FLUIDS AND ELECTROLYTES

OBJECTIVES
After this lecture/discussion, the learner should be able to: 1. Describe the mechanisms that maintain fluid, electrolyte and acid-base balance. 2. Compare the mechanisms and effects of fluid deficit and excess. 3. Discuss the mechanisms and effects of deficits and excess. 4. Describe the mechanisms that maintain acid-base balance. 5. Differentiate between metabolic and respiratory acidosis and alkalosis. 6. Apply the pathophysiologic principles of acid-base balance to the interpretation of ABG measurements. 7. Analyze the components of ABGs to identify the type of acidbase balance. 8. Describe the causes and effects of each type of acid-base balance. 9. Use ABG findings in formulating the care of the patient with an acid-base imbalance. 10. Describe the management of patients with a fluid, electrolyte, or acid-base imbalance.

HOW IMPORTANT IS WATER? Between 50% and 60% of the human body by weight is water Water provides a medium for transporting nutrients to cells and wastes from cells and for transporting substances such as hormones, enzymes, blood platelets, and red and white blood cells Water facilitates cellular metabolism and proper cellular chemical functioning

Water acts as a solvent for electrolytes and nonelectrolytes

Helps maintain normal body temperature Facilitates digestion and promotes elimination Acts as a tissue lubricant

VARIATIONS IN FLUID CONTENT

BODY FAT
Because fat cells contain little water and lean tissue is rich in water, the more obese the person, the smaller the percentage of total body water compared with body weight. This is also true between sexes because females tend to have proportionally more body fat than males.

There is also an increase in fat cells in older people

VARIATIONS IN FLUID CONTENT

AGE

AVENUES BY WHICH WATER ENTERS AND LEAVES THE BODY

ANTIDIURETIC HORMONE REGULATION MECHANISMS

Osmolarity

Osmoreceptors in hypothalamus Hypothalamus Posterior pituitary gland ADH Kidney tubules H2O reabsorption vascular volume and osmolarity

Blood volume or BP

Volume receptor Atria and great veins

Narcotics, Stress, Anesthetic agents, Heat, Nicotine, Antineoplastic agents, Surgery

ALDOSTERONE-RENIN-ANGIOTENSIN SYSTEM
Serum Sodium Blood volume Juxtaglomerular cells-kidney RENIN Angiotensinogen in plasma Angiotensin I
Angiotensinconverting enzyme

Sodium resorption (H2O resorbed with sodium); Blood volume

Via vasoconstriction of arterial smooth muscle

Angiotensin II
Kidney tubules
ALDOSTERONE

Adrenal Cortex Intestine, sweat glands, Salivary glands

FLUID BALANCE
The desirable amount of fluid intake and loss in adults ranges from 1500 to 3500 mL each 24 hours. Ave= 2500 mL Normally INTAKE = OUTPUT

FLUID IMBALANCE
Changes in ECF volume = alterations in sodium balance Change in sodium/water ratio = either hypoosmolarity or hyperosmolarity Fluid excess or deficit = loss of fluid balance As with all clinical problems, the same pathophysiologic change is not of equal significance to all people For example, consider two persons who have the same viral syndrome with associated nausea and vomiting

FLUID DEFICIT/HYPOVOLEMIA
May occur as a result of:
Reduced fluid intake Loss of body fluids Sequestration (compartmentalizing) of body fluids

Pathophysiology and Clinical Manifestations

DECREASED FLUID VOLUME Stimulation of thirst center in hypothalamus

ADH Secretion Water resorption Urine Output

Renin-AngiotensinAldosterone System Activation Sodium and Water Resorption

Person complains of thirst

Urine specific gravity except with osmotic diuresis

Pathophysiology and Clinical Manifestations

UNTREATED FLUID VOLUME DEFICIT

Depletion of fluids available BODY TEMPERATURE Dry mucous membranes

Cells become unable to continue providing water to replace ECF losses Signs of circulatory collapse
blood pressure
heart rate respiratory rate

Difficulty with speech

Restlessness and Apprehension

Collaborative Care Management

Identification of vulnerable patients and risk factors: * Compromised mental state * Physical limitations * Disease states * Limited access to adequate food and fluids

Development of a plan of care

Ongoing assessment and detailed action plan of fluid and serum electrolyte balance. Factors such as medications (particularly diuretics), hyperventilation, fever, burns, diarrhea, and diabetes with appropriate referral

Collaboration with the nurse, patient, family members, and other health care providers for continued assessment and treatment of problems

Family members should be educated about the importance of fluid and nutrition intake

Collaborative Care Key Points

1 Liter of water = 1 kg of water by weight Fluid replacement are calculated according to this ratio plus 1.5 L to fulfill the current daily needs For example, JUAN, a one-year-old, lost 1 kg of water from diarrhea as weighed from his diaper over the last 24 hours. Therefore, since 1 kg=1 L, fluid replacement therapy for him will involve 1 L of fluids + 1500 L. Oral fluid resuscitation is preferable but if the patient is unable to tolerate fluids, IV Therapy may be ordered Vital signs should be assessed regularly Postural hypotension is common for postural persons with fluid volume deficit. How do we assess this? For example, in the care of LOIDA, a 31 year old with severe DHN, you take her blood pressure (130/80) and pulse (75) while shes lying down. Then you ask her to sit at the edge of bed. When you take her blood pressure again, you get 115/80 and when you take her pulse, you get 80. This is consistent with intravascular volume depletion. Daily weighing is also useful to monitor fluid and electrolyte balance Laboratory results should be reviewed for various fluid and electrolyte disturbances so that appropriate adjustments to therapy can be initiated

FLUID EXCESS/HYPERVOLEMIA
Psychiatric Disorders, SIADH, Certain head injuries Dietary Sodium Indiscretion Renal and endocrine disturbances, malignancies, adenomas Failure of renal or hormonal regulatory functions

Overhydration

Excessive Sodium Intake

FLUID VOLUME EXCESS/HYPERVOLEMIA

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

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

WHAT DO ELECTROLYTES DO?

 Controls and regulates volume of body fluids

Its concentration is the major determinant of ECF volume

Is the chief electrolyte of ECF Influence ICF Volume

Participates in the generation and transmission of nerve impulses

Is an essential electrolyte in the sodium-potassium pump RDA: not known precisely. 500 mg

Eliminated primarily by the kidneys, smaller in feces and perspiration

Salt intake affects sodium concentrations Sodium is conserved through reabsorption in the kidneys, a process stimulated by aldosterone Normal value: 135-145 mEq/L

HYPONATREMIA
Refers to the serum sodium concentration less than 135 mEq/L Common with thiazide diuretic use, but may also be seen with loop and potassium-sparing diuretics as well Occurs with marked sodium restriction, vomiting and diarrhea, SIADH, etc. The etiology may be mulfactorial May also occur postop due to temporary alteration in hypothalamic function, loss of GI fluids by vomiting or suction, or hydration with nonelectrolyte solutions Postoperative hyponatremia is a more serious complication in premenopausal women. The reasons behind this is unknown Therefore monitoring serum levels is critical and careful assessment for symptoms of hyponatremia is important for all postoperative patients

PATHOPHYSIOLOGY OF HYPONATREMIA
Sodium loss from the intravascular compartment Diffusion of water into the interstitial spaces Sodium in the interstitial space is diluted

Decreased osmolarity of ECF

Water moves into the cell as a result of sodium loss

Water moves into the cell as a result of sodium loss

Extracellular compartment is depleted of water

CLINICAL SYMPTOMS

CLINICAL MANIFESTATIONS OF HYPONATREMIA

Muscle Weakness

APATHY

Postural hypotension

Nausea and

Abdominal Cramps

Weight Loss

In severe hyponatremia: mental confusion, delirium, shock and coma

COLLABORATIVE CARE MANAGEMENT

General goal: correct sodium imbalance and restore normal fluid and electrolyte homeostasis Recognition of people at risk for hyponatremia is essential for its prevention: athletes, persons working in hot environments Salt is always replaced along with water Management includes educating vulnerable people to recognize signs and symptoms of sodium depletion and maintaining sufficient sodium and water intake to replace skin and insensible fluid loss Generally, an increased sodium and water intake provides adequate treatment Education as the importance of sodium and fluid balance and the rationale for prescription medications to ensure compliance Daily weight. MIO Monitoring of sodium levels to determine extent of replacement Generally, PNSS or PLRS is prescribed Too rapid restoration of sodium balance, hypertonic sodium solutions may provoke brain injury

HYPERNATREMIA
A serum sodium level above 145 mEq/L is termed hypernatremia May occur as a result of fluid deficit or sodium excess Frequently occurs with fluid imbalance Develops when an excess of sodium occurs without a proportional increase in body fluid or when water loss occurs without proportional loss of sodium Risk Factors: excess dietary or parenteral sodium intake, watery diarrhea, diabetes insipidus, damage to thirst center, too young, too old, those with physical or mental status compromise, and people with hypothalamic dysfunction

PATHOPHYSIOLOGY OF HYPERNATREMIA
Increased Sodium concentration in ECF Osmolarity rises Water leaves the cell by osmosis and enters the the extracellular compartments Dilution of fluids in ECF Cells are water depleted

CLINICAL SYMPTOMS
Suppression of aldosterone secretion Sodium is exreted in the urine

CLINICAL MANIFESTATIONS

Dry, sticky mucous membranes

Firm, rubbery tissue turgor

DEATH Tachycardia Manic excitement

COLLABORATIVE CARE MANAGEMENT

Recognition of risk factors: bedridden and debilitated patients, diabetes insipidus, fluid deprivation, the elderly and the very young A careful and accurate record of MIO permits quick recognition of negative fluid balance People with kidney failure, CHF, or increased aldosterone production may require dietary sodium intake restriction Usually, osmolar balance can be restored with oral fluids. If not, the parenteral route may be necessary Fluid resuscitation must be undertaken with particular caution in patients with compromised cardiac or renal function The nurse should closely monitor the patients response to fluids and be alert to symptoms of fluid overload

 Major cation of the ICF. Chief regulator of cellular enzyme activity and cellular water content The more K, the less Na. The less K, the more Na Plays a vital role in such processes such as transmission of electrical impulses, particularly in nerve, heart, skeletal, intestinal and lung tissue; CHON and CHO metabolism; and cellular building; and maintenance of cellular metabolism and excitation Assists in regulation of acid-base balance by cellular exchange with H RDA: not known precisely. 50-100 mEq

Sources: bananas, peaches, kiwi, figs, dates, apricots, oranges, prunes, melons, raisins, broccoli, and potatoes, meat, dairy products
Excreted primarily by the kidneys. No effective conserving mechanism Conserved by sodium pump and kidneys when levels are low Aldosterone triggers K excretion in urine Normal value: 3.5 5 mEq/L

CAUSES AND EFFECTS OF HYPOKALEMIA

Known as a low level of serum potassium, less than 3.5 mEq/L
Decreased Intake
Food and Fluids as in starvation Failure to replace GI losses

Increased Loss
Aldosterone Gastrointestinal losses Potassium-losing diuretics Loss from cells as in trauma, burns

Shift of Potassium into Cells

(No change in total body potassium)

HYPOKALEMIA
GI Tract Anorexia N&V Abdominal distention CNS Lethargy, Diminished deep-tendon reflexes, Confusion, Mental depression Muscles Weakness, Flaccid paralysis, Weakness of respiratory muscles, Respiratory arrest CV System Decrease in standing BP, Dysrhythmias, ECG changes, Myocardial damage, Cardiac arrest Kidneys Capacity to concentrate waste, water loss, thirst, kidney damage

PATHOPHYSIOLOGY OF HYPOKALEMIA

= Action Potential

Nerve and Muscle Activity

Low Extracellular K+

Increase in resting membrane potential

The cell becomes less excitable

Aldosterone is secreted Sodium is retained in the body through resorption by the kidney tubules Potassium is excreted
Use of certain diuretics such as thiazides and furosemide, and corticosteroids Increased urinary output

Loss of potassium in urine

COLLABORATIVE CARE MANAGEMENT

Being alert to the conditions that cause potassium depletion such as vomiting, diarrhea and diuretics, by monitoring the patient for early warning signs No more than 3 enemas without consulting a physician Education about the importance of adequate dietary intake of potassium In severe hypokalemia, a patient may die unless potassium is administered promptly The safest way to administer K is orally. When K is given IV, the rate of flow must be monitored closely and should be diluted. Should not exceed 20 mEq/hr If PO, taken with at least glass of water Cardiac monitoring is useful Potassium sparing diuretics such as triamterene, spironolactone, etc Symptoms of K depletion: muscle weakness, anorexia, nausea and vomiting = appropriate referral

CAUSES AND EFFECTS OF HYPERKALEMIA

Serum potassium level greater than 5.5 mEq/L
Excess Intake Decreased Loss Potassium-sparing diuretics; Renal failure; Adrenal insufficiency Shift of Potassium out of the Cells Extensive injuries, crushing injuries, metabolic acidosis

Dietary intake of excess of kidneys ability to excrete; Excess parenteral administration

HYPERKALEMIA
CNS Numbness, paresthesias CV System Conduction disturbance, ventricular fibrillation, Cardiac Arrest

GI Tract N&V Diarrhea, Colic

Muscles Early: irritability

Kidneys Oliguria leading to anuria

Late: weakness leading to flaccid paralysis

COLLABORATIVE CARE MANAGEMENT

Patients at risk should be identified: impaired renal function to avoid OTC, esp. NSAIDS which provoke hyperkalemia; and salt substitutes that are high in potassium Severity guides therapy Mild: Withholding provoking agent (i.e., K supp) Severe (>6 mEq/L: cation-exchange resin such as Kayexalate (act by exchanging the cations in the resin for the potassium in the intestine potassium is then excreted in the stool; Continuous cardiac monitoring Bowel function must be maintained if Kayexelate therapy is to be effective Potassium-wasting diuretics may be prescribed to promote further potassium loss. Dialysis for patients with renal failure to eliminate excess potassium Intravenous Ca Gluconate may be prescribed to counteract the cardiac effects of hyperkalemia Insulin infusions and IV NaCO3 may be used to promote intracellular uptake of K

 Most abundant electrolyte in the body. 99% in bones and teeth

Close link between calcium and phosphorus. High PO4, Low Ca

Necessary for nerve impulse transmission and blood clotting and is also a catalyst for muscle contraction and other cellular activities Needed for Vitamin B12 absorption and use Necessary for strong bones and teeth and thickness and strength of cell membranes RDA: 1g for adults. Higher for children and pregnant and lactating women according to body weight, older people, esp. post-menopausal Found in milk, cheese, and dried beans; some in meat and vegetables Use is stimulated by Vitamin D. Excreted in urine, feces, bile, digestive secretions, and perspiration Dec. serum calcium = PTH hormone release = calcium reabsorption Normal value 8.5 10.5 mg/dl

CAUSES AND EFFECTS OF HYPOCALCEMIA

Decreased Ionized Ca Excess Loss Inadequate Intake Dietary Deficit
Decrease in GI Tract and Bone Absorption

Large tranfusion with citrated blood

Kidney Disease Draining fistula

Magnesium
Calcitonin Vitamin D Parathyroid Hormone

HYPOCALCEMIA
CNS Tingling

Bones
Osteoporosis leading to Fractures

Other Abnormal deposits of calcium in body tissues

Muscles Muscle spasm

Cardiovascular System

convulsions

Tetany

Dysrhythmias

Cardiac arrest

PATHOPHYSIOLOGY OF HYPOCALCEMIA
Calcium ions are thought to line the pores of cell membranes, especially neurons Calcium and Sodium repel each other When serum calcium levels are low, this blocking effect is minimized When Sodium moves more easily into the cell, depolarization takes place more easily
Sodium Calcium

This results in increased excitability of the nervous system leading to muscle spasm, tingling sensations, and if severe, convulsions and tetany
Skeletal, smooth, and cardiac muscle functions are all affected by overstimulation

CLINICAL MANIFESTATIONS OF HYPOCALCEMIA

PAINFUL MUSCULAR SPASMS (TETANY) ESPECIALLY OF FEET AND HANDS (CARPOPEDAL SPASMS), MUSCLE TWITCHING AND CONVULSIONS MAY FOLLOW

TREATMENT

COMPLAINT OF NUMBNESS AND TINGLING OF EARS, NOSE, FINGERTIPS OR TOES

TESTS USED TO ELICIT SIGNS OF CALCIUM DEFICIENCY

COLLABORATIVE CARE MANAGEMENT

Identify risk factors: Inadequate calcium intake, excess calcium loss, Vitamin D deficiency, patients with poor diets Education about the importance of adequate calcium and Vitamin D intake Patients undergoing thyroid, parathyroid, and radical neck surgery are particularly vulnerable to hypocalcemia secondary to parathyroid hormone deficit Monitoring of serum calcium levels and correction of deficits Citrate is added to store blood to prevent coagulation. Citrate + Transfusion = Citrate+Calcium Normally, Liver + Citrate = Quick metabolism Preexisting calcium deficit/hepatic dysfunction/large amounts of BT very rapidly = hypocalcemia With acute hypocalcemia, Ca Gluconate is used + Continuous cardiac monitoring Mild Hypocalcemia: High calcium diet or oral calcium salts If PTH or Vit D Deficiency is the cause: aluminum hydroxide gel is used because when serum phosphate level rises, calcium level falls Complication: Bone demineralization Therefore, careful ambulation should be encouraged to minimize bone resorption

HYPERCALCEMIA: Serum concentration > 10mg/dL Causes and Effects

Loss from bones Excess Intake Calcium diet (esp. milk) Antacids containing calcium

Immobilization, Carcinoma with bone metastases, Multiple myeloma

Increase in factors Causing Mobilization from bone PTH, Vitamin D, steroid therapy

HYPERCALCEMIA
CNS Muscles Muscle fatigue, hypotonia

Kidneys Stones

Bones Bone pain

CV System Depressed activity

Kidney Damage

Deep-tendon reflexes Lethargy

Osteoporosis Fractures

GI motility

Dysrhythmias Cardiac Arrest

Coma

HOW IT HAPPENS
HYPERCALCEMIA DEPRESSED NERVE AND MUSCLE ACTIVITY DEEP TENDON REFLEXES MAY BE DECREASED OR ABSENT MYOCARDIAL FUNCTION IS ALTERED

CLINICAL MANIFESTATIONS OF HYPERCALCEMIA

Constipation

Cardiac Dysrhythmias

Nausea Decreased GI Motility Mental status changes: lethargy, confusion, memory loss

CLINICAL MANIFESTATIONS OF HYPERCALCEMIA

Calcium accumulates in the ECF and passes through the kidneys
Immobilization Bone Demineralization

Calcium Stones

Ca Precipitation

COLLABORATIVE CARE MANAGEMENT

Mild hypercalcemia: hydration and education about avoiding foods high in calcium or medications that promote calcium elevation Ambulation as appropriate; weight-bearing exercises as tolerated Trapeze, resistance devices Marked hypercalcemia: prevention of pathologic fractures, individualized plan of care Prevention of renal calculi: encourage oral fluids to prevent concentrated urine: 3000 to 4000 mL/day unless contraindicated Acid-ash fruit juices: cranberry juice and prune juice Severe hypercalcemia: medical emergency: continuous cardiac monitoring, hydration, IV furosemide, Calcitonin and/or plicamycin (mithramycin), q2 serum and urinary electrolytes

 Mostly found within body cells: heart, bone, nerve, and muscle tissues Second most important cation in the ICF, 2nd to K+ Functions: Metabolism of CHO and CHON, protein and DNA synthesis, DNA and RNA transcription, and translation of RNA, maintains normal intracellular levels of potassium, helps maintain electric activity in nervous tissue membranes and muscle membranes RDA: about 18-30 mEq; children require larger amounts Sources: vegetables, nuts, fish, whole grains, peas, and beans Absorbed in the intestines and excreted by the kidneys Plasma concentrations of magnesium range from 1.5 2.5 mEq/L, with about one third of that amount bound to plasma proteins

HYPOMAGNESEMIA: Serum level < 1.5 mEq/L

Usually coexists with hypokalemia and les often with hypocalcemia
Decreased Intake Prolonged malnutrition, Starvation Impaired absorption from GI Tract
Malabsorption syndrome, Alcohol Withdrawal Syndrome, Hypercalcemia, Diarrhea, Draining gastrointestinal fistula

Excessive Excretion Aldosterone, Conditions causing large losses of urine

HYPOMAGNESEMIA
Mental Changes Muscles Cramps, Spasticity, Tetany

CNS

CV System Tachycardia, Hypotension, Dysrhythmias

Agitation, Depression, Confusion

Convulsions, Paresthesias, Tremor, Ataxia

HYPOKALEMIA

PATHOPHYSIOLOGY OF HYPOMAGNESEMIA
Low serum magnesium level Increased acetylcholine release Increased neuromuscular irritability Increased sensitivity to acetylcholine at the myoneural junction

Diminished threshold of excitation for the motor nerve

Enhancement of myofibril contraction

PATHOPHYSIOLOGY OF HYPOMAGNESEMIA
High Serum Calcium Increased acetylcholine release Increased neuromuscular irritability Increased sensitivity to acetylcholine at the myoneural junction

Diminished threshold of excitation for the motor nerve

Enhancement of myofibril contraction

Excretion of Magnesium

High Serum Calcium

By the GI tract

PATHOPHYSIOLOGY OF HYPOMAGNESEMIA
MAGNESIUM INHIBITS TRANSPORT OF PTH DECREASE IN THE AMOUNT OF CALCIUM BEING RELEASED FROM THE BONE POSSIBLE CALCIUM DEFICIT

CLINICAL MANIFESTATIONS OF HYPOMAGNESEMIA

DEPRESSION
CONFUSION CRAMPS

TETANY

CONVULSIONS

COLLABORATIVE CARE MANAGEMENT

Recognition of people at risk: people taking loop diuretics and digoxin should be encouraged to eat foods rich in magnesium, such as fruits, vegetables, cereals, and milk Recognition of signs and symptoms of magnesium deficiency Magnesium is essential for potassium resorption, so if hypokalemia does not respond to potassium replacement, hypomagnesemia should be suspected Treatment of the underlying cause is the first consideration in hypomagnesemia Severe: parenteral magnesium replacement is indicated IV therapy: continuous cardiac monitoring Safety measures for patients with mental status changes

HYPERMAGNESEMIA: Serum Mg level 2.5 mEq/L

Seldom develops in the presence of normal renal function May occur as a result of Mg replacement May occur when MgSO4 is administered to prevent seizures resulting from eclampsia Careful monitoring is imperative

PATHOPHYSIOLOGY
Renal failure, Excessive IV infusion of magnesium, Decreased GI elimination and/or absorption, etc. Accummulation of Mg in the body Mg Level Rises Altered Electrical Conduction Diminishing of reflexes, drowsiness, lethargy Severe Respiratory Depression RESPIRATORY ARREST may occur Peripheral vasodilation Slowed heart rate and AV Block

Hypotension, flushing, and increased skin warmth

COLLABORATIVE CARE MANAGEMENT

Identification of patients at risk: those with impaired renal function to avoid OTC that contain magnesium such as Milk of Magnesia and some Mg-containing antacids Any patient receiving parenteral magnesium therapy should be assessed frequently for signs of hypermagnesemia Mild hypermagnesemia: withholding magnesium-containing medications may suffice Renal failure: dialysis Severe: may require treatment with calcium gluconate (10-20 mL of 10% Ca Gluconate administered over 10 minutes) If cardiorespiratory collapse is imminent, the patient may require temporary pacemaker and ventilator support

NURSING MANAGEMENT OF PATIENT WITH FLUID AND ELECTROLYTE IMBALANCES

Parameter_____Fluid Excess___
Behavior

Fluid Loss/Electrolyte Imbalance____

Tires easily; Change in behavior, confusion, apathy

Head, neck Upper GI Skin edematous

Facial edema, distended neck Headache, thirst, dry mucous membranes veins Anorexia, nausea, vomiting Warm, moist, taut, cool feeling Dry, decreased turgor where

Respiration Dyspnea, orthopnea, productive cough, moist breath sounds Circulation Loss of sensation in edematous areas, pallor, bounding pulse, hypotension increased blood pressure Abdomen Increased girth, fluid wave Elimination Constipation

Changes in rate and depth of respiration Pulse rate changes, dysrhythmia, postural

Distention, abdominal cramps Diarrhea, constipation Muscle weakness, tingling, tetany ,

Extremities Dependent edema, pitting discomfort from weight of bedclothes

Pitting edema

Refractory Edema

Dependent edema

LABORATORY VALUES
FLUID DEFICIT Hemoconcentration Hct, BUN, E+ levels
Urine Specific Gravity

FLUID EXCESS Hemodilution Hct, BUN, E+ levels

Urine Specific Gravity

Determined from analysis of patient data

Diagnostic Title 1 Possible Etiologic Factors

Deficient fluid volume Active fluid volume loss (hemorrhage, diarrhea, gastric intubation, wounds, diaphoresis), inadequate fluid intake, failure of regulatory mechanisms, sequestration of body fluids

Excess Fluid Volume Excess fluid intake, excess sodium intake, compromised regulatory processes

EXPECTED PATIENT OUTCOMES

1,2. Will maintain functional fluid volume as evidenced by adequate urinary output, stable weight, normal vital signs, normal urine specific gravity, moist mucus membranes, balanced intake and output, elastic skin prompt capillary refill, and absence of edema 2 Will verbalize understanding of treatment plan and causative factors that led to the imbalance

turgor,

1,2

Intake and Output Monitoring - Type and amount of fluid the patient has received and the route by which they were administered - Record of solid food intake. Gelatin or Popsicles are recorded as fluids - Ice chips are recorded by dividing the amount of chips by (60 mL of chips = 30 mL water) - Accurate output record and described by color, content, and odor (Normally, gastric contents are watery and pale yellow-green; they usually have a sour odor) - With acid-base balance upset, gastric secretions may have a fruity odor because of ketone bodies - Bile: thicker than gastric juice, dark green to brown, acrid odor, bitter taste when vomiting - NGT irrigation added to intake - Stools: difficult to estimate amount; consistency, color, and number of stools provide a reasonable estimate - Peritoneal or pleural fluid drainage is recorded as output as with its amount, color, and clarity - Character and volume of urine. Place signs and materials so that an accurate record of UO is

1,2

Intake and Output Monitoring - Evaluate and refer urine specific gravity as appropriate (normal value is 1.003 1.030). The implications are: High Dehydration Low SIADH, overhydration - Drainage, fluid aspirated from any body cavity must be measured. With dressings, fluid loss is the difference between the wet dressings and the dry weight of the dressing - Accurate recording of the temperature to help the physician determine how much fluid should be replaced 1,2 Daily Weight - Evaluate trends in weight (An increase in 1kg in weight is equal to the retention of 1L of fluid in an edematous patient) Considerations: - Daily weights early in the morning after voiding but before he or she has eaten or defecated

1 Replacement of Fluid and Electrolytes General Principles: - Either by oral intake (healthiest way), tube feeding, intravenous infusion, and/or total parenteral nutrition - Normal saline solution and plain water should also be given by slow drip to replace daily fluid loss - IV administration per doctors orders - Fluid replacement considerations: * Most effective when apportioned over 24 hr period (Better regulation, potential for calculi formation and subsequent renal damage, potential for circulatory overload which may cause in fluid and electrolyte shifts) * Administer concentrated solutions of Na, Glucose or protein because they require body fluids for dilution * Consider the size of the patient (small adult has less fluid in each compartment, especially in the intravascular compartment) - Promote oral intake as appropriate * Caution with coffee, tea, and some colas

* small amount at frequent intervals is more useful than a large amount presented less often * Always give consideration to cultural and aesthetic aspects of eating Give mouth care to a dehydrated patient before and after meals and before bedtime (Xerostomia may lead to disruption of tissues in the oral cavity) Avoid irritating foods Stimulation of saliva may be aided by hard candy or chewing gum or carboxymethylcellulose (artificial saliva) Keep lips moist and well lubricated Give salty broth or soda crackers for sodium replacement and tea or orange juice for potassium replacement as appropriate. Bananas, citrus fruits and juices, some fresh vegetables, coffee, and tea are relatively high in potassium and low in sodium. Milk, meat, eggs, and nuts are high in protein, sodium and potassium. Offer milk for patients with draining fistulas from any portion of the GI tract. Lactose intolerance is not necessarily a contraindication (Lactase enzyme preparations are available) Increase usual daily requirement of foods when losses must be restored, as tolerated

* Patients with cardiac and renal impairments are instructed to avoid foods containing high levels of sodium, potassium and bicarbonate - Administer replacement solutions through tube feeding as is * Either water, physiologic solution of NaCl, high protein liquids, or a regular diet can be blended, diluted and given by gavage * The water content in the tube feeding needs to be increased if: 1 the patient complains of thirst 2 the protein or electrolyte content of the tube feeding is high 3 the patient has fever or disease causing an increased metabolic rate 4 UO is concentrated 5 signs of water deficit develop - Administer parenteral fluids as necessary

* Types of solutions - D5W (hypotonic) is given short-term for hyponatremia - D5NSS may be given depending on the serum levels of sodium and vascular volume + KCl to meet normal intake needs and replace losses for hyponatremia - Dextrose 5% in 0.2% normal saline is generally used as a maintenance fluid - Dextrose 5% in normal saline is generally used as a replacement solution for losses caused by gastrointestinal drainage - PNSS is given primarily when large amounts of sodium have been lost and for patients with hyponatremia - LRS is also isotonic because it remains in the extracellular space - Fructose or 10-20% glucose in distilled water are hypertonic solutions and may partially meet body needs for CHOs - Dextran (commonly-used plasma expander) increases plasma volume by increasing oncotic pressure. May cause prolonged bleeding time and is CI in patients with renal failure, bleeding disorders, or severe CHF

* Administration - The rate should be regulated according to the patients needs and condition per doctors orders - Monitor UO carefully. Refer marked decreases! - Verify orders for potassium administration in patients with renal failure and untreated adrenal insufficiency - Usual rate for fluid loss replacement: 3ml/min - Recognize signs of pulmonary edema (bounding pulse, engorged peripheral veins, hoarseness, dyspnea, cough, and rales) that can result from IV rate - If infiltration occurs, the infusion should be stopped immediately and relocated. Peripheral IV sites are generally rotated every 72 hours - For dextran and other plasma expanders, observe for anaphylactic reaction (apprehension, dyspnea, wheezing, tightness of chest, angioedema, itching, hives and hypotension). If this happens, switch infusion to nonprotein solution and run at KVO rate, notify physician and monitor VS - Pronounced and continued thirst despite administration of fluids is not normal and should be reported (may indicate DM or hypercalcemia)

* Patient/Family Education - Include the signs and symptoms of water excess in discharge instructions - With drug therapy, instruct patient and family regarding correct method of administration, correct dose, and therapeutic and adverse effects - Instruct to read labels for nutritional content * For K restriction: avoid organ meats, fresh and dried fruits, and salt substitutes - Skin assessment and care, positioning techniques for patients with mobility restrictions

* Achievement of outcomes is successful in disturbances in fluid and electrolyte balance: 1 Maintains functional fluid volume level with adequate UO, VS within the patients normal limits, sp gr of urine within 1.003-1.035, moist mucous membranes, stable weight, Intake=output, elastic skin turgor, and no edema 2 States possible causes of imbalance and plan to prevent recurrence of imbalances 3 Reports a decrease or absence of symptoms causing discomfort

DRAWING ARTERIAL BLOOD GASES

ARTERIAL PUNCTURE

ALLENS TEST

NORMAL ACID-BASE BALANCE

Parameter Normal Value Definition and Implications
Partial pressure of oxygen in arterial blood (decreases with age) In adults < 60 years: 60-80 mmHg = mild hypoxemia 40-60 mmHg = moderate hypoxemia < 40 mmHg = severe hypoxemia Identifies whether there is acidemia or alkalemia: pH<7.35 = acidosis; pH>7.45 = alkalosis Partial pressure of CO2 in the arterial blood: PCO2<35 mmHg = respiratory alkalosis PCO2>45 mmHg = respiratory acidosis Estimated HCO3 concentration after fully oxygenated arterial blood has been equilibrated with CO2 at a PCO2 of 40 mmHg at 38C; eliminates the influence of respiration on the plasma HCO3 concentration

PaO2

80-100 Hg

pH

7.35-7.45

PaCO2

21-30 mmHg

Standard HCO3

22-26 mEq/L

BASIC REGULATION OF ACID-BASE BALANCE

CO2

H2O H2CO3 H+

HCO3

The lungs help control acid-base balance by blowing off or retaining CO2. The kidneys help regulate acid-base balance by excreting or retaining HCO3

TYPES OF ACID-BASE DISTURBANCES

Depression of the central nervous system, as evidenced by disorientation followed by coma

Overexcitability of the nervous system; muscles may go into a state of tetany and convulsioons

INTERPRETING ARTERIAL BLOOD GASES RESULTS

CONDITION ACIDOSIS NORMAL ALKALOSIS

Is the pH acidic or alkaline? Look at the pCO2. Is it normal or abnormal?

7.35-7.45

21-30

Look at the HCO3 level. Is it normal or abnormal?

Decide as to what may be the direct cause of the change in pH. pCO2 or HCO3? If PCO2, its respiratory, if HCO3, its metabolic

22-26

Look at the unrelated value. Decide whether or not compensation is happening

RESPIRATORY ACIDOSIS: CARBONIC ACID EXCESS

Damage to the respiratory center in the medulla, drug or narcotic use, obstruction of respiratory passages, respiratory and respiratory muscle disorders

Decrease in the rate of pulmonary ventilation

Increase in the concentration of CO2, carbonic acid, and hydrogen ions

RESPIRATORY ACIDOSIS

Potassium moves out of the cells

HYPERKALEMIA
VENTRICULAR FIBRILLATION

NURSING MANAGEMENT OF RESPIRATORY ACIDOSIS

ASSESSMENT * Health Hx: complaints of headache, confusion, lethargy, nausea, irritability, nausea, irritability, anxiety, dyspnea, and blurred vision, preexisting conditions * Physical Examination: lethargy to stupor to coma, tachycardia, hypertension, cardiac dysrhythmias, airway patency

NURSING DIAGNOSES include but are not limited to: Diagnostic Title Possible Etiologic Factors 1 Impaired gas exchange Hypoventilation 2 Disturbed thought processes Central nervous system depression 3 Anxiety Hypoxia, hospitalization 4 Risk for ineffective family Illness of a family member coping 5 Ineffective airway clearance Hypoventilation, secretions 6 Ineffective breathing pattern Hypoventilation, dyspnea

NURSING MANAGEMENT OF RESPIRATORY ACIDOSIS

EXPECTED PATIENT OUTCOMES include but are not limited to: 1 Will maintain airway patency and adequate breathing rate and rhythm will return of ABGs to patients normal level 2 Will be alert and oriented to time, place, and person, or to his or her normal baseline level of consciousness 3 Will cope with anxiety 4 Will exhibit effective coping and awareness of effective support systems 5 Will have secretions that are normal for self in amount and can be raised 6 Will maintain adequate rate and depth of respirations using pursed lip and other breathing techniques when necessary (as in the patient with COPD)

NURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSIS INTERVENTIONS 1 Supporting effective gas exchange - Provide a position of comfort to allow ease of respiration - Obtain and monitor ABG results and VS. Refer accordingly - Provide and monitor supplemental oxygen as ordered - Turn the patient q2 and PRN - Provide pulmonary hygiene PRN - Maintain adequate hydration - Provide comfort measures such as mouth care - Assist with ADLs - Instruct patient regarding coughing and deep breathing and management of disease condition, especially COPD 2 Coping with disturbed thought processes - Do frequent neurologic assessments - Monitor and document persons baseline LOC frequently

NURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSIS

Reorient as necessary by providing calendars, clocks, etc.

Relieving anxiety
Provide a calm, relaxed environment Give clear, concise explanations of treatment plans

Encourage expression of feelings

Provide support and information to patient and family Teach relaxation techniques

Assist the patient to identify coping mechanisms to deal with anxiety and stress

Enhancing coping mechanisms Provide support and information to family members about the patients ongoing condition Reassure them that there is a physiologic cause for the patients behavior

NURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSIS

Encourage questions and open communication

Promote airway clearance Implement regular breathing and coughing exercises

Do suctioning as necessary
Maintain good hydration Do chest physiotherapy as appropriate

Promoting an effective breathing pattern

Maintain alveolar ventilation Teach the patient proper breathing techniques as well as panic control breathing

NURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSIS

EVALUATION. Achievement of outcomes is successful when the patient: 1a. Demonstrates improved ventilation and oxygenation 1b Has vital signs, ABGs, and cardiac rhythm within own normal range 2 3 4 5 6 Returns to baseline LOC Reports reduced anxiety Family uses adequate coping mechanisms Is able to raise secretions on own Demonstrate effective breathing techniques

RESPIRATORY ALKALOSIS: CARBONIC ACID DEFICIT

Anxiety, hysteria, fever, hypoxia, pain, pulmonary disorders, lesions affecting the respiratory center in the medulla, brain tumor, encephalitis, meningitis, hyperthyroidism, gram-negative sepsis

Hyperventilation: Excessive pulmonary ventilation

Decrease in hydrogen ion concentration

RESPIRATORY ALKALOSIS

NURSING MANAGEMENT OF RESPIRATORY ALKALOSIS

ASSESSMENT * Health Hx: anxiety, shortness of breath, muscle cramps or weakness, palpitations, panic, dyspnea * Physical Examination: light-headedness, confusion as a result of cerebral hypoxia, hyperventilation, tachycardia or arrhythmia, muscle weakness, (+) Chvosteks sign or Trousseaus sign indicating a low ionized serum calcium level secondary to hyperventilation and alkalosis, hyperactive deep tendon reflexes, unsteady gait, muscle spasms to tetany, agitation, psychosis, seizures in extreme cases, decreased potassium levels NURSING DIAGNOSES include but are not limited to: Diagnostic Title Possible Etiologic Factors 1 Anxiety Stress, fear 2 Ineffective breathing pattern Hyperventilation, anxiety 3 Disturbed thought processes CNS excitability; irritability 4 Risk for injury Change in LOC, and potential for seizures

NURSING MANAGEMENT OF RESPIRATORY ALKALOSIS

EXPECTED PATIENT OUTCOMES include but are not limited to: 1 Will report decreased anxiety; verbalizes methods to cope with anxiety 2 Will return to normal respiratory rate and rhythm or at least decreased hyperventilation, with return to baseline ABGs 3 Will exhibit reorientation to person, place, and time as per patients baseline 4 Will be free from injury

INTERVENTIONS 1 Allay anxiety - Give antianxiety medications as ordered - Have patient breath into a paper bag - Teach relaxation techniques when initial anxiety attack is over

NURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSIS INTERVENTIONS 2 Promoting an Effective Breathing Pattern - Encourage the patient to slow his or her RR - Maintain a calm and comforting attitude - Position the patient to promote maximal ease of inspiration - Assist the patient with relaxation techniques 3 Coping with Disturbed Thought Processes - Do frequent reorientation - Encourage family to participate in patients care - Use simple, direct statements or directions - Allow the patient adequate time to respond 4 Preventing injuries - Perform neurologic assessment frequently and document - Institute safety and seizure precautions - Assess frequently for muscle strength and coordination

NURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSIS

EVALUATION. Achievement of outcomes is successful when the patient: 1 Reports reduction in anxiety levels

2a Demonstrates effective normal breathing patterns 2b Has ABG results within patients normal baseline 3 4 Returns to normal baseline LOC and orientation level Remains free from injury; no seizure activity

METABOLIC ACIDOSIS: BICARBONATE DEFICIT

Increased acid production, uncontrolled diabetes mellitus, alcoholism, starvation, renal acidosis, lactic acidosis, increased acid ingestion, ethanol, salicylates, loss of bicarbonate, severe diarrhea, intestinal fistulas, adrenal insufficiency, hypoparathyroidism Excess organic acids are added to body fluids or bicarbonate is lost

Decrease in bicarbonate concentration

METABOLIC ACIDOSIS

NURSING MANAGEMENT OF METABOLIC ACIDOSIS

ASSESSMENT * Health Hx: anorexia, nausea, vomiting, abdominal pain, headache, thirst if the patient is dehydrated * Physical Examination: confusion, hyperventilation, warm, flushed skin, bradycardia and other dysrhythmias, decreasing LOC, nausea, vomiting, diarrhea, Kussmaul respirations, and acetone breath, especially if acidosis is due to ketoacidosis. Symptoms may progress to coma if untreated NURSING DIAGNOSES include but are not limited to: Diagnostic Title Possible Etiologic Factors 1 Disturbed thought processes Secondary to CNS depression 2 Decreased cardiac output Dysrhythmias 3 Risk for injury Secondary to altered mental state 4 Risk for imbalanced fluid Diarrhea, renal failure volume

NURSING MANAGEMENT OF METABOLIC ACIDOSIS

EXPECTED PATIENT OUTCOMES include but are not limited to: 1 Will return to usual baseline LOC 2 Will return to normal baseline parameters for vital signs with improved CO and decreased or resolved dysrhythmias 3 Will remain in a safe, secure environment without injury 4 Will maintain fluid and electrolyte balance and stable renal status INTERVENTIONS 1 Coping with disturbed thought processes - Monitor LOC and reorient as necessary - Monitor VS, esp. RRR, BP, and T - Monitor ABGs to assess the effects of treatment - Institute cardiac monitoring as ordered

NURSING MANAGEMENT OF PATIENT WITH METABOLIC ACIDOSIS 2 Supporting cardiac output - Monitor VS, MIO, and fluid and electrolyte balance - Institute cardiac monitoring to evaluate cardiac status Promoting safety - Provide a safe, secure and monitored environment - Institute safety precautions Promoting return of fluid and electrolyte balance - Monitor MIO - Administer medications per medical order

NURSING MANAGEMENT OF PATIENT WITH METABOLIC ACIDOSIS

EVALUATION. Achievement of outcomes is successful when the patient: 1 2 3 4 Exhibits baseline-level consciousness and orientation Returns to normal baseline parameters for vital signs and Cardiac Output with cardiac dysrhythmias resolved Remains free from injury Maintains fluid and electrolyte balance and stable renal function

METABOLIC ALKALOSIS: BICARBONATE EXCESS

Loss of stomach acid, gastric suctioning, persistent vomiting, excess alkali intake, intestinal fistulas, hypokalemia, Cushings syndrome or aldosteronism, potassium-diuretic therapy

Excessive amounts of acid substance and hydrogen ions are lost from the body or large amounts of bicarbonate or lactate are added orally or IV

Excess of base elements

METABOLIC ALKALOSIS

NURSING MANAGEMENT OF METABOLIC ALKALOSIS

ASSESSMENT * Health Hx: Prolonged vomiting or nasogastric suctioning,

frequent self-induced vomiting, muscle weakness, lightheadedness, ingestion of large amounts of licorice or antacids, use of diuretics, muscle cramping, twitching, or tingling Physical Examination: mental confusion, dizziness, changes in LOC, hyperreflexia, tetany, dysrhthmias, seizurees, respiratory failure, positive Chvosteks or Trosseaus sign if the patient has a low ionized serum calcium level, decreased hand grasps, generalized muscle weakness, decreased serum calcium or potassium level, impaired concentration, seizures, ECG changes consistent with hypokalemia

NURSING DIAGNOSES include but are not limited to: Diagnostic Title Possible Etiologic Factors 1 Disturbed thought processes CNS excitation 2 Decreased cardiac output Dysrhythmias and electrolyte imbalances 3 Risk for injury Muscle weakness, tetany, confusion and possible seizures 4 Risk for imbalanced fluid Nasogastric drainage, diuretic therapy volume fistula

NURSING MANAGEMENT OF METABOLIC ALKALOSIS

EXPECTED PATIENT OUTCOMES include but are not limited to: 1 Will return to usual baseline LOC and orientation 2 Will return to normal baseline parameters for vital signs with improved CO with resolution of electrolyte imbalances and decreased or resolved cardiac dysrhythmias 3 Will remain in a safe, secure environment without injury 4 Will maintain fluid and electrolyte balance INTERVENTIONS 1 Coping with disturbed thought processes - Monitor LOC and reorient as necessary - Monitor VS, esp. RRR, BP, and T - Monitor ABGs to assess the effects of treatment - Institute cardiac monitoring as ordered

NURSING MANAGEMENT OF PATIENT WITH METABOLIC ALKALOSIS 2 Supporting cardiac output - Monitor VS, MIO, and fluid and electrolyte balance - Institute cardiac monitoring to evaluate cardiac status Promoting safety - Provide a safe, secure and monitored environment - Institute safety precautions Promoting return of fluid and electrolyte balance - Monitor MIO - Administer medications per medical order

NURSING MANAGEMENT OF PATIENT WITH METABOLIC ALKALOSIS

EVALUATION. Achievement of outcomes is successful when the patient: 1 2 3 4 Manifests mental status has returned to baseline Is free from cardiac dysrhythmias Remains free from injury Maintains fluid balance at baseline level

CRITICAL THINKING EXERCISES

A patient on your unit has a diagnosis of dehydration. The physician has ordered force fluids. You must make a judgment as to the type and amount since these were not specified in the order. Identify the additional patient data needed to make an appropriate nursing decision

CRITICAL THINKING EXERCISES

A 32-year-old administrative assistant comes to the urgent care center with a 72-hour history of vomiting secondary to influenza. She is lethargic and states, My muscles are twitching. Her RR is 18/min and HR is 110 bpm, T=100.4F. Her blood pressure is 110/68 which she states is about normal for me. Her ABG values are as follows: pH: 7.57 PaO2: 92 PaCO2: 41 HCO3: 36 Describe her acid-base status, probable cause for the imbalance and treatment

EXPECTED DIRECTIONAL CHANGES WITH ACID-BASE IMBALANCES

CONDITION pH HCO3 PCO2

Respiratory Acidosis Uncompensated Partly Compensated Compensated Respiratory Alkalosis Uncompensated Partly Compensated Compensated Metabolic Acidosis Uncompensated Partly Compensated Compensated Metabolic Alkalosis Uncompensated Partly Compensated Compensated

Normal

Normal

Normal
Normal Normal

Normal

Normal Normal