Fluids and Electrolytes

Alteration in Fluids and Electrolytes

Terms
Osmosis
movement of water across cell membranes from less concentrated to more concentrated

Solutes
substances dissolved in a liquid

Osmolality
the concentration within a fluid

Terms
Diffusion movement of molecules in liquids from an area of higher concentration to lower concentration Filtration fluid and solutes move together across a membrane from area of higher pressure to one of lower pressure Active Transport substance moves across cell membranes from less concentrated solution to more concentrated - requires a carrier

Homeostasis
A delicate balance of fluids, electrolytes, and acids and bases is required to maintain good health. This balance is called Homeostasis.

Body Fluid and Electrolyte Compartments

Approximately 60% of a typical adult s weight consists of fluid (water and electrolytes). Factors Influence the amount of Body Fluid  Age  Gender Body Fat

80% of body weight

50 % of body weight

60 % of body weight

Compartments of Body Fluid

Intracellular Space- 70% Approximately two-third of the body, located in the skeletal muscle mass. Fluid within the cells themselves Provide nutrients for metabolism: High in K, Po4, protein Moderate levels of Mg, So4 Assists in cellular metabolism

Compartments of Body Fluid

Extracellular Space 1.Intravascular fluid- blood plasma 2.Interstitial fluid (tissue fluid)- ex. lymph 3.Transcellular fluid- ex. Cerebrospinal, pericardial, synovial, intraocular and pleural fluids, sweats and digestive secretions

Electrolytes in body fluids are active chemicals Cations- carry positive charges Anions- carry negative charges  Major Cations in body fluid: o sodium o potassium o calcium o magnesium o hydrogen  Major Anions in body fluid: o chloride o bicarbonate o phosphate o sulfate o proteinate

Approximate Major Electrolyte Content in Body Fluid

Electrolytes Extracellular Fluid (Plasma) Cations Sodium (Na) Potassium (K) Calcium (C ++) Magnesium (Mg++) Total Cations 142 5 5 2 154 MEQ/L Electrolytes Extracellular Fluid (Plasma) Anions Chloride (Cl-) Bicarbonate (HCO3-) Phosphate (HPO4-) Sulfate (SO4-) Organic Acids Proteinate Total Anions 103 26 2 1 5 17 154 MEQ/L

Approximate Major Electrolyte Content in Body Fluid

Electrolytes Intracellular Fluid Cations Potassium (K+) Magnesium (Mg++) Sodium (Na+) Total Cations 150 40 10 200 Electrolytes Intracellular Fluid Anions Phosphates and Sulfates 150 Bicarbonate (HCO3-) Proteinate Total Anions 10 40 200 MEQ/L MEQ/L

Functionsof Electrolytes
Promote neuromuscular irritability Maintain body fluid volume and osmolality Distribute body water between fluid compartments Regulate acid base balance

Average Daily Intake and Output in an Adult

Intake Oral Liquids Water in Food Water Poroduce by Metabolism 1,300 mL 1,000 mL 300 mL Output Urine Stool Insensible Lungs skin Total Gain 2,600 mL Total Loss 300 mL 600 mL 2,600 mL 1,500 mL 200 mL

Falling Systemic Blood Pressure/ Volume

Reduces Filtrate Volume or Solute content in Renal Tubules

Baroreceptors in Blood Vessels Sympathetic Nervous System

Hypothalamic Osmoreceptors

JG Cells of Kidney

Posterior Pituitary

Systemic Arterioles Renin Vasoconstriction

ADH (antidiuretic hormone

Collecting Ducts of Kidneys Angiotensin II Formed in Blood

Peripheral Resistance

Water Reabsorption

Systemic Arterioles

Adrenal Cortex

Vasoconstriction

Aldosterone

Peripheral Resistance

Kidney Tubules

Na Reabsorption (and Water Absorption)

Blood Volume

Rising Blood Pressure

Regulation of Body Fluid Compartments

When two different solutions are separated by a membrane that is impermeable to the dissolved substances, fluid shifts through te membrane from region of low concentration to the region of high solute concentration until the solutions are of equal concentration; this diffusion of water caused by a fluid concentration gradient is known as OSMOSIS

Regulation of Body Fluid Compartments

Diffusion- is the normal tendency of a substance to move from an area of higher concentration to one of lower concentration . It occurs through the random movement of ions and molecules. Example of diffusion are the exchange of oxygen and carbon dioxide between the pulmonary capillaries and alveoli and the tendency of sodium to move from the ECF compartment, where the sodium concentration is high, to the ICF where its concentration is low.

Laboratory Tests for Evaluating Fluid Status

Osmolality- reflects the concentration of fluid that affects the movement of water between fluid compartments by osmosis. measures the solute concentration per kilogram in blood and urine. measure of a solution s ability to create osmotic pressure and affect the movement of water. Serum osmolality- primarily reflects the concentration of Sodium Normal Serum Osmolality- 280 to 300 mOsm/kg Urine osmolality- is determined by urea, creatinine and uric acid. most reliable of urine concentration. Normal Urine Osmolality- 250 to 900 mOsm/kg mOsm/kg

Laboratory Tests for Evaluating Fluid Status

Osmolarity- describes the concentration of solutions, is measured in milliosmoles per liter (mOsm/L). Urine Specific Gravity- measures the kidney s ability to excrete or conserve water. Normal range- 1.010 to 1.025

Laboratory Tests for Evaluating Fluid Status

Blood Urea Notrogen (BUN)- is made up of urea, an end product of metabolism of protein by the liver. Amino acid breakdown produces large amounts of amonia molecules, which are absorbed into the bloodstream. Amonia molecules are converted to urea and excreted in the urine. Normal BUN- 10 to 20 mg/dL (3.5 to 7 mmol/L) Factors that Increase BUN include: Decrease Renal Function GI Bleeding Dehydration Increase Protein Intake Fever Sepsis

Laboratory Tests for Evaluating Fluid Status

Factors that Decrease BUN: End Stage Liver Disease Low Protein Intake Starvation Any condition that results in expanded fluid volume Example Pregnancy Creatinine- end product of muscle metabolism. Better indicator of Renal Function. Normal Serum Creatinine- 0.7 to 1.5 mg/dL Serum Creatinine levels increases when renal function decreases,

Laboratory Tests for Evaluating Fluid Status

Hematocrit- measures the volume percentage of RBC in whole blood. Normal value: Male- 44 % to 52 % Female- 39 % to 47 % Increase Hct: Dehydration and Polycythemia Decrease Hct: Overhydration and anemia Urine Sodium- values change with sodium intake and the status of fluid volume. Normal Urine Sodium levels: 50 to 220 mEq/24h used to assess volume status and are useful in the diagnosis of hyponatremia and acute renal failure.

Routes of Gains and Losses

Drinking Eating Parenteral Route Enteral Feeding

KIDNEYS the usual daily urine in the adult is 1 to 2 L. A general rule is that the output is approximately 1 mL of urine per kilogram of body weight per hour in all age groups.

Routes of Gains and Losses

SKIN Sensible perspiration refers to visible water and electrolyte loss through the skin (sweating). Continuous water loss by evaporation occurs through the skin as insensible perspiration, a nonvisible form of water loss. LUNGS lungs normally eliminate water vapor (insensible loss) at rate of approximately 400mL everyday.
.

Routes of Gains and Losses

GI TRACT the usual loss through the GIT is only 100 to 200 mL daily, even through approximately 8 L of fluid circulates through the GI system every 24 hours. Because the bulk of fluid is reabsorbed in the small intestine, diarrhea and fistulas cause larger losses. In healthy people, the daily average intake and output of water are approximately equal.

Homeostatic Mechanism
Kidney Functions vital to the regulation of fluid and electrolyte balance. kidneys normally filter 170 L of plasma every day in the adult. While excreting only 1.5 L of urine. Major functions of the kidneys in maintaining normal fluid balance include following: Regulation of ECF volume and osmolality by selective retention and excretion of body fluids.

Homeostatic Mechanism
Regulation of electrolyte levels in the ECF by selective retention of needed substances and excretion of unneeded substances. Regulation of pH of the ECF by retention of hydrogen ions Excretion of metabolic wastes and toxic substances Heart and Bood Vessel Functions the pumping action of the heart circulates blood through the kidneys under sufficient pressure to allow for urine formation. failure of this pumping action interferes with renal perfusion and thus with water and electrolyte regulation.

Homeostatic Mechanism
Lung Functions also vital in maintaining homeostasis. through exhalation, the lungs remove approximately 300 mL of water daily in the normal adult. also have a major role in maintaining acid-base balance. changes from normal aging result in decreased respiratory function causing increased difficulty in pH regulation in older adults with major illness or trauma.

Homeostatic Mechanism
Pituitary Functions the hypothalamus manufactures ADH, which is stored in the posterior pituitary gland and released as needed. ADH sometimes called the water-conserving hormone because it causes the body to retain water. functions of ADH include maintaining the osmotic pressure of the cells by controlling the retention or excretion of water by the kidneys and by regulating blood volume.

Homeostatic Mechanism
Adrenal Functions Aldosterone, a mineralococticoid secreted by the zona glomerulosa (outer zone) of the adrenal cortex, has profound effect on fluid balance. increased secretion of aldosterone causes sodium retention (and thus water retention) and potassium loss. conversely, decreased secretion of aldosterone causes sodium and water loss and potassium retention. Cortisol, another adrenocortical hormone, has only a fraction of the mineralocorticoid potency of aldosterone. When secreted in large quantities, however, it can also produce sodium retention and fluid retention and potassium deficit.

Homeostatic Mechanism
Parathyroid Functions embedded in the thyroid gland, regulated calcium and phosphate balance by means of parathyroid hormone (PTH). PTH influences bone resorption, calcium absorption from the intestines, and calcium reabsorption from the renal tubules.

Other Mechanism
Baroreceptors are small nerve receptors that detect changes in pressure within blood vessels and transmit this information to the central nervous system . responsible for monitoring the circulating volume, and they regulate sympathetic and parasympathetic neural activity as well as endocrine activities . Low- pressure baroreceptor- located in the cardiac atria, particularly the left atrium. High- pressure baroreceptor- nerve endings in the aortic arch and in the cardiac sinus. Also located in the afferent arteriole of the juxtaglomerular apparatus of the nephrons.

Other Mechanism
As arterial pressure decreases, baroreceptors transmit fewer impulses from the carotid sinuses and the aortic arch to the vasomotor center. A decrease in impulses stimulates the sympathetic nervous system and inhibits the parasympathetic nervous system. The outcome is an increase in cardiac rate, conduction and contractility and in circulating blood volume. Sympathetic stimulation constrict renal arterioles; this increases the release of aldosterone, decreases glomerular filtration, and increases sodium and water reabsorption.

Other Mechanism
Renin-Angiotensin- Aldosterone System is an enzyme that converts angiotensinogen, an inactive substance formed by the liver, into angiotensin 1. renin is released by the juxtaglomerular cells of the kidneys in response to decreased renal perfusion. Angiotensin-Converting Enzyme (ACE) converts angiotensin 1 to Angiotensin II. Angiotensin II, with its vasoconstrictor properties, increases arterial perfusion pressure and stimulates thirst. As the sympathetic nervous system is stimulated, aldosterone is released in response to an increased release of renin. Aldosterone is a volume regulator and is also released as serum potassium increases, serum sodium decreases, or adrenocorticotropic hormone increases.

Other Mechanism
ADH and Thirst important roles in maintaining sodium concentration and oral intake of fluids. Oral intake is controlled by the thirst center located in the hypothalamus. as serum concentration or osmolality increases or blood volume decreases, neuron in the hypothalamus are stimulated by intracellular dehydration; thirst then occurs, and the person increases oral intake of fluids. water excretion is controlled by ADH, aldosterone, and basoreceptors Absence or presence of ADH is the most significant factor in determining whether the urine that is excreted is concentrated or dilute.

Other Mechanism
Osmoreceptors Located on the surfaceof the hypothalamus, osmoreceptors sense changes in sodium concentration. as osmotic pressure increases,the neurons become dehydrated and quickly release impulses to the posterior pituitary, which increases the release of ADH. ADH travels in the blood to the kidneys, where it alters permeability to water, causing increased reabsorption of water and decreased urine output. The retained water dilutes the ECF and returns its concentration to normal. Restoration of normal osmotic pressure provides feedback to the osmoreceptors to inhibit further ADH release.

Release of Atrial Natriuretic Peptide ANP is released by cardiac cells in the atria of the heart in response to increased atrial pressure. any disorder that results in volume expansion or increased cardiac filling pressure will increase the release of ANP. action of ANP is the direct opposite of the reninangiotensin- aldosterone system and decrease blood pressure and volume. ANP measured in plasma is normally 20 to 70 pg/mL. this level increases in acute heart failure, paroxysmal atrial tachycardia, hyperthyroidism, subarachnoid hemorrhage, and small cell lung cancer. the level decreases in chronic heart failure and with the use of medications such as urea (ureaphil) and prazosin (minipress).

Fluid Volume Deficit

HYPOVELIMIA FVD occurs when loss of extracellular fluid volume exceeds the intake of fluid. It occurs when water and electrolytes are lost in the same proportion as they exist in normal body fluids, so that the ratio of serum electrolytes to water remains the same. Abnormally low volume of body fluid in intravascular and/or interstitial compartments Causes Vomiting Diarrhea Fever Excess sweating Burns Diabetes insipidus Uncontrolled diabetes mellitus

Fluid Volume Deficit

What happens Output > Intake -> Water extracted from ECF ECF hypertonic (water moves out of cell -> cell dehydration) + osmotic pressure increased (stimulates thirst preceptor in hypothalamus) ICF hypotonic with decreased osmotic pressure -> posterior pituitary secretes more ADH Decreased ECF volume -> adrenal glands secrete Aldosterone

Signs & Symptoms

Acute weight loss Decreased skin turgor Oliguria Concentrated urine Weak, rapid pulse Capillary filling time elongated Decreased BP Increased pulse Sensations of thirst, weakness, dizziness, muscle cramps

Pathophysiology
Decreased Fluid Volume
Stimulation of Thirst Center in Hypothalamus ADH Secretion Renin- AngiotensinAldosterone System Activation

Water Resorption Sodium and Water Resorption

Person Complains of Thirst

Urine Output Urine Specific Gravity Except with Osmotic Diuresis

Pathophysiology
Untreated Fluid Volume Deficit
Cells Become unable to continue providing water to replace ECF losses Depletion of Fluids Available

Signs of Circulatory Collapse: Decreased Blood Pressure Increased Heart Rate Increased Respiratory Rate

Body Temperature

Dry Mucus Membrane Restlessness And Apprehension Difficulty with Speech

Significant Points
Dehydration one of most common disturbances in infants and children Additional S/S Sunken eyeballs Depressed fontanels Significant wt loss

Laboratory
Increased HCT Increased BUN out of proportion to Creatinine High serum osmolality Increased urine osmolality Increased specific gravity Decreased urine volume, dark color

Intervention
Major goal prevent or correct abnormal fluid volume status before ARF occurs Encourage fluids IV fluids Isotonic solutions (0.9% NS or LR) until BP back to normal, then hypotonic (0.45% NS) Monitor I & O at least every 8 hrs Check urine specific gravity and urine concentration daily weights Check skin turgor

Intervention
Monitor skin turgor Monitor VS and mental status Evaluation Normal skin turgor, increased UOP with normal specific gravity, normal VS, clear sensorium, good oral intake of fluids

Fluid Volume Excess

Hypervolemia Isotonic expansion of ECF caused by abnormal retention of water and sodium Fluid moves out of ECF into cells and cells swell

Causes
Cardiovascular Heart failure Urinary Renal failure Hepatic Liver failure, cirrhosis Other Cancer, thrombus, PVD, drug therapy (i.e., corticosteriods), high sodium intake, protein malnutrition

Clinical Manifestation
Physical assessment Weight gain Distended neck veins Periorbital edema, pitting edema Adventitious lung sounds (mainly crackles) Dyspnea Mental status changes Generalized or dependent edema

Clinical Manifestation
VS High CVP/PAWP cardiac output Lab data Hct (dilutional) Low serum osmolality Low specific gravity BUN (dilutional) Radiography Pulmonary vascular congestion Pleural effusion Pericardial effusion Ascites

Pathophysiology
SIAD, Certain Head Injuries Dietary Sodium Indiscretion Excessive Sodium Intake Overhydration

Renal and Endocrine Disturbances, Malignancies, Adenomas

Failure of Renal or Hormonal Regulatory Functions

FLUID VOLUME EXCESS/ HYPERVOLEMIA Sodium

Since ECF become hypoosmolar, fluid moves into the cells to equalize the concentration on both sides of the cell membrane

Thus, there is increase in intracellular fluid The brain cells are particularly sensitive to the increase of intracellular water, most common signs of hypoosmolar overhydration are changes in mental status, confusion, ataxia, and convulsion may also occur. Other clinical manifestations include: Hypervertilation,sudden weight gain, warm, mosit skin, increased ICP: slow bounding pulse with an increase in systolic and descreased diastolic pressure and peripheral edema, usually not marked.

Intervention
Sodium restriction (foods/water high in sodium) Fluid restriction, if necessary Closely monitor IVF If dyspnea or orthopnea > Semi-Fowler s Strict I & O, lung sounds, daily weight, degree of edema, reposition q 2 hr Promote rest and diuresis

IV Fluid Replacement
IV Fluid to manage fluid volume imbalances Isotonic fluids (approximate normal serum plasma) Rapid ECF expansion needed D5W, NS, LR Hypotonic fluids Treatment of cellular dehydration .45% NS, .2% NS, 2.5% dextrose

IV Fluid Replacement
Hypertonic Treatment of water intoxication D5 NS, D10W, 3% NS Shifts fluids from ICF & ECF to intravascular component expands blood volume Now can be removed by kidneys

Sodium (Na+)
Normal 135-145 mEq/L Major cation in ECF Regulates voltage of action potential; transmission of impulses in nerve and muscle fibers, one of main factors in determining ECF volume Helps maintain acid-base balance Sodium is conserved through reabsorption in the kidneys, a process stimulated by aldosterone

Hyponatremia
Results from excess Na loss or water gain GI losses, diuretic therapy, severe renal dysfunction, severe diaphoresis, DKA, unregulated production of ADH associated with cerebral trauma, narcotic use, lung cancer, some drugs Clinical manifestations BP, confusion, headache, lethargy, seizures, decreased muscle tone, muscle twitching and tremors, vomiting, diarrhea, and cramps

Pathophysiology
Sodium Loss from the Intravascular Compartment Diffusion of water into the interstitial spaces Sodium in the interstitial spaces is diluted Decreased Osmolarity of ECF Water moves into the cell as a result of sodium loss Extracellular Compartment is depleted with water Clinical Manifestation

Clinical Manifestation

Headache

Muscle weakness

Nausea and vomiting

Abdominal Cramps

Weight loss Postural Hypotension

Assessment
Labs Increased HCT, K Decreased Na, Cl, Bicarbonate, UOP with low Na and Cl concentration Urine specific gravity 1.010

Colloborative Care Management

General Goal: Correct Sodium Imbalances and Restore Normal Fluid and Electrolyte Hemoestasis. Recognition of people at risk of hyponatremia is essential for its prevention: athletes, person working in hot environments. Salt is always replaced along with water. Management includes educating vulnerable people to recognize signs and symptoms of sodium depleation and maintaining sufficient sodium and water intake to replace skin and insensible loss. Generally, an increased sodium and water intake provides adequate treatment. Education as the importance of sodium and fluid balance and the rationale for prescription medications to ensure compliance Daily Weight Monitoring sodium levels to determine extent of replacement Too rapid restoration of sodium balance, hypertonic sodium solutions may provoke brain injury

Treatment
Interventions Mild Water restriction if water retention problem Increase Na in foods if loss of Na Moderate IV 0.9% NS, 0.45% NS, LR Severe 3% NS short-term therapy in ICU setting

Hypernatremia
Gain of Na in excess of water or loss of water in excess of Na Causes Deprivation of water; hypertonic tube feedings without water supplements, watery diarrhea, greatly increased insensible water loss, renal failure, inadequate blood circulation to kidneys, use of large doses of adrenal corticoids, excess sodium intake

Hypernatremia
Early: Generalized muscle weakness, faintness, muscle fatigue, HA Moderate: Confusion, thirst Late: Edema, restlessness, thirst, hyperreflexia, muscle twitching, irritability, seizures, possible coma Severe: Permanent brain damage, hypertension, tachycardia, N & V

Pathophysiology
Increased Sodium Concentration in ECF Osmolarity Rises

Water Leaves the Cell by Osmosis and Enters to the Extracellular Compartment

Dilution of Fluids in the ECF

Cells are depleted with water

Clinical Manifestation Sodium is Excreted in the Urine Suppression of Aldosterone Secretion

Clinical Manifestation

Excessive Thirst

Dry Sticky Mucous Membrane

Firm, Rubbery Skin Turgor

Manic Excitement

Death Tachycardia

Labs
Increased serum Na Increased serum osmolality Increased urine specific gravity

Treatment
Free water to replace ECF volume Gradual lowering with hypotonic saline Decrease by no more than 2 mEq/L/hr Offer fluids at regular intervals Supplement tube feedings with free water Teach about foods, medications high in Na Treat underlying problem

Potassium (K+)
Normal 3.5-5.5 mEq/L Major ICF cation Vital in maintaining normal cardiac and neuromuscular function, influences nerve impulse conduction, important in CHO metabolism, helps maintain acid-base balance, control fluid movement in and out of cells by osmosis Aldosterone triggers K+ excretion in Urine

Hypokalemia
Serum potassium level below 3.5 mEq/L Causes Loss of GI secretions Excessive renal excretion of K Movement of K into the cells (DKA) Prolonged fluid administration without K supplementation Diuretics (some)

Signs/Symptoms
Skeletal muscle weakness, smooth muscle function, DTR s BP, EKG changes, possible cardiac arrest N/V, paralytic ileus, diarrhea Metabolic alkalosis Mental depression and confusion

Causes and Effects of HypoK+

Decreased Intake Food & Fluid as in Starvation Failure to Replace GI Losses Increased Loss Aldosterone Gastrointestinal Losses Potassium Losing Diuretics Loss from the Cells as in Trauma, Burns Shift Potassium into Cells

HYPOKALEMIA

GI Tract Anorexia N/V Abdominal Distention

CNS Lethargy, Diminished Deep Tendon Reflexes, Confusion, Mental Depression

Muscles Weakness, Flaccid Paralysis, Weakness of Respiratory Muscles, Respiratory Arrest

Cardio Vascular Decreased BP, Dysrhythmias, ECG changes, Myocardial damage, Cardiac Arrest

Kidneys Decreased Capacity to Concentrate Waste, Water Loss, Thirst, Kidney damage

Pathophysiology
= ACTION POTENTIAL

Muscle and Nerve Activity

Low Extracellular Potassium

Increase in Resting Membrane Poetential

The Cell Become Less Excitable

Aldosterone is Secreted

Sodium is Retained in the Body through Resorption by the Kidney Tubules

Potassium is Excreted

Use of Certain Diuretics such as Thiazide and Furosemide and Corticosteroid

Increased Urinary Output

Loss of Potassium in Urine

Treatment
Hydrate if low urine output Oral replacement through high K diet No more than 3 enemas without consulting a doctor Potassium sparing diuretics such as spinorolacton, triamterene etc. Symptoms of K depletion : Muscle weakness, anorexia, nausea and vomiting= appropriate referral IV supplementation No more than 10 mEq/hr; for child 2-4 mEq/kg/24 h No more than 20 mEq/L

Treatment
Being alert to the condition that cause potassium depletion such as vomiting, diarrhea, diuretics, by monitoring the patient for early warning signs. Hypertonic glucose solution Monitor I & O Bowel sounds VS, cardiac rhythm Muscle strength Digoxin level if necessary

Hyperkalemia
Serum potassium level above 5.3 mEq/L Causes Excessive K intake (IV or PO) especially in renal failure Tissue trauma Acidosis Catabolic state

Signs/Symptoms
ECG changes tachycardia to bradycardia to possible cardiac arrest Tall, tented T waves Cardiac arrhythmias Muscle weakness, paralysis, paresthesia of tongue, face, hands, and feet, N/V, cramping, diarrhea, metabolic acidosis

Excess Intake Dietary Intake Excess of Kidney s ability to excrete; Excess in parenteral Administration

Decreased Loss Potassium-Sparing Diuretics Renal Failure Adrenal Insufficiency

Shift of Potassium out of the Cell Extensive Injuries, Crushing Injuries, Metabolic Acidosis

HYPERKALEMIA

CNS Numbness, Paresthesi a

Muscles Early: Irritability Late: Weakness leading to Flaccid Paralysis

Cardio Vascular Conduction Disturbance, Ventricular Fibrillation, Cardiac Arrest

Kidneys Oliguria leading to Anuria

GI Tract N/V Diarrhea Colic

Treatment
10% Calcium gluconate Sodium bicarbonate 50% glucose solution Kayexalate PO or PR Stop K supplements and avoid K in foods, fluids, salt substitutes

Calcium (Ca++)
Normal 4.5-5.5 mEq/L 99% of Ca in bones, other 1% in ECF and soft tissues Total Calcium bound to protein levels influenced by nutritional state Ionized Calcium used in physiologic activities crucial for neuromuscular activity

Calcium
Required for blood coagulation, neuromuscular contraction, enzymatic activity, and strength and durability of bones and teeth Nerve cell membranes less excitable with enough calcium Ca absorption and concentration influenced by Vit D, calcitriol (active form of Vitamin D), PTH, calcitonin, serum concentration of Ca and Phos

Causes of Hypocalcemia
Most common depressed function or surgical removal of the parathyroid gland Hypomagnesemia Hyperphosphatemia Administration of large quantities of stored blood (preserved with citrate) Renal insufficiency absorption of Vitamin D from intestines

Signs/Symptoms
Abdominal and/or extremity cramping Tingling and numbness Positive Chvostek or Trousseau signs Tetany; hyperactive reflexes Irritability, reduced cognitive ability, seizures Prolonged QT on ECG, hypotension, decreased myocardial contractility Abnormal clotting

Decreased Ionized Cacium Large Transfusion with citrated blood

Excess Loss Kidney Disease Draining Fistula

Inadequate Intake Dietary Deficit

Decrease In GI Tract and Bone Absorption Increase Magnesium Increase Calcitonin Decrease Vit. D Decrease Parathyroid Hormone

HYPOCALCEMIA

Bones Osteoporosis leading to fracture

CNS Tingling

Convulsion

Other Abnormal Deposits of Calcium in Body Tissues

Muscles Muscle Spasm

Cardiovascular Dysrhythmias

Tetany

Cardiac Arrest

Pathophysiology
Calcium ions are thought to line the pores of cell membrane, especially neurons. Calcium and Sodium repel each other When serum calcium is low, this blocking effect is minimal When sodium moves more easily into the cell, depolarization takes place more easily. This results in increased excitability of the nervous system leading to muscle spas, tingling sensation, and if severe, convulsion and tetany will occur Skeletal, smooth and cardiac muscle function are all affected by overstimulation

Treatment
High calcium diet or oral calcium salts (mild) formulas for calcium content IV calcium as 10% calcium chloride or 10% calcium gluconate give with caution Close monitoring of serum Ca and digitalis levels Phosphorus levels Magnesium levels Vitamin D therapy

Hypercalcemia
Causes Mobilization of Ca from bone Malignancy Hyperparathyroidism Immobilization causes bone loss Thiazide diuretics Thyrotoxicosis Excessive ingestion of Ca or Vit D

Signs/Symptoms
Anorexia, constipation Generalized muscle weakness, lethargy, loss of muscle tone, ataxia Depression, fatigue, confusion, coma Dysrhythmias and heart block Deep bone pain and demineralization Polyuria & predisposes to renal calculi Pathologic bone fractures

Loss from Bones Immobilization, Carcinoma with bone Metastasis, Multiple Myeloma

Excess Intake Increase Calcium Diet Antacid Containing Calcium

Increase in factors Causing Mobilization from Bone Increase PTH, Increase Vit. D, Steroid Therapy

HYPERCALCEMIA
Cardiovascular Depressed Nerve and MuscleActivity

CNS Deep Tendon Reflexes Lethargy

Bones Bone Pain

Muscles Muscle Fatigue Hypotonia

Kidneys Stones

Osteoporosis GI Motility Kidney Damage Dysrhythmias Cardiac Arrest

Coma

Fracture

Hypercalcemic Crisis
Emergency level of 8-9 mEq/L Intractable nausea, dehydration, stupor, coma, azotemia, hypokalemia, hypomagnesemia, hypernatremia High mortality rate from cardiac arrest

Treatment
NS IV match infusion rate to amount of UOP I&O hourlyLoop diuretics Corticosteroids and Mithramycin in cancer clients Phosphorus and/or calcitonin Encourage fluids Keep urine acid

Magnesium
Normal 1.5 to 2.5 mEq/L Mostly found within body cells: heart, bone, nerve and muscle tissue Ensures K and Na transport across cell membrane Important in CHO and protein metabolism Plays significant role in nerve cell conduction Important in transmitting CNS messages and maintaining neuromuscular activity

Magnesium
Causes vasodilatation Decreases peripheral vascular resistance Balance - closely related to K and Ca balance Intracellular compartment electrolyte Hypomagnesemia - < 1.5 mEq/L Hypermagnesemia - > 2.5 mEq/L

Hypomagnesemia
Causes Decreased intake or decreased absorption or excessive loss through urinary or bowel elimination Acute pancreatitis, starvation, malabsorption syndrome, chronic alcoholism, burns, prolonged hyperalimentation without adequate Mg Hypoparathyroidism with hypocalcemia Diuretic therapy

Signs/Symptoms
Tremors, tetany, reflexes, paresthesias of feet and legs, convulsions Positive Babinski, Chvostek and Trousseau signs Personality changes with agitation, depression or confusion, hallucinations ECG changes (PVC S, V-tach and V-fib)

Increased Intake Prolonged Malnutrition, Starvation

Impaired Absorption from GITract Malabsorption Syndrome, Alcohol Withdrawal Syndrome, Hypercalcemia, Diarrhea, Draining, Gastrointestinal Fistula

Excessive Excretion Increased Aldosterone, Conditions causing large losses of urine

HYPOMAGNESEMIA

CNS Convulsions, Paresthesia, Tremor, Ataxia

Mental Changes Agitation, Depression, Confusion

Hypokalemia

Muscles Cramps, Spascity, Tetany

Cardiovascular Tachycardia, Hypotension, Dysrhythmias

Low Serum Magnesiun Level

Increased Acetylcholine Release

Increased Neuromuscular Irritability

Increased Sensitivity to Acetylcholine at the myoneural Junction

Diminished Threshold of Excitation for the Motor Nerve

Enhancement of Myofibril Contraction

High Serum Calcium

Excretion of Magnesium by the GITract

Magnesium

InhibitsTransport of PTH Decrease in the Amount of Calcium being Released from the Bone Possible Calcium Deficit

Treatment
Mild Diet Best sources are unprocessed cereal grains, nuts, legumes, green leafy vegetables, dairy products, dried fruits, meat, fish Magnesium salts More severe MgSO4 IM MgSO4 IV slowly

Treatment
Monitor Mg q 12 hr Monitor VS, knee reflexes Precautions for seizures/confusion Check swallow reflex

Hypermagnesemia
Most common cause is renal failure, especially if taking large amounts of Mg-containing antacids or cathartics; DKA with severe water loss Signs and symptoms Hypotension, drowsiness, absent DTRs, respiratory depression, coma, cardiac arrest ECG Bradycardia, CHB, cardiac arrest, tall T waves

Renal Failure, Excessive IV Infusion of Magnesium, Decreased GI Elimination and/or Absorption

Accumulation of Magnesium in the Body

Serum Mg Level Rises

Altered Electrical Conduction

Diminishing of Reflexes, Drowsiness and Lethargy Severe Respiratory Distress

Slowed Heart Rate and AV Block

Peripheral Vasodilation Hypotension, Flushing, and Increased Skin Warm

Respiratory Arrest may occur

Treatment
Withhold Mg-containing products Calcium chloride or gluconate IV for acute symptoms IV hydration and diuretics Monitor VS, LOC Check patellar reflexes

Phosphorous
Normal 2.5-4.5 mg/dL Intracellular mineral Essential to tissue oxygenation, normal CNS function and movement of glucose into cells, assists in regulation of Ca and maintenance of acid-base balance Influenced by parathyroid hormone and has inverse relationship to Calcium

Hypophosphotemia
Causes Malnutrition Hyperparathyroidism Certain renal tubular defects Metabolic acidosis (esp. DKA) Disorders causing hypercalcemia

Signs/Symptoms
Impaired cardiac function Poor tissue oxygenation Muscle fatigue and weakness N/V, anorexia Disorientation, seizures, coma

Treatment
Closely monitor and correct imbalances oAdequate amounts of Phos oRecommended dietary allowance for formula-fed infants 300 mg Phos/day for 1st 6 mos. and 500 mg per day for latter of first year o1:1 ratio Phos and Ca recommended dietary allowance. Exception is infants, whose Ca requirements is 400 mg/day for 1st 6 mos and 500 mg/day for next 6 months

Treatment
Treatment of moderate to severe deficiency Oral or IV phosphate (do not exceed rate of 10 mEq/h) Identify clients at risk for disorder and monitor Prevent infections Monitor levels during treatment

Hyperphosphatemia
Causes Chronic renal failure (most common) Hyperthyroidism, hypoparathyroidism Severe catabolic states Conditions causing hypocalcemia

Signs/Symptoms
Muscle cramping and weakness HR Diarrhea, abdominal cramping, and nausea

Treatment
Prevention is the goal Restrict phosphate-containing foods Administer phosphate-binding agents Diuretics Treat cause Treatment may need to focus on correcting calcium levels