Fluid & Electrolyte Imbalance

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

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↓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 tubules

Angiotensin 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

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• Types of Transport

A. Active transport B. Passive transport

• Diffusion• Osmosis• Filtration

FLUID BALANCE• The desirable amount of fluid intake and loss in adults ranges from 1500 to 3500 mL

each 24 hours. Ave= 2500 mL• Normally INTAKE = OUTPUT

FLUID IMBALANCE• Changes in ECF volume = alterations in sodium balance• Change in sodium/water ratio = either hypoosmolarity or hyperosmolarity• Fluid excess or deficit = loss of fluid balance• As with all clinical problems, the same pathophysiologic change is not of equal

significance to all people• For example, consider two persons who have the same viral syndrome with associated

nausea and vomitingFLUID DEFICIT/HYPOVOLEMIA

• May occur as a result of:– Reduced fluid intake– Loss of body fluids– Sequestration (compartmentalizing) of body fluids

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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 Manifestations

UNTREATED 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 providing Cells become unable to continue providing water to replace ECF losseswater to replace ECF losses

Signs of circulatory collapse Signs of circulatory collapse

↓↓ blood pressureblood pressure

↑ ↑ heart rateheart rate

↑ ↑ respiratory raterespiratory rate

Restlessness and ApprehensionRestlessness and Apprehension

HypovolemiaFluid ImbalanceFluid Volume Deficit(Hypovolemia, Isotonic Dehydration) Common Causes– Hemorrhage– Vomiting – Diarrhea– Burns– Diuretic therapy– Fever– Impaired thirstClinical Manifestations Signs/Symptoms– Weight loss– Thirst– Orthostatic changes in pulse rate and bp– Weak, rapid pulse– Decreased urine output– Dry mucous membranes– Poor skin turgorTreatment/Interventions (FVD) Fluid Management– Diet therapy – Mild to moderate dehydration. Correct with oral fluid replacement. – Oral rehydration therapy – Solutions containing glucose and electrolytes. E.g., Pedialyte, Rehydralyte.– IV therapy – Type of fluid ordered depends on the type of dehydration and the clients cardiovascular status.

• 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

• Warning Signs– Cool pale skin over the arms and legs– Decreased central venous pressure– Delayed capillary refill

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– 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

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

• Thus there, is an increase in intracellular fluid• The brain cells are particularly sensitive to the increase of intracellular water, the most

common signs of hypoosmolar overhydration are changes in mental status. Confusion, ataxia, and convulsions may also occur.

• Other clinical manifestations include: hyperventilation, sudden weight gain, warm, moist skin, increased ICP: slow bounding pulse with an increase in systolic and decrease in diastolic pressue and peripheral edema, usually not marked

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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 * Disease Physical limitations * Disease states * Limited access to states * Limited access to adequate food and fluidsadequate food and fluids

Development of a plan of careDevelopment of a plan of care

Family members should be Family members should be educated about the importance educated about the importance

of fluid and nutrition intakeof fluid and nutrition intake

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

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

FLUID EXCESS/HYPERVOLEMIAFLUID EXCESS/HYPERVOLEMIAPsychiatric Disorders, Psychiatric Disorders,

SIADH, Certain head injuriesSIADH, Certain head injuries Dietary Sodium IndiscretionDietary Sodium IndiscretionRenal and endocrine disturbances, Renal and endocrine disturbances,

malignancies, adenomasmalignancies, adenomas

OverhydrationOverhydration Excessive Sodium IntakeExcessive Sodium Intake Failure of renal or hormonal Failure of renal or hormonal regulatory functionsregulatory functions

FLUID VOLUME EXCESS/HYPERVOLEMIAFLUID VOLUME EXCESS/HYPERVOLEMIA

Common Causes:– Congestive Heart Failure– Early renal failure– IV therapy– Excessive sodium ingestion– SIADH– CorticosteroidClinical Manifestations Signs/Symptoms – Increased BP– Bounding pulse– Venous distention– Pulmonary edema Dyspnea Orthopnea (diff. breathing when supine) cracklesTreatment/Interventions (FVE) Drug therapy– Diuretics may be ordered if renal failure is not the cause. Restriction of sodium and saline intakeNursing 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

ElectrolyteImbalance

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Anions and Cations

AnionsCations

BicarbonateChloride

Phosphorous

CalciumMagnesiumPotassiumSodium

HYPONATREMIA• Refers to the serum sodium concentration less than 135 mEq/L• Common with thiazide diuretic use, but may also be seen with loop and potassium-

sparing diuretics as well• Occurs with marked sodium restriction, vomiting and diarrhea, SIADH, etc. The etiology

may be mulfactorial• May also occur postop due to temporary alteration in hypothalamic function, loss of GI

fluids by vomiting or suction, or hydration with nonelectrolyte solutions• Postoperative hyponatremia is a more serious complication in premenopausal women.

The reasons behind this is unknown• Therefore monitoring serum levels is critical and careful assessment for symptoms of

hyponatremia is important for all postoperative patients

Hyponatremia (<135mEq/L) Contributing Factors– Excessive diaphoresis– Wound Drainage– NPO– CHF– Low salt diet– Renal Disease– DiureticsHyponatremia (<135mEq/L) Assessment findings:

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PATHOPHYSIOLOGY OF HYPONATREMIAPATHOPHYSIOLOGY OF HYPONATREMIA

Sodium loss from the intravascular compartmentSodium loss from the intravascular compartment

Diffusion of water intDiffusion of water int Diffusion of water into the interstitial spacesDiffusion of water into the interstitial spaces

o the interstitial spaceso the interstitial spacesSodium in the interstitSodium in the interstitial ial Sodium in the interstitial space is dilutedSodium in the interstitial space is diluted

odium in the interstitial space is dilutedodium in the interstitial space is diluted

ial space is dilutedial space is dilutedDecreased osmolarity of ECFDecreased osmolarity of ECF

eased osmolarity of ECFeased osmolarity of ECFWater moves into theWater moves into the Water moves into the cell as a result of sodium lossWater moves into the cell as a result of sodium loss

cell as a result of sodium losscell as a result of sodium loss

Extracellular compartment is depleted of waterExtracellular compartment is depleted of water

t is depleted of watert is depleted of water CLINICAL SYMPTOMSCLINICAL SYMPTOMS

LINICAL SYMPTOMSLINICAL SYMPTOMS

– Neuro - Generalized skeletal muscle weakness. Headache / personality changes.– Resp.- Shallow respirations– CV - Cardiac changes depend on fluid volume– GI – Increased GI motility, Nausea, Diarrhea (explosive)– GU - Increased urine outputHyponatremia (<135mEq/L) Interventions/Treatment– Restore Na levels to normal and prevent further decreases in Na.– Drug Therapy – (FVD) - IV therapy to restore both fluid and Na. If severe may see 2-3% saline. (FVE) – Administer osmotic diuretic (Mannitol) to excrete the water rather than the sodium.– Increase oral sodium intake and restrict oral fluid intake.HYPERNATREMIA

• A serum sodium level above 145 mEq/L is termed hypernatremia• May occur as a result of fluid deficit or sodium excess• Frequently occurs with fluid imbalance• Develops when an excess of sodium occurs without a proportional increase in body fluid

or when water loss occurs without proportional loss of sodium• Risk Factors: excess dietary or parenteral sodium intake, watery diarrhea, diabetes

insipidus, damage to thirst center, those with physical or mental status compromise, and people with hypothalamic dysfunction

Hypernatremia (>145mEq/L) Contributing Factors– Hyperaldosteronism– Renal failure– Corticosteroids

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PATHOPHYSIOLOGY OF HYPERNATREMIAPATHOPHYSIOLOGY OF HYPERNATREMIA

Increased Sodium concentration in ECFIncreased Sodium concentration in ECF

Osmolarity risesOsmolarity rises

Water leaves the cell by osmosis and enters the the Water leaves the cell by osmosis and enters the the extracellular compartmentsextracellular 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 urineSodium is exreted in the urine

CLINICAL SYMPTOMSCLINICAL SYMPTOMS

– Increase in oral Na intake– Na containing IV fluids– Decreased urine output with increased urine concentration

Hypernatremia (>145mEq/L) Contributing factors (cont’d):– Diarrhea– Dehydration– Fever– Hyperventilation

Hypernatremia (>145mEq/L) Assessment findings: – Neuro - Spontaneous muscle twitches. Irregular contractions. Skeletal muscle wkness. Diminished deep tendon reflexes– Resp. – Pulmonary edema– CV – Diminished CO. HR and BP depend on vascular volume.Hypernatremia (>145mEq/L)

GU – Dec. urine output. Inc. specific gravity

Skin – Dry, flaky skin. Edema r/t fluid volume changes.

Hypernatremia (>145mEq/L) Interventions/Treatment– Drug therapy (FVD) .45% NSS. If caused by both Na and fluid loss, will administer NaCL. If inadequate renal excretion of sodium, will administer diuretics.– Diet therapy Mild – Ensure water intake

• Major cation of the ICF. Chief regulator of cellular enzyme activity and cellular water content

• The more K, the less Na. The less K, the more Na• Plays a vital role in such processes such as transmission of electrical impulses,

particularly in nerve, heart, skeletal, intestinal and lung tissue; CHON and CHO metabolism; and cellular building; and maintenance of cellular metabolism and excitation

• Assists in regulation of acid-base balance by cellular exchange with H• RDA: not known precisely. 50-100 mEq• Sources: bananas, peaches, kiwi, figs, dates, apricots, oranges, prunes, melons, raisins,

broccoli, and potatoes, meat, dairy products• Excreted primarily by the kidneys. No effective conserving mechanism• Conserved by sodium pump and kidneys when levels are low• Aldosterone triggers K excretion in urine• Normal value: 3.5 – 5 mEq/L

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CAUSES AND EFFECTS OF HYPOKALEMIACAUSES AND EFFECTS OF HYPOKALEMIAKnown 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 lossesPotassium-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 System-CV 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 Extracellular K+Low Extracellular K+ Increase in resting Increase in resting membrane potentialmembrane potential

The cell becomes The cell becomes less excitableless excitable

Sodium is retained in the body through resorption by the kidney tubulesSodium is retained in the body through resorption by the kidney tubules

Potassium is excretedPotassium is excreted

Aldosterone is secretedAldosterone is secreted

Use of certain diuretics such as thiazides and furosemide, and corticosteroidsUse of certain diuretics such as thiazides and furosemide, and corticosteroids

Increased urinary outputIncreased urinary output

Loss of potassium in urineLoss of potassium in urine

Hypokalemia (<3.5mEq/L) Pathophysiology – – Decrease in K+ causes decreased excitability of cells, therefore cells are less responsive to normal stimuliHypokalemia (<3.5mEq/L) Contributing factors:– Diuretics– Shift into cells– Digitalis– Water intoxication– Corticosteroids– Diarrhea– Vomiting Interventions– Assess and identify those at risk– Encourage potassium-rich foods– K+ replacement (IV or PO)– Monitor lab values– D/c potassium-wasting diuretics– Treat underlying causeHyperkalemia (>5.0mEq/L)

Pathophysiology – An inc. in K+ causes increased excitability of cells.Hyperkalemia (>5.0mEq/L) Contributing factors:– Increase in K+ intake– Renal failure– K+ sparing diuretics

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CAUSES AND EFFECTS OF HYPERKALEMIACAUSES AND EFFECTS OF HYPERKALEMIASerum potassium level greater than 5.5 mEq/LSerum potassium level greater than 5.5 mEq/L

Excess IntakeExcess IntakeDietary intake of excess of kidney’s ability to

excrete; Excess parenteral administration

Decreased LossDecreased LossPotassium-Potassium-sparing diuretics; Renal failure; sparing diuretics; Renal failure;

Adrenal insufficiencyAdrenal insufficiency

Shift of Potassium Shift of Potassium out of the Cells-out of the Cells-Extensive injuries, Extensive injuries, crushing injuries, crushing injuries,

metabolic acidosismetabolic acidosis

HYPERKALEMIAHYPERKALEMIA

GI GI TractTractN&V

Diarrhea,

Colic

CNSCNSNumbness, paresthesias

MusclesMusclesEarly: irritability..Late:

weakness leading to flaccid paralysis

CV CV SystemSystemConductio

n disturbance, ventricular fibrillation,

Cardiac Arrest

KidneysKidneysOliguria leading to

anuria

– Shift of K+ out of the cellsHyperkalemia (>5.0mEq/L) Interventions– Need to restore normal K+ balance:– Eliminate K+ administration– Inc. K+ excretion Lasix Kayexalate (Polystyrene sulfonate)– Infuse glucose and insulin– Cardiac Monitoring

• Most abundant electrolyte in the body. 99% in bones and teeth• Close link between calcium and phosphorus. High PO4, Low Ca• Necessary for nerve impulse transmission and blood clotting and is also a catalyst for

muscle contraction and other cellular activities• Needed for Vitamin B12 absorption and use• Necessary for strong bones and teeth and thickness and strength of cell membranes• RDA: 1g for adults. Higher for children and pregnant and lactating women according to

body weight, older people, esp. post-menopausal • Found in milk, cheese, and dried beans; some in meat and vegetables• Use is stimulated by Vitamin D. Excreted in urine, feces, bile, digestive secretions, and

perspiration• Normal value 8.5 – 10.5 mg/dl

PATHOPHYSIOLOGY OF HYPOCALCEMIA

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

Contributing factors:– Dec. oral intake– Lactose intolerance– Dec. Vitamin D intake– End stage renal disease– DiarrheaContributing factors (cont’d):

Acute pancreatitisHyperphosphatemiaImmobilityRemoval or destruction of parathyroid gland

Hypocalcemia (<9.0mg/dL) Assessment findings: CLINICAL MANIFESTATIONS OF HYPOCALCEMIA

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CAUSES AND EFFECTS OF HYPOCALCEMIACAUSES AND EFFECTS OF HYPOCALCEMIA

Decreased Ionized Decreased Ionized CaCaLarge tranfusion with citrated blood

Excess LossExcess Loss

Kidney DiseaseKidney Disease

Decrease in GI Tract and Bone Decrease in GI Tract and Bone AbsorptionAbsorption

↑↑Magnesium, ↑Calcitonin Magnesium, ↑Calcitonin ↓Vitamin D, , ↓Parathyroid Hormone

HYPOCALCEMIAHYPOCALCEMIA

BonesBones

Osteoporosis leading to

Fractures

CNSCNS

Tingling

↓ convulsions

OtherOther

Abnormal deposits of calcium in

body tissues

MusclesMuscles

Muscle spasm ↓ Tetany

Cardiovascular Cardiovascular SystemSystemDysrhyt

hmias

↓Cardiac arrest

Inadequate IntakeInadequate Intake

Dietary DeficitDietary Deficit

PAINFUL MUSCULAR SPASMS (TETANY) ESPECIALLY OF FEET AND HANDS (CARPOPEDAL SPASMS), MUSCLE TWITCHING AND CONVULSIONS MAY FOLLOWHypocalcemia (<9.0mg/dL)– Neuro –Irritable muscle twitches. Positive Trousseau’s sign. Positive Chvostek’s sign.– Resp. – Resp. failure d/t muscle tetany.– CV – Dec. HR., dec. BP, diminished peripheral pulses– GI – Inc. motility. Inc. BS. DiarrheaPositive Trousseau’s Sign Positive Chvostek’s SignHypocalcemia (<9.0mg/dL) Interventions/Treatment– Drug Therapy Calcium supplements Vitamin D– Diet Therapy High calcium diet– Prevention of Injury Seizure precautions

Hypercalcemia (>10.5mg/dL)

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HOW IT HAPPENSHYPERCALCEMIA

DEPRESSED NERVE AND MUSCLE ACTIVITY

DEEP TENDON REFLEXES MAY BE DECREASED OR ABSENTMYOCARDIAL FUNCTION IS ALTERED

Contributing factors:– Excessive calcium intake– Excessive vitamin D intake– Renal failure– Hyperparathyroidism– Malignancy– Hyperthyroidism Assessment findings:– Neuro – Disorientation, lethargy, coma, profound muscle weakness– Resp. – Ineffective resp. movement– CV - Inc. HR, Inc. BP. , Bounding peripheral pulses, Positive Homan’s sign. Late Phase – Bradycardia, Cardiac arrest– GI – Dec. motility. Dec. BS. Constipation– GU – Inc. urine output. Formation of renal calculi

Interventions/Treatment

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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 Causing Increase in factors Causing Mobilization from boneMobilization from 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

– Eliminate calcium administration– Drug Therapy– Isotonic NaCL (Inc. the excretion of Ca)– Diuretics– Calcium reabsorption inhibitors (Phosphorus)– Cardiac Monitoring

Hypophosphatemia (<2.5mg/L) Contributing Factors:– Malnutrition– Starvation– Hypercalcemia– Renal failure– Uncontrolled DMAssessment findings: (Chart 13-7)

Neuro – Irritability, confusionCV – Dec. contractilityResp. – Shallow respirationsMusculoskeletal - RhabdomyolysisHematologic – Inc. bleeding

Dec. platelet aggregation Interventions– Treat underlying cause– Oral replacement with vit. D– IV phosphorus (Severe)– Diet therapy Foods high in oral phosphateHyperphosphatemia (>4.5mg/L) Causes few direct problems with body function. Care is directed to hypocalcemia. Rarely occurs

• Mostly found within body cells: heart, bone, nerve, and muscle tissues• Second most important cation in the ICF, 2nd to K+• Functions: Metabolism of CHO and CHON, protein and DNA synthesis, DNA and RNA

transcription, and translation of RNA, maintains normal intracellular levels of potassium, helps maintain electric activity in nervous tissue membranes and muscle membranes

• RDA: about 18-30 mEq; children require larger amounts• Sources: vegetables, nuts, fish, whole grains, peas, and beans• Absorbed in the intestines and excreted by the kidneys• Plasma concentrations of magnesium range from 1.5 – 2.5 mEq/L, with about one third

of that amount bound to plasma proteins

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PATHOPHYSIOLOGY OF HYPOMAGNESEMIA Low serum magnesium level

Increased acetylcholine release

Increased neuromuscular irritability

Increased sensitivity to acetylcholine at the myoneural junction

Diminished threshold of Enhancement ofexcitation for the motor nerve myofibril contraction

PATHOPHYSIOLOGY OF HYPOMAGNESEMIA High Serum Calcium

Increased acetylcholine release

Increased neuromuscular irritability Increased sensitivity to acetylcholine at the myoneural junction

Diminished threshold of Enhancement of myofibril excitation for the motor nerve contraction

High Serum Calciu Excretion of Magnesium By the GI tract

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HYPOMAGNESEMIA: Serum level < 1.5 mEq/LHYPOMAGNESEMIA: Serum level < 1.5 mEq/L

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, Draining Syndrome, Hypercalcemia, Diarrhea, Draining

gastrointestinal fistulagastrointestinal fistula

Excessive Excessive ExcretionExcretion

↑↑Aldosterone, Aldosterone, Conditions causing Conditions causing large losses of urinelarge losses 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

• Usually coexists with hypokalemia and less often with hypocalcemia

MAGNESIUM

INHIBITS TRANSPORT OF PTH

DECREASE IN THE AMOUNT OF CALCIUM BEING RELEASED FROM THE BONE

POSSIBLE CALCIUM DEFICITHypomagnesemia (<1.4mEq/L) Contributing factors:– Malnutrition– Starvation– Diuretics– Aminoglcoside antibiotics– Hyperglycemia– Insulin administration

Assessment findings: *Neuro - Positive Trousseau’s sign. Positive Chvostek’s sign. Hyperreflexia. Seizures*CV – ECG changes. Dysrhythmias. HTN*Resp. – Shallow resp.*GI – Dec. motility. Anorexia. Nausea

Hypomagnesemia (<1.4mEq/L) Interventions:– Eliminate contributing drugs– IV MgSO4– Assess DTR’s hourly with MgSO4– Diet Therapy

HYPERMAGNESEMIA: Serum Mg level 2.5 mEq/L• Seldom develops in the presence of normal renal function• May occur as a result of Mg replacement• May occur when MgSO4 is administered to prevent seizures resulting from eclampsia• Careful monitoring is imperative

PATHOPHYSIOLOGYRenal failure, Excessive IV infusion of magnesium, Decreased GI elimination and/or

absorption, etc.

Accummulation of Mg in the body

Mg Level Rises

Altered Electrical Conduction

Diminishing of reflexes, drowsiness, lethargy Slowed heart rate and AV Block

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Severe Respiratory Depression Peripheral vasodilation

RESPIRATORY ARREST may occur Hypotension, flushing, and increased skin warmth

Contributing factors:– Increased Mag intake– Decreased renal excretionHypermagnesemia (>2.0mEq/L) Assessment findings:

Neuro – Reduced or weak DTR’s. Weak voluntary muscle contractions. Drowsy to the point of lethargy

CV – Bradycardia, peripheral vasodilatation, hypotension. ECG changes.

Hypermagnesemia (>2.0mg/dL) Interventions– Eliminate contributing drugs– Administer diuretic– Calcium gluconate reverses cardiac effects– Diet restrictions NURSING MANAGEMENT OF PATIENT WITH FLUID AND ELECTROLYTE IMBALANCESParameter_____Fluid Excess___ Fluid Loss/Electrolyte Imbalance____ Behavior Tires easily; Change in behavior, confusion, apathy

Head, neck Facial edema, distended neck ,Headache thirst, dry mucous membrane veinsUpper GI Anorexia, nausea, vomiting Skin Warm, moist, taut, cool feeling Dry, decreased turgor where edematousRespiration Dyspnea, orthopnea, productive Changes in rate and depth of respiration

cough, moist breath sounds

Circulation Loss of sensation in edematous Pulse rate changes, dysrhythmia, increased blood pressure postural areas, pallor,

bounding pulse, hypotension

Abdomen Increased girth, fluid wave Distention, abdominal crampsElimination Constipation Diarrhea, constipationExtremities Dependent edema, “pitting” Muscle weakness, tingling, tetany

, discomfort from weight of bedclothes

LABORATORY VALUESFLUID DEFICIT FLUID EXCESSHemoconcentration Hemodilution

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↑ Hct, BUN, E+ levels ↓ Hct, BUN, E+ levels ↑ Urine Specific Gravity ↓ Urine Specific Gravity

Determined from analysis of patient dataDiagnostic Title Possible Etiologic Factors

1 Deficient fluid volume Active fluid volume loss (hemorrhage, diarrhea, gastric

intubation, wounds, diaphoresis), inadequate fluid intake, failure of regulatory mechanisms, sequestration of body fluids

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

processesIntake and Output Monitoring

a. Type and amount of fluid the patient has received and the route by which they were administered

b. Record of solid food intake. Gelatin or Popsicles are recorded as fluidsc. Ice chips are recorded by dividing the amount of chips by ½ (60 mL of chips = 30

mL water)d. Accurate output record and described by color, content, and odor (Normally,

gastric contents are watery and pale yellow-green; they usually have a sour odor)e. With acid-base balance upset, gastric secretions may have a fruity odor because of

ketone bodiesf. Bile: thicker than gastric juice, dark green to brown, acrid odor, bitter taste when

vomitingg. NGT irrigation added to intakeh. Stools: difficult to estimate amount; consistency, color, and number of stools

provide a reasonable estimatei. Peritoneal or pleural fluid drainage is recorded as output as with its amount, color,

and clarityj. Character and volume of urine. Place signs and materials so that an accurate

record of UO is maintainedIntake and Output Monitoring

1.Evaluate and refer urine specific gravity as appropriate (normal value is 1.003 – 1.030). The implications are:

High DehydrationLow SIADH, overhydrationDrainage, fluid aspirated from any body cavity must be measured. With dressings, fluid loss is the difference between the wet dressings and the dry weight of the dressingAccurate recording of the temperature to help the physician determine how much fluid should be replaced

2. Daily Weight

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Evaluate trends in weight (An increase in 1kg in weight is equal to the retention of 1L of fluid in an edematous patient)Considerations: Daily weights early in the morning after voiding

but before he or she has eaten or defecatedReplacement of Fluid and Electrolytes

General Principles: Either by oral intake (healthiest way), tube feeding, intravenous infusion, and/or total

parenteral nutrition Normal saline solution and plain water should also be given by slow drip to replace daily

fluid loss IV administration per doctor’s orders

Fluid replacement considerations: Most effective when apportioned over 24 hr period (Better regulation, ↓potential for

calculi formation and subsequent renal damage, ↓potential for circulatory overload which may cause in fluid and electrolyte shifts)

Administer concentrated solutions of Na, Glucose or protein because they require body fluids for dilution

Consider the size of the patient (small adult has less fluid in each compartment, especially in the intravascular compartment)

Promote oral intake as appropriate Caution with coffee, tea, and some colaso small amount at frequent intervals is more useful than a large amount presented

less ofteno Always give consideration to cultural and aesthetic aspects of eating

Give mouth care to a dehydrated patient before and after meals and before bedtime (Xerostomia may lead to disruption of tissues in the oral cavity)

o Avoid irritating foods Stimulation of saliva may be aided by hard candy or chewing gum or

carboxymethylcellulose (artificial saliva)o Keep lips moist and well lubricated

Give salty broth or soda crackers for sodium replacement and tea or orange juice for potassium replacement as appropriate. Bananas, citrus fruits and juices, some fresh vegetables, coffee, and tea are relatively high in potassium and low in sodium. Milk, meat, eggs, and nuts are high in protein, sodium and potassium.

o Offer milk for patients with draining fistulas from any portion of the GI tract. Lactose intolerance is not necessarily a contraindication (Lactase enzyme preparations are available)

o Increase usual daily requirement of foods when losses must be restored, as tolerated

o Patients with cardiac and renal impairments are instructed to avoid foods containing high levels of sodium, potassium and bicarbonate

o Administer replacement solutions through tube feeding as is*Either water, physiologic solution of NaCl, high protein liquids, or a regular diet can be blended, diluted and given by gavage*The water content in the tube feeding needs to be increased if:1 the patient complains of thirst

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2 the protein or electrolyte content of the tube feeding is high3 the patient has fever or disease causing an increased metabolic rate4 UO is concentrated5 signs of water deficit develop- Administer parenteral fluids as necessary

* Types of solutions- D5W (hypotonic) is given short-term for hyponatremia- D5NSS may be given depending on the serum levels of sodium and vascular volume + KCl to meet normal intake needs and replace losses for hyponatremia- Dextrose 5% in 0.2% normal saline is generally used as a maintenance fluid- Dextrose 5% in ½ normal saline is generally used as a replacement solution for losses caused by gastrointestinal drainage- PNSS is given primarily when large amounts of sodium have been lost and for patients with hyponatremia- LRS is also isotonic because it remains in the extracellular space- Fructose or 10-20% glucose in distilled water are hypertonic solutions and may partially meet body needs for CHOs- Dextran (commonly-used plasma expander) increases plasma volume by increasing oncotic pressure. May cause prolonged bleeding time and is CI in patients with renal failure, bleeding disorders, or severe CHF*Administration-The rate should be regulated according to the patient’s needs and condition per doctor’s orders-Monitor UO carefully. Refer marked decreases!-Verify orders for potassium administration in patients with renal failure and untreated adrenal insufficiency-Usual rate for fluid loss replacement: 3ml/min-Recognize signs of pulmonary edema (bounding pulse, engorged peripheral veins, hoarseness, dyspnea, cough, and rales) that can result from ↑IV rate-If infiltration occurs, the infusion should be stopped immediately and relocated. Peripheral IV sites are generally rotated every 72 hours-For dextran and other plasma expanders, observe for anaphylactic reaction (apprehension, dyspnea, wheezing, tightness of chest, angioedema, itching, hives and hypotension). If this happens, switch infusion to nonprotein solution and run at KVO rate, notify physician and monitor VS-Pronounced and continued thirst despite administration of fluids is not normal and should be reported (may indicate DM or hypercalcemia)*Patient/Family Education-Include the signs and symptoms of water excess in discharge instructions-With drug therapy, instruct patient and family regarding correct method of administration, correct dose, and therapeutic and adverse effects-Instruct to read labels for nutritional content* For K restriction: avoid organ meats, fresh and dried fruits, and salt substitutes-Skin assessment and care, positioning techniques for patients with mobility restrictions

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Acid-base balanceNORMAL ACID-BASE BALANCE

TYPES OF ACID-BASE DISTURBANCES

ACIDOSIS

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Estimated HCO3 concentration after fully oxygenated Estimated HCO3 concentration after fully oxygenated arterial blood has been equilibrated with CO2 at a arterial blood has been equilibrated with CO2 at a

PCO2 of 40 mmHg at 38C; eliminates the influence PCO2 of 40 mmHg at 38C; eliminates the influence

of respiration on the plasma HCO3 concentrationof respiration on the plasma HCO3 concentration

22-26 mEq/L22-26 mEq/LStandard HCO3Standard HCO3

Partial pressure of CO2 in the arterial blood:Partial pressure of CO2 in the arterial blood:

PCO2<35 mmHg = respiratory alkalosisPCO2<35 mmHg = respiratory alkalosis

PCO2>45 mmHg = respiratory acidosisPCO2>45 mmHg = respiratory acidosis

35-45 mmHg35-45 mmHgPaCO2PaCO2

Identifies whether there is acidemia or alkalemia:Identifies whether there is acidemia or alkalemia:

pH<7.35 = acidosis; pH>7.45 = alkalosispH<7.35 = acidosis; pH>7.45 = alkalosis7.35-7.457.35-7.45pHpH

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

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

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

RESPIRATORY ACIDOSIS: CARBONIC ACID EXCESDamage to the respiratory center in the medulla, drug or narcotic use, obstruction of respiratory passages, respiratory and respiratory muscle disorders

Decrease in the rate of pulmonary ventilation

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

RESPIRATORY ACIDOSIS

Potassium moves out of the cells

HYPERKALEMIA

VENTRICULAR FIBRILLATIONNURSING MANAGEMENT OF RESPIRATORY ACIDOSISASSESSMENTHealth Hx: complaints of headache, confusion, lethargy, nausea, irritability, nausea, irritability, anxiety, dyspnea, and blurred vision, preexisting conditions

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↑

↑

↑

↓

↓

↓

Normal

↓

↓

Normal

↑

↑

HCO3HCO3

Normal

↑

↑

↑

↑

Normal

Metabolic Alkalosis

Uncompensated

Partly Compensated

Compensated

Normal

↓

↓

↓

↓

Normal

Metabolic Acidosis

Uncompensated

Partly Compensated

Compensated

↓

↓

↓

↑

↑

Normal

Respiratory Alkalosis

Uncompensated

Partly Compensated

Compensated

↑

↑

↑

↓

↓

Normal

Respiratory Acidosis

Uncompensated

Partly Compensated

Compensated

PCO2PCO2pHpHCONDITIONCONDITION

*Physical Examination: lethargy to stupor to coma, tachycardia, hypertension, cardiac dysrhythmias, airway patencyNURSING DIAGNOSES include but are not limited to:

Diagnostic Title Possible Etiologic Factors1 Impaired gas exchange Hypoventilation2 Disturbed thought processes Central nervous system depression3 Anxiety Hypoxia, hospitalization4 Risk for ineffective family Illness of a family member coping5 Ineffective airway clearance Hypoventilation, secretions6 Ineffective breathing pattern Hypoventilation, dyspneaNURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSISINTERVENTIONS1 Supporting effective gas exchange- Provide a position of comfort to allow ease of respiration- Obtain and monitor ABG results and VS. Refer accordingly- Provide and monitor supplemental oxygen as ordered- Turn the patient q2 and PRN- Provide pulmonary hygiene PRN- Maintain adequate hydration- Provide comfort measures such as mouth care- Assist with ADLs- Instruct patient regarding coughing and deep breathing and management of disease condition, especially COPD2 Coping with disturbed thought processes- Do frequent neurologic assessments- Monitor and document person’s baseline LOC frequently- Reorient as necessary by providing calendars, clocks, etc.3 Relieving anxiety- Provide a calm, relaxed environment- Give clear, concise explanations of treatment plans- Encourage expression of feelings- Provide support and information to patient and family- Teach relaxation techniques- Assist the patient to identify coping mechanisms to deal with anxiety and stress4 Enhancing coping mechanisms- Provide support and information to family members about the patient’s ongoing condition- Reassure them that there is a physiologic cause for the patient’s behavior- Encourage questions and open communication5 Promote airway clearance- Implement regular breathing and coughing exercises- Do suctioning as necessary- Maintain good hydration- Do chest physiotherapy as appropriate6 Promoting an effective breathing pattern- Maintain alveolar ventilation- Teach the patient proper breathing techniques as well as panic control breathing

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RESPIRATORY ALKALOSIS: CARBONIC ACID DEFICITAnxiety, hysteria, fever, hypoxia, pain, pulmonary disorders, lesions affecting the respiratory center in the medulla, brain tumor, encephalitis, meningitis, hyperthyroidism, gram-negative sepsis

Hyperventilation: Excessive pulmonary ventilation

Decrease in hydrogen ion concentration

RESPIRATORY ALKALOSISNURSING MANAGEMENT OF RESPIRATORY ALKALOSISASSESSMENTHealth Hx: anxiety, shortness of breath, muscle cramps or weakness, palpitations, panic, dyspneaPhysical Examination: light-headedness, confusion as a result of cerebral hypoxia, hyperventilation, tachycardia or arrhythmia, muscle weakness, (+) Chvostek’s sign or Trousseau’s sign indicating a low ionized serum calcium level secondary to hyperventilation and alkalosis, hyperactive deep tendon reflexes, unsteady gait, muscle spasms to tetany, agitation, psychosis, seizures in extreme cases, decreased potassium levelsINTERVENTIONS1 Allay anxiety- Give antianxiety medications as ordered- Have patient breath into a paper bag- Teach relaxation techniques when initial anxiety attack is over2 Promoting an Effective Breathing Pattern-Encourage the patient to slow his or her RR-Maintain a calm and comforting attitude-Position the patient to promote maximal ease of inspiration-Assist the patient with relaxation techniques3 Coping with Disturbed Thought Processes-Do frequent reorientation-Encourage family to participate in patient’s care-Use simple, direct statements or directions-Allow the patient adequate time to respond4 Preventing injuries-Perform neurologic assessment frequently and document-Institute safety and seizure precautions-Assess frequently for muscle strength and coordination

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