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Fluids and Electrolytes

Ma. Tosca Cybil A. Torres, RN

OBJECTIVES
After this lecture/discussion, the learner should be able to: 1. Describe the mechanisms that maintain fluid, electrolyte and acid-base balance. acid2. 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 acidbalance. 5. Differentiate between metabolic and respiratory acidosis and alkalosis. 6. Apply the pathophysiologic principles of acid-base acidbalance to the interpretation of ABG measurements. 7. Analyze the components of ABGs to identify the type of acidacid-base balance. 8. Describe the causes and effects of each type of acidacidbase balance. 9. Use ABG findings in formulating the care of the patient with an acid-base imbalance. acid10. Describe the management of patients with a fluid, electrolyte, or acid-base imbalance. acid-

Fluids

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 ADH Posterior pituitary gland 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 ALDOSTERONE-RENINSerum Sodium Blood volume Juxtaglomerular cells-kidney RENIN Angiotensinogen in plasma Angiotensin I
AngiotensinAngiotensinconverting 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 Types
Fluids in the body generally arent found in pure forms Isotonic, hypotonic, and hypertonic types Defined in terms of the amount of solute or dissolve substances in the solution Balancing these fluids involves the shifting of fluid not the solute involved

Isotonic Solutions

No net fluid shifts occur between isotonic solutions because the solution are equally concentrated Ex. NSS or 0.9SS

Hypotonic Solutions
Has a lower solute concentration than another solution Fluid from the hypotonic solution would shift into the second solution until the two solutions had equal concentrations Ex. Half normal or 0.45%SS

Hypertonic Solutions
Has a higher solute concentration than another solution Fluid from the second solution would shift into the hypertonic solution until the two solutions had equal concentrations Ex. D5NSS

Fluid Movements
Fluids and solutes constantly move within the body, which allows the body to maintain homeostasis Fluids along with nutrients and waste products constantly shift within the bodys compartments from the cell to the interstitial spaces, to the blood vessels and back again

Fluid Movements
Types of Transport
A. Active transport B. Passive transport
Diffusion Osmosis Filtration

CLINICAL MEASUREMENT
Daily weights
Each kg = 1 L of fluid To gain accuracy:

Assessment

Balance the scale before each use and weigh the client; At same time each day before breakfast after the first void Wear the same or similar clothing On the same scale

Vital signs
Tachycardia first sign of hypovolemia

Fluid I & O
Oral fluids Ice chips Foods that tend to become fluid at room temperature Tube feedings Parenteral fluids IV meds Catheter or tube irrigant Urinary output if with diaper, 1 g = 1 mL Vomitus or liquid feces Diaphoresis Tube drainage Wound dressing or wound fistula

LABORATORY TESTS FOR EVALUATING FLUID STATUS


Osmolality measures the solute concentration per kilogram in blood and urine. Osmolarity concentration of solution per liter. BUN (10-20 mg/dL)made up of urea, an end product of protein metabolism by the liver. Creatinine (0.7 to 1.5 mg/dL)- end product of muscle metabolism Serum electrolytes CBC

Diagnosis
Fluid volume deficit High risk for Fluid volume deficit Fluid volume excess Altered oral mucous membrane

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 Urine specific gravity

Renin-AngiotensinRenin-AngiotensinAldosterone System Activation Sodium and Water Resorption

Person complains of thirst

Pathophysiology and Clinical Manifestations


UNTREATED FLUID VOLUME DEFICIT

Depletion of fluids available BODY TEMPERATURE Dry mucous membranes Difficulty with speech blood pressure
heart rate respiratory rate

Cells become unable to continue providing water to replace ECF losses Signs of circulatory collapse

Restlessness and Apprehension

Hypovolemia
Nursing Intervention
Monitor fluid intake and output Checked daily weight (a 1lb(0.45kg) weight loss equals a 500 ml fluid loss) Monitor hemodynamic values such as CVP Monitor results of laboratory studies Assess level of consciousness Administer and monitor I.V. fluids Apply and adjust oxygen therapy as ordered If patient is bleeding, apply direct continuous pressure to the area and elevate it if possible Assess skin turgor Assess oral mucous membranes Turn the patient at least every 2 hours to prevent skin breakdown Encourage oral fluids

Hypovolemia
Warning Signs
Cool pale skin over the arms and legs Decreased central venous pressure Delayed capillary refill Deterioration in mental status flat jugular veins Orthostatic hypotension Tachycardia Urine output initially more than 30ml/min, then dropping below 10ml/hour Weak or absent peripheral pulses Weight loss

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 one-yearweighed 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 Replacement Therapy


Aimed at restoring and maintaining homeostasis Methods:
Oral and gastric feeding Parenteral therapy

Choice of therapy affected by several factors


Type and severity of imbalance Patients overall health status, age, renal and cardiovascular status Usual maintenance requirements

Fluid Replacement Therapy


Advantages
Provides the patient with life-sustaining fluids, electrolytes, and drugs Immediate and predictable therapeutic effects Preferred for administering fluids, electrolytes, and drugs in emergency situations Allows fluid intake when a patient has GI malabsorption Permits accurate dosage titration for analgesics and other drugs

Fluid Replacement Therapy


Disadvantages
Solution incompatibility Adverse reactions Infection

Fluid Replacement Therapy


Administration routes
Oral route : oral ingestion of fluids and electrolytes as liquids or solids administered directly into the GI tract Nasogastric route: instillation of fluids and electrolytes through feeding tubes, such as NG, gastrostomy and jejunostomy tubes I.V. route: administration of fluids and electrolytes directly into the bloodstream using continuous infusion, bolus, or I.V. push injection through peripheral or central venous site

Which among the following IV solutions contains the highest potassium content? A. D5 IMB B. Lactated Ringer's Solution C. D5 LRS D. D5 0.3 NaCl

Composition of Different Intravenous Solution


IVF D5 0.9% NaCl D5 0.15% NaCl D5 0.3% NaCl D5 0.45% NaCl D5 IMB LRS NSS D5LRS Dextrose (g/L) 50 50 50 50 50 0 0 50 Na (meq/L) 154 25 51 77 25 130 154 130 Cl (meq/L) 154 25 51 77 22 109 154 109 4 28 20 4 23 28 K (meq/L) Lactate (meq/L)

Fluid Replacement Therapy

ISOTONIC SOLUTION
Facts -same osmolality as plasma (app. 275 to 295 mOsm/kg) -vascular space osmolality not altered by infusion -expand intracellular and extracellular space equally; degree of expansion correlates with amount of fluid infused -no solution-related shifting solutionbetween ICF and ECF spaces -cells neither shrink nor swell with fluid movement Examples Dextrose 5% in water, Uses -Fluid loss and dehydration -Hypernatremia -Blood transfusion, fluid challenges, resuscitation, shock, metabolic alkalosis, hypercalcemia, hyponatremia

Normal Saline Solution,

Lactated Ringers Solution

-Acute blood loss, burns, dehydration, hypovolemia

Fluid Replacement Therapy

HYPOTONIC SOLUTION

Fluid Replacement Therapy

HYPERTONIC SOLUTION

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

Hypervolemia
Evaluating pitting edema
Press your fingertip firmly into the patients skin over a bony surface for a few seconds. Then note the depth of the imprint your finger leaves on the skin
A slight imprint indicates +1 pitting edema A deep imprint, with the skin slow to return to its original contour, indicates a +4 pitting edema When the skin resists pressure and appears distended, the condition is called brawny edema, which causes the skin to swell so much that fluid cant be displaced

Hypervolemia
Diagnostic Findings:
Decreased hematocrit resulting from hemodilution Normal serum Na level Low serum K and BUN levels
either due to hemodilution or higher levels may indicate renal failure

Low oxygen level Abnormal chest x-ray


Indicates fluid accumulation May reveal pulmonary edema or pleural effusions

Hypervolemia
Treatment
Na and fluid intake restriction Diuretics to promote excess fluid excretion Morphine and nitroglycerin (Nitro-Dur) for pulmonary edema
Dilate blood vessels Reduce pulmonary congestion and amount of blood returning to the heart

Digoxin for heart failure


Strengthens cardiac contractions

Hypervolemia
Treatment
Supportive measures
Oxygen administration Bed rest

Hemodialysis or continuous renal replacement therapy for renal dysfunction

Hypervolemia
Nursing Interventions
Monitor fluid intake and output Monitor daily weight Monitor cardiopulmonary status Auscultate breathe sounds Assess for complaints of dyspnea Monitor chest x-ray results Monitor arterial blood gas values Assess for peripheral edema Inspect the patient for sacral edema Monitor infusion of I.V. solutions Monitor the effects of prescribed medications

BURN

General Information

Involve destruction of the epidermis, dermis, or subcutaneous layers of the skin Can be permanently disfiguring and incapacitating and possibly life-threatening

General Information

Associated imbalances result from alterations in skin integrity and internal body membranes, and from effect of heat on body water and solute loss that may result from cellular destruction

General Information

Type and severity of imbalance depends on burn type and depth, percentage body surface area involved and burn phase

Pathophysiology
Burn Phase:
Refer to stages that describe physiologic changes occurring after a burn

Burn phase

Fluidaccumulation phase Fluidremobilization phase

Convalescent phase

Pathophysiology
Fluid-accumulation phase:
y Last fro 36 to 48 hours after a burn injury y Fluid shifts from vascular compartment to interstitial space third-space shift y Edema caused by shifted fluid, which typically reaches maximum within 8 hours after injury y Circulation possibly compromised and pulses diminished from severe edema

Burn phase

Fluidaccumulation phase Fluidremobilization phase

Convalescent phase

Pathophysiology
Several reasons for fluid imbalances during fluidaccumulation phase
Damage to capillaries causing altered vessel permeability Diminished kidney perfusion Production and release of stress hormones such as aldosterone and ADH

Burn phase

Fluidaccumulation phase Fluidremobilization phase

Convalescent phase

Pathophysiology
Respiratory problems Muscle and tissue injuries GI problems Electrolyte imbalances:
y Common during fluid accumulation phase due to bodys hypermetabolic needs and priority that fluid replacement takes over nutritional needs during emergency phase

Burn phase

Fluidaccumulation phase Fluidremobilization phase

Convalescent phase

Pathophysiology
Fluid- remobilization phase :
y Also known as diuresis stage y Starts about 48 hours after initial burn y Fluid shifted back to vascular compartment y Edema at burn site decreased, blood flow to kidneys increased, increased urine output y Fluid and electrolyte imbalances can still occur

Burn phase

Fluidaccumulation phase Fluidremobilization phase

Convalescent phase

Pathophysiology
Convalescent phase:
y Begins after first two phases has been resolved y Characterized by healing or reconstruction of burn wound y Major fluid shifts now resolved but possible further fluid and electrolyte imbalances exist as a result of inadequate dietary intake y Anemia is common severe burns typically destroy red blood cells

Burn phase

Fluidaccumulation phase Fluidremobilization phase

Convalescent phase

Characteristics
1. Minor Burns
a. Partial thickness burns are no greater than 15% of the TBSA in the adult b. Full thickness burns are < 2% of the TBSA in the adult c. Burn areas do not involve the eyes, ears, hands, face, feet, or perineum d. There are no electrical burns or inhalation injuries e. The client is an adult younger than 60 y.o. f. The client has no preexisting medical condition at the time of the burn injury g. No other injury occurred with the burn

Characteristics
2. Moderate Burns
a. Partial thickness burns are deep and are 15% to 25% of the TBSA in the adult b. Full thickness burns are 2% to 10% of the TBSA in the adult c. Burn areas do not involve the eyes, ears, hands, face, feet, or perineum d. There are no electrical burns or inhalation injuries e. The client is an adult younger than 60 y.o. f. The client has no chronic cardiac, pulmonary, or endocrine disorder at the time of the burn injury g. No other complicated injury occurred with the burn

Characteristics
3. Major Burns
a. Partial thickness burns are > 25% of the TBSA in the adult b. Full thickness burns are > 10% of the TBSA c. Burn areas involve the eyes, ears, hands, face, feet, or perineum d. The burn injury was an electrical or inhalation injury e. The client is older than 60 y.o. f. The client has a chronic cardiac, pulmonary, or metabolic disorder at the time of the burn injury g. Burns are accompanied by other injuries

Assessment of Burn Injury


Extent / Degree First Degree Assessment of Extent Reparative Process

Pink to red: slight edema, which subsides quickly. Pain may last up to 48 hours. Relieved by cooling. Sunburn is a typical example.

In about 5 days, epidermis peels, heals spontaneously. Itching and pink skin persist for about a week. No scarring. Heals spont. If it does not become infected w/in 10 days - 2 weeks.

Second degree

Superficial: Pink or red; blisters form (vesicles); weeping, edematous, elastic. Superficial layers of skin are destroyed; wound moist and painful. Deep dermal: Mottled white and red: edematous reddened areas blanch on pressure. May be yellowish but soft and elastic may or may not be sensitive to touch; sensitive to cold air. Hair does not pull out easily

Takes several weeks to heal. Scarring may occur.

Takes several weeks to heal. Scarring may occur.

Assessment of Burn Injury


Extent / Degree Assessment of Extent

Reparative Process
Eschar must be removed. Granulation tissue forms to nearest epithelium from wound margins or support graft. For areas larger than 3-5 cm, grafting is required. Expect scarring and loss of skin function. Area requires debridement, formation of granulation tissue, and grafting.

Third degree

Destruction of epithelial cells epidermis and dermis destroyed Reddened areas do not blanch with pressure. Not painful; inelastic; coloration varies from waxy white to brown; leathery devitalized tissue is called eschar. Destruction of epithelium, fat, muscles, and bone.

Burn:Classification Superficial (1 burns)

Involve only the epidermal layer of the skin. sunburns are commonly first-degree burns.

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1 burn

2 burn

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Superficial burn (1 burn)

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Partial thickness (2burn)


Present of blisters indicates superficial partial-thickness injury. Blister may size because continuous exudation and collection of tissue fluid. Healing phase of partial thickness, itching and dryness because vascularization of sebaceous glands, reduction of secretions and perspiration.
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2 burn

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Partial thickness (2burn)

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Burn:Classification
3.Full thickness (third-degree burn) Destruction of the epidermis and the entire dermis, subcutaneous layer, muscle and bone. Nerve ending are destroyed-painless wound. Eschar may be formed due to surface dehydration. Black networks of coagulate capillaries may be seen. Need skin grafting because the destroyed tissue is unable to epithelialize. Deep partial-thickness burn may convert to a full-thickness burn because of infection, trauma or blood supply.
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3 burn

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Eschar:composed of denatured protein


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Full thickness (3burn)

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Extent of surface area burned


Rule of nines-An estimated of the TBSA involved as a result of a burn. The rule of nines measures the percentage of the body burned by dividing the body into multiples of nine. The initial evaluation is made upon arrival at the hospital.
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Lund and Browder


More precise method of estimating Recognizes that the percentage of BSA of various anatomic parts. By dividing the body into very small areas and providing an estimate of proportion of BSA accounted for by such body parts Includes, a table indicating the adjustment for different ages Head and trunk represent larger proportions of body surface in children.
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Lund and Browder chart

Age in years A-head (back or front)

10 15 Adult

9 8

6 5 4 3 4 4 4 4 3 3

B-1 thigh (back or 2 3 front) C-1 leg (back or front) 2 2

2 3

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TYPES OF BURNS
Thermal Burns:
caused by exposure to flames, hot liquids, steam or hot objects

Chemical Burns:
Caused by tissue contact with strong alkali, or organic compounds Systemic toxicity from cutaneous absorption can occur

Radiation Burns:
source caused by exposure to UV light, x-rays, or radioactive

TYPES OF BURNS
Electrical Burns:
Caused by heat generated by electrical energy as it passes through the body Results in internal tissue damage Cutaneous burns cause muscle and soft tissue damage that may be extensive, particularly in high voltage electrical injuries Alternating current is more dangerous than direct current because it is associated with CP arrest, ventricular fibrillation, tetanic muscle contractions, and long bone or vertebral fractures

Potential Imbalance
Hypovolemia
y Approximately 10% of plasma volume lost into tissue soon after a severe burn y Occurs because of the third space shift causes multiple effects: y With burns damage to the skin surface, decrease in skins ability to prevent water loss; patient can lose up to 8L of fluid per day (400ml/hour) y Potential for blood loss, adding to fluid volume losses

Potential Imbalance
Hypervolemia
Usually develops 3 to 5 days after a major burn injury Occurs during the fluid remobilization phase, as fluid shifts from the interstitial space back to the vascular compartment May be exacerbated by excessive administration of I.V. fluids

Potential Imbalance
Hyperkalemia / Hypokalemia Hypocalcemia Hyponatremia / Hypernatremia Metabolic acidosis Respiratory acidosis

Burns
NURSING PRIORITY: The client with burn injury is often awake, mentally alert, and cooperative at first. The level of consciousness may change as respiratory status change or as the fluid shift occurs, precipitating hypovolemia. If the client is unconscious or confused, assess him or her for the possibility of a head injury.

Burns
Assess for
Patent airway Presence of adequate breath sounds Symptoms of hypoxia Pulmonary damage
Burns around the face, neck, mouth or in the oral mucosal area Tachycardia and hypotension occur early Elevate UO

Circulatory status

Burns
Assess for
GI function check last time client ate Fluid status
UO (30 ml/hr) Hypotension (< 90/60) Confusion / disorientation

Circulatory status of the extremities

Burns
Treatment
y Respiratory status takes priority over the treatment of the burn injury y If burn area is small cold compress or not ice) immerse in cool water (not ice to heat y May have ointment on the burn area y Analgesics IV, IM, SQ. oral forms may not be absorbed effectively

Burns
Nursing intervention
Maintain patent airway; prevent hypoxia Evaluate fluid status; determine circulatory status Prevent of decrease infection Maintain nutrition Prevent contractures and scarring Promote acceptance and adaptation to alterations in body image

Burns
First 24 hours
Formula name ElectrolyteContaining solution Colloid-Containing Solution Dextrose in Water

Evans Brooke Modified Brooke Parkland Hypertonic Saline

NSS 1 ml/kg/%burn LR 1.5 ml/kg/%burn LR 2 ml/kg/%burn LR 4 ml/kg/%burn Fluid containing 250 mEq of Na/L to maintain hourly urine output of 70 ml in adults

NSS 1 ml/kg/%burn 0.5 ml/kg/%burn None None None

2000 ml 2000 ml None None None

Burns
Second 24 hours
Formula name Evans Brooke Modified Brooke ElectrolyteContaining solution of first 24-hr requirement - of first 24-hr requirement None Colloid-Containing Solution of first 24-hr requirement - of first 24-hr requirement 0.3-0.5 ml/kg/%burn Dextrose in Water 2000 ml 2000 ml Titrate to maintain urine output Titrate to maintain urine output None

Parkland

None

0.3-0.5 ml/kg/%burn

Hypertonic Saline

Same solution to maintain hourly urine output of 30 ml in adults

None

Considerations AGE AND GENERAL HEALTH


Mortality rates are higher for children < 4 y.o,
particularly those < 1 y.o., and for clients over the age of 60 years. Debilitating disorders, such as cardiac, respiratory, endocrine, and renal d/o, negatively influence the client s response to injury and treatment. Mortality rate is higher when the client has a preexisting disorder at the time of the burn injury

Electrolytes

Which one is not a cation?


A. Calcium B. Magnesium C. Phosphorous D. Sodium

Anions and Cations


Anions Cations

Bicarbonate Chloride Phosphorous

Calcium Magnesium Potassium Sodium

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 sodium 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 135-

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

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, 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 acid RDA: not known precisely. 50-100 mEq 50 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 PotassiumPotassium-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 Dietary intake of excess of kidneys ability to excrete; Excess parenteral administration Decreased Loss PotassiumPotassium-sparing diuretics; Renal failure; Adrenal insufficiency Shift of Potassium out of the Cells Extensive injuries, crushing injuries, metabolic acidosis

HYPERKALEMIA
GI Tract N&V Diarrhea, Colic CNS Numbness, paresthesias Muscles Early: irritability Late: weakness leading to flaccid paralysis CV System Conduction disturbance, ventricular fibrillation, Cardiac Arrest Kidneys Oliguria leading to anuria

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 cationKayexalate (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 Potassiumfurther 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 post 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 Normal value 8.5 10.5 mg/dl

CAUSES AND EFFECTS OF HYPOCALCEMIA


Decreased Ionized Ca Large tranfusion with citrated blood Excess Loss Kidney Disease Dietary Deficit Inadequate Intake
Decrease in GI Tract and Bone Absorption Magnesium Calcitonin Vitamin D Parathyroid Hormone

HYPOCALCEMIA
Bones
Osteoporosis leading to Fractures

CNS Tingling convulsions

Other Abnormal deposits of calcium in body tissues

Muscles Muscle spasm

Cardiovascular System Dysrhythmias

Tetany
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 Immobilization, Carcinoma with bone metastases, Multiple myeloma Excess Intake Calcium diet (esp. milk) Antacids containing calcium Increase in factors Causing Mobilization from bone PTH, Vitamin D, steroid therapy

HYPERCALCEMIA
Kidneys Stones CNS Bones Bone pain Muscles Muscle fatigue, hypotonia CV System Depressed activity

Deep-tendon reflexes

Kidney Damage

Osteoporosis Lethargy Fractures Coma Cardiac Arrest GI motility Dysrhythmias

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 18 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 less 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 CV System Tachycardia, Hypotension, Dysrhythmias

CNS Convulsions, Paresthesias, Tremor, Ataxia

Agitation, Depression, Confusion

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 Mg Any patient receiving parenteral magnesium therapy should be assessed frequently for signs of hypermagnesemia Mild hypermagnesemia: withholding magnesium-containing magnesiummedications may suffice Renal failure: dialysis Severe: may require treatment with calcium gluconate (10-20 (10mL 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 Tires easily; Change in behavior,

Fluid Loss/Electrolyte Imbalance____


confusion, apathy

Head, neck veins Upper GI Skin edematous

Facial edema, distended neck Headache, Anorexia, nausea, vomiting Warm, moist, taut, cool feeling

thirst, dry mucous membranes

Dry, decreased turgor

where

Respiration Dyspnea, orthopnea, productive cough, moist breath sounds Circulation Loss of sensation in edematous increased blood pressure Abdomen Elimination Extremities Increased girth, fluid wave Constipation Dependent edema, pitting discomfort from weight of bedclothes

Changes in rate and depth of respiration Pulse rate changes, dysrhythmia, postural areas, pallor, bounding pulse, hypotension Distention, abdominal cramps Diarrhea, constipation Muscle weakness, tingling, tetany ,

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 Deficient fluid volume Possible Etiologic Factors Active fluid volume loss (hemorrhage, diarrhea, gastric intubation, wounds, diaphoresis), inadequate fluid intake, failure of regulatory mechanisms, sequestration of body fluids Excess fluid intake, excess sodium intake, compromised regulatory processes

Excess Fluid Volume

EXPECTED PATIENT OUTCOMES


1. 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 turgor, prompt capillary refill, and absence of edema 2. Will verbalize understanding of treatment plan and causative factors that led to the imbalance

1,2Intake 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 yellowyellow -green; they usually have a sour odor) - With acid-base balance upset, gastric secretions may acidhave 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 maintained

1,2

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 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 short- 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 10hypertonic solutions and may partially meet body needs for CHOs - Dextran (commonly-used plasma expander) increases (commonlyplasma 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 1.003weight, 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

Fluids and Electrolytes

Acid-base balance

DRAWING ARTERIAL BLOOD GASES

ARTERIAL PUNCTURE

ALLENS TEST

NORMAL ACID-BASE BALANCE ACIDParameter Normal Value Definition and Implications Partial pressure of oxygen in arterial blood (decreases with age) In adults < 60 years: 6060-80 mmHg = mild hypoxemia 4040-60 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

8080-100 Hg

pH

7.357.35-7.45

PaCO2

3535-45 mmHg

Standard HCO3

2222-26 mEq/L

BASIC REGULATION OF ACID-BASE BALANCE ACID-

CO2

H2O

H2CO3

H+

HCO3

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

TYPES OF ACID-BASE DISTURBANCES ACIDDepression 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

EXPECTED DIRECTIONAL CHANGES WITH ACID-BASE IMBALANCES ACIDCONDITION 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

Compensation

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: Possible Etiologic Factors Diagnostic Title 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

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 4 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 gram-

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 lightresult 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 ordered anxiety attack is

Give antianxiety medications as Have patient breath into a paper bag Teach relaxation techniques when initial 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

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: Possible Etiologic Factors Diagnostic Title 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 balance Institute cardiac monitoring to evaluate cardiac status 3 Promoting safety Provide a safe, secure and monitored environment Institute safety precautions 4 Promoting return of fluid and electrolyte balance Monitor MIO Administer medications per medical order Supporting cardiac output Monitor VS, MIO, and fluid and electrolyte

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 baselineReturns 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 potassium-

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, Hx:

weakness, lightlightof large amounts of licorice or antacids, use of diuretics, muscle cramping, twitching, or tingling * Physical Examination: mental confusion, dizziness, changes in Examination: 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

frequent self-induced vomiting, muscle selfheadedness, ingestion

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 balance Institute cardiac monitoring to evaluate cardiac status 3 Promoting safety Provide a safe, secure and monitored environment Institute safety precautions 4 Promoting return of fluid and electrolyte balance Monitor MIO Administer medications per medical order Supporting cardiac output Monitor VS, MIO, and fluid and electrolyte

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 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

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