Fluids and Electrolytes Fa 2010

8/4/2019 Fluids and Electrolytes Fa 2010

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FLUIDS AND ELECTROLYTES

CH.14

GLORIA PHILLIPS, RN

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OBJECTIVES

1. DISCUSS OSMOSIS, DIFFUSION, OSMOALITY, FILTRATION

2. DISCUSS THE NA-K PUMP

3. DISCUSS THE BODYS HOMEOSTATIC MECHANISM

4. DESCRIBE F/E EFFECTS IN RELATION TO AGING

5. EXPLAIN FLUID/VOLUME DISTURBANCES

6. DISCUSS ELECTROLYTE IMBALANCES

7. DESCRIBE ISOTONIC, HYPERTONIC, AND HYPOTONIC

SOLUTIONS

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TERMINOLOGY

1. HYDROSTATIC PRESSURE

2. HYPOVOLEMIA

3. ISOTONIC 4. TROUSSEAUS SIGN

5. CHVOSTEKS SIGN

6. FLUID VOLUME EXCESS 7. ACTIVE TRANSPORT

8. PASSIVE TRANSPORT

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FLUIDS AND ELECTROLYTES

BODY FLUIDS: 2 MAIN COMPARTMENTS

INTRACELLULAR (ICF): WITHIN THE CELL

a. Cations b. Anions

EXTRACELLULAR (ECF): FLUID OUTSIDE THE CELL

a. Cations b. Anions

INTERSTITIAL FLUID (B/W CELLS)

INTRAVASCULAR FLUID (WITHIN BLOOD VESSELS)

TRANSCELLULAR FLUID: (FLUIDS SEPARATED BY A LAYER OF EPITHELIAL CELLS FROM

OTHER ECF)

DIGESTIVE JUICES, INTRAOCULAR FLUID, CEREBRO-SPINAL FLUID (CSF), AND

THE WATER AND SOLUTE IN THE RENAL TUBULES

Third Spacing

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FLUID DISTRIBUTION

WATER: MAJOR COMPONENT OF BODY TISSUE

45-75% OF TOTAL BODY WEIGHT

ICF: 75% OF TOTAL BODY WATER

ECF: 25% OF TOTAL BODY WATER

What is Hydrostatic Pressure?

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COMPOSITION OF BODY FLUIDS

ALL BODY FLUIDS CONTAIN ELECTROLYTES ELECTROLYTES: CHEMICAL COMPOUNDS CAPABLE OF CONDUCTING

ELECTRICITY WHEN DISSOLVED IN H2O

IONS: SHORT AN ELECTRON OR HAVE AN EXTRA ELECTRON

CATION: ELECTRON WITH A POSITIVE CHARGE

ANIONS: ELECTRON WITH A NEGATIVE CHARGE

DYNAMIC PROCESS: IONS MOVE B/W COMPARTMENTS TO MAINAINBALANCE

CONCENTRATION VARIES WITH THE COMPARTMENT.

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CONTINUATION

REPLACEMENT OF FLUIDS AND ELECTROLYTES

IS NECESSARY AS LOSS OF ELECTROLYTES IS

CONTINOUS WITH WATER LOSS

Osmosis is:

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ELECTROLYTE CONCENTRATION

MEASURED IN MILLI-EQUIVALENTS (mEq.) PER LITEROF FLUID

NUMBERS OF POSITIVE AND NEGATIVE IONS AREEQUAL IN SOLUTION

MEASUREMENT OF ELECTROLYTE CONCENTRATION OSMOLALITY: ONE GRAM MOLE OF SOLUTE DISSOLVED IN

1000 GRAMS OF WATER; YIELD IS GREATER THAN 1000ML

UNAFFECTED BY TEMPERATURE OR AMOUNT OFSOLUTE,

BASED ON A CERTAIN WEIGHT OF SOLUTE

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ELECTROLYTE CONCENTRATION

CONTINUED OSMOLARITY = OSMOTIC PRESSURE (PULLINGPOWER OF WATER) OF A SOLUTION EXPRESSED ASOSMOLS OR MILLIOSMOLS/KG (mOsm/Kg)

CONCENTRATION OF SOLUTE IN 1000ML OF SOLUTION (>SOLUTE = > ABILITY TO PULL WATER INTO IT)

AMOUNT OF SOLUTE PLUS ENOUGH WATER TO YEILD1000ML. OF SOLUTION

USED INTERCHANGEABLY WITH OSMOLALITY; NOT

EXACTLY THE SAME

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TYPES OF SOLUTIONS

ISOTONIC SOLUTIONS = SAME OSMOLALITY ASBLOOD (0.9% NACL)

HYPER-OSMOLARSOLUTIONS: EXCESS SOLUTE IN

1000ML; MORE SOLUTE THAN BLOOD; PULLS H20OUT OF THE CELLS; SHRIVELS CELLS (3% NACL)

HYPO-OSMOLAR SOLUTIONS: LESS THAN NORMALAMOUNTS OF SOLUTE/1000ML; LESS SOLUTE THAN

BLOOD; WATER IS PULLED INTO THECELLS(SWELLING/EDEMA); (0.2NACL)

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GENERAL FUNCTIONS OF ELECTROLYTES

PROMOTE NEUROMUSCULAR IRRITABILITY

MAINTAIN BODY WATER B/W COMPARTMENTS

DISTRIBUTE BODY WATER B/W COMPARTMENTS

REGULATE ACID/BASE BALANCE

EACH ELECTROLYTE HAS SPECIFIC FUNCTIONS IN THE

BODY

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REGULATION OF F AND E BALANCE

WATER LOSS: KIDNEYS, INSENSIBLE LOSS

(LUNGS, GI TRACT, SKIN)

INSENSIBLE LOSS: 500-800ML/24HR

CONTROL OF BODY TEMPERATURE AND

EXCRETION OF METABOLIC WASTES REQUIRES

CONTINUAL WATER LOSS AND REPLACEMENT

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INTERNAL CONTROL OF WATER

BALANCE

INTAKE AND OUTPUT: approx. EQUAL

FLUID LOSS: INFLUENCED BY EXTERNALTEMPERATURE, HUMIDITY, METABOLIC RATE,

PHYSICAL ACTIVITY INTAKE: CONTROLLED BY THIRST

> SERUM OSMOLALITY STIMULATES OSMORECEPTORSIN THE HYPOTHALMUS, TRIGGERING FLUID INTAKE

HYPOTHALMUS STIMULATES POST. PITUITARY TORELEASE ADH RESULTING IN RETENTION OF WATER BYTHE KIDNEY

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INTERNAL CONTROL: WATER BALANCE CONT.

REABSORPTION OF NA+ AND H20 RESULTS IN > K+

LOSS AND DECREASED URINE OUTPUT

> FLUID INTAKE AND RETENTION OF NA+ AND

WATER LEAD TO INCREASED CBV,

DECREASED SERUM OSMOLALITY,

DECREASED THIRST

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INTERNAL CONTROL: FLUID BALANCE CONT.

OUTPUT: MAJOR CONTROL = KIDNEY

KIDNEY REGULATES VOLUME AND OSMOLALITY (PRIMARILY NA+)

NA+ AND H20 BALANCE DEPENDS ON:

GLOMERULAR FILTRATION RATE (GFR) DETERMINED BY: GLOMERULAR CAP. BP, HYDROSTATIC PRESSURE IN BOWMANS

CAPSULE AND PLASMA PROTEIN CONCENTRATION.

ALL AFFECTED BY VARIETY OF FACTORS AND DISEASE STATES

EXAMPLES:

SHOCK = DECREASE IN GLOM. CAP.BLOOD PRESSURE,

HTN = INCREASE IN GLOM. CAP. BLOOD PRESSURE,

URINARY OBSTRUCTION = INCREASE IN HYDROSTATIC PRESSURE INBOWMANS CAPSULE,

LOSS OF PROTEIN FROM THE BODY = DECREASED PLASMA PROTEIN

LEADS TO NON-PITTING EDEMA AND HYPOTENSION.

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INTERNAL CONTROL OF FLUID

BALANCE: CONT.

LOW SERUM PROTEIN

CAUSES:

ACUTE GLOMERULAR NEPHRITIS

NEPHROSIS

DECREASED INTAKE OF PROTEIN

DECREASED PRODUCTION (LIVER DISEASE)

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OTHER FACTORS INFLUENCING

OUTPUT

STIMULATION OF VOL. RECEPTORS IN ATRIA,

VENA CAVA AND OSMORECEPTORS IN THE

HYPOTHALMUS LEADS TO STIMULATION OF

POSTERIOR Pituitary TO < PRODUCTION ANDSECRETION OF ADH RESULTING IN > RENAL

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OTHER FACTORS INFLUENCING OUTPUT

< IN CELL SIZE (DEHYDRATION) STIMULATESOSMORECEPTORS IN THE HYPOTHALMUS TOTRIGGER RELEASE OF ADH FROM THE PITUITARY(water retention)

> IN CELL SIZE (EDEMA OR SWELLING OF CELLS)CAUSES < IN ADH SECRETION

OTHER CONTRIBUTING FACTORS WHICH >ADHSECRETION

NARCOTICS, STRESS, ANESTHESIA, HEAT, NICOTINE,ANTINEOPLASTIC DRUGS, ANGIOTENSIN (A POTENTVASOCONSTRICTOR)

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RENIN-ANGIOTENSIN-

ALDOSTERONE SYSTEM ALDOSTERONE: PRODUCED IN ADRENAL

CORTEX; CAUSES > RENAL REABSORPTION OFSODIUM (> K+ excretion)

RENAL CELLS MONITOR NA+ LEVELS ANDBLOOD VOLUME

< CBV OR NA+ RESULTS IN RELEASE OF RENIN

FROM THE JUXTAGLOMERULAR APPARATUS

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RAAS CONT.

RENIN STIMULATES CONVERSION OFANGIOTENSIN I TO ANGIOITENSIN II

ANGIOTENSIN II STIMULATES THE ADRENAL

GLAND TO RELEASE ALDOSTERONE = NA+RETENTION = INCREASED OSMOLALITY OFTHE SERUM.

TOGETHER CAUSE THE CYCLE TO BEGIN ALL OVER.

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FACTORS AFFECTING FLUID

BALANCE AGE: REQUIREMENTS VARY;

INFANTS AND SMALL CHILDREN HAVE > NEED

ELDERLY = < RENAL ABILITY TO CONCENTRATE URINE

ENVIRONMENTAL TEMPERATURE SNS STIMULATION: SWEATING

CAN CAUSE COPIOUS FLUID LOSSES (UNACCUSTOMED TO

HIGH TEMP AND HUMIDITY)

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CONT. FACTORS AFFECTING FLUID

BALANCE DIET: INADEQUATE INTAKE OF PROTEIN LEADS TO >

BREAKDOWN OF GLYCOGEN AND FAT; WHEN SUPPLY

IS EXHAUSTED, BODYUSES ITS OWN PROTEIN

STORES (MUSCLE) FOR ENERGY LOW SERUM PROTEIN (ALBUMIN)

< COP

HYPOTENSION

INTERSTITIAL EDEMA (non-pitting)

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CONT. FACTORS AFFECTING FLUID

BALANCE

STRESS: > CELLULAR METABOLISM, GLUCOSE

LEVELS AND MUSCLE GLYCOGENOLYSIS

(BREAKDOWN TO GLUCOSE)

NA+ AND H2O RETENTION

DECREASED U/O, > CBV, > BP

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FACTORS CONT.

ILLNESS: EXTENSIVE SURGERY OR TRAUMA AFFECT F

& E BALANCE

EXAMPLES:

BURNS ( LOSS OF F &E FROM PLASMA AND INTERSTITIALFLUID),

CARDIAC DISORDERS (IMPAIRED CARDIAC MUSCLE

FUNCTION) CAUSES < ELIMINATION OF WASTE PRODUCTS

OF METABOLISM AND NA+ AND WATER

RESULTS IN IMPAIRED RENAL PERFUSION

< U/O, HYPERVOLEMIA, AND PULMONARY EDEMA

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MOVEMENT OF F & E

FLUIDS MOVE B/W ECF COMPARTMENT AND THE ICFCOMPARTMENT

PROCESS

DIFFUSION: MOVEMENT OF SOLID PARTICLES ACROSS A

MEMBRANE FROM A SOLUTION OF HIGHERCONCENTRATION TO SOLUTION OF LESSER CONCENTRATION

OSMOSIS: MOVEMENT OF WATER ACROSS A MEMBRANEFROM A SOLUTION OF LESSER CONCENTRATION TO ONE OFGREATER CONCENTRATION

FILTRATION: MOVEMENT OF SOLUTE AND WATER ACROSS AMEMBRANE FROM ONE COMPARTMENT TO ANOTHER

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MOVEMENT OF FLUIDS AND

ELECTROLYTES

PROCESS CONT.

ACTIVE TRANSPORT = MOVEMENT OF

SUBSTANCES ACROSS A MEMBRANE FROM A

LESSER CONCENTRATION TO A SOLUTION OFGREATER CONCENTRATION USING A SPECIFIC

CARRIER (REQUIRES ENZYME ACTIVITY) EXAMPLE

= K+ BINDS WITH INSULIN TO CARRY IT ACROSS

THE CELL MEMBRANE SO THE CELL CAN USE IT.

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CONT. F & E MOVEMENT

ACTIVE TRANSPORT = VERY IMPORTANT IN

MAINTAINING DIFFERENCE B/W NA+ AND K +

ION CONCENTRATION OF ECF AND ICF

NA+: LEVELS HIGHER IN ECF

K+: LEVELS HIGHER IN ICF

BOTH REGULATED BY THE SODIUM/POTASSIUM

PUMP

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CATEGORIES OF FLUID

IMBALANCES 5 Fluid Imbalances

EXTRACELLULAR FLUID VOLUME DEFICIT (ECFVD)Decrease in intravascular & interstitial fluids

Common & serious imbalance

Vascular volume loss hypovolemia

Can lead to cellular fluid loss from fluid shifting from cells intovascular fluid to restore fluid balance

ECVD

2 major types

Hyperosmolar fluid volume deficit Fluid loss greater than solute (NA+) loss

Iso osmolar fluid volume deficit Equal proportion of fluid & solute (Na+) loss

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EXTRACELLULAR FLUID VOLUME DEFICIT

Pathophysiology: HYPEROSMOLAR ECFVD Changes in Na+ level

Serum Na+ concentration is increased with ECFVD caused by

insufficient water intake or massive water loss

Shifting water from cells into vascular space to decrease

hyperosmolality that occurrs with water loss

EXCESS NA+ causes cells to shrink and cellular dehydration to

occur

Thirst

Cells shrink stimulating thirst osmoreceptors in

hypothalamus

with iso-osmolar fluid loss, thirst usually does not occur

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ECFVD: HYPEROSMOLAR

PATHOPHYSIOLOGY CONT.

Decreased skin turgor

< interstitial fluid volume skin tissues stick

together (tenting) when pinched up

Dry mucous membranes, dry, cracked

lips/tongue

Soft sunken eyeballs = severe deficit

< eye ball water tension (dehydration)

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ECFVD: HYPEROSMOLAR

Signs/symptoms Apprehension & restlessness (effect of high sodium levels

on CNS)

Cerebral dehydration (high sodium levels, osmotic diuresis)

Elevated temperature Less water available for evaporation to cool the body

Tachycardia ( fever, compensation for decreased CBV fromfluid loss)

Pulse greater than 100 fever, circulatory compensation

Postural systolic B/P drop > 15 mmHg and diastolic drop >10 mmHg with position changes, drops are greater onstanding (postural hypotension)

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ECFVD:ISO-OSMOLAR

Iso-osmolar fluid loss = inadequate plasma volume due to proportional losses ofNa + and water resulting in beginning decrease in systolic blood pressure

Signs/symptoms Narrowed pulse pressure = systolic and diastolic become closer in numbers

(ex. 110/90), < Central Venous Pressure (reflects fluid volume status &Pulmonary Capillary Wedge Pressure (reflects left heart function

Decreased venous return 2ndary to < CBV

Flattened neck veins Decreased venous return

Weight loss Lack of water component of body fluids

Oliguria= < 30ccs urine output per hour

Renal response to hypovolemia (RAAS)

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ECFVD

Lab. Values

Increased osmolality > 295 * Normal Range: 285-295

> or normal Na+ level

Hyper-Osmolar fluid volume DEFICIT Na+ greater than 145, water loss greater than amount Na+

loss (disproportionate)

Iso-osmolar Fluid Volume Deficit serum Na+ levels

= 135-145 mEq/LITER

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ECFVD : LAB CONT.

> Bun > 25 mg/dl

25 to 35 * hemoconcentration

Hyperglycemia sugar increases serum osmolality causingdiuresis and water loss (worsens the problem)

Glucose >ed due to hemoconcentration

> HCT > 55%

Hyperosmolar loss = Elevated HCT * hemoconcentration

Iso-osmolar loss hemorrhage, initially HCT normal rangeequal amounts of cells lost to plasma loss, Increased specificgravity of urine increased solute to solvent ratio

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Extracellular fluid vol. deficit

Mild ECFVD 1-2 liters of body water lost & 2% body weight lost

Moderate

3 - 5 liters body water lost & 5% body weight lost

Severe 5 -10 liters body water lost & up to 8% body weight lost

Systolic blood pressure alarmingly low -- < 70mm Hg (no renal perfusion) less than 80 systolic= no renal perfusion, shock ensues

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Medical Management

Hyper-osmolar fluid volume deficit

D-5-W IV if deficit present less than 24 hours

D-5-w in 0.2% NaCl

If deficit present more than 24 hours, dangerous to

correct too fast

Maximal rate at which Na+ solution infused 2mEq /L

per hour too fast cerebral edema can occur

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Medical Management

ECVD

Hemorrhage

Blood replacement when loss greater than 1 L usuallywhole blood

Blood loss < than 1 L.

Normal saline

Lactated ringers to restore volume

fluid needs assessed within context of overall condition

Severe ECFVD & heart or kidney condition

Cannot be given large amounts of fluid or sodium

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Medical Management

Dietary management

Fluid loss from diarrhea:

TEACH

Avoid fatty or fried foods & milk products Avoid fruit juices as they may compound the problem

INCREASE FIBER IN THE DIET SLOWLY UNLESS CONTRAINDICATED;

HELPS PREVENT DIARRHEA;

TOO MUCH CAN CAUSE CONSTIPATION (TOO LITTLE WATER

INTAKE)

OR DIARRHEA IF NOT USED TO EATING MORE FIBER.

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Nursing Management

Assessment: FVD

Typical S/S: mucous membranes, skin turgor, wt. loss,

N/V/D, fever

Ability to participate in tx. Plan Abilitly to Swallow

Where to insert the IV & size angio-cath

Nursing Diagnosis

FVD R/T insufficient fluid intake, excessive fluid losses(vomitus, diarrhea, hemorrhage), physiologic third space

fluid loss (burns or ascites, or pleural effusion)

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Nursing Management

Planning: expected outcomes Patient will exhibit signs of improved fluid balance AEB:

VS WNL

Weight gain 1-2 pounds/day or return to baseline

Absence of causative factors

Equal I & O

Urine output greater than 600 cc/day

Absence of tenting of skin over sternum

Moist mucous membranes

Critical element absence of adequate renal perfusion for several hours= permanent renal damage

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Nursing Management

IMPLEMENTATION Take vital signs q 2 4 hours depending on severity of loss

Compare with baseline

Report marked differences to MD

If safe to do so, determine orthostatic VS Degree of orthostasis

Standing 15 mm Hg or greater drop in systolic, report result to MD

Protect from injury if ambulated

Urine output

Assessed hourly in severe cases

Mild cases q 4

Compare I & O for 24 hour period; Should be relatively equal

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Nursing Management: Implementation

cont.

Absence of urine output in 8 -12 hours = renal insufficiency *

decreased renal perfusion

Check Urine sp. Gr. Q shift provides objective data on

osmolality

Daily weight

Loss of 1 kg= 1 Liter fluid loss

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cont.

Skin care

Apply Lotion (preserve skin integrity)

Position changes q 2 hours (prevent

pressure/breakdown)

Oral care q 2 hours use non alcohol based solution

Moisten lips q 1 hour

Labs

Monitor

Na+, BUN, glucose and HCT levels

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cont.

Mild FVD

Oral fluid replacements

Moderate to severe

IV fluids (D-5-W, D-5-0.2 NaCl) indicated but

monitored very closely

Over hydration from excessive & rapidly infused fluid or

in those with renal or cardiac disorders Symptoms of dyspnea, crackles, jugular vein engorgement

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Nursing Management: EVALUATION

Degree of achievement of expected outcome

monitored after 8 hours and ongoing to determine ECFVD

correction

modification of plan for elderly

Rehydrate slowly

renal & cardiac disease

Monitor Skin impairment

more common in elderly Position changes more frequently; rise slowly from

recumbent to standing

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Nursing Management

Education

Follow up Care

Responsible person taught how to be sure adequate

fluid intake is provided (1500-2000ml per day); how tomeasure and record I & O

Tube feedings water between feedings to equal the

total 1500-2000ml/day

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ECFVD: FLUID SHIFT

ECF volume shift: 3rd space fluid Volume shift change in location of ECF between

intravascular and interstitial spaces

2 types of fluid shiftsVascular fluid to interstitial space

Fluid shifts into interstitial space & remain there(consolidate) 3rd space fluid

Occurs with tissue injury resulting from altered capillarypermeability i.e. inflammation, traumatic injury & fromincreased vascular fluid volume

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ECFVD: Extracellular Fluid Shifts

Interstitial fluid to vascular fluid space Increased vascular fluid volume appears in

abdominal cavity

ascites Pleural cavity

Peritoneal cavity

Pericardial sac

Basically useless does not circulate to provide

nutrients to cells

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Extracellular Fluid Shifts Third space accumulation 3rd spacing Abnormal accumulation of fluid and electrolytes including

protein within a body space thats not normally a fluidcompartment

Ascites Complication of Cirrhosis = fluid and protein in the abd. cavity

CHF (pitting edema)

Kidney disease (edema)

Abdominal tumor growth

As much as 20 liters can accumulate in abdominal cavity Blisters

Accumulation of fluid in lungs

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Extracellular Fluid Shifts

Clinical manifestations of fluid shift fromvascular to interstitial space similar to thoseof shock

Skin pallor Cold extremities

Weak & rapid pulse

Hypotension

Oliguria

< LOC

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Extracellular Fluid Shifts

When fluid returns to blood vessels, signs/

symptoms similar to those of fluid overload

occur

Bounding pulse

Crackles

Engorged peripheral & jugular veins

Increased blood pressure

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Extracellular Fluid Shifts: MEDICAL

MANAGEMENT

Based on cause: Hypovolemia from tissue injury i.e. burns, crushing injury

Iso-osmolar fluid volume infused

May be 3 xs greater than UO

Over-zealous fluid Replacement

Fluid overload could occur

During 2nd phase, fluid administration & intake may need tobe limited because of fluid influx from tissue spaces INTOvessels

If third space fluid is the result of other processes SUCH aspericarditits or bowel obstruction or ascites

Fluid is removed so organ can retain function

(Pericardiocentesis, thoracentesis, paracentesis)

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Nursing management

Vital signs q 1-8 hours depending on patients condition Loss into peritoneum ascites or extremities peripheral

edema fluid shift slower & vital sign changes can be subtle

IV fluid replacement monitored Too fast hypervolemia

Auscultate chest for crackles

Difficulty breathing

Neck vein engorgement

Elevate head of bed 30-45 degrees; O2 if indicated

Measure abdominal girth ascites Weigh patient

Measure and record I & O

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Nursing management

Extremities involved measure circumference ofextremities & check peripheral pulses

Loc monitored

Seizure activity

Skin care to edematous areas

As fluids shifts back with tissue repair, IV fluid rate decreased

Measure UO q 1hour to ensure at least 25 ccs hour

Decreased because of renal circulation and fluid shift into injuredspaces

3 5 days post-injury, fluid returns into circulation unlessrenal impairment has occurred

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Nursing management

Monitor Bun and ammonia levels in patients

with ascites

Compare fluid volume administered with UO

and VS to monitor progress or deterioration

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ICFVE: HYPO-OSMOLAR

Intracellular fluid volume excess

water intoxication

hypo-osmolar disorders

Water excess

Amount of solute remains normal

Solute deficit

Mainly due to na+ loss

Amount of water normal but too few particles per liter ofwater

Both cause hypo-osmolality of vascular fluids and

cellular swelling occurs

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ICFVE

Not as common as ECFVD or ECFVE Presents serious problem if unrecognized & untreated

Common causes Excessive amounts of hypo-osmolar IV fluids

0.45 NACL

D-5W

Brain injury or disease that causes an > production of ADH thatincreases water reabsorption from renal tubules

Elderly who consume excessive amounts of tap water withoutadequate nutrient intake

Increased ADH secretion can follow surgery, pain, narcotic use REACTION CALLED Syndrome of Inappropriate Antidiuretic Hormone

Secretion = SIADH

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ICFVE

Hypo-osmolar fluid moves by osmosis to forcefluid movement from the lesser concentrationin vessels to higher concentration in cells

Too much hypo-osmolar fluid accumulates incells causing intracellular edema

Urine output may be normal or decreased

Serum Na+ decreased = hemodilution

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ICFVE

Clinical manifestations Headache, nausea, vomiting

CNS changes due to > ICP, as cerebral cells absorb hypo-osmolar fluid more quickly than other cells

Pupillary changes

pressure on 3rd cranial nerve from ICP

Decreased muscle strength, unequal grasp,

pronation drift Due to cerebral basal ganglia swelling

Weight gain excess water retention

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ICFVE

Clinical Manifestations Vital sign:

Bradycardia with > systolic B/P

Widened pulse pressure (BP 170/50)

Increased respirations

Neuro-excitability (muscle twitching)

POSITIVE Babinskis reflex (abnormal) Flaccidity

Projectile vomiting

Papilledema, delirium

Convulsions to coma

Vital sign changes = ominous indicator of increased intracranial pressure and

herniation of brain stem (death)

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ICFVE

Labs

Na+ Less than 125 associated with hypo-

osmolality

< HCT hemodilution, ECFE often accompanied byICF fluid excess

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ICFVE: MEDICAL MANAGEMENT

Addition of solutes to IV fluids

D-5-0.45 helps correct ICFE when cause iswater excess

Juices, soft drinks given in addition to waterand ice chips

Notify MD of changes in sensorium

Assess reflexes and pupillary response

Offer fluids containing solutes

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EXTRACELLULAR FLUID VOLUME EXCESS

Increased fluid retention in intravascular & interstitialspaces

Na+ & water retained in same proportion = iso-osmolar fluid volume excess

Serum Na+ level may be WNL even though actualsodium level is increased because of excess waterretention

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ECFVE

Etiology > in total body Na+ content

Heart failure

Kidney disorders

Cirrhosis of liver

Foods with high sodium content

Excessive water enemas

Excessive IV fluids containing sodium

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ECFVE: ISO-OSMOLAR

Risk factors Kidney, heart, liver disorders

Hyper-aldosteronism or Cushings syndrome

Use of glucocortiocoids

Use of hypotonic fluid for irrigation

Men who have undergone TURP receiving CBI postoperatively

Prevention Decreasing salt intake

Initiating medical treatment with digoxin or diuretics

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ECFVE: ISO-OSMOLAR

Pathophysiology Fluid overload fluid pressure greater than normal at the arterial

end of capillary

Fluid pushed into tissue spaces with greater force because venouspressure also exceeds oncotic pressure

Pulmonary and peripheral edema can result Fluid overload results from renal problems decrease in sodium and

water excretion

Fluid volume rises & heart must compensate for increasingpressures; heart failure can result

Cirrhosis of liver serum protein & albumin levels 145 low, normal, high

Depending on amount of NA+ retention or water retention

< HCT hemodilution

Sp. Gr. < 1.010 solvent exceeds solute

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ECFVE

Complications

Pulmonary Edema

Medical emergency requiring immediate intervention

to prevent further respiratory distress

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ECFVE: Medical Management

Pharmacologic management Loop and potassium-wasting diuretics (Lasix)

Potent diuretics cause K+ excretion along with Na+and water

a combination of potassium wasting and sparing diureticprescribed to conserve K+ (lasix, aldosterone)

Digitalis preparation (Lanoxin, Digoxin)

increase force of myocardial contraction and slowheart hate if heart failure is a cause of ECFVE

Dietary management Low Na+diet

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ECFVE: Nursing Management

Assessment Auscultate breath sounds at least q shift

Palpate lower extremities for edema (pitting)

Check neck veins for engorgement with patient insemi-fowlers position; if the jugular veins stillengorged, indicates fluid overload

Check Vital signs

Check hands for VENOUS engorgement

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ECFVE: Nursing Management

Check serum electrolytes for abnormalities

especially if receiving diuretics

If taking digoxin and potassium wasting

diuretic, observe for digitalis toxicity andhypokalemia (use of digoxin in presence of

hypokalemia = AV block)

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NURSING PROCESS: ECFVE

Nursing Diagnosis

FVE R/T compromised regulatory mechanisms,

inadequate myocardial pump,

excessive fluid intake

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NURSING PROCESS

Planning: GOALS/OUTCOMES Patient will demonstrate signs of fluid balance

AEB:

Absence of dyspnea

Clear,equal Bilateral breath sounds

Absence of dependent edema

Flat neck veins at 45 degrees

Peripheral veins emptying in 3 -5 seconds

Weight loss 1-2 pounds/day or absence of edema

Urine output exceeds intake

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NURSING PROCESS

IMPLEMENTATION Monitor for bounding pulse

Check BP,AP,. Respirations q 4 hours

Auscultate breath sounds q 4 -8 hours for crackles, note

changes in location of adventitious sounds Notify physician of increase crackles

Check for neck vein distention q 8

Daily weight

Edema with 3 Liters or more accumulation Strict Intake and output: monitor and record q 4-8 hours

O2 if indicated, check 02 sats to keep 92% or >

76

NURSING PROCESS: IMPLEMENTATION


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CONT.

Note changes in LOC (cerebral edema) Palpate lower extremities & sacrum q AM for dependent

pitting edema

Monitor labs

Restrict fluids & Na+ Explain rationale

Include fluids on meal trays as part of total fluids

Work with dietitian regardingfluid restrictions

77



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NURSING PROCESS: IMPLEMENTATIONCONT.

Schedule oral meds at meal times if possible

OFFER Very cold fluids deceases thirst

sensation

Frequent oral care

Generalized edema skin care important to

prevent pressure ulcers

78


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NURSING PROCESS

Evaluation

Note improvement or deterioration according to

outcomes q shift

Revise POC as indicated

Care plan modification for Elderly patients

Respond more slowly to interventions

Potential for drug-drug interactions

79


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NURSING PROCESS

Education Low na+ diet review foods allowed

Avoid canned foods fresh or frozen permitted

Use frozen foods cautiously

Read labels; look for sodium, salt ? Drinks soft drinkshigh in Na+

Weigh daily when edema is present; record weight

Weight gain 2 pounds or > 2 consecutive days, notify MDand keep record for MD

80

C O S SO U


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ELECTROLYTES: SODIUM

SODIUM FUNCTIONS: CONTROL AND REGULATIONOF BODY FLUID

MAJOR CATION IN EXTRACELLULAR FLUID

CHLORIDE GOES WITH NA+: REABSORBED OREXCRETED

WORKS WITH K+ TO MAINTAIN ELECTROLYTE

BALANCE

USUAL SERUM RANGE: 135-145mEQ/L

81

ELECTROLYTES SODIUM


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ELECTROLYTES: SODIUM

Sodium concentration in ECF assists inmaintaining water balance

Sodium Homeostatic Mechanisms

Sodium balance regulated by

Afferent & efferent mechanisms

Afferent sensing mechanisms in nerve endingsrecognize changes in Na+ intake & ECF volume by

sensing increase or decrease in pressure

These found in atria, carotid sinus, liver, kidneys

82

l i


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ELECTROLYTES: SODIUM regulation

Central nervous system receptors that respond to changes inNa+ concentration in cerebrospinal fluid

Mechanisms contd

Efferent mechanisms include: Glomerular filtration rate in kidney

Blood enters glomerulus & driven by systemic blood pressure High pressure of Entering blood favors filtration across the membrane

Blood proteins remaining in the vessel exert oncotic pressure to draw fluid backinto vessel

About 99% sodium thats filtered by glomerulus isreabsorbed by renal tubules

Renal function impacts sodium homeostasis

83

ELECTROLYTES SODIUM l i


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Hormonal factors Control Na+ homeostasis

Renin-angiotensin-aldosterone

Renin excreted in response to hypotension

Results in increased angiotensinogen to angiotensin to increase

aldosterone production Aldosterone stimulates net Na+ reabsorption across the tubules

Prostaglandins

secreted by kidney and stimulates production of renin; Act to

maintain renal blood flow during reduced blood volume period

84

ELECTROLYTES SODIUM l i


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Kallikerin = proteins of high molecular weight & areproduced by distal convoluted tubule and secrete

kinin

Kinin a potent renal vasodilator and increases renal

excretion of Na+ Naturetic hormones

Function of Natriurtic hormone not fully understood

85

ELECTROLYTE IMBALANCES SODIUM


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ELECTROLYTE IMBALANCES: SODIUM

HYPONATREMIA SODIUM DEFICIT IN PLASMA

One of the most common electrolyte disorders

CAUSES:

Renal loss from diuretics

Diabetic glycosuria

Aldosterone deficiency

Intrinsic renal disease

Extra renal loss from vomiting, diarrhea, increased sweating

SIADH

Continued secretion of due to pain, emotion, medications

Edematous disorders __

CHF, Cirrhosis, nephrotic syndrome, acute and chronic renal failure

Hyperglycemia, hyperlipidemia

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HYPONATREMIA


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HYPONATREMIA

Hyponatremia risk factors More prominent in :

Elderly

Infants, Small children

Because variation in TBW Clinical conditions

Vomiting

Diarrhea

Cardiac and renal disorders

Addisons disease NPO, receiving IV solutions

Diuretics without Na+ replacement

87

HYPONATREMIA


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HYPONATREMIA

Pathophysiology

ECF Na+ concentration decreases, the Na+concentration Gradient (difference) between the ECF &

ICF decreases Hypo-osmolality leads to intracellular edema

Water in In ECF moves by osmosis into cells

less Na+ available to move across the excitable membrane

(delayed membrane depolarization) Excitable tissues vary in response to decreased Na+

Most sensitive - CNS cell- leading to cerebral edema

Clinical manifestations reflect decreased excitability orirritability of membranes

If hyponatremia and volume are not corrected, K+, Ca++,

Cl-, and bicarbonate imbalances can occur 88


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HYPONATREMIA CONT


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HYPONATREMIA CONT.

PATHOPHYSIOLOGY AND S/S Gastrointestinal

Nausea, vomiting, hyperactive bowel sounds, abdominalcramping

Na+ abundant in GI tract; loss of GI secretions cause Na+ loss

90

HYPONATREMIA CONT


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HYPONATREMIA CONT.

Cardiovascular S/S Decrease in diastolic blood pressure, tachycardia,

profound orthostatic hypotension, weak pulse

Loss of Na+ & water decrease circulatingvolume with shock like state

Elevated SYSTOLIC B/P with full, rapid pulse

EXCESSIVE CIRC. BLD. VOL. 2NDARY TO

Dilutional hypo-natremia with excessive fluidvolume

91

HYPONATREMIA CONT


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HYPONATREMIA CONT.

Pulmonary S/S Changes in respiratory rate

Adventitious lung sounds

Fluid overload, CHF

Neurologic S/S Headache, apprehension, lethargy, slow problem solving,

flat affect, diminished muscle tone in extremities,decreased deep tendon reflexes, weakness & tremors

Diluted fluids move into brain cells, affecting cognition

and reflexes; excitable membranes less responsive tostimuli

92

HYPONATREMIA CONT


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HYPONATREMIA CONT.

Integumentary S/S

Dry pale skin;

Dry mucous membranes

Decreased interstitial fluids

93


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HYPONATREMIA CONT. Lab findings

NA+ Less than 135 mEq/L

Symptoms apparent Na+ < 125

Urine Na+ < 40 Body Na losses result in a compensatory decrease in

urinary excretion of Na+

Serum osmolality < 275 due to:

Na+ losses resulting in decreased Na+ concentration in

body fluids

94

HYPONATREMIA CONT


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HYPONATREMIA CON T.

Diagnostic assessment Based on combination of clinical manifestations and lab

values

Acute hypo-natremia concentration less than 120 with

CNS manifestations

Less than 115 causes severe neurologic impairment

Confusion

Convulsions

May result in death due to excessive water shift to theintracellular compartment

95

HYPONATREMIA: TREATMENT


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HYPONATREMIA: TREATMENT

TREATMENT DEPENDS ON CAUSE

Goal

Correct body water osmolality and restore cell volume

by raising the ratio of Na+ to water in ECF Increased ECF osmolality draws water from cells and

decreases cellular edema

If due to fluid excess FLUID RESTRICTION to allow

Na+ to regain balance If Na+ less that 125 Na+ replacement needed

96

HYPONATREMIA TREATMENT


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Pharmacologic management Moderate hypo-Na+ 125

IV normal saline or LR may be ordered

SEVERE 115 or less 3 % NaCl generally indicated

Hypertonic solution

Irritating to peripheral veins

Monitor closely for over-hydration or hyper-Na+ Especially cardiac problems or renal disease

97



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Pharmacologic Management Normal saline in conjunction with diuretic to

increase urinary Na+ loss and reduce risk of ECFvolume expansion

Urine excreted with Lasix-induced diuresis hasmuch less Na than does the ECF which raises theurinary Na+ level

Drug therapy for hypoNa+ from SIADH includeagents that antagonize ADHdemeclocycline andlithium

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Dietary Management: Balanced diet for mildcases

More severe cases Na+ replacement

Foods high in Na Hyponatremia due to excess fluids restrict fluids

restriction 800 to 1000 cc/day

99

HYPONATREMIA NURSING


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MANAGEMENT

ASSESSMENT: Data collection R/T health problems Signs/ symptoms

History of cause emesis, diarrhea etc

History of Addison's disease, steroid use, CVA, renal,

cardiac or hepatic failure noted

Check serum Na+ levels

If conditions from Hypervolemic hyponatremia, serum Na+

levels may normal or low

misleading reading in response to conditions that cause water to be

retained

100



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MANAGEMENT

Data collection cont. Note usual medications and OTC meds.

Drug drug interactions

UO and fluctuations in body weight

Assess amount Na+ consumed

Ask about behavioral changes, headaches,

increased sleepiness Note turgor and peripheral vein filling

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MANAGEMENT

Nursing diagnosis, planning & implementation Alteration in F&E R/T vomiting, diarrhea, gastric

suctioning, burns, SIADH, surgery Monitor Na levels to return to 135 or greater

Suspicious in those :

NPO NPO without Na+ replacement

N/V, changes in mucous membranes, skin turgor MONITOR FOR Neurologic changes

Estimate serum osmolality by doubling the value of the Na+ level

Na+ level of less than 125 need prompt medical attention

102

HYPONATREMIA: NURSING


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MANAGEMENT

Monitor dietary intake of sodium; include broth,juices, ice chips made of Na+

IV of 3% NaCl if indicated based on Na+ levels

Assess for hypervolemia

Dyspnea Crackles

Neck vein engorgement

Use IV pump safety

Irrigate NG tubes & wound sites with NACL Strict I&O - hourly if acutely ill

103

HYPONATREMIA: NURSING


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MANAGEMENT

Daily weight monitor for fluid balance Fluid restriction 1000ml or less if from FVE

Coordinate with dietitian

Schedule medications at meal times if possible

Confused or agitated Reorient

Safety measures

Keep noise down

Side rails elevated

Bed in low position

Padded side rails if seizure prone/tongue blades

104

ELECTROLYTE IMBALANCE: SODIUM


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EXCESS

HYPERNATREMIA

Serum Na+ level above 145 mEq/L

Etiology: HYPOVOLEMIC HYPERNATREMIA

renal losses: osmotic diuresis

severe hyperglycemia

Extrarenal losses: profuse diaphoresis,

decreased thirst, diarrhea occurring with inadequate

volume replacement or fluid replacement with

hyperosmolar fluids

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EXCESS

Euvolemic hypernatremia CAUSES

Excess fluid losses from skin and lungs

Hypodispia in elderly & infants

Diabetes Insipidus

Hypervolemic hypernatremia

Administration of concentrated saline solutions; hypertonicfeedings, excess mineral corticicoids,

Accidental or intentional salt ingestion; commerciallyprepared soups and canned vegetables

Clinical manifestations and Patho-physiologic Bases Gastrointestinal

Anorexia, nausea, vomiting

Fluid retention in gastric cells

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EXCESS:HYPERNATREMIA

Integumentary S/S Dry, flushed skin

Mucous membranes dry and sticky

Decrease of interstitial fluid in tissues

Thirst; tongue dry and rough; body temp elevated Less interstitial fluids to cool body by evaporation

Neurological S/S Restlessness, agitation, irritability, stupor, coma

From cerebral cellular dehydration

Muscle twitching, tremor, hype-rreflexia, seizures, rigidparalysis in late stages

Neuromuscular irritability

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EXCESS

Cardiovascular S/S Tachycardia, hypotension or hypertension

Blood pressure relative to type of hypernatremia

Hypovolemic- pressure decreased

Hypervolemic blood pressure elevated

Erratic heart rate and blood pressure dependenton fluid status

Myocardial depression as Na+ ions compete withCa++ ions in slow channels of heart

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EXCESS

Renal S/S Oliguria, dark, concentrated urine

Compensatory mechanism to conserve fluid

Lab values Na+ > 145

Serum osmolality

109

Medical Management HYPERNATREMIA


110/184


High mortality if untreated Death can result from: cellular dehydration

Vascular volume decreases, pulse increases and

B/P drops Progresses: seizures, coma or both or death

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GOAL: To decrease total body Na+ and replace fluidloss

Hypo-osmolar electrolyte solution

0.2% or 0.45 NACl

D-5-W Will not cause considerable dilution of body Na+

Serum level gradually decreased

D-5-W = hypo-osmolar in the body due to rapid

metabolism of dextrose only free water remains Given slowly to prevent osmotic diuresis which aggravates

hypertonic state

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Occ. NaCl used Volume depleted person for fluid resuscitation

Saline hypotonic in comparison with the serumand will allow the Na+ level to decrease slowly

If serum Na+ lowered to fast, fluid will shift fromvascular space into the cerebral cells causing cerebraledema

General rule of thumb: water replacement should be

administered to reduce Na+ levels not more than 2mEq/L/hour for the first 48 hours

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Pharmacologic management Hypernatremia from Na+ excess treated with:

D-5-W and a diuretic i.e. furosemide

Dietary management:

Dietary restrictions

Dietary restriction alone may not bring Na+ level down to normal

Renal disease Na= restricted to 500 to 2000

mg/day

Often fluids must be restricted

Compliance - difficult

113

Nursing management: HYPERNATREMIA


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Assessment Assess for usual manifestations

Suspicion

Head injuries + others high risk

Medication history Those with Na+

Cough medications

Corticosteroids

Dietary history Mucous membranes

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Nursing diagnosis: Alteration in fluid &electrolyte balance r/t decreased thirst or

excessive administration of salt solutions or

impaired secretion of Na+ and water

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Planning: goal: Pt will exhibit signs improved F & E balance AEB: absenceof S/S of hypernatremia, Return of normal Na+ levels

INTERVENTION monitor for response to IV fluid replacement of hypo-osmolar electrolyte

solutions

MONITOR LOC, IRRITABILITY

CHECK TPR AND BP Q 2-4 HOURS ORAL CARE Q 2 HOURS

DTRS Q 4 HOURS

QUIET, DARKENED ENVIRONMENT

PADDED SIDE RAILS

FREQUENT OBSERVATION

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INTERVENTION CONT. Water/fluids offered frequently to elderly and debilitated

To prevent loss and hypernatremia

Increasing fluid intake with CHF or severe disease usually

contraindicated

Decaffeniated fluids

Avoid ETOH

Caffeinated fluids and ETOH increase fluid loss can increase

Na+ level

Over use of fruit juices can increase fluid volume

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Interventions cont. Skin care q 2-4 hours

I&O at least q 2 hours until stable

Weight daily

Monitor for early signs/symptoms of altered mental status

Prevent progression of condition

Seizure precautions initiated

Fluid replacement monitored closely

Assess for osmotic diuresis if D-5-w continuous

Symptoms of cerebral edema

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u s g a age e t

Oral care with nonalcoholic mouth wash Avoid lemon glycerin swabs drying

Soft tooth brush

Lips water soluble lubricant Cool nonacidic fluids

Apple juice tolerated

119



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g g

PATIENT TEACHING reinforce need for SODIUM restriction

Avoid OTC drugs high in Na+

Recognize signs of hypo or hypernatremia

120

ELECTROLYTES: CHLORIDE


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ELECTROLYTES: CHLORIDE

A MAJOR ANION IN ECF: BLOOD, LYMPH,INTERSTITIAL FLUID

FUNCTION: MAINTAIN OSMOTIC PRESSURE OF

BLOOD,BUFFER FOR O2-CO2 EXCHANGE INRBCS, REGULATES ACIC-BASE BALANCE

EACH NA+ ION IS ACCOMPANIED BY A CL- ORHCO3- ION

USUAL RANGE: 95-105mEq/L

121

ELECTROLYTE IMBALANCE


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ELECTROLYTE IMBALANCE

HYPOCHLOREMIA A DEFICIT IN SERUM CHLORIDE


123/184

HYPERCHLOREMIA AN EXCESS OF CHLORIDE IN THE BLOOD >105mEq/L

CAUSES: EXCESSIVE REPLACEMENT OF NACL OR KCL;ANYTHING THAT CAUSES EXCESS NA+ RETENTION

SIGNS /SYMPTOMS: ACIDOSIS, WEAKNESS & LETHARGY,RISK FOR DYSRRHYTHMIAS AND COMA

BOTH HYPOCHLOREMIA AND HYPERCHLOREMIA USUALLYDEVELOP WITH SODIUM DISORDERS.

123

ELECTROLYTES: POTASSIUM


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MAJOR INTRACELLULAR CATION REGULATES INTRACELLULAR OSMOLALITY.

IMPORTANT IN NERVE CONDUCTION

REGULATES CARDIAC NERVE CONDUCTION AND

MUSCLE ACTIVITY IMPORTANT IN SKELETAL AND SMOOTH MUSCLE

FUNCTION

REQUIRES EXTRACELLULAR K+ LEVELS IN RANGE: 3.5-5mEq/L

EXCRETED PRIMARILY BY THE KIDNEY

REABSORBED IN PROXIMAL TUBULES/EXCRETED IN DISTALTUBULES

124

ELECTROLYTE IMBALANCE: POTASSIUM


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Potassium Homeostatic mechanisms Assist in regulation of intracellular osmolality

Promotes transmission & conduction of nerve impulses &contraction of skeletal, cardiac and smooth muscles

Promotes enzyme action for cellular metabolism

Promotes glycogen storage in live

Assist with maintenance of acid base balance

125


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ELECTROLYTE IMBALANCES:

POTASSIUM DEFICIT


127/184

POTASSIUM DEFICIT

HYPOKALEMIA: S/S

Musculoskeletal S/S

Muscle weakness, paralysis, leg cramps muscle

flabbiness

Slowed smooth and skeletal muscle contraction

127


POTASSIUM DEFICIT


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POTASSIUM DEFICIT

Hypokalemia contd Cardiovascular S/S

Dysrhythmias,

Vertigo

Postural hypotension

Flattened T wave, prominent U wave

Slow weak pulse

Increase in cell excitability; prolongation of myocardial

repolarization Dysrhythmias more pronounced when taking digitalis

128


POTASSIUM DEFICIT


129/184

POTASSIUM DEFICIT

Hypokalemia contd Respiratory S/S

Shallow respirations

SOB Weakness of respiratory muscles due to a decrease in muscle

contractions

129

ELECTROLYTE IMBALANCES: POTASSIUM

DEFICIT: Hypokalemia


130/184

DEFICIT: Hypokalemia

Neurologic S/S Fatigue, lethargy, decreased tendon reflexes,

confusion, depression

Decreased transmission and conduction of nerve

impulses Renal S/S

Polyuria, decreased serum osmolality, nocturia

Inhibition of kidneys ability to concentrate urine

Hypokalemia medical management Determine and correct cause/replacement

130

ELECTROLYTE IMBALANCES: POTASSIUM

DEFICIT:TREATMENT


131/184

DEFICIT:TREATMENT

RX DEPENDS ON K+ level and PT. S/S SEVERE hypokalemia cardiac monitoring

Pharmacologic Management

Oral supplement K= 3.3 -3.5 preventive purposes

Liquid, powder, tablet

Very irritating to gastric mucosa

Given with glass of glass water or juice & with meals

IV for moderate or severe K+ deficit

Not given IM and never IV PUSH

always diluted in IV fluids

K+ runs 10 to 20 mEq/hr in 100 cc IVF

Patient must be on a cardiac monitor

131

ELECTROLYTE IMBALANCES: HYPOKALEMIA:

TREATMENT


132/184

TREATMENT

Recommended 20 40 mEq K+ mixed in Liter of IVfluid mild to moderate hypoK+

Severe 40 80 mEq / L

High K+ concentrations very irritating to heart muscle

deficit may take several days to correct; also veryirritating to peripheral veins

NPO Need 40 mEq per day

hypoK+ slight peaked P wave, slightly prolonged PRinterval, ST depression and prolongation, DepressedT wave or inverted, prominent U wave following theT-wave

132

NURSING MANAGEMENT: HYPOKALEMIA


133/184

Assessment Focus on data collection r/t

Health problems

Clinical manifestations

Lab findings

Detailed history to ascertain cause of


134/184

Planning: Goal: Pt. will exhibit signs ofelectrolyte balance AEB

serum K+ WNL

Absence of Dysrhythmias

Pulse of normal range and strength

Absence of neurological deficits

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Implementation IV K + diluted in IV fluid on IV pump at controlled rate

Large loading IV dose cardiac arrest never IVP

Assess venous siteirritating phlebitis

Monitor K+ serum level

Auscultate bowel sounds; monitor bowel function ileus

Apical pulse especially on Digitalis dig. Toxicityassess

for Dysrhythmias

Renal function: intake and output

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Dietary management Foods high in K+

Prevention of further loss

Correction of problem

Need 1875-5625 mg daily due to loss through kidneys

and remainder in feces

Vegetables broccoli, cabbage, greens, mushrooms,

tomatoes, baked potato with skin

Fruits, apricots, banana, cantaloupe, honeydew,

orange, prunes, strawberries, watermelon

136

DIETARY MANAGEMENT CONT.


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Beverages Coffee

Tomato juice

Juice cocktail unsalted

Foods low in K+

Corn

Sweet potato

Lima beans

Fried potatoes

Beverages low in K+

Instant coffee, cola, cranberry juice cocktail, ginger ale, non-carbonated drinks, root beer, lemon lime soda

137

NURSING MANAGEMENT


138/184

Alteration in nutrition less than body requirement r/t insufficient intake of K+rich foods

Planning

GOAL: Remain free of injury

INTERVENTION: Safety measures

Bed low position, side rails up, Wear shoes to prevent slipping

Ambulation belt to be used by nurse

Restraints if absolutely needed

Instruction on foods high in K+

Taking supplement take with meals and with at least glasswater or juice

138

NURSING MANAGEMENT


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Patient Teaching Foods high in K+

Prolonged cooking result in K+ and vitamin

loss Steam or cook quickly.

Level over 5.0 to 5.5

rare in those with normal kidney function

K+ excreted in urine

139

HYPERKALEMIA


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Severe trauma K+ leaves the intracellular space i.e.burns, crushing injuries develop hyperkalemia

Presence of shock compounds problem lowcirculating vascular fluids & decreased kidney

function hyperkalemia

Hyperkalemia clinical manifestation andpathophysiologic base

Decreases the cell membranes threshold calling the cell tobecome more excitable

140

HYPERKALEMIA


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PATHOPHYSIOLOGY AND S/S Cardiovascular S/S

First tachycardia and then Bradycardia

Disturbances in cardiac conduction the Purkinje fibers &

atrioventricular node which can lead to ectopic beats;prolonged diastole

EKG changes: peaked narrow T waves; wide QRS complex;depressed St segment; widened PR interval

Hypotension

Weaker cardiac contraction Cardiac arrest with severe K+ elevation

141

HYPERKALEMIA


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PATHO CONT. GI S/S

N/V, explosive diarrhea, intestinal colic, hyperactive bowel soundsespecially over splenic flexure

Increased smooth muscle contractions; increased peristalsis

Neuromuscular S/S Paresthesiatingling sensation; muscle weakness and later flaccid

muscle paralysis

Muscle cramps

Increased neuromuscular irritability of skeletal muscles; muscles become

weaker from depolarization block in the muscle

142

HYPERKALEMIA


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PATHO CONT.

Renal S/S

Oliguria and later anuria

Usually due to preexisting renal dysfunction;

Labs K+ over 5.0

Serum osmolality > 295

Oliguria or anuria causes accumulation of K+ & other solutesincreasing osmolality of body fluids

Serum creatinine > 1.5 and BUN >2.5

Oliguria or anuria causes elevation of those in Intravascular fluids

143

HYPERKALEMIA


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Etiology and clinical conditions associatedwith hyperkalemia

K+ retention

Renal insufficiency, renal failure, decreased urineoutput post op., adrenal insufficiency, Addisons

disease, hypoaldosteronism, K+ sparing diuretics, blood

for transfusion that is more than 2 weeks old

(hemolysis) releases intracellular K+ into surrounding

fluids

144

HYPERKALEMIA


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Excessive release of cellular K+ into the blood Severe traumatic injuries, crushing injuries. Burns,

severe infection, metabolic acidosis, after open

heart surgery or surgery requiring a perfusion

pump

Exc. IV fluids or oral K

145

Medical management HYPERKALEMIA


146/184

Dietary restriction If due to metabolic acidosis correction with sodium

bicarbonate promotes K+ movement into cells

Improving urine outputdiuretic

Severe IV calcium gluconate to decrease antagonistic effect of K+

on heart

Infusion of insulin and glucose or Na-bicarb. To promote K+up into cells

Repeating measures may be necessary

146

Medical management HYPERKALEMIA


147/184

Cation exchange resin polystyrene sulfonate(Kayexalate) with sorbitol to stimulate

diarrhea orally or rectally

Stimulates the exchange of K+ ions for Na+ inthe intestinal tract; K+ excreted n stool

Marked renal failure peritoneal dialysis or

hemodialysis

147

NURSING MANAGEMENT

HYPERKALEMIA


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HYPERKALEMIA

Focuses on clinical manifestations of and lab findings Asses UO if receiving K+ preparations

Report decrease in urine output

Monitor levels in high risk patient

Greater than 7.0 cardiac disturbances

Ekg strips needed to assess for abnormalities Monitor IV fluids with K+

Symptoms of K+ excess

IV site for irritation vein & subq. Tissue irritation

Phlebitis and infiltration into subcutaneous tissues Can cause sloughingand tissue necrosis

148

NURSING MANAGEMENT

HYPERKALEMIA


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HYPERKALEMIA

Numbness & tingling of extremities early signs

Muscle weakness and flaccid muscle paralysis with

more severe hyperkalemia

Urine output less than 25 cc/h or less than

600cc/day report immediately

If receive blood transfusion and at risk for

hyperkalemia notify blood bank so that blood more

than 2 weeks old not given for the patient

149

NURSING MANAGEMENT

HYPERKALEMIA


150/184

HYPERKALEMIA

Patient Education Adhere to diet low in K+

Knowledge of food preparation important as

cooking styles can affect K+ levels

150

ELECTROLYTES IMBALANCES: CALCIUM


151/184

Extracellular & intracellular cation Normal range 4.5 to 5.5 mEq/L or 9-11mg/dL

99% in bone and teeth

Other 1% in tissue and intravascular fluid which is boundto protein mostly albumin and remaining one half % is free

ionized Ca++ Albumin low may give a false normal serum Ca+ level

Ionized Ca+ can be used to determine Ca++ deficit orexcess in critically ill

Ca++ FUNCTIONS Promotes coagulation of blood in all phases but mostly the

prothrombin to thrombin phase

151

CALCIUM


152/184

CALCIUM

Functions cont. Catalyst in transmission & conduction of nerve impulses &

stimulates skeletal smooth muscles and cardiac muscles.

Maintains normal cellular permeability

Increased Ca++ levels decrease cellular permeabilityand decrease Ca++ level increase cellular permeability

Promotes absorption & utilization of vitamin B 1

Excreted in urine & feces

152

CALCIUM


153/184

Disorders that cause CALCIUM IMBALANCE Renal failure with hyper-phosphatemia, acute pancreatitis

(which causes release of lipases into soft tissue spaces, so

that free fatty acids are formed bind with Ca++)

Burns, Cushings disease, hypoparathyroidism, liverdisease, removal parathyroid glands

Medications

Magnesium sulfate, colchicine, neomycin inhibits

parathyroid hormone secretion, aspirin, anticonvulsants,estrogen alter Vit. D metabolism, loop diuretics reduce Ca++

absorption from renal tubules, antacids & laxatives decrease

Ca++ absorption

153

CALCIUM


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CAUSES CONT. Vitamin D promotes Ca++ absorption from GI Tract where phosphorus

inhibits its absorption counterbalance each other

hypocalcaemia

Less than 4.5 mEq/L or 8.5 mg/dL

Common & potentially serious imbalance in children & elderly

Over correction of acidosis can lead to hypocalcemia because toomuch Ca++ bound to protein

Causes of Hypocalcemia Dietary changes

Inadequate Ca++ intake, Vitamin D deficiency or both; excess intake ofphosphorous combines with Ca++ so neither is absorbed

154

HYPOCALCEMIA


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PATHOPHYSIOLOGY GI changes

Malabsorption of fat in intestine

Calcium binding

Metabolic alkalosis because of less ionized Ca++;

multiple transfusions of stored blood which is

combined with citrate for storage

155

HYPOCALCEMIA


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Pathophysiology - hypocalcemia Lack of PTH

Inactivity of osteoclasts and consequent fall in serum Ca++

Nerve fibers more excitable & can discharge spontaneously causingmuscle twitching , spasms and tetany

Laryngeal spasm interfere with respirations

Bone stimulated to release Ca+ -- bone becomesosteoporotic and subject to fracture

Increases capillary permeability; neuromuscular excitabilityof skeletal, smooth, and cardiac muscles and decreases

blood coagulation If untreated seizures & death can occur

156

HYPOCALCEMIA


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PATHO SIGNS/SYMPTOMS Neuromuscular S/S

Tetany symptoms: twitching around mouth, tingling

and numbness of fingers; carpopedal spasms, facial &

laryngospasm and later convulsions

Increased neuromuscular excitability/irritability

producing hyperactivity of motor and sensory nerves

Presence of Trousseaus & CHVOSTEKS SIGN

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HYPOCALCEMIA


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Respiratory S/S Dyspnea, laryngeal spasm

Increased nerve conduction

GI S/S Increased peristalsis, diarrhea

Decreased Ca++ absorption in GI tract increases

smooth muscle contraction

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HYPOCALCEMIA


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Cardiovascular S/S Dysrhythmias, palpitations

Increased cell excitability

Musculoskeletal S/S

Pathologic fractures

Ca++ loss from bone * osteoporosis causing brittle bones

Hematologic S/S

Prolonged bleeding time

Intrinsic pathway for blood coagulation inhibition

159

MEDICAL MANAGEMENT

HYPOCALCEMIA


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Pharmacologic management Asymptomatic

Corrected with oral CA++ gluconate, calcium lactate or

calcium chloride

Best administered 30 minutes before meals for better

absorption and with a glass of milk because Vit D

needed for absorption of CA++ from intestines

160

MEDICAL MANAGEMENT:

HYPOCALCEMIA


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HYPOCALCEMIA Acute hypocalcemia with tetany - immediate correction

IV CA++ chloride or gluconate 10% given slowly to avoid hypotension,Bradycardia, and other arrhythmias

Usually diluted in liter of D-5-w

Saline solutions not used- Na+ tends to promote Ca++ loss

Dietary management Chronic or mild

Diet high in Ca++

If due to PT deficiency Avoid high phosphate foods

milk & milk products

Carbonated beverages

Maintenance Ca++ and Vit. D. supplements

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HYPERCALCEMIA


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Hypercalcemia Serum level over 5l5mEq or 11 mg/dL

3 common causes:

Metastatic malignancy

Certain ones will cause bone destruction from metastasis or

increase secretion of ectopic PTH Hyperparathyroidism

Thiazide diuretic therapy

Other causes

Prolonged immobilization

Excessive intake of Ca++ supplements and Vit D Ca++ containing antacids

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HYPERCALCEMIA


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Hypercalcemic Crisis Serum level reaching 15 mg/dL

Cardiac Dysrhythmias widened T wave and short QT

interval

Hypokalemia as body wasting K+ rather than Ca++

Usual tx- hydration about 200 250 cc/h

LITHIUM

Dironel therapy

Designed to lower Ca++ in 36 to 48 hours

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HYPERCALCEMIA


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Clinical manifestations Determined by level but in general are non specific

Mild near 11.5 mg/dL or 5.5mEq/L May increase momentarily when consumes ca++ containing

antacids

Large dose of oral Ca++ supplement

Kidney initially unable to eliminate excess Moderate 13 mg/dL or 6.2 mEq/L

Anorexia, N/V, Polyuria, fatigue, lethargy, dehydration

Slowed GI transit time

Severe lethargic, confused, coma may result & some

complain of deep bone pain

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HYPERCALCEMIA


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Neuromuscular S/S Mild to moderate

Weakness, fatigue, depression, difficulty concentrating Neurologic depression

Severe lethargy, depressed sensorium, confusion, coma

Cardiovascular S/S Dysrhythmias, heart block, EKG changes, lengthened QT

interval

dig toxicity

Critical - cardiac arrest

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HYPERCALCEMIA


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Renal S/S Polyuria. Kidney stones, renal failure

Decreases Glomerular filtration rate; causes osmotic

diuresis & volume depletion; reduces kidneys ability to

concentrate urine RESULTING in Polyuria

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HYPERCALCEMIA


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Musculoskeletal S/S Bone pain, fracture

Metastatic cancer causes bone pain, decalcification of bones osteoporosis andspontaneous fractures

Pharmacologic management IV normal saline rapidly with furosemide to prevent fluid overload promote urinary

Ca++ excretion

Antitumor antibiotics Mithramycin inhibit action of PTH on osteoclasts and reduction of decalcification

Calcitonin inhibits effects of PTH

Corticosteroid competing with vitamin D resulting in decr4ased intestinalabsorption

IV phosphate decrease Ca++ serum level Avoid usage or in reduced dosage of Ca++, Vit. D or Ca++ containing antacids

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HYPERCALCEMIA


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Surgical TREATMENT Remove an ectopic PTH secreting tumors

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Nursing management HYPERCALCEMIA


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Assessment Vital signs

EKG q 4-6 hours

Telemetry monitoring

Presence of Dysrhythmias

Changes in sensorium

Bowel sounds

Serum CALCIUM levels monitored

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NURSING MANAGEMENT:

HYPERCALCEMIA


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Fluid intake increased unless contraindicated Acidash foods & fluids that contain acid

Cranberry & prune juices

Strain urine stone

Caution with mobilization to reduce fractures risk

Caution / education with use of antacids Ca++ free antacids

High fiber foods to reduce constipation

Increase na+ intake unless contraindicated promotes ca++excretion per kidney

Safety when confused, lethargic or comatose

170

NURSING MANAGEMENT:

HYPERCALCEMIA


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Turn & move with caution Have adequate assistance to prevent fractures

Use turn sheet

Back braces, tripod cane, walker to facilitatesafe ambulation

Bed in low position, side rails up

Report clinical manifestations of fracturesimmediately

171

MAGNESIUM


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Magnesium 2nd most abundant intracellular cation

Actions & clinical manifestations of imbalances similar toK+

Absorbed by small intestine

Excreted in urine

Transmits and conducts nerve impulses and contractionsof skeletal, smooth & cardiac muscle

Responsible for transportation of Na+, K+ and protein and

activates enzymes necessary for metabolism of CHO andprotein

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MAGNESIUM


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Functions Promotes vasodilation of peripheral arteries and arterioles

Increased Ca+ or Phosphorus intake can decrease

magnesium absorption from small intestines

A low Ca+ level increases level of Mg+ due to increasedabsorption

It inhibits PTH secretion resulting in < in amount of Ca++

released from bone promoting a ca+ deficit

Used to decrease Dysrhythmias especially digoxin inducedventricular arrhythmia

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MAGNESIUM


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Hypomagnesemia Commonly Overlooked not routinely diagnosed until severe

Risk factors

Inadequate intake of foods containing Mg++

Severe or chronic malnutrition

Alcoholism

Prolonged IV or hyperalimentation therapy without Mg++replacement

Leads to increased transmission of action potentials fromincreased release of acetylcholine

Can cause cardiac Dysrhythmias, irritability and neuromuscularchange such as tetany, and convulsions

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HYPOMAGNESEMIA


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RISK

Alcoholism with liver disease decreases intestinal absorption as theenzymes need for absorption are decreased

Excess phosphorus in intestine usually from antacids inhibit uptakefrom intestinal villi

Also at risk are losses of fluids from GI tract

Draining fistulas

Laxative abuse

Hyperthyroidism

Prolonged diuretic therapy Diuresis phase of acute renal failure

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HYPOMAGNESEMIA


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Drugs interfere with renal handling of Mg++ Diuretics

Lasix

Osmotic diuretic

thiazide diuretics Aminoglycoside antibiotics

Gentamicin, tobramycin

Amphotericin B.

Corticosteroids digitalis

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HYPOMAGNESEMIA


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Neuromuscular S/S Positive Chvosteks & Trousseaus signs

Tetany

Convulsions PVCs

Atrial or ventricular fibrillation

Causes hypokalemia interferes with Na+ & K+ pump

Inhibits PTH hypocalcemia can occur

177

MEDICAL MANAGEMENT

HYPOMAGNESEMIA


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Oral magnesium replacement in form of magnesiumcontaining antacids

Parenteral magnesium sulfate in IV fluid

Increase dietary intake of Mg ++

Vital signs Ekg q 4-6 hours

Telemetry

Report tachycardia and arrhythmias

Monitor Mg++, K+ and Ca++ levels

Protection from harm with constant monitoring

178

NURSING MANAGEMENT

HYPOMAGNESEMIA


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Monitor replacement closely

Slowly administer magnesium diluted in IV solution usingan IV pump

Rapid infusion can cause hot or flushed feeling

Monitor urine output; notify MD if less than 30ml/hr.

for 2 consecutive hours Teach foods rich in magnesium to correct mild deficit

Cashews

Chili with beans

Halibut

Tofu

Wheat germ toasted

Green leafy vegetables

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HYPERMAGNESEMIA


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HYPERMAGNESEMIA = EXCESSIVE AMOUNTS OF MAGNESIUM INTHE SERUM

CAUSES: RENAL FAILURE, EXCESSIVE INTAKE

SIGNS/SYMPTOMS: DEPRESSED DEEP TENDON RELFEXES, 2.5 mEq./L

UNLIKELY TO OCCUR IN THE PRESENCE OF NORMAL RENALFUNCTION

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QUESTIONS


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1. WOULD DEHYDRATION CAUSE AN INCREASE OR DECREASE IN ADH SECRETION?

2. WHEN A PERSONS BLOOD PRESSURE DROPS, THE KIDNEYS RESPOND BY A. SECRETING RENIN

B. PRODUCING ALDOSTERONE

C. SLOWING THE RELEASE OF ADH

3. The nurse encourages the patient who has been vomiting to drink fluids because, to maintain homeostasis, the body fluid

lost daily must match the amount of fluid taken in. This amount in an adult is about

1. 1000 ml.

2. 1500 ml.

3. 2050 ml.

4. 2500 ml.

Daily water intake and output is about 2500 ml the adult.

4. The nurse makes a point to weigh the patient at the same time of day with the same scale and same clothing as a simple

and accurate method of determining

1.an accurate weight.

2.water balance. 3.adequate nutrition.

4.urinary output.

A simple and accurate method of determining water balance is to weigh the patient under the same conditions each day.

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QUESTIONS CONTD


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5. The nurse explains to the patient that the drug Lasix will reduce his edema by drawing water from the interstitial space

into the intravascular space. This process is called 1.diffusion.

2.filtration.

3.osmosis.

4.homeostasis.

Osmosis is the movement of water from an area of lower concentration to an area of higher

6. As the nurse assesses the edematous cardiac patient, she is aware the condition is a result of retained fluid and the

patient is

1.hyponatremic.

2.hypokalemic.

3.hypernatremic.

4.hypercalcemic.

Hypernatremia is a greater-than-normal concentration of sodium, which leads to retained fluids and edema.

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QUESTIONS CONTD


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7. When the nurse assesses a calcium level of 6.2, she modifies the care plan for the immobilized patient to include

observation for possible 1.osteoporosis.

2.tooth loss.

3.renal calculi.

4.contractures.

Renal calculi may develop because of the excretion of high levels of calcium. Immobilized patients are especially prone to

this problem.

8. The nurse concludes there is no need for further instruction relative to the selection of foods with a high potassium

content when the patient chooses

1.apples and green beans.

2.kiwis and onions.

3. apricots and asparagus.

4.grapes and lima beans.

Apricots and asparagus are potassium-rich.

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ANSWERS


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Fluids and Electrolytes Fa 2010

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