FLUIDS AND ELECTROLYTES

CH.14

GLORIA PHILLIPS, RN

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

TERMINOLOGY
1. 2. 3. 4. 5. 6. 7. 8. HYDROSTATIC PRESSURE HYPOVOLEMIA ISOTONIC TROUSSEAUS SIGN CHVOSTEKS SIGN FLUID VOLUME EXCESS ACTIVE TRANSPORT 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

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?

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 MAINAIN BALANCE

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:

ELECTROLYTE CONCENTRATION
MEASURED IN MILLI-EQUIVALENTS (mEq.) PER LITER OF FLUID NUMBERS OF POSITIVE AND NEGATIVE IONS ARE EQUAL 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 OF SOLUTE, BASED ON A CERTAIN WEIGHT OF SOLUTE

 OSMOLARITY = OSMOTIC PRESSURE (PULLING POWER OF WATER) OF A SOLUTION EXPRESSED AS OSMOLS 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 YEILD 1000ML. OF SOLUTION USED INTERCHANGEABLY WITH OSMOLALITY; NOT EXACTLY THE SAME

ELECTROLYTE CONCENTRATION CONTINUED

TYPES OF SOLUTIONS
ISOTONIC SOLUTIONS = SAME OSMOLALITY AS BLOOD (0.9% NACL) HYPER-OSMOLARSOLUTIONS: EXCESS SOLUTE IN 1000ML; MORE SOLUTE THAN BLOOD; PULLS H20 OUT OF THE CELLS; SHRIVELS CELLS (3% NACL) HYPO-OSMOLAR SOLUTIONS: LESS THAN NORMAL AMOUNTS OF SOLUTE/1000ML; LESS SOLUTE THAN BLOOD; WATER IS PULLED INTO THE CELLS(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 EXTERNAL TEMPERATURE, HUMIDITY, METABOLIC RATE, PHYSICAL ACTIVITY INTAKE: CONTROLLED BY THIRST
> SERUM OSMOLALITY STIMULATES OSMORECEPTORS IN THE HYPOTHALMUS, TRIGGERING FLUID INTAKE HYPOTHALMUS STIMULATES POST. PITUITARY TO RELEASE ADH RESULTING IN RETENTION OF WATER BY THE 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 IN BOWMANS 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 AND SECRETION OF ADH RESULTING IN > RENAL EXCRETION OF NA+ AND WATER (<CBV,<BP, > U/O)

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OTHER FACTORS INFLUENCING OUTPUT

< IN CELL SIZE (DEHYDRATION) STIMULATES OSMORECEPTORS IN THE HYPOTHALMUS TO TRIGGER RELEASE OF ADH FROM THE PITUITARY (water retention) > IN CELL SIZE (EDEMA OR SWELLING OF CELLS) CAUSES < IN ADH SECRETION OTHER CONTRIBUTING FACTORS WHICH >ADH SECRETION
NARCOTICS, STRESS, ANESTHESIA, HEAT, NICOTINE, ANTINEOPLASTIC DRUGS, ANGIOTENSIN (A POTENT VASOCONSTRICTOR)

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RENIN-ANGIOTENSINALDOSTERONE SYSTEM
ALDOSTERONE: PRODUCED IN ADRENAL CORTEX; CAUSES > RENAL REABSORPTION OF SODIUM (> K+ excretion) RENAL CELLS MONITOR NA+ LEVELS AND BLOOD VOLUME < CBV OR NA+ RESULTS IN RELEASE OF RENIN FROM THE JUXTAGLOMERULAR APPARATUS

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RAAS CONT.
RENIN STIMULATES CONVERSION OF ANGIOTENSIN I TO ANGIOITENSIN II ANGIOTENSIN II STIMULATES THE ADRENAL GLAND TO RELEASE ALDOSTERONE = NA+ RETENTION = INCREASED OSMOLALITY OF THE 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 INTERSTITIAL FLUID), 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 ICF COMPARTMENT
PROCESS
DIFFUSION: MOVEMENT OF SOLID PARTICLES ACROSS A MEMBRANE FROM A SOLUTION OF HIGHER CONCENTRATION TO SOLUTION OF LESSER CONCENTRATION OSMOSIS: MOVEMENT OF WATER ACROSS A MEMBRANE FROM A SOLUTION OF LESSER CONCENTRATION TO ONE OF GREATER CONCENTRATION FILTRATION: MOVEMENT OF SOLUTE AND WATER ACROSS A MEMBRANE 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 OF GREATER 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 into vascular 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 from fluid 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 on standing (postural hypotension)
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ECFVD:ISO-OSMOLAR
Iso-osmolar fluid loss = inadequate plasma volume due to proportional losses of
Na + 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 causing diuresis 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 range equal amounts of cells lost to plasma loss, Increased specific gravity 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 -- < 70 mm 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 usually whole 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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Nursing Management: Implementation 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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Nursing Management: Implementation 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 to measure 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 shifts Vascular fluid to interstitial space

Fluid shifts into interstitial space & remain there (consolidate) 3rd space fluid Occurs with tissue injury resulting from altered capillary permeability i.e. inflammation, traumatic injury & from increased 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 fluid compartment 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 from vascular to interstitial space similar to those of 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 to be limited because of fluid influx from tissue spaces INTO vessels If third space fluid is the result of other processes SUCH as pericarditits 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 of extremities & 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 injured spaces

3 5 days post-injury, fluid returns into circulation unless renal 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 of water

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 that increases water reabsorption from renal tubules Elderly who consume excessive amounts of tap water without adequate 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 force fluid movement from the lesser concentration in vessels to higher concentration in cells Too much hypo-osmolar fluid accumulates in cells 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 hypoosmolar 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 hypoosmolality < HCT hemodilution, ECFE often accompanied by ICF fluid excess

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ICFVE: MEDICAL MANAGEMENT

Addition of solutes to IV fluids D-5-0.45 helps correct ICFE when cause is water excess Juices, soft drinks given in addition to water and 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 & interstitial spaces Na+ & water retained in same proportion = isoosmolar fluid volume excess Serum Na+ level may be WNL even though actual sodium level is increased because of excess water retention

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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 post operatively
Decreasing salt intake Initiating medical treatment with digoxin or diuretics

Prevention

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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 venous pressure 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 increasing pressures; heart failure can result
Cirrhosis of liver serum protein & albumin levels <
Oncotic pressure decreased in vascular fluids resulting in less fluid reabsorption from tissue spaces resulting in peripheral edema and ascites

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ECFVE: ISO-OSMOLAR
Pathophysiology cont. Obstructed lymph channels Tissue oncotic pressure rises result edema Tissue Edema can also result from increased capillary permeability

Uncorrected CHF can lead to kidney & liver failure can be fatal Clinical manifestations of ECFVE
Respiratory
Constant, irritating cough Fluid accumulation in alveolar sacs from hypervolemia Dyspnea congestion in lungs Crackles in lungs alveoli congestion with fluid 2ndary to increased hydrostatic pressure Cyanosis late symptom of pulmonary edema from impaired oxygen transport * to capillaries being filled with fluid

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ECFVE : ISO-OSMOLAR
Clinical manifestations of ECFVE
Cardiovascular Neck vein engorgement in semi Fowlers position Fluid overload & delayed right sided heart emptying/filling Hand vein engorgement Peripheral vascular fluid overload Bounding pulse, elevated B/P- PV overload S 3 gallop Delayed ventricular filling & over-distention of ventricles from rapid filling during early diastole Pitting edema in lower extremities Osmotic pressure in venous end of capillary exceeds interstitial pressure and fluid cannot return to blood stream Sacral edema Dependent edema because sacrum in lowest place on the body Weight gain fluid retention for every 1 kg. gained, 1 liter fluid retained

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ECFVE
Clinical Manifestations Cont.
Neurologic
Change in LOC Malaise, confusion, headache Cerebral edema Labs: < serum osmolaltity < 275 Serum Na+ < 135 to > 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 diuretic prescribed to conserve K+ (lasix, aldosterone) Digitalis preparation (Lanoxin, Digoxin) increase force of myocardial contraction and slow heart 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 in semi-fowlers position; if the jugular veins still engorged, 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 and hypokalemia (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 >
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NURSING PROCESS: IMPLEMENTATION 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 regarding fluid restrictions

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NURSING PROCESS: IMPLEMENTATION

CONT.
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

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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

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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 drinks high in Na+ Weigh daily when edema is present; record weight Weight gain 2 pounds or > 2 consecutive days, notify MD and keep record for MD

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ELECTROLYTES: SODIUM
SODIUM FUNCTIONS: CONTROL AND REGULATION OF BODY FLUID MAJOR CATION IN EXTRACELLULAR FLUID CHLORIDE GOES WITH NA+: REABSORBED OR EXCRETED WORKS WITH K+ TO MAINTAIN ELECTROLYTE BALANCE USUAL SERUM RANGE: 135-145mEQ/L

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ELECTROLYTES: SODIUM
Sodium concentration in ECF assists in maintaining water balance Sodium Homeostatic Mechanisms
Sodium balance regulated by

Afferent & efferent mechanisms

Afferent sensing mechanisms in nerve endings recognize changes in Na+ intake & ECF volume by sensing increase or decrease in pressure These found in atria, carotid sinus, liver, kidneys
82

ELECTROLYTES: SODIUM regulation

Central nervous system receptors that respond to changes in Na+ 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 back into vessel

About 99% sodium thats filtered by glomerulus is reabsorbed by renal tubules Renal function impacts sodium homeostasis

83

ELECTROLYTES: SODIUM regulation

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 regulation

Kallikerin = proteins of high molecular weight & are produced 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

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

86

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
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 or irritability of membranes If hyponatremia and volume are not corrected, K+, Ca++, 88 Cl-, and bicarbonate imbalances can occur

HYPONATREMIA
Uncorrected hypo-volemia from hyponatremia results in shock from continued ECF volume loss Severe hyponatremia neurologic changes vary from confusion to convulsion and coma Hypervolemic hyponatremia if not corrected results in ECF volume excess and edema

89

HYPONATREMIA CONT.
PATHOPHYSIOLOGY AND S/S
Gastrointestinal
Nausea, vomiting, hyperactive bowel sounds, abdominal cramping Na+ abundant in GI tract; loss of GI secretions cause Na+ loss

90

HYPONATREMIA CONT.
Cardiovascular S/S
Decrease in diastolic blood pressure, tachycardia, profound orthostatic hypotension, weak pulse Loss of Na+ & water decrease circulating volume with shock like state Elevated SYSTOLIC B/P with full, rapid pulse EXCESSIVE CIRC. BLD. VOL. 2NDARY TO Dilutional hypo-natremia with excessive fluid volume

91

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 to stimuli

92

HYPONATREMIA CONT.
Integumentary S/S
Dry pale skin; Dry mucous membranes
Decreased interstitial fluids

93

 Lab findings

HYPONATREMIA CONT.

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.
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 the intracellular compartment

95

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
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

HYPONATREMIA TREATMENT
Pharmacologic Management
Normal saline in conjunction with diuretic to increase urinary Na+ loss and reduce risk of ECF volume expansion Urine excreted with Lasix-induced diuresis has much less Na than does the ECF which raises the urinary Na+ level Drug therapy for hypoNa+ from SIADH include agents that antagonize ADH demeclocycline and lithium
98

HYPONATREMIA TREATMENT
Dietary Management: Balanced diet for mild cases
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 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

HYPONATREMIA NURSING 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
101

HYPONATREMIA NURSING 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 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 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 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

105

ELECTROLYTE IMBALANCE: SODIUM EXCESS

Euvolemic hypernatremia CAUSES

Excess fluid losses from skin and lungs Hypodispia in elderly & infants Diabetes Insipidus Hypervolemic hypernatremia Administration of concentrated saline solutions; hypertonic feedings, excess mineral corticicoids, Accidental or intentional salt ingestion; commercially prepared soups and canned vegetables
Clinical manifestations and Patho-physiologic Bases
Gastrointestinal Anorexia, nausea, vomiting Fluid retention in gastric cells

106

ELECTROLYTE IMBALANCE: SODIUM 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, rigid paralysis in late stages Neuromuscular irritability
107

ELECTROLYTE IMBALANCE: SODIUM 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 dependent on fluid status Myocardial depression as Na+ ions compete with Ca++ ions in slow channels of heart

108

ELECTROLYTE IMBALANCE: SODIUM EXCESS

Renal S/S
Oliguria, dark, concentrated urine
Compensatory mechanism to conserve fluid

Lab values
Na+ > 145 Serum osmolality

109

Medical Management HYPERNATREMIA

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

110

Medical Management HYPERNATREMIA

GOAL: To decrease total body Na+ and replace fluid loss
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

111

Medical Management HYPERNATREMIA

Occ. NaCl used
Volume depleted person for fluid resuscitation Saline hypotonic in comparison with the serum and will allow the Na+ level to decrease slowly If serum Na+ lowered to fast, fluid will shift from vascular space into the cerebral cells causing cerebral edema General rule of thumb: water replacement should be administered to reduce Na+ levels not more than 2 mEq/L/hour for the first 48 hours

112

Medical Management HYPERNATREMIA

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

Assessment Assess for usual manifestations
Suspicion
Head injuries + others high risk

Medication history
Those with Na+

Cough medications Corticosteroids Dietary history Mucous membranes

114

Nursing management: HYPERNATREMIA

Nursing diagnosis: Alteration in fluid & electrolyte balance r/t decreased thirst or excessive administration of salt solutions or impaired secretion of Na+ and water

115

Nursing management: HYPERNATREMIA

Planning: goal: Pt will exhibit signs improved F & E balance AEB: absence of 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

116

Nursing management: HYPERNATREMIA

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

117

Nursing management: HYPERNATREMIA

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

118

Nursing management: HYPERNATREMIA

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

Nursing management: HYPERNATREMIA

PATIENT TEACHING
reinforce need for SODIUM restriction Avoid OTC drugs high in Na+ Recognize signs of hypo or hypernatremia

120

ELECTROLYTES: CHLORIDE
A MAJOR ANION IN ECF: BLOOD, LYMPH, INTERSTITIAL FLUID FUNCTION: MAINTAIN OSMOTIC PRESSURE OF BLOOD,BUFFER FOR O2-CO2 EXCHANGE IN RBCS, REGULATES ACIC-BASE BALANCE EACH NA+ ION IS ACCOMPANIED BY A CL- OR HCO3- ION USUAL RANGE: 95-105mEq/L

121

ELECTROLYTE IMBALANCE
HYPOCHLOREMIA
A DEFICIT IN SERUM CHLORIDE <95mEq/L CAUSES: EXCESS LOSSES THROUGH THE G I TRACT, KIDNEYS, OR SWEATING, FISTULA DRAINAGE, LOOP AND THIAZIDE DIURETICS, EXC. GASTRIC SUCTION S/S: MUSCLE TWITCHING, TREMORS OR TETANY; AT RISK FOR ALKALOSIS

122

ELECTROLYTE IMBALANCES
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 USUALLY DEVELOP WITH SODIUM DISORDERS.

123

ELECTROLYTES: POTASSIUM
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: 3.55mEq/L EXCRETED PRIMARILY BY THE KIDNEY REABSORBED IN PROXIMAL TUBULES/EXCRETED IN DISTAL TUBULES
124

ELECTROLYTE IMBALANCE: POTASSIUM

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

ELECTROLYTE IMBALANCES: POTASSIUM CONT.

Critical to remember
K+ deficit associated with alkalosis K+ excess associated with acidosis K+ levels affected by acid base imbalance Alkalosis can cause hypokalemia Hydrogen moves out of cells to correct alkalosis & K+ shifts into cells to lower serum K+ level In acidosis, reverse true, and K+ level rises Hormonal influence Insulin promotes K+ uptake by cells Insulin deficient patients frequently develop hyperkalemia Hypokalemia etiology and clinical disorders-pathophysiologic bases

Less than 3.5 mEq/L GI anorexia, vomiting, diarrhea, ileus, distention Slow smooth muscle contract
126

ELECTROLYTE IMBALANCES: POTASSIUM DEFICIT

HYPOKALEMIA: S/S
Musculoskeletal S/S
Muscle weakness, paralysis, leg cramps muscle flabbiness Slowed smooth and skeletal muscle contraction

127

ELECTROLYTE IMBALANCES: 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

ELECTROLYTE IMBALANCES: 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

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

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

Recommended 20 40 mEq K+ mixed in Liter of IV fluid 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 very irritating to peripheral veins NPO Need 40 mEq per day hypoK+ slight peaked P wave, slightly prolonged PR interval, ST depression and prolongation, Depressed T wave or inverted, prominent U wave following the T-wave
132

NURSING MANAGEMENT: HYPOKALEMIA

Assessment
Focus on data collection r/t

Health problems Clinical manifestations Lab findings Detailed history to ascertain cause of <K+ Dietary history Sources of K+ loss GI losses, drugs, etc

Assess cardiac, GI and neuromuscular changes Suspicion for those with NG suction, NPO without K+ supplement or have renal disease

133

NURSING MANAGEMENT: HYPOKALEMIA

Planning: Goal: Pt. will exhibit signs of electrolyte balance AEB
serum K+ WNL Absence of Dysrhythmias Pulse of normal range and strength Absence of neurological deficits

134

NURSING MANAGEMENT: HYPOKALEMIA

Implementation
IV K + diluted in IV fluid on IV pump at controlled rate
Large loading IV dose cardiac arrest never IVP

Assess venous site irritating 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

135

NURSING MANAGEMENT: HYPOKALEMIA

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.

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, noncarbonated drinks, root beer, lemon lime soda
137

NURSING MANAGEMENT
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 glass water or juice

138

NURSING MANAGEMENT
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
Severe trauma K+ leaves the intracellular space i.e. burns, crushing injuries develop hyperkalemia Presence of shock compounds problem low circulating vascular fluids & decreased kidney function
hyperkalemia

Hyperkalemia clinical manifestation and pathophysiologic base

Decreases the cell membranes threshold calling the cell to become more excitable

140

HYPERKALEMIA
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
PATHO CONT. GI S/S
N/V, explosive diarrhea, intestinal colic, hyperactive bowel sounds especially over splenic flexure Increased smooth muscle contractions; increased peristalsis

Neuromuscular S/S
Paresthesia tingling 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
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 solutes increasing osmolality of body fluids

Serum creatinine > 1.5 and BUN >2.5

Oliguria or anuria causes elevation of those in Intravascular fluids

143

HYPERKALEMIA
Etiology and clinical conditions associated with hyperkalemia
K+ retention
Renal insufficiency, renal failure, decreased urine output 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
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

Dietary restriction If due to metabolic acidosis correction with sodium bicarbonate promotes K+ movement into cells Improving urine output diuretic 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

Cation exchange resin polystyrene sulfonate (Kayexalate) with sorbitol to stimulate diarrhea orally or rectally Stimulates the exchange of K+ ions for Na+ in the intestinal tract; K+ excreted n stool Marked renal failure peritoneal dialysis or hemodialysis

147

NURSING MANAGEMENT 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 sloughing and tissue necrosis

148

NURSING MANAGEMENT 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

Patient Education
Adhere to diet low in K+ Knowledge of food preparation important as cooking styles can affect K+ levels

150

ELECTROLYTES IMBALANCES: CALCIUM

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 bound to 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 or excess in critically ill

Ca++ FUNCTIONS
Promotes coagulation of blood in all phases but mostly the prothrombin to thrombin phase
151

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 permeability and decrease Ca++ level increase cellular permeability Promotes absorption & utilization of vitamin B 1 Excreted in urine & feces

152

CALCIUM
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, liver disease, 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
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 too much Ca++ bound to protein

Causes of Hypocalcemia
Dietary changes Inadequate Ca++ intake, Vitamin D deficiency or both; excess intake of phosphorous combines with Ca++ so neither is absorbed

154

HYPOCALCEMIA
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
Pathophysiology - hypocalcemia
Lack of PTH
Inactivity of osteoclasts and consequent fall in serum Ca++
Nerve fibers more excitable & can discharge spontaneously causing muscle twitching , spasms and tetany Laryngeal spasm interfere with respirations

Bone stimulated to release Ca+ -- bone becomes osteoporotic and subject to fracture Increases capillary permeability; neuromuscular excitability of skeletal, smooth, and cardiac muscles and decreases blood coagulation If untreated seizures & death can occur

156

HYPOCALCEMIA
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

157

HYPOCALCEMIA
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

158

HYPOCALCEMIA
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

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 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

161

HYPERCALCEMIA
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

162

HYPERCALCEMIA
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

163

HYPERCALCEMIA
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

164

HYPERCALCEMIA
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

165

HYPERCALCEMIA
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

166

HYPERCALCEMIA
Musculoskeletal S/S
Bone pain, fracture
Metastatic cancer causes bone pain, decalcification of bones osteoporosis and spontaneous 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 intestinal absorption 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
Surgical TREATMENT
Remove an ectopic PTH secreting tumors

168

Nursing management HYPERCALCEMIA

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

Fluid intake increased unless contraindicated Acid ash 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

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NURSING MANAGEMENT: HYPERCALCEMIA

Turn & move with caution
Have adequate assistance to prevent fractures
Use turn sheet

Back braces, tripod cane, walker to facilitate safe ambulation Bed in low position, side rails up Report clinical manifestations of fractures immediately
171

MAGNESIUM
Magnesium
2nd most abundant intracellular cation Actions & clinical manifestations of imbalances similar to K+ Absorbed by small intestine Excreted in urine Transmits and conducts nerve impulses and contractions of skeletal, smooth & cardiac muscle Responsible for transportation of Na+, K+ and protein and activates enzymes necessary for metabolism of CHO and protein
172

MAGNESIUM
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 increased absorption It inhibits PTH secretion resulting in < in amount of Ca++ released from bone promoting a ca+ deficit Used to decrease Dysrhythmias especially digoxin induced ventricular arrhythmia
173

MAGNESIUM
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 from increased release of acetylcholine
Can cause cardiac Dysrhythmias, irritability and neuromuscular change such as tetany, and convulsions

174

HYPOMAGNESEMIA
RISK
Alcoholism with liver disease decreases intestinal absorption as the enzymes need for absorption are decreased Excess phosphorus in intestine usually from antacids inhibit uptake from 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

175

HYPOMAGNESEMIA
Drugs interfere with renal handling of Mg++
Diuretics
Lasix
Osmotic diuretic

thiazide diuretics

Aminoglycoside antibiotics
Gentamicin, tobramycin

Amphotericin B. Corticosteroids digitalis

176

HYPOMAGNESEMIA
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

Oral magnesium replacement in form of magnesium containing 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

Monitor replacement closely Slowly administer magnesium diluted in IV solution using an 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
179

HYPERMAGNESEMIA
HYPERMAGNESEMIA = EXCESSIVE AMOUNTS OF MAGNESIUM IN THE SERUM CAUSES: RENAL FAILURE, EXCESSIVE INTAKE SIGNS/SYMPTOMS: DEPRESSED DEEP TENDON RELFEXES, < RATE AND DEPTH OF RESPIRATION, HYPOTENSION, FLUSHING AND DEPRESSED GAG REFLEX LAB DATA: SERUM MG++ > 2.5 mEq./L
UNLIKELY TO OCCUR IN THE PRESENCE OF NORMAL RENAL FUNCTION

180

QUESTIONS
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. 181

QUESTIONS CONTD
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.

182

QUESTIONS CONTD
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
1 2 3 4 5 6 7
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