back 16

• Thirst
• Sodium
• Protein, Albumin
• ADH (Antidiuretic hormone)
• Aldosterone
• Renin
• Lymphatics
• Kidneys
• Skin, Lungs
• GI tract
• Osmosis
• Diffusion
• Filtration
• Na+ - K+ pump

Front 17

Osmolarity is?

Back 17

the number of particles/L

Front 18

Osmolality is?

Back 18

number of particles/kg (Normal value = 280-295 mOsm/kg)

Front 19

Tonicity is ?

Back 19

Concentratin of IV solutions ( 2 things, think coffee and water)

Front 20

Isotonic is ?

Back 20

IV solution with nearly the same osmolality of blood

Front 21

Hypertonic is?

Back 21

IV solutions with osmolality higher than blood and therefore pull water into the vascular space to raise blood pressure, increase blood volume
Eg. D10W (10% dextrose in water), D5/0.45%NaCl

Front 22

Hypotonic is?

Back 22

: IV solutions with osmolality lower than blood which therefore moves fluid out of blood to intracellular spaces
Eg. O.45% NaCl
D5W (5% dextrose solution)—this solution is isotonic in the IV bag, however once the dextrose reaches the bloodstream it is metabolized very quickly which makes the solution hypotonic.

Front 23

Isotonic FVD causes?

Back 23

• Excessive losses from the GI tract eg. Vomiting, diarrhea, NG suctioning, fistulas
• Excessive losses through the skin eg. Profuse diaphoresis, fever
• Excessive losses through the kidney eg. Diuretics,
• Third space shifting: fluid shifts from the vascular space to an area where it is not readily accessible eg. Fluid sequestered in the bowel with a bowel obstruction, in the peritoneal cavity as ascites, blisters in burn injuries
• Hemorrhage
• Decreased oral intake eg. Oral trauma

Front 24

Hypertonic FVD causes?

Back 24

• Unconsciousness (inability to respond to thirst mechanism)
• Diabetes insipidus (↓ADH)
• Diabetic ketoacidosis, hyperglycemia
• Watery diarrhea
• Excessive administration of hypertonic IV fluids
• High osmolality enteral feeding formulas with inadequate water supplementation

Front 25

Hypotonic FVD causes?

Back 25

• Renal insufficiency (sodium is lost by the kidney)
• Excessive use of hypotonic IV solutions

Front 26

Pathophysiology of Isotonic FVD?

Back 26

-because Na+ and H2O ratio is essentially unchanged serum osmolality remains normal and regulatory mechanisms such as ADH do not respond.
-usually there is no fluid shift
-↓plasma volume may trigger aldosterone secretion
-when 3% of plasma volume is lost the sympathetic nervous system is activated
• Epinephrine and norepinephrine - ↑HR and myocardial contractility to increase cardiac output, constriction of small vessels shunts blood away from the periphery to major organs
• Hormonal response – rennin activates a process that lead to angiotensin II (vasoconstrictor) and stimulates release of aldosterone

Front 27

Pathophysiology of Hypertonic FVD?

Back 27

-excessive ECF loss of water = ↑Na+ concentration = ↑serum osmolality = hyperosmolar plasma
-hyperosmolar plasma = ↑osmotic pressure = fluid is pulled from ICF causing cells to shrink = cellular dehydration
-posterior pituitary gland releases more ADH to increase water reabsorption by the kidneys
-thirst center in the hypothalamus is activated to increase oral fluid intake

Front 28

Isotonic FVD Implications for the elderly?

Back 28

-compensatory mechanisms can lose their effectiveness as a result of the physiologic changes of aging eg. Renal function can ↓by 50%
-less body water means that the elderly more readily experience the signs and symptoms of dehydration.
-the elderly are at a higher risk for diseases that lead to dehydration eg. Intestinal obstruction
-diuretic medications are more commonly prescribed for the older population

Front 29

Isotonic FVD Implications for young children?

Back 29

percentage of total body water and the inability to control fluid intake makes this group very susceptible to isotonic dehydration.

Front 30

Assessing Isotonic FVD?

Back 30

• Weight
-determine % of dehydration:

% weight loss Litres

Mild 2% 1-2 L
Marked 5% 3-5L
Severe 8% 5-10L
Fatal 22 – 30%

Loss of 1/3 of ECF volume = vascular collapse

Front 31

Hypotonic FVE?

Back 31

also known as water intoxication
-the gain of body fluid is greater than the gain of body sodium = dilutional hyponatremia

Front 32

Hypotonic FVE Causes?

Back 32

• SIADH (syndrome of inappropriate ADH secretion, ↑ADH)
• Excessive water intake
• Congestive heart failure (CHF)

Front 33

Hypotonic FVE Pathophysiology?

Back 33

excess fluid is hpotonic = plasma osmolarity is decreased = fluid moves from ECF to ICF and into tissue spaces

Front 34

Isotonic FVE?

Back 34

relatively equal gains of sodium and water
-overhydration

Front 35

Isotonic FVE Causes?

Back 35

• Excessive administration of IV or oral fluids
• Chronic renal failure

Front 36

Isotonic FVE Pathophysiology?

Back 36

osmolarity is not significantly effected
-increasing ECF volume can shift into the interstitial space = edema

Front 37

Isotonic FVE Implications for Elderly?

Back 37

if cardiac function is impaired the excess fluid may lead to CHF or pulmonary edema

Front 38

Hyponatremia?

Back 38

-serum sodium < 135 mmol/L
-can be a result of:
a) direct loss of sodium from the body
b) excess water in ECF →dilutional hyponatremia

Front 39

Causes of Hypotnatremia?

Back 39

-Direct loss of Sodium:
-excessive losses from diaphoresis, vomiting, diarrhea and fistulas
-diuretic medications (thiazide and loop diuretics)
-aldosterone insufficiency
-renal disease
-decreased sodium diet

-Excess water in ECF:
-excessive oral intake without adequate output
-irrigation of body cavities with hypotonic solutions such as sterile water
-SIADH

Front 40

Hyponatremia Pathophysiology?

Back 40

low sodium levels impair nerve conduction

Front 41

Signs and Symptoms of Hyponatremia?

Back 41

muscle cramps, fatigue, abdominal discomfort or cramps with N/V

Front 42

Medical Treatment of Hyponatremia?

Back 42

-treat underlying cause
-if it is an isotonic loss – infusion of an isotonic IV solution eg. N/S, R/L
-excess fluid volume – hypertonic solution eg. 3% saline, fluid restriction, diuretics that promote water loss rather than sodium loss eg. Mannitol

Front 43

Nursing interventions of Hyponatremia?

Back 43

-ongoing assessment of all clients at risk of developing hyponatremia
-high sodium foods eg. Tomatoes, broth, processed foods, bacon, ham
-assess fluid balance: monitor I/O, weights, skin turgor, mucous membranes
-irrigations of GI and GU tracts should be done with N/S (not sterile water)
-monitor for manifestations of overcorrection eg. Edema, pulmonary edema

Front 44

Hypernatremia?

Back 44

-serum sodium > 145 mmol/L
-can be a result of:
a) ingestion of large amounts of sodium without proportionate water intake
b) loss of water exceeds loss of sodium

Front 45

Causes of Hypernatremia?

Back 45

-Ingestion of large amounts of sodium:
-in diet
-hypertonic tube feedings
-IV fluids
-salt watering near drowning
-Cushing’s Syndrome, hyperaldosteronism
-long term corticosteroids

-Loss of water exceeds loss of sodium:
-Diabetes Insipidus (decreased ADH)
-diminished thirst mechanism
-decreased ingestion of fluids

Front 46

Pathophyisiology of Hypernatremia?

Back 46

increased osmotic pressure causes a movement of fluid out of the cells into the extracellular space

changes in excitable cell membrane activity

decreased fluid volume
Increased serum sodium concentration prevents movement of calcium into the myocardium

Front 47

Signs and Symptoms of Hypernatremia?

Back 47

-weakness, agitation
-twitching, irregular muscle contractions, seizures
decreased myocardial contractility → ↓cardiac output → heart failure

Front 48

Medical Management Hypernatremia?

Back 48

increase water intake either orally or through salt-free IV solutions eg. D5W

Front 49

Nursing Interventions of Hypernatremia?

Back 49

assessment and ongoing monitoring for those at risk
-review dietary restrictions
-ensure water flush accompanies tube feedings
-monitor I/O etc.

Front 50

Hypokalemia?

Back 50

-serum potassium < 3.5 mmol/L
-can be a result of:
a) excessive loss of potassium
b) movement of potassium from ECF → ICF

Front 51

Causes of Hypokalemia?

Back 51

-Actual Deficit – excessive loss of K+
-excessive use of loop and thiazide diuretics
-excessive use of corticosteroids
-increased secretion of aldosterone (Cushing’s Disease)
-excessive GI losses – vomiting, diarrhea, prolonged nasogastric drainage
-wound drainage
-renal disease impairing reabsorption of potassium
-inadequate intake

-Relative Deficit – movement of K+ from ECF → ICF
-alkalosis
-treatment of diabetic ketoacidosis with insulin

Front 52

Pathophysiology of Hypokalemia?

Back 52

interferes with neuromuscular functioning…normally interacts with enzymes for muscle contraction
ICF levels of potassium are insufficient to maintain cellular metabolism

Potassium maintains ability of nerves to carry an electrical charge

decreased GI motlity

weak respiratory muscles
renal function may be impaired in severe cases because of failure to concentrate urine

Front 53

Signs and Symptoms of Hypokalemia?

Back 53

-fatigue, muscle weakness, cramps
paresthesis “pins and needles”
-fatigue and lack of strength are early indicators
-cardiac dysrhthmias, decreased cardiac contractility that can lead to cardiac arrest (particularly a risk with serum potassium <2.5 mmol/L) -
EKG changes – elevated U waves, flat T wave, depressed ST segment

Front 54

Medical Management Hypokalemia

Back 54

-replacement orally or IV
-IV concentration should not exceed 40 mmol of potassium/L of fluid
-can give emergency bolus doses of 40mmol of potassium in 100 mL of IV fluid under monitored conditions

Front 55

Nursing Interventions of Hypokalemia

Back 55

-monitor at risk patients closely (eg. pt receiving Digoxin)
-IV assessment for patient receiving supplemental potassium
-health teaching re diet for increasing potassium eg. Bananas, tomatoes,
Fruits, vegetables, nuts, cocoa, cola

Front 56

Hyperkalemia?

Back 56

-serum potassium > 5.0 mmol/L

Front 57

Causes of Hyperkalemia?

Back 57

renal failure
-excessive oral or intravenous administration of potassium to correct a deficit
-excessive use of salt substitutes
-Addison’s disease, deficit of aldosterone
-use of potassium sparing diuretics
-Crushing injuries, burns (K+ is released from damaged cells)
-Metabolic acidosis (promotes movement of K+ from ICF → ECF

Front 58

Patjophysiology of Hyperkalemia

Back 58

neuromuscular irritability
slowed GI muscular contraction
depresses action of the heart, slows impulse formation and transmission)
ECG changes – tall tented T waves

Front 59

Signs and Symptoms of Hyperkalemia

Back 59

vague muscle weakness starting in the legs progressing to the trunk and arms. Involvement of facial and respiratory muscles is a late symptom , paresthesias
-flaccid paralyis

Front 60

Medical Management of Hyperkalemia?

Back 60

-Non-emergency:
-restrict dietary potassium
- Kayexelate (cation exhange resin- potassium is absorbed in the GI tract and is exchanged for sodium)
-Furosemide (lasix) – loop diuretic

-Emergency – K+ > 6.5 mmol/L
-IV insulin, glucose and sodium bicarbonate
-usually hypertonic glucose is used D10W or D20W
-insulin facilitates the movement of glucose and potassium into the cell, the glucose prevents the hypoglycemia that would accompany the insulin administration
-sodium bicarbonate corrects the acidosis

-IV Calcium chloride
-stimulates the heart (hyperkalemia depresses the action of the heart)

-Kayexlate
-Dialysis

Front 61

Nursing INterventions of Hyperkalemia?

Back 61

close monitoring of patients at risk eg. Oliguric/anuric patients
-health teaching dietary restrictions and avoidance of salt substitutes

Front 62

Hypoglycemia?

Back 62

-serum calcium < 2.15 mmol/L
(some sources say < 2.2 mmol/L)
-most of the calcium in our bodies is located in bones, teeth and nails
-the remainder is in serum
-serum calcium travels either bound to protein (usually albumin) or travels freely (ionized)
-serum calcium levels measure both bound and ionized calcium
-ionized calcium can be measured and is not affected by changes in levels of serum albumin

Front 63

Causes of Hypoglycemia?

Back 63

inadequate dietary intake
-malabsorption disorders
-hypoparathyroidism (decreased PTH)
-renal failure (retention of phosphate which causes loss of calcium, also vitamin D is not activated therefore intestinal absorption is decreased)
-decreased albumin (~ 46% of calcium is bound to protein, primarily albumin therefore a decrease in albumin can cause a decrease in calcium)
-increase in dietary protein (causes calcium to move out of bones and is then excreted in urine)
-decreased vitamin D
-long term effect of immobilization and bone demineralization
-can be lost in GI tract

Front 64

Pathophysiology of Hypoglycemia?

Back 64

increased permeability and excitability of nerve membranes leading to spontaneous stimulation of skeletal muscle

weak heart contractions because of insufficient calcium for muscle action and conduction is delayed

calcium is part of the clotting cascade converting prothrombin to thrombin and therefore functions in the coagulation of blood)

99% of body calcium is located in bones, teeth and nails

Front 65

Signs and Symptoms of Hypoglycemia?

Back 65

muscle twitching, carpopedal spasm, Chvostek’s sign, Trousseau’s sign, hyperactive reflexes, tetany paresthesias, abdominal cramps

arrythmias
renal or GI bleeding, impaired clotting time and impaired clot formation

Front 66

Medical Management of Hypoglycemia?

Back 66

-administration of calcium orally or intravenously (with IV replacement should use D5W not N/S as sodium encourages calcium loss)
-administration of vitamin D to aid in absorption of calcium from the GI tract

Front 67

Nursing Interventions of Hypoglycemia

Back 67

health teaching about increasing dietary calcium (dairy products, green leafy vegetables, salmon
-quiet environment where patient is not overstimulated
-seizure precautions
-ongoing monitoring and assessment
-Medications eg. Bisphosphanates eg. Actonel, Alendronate

Front 68

Hyperglycemia?

Back 68

serum levels of calcium > 2.65mmol/L

Front 69

Causes of Hyperglycemia?

Back 69

-hyperparathyroidism
-immobility
-neoplasms (can cause uncontrolled release of calcium ions from the bones and some tumors can secrete PTH)
-excessive intake
-milk-alkali syndrome – increased ingestion of milk and antacids
-renal dysfunction use of thiazide diuretics decrease excretion of calcium
-corticosteroids mobilize calcium absorption from bone

Front 70

Pathophysiology of Hyperglycemia?

Back 70

depresses neuromuscular activity—high levels of ionized calcium have a sedative effect on the neuromuscular system

interferes with function of ADH in the kidneys resulting in less absorption of water
(increased myocardial contractility, altered action of the cardiac muscle)

Front 71

Signs and Symptoms of Hyperglycemia

Back 71

-muscle weakness, loss of muscle tone, lethargy, stupor, personality changes, depression, apathy, anorexia and nausea

-dysrhythmias

Front 72

Hyperglycemia Knowledge?

Back 72

bone changes
—if excess PTH is the problem = bone density will decrease and pathological fractures may occur
-if calcium intake is high then PTH will be low and more calcium will be stored in the bone maintaining bone strength
-flank pain (renal calculi)

Front 73

Medical Management of Hyperglycemia?

Back 73

dietary restriction of calcium
-diuresis (intravenous N/S and Furosemide)
-increase fluid intake

Front 74

Nursing Interventions of Hyperglycemia?

Back 74

-prevent hypercalcemia in the immobilized patient
-observe for S&S that accompany the passing of a renal calculus
-teach re diet to temporarily avoid calcium
-monitor urinary output and urinary pH (calcium precipitates in alkaline urine leading to the formation of renal calculi)
-encourage cranberry juice to increase the acidity of urine

Front 75

Acid-Base Balcne is?

Back 75

-refers to homeostasis of H+ ion concentration
-even a slight deviation from normal results in pronounced changes of cellular chemical reactions which threaten survival.
-maintaining a balance is an ongoing process due to the continuous formation and expulsion of the acid end products of metabolism

Front 76

Acid-Base Balance

Back 76

-acid-base balance is maintained by controlling H+ ion concentration
-numerous homeostatic mechanisms are in place to maintain this balance:
• Chemical buffer systems (eg. Bicarbonate-carbonic acid system…respond immediately to imbalances but the effect is temporary and they cannot completely restore homeostasis)
• Respiratory regulation (stimulation of respiratory centers to alter respiratory rate adjust amount of CO2 being exhaled…responds within minutes to hours to correct an imbalance)
• Cellular regulation (exchange of H+ and K+… with acidosis H+ moves into the cell and K+ moves out which explains the hyperkalemia that occurs with acidosis)
• Renal regulation (maintains homeostasis through HCO3- reabsorption and H+ secretion….responds within hours therefore is the slowest to respond but is the most thorough and is the only system that can make a permanent adjustment in acid-base balance)

Front 77

Acidosis
alkalosis

Back 77

Respiratory
Metabolic

Front 78

Evaluation of Acid-Base Balance?

Back 78

-measured through ABG’s (arterial blood gases)
pH -represents the H+ ion concentration of a solution
-reflects acidity or alkalinity of the solution
-inverse relationship between concentration of H+ ions and pH
• ↓ pH = ↑ H+ ion concentration = acidosis
• ↑ pH = ↓ H+ ion concentration = alkalosis

Front 79

Acid-Base Balance Compensation

Back 79

-maintaining acid-base homeostasis is essential for the functioning of cells
-when a problem arises that alters acid base balance, homeostatic mechanisms begin functioning

Front 80

Eg of Acid-Base Balance Compensation

Back 80

- Pt has a diagnosis of COPD and has a category of this disorder that causes the individual to retain CO2.
- ↑ pCO2 = acidosis = ↓ pH
- As the problem has started with a change in pCO2 (the respiratory parameter) the problem is respiratory acidosis.
- As the problem has started in the lungs compensation (to correct the problem) will have to come from the other mechanisms eg. Renal regulation
- The kidneys will increase the excretion of H+ ions and increase the reabsorption of bicarbonate

Front 81

Eg of Acid-Base Balance Compensation

Back 81

Pt has persistent vomiting which led to the insertion of an NGT attached to suction.
-Loss of gastric fluids means there is also a loss of HCl acid (hydrochloric acid)
-this loss of acidity causes alkalinity and the problem is metabolic alkalosis
-as this is a metabolic problem compensation must be achieved by other mechanisms eg. Respiratory regulation
-the decrease in H+ ion concentration triggers the respiratory center to slow the respiratory rate to increase pCO2

Front 82

Steps in Interpreting Arterial Blood Gases?

Back 82

1. Evaluate pH, PCO2, and HCO3- to determine acidity or alkalinity
2. Identify cause of imbalance as either acidosis or alkalosis by the pH
3. Determine if the problem is respiratory or metabolic
➢ Check pCO2 and HCO3- to see which one has the same acid-base status as the pH
➢ If pCO2 matches then the problem is respiratory
➢ If HCO3- matches then the problem is metabolic

4. Determine extent of compensation
➢ Check the value that doesn’t match the pH
➢ If value is normal then no compensation has occurred = uncompensated
➢ Partial compensation = pH abnormal, buffer value out of normal range
➢ Full compensation = pH normal and both other values are out of normal range