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Fluids and Electrolytes

Alteration in Fluids and Electrolytes



Terms

Osmosis

± movement of water across cell membranesfrom 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 lessconcentrated 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 adults weight

consists of fluid (water and electrolytes).

Factors Influence the amount of Body Fluid

Age

Gender

Body Fat



80% of body weight

60 % of body weight

50 % 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 themselvesProvide nutrients for metabolism:

High in K, Po4, protein

Moderate levels of Mg, So4

Assists in cellular metabolism



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

Compartments of Body Fluid



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 calciumo magnesium

o hydrogen

Major Anions in body fluid:

o chlorideo bicarbonate

o phosphate

o sulfate

o proteinate



Electrolytes MEQ/L

Extracellular Fluid

(Plasma)

Cations

Sodium (Na) 142

Potassium (K) 5

Calcium (C ++) 5

Magnesium (Mg++) 2

Total Cations 154

Electrolytes MEQ/L

Extracellular Fluid

(Plasma)

Anions

Chloride (Cl-) 103

Bicarbonate (HCO3-) 26

Phosphate (HPO4-) 2

Sulfate (SO4-) 1

Organic Acids 5

Proteinate 17

Total Anions 154

Approximate Major Electrolyte

Content inB

ody Fluid



Approximate Major Electrolyte

Content inB

ody FluidElectrolytes MEQ/L

Intracellular Fluid

Cations

Potassium (K+) 150

Magnesium (Mg++) 40

Sodium (Na+) 10

Total Cations 200Electrolytes MEQ/L

Intracellular Fluid

Anions

Phosphates and Sulfates 150

Bicarbonate (HCO3-) 10

Proteinate 40

Total Anions 200



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 AdultIntake Output

Oral Liquids 1,300 mL Urine 1,500 mL

Water in Food 1,000 mL Stool 200 mL

Water Poroduce

by Metabolism

300 mL Insensible

Lungs 300 mL

skin 600 mL

Total Gain 2,600 mL Total Loss 2,600 mL



Falling Systemic Blood

Pressure/ Volume

Reduces Filtrate

Volume or Solute

content in Renal

Tubules

JG Cells of Kidney

Renin

Angiotensin II

Formed in Blood

Baroreceptors in

Blood Vessels

Sympathetic

Nervous System

Systemic Arterioles

Vasoconstriction

Peripheral Resistance

Hypothalamic

Osmoreceptors

Posterior

Pituitary

ADH (antidiuretic

hormone

Collecting Ducts

of Kidneys

Water Reabsorption



Systemic

Arterioles

Vasoconstriction

Peripheral

Resistance

Adrenal Cortex

Aldosterone

Kidney Tubules

Na Reabsorption

(and Water

Absorption)

Blood Volume

Rising Blood

Pressure



Regulation of Body Fluid

CompartmentsWhen 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 soluteconcentration 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

CompartmentsDiffusion- 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 pulmonarycapillaries 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 StatusOsmolality- 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 solutions ability to create osmotic pressureand affect the movement of water.

Serum osmolality- primarily reflects the concentration of

Sodium

Normal Serum Osmolality- 28

0 to 300 mOsm/kgUrine osmolality- is determined by urea, creatinine and uric

acid. most reliable of urine concentration.

Normal Urine Osmolality- 250 to 900 mOsm/kg

mOsm/kg




Fluid Status

Osmolarity- describes the concentration of solutions,

is measured in milliosmoles per liter (mOsm/L).

Urine Specific Gravity- measures the kidneys abilityto excrete or conserve water.

Normal range- 1.010 to 1.025



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 BleedingDehydration

Increase Protein Intake

Fever

Sepsis


Fluid Status




Fluid Status

Factors that Decrease BUN:

End Stage Liver Disease

Low Protein Intake

StarvationAny 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,



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/24hused to assess volume status and are useful in the

diagnosis of hyponatremia and acute renal failure.


Fluid Status



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.



LUNGS

lungs normally eliminate water vapor (insensible

loss) at rate of approximately 400mL everyday.

.

SKIN

Sensible perspiration refers to visible water and

electrolyte loss through the skin (sweating).

Continuous water loss by evaporation occursthrough the skin as insensible perspiration, a

nonvisible form of water loss.





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.




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.



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-basebalance.

changes from normal aging result in decreased

respiratory function causing increased difficulty in pH

regulation in older adults with major illness or trauma.





Pituitary Functions

the hypothalamus manufactures ADH, which is stored in

the posterior pituitary gland and released as needed.

ADH sometimes called the water-conserving hormonebecause 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 MechanismAdrenal 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 sodiumretention (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.



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, andthey 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.



R

enin-Angiotensin- Aldosterone Systemis 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) convertsangiotensin 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 Thirstimportant 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, andbasoreceptors

Absence or presence of ADH is the most significant

factor in determining whether the urine that is excreted is

concentrated or dilute.

Other Mechanism



Other MechanismOsmoreceptors

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 posteriorpituitary, 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 itsconcentration 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 renin-angiotensin- 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, subarachnoidhemorrhage, 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 DeficitHYPOVELIMIAFVD 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 compartmentsCauses

VomitingDiarrhea

FeverExcess sweatingBurnsDiabetes insipidusUncontrolled 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 lossDecreased skin turgorOliguriaConcentrated urine

Weak, rapid pulseCapillary filling time elongatedDecreased BPIncreased pulseSensations of thirst, weakness, dizziness, muscle

cramps



Pathophysiology

Decreased Fluid Volume

ADH SecretionStimulation of Thirst

Center in Hypothalamus

Person Complains of Thirst

Water Resorption

Renin- Angiotensin-

Aldosterone System

Activation

Sodium and Water

Resorption

Urine Output

Urine Specific Gravity

Except with Osmotic Diuresis



PathophysiologyUntreated Fluid Volume Deficit

Depletion of Fluids

Available

Body Temperature

Dry Mucus Membrane

Difficulty with Speech

Cells Become unable to

continue providing water to

replace ECF losses

Signs of Circulatory Collapse:

Decreased Blood Pressure

Increased Heart Rate

Increased Respiratory Rate

Restlessness And Apprehension



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 osmolalityIncreased specific gravity

Decreased urine volume, dark color



Intervention

Major goal prevent or correct abnormal fluid volumestatus before ARF occursEncourage fluidsIV fluids

Isotonic solutions (0.9% NS or LR) until BP back tonormal, then hypotonic (0.45% NS)

Monitor I & O at least every 8 hrsCheck urine specific gravity and urine concentrationdaily weightsCheck skin turgor



Intervention

Monitor skin turgor

Monitor VS and mental status

Evaluation

Normal skin turgor, increased UOP with normalspecific 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




VSHigh CVP/PAWP

cardiac output

Lab data

Hct (dilutional)Low serum osmolality

Low specific gravity

BUN (dilutional)

RadiographyPulmonary vascular

congestion

Pleural effusion

Pericardial effusionAscites



PathophysiologySIAD, Certain Head

Injuries

Overhydration

Dietary Sodium

Indiscretion

Excessive Sodium

Intake

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 descreaseddiastolic 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-Fowlers

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 imbalancesIsotonic fluids (approximate normal serum plasma)Rapid ECF expansion needed

D5W, NS, LRHypotonic fluids

Treatment of cellular dehydration.45% NS, .2% NS, 2.5% dextrose



IV Fluid Replacement

Hypertonic

Treatment of water intoxication

D5 ½ NS, D10W, 3% NS

Shifts fluids from ICF &E

CF to intravascularcomponent 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; transmissionof 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 thekidneys, a process stimulated by aldosterone



Hyponatremia

Results from excess Na loss or water gainGI losses, diuretic therapy, severe renal dysfunction,severe diaphoresis, DKA, unregulated production of

ADH associated with cerebral trauma, narcotic use,lung cancer, some drugsClinical manifestations

BP, confusion, headache, lethargy, seizures,decreased muscle tone, muscle twitching and

tremors, vomiting, diarrhea, and cramps



PathophysiologySodium 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





Headache

Muscle weakness

Postural Hypotension

Nausea

and

vomiting Abdominal CrampsWeight loss



Assessment

Labs

Increased HCT, K

Decreased Na, Cl, Bicarbonate, UOP with low Na and

Cl concentrationUrine specific gravity 1.010



Colloborative Care Management

General Goal: Correct Sodium Imbalances and Restore Normal Fluid andElectrolyte 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 intaketo 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 feedingswithout water supplements, watery diarrhea,

greatly increased insensible water loss, renal failure,

inadequate blood circulation to kidneys, use of

large doses of adrenal corticoids, excess sodiumintake



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



PathophysiologyIncreased Sodium Concentration in ECF

Osmolarity Rises

Water Leaves the Cell by Osmosis and Enters to the ExtracellularCompartment

Dilution of Fluids in the ECF Cells are depleted with water


Suppression of Aldosterone

Secretion

Sodium is Excreted in the

Urine




Excessive Thirst Dry Sticky Mucous

Membrane

Firm, Rubbery

Skin Turgor

Manic Excitement

Tachycardia

Death



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, DTRs

BP, EKG changes, possible cardiac arrest

N/V, paralytic ileus, diarrheaMetabolic alkalosis

Mental depression and confusion



Causes and Effects of HypoK+

HYPOKALEMIA

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

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 VascularDecreased BP,

Dysrhythmias,

ECG changes,

Myocardial

damage,

Cardiac Arrest

Kidneys

Decreased

Capacity to

Concentrate

Waste, Water

Loss, Thirst,

Kidney

damage

P h h i l



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

Increased Urinary Output

Use of Certain Diuretics such as Thiazide and Furosemide and

Corticosteroid

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 potassiumdepletion such as vomiting, diarrhea, diuretics, by

monitoring the patient for early warning signs.

Hypertonic glucose solution

MonitorI & 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

failureTissue trauma

Acidosis

Catabolic state



Signs/Symptoms

ECG changes tachycardia to bradycardia to possible

cardiac arrest

Tall, tented T waves

Cardiac arrhythmiasMuscle weakness, paralysis, paresthesia of tongue,

face, hands, and feet, N/V, cramping, diarrhea, metabolic

acidosis



HYPERKALEMIA

Decreased Loss

Potassium-Sparing Diuretics

Renal Failure

Adrenal Insufficiency

Shift of Potassium out

of the CellExtensive Injuries,

Crushing Injuries,

Metabolic Acidosis

CNS

Numbness,

Paresthesi

a

Muscles

Early: Irritability

Late: Weakness

leading to

Flaccid Paralysis

Cardio Vascular

ConductionDisturbance,

Ventricular

Fibrillation,

Cardiac Arrest

KidneysOliguria

leading to

Anuria

Excess Intake

Dietary Intake Excess of

Kidneys ability to

excrete; Excess in

parenteral

Administration

GI TractN/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 stateIonized 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 reflexesIrritability, reduced cognitive ability, seizures

Prolonged QT on ECG, hypotension, decreased

myocardial contractilityAbnormal clotting



HYPOCALCEMIA

Inadequate

IntakeDietary Deficit

Decrease In GI Tract and

Bone Absorption

Increase Magnesium

Increase CalcitoninDecrease Vit. D

Decrease Parathyroid

Hormone

BonesOsteoporosis

leading to

fracture

CNS

Tingling

Convulsion

Other

Abnormal

Deposits of

Calcium in

Body Tissues

Muscles

Muscle Spasm

Tetany

Decreased Ionized

CaciumLarge Transfusion

with citrated blood

Cardiovascular

Dysrhythmias

Cardiac Arrest

Excess Loss

Kidney DiseaseDraining

Fistula

P h h i l



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 cautionClose 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

ThyrotoxicosisExcessive ingestion of Ca or Vit D



Signs/Symptoms

Anorexia, constipationGeneralized muscle weakness, lethargy, loss of

muscle tone, ataxia

Depression, fatigue, confusion, comaDysrhythmias and heart blockDeep bone pain and demineralizationPolyuria & predisposes to renal calculiPathologic bone fractures



HYPERCALCEMIA

Excess IntakeIncrease Calcium Diet

Antacid Containing Calcium

Increase in factors

Causing Mobilizationfrom Bone

Increase PTH, Increase

Vit. D, Steroid Therapy

CNS

Deep Tendon

Reflexes

Lethargy

Coma

Bones

Bone Pain

Osteoporosis

Fracture

Muscles

MuscleFatigue

Hypotonia

GI Motility

Kidneys

Stones

Kidney

Damage

Loss from Bones

Immobilization,Carcinoma with bone

Metastasis, Multiple

Myeloma

Cardiovascular

Depressed

Nerve andMuscleActivity

Dysrhythmias

Cardiac Arrest



Hyper calcemic Cr isis

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 calcitoninEncourage 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 conductionImportant 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

CausesDecreased intake or decreased absorption orexcessive loss through urinary or bowel

eliminationAcute pancreatitis, starvation, malabsorptionsyndrome, chronic alcoholism, burns,prolonged hyperalimentation withoutadequate MgHypoparathyroidism with hypocalcemiaDiuretic therapy



Signs/Symptoms

Tremors, tetany, reflexes, paresthesias of feet

and legs, convulsions

Positive Babinski, Chvostek and Trousseau signsPersonality changes with agitation, depression

or confusion, hallucinations

ECG changes (PVCS, V-tach and V-fib)



HYPOMAGNESEMIA

Impaired Absorption from GITract

Malabsorption Syndrome, AlcoholWithdrawal Syndrome,

Hypercalcemia, Diarrhea, Draining,

Gastrointestinal Fistula

Excessive Excretion

Increased Aldosterone,Conditions causing large

losses of urine

CNS

Convulsions,Paresthesia,

Tremor, Ataxia

Mental

ChangesAgitation,

Depression,

Confusion

Hypokalemia

Muscles

Cramps,

Spascity,

Tetany

Increased Intake

Prolonged

Malnutrition,

Starvation

Cardiovascular

Tachycardia,

Hypotension,

Dysrhythmias

L S M i L l



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

Excretion of Magnesium by the

GITractHigh Serum Calcium

Magnesium



Magnesium

InhibitsTransport of PTH

Decrease in the Amount of Calcium being Released

from the Bone

Possible Calcium Deficit

T



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 IMMgSO4 IV slowly

T t t



Treatment

Monitor Mg q 12 hr

Monitor VS, knee reflexes

Precautions for seizures/confusion Check swallow reflex

H i



Hypermagnesemia

Most common cause is renal failure, especiallyif taking large amounts of Mg-containingantacids or cathartics; DKA with severe waterloss

Signs and symptomsHypotension, drowsiness, absent DTRs,respiratory depression, coma, cardiac arrestECG Bradycardia, CHB, cardiac arrest, tall Twaves

Renal Failure, Excessive IV Infusion of Magnesium, Decreased

GI Eli i i d/ Ab i



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

Respiratory Arrest may occur

Slowed Heart Rate and AV Block

Peripheral Vasodilation

Hypotension, Flushing, and Increased Skin

Warm

T t t



Treatment

Withhold Mg-containing products

Calcium chloride or gluconate IV for acute

symptoms

IV hydration and diuretics

Monitor VS, LOC

Check patellar reflexes

Ph h



Phosphor ous

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 hasinverse relationship to Calcium

H h h t i



Hypophosphotemia

Causes

Malnutrition

Hyperparathyroidism

Certain renal tubular defects

Metabolic acidosis (esp. DKA)

Disorders causing hypercalcemia

Si /S t



Signs/Symptoms

Impaired cardiac function

Poor tissue oxygenation

Muscle fatigue and weakness

N/V, anorexia

Disorientation, seizures, coma

T t t



Treatment

Closely monitor and correct imbalancesoAdequate amounts of Phos

oRecommended dietary allowance for

formula-fed infants 300 mg Phos/day for 1st

6mos. and 500 mg per day for latter ½ 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

T t t



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

H h h t i



Hyperphosphatemia

Causes

Chronic renal failure (most common)

Hyperthyroidism, hypoparathyroidismSevere catabolic states

Conditions causing hypocalcemia

Signs/S mptoms



Signs/Symptoms

Muscle cramping and weakness

HR

Diarrhea, abdominal cramping, and nausea

Treatment



Treatment

Prevention is the goal

Restrict phosphate-containing foods

Administer phosphate-binding agentsDiuretics

Treat cause

Treatment may need to focus on correcting

calcium levels

my report f and e

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