fluids and electrolytes
TRANSCRIPT
Fluids Fluids andand
ElectrolytesElectrolytesMa. Tosca Cybil A. Torres, RN
OBJECTIVESOBJECTIVESAfter this lecture/discussion, the learner should be able to:After this lecture/discussion, the learner should be able to:
1.1. Describe the mechanisms that maintain fluid, electrolyte Describe the mechanisms that maintain fluid, electrolyte and and acid-base balance.acid-base balance.
2.2. Compare the mechanisms and effects of fluid deficit and Compare the mechanisms and effects of fluid deficit and excess.excess.3.3. Discuss the mechanisms and effects of deficits and excess.Discuss the mechanisms and effects of deficits and excess.4.4. Describe the mechanisms that maintain acid-base balance.Describe the mechanisms that maintain acid-base balance.5.5. Differentiate between metabolic and respiratory acidosis and Differentiate between metabolic and respiratory acidosis and alkalosis.alkalosis.6.6. Apply the pathophysiologic principles of acid-base balance to Apply the pathophysiologic principles of acid-base balance to the the interpretation of ABG measurements.interpretation of ABG measurements.7.7. Analyze the components of ABGs to identify the type of acid-base Analyze the components of ABGs to identify the type of acid-base balance.balance.8.8. Describe the causes and effects of each type of acid-base Describe the causes and effects of each type of acid-base balance.balance.9.9. Use ABG findings in formulating the care of the patient with an Use ABG findings in formulating the care of the patient with an
acid-base imbalance.acid-base imbalance.10.10. Describe the management of patients with a fluid, electrolyte, or Describe the management of patients with a fluid, electrolyte, or
acid-base imbalance.acid-base imbalance.
Fluids
HOW IMPORTANT IS WATER?HOW IMPORTANT IS WATER?
• Between 50% and 60% of the human Between 50% and 60% of the human body by weight is waterbody by weight is water
• Water provides a medium for Water provides a medium for transporting nutrients to cells and wastes transporting nutrients to cells and wastes from cells and for transporting from cells and for transporting substances such as hormones, enzymes, substances such as hormones, enzymes, blood platelets, and red and white blood blood platelets, and red and white blood cellscells
• Water facilitates cellular metabolism and Water facilitates cellular metabolism and proper cellular chemical functioningproper cellular chemical functioning
• Water acts as a solvent for electrolytes Water acts as a solvent for electrolytes and nonelectrolytesand nonelectrolytes
• Helps maintain normal body temperatureHelps maintain normal body temperature
• Facilitates digestion and promotes Facilitates digestion and promotes eliminationelimination
• Acts as a tissue lubricantActs as a tissue lubricant
VARIATIONS IN FLUID CONTENTVARIATIONS IN FLUID CONTENT
BODY FATBODY FATBecause fat cells contain little Because fat cells contain little water and lean tissue is rich in water and lean tissue is rich in water, the more obese the water, the more obese the person, the smaller the person, the smaller the percentage of total body water percentage of total body water compared with body weight.compared with body weight.
This is also true between sexes This is also true between sexes because females tend to have because females tend to have proportionally more body fat proportionally more body fat than males.than males.
There is also an increase in fat There is also an increase in fat cells in older peoplecells in older people
VARIATIONS IN FLUID CONTENTVARIATIONS IN FLUID CONTENT
AGEAGE
AVENUES BY WHICH WATER AVENUES BY WHICH WATER ENTERS AND LEAVES THE BODYENTERS AND LEAVES THE BODY
↓Blood volume or ↓BP
Volume receptor
Atria and great veins
Hypothalamus
↓
Posterior pituitary gland
Osmoreceptors in hypothalamus
↑Osmolarity
↑ADH Kidney tubules
↑H2O reabsorption
↑vascular volume and ↓osmolarity
Narcotics, Stress, Anesthetic agents, Heat, Nicotine, Antineoplastic
agents, Surgery
ANTIDIURETIC HORMONE REGULATION MECHANISMSANTIDIURETIC HORMONE REGULATION MECHANISMS
Juxtaglomerular cells-kidney
↓Serum Sodium ↓Blood volume
Angiotensin I
Kidney tubulesAngiotensin II
Adrenal Cortex
↑Sodium resorption
(H2O resorbed with sodium); ↑ Blood volume
Angiotensinogen in plasma
RENIN
Angiotensin-Angiotensin-converting converting
enzymeenzyme
ALDOSTERONE
Intestine, sweat glands, Salivary
glands
Via vasoconstriction of arterial smooth muscle
ALDOSTERONE-RENIN-ANGIOTENSIN SYSTEMALDOSTERONE-RENIN-ANGIOTENSIN SYSTEM
Fluid Types
• Fluids in the body generally aren’t 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 body’s 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
Assessment• CLINICAL MEASUREMENT
– Daily weights• Each kg = 1 L of fluid• To gain accuracy:
– 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 BALANCEFLUID 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 IMBALANCEFLUID 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/HYPOVOLEMIAFLUID DEFICIT/HYPOVOLEMIA• May occur as a result of:May occur as a result of:
– Reduced fluid intakeReduced fluid intake– Loss of body fluidsLoss of body fluids– Sequestration (compartmentalizing) of body fluidsSequestration (compartmentalizing) of body fluids
Pathophysiology and Clinical ManifestationsPathophysiology and Clinical Manifestations
DECREASED FLUID VOLUMEDECREASED FLUID VOLUME
Stimulation of thirst Stimulation of thirst center in hypothalamuscenter in hypothalamus
Person complains of thirstPerson complains of thirst
↑ ↑ ADH SecretionADH Secretion
↑ ↑ Water resorptionWater resorption
↓ ↓ Urine OutputUrine Output
Renin-Angiotensin-Renin-Angiotensin-Aldosterone System Aldosterone System
ActivationActivation
↑ ↑ Sodium and Sodium and Water ResorptionWater Resorption
↑ ↑ Urine specific gravity Urine specific gravity
Pathophysiology and Clinical ManifestationsPathophysiology and Clinical ManifestationsUNTREATED FLUID VOLUME DEFICITUNTREATED FLUID VOLUME DEFICIT
Depletion of fluids availableDepletion of fluids available
↑ ↑ BODY TEMPERATUREBODY TEMPERATURE
Dry mucous membranesDry mucous membranes
Difficulty with speechDifficulty with speech
Cells become unable to continue Cells become unable to continue providing water to replace ECF providing water to replace ECF
losseslosses
Signs of circulatory collapse Signs of circulatory collapse
↓↓ blood pressureblood pressure
↑ ↑ heart rateheart rate
↑ ↑ respiratory raterespiratory rate
Restlessness and ApprehensionRestlessness 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 ManagementCollaborative Care ManagementIdentification of vulnerable patients and risk factors:Identification of vulnerable patients and risk factors:
* Compromised mental state * Compromised mental state * Physical limitations * Physical limitations * Disease states * Disease states * Limited access to adequate food and fluids* Limited access to adequate food and fluids
Development of a plan of careDevelopment of a plan of care
Family members should Family members should be educated about the be educated about the
importance of fluid and importance of fluid and nutrition intakenutrition intake
Collaboration with the Collaboration with the nurse, patient, family nurse, patient, family members, and other members, and other
health care providers health care providers for continued for continued
assessment and assessment and treatment of problemstreatment of problems
Ongoing assessment and Ongoing assessment and detailed action plan of detailed action plan of
fluid and serum fluid and serum electrolyte balance. electrolyte balance.
Factors such as Factors such as medications (particularly medications (particularly
diuretics), diuretics), hyperventilation, fever, hyperventilation, fever,
burns, diarrhea, and burns, diarrhea, and diabetes with diabetes with
appropriate referralappropriate referral
Collaborative Care Key PointsCollaborative Care Key Points• 1 Liter of water = 1 kg of water by weight1 Liter of water = 1 kg of water by weight• Fluid replacement are calculated according to this ratio plus 1.5 L to Fluid replacement are calculated according to this ratio plus 1.5 L to
fulfill the current daily needsfulfill the current daily needs• For example, JUAN, a one-year-old, lost 1 kg of water from diarrhea as 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 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 + kg=1 L, fluid replacement therapy for him will involve 1 L of fluids + 1500 L.1500 L.
• Oral fluid resuscitation is preferable but if the patient is unable to Oral fluid resuscitation is preferable but if the patient is unable to tolerate fluids, IV Therapy may be orderedtolerate fluids, IV Therapy may be ordered
• Vital signs should be assessed regularlyVital signs should be assessed regularly• Postural hypotension is common for postural persons with fluid Postural hypotension is common for postural persons with fluid
volume deficit. How do we assess this?volume deficit. How do we assess this?• For example, in the care of LOIDA, a 31 year old with severe DHN, you 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 she’s lying take her blood pressure (130/80) and pulse (75) while she’s lying down. Then you ask her to sit at the edge of bed. When you take her 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, blood pressure again, you get 115/80 and when you take her pulse, you get 80. This is consistent with intravascular volume depletion.you get 80. This is consistent with intravascular volume depletion.
• Daily weighing is also useful to monitor fluid and electrolyte balanceDaily weighing is also useful to monitor fluid and electrolyte balance• Laboratory results should be reviewed for various fluid and electrolyte Laboratory results should be reviewed for various fluid and electrolyte
disturbances so that appropriate adjustments to therapy can be disturbances so that appropriate adjustments to therapy can be initiatedinitiated
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– Patient’s overall health status, age, renal and
cardiovascular status– Usual maintenance requirements
Fluid Replacement TherapyAdvantages
– 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 TherapyAdministration 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 IMBB. Lactated Ringer's SolutionC. D5 LRSD. D5 0.3 NaCl
Composition of Different Intravenous Solution
IVF Dextrose (g/L)
Na (meq/L)
Cl (meq/L)
K (meq/L)
Lactate (meq/L)
D5 0.9% NaCl 50 154 154
D5 0.15% NaCl 50 25 25
D5 0.3% NaCl 50 51 51
D5 0.45% NaCl 50 77 77
D5 IMB 50 25 22 20 23
LRS 0 130 109 4 28
NSS 0 154 154
D5LRS 50 130 109 4 28
Fluid Replacement TherapyISOTONIC SOLUTION
FactsFacts ExamplesExamples UsesUses
-same osmolality as plasma -same osmolality as plasma (app. 275 to 295 mOsm/kg)(app. 275 to 295 mOsm/kg)-vascular space osmolality not -vascular space osmolality not altered by infusionaltered by infusion-expand intracellular and -expand intracellular and extracellular space equally; extracellular space equally; degree of expansion correlates degree of expansion correlates with amount of fluid infusedwith amount of fluid infused-no solution-related shifting -no solution-related shifting between ICF and ECF spacesbetween ICF and ECF spaces-cells neither shrink nor swell -cells neither shrink nor swell with fluid movementwith fluid movement
Dextrose 5% in Dextrose 5% in water,water,
Normal Saline Normal Saline Solution,Solution,
Lactated Ringers Lactated Ringers SolutionSolution
-Fluid loss and Fluid loss and dehydrationdehydration-HypernatremiaHypernatremia
-Blood transfusion, Blood transfusion, fluid challenges, fluid challenges, resuscitation, shock, resuscitation, shock, metabolic alkalosis, metabolic alkalosis, hypercalcemia, hypercalcemia, hyponatremiahyponatremia
-Acute blood loss, Acute blood loss, burns, dehydration, burns, dehydration, hypovolemiahypovolemia
Fluid Replacement Therapy HYPOTONIC SOLUTION
Fluid Replacement TherapyHYPERTONIC SOLUTION
FLUID EXCESS/HYPERVOLEMIAFLUID EXCESS/HYPERVOLEMIAPsychiatric Psychiatric
Disorders, SIADH, Disorders, SIADH, Certain head injuriesCertain head injuries
Dietary Sodium Dietary Sodium IndiscretionIndiscretion
Renal and endocrine Renal and endocrine disturbances, disturbances,
malignancies, adenomasmalignancies, adenomas
OverhydrationOverhydrationExcessive Sodium Excessive Sodium
IntakeIntake
Failure of renal or Failure of renal or hormonal regulatory hormonal regulatory
functionsfunctions
FLUID VOLUME EXCESS/HYPERVOLEMIAFLUID VOLUME EXCESS/HYPERVOLEMIA
• Since ECF becomes hypoosmolar, fluid moves into the cells to equalize Since ECF becomes hypoosmolar, fluid moves into the cells to equalize the concentration on both sides of the cell membranethe concentration on both sides of the cell membrane
• Thus there, is an increase in intracellular fluidThus there, is an increase in intracellular fluid• The brain cells are particularly sensitive to the increase of The brain cells are particularly sensitive to the increase of
intracellular water, the most common signs of hypoosmolar intracellular water, the most common signs of hypoosmolar overhydration are changes in mental status. Confusion, ataxia, and overhydration are changes in mental status. Confusion, ataxia, and convulsions may also occur.convulsions may also occur.
• Other clinical manifestations include: hyperventilation, sudden weight Other clinical manifestations include: hyperventilation, sudden weight gain, warm, moist skin, increased ICP: slow bounding pulse with an gain, warm, moist skin, increased ICP: slow bounding pulse with an increase in systolic and decrease in diastolic pressue and peripheral increase in systolic and decrease in diastolic pressue and peripheral edema, usually not markededema, 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
Fluid- accumulation
phase
Fluid-remobilization
phase
Convalescent phase
Pathophysiology
Fluid-accumulation phase:Last fro 36 to 48 hours after a
burn injuryFluid shifts from vascular
compartment to interstitial space – third-space shift
Edema caused by shifted fluid, which typically reaches maximum within 8 hours after injury
Circulation possibly compromised and pulses diminished from severe edema
Burn phase
Fluid- accumulation
phase
Fluid-remobilization
phase
Convalescent phase
Pathophysiology
• Several reasons for fluid imbalances during fluid-accumulation phase– Damage to capillaries causing
altered vessel permeability– Diminished kidney perfusion– Production and release of
stress hormones such as aldosterone and ADH
Burn phase
Fluid- accumulation
phase
Fluid-remobilization
phase
Convalescent phase
Pathophysiology
Respiratory problems Muscle and tissue injuries GI problems Electrolyte imbalances:
Common during fluid accumulation phase due to body’s hypermetabolic needs and priority that fluid replacement takes over nutritional needs during emergency phase
Burn phase
Fluid- accumulation
phase
Fluid-remobilization
phase
Convalescent phase
Pathophysiology
Fluid- remobilization phase : Also known as diuresis stageStarts about 48 hours after initial
burnFluid shifted back to vascular
compartmentEdema at burn site decreased,
blood flow to kidneys increased, increased urine output
Fluid and electrolyte imbalances can still occur
Burn phase
Fluid- accumulation
phase
Fluid-remobilization
phase
Convalescent phase
Pathophysiology
Convalescent phase:Begins after first two phases has
been resolvedCharacterized by healing or
reconstruction of burn woundMajor fluid shifts now resolved but
possible further fluid and electrolyte imbalances exist as a result of inadequate dietary intake
Anemia is common – severe burns typically destroy red blood cells
Burn phase
Fluid- accumulation
phase
Fluid-remobilization
phase
Convalescent phase
Characteristics
1. Minor Burnsa. Partial thickness burns are no greater than 15%
of the TBSA in the adultb. Full thickness burns are < 2% of the TBSA in the
adultc. Burn areas do not involve the eyes, ears, hands,
face, feet, or perineumd. There are no electrical burns or inhalation
injuriese. The client is an adult younger than 60 y.o.f. The client has no preexisting medical condition
at the time of the burn injuryg. No other injury occurred with the burn
Characteristics2. 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 injuriese. 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 injuryg. No other complicated injury occurred with the
burn
Characteristics
3. Major Burnsa. Partial thickness burns are > 25% of the TBSA
in the adultb. Full thickness burns are > 10% of the TBSA c. Burn areas involve the eyes, ears, hands, face,
feet, or perineumd. The burn injury was an electrical or inhalation
injurye. 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 injuryg. Burns are accompanied by other injuries
Assessment of Burn Injury
Takes several weeks to heal.Scarring may occur.
Takes several weeks to heal.Scarring may occur.
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
Second degree
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.
Pink to red: slight edema, which subsides quickly.Pain may last up to 48 hours.Relieved by cooling.Sunburn is a typical example.
First Degree
Reparative ProcessAssessment of ExtentExtent / Degree
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.
Destruction of epithelial cells – epidermis and dermis destroyedReddened 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.
Third degreeReparative ProcessAssessment of ExtentExtent / Degree
Assessment of Burn Injury
59
Burn:Classification
Superficial (1° burns)
• Involve only the epidermal layer of the skin.• sunburns are commonly first-degree burns.
60
1° burn
2° burn
61
Superficial burn (1° burn)
62
• 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.
Partial thickness (2°burn)
63
2° burn
64
Partial thickness (2°burn)
65
Burn:Classification3.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.
66
3° burn
67
Eschar:composed of denatured protein
68
Full thickness (3°burn)
69
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.
70
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.
71
72
Age in years Age in years 0 0 1 1 5 5 10 10 15 15 Adult Adult
A-head (back or A-head (back or front) front)
9½ 9½ 88½ ½
6½ 6½ 5½ 5½ 4½ 4½ 3½ 3½
B-1 thigh (back or B-1 thigh (back or front) front)
2¾ 2¾ 33¼ ¼
4 4 4¼ 4¼ 4½ 4½ 4¾ 4¾
C-1 leg (back or C-1 leg (back or front) front)
2½ 2½ 22½ ½
2¾ 2¾ 3 3 3¼ 3¼ 3½ 3½
Lund and Browder chart
TYPES OF BURNSThermal Burns:
caused by exposure to flames, hot liquids, steam or hot objects
Chemical Burns:Caused by tissue contact with strong alkali, or organic compoundsSystemic toxicity from cutaneous absorption can occur
Radiation Burns: caused by exposure to UV light, x-rays, or radioactive source
TYPES OF BURNSElectrical Burns:
Caused by heat generated by electrical energy as it passes through the bodyResults 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
HypovolemiaApproximately 10% of plasma volume lost into
tissue soon after a severe burnOccurs because of the third space shift causes
multiple effects:With burn’s 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)
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
– Circulatory status• Tachycardia and hypotension occur early• Elevate UO
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 Respiratory status takes priority over the
treatment of the burn injury If burn area is small cold compress or
immerse in cool water (not icenot ice) to ↓ heat May have ointment on the burn area 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
Formula name Electrolyte- Containing solution
Colloid-Containing Solution
Dextrose in Water
Evans NSS 1 ml/kg/%burn NSS 1 ml/kg/%burn 2000 ml
Brooke LR 1.5 ml/kg/%burn 0.5 ml/kg/%burn 2000 ml
Modified Brooke LR 2 ml/kg/%burn None None
Parkland LR 4 ml/kg/%burn None None
Hypertonic Saline
Fluid containing 250 mEq of Na/L to maintain hourly urine output of 70 ml in adults
None None
First 24 hours
Burns
Formula name Electrolyte- Containing solution
Colloid-Containing Solution
Dextrose in Water
Evans ½ of first 24-hr requirement
½ of first 24-hr requirement
2000 ml
Brooke ½ - ¾ of first 24-hr requirement
½ - ¾ of first 24-hr requirement
2000 ml
Modified Brooke None 0.3-0.5 ml/kg/%burn Titrate to maintain urine output
Parkland None 0.3-0.5 ml/kg/%burn Titrate to maintain urine output
Hypertonic Saline
Same solution to maintain hourly urine output of 30 ml in adults
None None
Second 24 hours
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 pre-existing 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
BicarbonateChloride
Phosphorous
CalciumMagnesiumPotassium
Sodium
WHAT DO ELECTROLYTES DO?WHAT DO ELECTROLYTES DO?
• Controls and regulates volume of body fluidsControls and regulates volume of body fluids
• Its concentration is the major determinant of ECF volumeIts concentration is the major determinant of ECF volume
• Is the chief electrolyte of ECFIs the chief electrolyte of ECF
• Influence ICF VolumeInfluence ICF Volume
•Participates in the generation and transmission of nerve impulsesParticipates in the generation and transmission of nerve impulses
• Is an essential electrolyte in the sodium-potassium pumpIs an essential electrolyte in the sodium-potassium pump
• RDA: not known precisely. 500 mgRDA: not known precisely. 500 mg
• Eliminated primarily by the kidneys, smaller in feces and perspirationEliminated primarily by the kidneys, smaller in feces and perspiration
• Salt intake affects sodium concentrationsSalt intake affects sodium concentrations
• Sodium is conserved through reabsorption in the kidneys, a process Sodium is conserved through reabsorption in the kidneys, a process stimulated by aldosteronestimulated by aldosterone
• Normal value: 135-145 mEq/LNormal value: 135-145 mEq/L
HYPONATREMIAHYPONATREMIA• 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 HYPONATREMIAPATHOPHYSIOLOGY OF HYPONATREMIASodium loss from the intravascular compartmentSodium loss from the intravascular compartment
Diffusion of water into the interstitial spacesDiffusion of water into the interstitial spaces
Sodium in the interstitial space is dilutedSodium in the interstitial space is diluted
Decreased osmolarity of ECFDecreased osmolarity of ECF
Water moves into the cell as a result of sodium lossWater moves into the cell as a result of sodium loss
Extracellular compartment is depleted of waterExtracellular compartment is depleted of water
CLINICAL SYMPTOMSCLINICAL SYMPTOMS
CLINICAL MANIFESTATIONS OF HYPONATREMIACLINICAL MANIFESTATIONS OF HYPONATREMIA
Muscle Weakness
APATHY
Postural hypotensio
nNausea and
Abdominal Cramps
Weight Loss
In severe hyponatremia: mental confusion, delirium, shock and comaIn severe hyponatremia: mental confusion, delirium, shock and coma
COLLABORATIVE CARE MANAGEMENTCOLLABORATIVE CARE MANAGEMENT• General goal: correct sodium imbalance and restore normal fluid and General goal: correct sodium imbalance and restore normal fluid and
electrolyte homeostasiselectrolyte homeostasis• Recognition of people at risk for hyponatremia is essential for its Recognition of people at risk for hyponatremia is essential for its
prevention: athletes, persons working in hot environmentsprevention: athletes, persons working in hot environments• Salt is always replaced along with waterSalt is always replaced along with water• Management includes educating vulnerable people to recognize signs Management includes educating vulnerable people to recognize signs
and symptoms of sodium depletion and maintaining sufficient sodium and symptoms of sodium depletion and maintaining sufficient sodium and water intake to replace skin and insensible fluid lossand water intake to replace skin and insensible fluid loss
• Generally, an increased sodium and water intake provides adequate Generally, an increased sodium and water intake provides adequate treatmenttreatment
• Education as the importance of sodium and fluid balance and the Education as the importance of sodium and fluid balance and the rationale for prescription medications to ensure compliancerationale for prescription medications to ensure compliance
• Daily weight. MIODaily weight. MIO• Monitoring of sodium levels to determine extent of replacementMonitoring of sodium levels to determine extent of replacement• Generally, PNSS or PLRS is prescribedGenerally, PNSS or PLRS is prescribed• Too rapid restoration of sodium balance, hypertonic sodium solutions Too rapid restoration of sodium balance, hypertonic sodium solutions
may provoke brain injury may provoke brain injury
HYPERNATREMIAHYPERNATREMIA
• A serum sodium level above 145 mEq/L is termed hypernatremiaA serum sodium level above 145 mEq/L is termed hypernatremia• May occur as a result of fluid deficit or sodium excessMay occur as a result of fluid deficit or sodium excess• Frequently occurs with fluid imbalanceFrequently occurs with fluid imbalance• Develops when an excess of sodium occurs without a proportional Develops when an excess of sodium occurs without a proportional
increase in body fluid or when water loss occurs without increase in body fluid or when water loss occurs without proportional loss of sodiumproportional loss of sodium
• Risk Factors: excess dietary or parenteral sodium intake, watery Risk Factors: excess dietary or parenteral sodium intake, watery diarrhea, diabetes insipidus, damage to thirst center, those with diarrhea, diabetes insipidus, damage to thirst center, those with physical or mental status compromise, and people with physical or mental status compromise, and people with hypothalamic dysfunctionhypothalamic dysfunction
PATHOPHYSIOLOGY OF HYPERNATREMIAPATHOPHYSIOLOGY OF HYPERNATREMIAIncreased Sodium concentration in ECFIncreased Sodium concentration in ECF
Osmolarity risesOsmolarity rises
Water leaves the cell by osmosis and enters Water leaves the cell by osmosis and enters the the extracellular compartmentsthe the extracellular compartments
Dilution of fluids in ECFDilution of fluids in ECF Cells are water depletedCells are water depleted
Suppression of aldosterone Suppression of aldosterone secretionsecretion
Sodium is exreted in the Sodium is exreted in the urineurine
CLINICAL SYMPTOMSCLINICAL SYMPTOMS
CLINICAL MANIFESTATIONSCLINICAL MANIFESTATIONS
Dry, sticky Dry, sticky mucous mucous
membranesmembranes
Firm, rubbery Firm, rubbery tissue turgortissue turgor
Manic Manic excitementexcitement
TachycardiaTachycardiaDEATHDEATH
COLLABORATIVE CARE MANAGEMENTCOLLABORATIVE CARE MANAGEMENT• Recognition of risk factors: bedridden and debilitated patients, Recognition of risk factors: bedridden and debilitated patients,
diabetes insipidus, fluid deprivation, the elderly and the very diabetes insipidus, fluid deprivation, the elderly and the very youngyoung
• A careful and accurate record of MIO permits quick recognition A careful and accurate record of MIO permits quick recognition of negative fluid balanceof negative fluid balance
• People with kidney failure, CHF, or increased aldosterone People with kidney failure, CHF, or increased aldosterone production may require dietary sodium intake restrictionproduction may require dietary sodium intake restriction
• Usually, osmolar balance can be restored with oral fluids. If Usually, osmolar balance can be restored with oral fluids. If not, the parenteral route may be necessarynot, the parenteral route may be necessary
• Fluid resuscitation must be undertaken with particular caution Fluid resuscitation must be undertaken with particular caution in patients with compromised cardiac or renal functionin patients with compromised cardiac or renal function
• The nurse should closely monitor the patient’s response to The nurse should closely monitor the patient’s response to fluids and be alert to symptoms of fluid overloadfluids and be alert to symptoms of fluid overload
• Major cation of the ICF. Chief regulator of cellular enzyme activity and Major cation of the ICF. Chief regulator of cellular enzyme activity and cellular water content cellular water content
• The more K, the less Na. The less K, the more NaThe more K, the less Na. The less K, the more Na
• Plays a vital role in such processes such as transmission of electrical Plays a vital role in such processes such as transmission of electrical impulses, particularly in nerve, heart, skeletal, intestinal and lung tissue; impulses, particularly in nerve, heart, skeletal, intestinal and lung tissue; CHON and CHO metabolism; and cellular building; and maintenance of CHON and CHO metabolism; and cellular building; and maintenance of cellular metabolism and excitationcellular metabolism and excitation
• Assists in regulation of acid-base balance by cellular exchange with HAssists in regulation of acid-base balance by cellular exchange with H
• RDA: not known precisely. 50-100 mEqRDA: not known precisely. 50-100 mEq
• Sources: bananas, peaches, kiwi, figs, dates, apricots, oranges, Sources: bananas, peaches, kiwi, figs, dates, apricots, oranges, prunes, melons, raisins, broccoli, and potatoes, meat, dairy productsprunes, melons, raisins, broccoli, and potatoes, meat, dairy products
• Excreted primarily by the kidneys. No effective conserving mechanismExcreted primarily by the kidneys. No effective conserving mechanism
• Conserved by sodium pump and kidneys when levels are lowConserved by sodium pump and kidneys when levels are low
• Aldosterone triggers K excretion in urineAldosterone triggers K excretion in urine
• Normal value: 3.5 – 5 mEq/LNormal value: 3.5 – 5 mEq/L
CAUSES AND EFFECTS OF HYPOKALEMIACAUSES AND EFFECTS OF HYPOKALEMIA• Known as a low level of serum potassium, less than 3.5 mEq/L Known as a low level of serum potassium, less than 3.5 mEq/L
Decreased IntakeDecreased Intake
↓ Food and Fluids as in starvation
Failure to replace GI losses
Increased LossIncreased Loss
↑ ↑ AldosteroneAldosteroneGastrointestinal lossesGastrointestinal losses
Potassium-losing diureticsPotassium-losing diureticsLoss from cells as in trauma, Loss from cells as in trauma,
burnsburns
Shift of Potassium Shift of Potassium into Cellsinto Cells
(No change in total (No change in total body potassium)body potassium)
HYPOKALEMIAHYPOKALEMIA
GI TractGI Tract
Anorexia
N&V
Abdominal distention
CNSCNS
Lethargy, Diminished
deep-tendon reflexes,
Confusion, Mental
depression
MusclesMuscles
Weakness, Flaccid paralysis,
Weakness of respiratory muscles,
Respiratory arrest
CV SystemCV System
Decrease in standing BP,
Dysrhythmias, ECG changes,
Myocardial damage, Cardiac
arrest
KidneysKidneys
↓Capacity to concentrate waste, water loss, thirst,
kidney damage
PATHOPHYSIOLOGY OF HYPOKALEMIAPATHOPHYSIOLOGY OF HYPOKALEMIA
= Action Potential= Action Potential
Nerve and Muscle ActivityNerve and Muscle Activity
Low Low Extracellular Extracellular
K+K+
Increase in Increase in resting resting
membrane membrane potentialpotential
The cell The cell becomes becomes
less less excitableexcitable
Sodium is retained in the body through resorption by Sodium is retained in the body through resorption by the kidney tubulesthe kidney tubules
Potassium is excretedPotassium is excreted
Aldosterone is secretedAldosterone is secreted
Use of certain diuretics such as thiazides and furosemide, and Use of certain diuretics such as thiazides and furosemide, and corticosteroidscorticosteroids
Increased urinary outputIncreased urinary output
Loss of potassium in urineLoss of potassium in urine
COLLABORATIVE CARE MANAGEMENTCOLLABORATIVE 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 ½ 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 HYPERKALEMIACAUSES AND EFFECTS OF HYPERKALEMIA• Serum potassium level greater than 5.5 mEq/LSerum potassium level greater than 5.5 mEq/L
Excess IntakeExcess Intake
Dietary intake of excess of kidney’s ability to
excrete; Excess parenteral administration
Decreased LossDecreased Loss
Potassium-sparing diuretics; Potassium-sparing diuretics; Renal failure; Adrenal Renal failure; Adrenal
insufficiencyinsufficiency
Shift of Potassium Shift of Potassium out of the Cellsout of the Cells
Extensive injuries, Extensive injuries, crushing injuries, crushing injuries,
metabolic acidosismetabolic acidosis
HYPERKALEMIAHYPERKALEMIA
GI TractGI Tract
N&V
Diarrhea, Colic
CNSCNS
Numbness, paresthesias
MusclesMuscles
Early: irritability
Late: weakness leading to flaccid
paralysis
CV SystemCV System
Conduction disturbance, ventricular fibrillation,
Cardiac Arrest
KidneysKidneys
Oliguria leading to
anuria
COLLABORATIVE CARE MANAGEMENTCOLLABORATIVE CARE MANAGEMENT• Patients at risk should be identified: impaired renal function to Patients at risk should be identified: impaired renal function to
avoid OTC, esp. NSAIDS which provoke hyperkalemia; and salt avoid OTC, esp. NSAIDS which provoke hyperkalemia; and salt substitutes that are high in potassiumsubstitutes that are high in potassium
• Severity guides therapySeverity guides therapy– Mild: Withholding provoking agent (i.e., K supp)Mild: Withholding provoking agent (i.e., K supp)– Severe (>6 mEq/L: cation-exchange resin such as Severe (>6 mEq/L: cation-exchange resin such as
Kayexalate (act by exchanging the cations in the resin for Kayexalate (act by exchanging the cations in the resin for the potassium in the intestine the potassium in the intestine potassium is then excreted potassium is then excreted in the stool; Continuous cardiac monitoringin the stool; Continuous cardiac monitoring
• Bowel function must be maintained if Kayexelate therapy is to Bowel function must be maintained if Kayexelate therapy is to be effectivebe effective
• Potassium-wasting diuretics may be prescribed to promote Potassium-wasting diuretics may be prescribed to promote further potassium loss. Dialysis for patients with renal failure to further potassium loss. Dialysis for patients with renal failure to eliminate excess potassiumeliminate excess potassium
• Intravenous Ca Gluconate may be prescribed to counteract the Intravenous Ca Gluconate may be prescribed to counteract the cardiac effects of hyperkalemiacardiac effects of hyperkalemia
• Insulin infusions and IV NaCO3 may be used to promote Insulin infusions and IV NaCO3 may be used to promote intracellular uptake of Kintracellular uptake of K
• Most abundant electrolyte in the body. 99% in bones and teethMost abundant electrolyte in the body. 99% in bones and teeth
• Close link between calcium and phosphorus. High PO4, Low CaClose link between calcium and phosphorus. High PO4, Low Ca
• Necessary for nerve impulse transmission and blood clotting and is Necessary for nerve impulse transmission and blood clotting and is also a catalyst for muscle contraction and other cellular activitiesalso a catalyst for muscle contraction and other cellular activities
• Needed for Vitamin B12 absorption and useNeeded for Vitamin B12 absorption and use
• Necessary for strong bones and teeth and thickness and strength of Necessary for strong bones and teeth and thickness and strength of cell membranescell membranes
• RDA: 1g for adults. Higher for children and pregnant and lactating RDA: 1g for adults. Higher for children and pregnant and lactating women according to body weight, older people, esp. post-menopausal women according to body weight, older people, esp. post-menopausal
• Found in milk, cheese, and dried beans; some in meat and vegetablesFound in milk, cheese, and dried beans; some in meat and vegetables
• Use is stimulated by Vitamin D. Excreted in urine, feces, bile, digestive Use is stimulated by Vitamin D. Excreted in urine, feces, bile, digestive secretions, and perspirationsecretions, and perspiration
• Normal value 8.5 – 10.5 mg/dlNormal value 8.5 – 10.5 mg/dl
CAUSES AND EFFECTS OF HYPOCALCEMIACAUSES AND EFFECTS OF HYPOCALCEMIADecreased Decreased Ionized CaIonized Ca
Large tranfusion with citrated blood
Excess LossExcess Loss
Kidney DiseaseKidney Disease
Decrease in GI Tract Decrease in GI Tract and Bone Absorptionand Bone Absorption
↑↑MagnesiumMagnesium
↑↑CalcitoninCalcitonin
↓Vitamin D↓Parathyroid Hormone
HYPOCALCEMIAHYPOCALCEMIA
BonesBonesOsteoporosis
leading to Fractures
CNSCNS
Tingling
↓ convulsions
OtherOther
Abnormal deposits
of calcium in body tissues
MusclesMuscles
Muscle spasm
↓
Tetany
Cardiovascular Cardiovascular SystemSystem
Dysrhythmias
↓
Cardiac arrest
Inadequate Inadequate IntakeIntake
Dietary DeficitDietary Deficit
PATHOPHYSIOLOGY OF HYPOCALCEMIAPATHOPHYSIOLOGY 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
•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
Sodium Calcium
CLINICAL MANIFESTATIONS OF HYPOCALCEMIACLINICAL MANIFESTATIONS OF HYPOCALCEMIA
COMPLAINT OF NUMBNESS AND TINGLING OF EARS, NOSE, COMPLAINT OF NUMBNESS AND TINGLING OF EARS, NOSE, FINGERTIPS OR TOESFINGERTIPS OR TOES
TREATMENTTREATMENT
PAINFUL MUSCULAR SPASMS (TETANY) PAINFUL MUSCULAR SPASMS (TETANY) ESPECIALLY OF FEET AND HANDS ESPECIALLY OF FEET AND HANDS
(CARPOPEDAL SPASMS), MUSCLE TWITCHING (CARPOPEDAL SPASMS), MUSCLE TWITCHING AND CONVULSIONS MAY FOLLOWAND CONVULSIONS MAY FOLLOW
TESTS USED TO ELICIT SIGNS OF CALCIUM DEFICIENCYTESTS USED TO ELICIT SIGNS OF CALCIUM DEFICIENCY
COLLABORATIVE CARE MANAGEMENTCOLLABORATIVE CARE MANAGEMENT• Identify risk factors: Inadequate calcium intake, excess calcium loss, Identify risk factors: Inadequate calcium intake, excess calcium loss,
Vitamin D deficiency, patients with poor dietsVitamin D deficiency, patients with poor diets• Education about the importance of adequate calcium and Vitamin D Education about the importance of adequate calcium and Vitamin D
intakeintake• Patients undergoing thyroid, parathyroid, and radical neck surgery are Patients undergoing thyroid, parathyroid, and radical neck surgery are
particularly vulnerable to hypocalcemia secondary to parathyroid particularly vulnerable to hypocalcemia secondary to parathyroid hormone deficithormone deficit
• Monitoring of serum calcium levels and correction of deficitsMonitoring of serum calcium levels and correction of deficits• Citrate is added to store blood to prevent coagulation. Citrate is added to store blood to prevent coagulation. • Citrate + Transfusion = Citrate+CalciumCitrate + Transfusion = Citrate+Calcium• Normally, Liver + Citrate = Quick metabolismNormally, Liver + Citrate = Quick metabolism• Preexisting calcium deficit/hepatic dysfunction/large amounts of BT Preexisting calcium deficit/hepatic dysfunction/large amounts of BT
very rapidly = hypocalcemiavery rapidly = hypocalcemia• With acute hypocalcemia, Ca Gluconate is used + Continuous cardiac With acute hypocalcemia, Ca Gluconate is used + Continuous cardiac
monitoringmonitoring• Mild Hypocalcemia: High calcium diet or oral calcium saltsMild Hypocalcemia: High calcium diet or oral calcium salts• If PTH or Vit D Deficiency is the cause: aluminum hydroxide gel is If PTH or Vit D Deficiency is the cause: aluminum hydroxide gel is
used because when serum phosphate level rises, calcium level fallsused because when serum phosphate level rises, calcium level falls• Complication: Bone demineralizationComplication: Bone demineralization• Therefore, careful ambulation should be encouraged to minimize bone Therefore, careful ambulation should be encouraged to minimize bone
resorptionresorption
HYPERCALCEMIA: Serum concentration > 10mg/dLHYPERCALCEMIA: Serum concentration > 10mg/dLCauses and EffectsCauses and Effects
Loss from bonesLoss from bones
Immobilization, Carcinoma with bone metastases, Multiple
myeloma
Excess IntakeExcess Intake
↑ ↑ Calcium diet (esp. milk)Calcium diet (esp. milk)Antacids containing calciumAntacids containing calcium
Increase in factors Increase in factors Causing Mobilization Causing Mobilization
from bonefrom bone
↑↑PTH, ↑PTH, ↑ Vitamin D, steroid therapy
HYPERCALCEMIAHYPERCALCEMIA
KidneysKidneys
Stones
↓
Kidney Damage
CNSCNS
↓Deep-tendon reflexes
↓
Lethargy
↓
Coma
BonesBones
Bone pain
↓
Osteoporosis
↓
Fractures
MusclesMuscles
Muscle fatigue, hypotonia
↓
↓ GI motility
CV SystemCV System
Depressed activity
↓
Dysrhythmias
↓
Cardiac Arrest
HOW IT HAPPENSHOW IT HAPPENSHYPERCALCEMIAHYPERCALCEMIA
DEPRESSED NERVE DEPRESSED NERVE AND MUSCLE AND MUSCLE
ACTIVITYACTIVITY
DEEP TENDON DEEP TENDON REFLEXES MAY BE REFLEXES MAY BE
DECREASED OR DECREASED OR ABSENTABSENT
MYOCARDIAL MYOCARDIAL FUNCTION IS FUNCTION IS
ALTEREDALTERED
CLINICAL MANIFESTATIONS OF HYPERCALCEMIACLINICAL MANIFESTATIONS OF HYPERCALCEMIA
Decreased GI Decreased GI MotilityMotility
Cardiac DysrhythmiasCardiac Dysrhythmias
ConstipationConstipation
NauseaNausea
Mental status changes: Mental status changes: lethargy, confusion, lethargy, confusion,
memory lossmemory loss
CLINICAL MANIFESTATIONS OF HYPERCALCEMIACLINICAL MANIFESTATIONS OF HYPERCALCEMIA
ImmobilizationImmobilization Bone Bone DemineralizationDemineralization
Calcium Calcium accumulates in accumulates in
the ECF and the ECF and passes through passes through
the kidneysthe kidneys
Ca PrecipitationCa PrecipitationCalcium StonesCalcium Stones
COLLABORATIVE CARE MANAGEMENTCOLLABORATIVE 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 tissuesMostly found within body cells: heart, bone, nerve, and muscle tissues
• Second most important cation in the ICF, 2Second most important cation in the ICF, 2ndnd to K+ to K+
• Functions: Metabolism of CHO and CHON, protein and DNA synthesis, Functions: Metabolism of CHO and CHON, protein and DNA synthesis, DNA and RNA transcription, and translation of RNA, maintains normal DNA and RNA transcription, and translation of RNA, maintains normal intracellular levels of potassium, helps maintain electric activity in intracellular levels of potassium, helps maintain electric activity in nervous tissue membranes and muscle membranesnervous tissue membranes and muscle membranes
• RDA: about 18-30 mEq; children require larger amountsRDA: about 18-30 mEq; children require larger amounts
• Sources: vegetables, nuts, fish, whole grains, peas, and beansSources: vegetables, nuts, fish, whole grains, peas, and beans
• Absorbed in the intestines and excreted by the kidneysAbsorbed in the intestines and excreted by the kidneys
• Plasma concentrations of magnesium range from 1.5 – 2.5 mEq/L, with Plasma concentrations of magnesium range from 1.5 – 2.5 mEq/L, with about one third of that amount bound to plasma proteinsabout one third of that amount bound to plasma proteins
HYPOMAGNESEMIA: Serum level < 1.5 mEq/LHYPOMAGNESEMIA: Serum level < 1.5 mEq/L• Usually coexists with hypokalemia and less often with hypocalcemia
Decreased IntakeDecreased Intake
Prolonged malnutrition, Starvation
Impaired absorption from GI TractImpaired absorption from GI Tract
Malabsorption syndrome, Alcohol Withdrawal Malabsorption syndrome, Alcohol Withdrawal Syndrome, Hypercalcemia, Diarrhea, Syndrome, Hypercalcemia, Diarrhea,
Draining gastrointestinal fistulaDraining gastrointestinal fistula
Excessive Excessive ExcretionExcretion
↑↑Aldosterone, Aldosterone, Conditions Conditions
causing large causing large losses of urinelosses of urine
HYPOMAGNESEMIAHYPOMAGNESEMIA
Mental ChangesMental Changes
Agitation, Depression, Confusion
CNSCNS
Convulsions, Paresthesias, Tremor, Ataxia
MusclesMuscles
Cramps, Spasticity, Tetany
CV SystemCV System
Tachycardia, Hypotension, Dysrhythmias
HYPOKALEMIAHYPOKALEMIA
PATHOPHYSIOLOGY OF HYPOMAGNESEMIAPATHOPHYSIOLOGY OF HYPOMAGNESEMIA
Low serum magnesium levelLow serum magnesium level
Increased acetylcholine releaseIncreased acetylcholine release
Increased neuromuscular irritabilityIncreased neuromuscular irritability
Increased sensitivity to acetylcholine at the myoneural junctionIncreased sensitivity to acetylcholine at the myoneural junction
Diminished threshold of Diminished threshold of excitation for the motor excitation for the motor
nervenerve
Enhancement of myofibril Enhancement of myofibril contractioncontraction
PATHOPHYSIOLOGY OF HYPOMAGNESEMIAPATHOPHYSIOLOGY OF HYPOMAGNESEMIA
High Serum CalciumHigh Serum Calcium
Increased acetylcholine releaseIncreased acetylcholine release
Increased neuromuscular irritabilityIncreased neuromuscular irritability
Increased sensitivity to acetylcholine at the myoneural junctionIncreased sensitivity to acetylcholine at the myoneural junction
Diminished threshold of Diminished threshold of excitation for the motor excitation for the motor
nervenerve
Enhancement of myofibril Enhancement of myofibril contractioncontraction
High Serum CalciumHigh Serum CalciumExcretion of MagnesiumExcretion of Magnesium
By the GI tractBy the GI tract
PATHOPHYSIOLOGY OF HYPOMAGNESEMIAPATHOPHYSIOLOGY OF HYPOMAGNESEMIA
MAGNESIUMMAGNESIUM
INHIBITS TRANSPORT OF PTHINHIBITS TRANSPORT OF PTH
DECREASE IN THE AMOUNT OF CALCIUM BEING RELEASED DECREASE IN THE AMOUNT OF CALCIUM BEING RELEASED FROM THE BONEFROM THE BONE
POSSIBLE CALCIUM DEFICITPOSSIBLE CALCIUM DEFICIT
CLINICAL MANIFESTATIONS OF HYPOMAGNESEMIACLINICAL MANIFESTATIONS OF HYPOMAGNESEMIA
CONFUSIONCONFUSION
DEPRESSIONDEPRESSION
CRAMPSCRAMPS
TETANYTETANY CONVULSIONSCONVULSIONS
COLLABORATIVE CARE MANAGEMENTCOLLABORATIVE CARE MANAGEMENT• Recognition of people at risk: people taking loop diuretics and Recognition of people at risk: people taking loop diuretics and
digoxin should be encouraged to eat foods rich in magnesium, digoxin should be encouraged to eat foods rich in magnesium, such as fruits, vegetables, cereals, and milksuch as fruits, vegetables, cereals, and milk
• Recognition of signs and symptoms of magnesium deficiencyRecognition of signs and symptoms of magnesium deficiency• Magnesium is essential for potassium resorption, so if Magnesium is essential for potassium resorption, so if
hypokalemia does not respond to potassium replacement, hypokalemia does not respond to potassium replacement, hypomagnesemia should be suspectedhypomagnesemia should be suspected
• Treatment of the underlying cause is the first consideration in Treatment of the underlying cause is the first consideration in hypomagnesemiahypomagnesemia
• Severe: parenteral magnesium replacement is indicatedSevere: parenteral magnesium replacement is indicated• IV therapy: continuous cardiac monitoringIV therapy: continuous cardiac monitoring• Safety measures for patients with mental status changesSafety measures for patients with mental status changes
HYPERMAGNESEMIA: Serum Mg level 2.5 mEq/LHYPERMAGNESEMIA: Serum Mg level 2.5 mEq/L• Seldom develops in the presence of normal renal functionSeldom develops in the presence of normal renal function• May occur as a result of Mg replacementMay occur as a result of Mg replacement• May occur when MgSO4 is administered to prevent seizures May occur when MgSO4 is administered to prevent seizures
resulting from eclampsiaresulting from eclampsia• Careful monitoring is imperativeCareful monitoring is imperative
PATHOPHYSIOLOGYPATHOPHYSIOLOGYRenal failure, Excessive IV infusion of Renal failure, Excessive IV infusion of
magnesium, Decreased GI elimination magnesium, Decreased GI elimination and/or absorption, etc.and/or absorption, etc.
Accummulation of Mg in the bodyAccummulation of Mg in the body
Diminishing of reflexes, drowsiness, lethargyDiminishing of reflexes, drowsiness, lethargy
Mg Level RisesMg Level Rises
Severe Respiratory DepressionSevere Respiratory Depression
RESPIRATORY ARREST may occurRESPIRATORY ARREST may occur
Altered Electrical ConductionAltered Electrical Conduction
Slowed heart Slowed heart rate and AV rate and AV
BlockBlock
Peripheral Peripheral vasodilationvasodilation
Hypotension, flushing, and Hypotension, flushing, and increased skin warmthincreased skin warmth
COLLABORATIVE CARE MANAGEMENTCOLLABORATIVE CARE MANAGEMENT• Identification of patients at risk: those with impaired renal Identification of patients at risk: those with impaired renal
function to avoid OTC that contain magnesium such as Milk of function to avoid OTC that contain magnesium such as Milk of Magnesia and some Mg-containing antacidsMagnesia and some Mg-containing antacids
• Any patient receiving parenteral magnesium therapy should be Any patient receiving parenteral magnesium therapy should be assessed frequently for signs of hypermagnesemiaassessed frequently for signs of hypermagnesemia
• Mild hypermagnesemia: withholding magnesium-containing Mild hypermagnesemia: withholding magnesium-containing medications may sufficemedications may suffice
• Renal failure: dialysisRenal failure: dialysis• Severe: may require treatment with calcium gluconate (10-20 Severe: may require treatment with calcium gluconate (10-20
mL of 10% Ca Gluconate administered over 10 minutes)mL of 10% Ca Gluconate administered over 10 minutes)• If cardiorespiratory collapse is imminent, the patient may If cardiorespiratory collapse is imminent, the patient may
require temporary pacemaker and ventilator supportrequire temporary pacemaker and ventilator support
NURSING MANAGEMENT OF NURSING MANAGEMENT OF PATIENT WITH FLUID AND PATIENT WITH FLUID AND
ELECTROLYTE IMBALANCESELECTROLYTE IMBALANCES
Parameter_____Fluid Excess___ Parameter_____Fluid Excess___ Fluid Loss/Electrolyte Imbalance____Fluid Loss/Electrolyte Imbalance____Behavior Tires easily; Change in behavior, confusion, apathy
Head, neck Facial edema, distended neck Headache, thirst, dry mucous membranes veins
Upper GI Anorexia, nausea, vomiting
Skin Warm, moist, taut, cool feeling Dry, decreased turgor where edematous
Respiration Dyspnea, orthopnea, productive Changes in rate and depth of respirationcough, moist breath sounds
Circulation Loss of sensation in edematous Pulse rate changes, dysrhythmia, postural areas, pallor, bounding pulse,
increased blood pressure hypotension
Abdomen Increased girth, fluid wave Distention, abdominal cramps
Elimination Constipation Diarrhea, constipation
Extremities Dependent edema, “pitting” Muscle weakness, tingling, tetany , discomfort from weight of
bedclothes
Pitting edemaPitting edema
Dependent edemaDependent edema
Refractory EdemaRefractory Edema
LABORATORY VALUESLABORATORY VALUESFLUID DEFICITFLUID DEFICIT FLUID EXCESSFLUID EXCESS
HemoconcentrationHemoconcentration HemodilutionHemodilution
↑ ↑ Hct, BUN, E+ levelsHct, BUN, E+ levels ↓ ↓ Hct, BUN, E+ levelsHct, BUN, E+ levels
↑ ↑ Urine Specific GravityUrine Specific Gravity ↓ Urine Specific Gravity ↓ Urine Specific Gravity
Determined from analysis of patient dataDetermined from analysis of patient data
Diagnostic TitleDiagnostic Title Possible Etiologic FactorsPossible Etiologic Factors
11 Deficient fluid volumeDeficient fluid volume Active fluid volume loss Active fluid volume loss (hemorrhage, diarrhea, gastric (hemorrhage, diarrhea, gastric
intubation, wounds, diaphoresis), intubation, wounds, diaphoresis), inadequate fluid intake, failure of inadequate fluid intake, failure of
regulatory mechanisms, regulatory mechanisms, sequestration of body fluidssequestration of body fluids
22 Excess Fluid Volume Excess Fluid Volume Excess fluid intake, excess sodium Excess fluid intake, excess sodium intake, compromised regulatory intake, compromised regulatory
processesprocesses
EXPECTED PATIENT OUTCOMESEXPECTED PATIENT OUTCOMES
1.1. Will maintain functional fluid volume as evidenced by Will maintain functional fluid volume as evidenced by adequate urinary output, stable weight, normal vital adequate urinary output, stable weight, normal vital
signs, normal urine specific gravity, moist mucus signs, normal urine specific gravity, moist mucus membranes, balanced intake and output, elastic skin turgor, membranes, balanced intake and output, elastic skin turgor,
prompt capillary refill, and absence of edemaprompt capillary refill, and absence of edema
2.2. Will verbalize understanding of treatment plan and Will verbalize understanding of treatment plan and causative factors that led to the imbalancecausative factors that led to the imbalance
1,21,2 Intake and Output MonitoringIntake and Output Monitoring- Type and amount of fluid the patient has received and the - Type and amount of fluid the patient has received and the route by which they were administeredroute by which they were administered-- Record of solid food intake. Gelatin or Popsicles are Record of solid food intake. Gelatin or Popsicles are recorded as fluidsrecorded as fluids-- Ice chips are recorded by dividing the amount of chips Ice chips are recorded by dividing the amount of chips by ½ (60 mL of chips = 30 mL water)by ½ (60 mL of chips = 30 mL water)-- Accurate output record and described by color, content, Accurate output record and described by color, content, and odor (Normally, gastric contents are watery and pale and odor (Normally, gastric contents are watery and pale yellow-green; they usually have a sour odor)yellow-green; they usually have a sour odor)-- With acid-base balance upset, gastric secretions may With acid-base balance upset, gastric secretions may have a fruity odor because of ketone bodieshave a fruity odor because of ketone bodies-- Bile: thicker than gastric juice, dark green to brown, Bile: thicker than gastric juice, dark green to brown, acrid odor, bitter taste when vomitingacrid odor, bitter taste when vomiting-- NGT irrigation added to intakeNGT irrigation added to intake-- Stools: difficult to estimate amount; consistency, color, Stools: difficult to estimate amount; consistency, color, and number of stools provide a reasonable estimateand number of stools provide a reasonable estimate-- Peritoneal or pleural fluid drainage is recorded as output Peritoneal or pleural fluid drainage is recorded as output as with its amount, color, and clarity as with its amount, color, and clarity -- Character and volume of urine. Place signs and Character and volume of urine. Place signs and materials so materials so that an accurate record of UO is maintainedthat an accurate record of UO is maintained
1,21,2 Intake and Output MonitoringIntake and Output Monitoring- Evaluate and refer urine specific gravity as appropriate - Evaluate and refer urine specific gravity as appropriate
(normal value is 1.003 – 1.030). The implications are:(normal value is 1.003 – 1.030). The implications are:HighHigh DehydrationDehydrationLowLow SIADH, overhydrationSIADH, overhydration
-- Drainage, fluid aspirated from any body cavity must be Drainage, fluid aspirated from any body cavity must be measured. With dressings, fluid loss is the difference measured. With dressings, fluid loss is the difference between the wet dressings and the dry weight of the between the wet dressings and the dry weight of the
dressingdressing-- Accurate recording of the temperature to help the Accurate recording of the temperature to help the
physician determine how much fluid should be replaced physician determine how much fluid should be replaced 1,21,2 Daily WeightDaily Weight
-- Evaluate trends in weight (An increase in 1kg in weight Evaluate trends in weight (An increase in 1kg in weight is equal to the retention of 1L of fluid in an edematous is equal to the retention of 1L of fluid in an edematous patient)patient)
Considerations: Considerations: -- Daily weights early in the morning after voiding Daily weights early in the morning after voiding
but before he or she has eaten or defecatedbut before he or she has eaten or defecated
11 Replacement of Fluid and ElectrolytesReplacement of Fluid and ElectrolytesGeneral Principles:General Principles:
-- Either by oral intake (healthiest way), tube feeding, Either by oral intake (healthiest way), tube feeding, intravenous infusion, and/or total parenteral nutritionintravenous infusion, and/or total parenteral nutrition
-- Normal saline solution and plain water should also be Normal saline solution and plain water should also be given by slow drip to replace daily fluid lossgiven by slow drip to replace daily fluid loss-- IV administration per doctor’s ordersIV administration per doctor’s orders-- Fluid replacement considerations:Fluid replacement considerations:
** Most effective when apportioned over 24 hr period Most effective when apportioned over 24 hr period (Better regulation, (Better regulation, ↓potential for calculi formation and ↓potential for calculi formation and
subsequent renal damage, ↓potential for circulatory subsequent renal damage, ↓potential for circulatory overload which may cause in fluid and electrolyte overload which may cause in fluid and electrolyte shifts)shifts)
** Administer concentrated solutions of Na, Glucose or Administer concentrated solutions of Na, Glucose or protein because they require body fluids for dilutionprotein because they require body fluids for dilution
** Consider the size of the patient (small adult has less Consider the size of the patient (small adult has less fluid in each compartment, especially in the fluid in each compartment, especially in the intravascular compartment)intravascular compartment)
-- Promote oral intake as appropriatePromote oral intake as appropriate** Caution with coffee, tea, and some colasCaution with coffee, tea, and some colas
** small amount at frequent intervals is more useful than a small amount at frequent intervals is more useful than a large amount presented less oftenlarge amount presented less often
** Always give consideration to cultural and aesthetic Always give consideration to cultural and aesthetic aspects of eatingaspects of eating-- Give mouth care to a dehydrated patient before and after Give mouth care to a dehydrated patient before and after
meals and before bedtime (Xerostomia may lead to meals and before bedtime (Xerostomia may lead to disruption disruption of tissues in the oral cavity)of tissues in the oral cavity)
-- Avoid irritating foodsAvoid irritating foods-- Stimulation of saliva may be aided by hard candy or chewing Stimulation of saliva may be aided by hard candy or chewing
gum or carboxymethylcellulose (artificial saliva)gum or carboxymethylcellulose (artificial saliva)-- Keep lips moist and well lubricatedKeep lips moist and well lubricated-- Give salty broth or soda crackers for sodium replacement Give salty broth or soda crackers for sodium replacement
and tea or orange juice for potassium replacement as and tea or orange juice for potassium replacement as appropriate. Bananas, citrus fruits and juices, some fresh appropriate. Bananas, citrus fruits and juices, some fresh vegetables, vegetables, coffee, and tea are relatively high in potassium coffee, and tea are relatively high in potassium and low in sodium. and low in sodium. Milk, meat, eggs, and nuts are high in Milk, meat, eggs, and nuts are high in protein, sodium and protein, sodium and potassium.potassium.-- Offer milk for patients with draining fistulas from any portion Offer milk for patients with draining fistulas from any portion of of the GI tract. Lactose intolerance is not necessarily a the GI tract. Lactose intolerance is not necessarily a contraindication (Lactase enzyme preparations are available)contraindication (Lactase enzyme preparations are available)- - Increase usual daily requirement of foods when losses must Increase usual daily requirement of foods when losses must be be restored, as toleratedrestored, as tolerated
** Patients with cardiac and renal impairments are Patients with cardiac and renal impairments are instructed to avoid foods containing high levels instructed to avoid foods containing high levels of sodium, potassium and bicarbonateof sodium, potassium and bicarbonate
-- Administer replacement solutions through tube feeding as isAdminister replacement solutions through tube feeding as is** Either water, physiologic solution of NaCl, high protein Either water, physiologic solution of NaCl, high protein
liquids, or a regular diet can be blended, diluted and liquids, or a regular diet can be blended, diluted and given by gavagegiven by gavage** The water content in the tube feeding needs to be The water content in the tube feeding needs to be
increased if:increased if:11 the patient complains of thirstthe patient complains of thirst22 the protein or electrolyte content of the tube the protein or electrolyte content of the tube
feeding is highfeeding is high33 the patient has fever or disease causing an the patient has fever or disease causing an
increased metabolic rateincreased metabolic rate44 UO is concentratedUO is concentrated55 signs of water deficit developsigns of water deficit develop
-- Administer parenteral fluids as necessaryAdminister parenteral fluids as necessary
** Types of solutionsTypes of solutions-- D5W (hypotonic) is given short-term for hyponatremiaD5W (hypotonic) is given short-term for hyponatremia-- D5NSS may be given depending on the serum levels of D5NSS may be given depending on the serum levels of
sodium and vascular volume + KCl to meet normal sodium and vascular volume + KCl to meet normal intake needs and replace losses for hyponatremiaintake needs and replace losses for hyponatremia
-- Dextrose 5% in 0.2% normal saline is generally used as Dextrose 5% in 0.2% normal saline is generally used as a maintenance fluida maintenance fluid
-- Dextrose 5% in ½ normal saline is generally used as a Dextrose 5% in ½ normal saline is generally used as a replacement solution for losses caused by replacement solution for losses caused by gastrointestinal drainagegastrointestinal drainage
-- PNSS is given primarily when large amounts of sodium PNSS is given primarily when large amounts of sodium have been lost and for patients with hyponatremiahave been lost and for patients with hyponatremia
-- LRS is also isotonic because it remains in the LRS is also isotonic because it remains in the extracellular spaceextracellular space
-- Fructose or 10-20% glucose in distilled water are Fructose or 10-20% glucose in distilled water are hypertonic solutions and may partially meet body hypertonic solutions and may partially meet body needs for CHOsneeds for CHOs
-- Dextran (commonly-used plasma expander) increases Dextran (commonly-used plasma expander) increases plasma volume by increasing oncotic pressure. May plasma volume by increasing oncotic pressure. May cause prolonged bleeding time and is CI in patients cause prolonged bleeding time and is CI in patients with renal failure, bleeding disorders, or severe CHFwith renal failure, bleeding disorders, or severe CHF
** AdministrationAdministration-- The rate should be regulated according to the patient’s The rate should be regulated according to the patient’s
needs and condition per doctor’s ordersneeds and condition per doctor’s orders-- Monitor UO carefully. Refer marked decreases!Monitor UO carefully. Refer marked decreases!-- Verify orders for potassium administration in patients Verify orders for potassium administration in patients
with renal failure and untreated adrenal insufficiencywith renal failure and untreated adrenal insufficiency-- Usual rate for fluid loss replacement: 3ml/minUsual rate for fluid loss replacement: 3ml/min-- Recognize signs of pulmonary edema (bounding pulse, Recognize signs of pulmonary edema (bounding pulse, engorged peripheral veins, hoarseness, dyspnea, engorged peripheral veins, hoarseness, dyspnea, cough, and rales) that can result from cough, and rales) that can result from ↑IV rate↑IV rate-- If infiltration occurs, the infusion should be stopped If infiltration occurs, the infusion should be stopped
immediately and relocated. Peripheral IV sites are immediately and relocated. Peripheral IV sites are generally rotated every 72 hoursgenerally rotated every 72 hours
-- For dextran and other plasma expanders, observe for For dextran and other plasma expanders, observe for anaphylactic reaction (apprehension, dyspnea, anaphylactic reaction (apprehension, dyspnea,
wheezing, tightness of chest, angioedema, wheezing, tightness of chest, angioedema, itching, hives and hypotension). If this happens, itching, hives and hypotension). If this happens, switch infusion to nonprotein solution and run at KVO switch infusion to nonprotein solution and run at KVO
rate, notify physician and monitor VSrate, notify physician and monitor VS-- Pronounced and continued thirst despite administration Pronounced and continued thirst despite administration of fluids is not normal and should be reported (may of fluids is not normal and should be reported (may
indicate DM or hypercalcemia)indicate DM or hypercalcemia)
** Patient/Family EducationPatient/Family Education-- Include the signs and symptoms of water excess in Include the signs and symptoms of water excess in
discharge instructionsdischarge instructions-- With drug therapy, instruct patient and family regarding With drug therapy, instruct patient and family regarding
correct method of administration, correct dose, and correct method of administration, correct dose, and therapeutic and adverse effectstherapeutic and adverse effects
-- Instruct to read labels for nutritional contentInstruct to read labels for nutritional content* For K restriction: avoid organ meats, fresh and dried * For K restriction: avoid organ meats, fresh and dried
fruits, and salt substitutesfruits, and salt substitutes-- Skin assessment and care, positioning techniques for Skin assessment and care, positioning techniques for
patients with mobility restrictionspatients with mobility restrictions
** Achievement of outcomes is successful in disturbances in Achievement of outcomes is successful in disturbances in fluid fluid and electrolyte balance:and electrolyte balance:
11 Maintains functional fluid volume level with adequate UO, Maintains functional fluid volume level with adequate UO, VS within the patient’s normal limits, sp gr of urine VS within the patient’s normal limits, sp gr of urine within 1.003-1.035, moist mucous membranes, stable within 1.003-1.035, moist mucous membranes, stable weight, Intake=output, elastic skin turgor, and no edemaweight, Intake=output, elastic skin turgor, and no edema
22 States possible causes of imbalance and plan to prevent States possible causes of imbalance and plan to prevent recurrence of imbalancesrecurrence of imbalances
33 Reports a decrease or absence of symptoms causing Reports a decrease or absence of symptoms causing discomfortdiscomfort
Fluids and Electrolytes
Acid-base balance
DRAWING ARTERIAL BLOOD GASESDRAWING ARTERIAL BLOOD GASES
ALLEN’S TESTALLEN’S TESTARTERIAL PUNCTUREARTERIAL PUNCTURE
NORMAL ACID-BASE BALANCENORMAL ACID-BASE BALANCE
Estimated HCO3 concentration after fully Estimated HCO3 concentration after fully oxygenated arterial blood has been oxygenated arterial blood has been equilibrated with CO2 at a PCO2 of 40 equilibrated with CO2 at a PCO2 of 40 mmHg at 38C; eliminates the influence of mmHg at 38C; eliminates the influence of respiration on the plasma HCO3 respiration on the plasma HCO3 concentrationconcentration
22-2622-26 mEq/L mEq/LStandard HCO3Standard HCO3
Partial pressure of CO2 in the arterial Partial pressure of CO2 in the arterial blood:blood:PCO2<35 mmHg = respiratory alkalosisPCO2<35 mmHg = respiratory alkalosisPCO2>45 mmHg = respiratory acidosisPCO2>45 mmHg = respiratory acidosis
35-45 mmHg35-45 mmHgPaCO2PaCO2
Identifies whether there is acidemia or Identifies whether there is acidemia or alkalemia:alkalemia:pH<7.35 = acidosis; pH>7.45 = alkalosispH<7.35 = acidosis; pH>7.45 = alkalosis
7.35-7.457.35-7.45pHpH
Partial pressure of oxygen in arterial Partial pressure of oxygen in arterial blood (decreases with age)blood (decreases with age)In adults < 60 years:In adults < 60 years: 60-80 mmHg = mild hypoxemia60-80 mmHg = mild hypoxemia 40-60 mmHg = moderate hypoxemia40-60 mmHg = moderate hypoxemia < 40 mmHg = severe hypoxemia< 40 mmHg = severe hypoxemia
80-100 Hg80-100 HgPaO2PaO2
Definition and ImplicationsDefinition and ImplicationsNormal ValueNormal ValueParameterParameter
BASIC REGULATION OF ACID-BASE BALANCEBASIC REGULATION OF ACID-BASE BALANCE
CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3
The lungs help control acid-base balance by blowing off or The lungs help control acid-base balance by blowing off or retaining CO2. The kidneys help regulate acid-base balance by retaining CO2. The kidneys help regulate acid-base balance by
excreting or retaining HCO3excreting or retaining HCO3
TYPES OF ACID-BASE DISTURBANCESTYPES OF ACID-BASE DISTURBANCES
Depression of the central Depression of the central nervous system, as nervous system, as evidenced by disorientation evidenced by disorientation followed by comafollowed by coma
Overexcitability of the Overexcitability of the nervous system; muscles nervous system; muscles
may go into a state of tetany may go into a state of tetany and convulsioonsand convulsioons
EXPECTED DIRECTIONAL CHANGES WITH ACID-BASE IMBALANCESEXPECTED DIRECTIONAL CHANGES WITH ACID-BASE IMBALANCES
↑↑↑
↓↓↓
Normal↓↓
Normal↑↑
HCO3HCO3
Normal↑↑
↑↑
Normal
Metabolic AlkalosisUncompensatedPartly CompensatedCompensated
Normal↓↓
↓↓
Normal
Metabolic AcidosisUncompensatedPartly CompensatedCompensated
↓↓↓
↑↑
Normal
Respiratory AlkalosisUncompensatedPartly CompensatedCompensated
↑↑↑
↓↓
Normal
Respiratory AcidosisUncompensatedPartly CompensatedCompensated
PCO2PCO2pHpHCONDITIONCONDITION
Compensation
RESPIRATORY ACIDOSIS: CARBONIC ACID EXCESSRESPIRATORY ACIDOSIS: CARBONIC ACID EXCESSDamage to the respiratory center in the medulla, drug or narcotic use, obstruction Damage to the respiratory center in the medulla, drug or narcotic use, obstruction
of respiratory passages, respiratory and respiratory muscle disordersof respiratory passages, respiratory and respiratory muscle disorders
Decrease in the rate of pulmonary ventilationDecrease in the rate of pulmonary ventilation
Increase in the concentration of CO2, carbonic acid, Increase in the concentration of CO2, carbonic acid, and hydrogen ionsand hydrogen ions
RESPIRATORY ACIDOSISRESPIRATORY ACIDOSIS
Potassium moves out of the cellsPotassium moves out of the cells
HYPERKALEMIAHYPERKALEMIA
VENTRICULAR FIBRILLATIONVENTRICULAR FIBRILLATION
NURSING MANAGEMENT OF RESPIRATORY ACIDOSISNURSING MANAGEMENT OF RESPIRATORY ACIDOSISASSESSMENTASSESSMENT** Health Hx: complaints of headache, confusion, lethargy, Health Hx: complaints of headache, confusion, lethargy,
nausea, irritability, nausea, irritability, anxiety, dyspnea, and nausea, irritability, nausea, irritability, anxiety, dyspnea, and blurred vision, preexisting conditionsblurred vision, preexisting conditions** Physical Examination: lethargy to stupor to coma, tachycardia, Physical Examination: lethargy to stupor to coma, tachycardia, hypertension, cardiac dysrhythmias, airway patencyhypertension, cardiac dysrhythmias, airway patency
NURSING DIAGNOSES include but are not limited to:NURSING DIAGNOSES include but are not limited to:Diagnostic TitleDiagnostic Title Possible Etiologic FactorsPossible Etiologic Factors
11 Impaired gas exchangeImpaired gas exchange HypoventilationHypoventilation22 Disturbed thought processesDisturbed thought processes Central nervous system depressionCentral nervous system depression33 AnxietyAnxiety Hypoxia, hospitalizationHypoxia, hospitalization44 Risk for ineffective familyRisk for ineffective family Illness of a family member Illness of a family member copingcoping55 Ineffective airway clearanceIneffective airway clearance Hypoventilation, secretionsHypoventilation, secretions66 Ineffective breathing patternIneffective breathing pattern Hypoventilation, dyspneaHypoventilation, dyspnea
NURSING MANAGEMENT OF RESPIRATORY ACIDOSISNURSING MANAGEMENT OF RESPIRATORY ACIDOSIS
EXPECTED PATIENT OUTCOMES include but are not limited to:EXPECTED PATIENT OUTCOMES include but are not limited to:11 Will maintain airway patency and adequate breathing rate and Will maintain airway patency and adequate breathing rate and
rhythm will return of ABGs to patient’s normal levelrhythm will return of ABGs to patient’s normal level22 Will be alert and oriented to time, place, and person, or to his Will be alert and oriented to time, place, and person, or to his
or her normal baseline level of consciousnessor her normal baseline level of consciousness33 Will cope with anxietyWill cope with anxiety44 Will exhibit effective coping and awareness of effective Will exhibit effective coping and awareness of effective support systemssupport systems55 Will have secretions that are normal for self in amount and can Will have secretions that are normal for self in amount and can
be raisedbe raised66 Will maintain adequate rate and depth of respirations using Will maintain adequate rate and depth of respirations using
pursed lip and other breathing techniques when necessary (as pursed lip and other breathing techniques when necessary (as in the patient with COPD)in the patient with COPD)
NURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSISNURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSIS
INTERVENTIONSINTERVENTIONS11 Supporting effective gas exchangeSupporting effective gas exchange
-- Provide a position of comfort to allow ease of respirationProvide a position of comfort to allow ease of respiration-- Obtain and monitor ABG results and VS. Refer accordinglyObtain and monitor ABG results and VS. Refer accordingly-- Provide and monitor supplemental oxygen as orderedProvide and monitor supplemental oxygen as ordered-- Turn the patient q2 and PRNTurn the patient q2 and PRN-- Provide pulmonary hygiene PRNProvide pulmonary hygiene PRN-- Maintain adequate hydrationMaintain adequate hydration-- Provide comfort measures such as mouth careProvide comfort measures such as mouth care-- Assist with ADLsAssist with ADLs-- Instruct patient regarding coughing and deep breathing and Instruct patient regarding coughing and deep breathing and
management of disease condition, especially COPDmanagement of disease condition, especially COPD22 Coping with disturbed thought processesCoping with disturbed thought processes
-- Do frequent neurologic assessmentsDo frequent neurologic assessments-- Monitor and document person’s baseline LOC frequentlyMonitor and document person’s baseline LOC frequently
NURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSISNURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSIS
-- Reorient as necessary by providing calendars, clocks, etc.Reorient as necessary by providing calendars, clocks, etc.
33 Relieving anxietyRelieving anxiety
-- Provide a calm, relaxed environmentProvide a calm, relaxed environment
-- Give clear, concise explanations of treatment plansGive clear, concise explanations of treatment plans
-- Encourage expression of feelingsEncourage expression of feelings
-- Provide support and information to patient and familyProvide support and information to patient and family
-- Teach relaxation techniquesTeach relaxation techniques
-- Assist the patient to identify coping mechanisms to deal with Assist the patient to identify coping mechanisms to deal with anxiety and stressanxiety and stress
44 Enhancing coping mechanismsEnhancing coping mechanisms
-- Provide support and information to family members about the Provide support and information to family members about the patient’s ongoing conditionpatient’s ongoing condition
-- Reassure them that there is a physiologic cause for the Reassure them that there is a physiologic cause for the patient’s behaviorpatient’s behavior
NURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSISNURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSIS
-- Encourage questions and open communicationEncourage questions and open communication
55 Promote airway clearancePromote airway clearance
-- Implement regular breathing and coughing exercisesImplement regular breathing and coughing exercises
-- Do suctioning as necessaryDo suctioning as necessary
-- Maintain good hydrationMaintain good hydration
-- Do chest physiotherapy as appropriateDo chest physiotherapy as appropriate
66 Promoting an effective breathing patternPromoting an effective breathing pattern
-- Maintain alveolar ventilationMaintain alveolar ventilation
-- Teach the patient proper breathing techniques as well as Teach the patient proper breathing techniques as well as panic panic control breathingcontrol breathing
NURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSISNURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSIS
EVALUATION. Achievement of outcomes is successful when the patient:EVALUATION. Achievement of outcomes is successful when the patient:
1a.1a. Demonstrates improved ventilation and oxygenationDemonstrates improved ventilation and oxygenation
1b1b Has vital signs, ABGs, and cardiac rhythm within own normal Has vital signs, ABGs, and cardiac rhythm within own normal rangerange
22 Returns to baseline LOCReturns to baseline LOC
33 Reports reduced anxietyReports reduced anxiety
44 Family uses adequate coping mechanismsFamily uses adequate coping mechanisms
55 Is able to raise secretions on ownIs able to raise secretions on own
66 Demonstrate effective breathing techniquesDemonstrate effective breathing techniques
RESPIRATORY ALKALOSIS: CARBONIC ACID DEFICITRESPIRATORY ALKALOSIS: CARBONIC ACID DEFICIT
Anxiety, hysteria, fever, hypoxia, pain, pulmonary disorders, lesions Anxiety, hysteria, fever, hypoxia, pain, pulmonary disorders, lesions affecting the respiratory center in the medulla, brain tumor, affecting the respiratory center in the medulla, brain tumor,
encephalitis, meningitis, hyperthyroidism, gram-negative sepsisencephalitis, meningitis, hyperthyroidism, gram-negative sepsis
Hyperventilation: Excessive pulmonary ventilationHyperventilation: Excessive pulmonary ventilation
Decrease in hydrogen ion concentrationDecrease in hydrogen ion concentration
RESPIRATORY ALKALOSISRESPIRATORY ALKALOSIS
NURSING MANAGEMENT OF RESPIRATORY ALKALOSISNURSING MANAGEMENT OF RESPIRATORY ALKALOSISASSESSMENTASSESSMENT** Health Hx: anxiety, shortness of breath, muscle cramps or Health Hx: anxiety, shortness of breath, muscle cramps or weakness, palpitations, panic, dyspneaweakness, palpitations, panic, dyspnea** Physical Examination: light-headedness, confusion as a result of Physical Examination: light-headedness, confusion as a result of
cerebral hypoxia, hyperventilation, tachycardia or arrhythmia, cerebral hypoxia, hyperventilation, tachycardia or arrhythmia, muscle weakness, (+) Chvostek’s sign or Trousseau’s sign muscle weakness, (+) Chvostek’s sign or Trousseau’s sign
indicating a low ionized serum calcium level secondary to indicating a low ionized serum calcium level secondary to hyperventilation and alkalosis, hyperactive deep tendon reflexes, hyperventilation and alkalosis, hyperactive deep tendon reflexes, unsteady gait, muscle spasms to tetany, agitation, psychosis, unsteady gait, muscle spasms to tetany, agitation, psychosis, seizures in extreme cases, decreased potassium levelsseizures in extreme cases, decreased potassium levels
NURSING DIAGNOSES include but are not limited to:NURSING DIAGNOSES include but are not limited to:Diagnostic TitleDiagnostic Title Possible Etiologic FactorsPossible Etiologic Factors
11 AnxietyAnxiety Stress, fearStress, fear22 Ineffective breathing patternIneffective breathing pattern Hyperventilation, anxietyHyperventilation, anxiety33 Disturbed thought processesDisturbed thought processes CNS excitability; irritabilityCNS excitability; irritability44 Risk for injuryRisk for injury Change in LOC, and potential for Change in LOC, and potential for seizuresseizures
NURSING MANAGEMENT OF RESPIRATORY ALKALOSISNURSING MANAGEMENT OF RESPIRATORY ALKALOSIS
EXPECTED PATIENT OUTCOMES include but are not limited to:EXPECTED PATIENT OUTCOMES include but are not limited to:11 Will report decreased anxiety; verbalizes methods to cope with Will report decreased anxiety; verbalizes methods to cope with
anxietyanxiety22 Will return to normal respiratory rate and rhythm or at least Will return to normal respiratory rate and rhythm or at least decreased hyperventilation, with return to baseline ABGsdecreased hyperventilation, with return to baseline ABGs33 Will exhibit reorientation to person, place, and time as per Will exhibit reorientation to person, place, and time as per patient’s baselinepatient’s baseline44 Will be free from injuryWill be free from injury
INTERVENTIONSINTERVENTIONS11 Allay anxietyAllay anxiety
-- Give antianxiety medications as orderedGive antianxiety medications as ordered-- Have patient breath into a paper bagHave patient breath into a paper bag-- Teach relaxation techniques when initial anxiety attack Teach relaxation techniques when initial anxiety attack
is is overover
NURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSISNURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSIS
INTERVENTIONSINTERVENTIONS22 Promoting an Effective Breathing PatternPromoting an Effective Breathing Pattern
-- Encourage the patient to slow his or her RREncourage the patient to slow his or her RR-- Maintain a calm and comforting attitudeMaintain a calm and comforting attitude-- Position the patient to promote maximal ease of inspirationPosition the patient to promote maximal ease of inspiration-- Assist the patient with relaxation techniquesAssist the patient with relaxation techniques
33 Coping with Disturbed Thought ProcessesCoping with Disturbed Thought Processes-- Do frequent reorientationDo frequent reorientation-- Encourage family to participate in patient’s careEncourage family to participate in patient’s care-- Use simple, direct statements or directionsUse simple, direct statements or directions-- Allow the patient adequate time to respondAllow the patient adequate time to respond
44 Preventing injuriesPreventing injuries-- Perform neurologic assessment frequently and documentPerform neurologic assessment frequently and document-- Institute safety and seizure precautionsInstitute safety and seizure precautions-- Assess frequently for muscle strength and coordinationAssess frequently for muscle strength and coordination
NURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSISNURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSIS
EVALUATION. Achievement of outcomes is successful when the patient:EVALUATION. Achievement of outcomes is successful when the patient:
11 Reports reduction in anxiety levelsReports reduction in anxiety levels
2a2a Demonstrates effective normal breathing patternsDemonstrates effective normal breathing patterns
2b2b Has ABG results within patient’s normal baselineHas ABG results within patient’s normal baseline
33 Returns to normal baseline LOC and orientation levelReturns to normal baseline LOC and orientation level
44 Remains free from injury; no seizure activityRemains free from injury; no seizure activity
METABOLIC ACIDOSIS: BICARBONATE DEFICITMETABOLIC ACIDOSIS: BICARBONATE DEFICIT
Increased acid production, uncontrolled diabetes mellitus, Increased acid production, uncontrolled diabetes mellitus, alcoholism, starvation, renal acidosis, lactic acidosis, increased acid alcoholism, starvation, renal acidosis, lactic acidosis, increased acid ingestion, ethanol, salicylates, loss of bicarbonate, severe diarrhea, ingestion, ethanol, salicylates, loss of bicarbonate, severe diarrhea,
intestinal fistulas, adrenal insufficiency, hypoparathyroidismintestinal fistulas, adrenal insufficiency, hypoparathyroidism
Excess organic acids are added to body fluids or Excess organic acids are added to body fluids or bicarbonate is lostbicarbonate is lost
Decrease in bicarbonate concentrationDecrease in bicarbonate concentration
METABOLIC ACIDOSISMETABOLIC ACIDOSIS
NURSING MANAGEMENT OF METABOLIC ACIDOSISNURSING MANAGEMENT OF METABOLIC ACIDOSISASSESSMENTASSESSMENT** Health Hx: anorexia, nausea, vomiting, abdominal pain, Health Hx: anorexia, nausea, vomiting, abdominal pain,
headache, thirst if the patient is dehydratedheadache, thirst if the patient is dehydrated** Physical Examination: confusion, hyperventilation, warm, Physical Examination: confusion, hyperventilation, warm, flushed skin, bradycardia and other dysrhythmias, decreasing flushed skin, bradycardia and other dysrhythmias, decreasing
LOC, nausea, vomiting, diarrhea, Kussmaul respirations, and LOC, nausea, vomiting, diarrhea, Kussmaul respirations, and acetone breath, especially if acidosis is due to ketoacidosis. acetone breath, especially if acidosis is due to ketoacidosis. Symptoms may progress to coma if untreatedSymptoms may progress to coma if untreated
NURSING DIAGNOSES include but are not limited to:NURSING DIAGNOSES include but are not limited to:Diagnostic TitleDiagnostic Title Possible Etiologic FactorsPossible Etiologic Factors
11 Disturbed thought processesDisturbed thought processes Secondary to CNS depressionSecondary to CNS depression22 Decreased cardiac outputDecreased cardiac output DysrhythmiasDysrhythmias33 Risk for injuryRisk for injury Secondary to altered mental stateSecondary to altered mental state44 Risk for imbalanced fluid Risk for imbalanced fluid Diarrhea, renal failureDiarrhea, renal failurevolumevolume
NURSING MANAGEMENT OF METABOLIC ACIDOSISNURSING MANAGEMENT OF METABOLIC ACIDOSIS
EXPECTED PATIENT OUTCOMES include but are not limited to:EXPECTED PATIENT OUTCOMES include but are not limited to:11 Will return to usual baseline LOCWill return to usual baseline LOC22 Will return to normal baseline parameters for vital signs with Will return to normal baseline parameters for vital signs with
improved CO and decreased or resolved dysrhythmiasimproved CO and decreased or resolved dysrhythmias33 Will remain in a safe, secure environment without injuryWill remain in a safe, secure environment without injury44 Will maintain fluid and electrolyte balance and stable renal Will maintain fluid and electrolyte balance and stable renal statusstatus
INTERVENTIONSINTERVENTIONS11 Coping with disturbed thought processesCoping with disturbed thought processes
-- Monitor LOC and reorient as necessaryMonitor LOC and reorient as necessary-- Monitor VS, esp. RRR, BP, and TMonitor VS, esp. RRR, BP, and T-- Monitor ABGs to assess the effects of treatmentMonitor ABGs to assess the effects of treatment-- Institute cardiac monitoring as orderedInstitute cardiac monitoring as ordered
NURSING MANAGEMENT OF PATIENT WITH METABOLIC ACIDOSISNURSING MANAGEMENT OF PATIENT WITH METABOLIC ACIDOSIS
22 Supporting cardiac outputSupporting cardiac output-- Monitor VS, MIO, and fluid and electrolyte balanceMonitor VS, MIO, and fluid and electrolyte balance-- Institute cardiac monitoring to evaluate cardiac statusInstitute cardiac monitoring to evaluate cardiac status
33 Promoting safetyPromoting safety-- Provide a safe, secure and monitored environmentProvide a safe, secure and monitored environment-- Institute safety precautionsInstitute safety precautions
44 Promoting return of fluid and electrolyte balancePromoting return of fluid and electrolyte balance-- Monitor MIOMonitor MIO-- Administer medications per medical orderAdminister medications per medical order
NURSING MANAGEMENT OF PATIENT WITH METABOLIC ACIDOSISNURSING MANAGEMENT OF PATIENT WITH METABOLIC ACIDOSIS
EVALUATION. Achievement of outcomes is successful when the patient:EVALUATION. Achievement of outcomes is successful when the patient:
11 Exhibits baseline-level consciousness and orientationExhibits baseline-level consciousness and orientation
22 Returns to normal baseline parameters for vital signs and Returns to normal baseline parameters for vital signs and Cardiac Output with cardiac dysrhythmias resolvedCardiac Output with cardiac dysrhythmias resolved
33 Remains free from injuryRemains free from injury
44 Maintains fluid and electrolyte balance and stable renal functionMaintains fluid and electrolyte balance and stable renal function
METABOLIC ALKALOSIS: BICARBONATE EXCESSMETABOLIC ALKALOSIS: BICARBONATE EXCESS
Loss of stomach acid, gastric suctioning, persistent vomiting, excess Loss of stomach acid, gastric suctioning, persistent vomiting, excess alkali intake, intestinal fistulas, hypokalemia, Cushing’s syndrome or alkali intake, intestinal fistulas, hypokalemia, Cushing’s syndrome or
aldosteronism, potassium-diuretic therapyaldosteronism, potassium-diuretic therapy
Excessive amounts of acid substance and Excessive amounts of acid substance and hydrogen ions are lost from the body or large hydrogen ions are lost from the body or large
amounts of bicarbonate or lactate are added orally amounts of bicarbonate or lactate are added orally or IVor IV
Excess of base elementsExcess of base elements
METABOLIC ALKALOSISMETABOLIC ALKALOSIS
NURSING MANAGEMENT OF METABOLIC ALKALOSISNURSING MANAGEMENT OF METABOLIC ALKALOSISASSESSMENTASSESSMENT
** Health HxHealth Hx: Prolonged vomiting or nasogastric suctioning, : Prolonged vomiting or nasogastric suctioning, frequent self-induced vomiting, muscle weakness, light-frequent self-induced vomiting, muscle weakness, light-
headedness, ingestion of large amounts of licorice or headedness, ingestion of large amounts of licorice or antacids, use of diuretics, muscle cramping, twitching, or antacids, use of diuretics, muscle cramping, twitching, or tinglingtingling** Physical ExaminationPhysical Examination: mental confusion, dizziness, changes in : mental confusion, dizziness, changes in
LOC, hyperreflexia, tetany, dysrhthmias, seizurees, respiratory LOC, hyperreflexia, tetany, dysrhthmias, seizurees, respiratory failure, positive Chvostek’s or Trosseau’s sign if the patient has failure, positive Chvostek’s or Trosseau’s sign if the patient has a low ionized serum calcium level, decreased hand grasps, a low ionized serum calcium level, decreased hand grasps,
generalized muscle weakness, decreased serum calcium or generalized muscle weakness, decreased serum calcium or potassium level, impaired concentration, seizures, ECG changes potassium level, impaired concentration, seizures, ECG changes consistent with hypokalemiaconsistent with hypokalemia
NURSING DIAGNOSES include but are not limited to:NURSING DIAGNOSES include but are not limited to:Diagnostic TitleDiagnostic Title Possible Etiologic FactorsPossible Etiologic Factors
11 Disturbed thought processesDisturbed thought processes CNS excitationCNS excitation22 Decreased cardiac output Dysrhythmias and electrolyte Decreased cardiac output Dysrhythmias and electrolyte imbalancesimbalances
33 Risk for injuryRisk for injury Muscle weakness, tetany, confusion and possible Muscle weakness, tetany, confusion and possible seizuresseizures
44 Risk for imbalanced fluid Nasogastric drainage, diuretic therapyRisk for imbalanced fluid Nasogastric drainage, diuretic therapyvolumevolume fistulafistula
NURSING MANAGEMENT OF METABOLIC ALKALOSISNURSING MANAGEMENT OF METABOLIC ALKALOSISEXPECTED PATIENT OUTCOMES include but are not limited to:EXPECTED PATIENT OUTCOMES include but are not limited to:
11 Will return to usual baseline LOC and orientationWill return to usual baseline LOC and orientation22 Will return to normal baseline parameters for vital signs with Will return to normal baseline parameters for vital signs with
improved CO with resolution of electrolyte imbalances and improved CO with resolution of electrolyte imbalances and decreased or resolved cardiac dysrhythmiasdecreased or resolved cardiac dysrhythmias33 Will remain in a safe, secure environment without injuryWill remain in a safe, secure environment without injury44 Will maintain fluid and electrolyte balance Will maintain fluid and electrolyte balance
INTERVENTIONSINTERVENTIONS11 Coping with disturbed thought processesCoping with disturbed thought processes
-- Monitor LOC and reorient as necessaryMonitor LOC and reorient as necessary-- Monitor VS, esp. RRR, BP, and TMonitor VS, esp. RRR, BP, and T-- Monitor ABGs to assess the effects of treatmentMonitor ABGs to assess the effects of treatment-- Institute cardiac monitoring as orderedInstitute cardiac monitoring as ordered
NURSING MANAGEMENT OF PATIENT WITH METABOLIC ALKALOSISNURSING MANAGEMENT OF PATIENT WITH METABOLIC ALKALOSIS
22 Supporting cardiac outputSupporting cardiac output-- Monitor VS, MIO, and fluid and electrolyte balanceMonitor VS, MIO, and fluid and electrolyte balance-- Institute cardiac monitoring to evaluate cardiac statusInstitute cardiac monitoring to evaluate cardiac status
33 Promoting safetyPromoting safety-- Provide a safe, secure and monitored environmentProvide a safe, secure and monitored environment-- Institute safety precautionsInstitute safety precautions
44 Promoting return of fluid and electrolyte balancePromoting return of fluid and electrolyte balance-- Monitor MIOMonitor MIO-- Administer medications per medical orderAdminister medications per medical order
NURSING MANAGEMENT OF PATIENT WITH METABOLIC NURSING MANAGEMENT OF PATIENT WITH METABOLIC ALKALOSISALKALOSIS
EVALUATION. Achievement of outcomes is successful when EVALUATION. Achievement of outcomes is successful when the patient:the patient:
11 Manifests mental status has returned to baselineManifests mental status has returned to baseline
22 Is free from cardiac dysrhythmiasIs free from cardiac dysrhythmias
33 Remains free from injuryRemains free from injury
44 Maintains fluid balance at baseline levelMaintains fluid balance at baseline level
CRITICAL THINKING EXERCISESA 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: 7.57PaO2: 92PaCO2: 41HCO3: 36
Describe her acid-base status, probable cause for the imbalance and treatment