Homeostasis (Fluid and Electrolyte Balance) WYNESS GONDWE 2011

LESSON PLAN
Student Level: BSc Genercic Year 4 Subject: Critical Care Nursing (NUR 403) Topic: Homeostasis (Fluid and Electrolyte Balance) Date:31st -03-2011 Time: 10.00am-12.00noon Number of Hours: 2 Hours Mode of Teaching: Lecture/Discussion Teaching and Learning Aids: White Board, marker

LEARNING OUTCOMES
At the end of the discussion, students should be able to: 1. Review common terms used in fluids and electrolytes. 2.Describe homeostasis. 3.Describe Factor influencing fluid and electrolyte balance. 4.Discuss Types of fluids therapy

Learningoutcomes cont,
Discuss electrolyte requirements in critically ill patients Explain the Heamodynamic Monitoring in ICU

Review

the

following

terms

Electrolytes Osmosis Osmotic pressure Solute Osmolality Hydrostatic pressure

Diffusion Active transport Solvent Filtration

What is homeostasis
Homeostasis =constancy of body fluid and electrolyte levels or fluid and electrolyte balance. Means that both the amount and distribution of body fluids and electrolytes is normal and constant. For homeostasis to be maintained, body input of water and electrolytes must by balanced by output.
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Cont,
If water and electrolytes in excess of requirements enter the body, they must be selectively eliminated, andshould excess losses occurprompt replacement is critical. The volume of fluid and the electrolyte levels inside the cells, in the interstitial spaces, and in the blood vessels all remain relatively constant when a condition of homeostasis exists.
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 Fluid and electrolyte imbalance, then, means that both the total volume of water or level of electrolytes in the body or the amounts in one or more of its fluid compartments have increased or decreased beyond normal limits. Electrolytes are salts that conduct electricity and are found in the body fluid, tissue, and blood. Examples are chloride, calcium, phosphate, sodium, 8 magnesium and potassium.

Cont,

cont,
Proper balance is essential for muscle coordination, heart function, fluid absorption and excretion, nerve function, and concentration. Too much or too little electrolytes, caused by poor diet, dehydration, medication, and disease, results in an imbalance These are common causes of fluid and electrolyte imbalance in ICU.

Body Fluid Compartments

2/3 (65%) of Total Body Water (TBW) is intracellular (ICF) 1/3 extracellular water
25 % interstitial fluid (ISF) 5- 8 % in plasma (IVF intravascular fluid) 1- 2 % in transcellular fluids CSF, intraocular fluids, serous membranes, and in GI, respiratory and urinary tracts (third space) 10

Balance
Fluid and electrolyte homeostasis is maintained in the body Neutral balance: input = output Positive balance: input > output Negative balance: input < output

Review how these are maintained

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Factor influencing fluid and electrolyte balance

AGE Infants and children have much greater fluid turnover than adults due to higher metabolic rate, increasing fluid loss. Infants lose more fluid through the kidneys because immature kidneys are less able to conserve water than adult kidneys. Infants respirations are more rapid increasing insensible fluid losses.
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Cont.
Rapid turnover of fluid plus the losses produced by disease can create critical fluid imbalances in children much more rapidly than in adults. In elderly people, the normal aging process may affect fluid balance. The thirst response often is blunted. Antidiuretic hormone levels remain normal or may even be elevated, but the nephrons become less able to conserve 13 water in response to ADH

GENDER AND BODY SIZE

Because fat cells contain little or no water and lean tissue has a high water content, people with a higher percentage of body fat have less body fluid. Women have proportionately more body fat and less body water than men. 60% in men but only 52% women. In an obese individual this may be even less, with water responsible for only 30% to 40% of the persons weight.
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ENVIRONMENTAL TEMPERATURE
People with an illness are at risk for fluid and electrolyte imbalances when the environmental temperature is high or due to increased metabolic rate. Fluid losses through sweating are increased in hot environments as the body attempts to dissipate heat. Both salt and water are lost through sweating. When only water is replaced, 15 salt depletion is a risk

Diet,
The intake of fluids and electrolytes is affected by diet. People on nothing per os are at risk for severe fluid and electrolyte imbalance because of inadequate intake Starving pts have decreased serum albumin, and may develop edema because the osmotic draw of fluid into the vascular compartment is reduced. When calorie intake is not adequate to meet the bodys needs, fat stores are broken down and fatty acids are released,16 increasing the risk of acidosis.

Stress,
Stress increases cellular metabolism, blood glucose concentration and catecholamine levels. In addition, stress can increase production of ADH, which in turn decreases urine production. The overall response of the body to stress is to increase the blood volume for increased metabolism.
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Types of fluids therapy

TONICITY Hypotonic Isotonic Hypertonic OSMOLALITY < 270 mOsm/kg 275-295 mOsm/kg > 300 mOsm/kg CELL Swelling Nothing Shrinking

ISOTONIC
ISO - means alike TONICITY - refers to osmotic activity of body fluids; tells the extent that fluid will allow movement of water in & out cell Means that solutions on both sides of selectively permeable membrane have established equilibrium Any solution put into body with the same osmolality as blood plasma

HYPOTONIC HYPERTONIC
Solution of lower osmotic pressure Less salt or more water than isotonic If infused into blood, RBCs draw water into cells ( can swell & burst ) Solutions move into cells causing them to swell Solution of higher osmotic pressure 3% sodium chloride is example If infused into blood, water moves out of cells & into solution (cells wrinkle or shrivel) Solutions pull fluid from cells causing them to shrink

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ISOTONIC SOLUTIONS p.211

0.9% Sodium Chloride Solution Ringers Solution Lactated Ringers Solution 5% dextrose in water

Cell in a hypertonic solution

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HYPERTONIC SOLUTIONS
3% SODIUM CHLORIDE 5% SODIUM CHLORIDE WHOLE BLOOD ALBUMIN TOTAL PARENTERAL NUTRITION TUBE FEEDINGS CONCENTRATED

Cell in a hypotonic solution

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HYPOTONIC SOLUTIONS
0.45% SODIUM CHLORIDE 0.33% SODIUM CHLORIDE 0.5% dextrose

Electrolyte requirements,
Electroltes, dissolved separates into ions, carries electric current CATION - positively charged electrolyte-Na+, K+ , Ca++, H+ ANION - negatively charged electrolyte -Cl-, HCO3- , PO43 # Cations must = # Anions for homeostatsis to exist in each fluid compartment Measured in milliequivalents / liter (mEq/L) or millimoles/liter (mmol/L)

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SODIUM (NA+)
DOMINANT EXTRACELLULAR ELECTROLYTE CHIEF BASE OF BLOOD NL SERUM LEVEL 135-145 mEq/L

SODIUM (NA+)
SODIUM AFFECTS FLUID VOLUME & CONCENTRATION IN ECF IS REGULATED BY: Aldosterone Renal blood flow Renin secretion Antidiuretic hormone (ADH) due to its effect on water EstrogenCarbonic anhydrase enzyme

SODIUM

(NA)*

Main extracellular fluid (ECF) cation Helps govern normal ECF osmolality Helps maintain acid-base balance Activates nerve & muscle cells Influences water distribution (with chloride)

Signs and symptoms of Hypernatremia,

*Agitation, restlessness, fever, low LOC due to altered cellular metabolism *Hypertension, tachycardia,pitting edema, and excessive wt gain due to water shift from intracellular to extracellular fluid *Thirst, increased viscosity of saliva, rough tongue due to fluid shift *Dyspnea, respiratory arrest, and death from dramatic increase in in osmotic 33

HYPERNATREMIA
Serum Na + level > 148 mEq/L serum osmolality > 295 mOsm/kg & urine sp gr > 1.030 with nl kidneys Collaborative management tries to gradually lower serum sodium by *infusion of 0.45% NaCl *monitoring U/O & serum sodium levels *administering fluids carefully *restricting sodium intake The thirsty person will not get this !!!!

Signs and symptoms of Hyponatreamia

*Muscle twitching and weakness due to osmotic swelling of cells *Lethargy, confusion, seizures,and coma due to altered neurotransmission *Hypertension and tachycardia due to decreased extracellular circulating volume *Nausea,vomiting, and abdominal cramps due to edema affecting receptors in the brain or vomiting center of the brain stem *Oliguria or anuria due to renal dysfunction

 Serum Na+ < 135 mEq/L (pt may be asymptomatic until level drops below 125) Collaborative management seeks to correct cause & give sodium with caution due to possible rebound fluid excess by : *infusing isotonic saline in IV fluids *restricting oral & IV water intake *increasing dietary sodium *monitoring for signs of hypervolemia

HYPONATREMIA

POTASSIUM (K+)
DOMINANT INTRACELLULAR ELECTROLYTE PRIMARY BUFFER IN CELL NL SERUM LEVEL 3.5-5.5 *mEq/L

POTASSIUM (K)*
Dominant cation in intracellular fluid (ICF) Regulates cell excitability Permeates cell membranes, thereby affecting cells electrical status Helps control ICF osmolality & ICF osmotic pressure

POTASSIUM (K+)
MOVEMENT INFLUENCED BY:Changes in pH Insulin Adrenal hormones Changes in serum sodium IMPORTANT IN: Neuromuscular irritability Intracellular osmotic activity Acid-base balance

HYPERKALEMIA
K+ > 5.5 mEq/L Dangerous due to potential for fatal dysrhythmias, cardiac arrest Major cause is renal disease EKG shows tall, peaked T waves & dysrthythmias Beware of pseudohyperkalemia due to prolonged tourniquet, hemolysis of blood, sampling above KCl

Signs and symptoms of Hyperkalemia

*Tachycardia changing to bradycardia, ECG changes, and cardiac arrest due to hypopolarization and alterations in repolarization *Nausea, diarrhea, and abdominal cramps due to decreased gastric motility *Muscle weakness and flaccid paralysis due to inactivation of membrane sodium channels
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HYPERKALEMIA TX
Watch EKG for dysrthymias or cardiac arrest Collaborative management include: -Calcium to counteract effect on heart -Sodium bicarbonate to alkalinize fluids -Hemodialysis or peritoneal dialysis -Cation exchange resins (Kayexalate) by mouth or enema -Small dose of insulin & dextrose -Restrict dietary K+

HYPOKALEMIA
K+ < 3.5mEq/L Most common type of electrolyte imbalance Major cause is increase renal loss most often associated with diuretics EKG shows dysrhythmias, flattened T wave Can increase the action of digitalis NEVER GIVE K+ IV PUSH & ALWAYS

Signs and symptoms of Hypokalemia

*Dizziness, hypotension, arrhythmias, electrocardiogram (ECG) changes, and cardiac arrest due to changes in membrane excitability *Serum potassium < 3.5 mEq/l *coexisting low serum calcium and magnesium levels not responsive to treatment for hypokalemia usually suggest hypomagnesemia
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Cont,
*Nausea, vomiting, anorexia, diarrhea, decreased peristalsis, and abdominal distention due to decreased bowel motility *Muscle weakness, fatigue, and leg cramps due to decreased neuromuscular excitability

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HYPOKALEMIA TX
Correct the cause Oral or IV administration of potassium Salt substitutes containing K+ Foods high in potassium : bananas, pears, dried apricots; fruit juices; tea, cola beverages; milk; meat, fish; baked potato; dried beans (cooked)

Calcium Imbalances- self study

Most in ECF Regulated by: Parathyroid hormone Blood Ca++ by stimulating osteoclasts GI absorption and renal retention Calcitonin from the thyroid gland Promotes bone formation renal excretion
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Hypercalcemia
Results from:
Hyperparathyroidism Hypothyroid states Renal disease Excessive intake of vitamin D/ calcium Malignant tumors hypercalcemia of malignancy Tumor products promote bone breakdown Tumor growth in bone causing Ca++ release

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Hypercalcemia
Usually also see hypophosphatemia Signs and symptoms: *Drowsiness, lethargy, headaches, irritability, confusion, depression, or apathy
Muscle cramps Bradycardia, cardiac arrest GI activity also common
Nausea, abdominal cramps Diarrhea / constipation

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Treatment
0.9% saline for rehydration Check osmolarity Forced diuresis to excrete it-frusemide Calcinotonin 4ug/kg sub cut 12 hourly to reduce rate of calcium and phosphate release from bones Cortcosteroids in malignancy
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Hypocalcemia
Hyperactive neuromuscular reflexes and tetany differentiate it from hypercalcemia Convulsions in severe cases Caused by:
Renal failure Lack of vitamin D Suppression of parathyroid function Hypersecretion of calcitonin Malabsorption states Large blood transfusion due to citrate accumulation. 52 Widespread infection or peritoneal inflammation

Hypocalcemia
Signs and symptoms: *Anxiety, irritability, twitching around the mouth, laryngospasm,seizures, Chvostek's and Trousseau's signs due to enhanced neuromuscular irritability *Hypotension and arrhythmias due to decreased calcium influx Treatment
IV 10mls of 10 % calcium chloride as slow IV bolus for acute, repeat as necessary and 53 consider slow IV.

phosphate
Normal range=07-1.25mmol/L HYPERPHOSPHATe *Usually asymptomatic unless leading to hypocalcemia, with tetany and seizures Tests Serum phosphates > 4.5 mg/dl *Serum calcium < 9mg/dl *Urine phosphorus < 0.9 g/24

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Hypophosphatemia
*Muscle weakness, tremor, and paresthesia due to deficiency of adenosine triphasphate *Peripheral hypoxia due to 2,3 diphosphoglycerate deficiency Tests *Serum phosphates < 2.5mg/dl *Urine phosphate > 1.3 g/24 hours
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HYPOCHLOREMIA
Signs and symptoms *Muscle hypertonicity and tetany *Shallow, depressed breathing *Usually associated with hyponatremia and its characteristic symptoms, such as muscle weakness and twitching Tests *Serum chloride <98 mEq/l
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HYPERCHLOREMIA
*Deep, rapid breathing *Weakness *Diminished cognitive ability, possibly leading to coma

Tests *Serum chloride > 108 mEq/l

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HYPOMAGNESEMIA
*coexists with hypokalemia & hypocalcemia *Hyperirritability, tetany, leg and foot cramps, positive Chvostek's and Trousseau's signs confusion in neuromuscular transmission *Arrhythmias, vasodilation, and hypotension due to enhanced inward sodium current or concurrent effects of calcium and potassium imbalance Tests*Serum magnesium < 1.5 mEq/l *Coexisting low serum potassium and 58

HYPERMAGNESEMIA
*caused by decreased renal excretion (renal failure) or increased intake of magnesium *Diminished reflexes, muscle weakness to flaccid paralysis due to suppression of acetylcholine release of the myoneural junction, blocking cell excitability *respiratory distress secondary to respiratory muscle paralysis *Heart block, bradycordia due to decreased inward sodium current 59

Cont,
*Hypotension due to relaxation of vascular smooth muscle and reduction of vascular wall surface Tests *Serum magnesium > 2.5 mEq/l *Coexisting elevated potassium and calcium levels
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Heamodynamic Monitoring in ICU

Aim to keep pt hydrated with adequate circulating volume and normal electrolytes. Exact fluid regimes depends on pts clinical state of hydration and electrolyte deficit Measure 24 hour fluid balance accurately. -Add insensible loss Measure serum electrolytes daily or more frequent depending on hospital protocol.
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Cont,
Vitals signs: BP, HR, Respirations and temperature , o2saturation Level of consciousness Crackles & wheezes CVP 5-10 cm H2O or 0-7mm Hg Jugular Vein Skin Mucous membranes Tongue/oral mucosa Urine output Edema & weight gain

Cont,
BUN - blood urea nitrogen; made up of urea an end-product of protein metabolism; Nl 10-20 mg/dL; inc. with GI bleeding, dehydration, inc. protein intake, fever, & sepsis; dec. with starvation, endstage liver dx., low protein diet, expanded fluid vol. (as with pregnancy) Creatinine - end product of muscle metabolism; better indicator of renal function; nl 0.7-1.5 mg/dL
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Cont,
Hematocrit - vol. % of RBCs in whole blood; m- 44-52%, f- 39-47% Urine specific gravity measures the kidneys ability to excrete or conserve water Nl range 1.010 to 1.025 (compared to weight of distilled water with sp g of 1.000) Electrolyte investigations

OSMOLALITY
Measure of solutions ability to create osmotic pressure & thus affect movement of water Number of osmotically active particles per kilogram of water ECF osmolality is determined by sodium Serum 280-300mOsm/kg; Urine 50-1400mOsm/kg

References
Morton, P.G., Fontaine, D. K., Hudak, C.M. & Gallo, B.M. (2005). Critical Care Nursing: A Holistic Approach 8th edition Lippincott Williams & Wilkins Urden, L. D; Stancy, K. M. & Lough, M.E. (2006). Thelans Critical Care Nursing Diagnosis and Management 5th edition Elsevier st Loius Whiteley, S. M., Bodenham, Bellamy, M. C. (2004). Intensive Care Elsevier Churchill Livingstone 66