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Fluids

and

Electrolytes

Ma. Tosca Cybil A. Torres, RN

HYPERPOLMIA



OBJECTIVESAfter this lecture/discussion, the learner should be able to:

1. Describe the mechanisms that maintain fluid, electrolyte and

acid-base balance.2. Compare the mechanisms and effects of fluid deficit andexcess.

3. Discuss the mechanisms and effects of deficits and excess.

4. Describe the mechanisms that maintain acid-base balance.

5. Differentiate between metabolic and respiratory acidosis andalkalosis.

6. Apply the pathophysiologic principles of acid-base balance tothe interpretation of ABG measurements.

7. Analyze the components of ABGs to identify the type of acid-base balance.

8. Describe the causes and effects of each type of acid-basebalance.

9. Use ABG findings in formulating the care of the patient with anacid-base imbalance.

10. Describe the management of patients with a fluid, electrolyte, or

acid-base imbalance.



Fluids



↓Bloodvolumeor ↓BP

Volume receptorAtria and great veins

Hypothalamus

↓

Posteriorpituitary gland

Osmoreceptors inhypothalamus

↑Osmolarity

↑ADH Kidneytubules

↑H2O

reabsorption

↑vascular

volume and↓osmolarity

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

agents, Surgery

ANTIDIURETIC HORMONE REGULATION MECHANISMS



Juxtaglomerularcells-kidney

↓Serum Sodium

↓Blood volume

Angiotensin I

Kidney tubules

Angiotensin II

Adrenal Cortex

↑Sodium

resorption(H2O resorbed

with sodium); ↑Blood volume

Angiotensinogen inplasma

RENIN

Angiotensin-converting

enzyme

ALDOSTERONE

Intestine, sweatglands, Salivary

glands

Via vasoconstriction of arterial smooth muscle

ALDOSTERONE-RENIN-ANGIOTENSIN SYSTEM



Fluid Types

• Fluids in the body generally aren’t

found in pure forms

• Isotonic, hypotonic, and hypertonictypes

• Defined in terms of the amount ofsolute or dissolve substances in thesolution

• Balancing these fluids involves theshifting of fluid not the solute involved



Isotonic Solutions

• No net fluid shiftsoccur between isotonic

solutions because thesolution are equallyconcentrated

• Ex. NSS or 0.9SS



Hypotonic Solutions

• Has a lower soluteconcentration thananother solution

• Fluid from thehypotonic solutionwould shift into thesecond solution until

the two solutions hadequal concentrations

• Ex. Half normal or0.45%SS



Hypertonic Solutions

• Has a higher soluteconcentration thananother solution

• Fluid from the secondsolution would shiftinto the hypertonicsolution until the two

solutions had equalconcentrations

• Ex. D5NSS



Fluid Movements

• Fluids and solutes constantly move withinthe body, which allows the body to maintainhomeostasis

• Fluids along with nutrients and wasteproducts 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 EVALUATINGFLUID STATUS

• Osmolality – measures the solute concentration perkilogram 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 musclemetabolism

• Serum electrolytes• CBC



Diagnosis

• Fluid volume deficit

• High risk for Fluid volume deficit

• Fluid volume excess

• Altered oral mucous membrane



FLUID BALANCE• The desirable amount of fluid intake and loss in adults ranges from

1500 to 3500 mL each 24 hours. Ave= 2500 mL

• Normally INTAKE = OUTPUT

FLUID IMBALANCE• Changes in ECF volume = alterations in sodium balance

• Change in sodium/water ratio = either hypoosmolarity orhyperosmolarity

• Fluid excess or deficit = loss of fluid balance

• As with all clinical problems, the same pathophysiologic change isnot of equal significance to all people

• For example, consider two persons who have the same viral

syndrome with associated nausea and vomiting



FLUID DEFICIT/HYPOVOLEMIA

• May occur as a result of:

– Reduced fluid intake

– Loss of body fluids – Sequestration (compartmentalizing) of body fluids

Pathophysiology and Clinical Manifestations

DECREASED FLUID VOLUME

Stimulation of thirstcenter in hypothalamus

Person complains of thirst

↑ ADH Secretion

↑ Water resorption

↓ Urine Output

Renin-Angiotensin-

Aldosterone System

Activation

↑ Sodium and

Water Resorption

↑ Urine specific gravity



Pathophysiology and Clinical Manifestations

UNTREATED FLUID VOLUME DEFICIT

Depletion of fluids available

↑ BODY TEMPERATURE

Dry mucous membranes

Difficulty with speech

Cells become unable to continue

providing water to replace ECF

losses

Signs of circulatory collapse

↓ blood pressure

↑ heart rate

↑ respiratory rate

Restlessness and Apprehension



Hypovolemia

• Nursing Intervention – Monitor fluid intake and output – Checked daily weight (a 1lb(0.45kg) weight loss equals a 500 ml

fluid loss) – Monitor hemodynamic values such as CVP

– Monitor results of laboratory studies – Assess level of consciousness – Administer and monitor I.V. fluids – Apply and adjust oxygen therapy as ordered – If patient is bleeding, apply direct continuous pressure to the area

and elevate it if possible – Assess skin turgor – Assess oral mucous membranes – Turn the patient at least every 2 hours to prevent skin breakdown

– Encourage oral fluids



Hypovolemia

• Warning Signs – Cool pale skin over the arms and legs

– Decreased central venous pressure

– Delayed capillary refill

– Deterioration in mental status flat jugular veins – Orthostatic hypotension

– Tachycardia

– Urine output initially more than 30ml/min, then dropping below10ml/hour

– Weak or absent peripheral pulses

– Weight loss



Collaborative Care Management

Identification of vulnerable patients and risk factors:

* Compromised mental state

* Physical limitations* Disease states

* Limited access to adequate food and fluids

Development of a plan of care

Family members should

be educated about the

importance of fluid and

nutrition intake

Collaboration with the

nurse, patient, family

members, and other

health care providers

for continuedassessment and

treatment of problems

Ongoing assessment and

detailed action plan of

fluid and serum

electrolyte balance.

Factors such asmedications (particularly

diuretics),

hyperventilation, fever,

burns, diarrhea, and

diabetes with

appropriate referral



Collaborative Care Key Points• 1 Liter of water = 1 kg of water by weight

• Fluid replacement are calculated according to this ratio plus 1.5 L tofulfill the current daily needs

• For example, JUAN, a one-year-old, lost 1 kg of water from diarrhea asweighed from his diaper over the last 24 hours. Therefore, since 1kg=1 L, fluid replacement therapy for him will involve 1 L of fluids +1500 L.

• Oral fluid resuscitation is preferable but if the patient is unable totolerate fluids, IV Therapy may be ordered

• Vital signs should be assessed regularly• Postural hypotension is common for postural persons with fluid

volume deficit. How do we assess this?

• For example, in the care of LOIDA, a 31 year old with severe DHN, youtake her blood pressure (130/80) and pulse (75) while she’s lyingdown. Then you ask her to sit at the edge of bed. When you take her

blood pressure again, you get 115/80 and when you take her pulse,you get 80. This is consistent with intravascular volume depletion.

• Daily weighing is also useful to monitor fluid and electrolyte balance

• Laboratory results should be reviewed for various fluid and electrolytedisturbances so that appropriate adjustments to therapy can beinitiated



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




Advantages – Provides the patient with life-sustainingfluids, electrolytes, and drugs

– Immediate and predictable therapeutic

effects – Preferred for administering fluids,

electrolytes, and drugs in emergencysituations

– Allows fluid intake when a patient has GImalabsorption

– Permits accurate dosage titration foranalgesics and other drugs




Disadvantages

– Solution incompatibility

– Adverse reactions

– Infection




Administration routes

– Oral route : oral ingestion of fluids and electrolytes asliquids or solids administered directly into the GI tract

– Nasogastric route: instillation of fluids and electrolytesthrough feeding tubes, such as NG, gastrostomy andjejunostomy tubes

– I.V. route: administration of fluids and electrolytesdirectly into the bloodstream using continuousinfusion, bolus, or I.V. push injection throughperipheral or central venous site



Which among the following IV

solutions contains the highestpotassium content?

A. D5 IMBB. Lactated Ringer's Solution

C. 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





ISOTONIC SOLUTION

Facts Examples Uses

-same osmolality as plasma(app. 275 to 295 mOsm/kg)

-vascular space osmolality notaltered by infusion

-expand intracellular andextracellular space equally;degree of expansion correlateswith amount of fluid infused

-no solution-related shifting

between ICF and ECF spaces

-cells neither shrink nor swellwith fluid movement

Dextrose 5% inwater,

Normal SalineSolution,

Lactated RingersSolution

-Fluid loss anddehydration

-Hypernatremia

-Blood transfusion,fluid challenges,resuscitation, shock,metabolic alkalosis,hypercalcemia,

hyponatremia

-Acute blood loss,

burns, dehydration,hypovolemia



Fluid Replacement Therapy HYPOTONIC SOLUTION

Facts Examples Uses

-lower osmolality thanplasma (usually lessthan 275 mOsm/kg)

-hypo-osmolalitypossible with infusionbecause solutions havea lower concentration ofelectrolytes than plasmadoes

-transcend allmembranes fromvascular space to tissueto cell

-cell swells

0.45% sodiumchloride (half-normal salinesolution)

0.3% sodiumchloride

-DKA after initial NSS andbefore dextrose infusion

-gastric fluid loss fromnasogastric suctioning orvomiting

-hypertonic dehydration

-sodium and chloridedepletion

-water replacement




HYPERTONIC SOLUTION

Facts Examples Uses

-higher osmolality thanplasma (usually > 295mOsm/kg)

-Infusion cansignificantly raisedplasma osmolality

-can cause vascularvolume expansion and

ICF deficit

-Cell shrinks

Dextrose 5% in halfnormal saline solution

Dextrose 5% in normalsaline solution

Dextrose 10% in water

DKA

Addisonian crisis

Hypotonic dehydration

SIADH

Water replacement

FLUID EXCESS/HYPERVOLEMIA



FLUID EXCESS/HYPERVOLEMIA

PsychiatricDisorders, SIADH,

Certain head injuries

Dietary SodiumIndiscretion

Renal and endocrinedisturbances,

malignancies, adenomas

OverhydrationExcessive Sodium

Intake

Failure of renal orhormonal regulatory

functions

FLUID VOLUME EXCESS/HYPERVOLEMIA

Si C f i i i



• Since ECF becomes hypoosmolar, fluid moves into the cells to equalize

the concentration on both sides of the cell membrane

• Thus there, is an increase in intracellular fluid

• The brain cells are particularly sensitive to the increase of intracellular

water, the most common signs of hypoosmolar overhydration are

changes in mental status. Confusion, ataxia, and convulsions may also

occur.

• Other clinical manifestations include: hyperventilation, sudden weight

gain, warm, moist skin, increased ICP: slow bounding pulse with an

increase in systolic and decrease in diastolic pressue and peripheral

edema, usually not marked



Hypervolemia

• Evaluating pitting edema

– Press your fingertip firmly into the patients skin over abony 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 originalcontour, indicates a +4 pitting edema

• When the skin resists pressure and appears distended, thecondition is called brawny edema, which causes the skin toswell 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 renalfailure

– 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) forpulmonary 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

http://images.google.com.ph/imgres?imgurl=http://newsimg.bbc.co.uk/media/images/41923000/jpg/_41923842_afp416oxygen.jpg&imgrefurl=http://news.bbc.co.uk/2/hi/in_pictures/5210194.stm&h=300&w=416&sz=22&hl=en&start=10&sig2=RceaZqersCx9FHSglrZVhA&tbnid=02oKp4zISWIdZM:&tbnh=90&tbnw=125&ei=0iYxSN_eLZOy6wOl7MynDw&prev=/images?q=oxygen&gbv=2&hl=en&sa=G



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



Electrolytes



Which one isnot a cation?A. CalciumB. MagnesiumC. PhosphorousD. Sodium



Anions and Cations

• Anions • Cations

BicarbonateChloride

Phosphorous

CalciumMagnesiumPotassiumSodium



WHAT DO ELECTROLYTES DO?



• Controls and regulates volume of body fluids

• Its concentration is the major determinant of ECF volume

• Is the chief electrolyte of ECF

• Influence ICF Volume

•Participates in the generation and transmission of nerve impulses

• Is an essential electrolyte in the sodium-potassium pump

• RDA: not known precisely. 500 mg

• Eliminated primarily by the kidneys, smaller in feces and perspiration

• Salt intake affects sodium concentrations

• Sodium is conserved through reabsorption in the kidneys, a processstimulated by aldosterone

• Normal value: 135-145 mEq/L

HYPONATREMIA



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 inhypothalamic function, loss of GI fluids by vomiting or suction, orhydration with nonelectrolyte solutions

• Postoperative hyponatremia is a more serious complication inpremenopausal women. The reasons behind this is unknown

• Therefore monitoring serum levels is critical and careful

assessment for symptoms of hyponatremia is important for allpostoperative patients

PATHOPHYSIOLOGY OF HYPONATREMIA



PATHOPHYSIOLOGY OF HYPONATREMIASodium loss from the intravascular compartment

Diffusion of water into the interstitial spaces

Sodium in the interstitial space is diluted

Decreased osmolarity of ECF

Water moves into the cell as a result of sodium loss

Extracellular compartment is depleted of water

CLINICAL SYMPTOMS



CLINICAL MANIFESTATIONS OF HYPONATREMIA

Muscle

Weakness

APATHY

Posturalhypotension

Nausea and

AbdominalCramps

Weight Loss

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



COLLABORATIVE CARE MANAGEMENT• General goal: correct sodium imbalance and restore normal fluid and

electrolyte homeostasis

• Recognition of people at risk for hyponatremia is essential for itsprevention: athletes, persons working in hot environments

• Salt is always replaced along with water

• Management includes educating vulnerable people to recognize signsand symptoms of sodium depletion and maintaining sufficient sodium

and water intake to replace skin and insensible fluid loss• Generally, an increased sodium and water intake provides adequate

treatment

• Education as the importance of sodium and fluid balance and therationale for prescription medications to ensure compliance

• Daily weight. MIO

• Monitoring of sodium levels to determine extent of replacement

• Generally, PNSS or PLRS is prescribed

• Too rapid restoration of sodium balance, hypertonic sodium solutionsmay provoke brain injury

HYPERNATREMIA



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 proportionalincrease in body fluid or when water loss occurs withoutproportional loss of sodium

• Risk Factors: excess dietary or parenteral sodium intake, waterydiarrhea, diabetes insipidus, damage to thirst center, those withphysical or mental status compromise, and people withhypothalamic dysfunction



PATHOPHYSIOLOGY OF HYPERNATREMIA

Increased Sodium concentration in ECF

Osmolarity rises

Water leaves the cell by osmosis and enters thethe extracellular compartments

Dilution of fluids in ECF Cells are water depleted

Suppression of aldosteronesecretion Sodium is exreted in theurine

CLINICAL SYMPTOMS

CLINICAL MANIFESTATIONS



CLINICAL MANIFESTATIONS

Dry, sticky mucousmembranes

Firm, rubberytissue turgor

Manic excitement

Tachycardia

DEATH

COLLABORATIVE CARE MANAGEMENT




• Recognition of risk factors: bedridden and debilitated patients,diabetes insipidus, fluid deprivation, the elderly and the very

young• A careful and accurate record of MIO permits quick recognition

of negative fluid balance

• People with kidney failure, CHF, or increased aldosteroneproduction may require dietary sodium intake restriction

• Usually, osmolar balance can be restored with oral fluids. If not,the parenteral route may be necessary

• Fluid resuscitation must be undertaken with particular cautionin patients with compromised cardiac or renal function

• The nurse should closely monitor the patient’s response to

fluids and be alert to symptoms of fluid overload



• Major cation of the ICF. Chief regulator of cellular enzyme activity andcellular 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 electricalimpulses, particularly in nerve, heart, skeletal, intestinal and lung tissue;CHON and CHO metabolism; and cellular building; and maintenance ofcellular 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

O O



CAUSES AND EFFECTS OF HYPOKALEMIA• Known as a low level of serum potassium, less than 3.5 mEq/L

Decreased Intake

↓ Food and Fluids as in

starvation

Failure to replace GIlosses

Increased Loss

↑ Aldosterone Gastrointestinal losses

Potassium-losing diureticsLoss from cells as in trauma,

burns

Shift of Potassium

into Cells

(No change in totalbody potassium)

HYPOKALEMIA

GI Tract

AnorexiaN&V

Abdominal

distention

CNS

Lethargy,Diminished

deep-tendonreflexes,

Confusion,Mental

depression

Muscles

Weakness,Flaccid paralysis,

Weakness ofrespiratorymuscles,

Respiratory arrest

CV System

Decrease instanding BP,

Dysrhythmias,ECG changes,

Myocardialdamage, Cardiac

arrest

Kidneys

↓Capacity to

concentratewaste, waterloss, thirst,

kidneydamage

PATHOPHYSIOLOGY OF HYPOKALEMIA



= Action Potential

Nerve and Muscle Activity

Low

ExtracellularK+

Increase in

restingmembranepotential

The cellbecomes

lessexcitable

Ald t i t d



Sodium is retained in the body through resorption by

the kidney tubules

Potassium is excreted

Aldosterone is secreted

Use of certain diuretics such as thiazides and furosemide, andcorticosteroids

Increased urinary output

Loss of potassium in urine





• Being alert to the conditions that cause potassium depletion such asvomiting, diarrhea and diuretics, by monitoring the patient for earlywarning signs

• No more than 3 enemas without consulting a physician

• Education about the importance of adequate dietary intake ofpotassium

• In severe hypokalemia, a patient may die unless potassium isadministered promptly

• The safest way to administer K is orally. When K is given IV, the rateof flow must be monitored closely and should be diluted. Should notexceed 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 HYPERKALEMIA



• Serum potassium level greater than 5.5 mEq/L

Excess Intake

Dietary intake of excess

of kidney’s ability toexcrete; Excess

parenteral administration

Decreased Loss

Potassium-sparing diuretics;Renal failure; Adrenal

insufficiency

Shift of Potassiumout of the Cells

Extensive injuries,crushing injuries,

metabolic acidosis

HYPERKALEMIA

GI Tract

N&VDiarrhea,

Colic

CNS

Numbness,paresthesias

Muscles

Early: irritability

Late: weaknessleading to flaccid

paralysis

CV System

Conductiondisturbance,ventricular

fibrillation,Cardiac Arrest

Kidneys

Oligurialeading to

anuria




• Patients at risk should be identified: impaired renal function toavoid OTC, esp. NSAIDS which provoke hyperkalemia; and saltsubstitutes that are high in potassium

• Severity guides therapy

– Mild: Withholding provoking agent (i.e., K supp)

– Severe (>6 mEq/L: cation-exchange resin such asKayexalate (act by exchanging the cations in the resin forthe potassium in the intestine potassium is then excretedin the stool; Continuous cardiac monitoring

• Bowel function must be maintained if Kayexelate therapy is tobe effective

• Potassium-wasting diuretics may be prescribed to promotefurther potassium loss. Dialysis for patients with renal failure to

eliminate excess potassium

• Intravenous Ca Gluconate may be prescribed to counteract thecardiac effects of hyperkalemia

• Insulin infusions and IV NaCO3 may be used to promoteintracellular uptake of K



CAUSES AND EFFECTS OF HYPOCALCEMIA



DecreasedIonized Ca

Large

tranfusion withcitrated blood

Excess Loss

Kidney Disease

Decrease in GI Tractand Bone Absorption

↑Magnesium

↑Calcitonin

↓Vitamin D ↓Parathyroid Hormone

HYPOCALCEMIA

Bones

Osteoporosisleading to

Fractures

CNS

Tingling

↓convulsions

Other

Abnormaldeposits

of calcium

in bodytissues

Muscles

Muscle spasm

↓

Tetany

CardiovascularSystem

Dysrhythmias

↓ Cardiac arrest

InadequateIntake

Dietary Deficit

PATHOPHYSIOLOGY OF HYPOCALCEMIA



PATHOPHYSIOLOGY OF HYPOCALCEMIA•Calcium ions are thought to line thepores of cell membranes, especially

neurons•Calcium and Sodium repel each other

•When serum calcium levels are low, thisblocking effect is minimized

•When Sodium moves more easily intothe cell, depolarization takes place moreeasily

•This results in increased excitability ofthe nervous system leading to musclespasm, tingling sensations, and if severe,convulsions and tetany

•Skeletal, smooth, and cardiac musclefunctions are all affected by

overstimulation

Sodium Calcium

CLINICAL MANIFESTATIONS OF HYPOCALCEMIA



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

TREATMENT

PAINFUL MUSCULAR SPASMS (TETANY)ESPECIALLY OF FEET AND HANDS

(CARPOPEDAL SPASMS), MUSCLE TWITCHINGAND CONVULSIONS MAY FOLLOW

TESTS USED TO ELICIT SIGNS OF CALCIUM DEFICIENCY



TESTS USED TO ELICIT SIGNS OF CALCIUM DEFICIENCY




• Identify risk factors: Inadequate calcium intake, excess calcium loss,Vitamin D deficiency, patients with poor diets

• Education about the importance of adequate calcium and Vitamin Dintake

• Patients undergoing thyroid, parathyroid, and radical neck surgery areparticularly vulnerable to hypocalcemia secondary to parathyroidhormone deficit

• Monitoring of serum calcium levels and correction of deficits

• Citrate is added to store blood to prevent coagulation.

• Citrate + Transfusion = Citrate+Calcium• Normally, Liver + Citrate = Quick metabolism

• Preexisting calcium deficit/hepatic dysfunction/large amounts of BTvery rapidly = hypocalcemia

• With acute hypocalcemia, Ca Gluconate is used + Continuous cardiacmonitoring

• Mild Hypocalcemia: High calcium diet or oral calcium salts

• If PTH or Vit D Deficiency is the cause: aluminum hydroxide gel isused because when serum phosphate level rises, calcium level falls

• Complication: Bone demineralization

• Therefore, careful ambulation should be encouraged to minimize bone

resorption

HYPERCALCEMIA: Serum concentration > 10mg/dLCauses and Effects



Causes and Effects

Loss from bones

Immobilization,

Carcinoma with bonemetastases, Multiple

myeloma

Excess Intake

↑ Calcium diet (esp. milk) Antacids containing calcium

Increase in factorsCausing Mobilization

from bone↑PTH, ↑ Vitamin D,

steroid therapy

HYPERCALCEMIA

Kidneys

Stones

↓

KidneyDamage

CNS

↓Deep-tendonreflexes

↓ Lethargy

↓

Coma

Bones

Bone pain

↓

Osteoporosis

↓

Fractures

Muscles

Muscle fatigue,hypotonia

↓

↓ GI motility

CV System

Depressedactivity

↓ Dysrhythmias

↓

Cardiac Arrest

CLINICAL MANIFESTATIONS OF HYPERCALCEMIA



Decreased GIMotility

Cardiac Dysrhythmias

Constipation

Nausea

Mental status changes:lethargy, confusion,

memory loss

CLINICAL MANIFESTATIONS OF HYPERCALCEMIA



Immobilization BoneDemineralization

Calciumaccumulates in

the ECF andpasses through

the kidneys

Ca PrecipitationCalcium Stones




• 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 preventconcentrated urine: 3000 to 4000 mL/day unless contraindicated

• Acid-ash fruit juices: cranberry juice and prune juice

• Severe hypercalcemia: medical emergency: continuous cardiac

monitoring, hydration, IV furosemide, Calcitonin and/or plicamycin(mithramycin), q2 serum and urinary electrolytes



• Mostly found within body cells: heart, bone, nerve, and muscle tissues

• Second most important cation in the ICF, 2nd to K+

• Functions: Metabolism of CHO and CHON, protein and DNA synthesis,DNA and RNA transcription, and translation of RNA, maintains normalintracellular levels of potassium, helps maintain electric activity innervous 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, withabout one third of that amount bound to plasma proteins

HYPOMAGNESEMIA: Serum level < 1.5 mEq/L



HYPOMAGNESEMIA: Serum level < 1.5 mEq/L• Usually coexists with hypokalemia and less often with hypocalcemia

Decreased Intake

Prolongedmalnutrition,Starvation

Impaired absorption from GI Tract

Malabsorption syndrome, Alcohol WithdrawalSyndrome, Hypercalcemia, Diarrhea,

Draining gastrointestinal fistula

ExcessiveExcretion

↑Aldosterone,

Conditionscausing largelosses of urine

HYPOMAGNESEMIA

Mental Changes

Agitation,Depression,

Confusion

CNS

Convulsions,Paresthesias,

Tremor, Ataxia

Muscles

Cramps,Spasticity, Tetany

CV System

Tachycardia,Hypotension,

Dysrhythmias

HYPOKALEMIA



PATHOPHYSIOLOGY OF HYPOMAGNESEMIA



High Serum Calcium

Increased acetylcholine release

Increased neuromuscular irritability

Increased sensitivity to acetylcholine at the myoneural junction

Diminished threshold ofexcitation for the motor

nerve

Enhancement of myofibrilcontraction

High Serum CalciumExcretion of Magnesium

By the GI tract



PATHOPHYSIOLOGY OF HYPOMAGNESEMIA

MAGNESIUM

INHIBITS TRANSPORT OF PTH

DECREASE IN THE AMOUNT OF CALCIUM BEING RELEASEDFROM THE BONE

POSSIBLE CALCIUM DEFICIT

CLINICAL MANIFESTATIONS OF HYPOMAGNESEMIA



CONFUSION

DEPRESSION

CRAMPS

TETANY CONVULSIONS




• Recognition of people at risk: people taking loop diuretics and

digoxin should be encouraged to eat foods rich in magnesium,such as fruits, vegetables, cereals, and milk

• Recognition of signs and symptoms of magnesium deficiency

• Magnesium is essential for potassium resorption, so ifhypokalemia does not respond to potassium replacement,

hypomagnesemia should be suspected

• Treatment of the underlying cause is the first consideration inhypomagnesemia

• Severe: parenteral magnesium replacement is indicated

• IV therapy: continuous cardiac monitoring• Safety measures for patients with mental status changes



HYPERMAGNESEMIA: Serum Mg level 2.5 mEq/L

• Seldom develops in the presence of normal renal function

• May occur as a result of Mg replacement

• May occur when MgSO4 is administered to prevent seizuresresulting from eclampsia

• Careful monitoring is imperative

PATHOPHYSIOLOGY

R l f il E i IV i f i f



Renal failure, Excessive IV infusion ofmagnesium, Decreased GI elimination

and/or absorption, etc.

Accummulation of Mg in the body

Diminishing of reflexes, drowsiness, lethargy

Mg Level Rises

Severe Respiratory Depression

RESPIRATORY ARREST may occur

Altered Electrical Conduction

Slowed heartrate and AV

Block

Peripheralvasodilation

Hypotension, flushing, andincreased skin warmth



COLLABORATIVE CARE MANAGEMENT• Identification of patients at risk: those with impaired renal

function to avoid OTC that contain magnesium such as Milk ofMagnesia and some Mg-containing antacids

• Any patient receiving parenteral magnesium therapy should beassessed frequently for signs of hypermagnesemia

• Mild hypermagnesemia: withholding magnesium-containing

medications may suffice• Renal failure: dialysis

• Severe: may require treatment with calcium gluconate (10-20mL of 10% Ca Gluconate administered over 10 minutes)

• If cardiorespiratory collapse is imminent, the patient may

require temporary pacemaker and ventilator support



NURSING MANAGEMENT OFPATIENT WITH FLUID AND

ELECTROLYTE IMBALANCES



Parameter_____Fluid Excess___ Fluid Loss/Electrolyte Imbalance____

Behavior Tires easily; Change in behavior, confusion, apathy

Head, neck Facial edema, distended neck Headache, thirst, dry mucous membranesveins

Upper GI Anorexia, nausea, vomiting

Skin Warm, moist, taut, cool feeling Dry, decreased turgor whereedematous

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 ofbedclothes



Pitting edema

Dependent edema

Refractory Edema



LABORATORY VALUES

FLUID DEFICIT FLUID EXCESS

Hemoconcentration Hemodilution

↑ Hct, BUN, E+ levels ↓ Hct, BUN, E+ levels

↑ Urine Specific Gravity ↓ Urine Specific Gravity



Determined from analysis of patient data

Diagnostic Title Possible Etiologic Factors

1 Deficient fluid volume Active fluid volume loss

(hemorrhage, diarrhea, gastricintubation, wounds, diaphoresis),inadequate fluid intake, failure ofregulatory mechanisms,sequestration of body fluids

2 Excess Fluid Volume Excess fluid intake, excess sodium

intake, compromised regulatoryprocesses



EXPECTED PATIENT OUTCOMES

1. Will maintain functional fluid volume as evidenced byadequate urinary output, stable weight, normal vital

signs, normal urine specific gravity, moist mucus

membranes, balanced intake and output, elastic skin turgor,prompt capillary refill, and absence of edema

2. Will verbalize understanding of treatment plan andcausative factors that led to the imbalance

1,2 Intake and Output Monitoring

- Type and amount of fluid the patient has received and the



yp proute by which they were administered

- Record of solid food intake. Gelatin or Popsicles arerecorded as fluids

- Ice chips are recorded by dividing the amount of chipsby ½ (60 mL of chips = 30 mL water)

- Accurate output record and described by color, content,and odor (Normally, gastric contents are watery and paleyellow-green; they usually have a sour odor)

- With acid-base balance upset, gastric secretions may

have a fruity odor because of ketone bodies- Bile: thicker than gastric juice, dark green to brown,

acrid odor, bitter taste when vomiting

- NGT irrigation added to intake

- Stools: difficult to estimate amount; consistency, color,and number of stools provide a reasonable estimate

- Peritoneal or pleural fluid drainage is recorded as outputas with its amount, color, and clarity

- Character and volume of urine. Place signs andmaterials so that an accurate record of UO is

maintained

1,2 Intake and Output Monitoring



, p g

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

High Dehydration

Low SIADH, overhydration

- Drainage, fluid aspirated from any body cavity must bemeasured. With dressings, fluid loss is the differencebetween the wet dressings and the dry weight of thedressing

- Accurate recording of the temperature to help thephysician determine how much fluid should be

replaced

1,2 Daily Weight

- Evaluate trends in weight (An increase in 1kg in weight

is equal to the retention of 1L of fluid in an edematouspatient)

Considerations:

- Daily weights early in the morning after voidingbut before he or she has eaten or defecated

1 Replacement of Fluid and Electrolytes

G l P i i l



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 begiven 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 andsubsequent renal damage, ↓potential for circulatoryoverload which may cause in fluid and electrolyte

shifts)

* Administer concentrated solutions of Na, Glucose orprotein because they require body fluids for dilution

* Consider the size of the patient (small adult has lessfluid in each compartment, especially in the

intravascular compartment)

- Promote oral intake as appropriate

* Caution with coffee, tea, and some colas

* small amount at frequent intervals is more useful than a



qlarge amount presented less often

* Always give consideration to cultural and aestheticaspects of eating

- Give mouth care to a dehydrated patient before and after mealsand before bedtime (Xerostomia may lead to disruption of tissues inthe oral cavity)

- Avoid irritating foods

- Stimulation of saliva may be aided by hard candy or chewinggum or carboxymethylcellulose (artificial saliva)

- Keep lips moist and well lubricated- Give salty broth or soda crackers for sodium replacement and

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

- Offer milk for patients with draining fistulas from any portion of theGI tract. Lactose intolerance is not necessarily a

contraindication (Lactase enzyme preparations are available)

- Increase usual daily requirement of foods when losses must berestored, as tolerated

* Patients with cardiac and renal impairments are



pinstructed to avoid foods containing high levelsof sodium, potassium and bicarbonate

- Administer replacement solutions through tube feeding as is

* Either water, physiologic solution of NaCl, high proteinliquids, or a regular diet can be blended, diluted andgiven by gavage

* The water content in the tube feeding needs to beincreased if:

1 the patient complains of thirst2 the protein or electrolyte content of the tube

feeding is high

3 the patient has fever or disease causing anincreased metabolic rate

4 UO is concentrated5 signs of water deficit develop

- Administer parenteral fluids as necessary

* Types of solutions

- D5W (hypotonic) is given short-term for hyponatremia



D5W (hypotonic) is given short term for hyponatremia

- D5NSS may be given depending on the serum levels ofsodium and vascular volume + KCl to meet normalintake needs and replace losses for hyponatremia

- Dextrose 5% in 0.2% normal saline is generally used asa maintenance fluid

- Dextrose 5% in ½ normal saline is generally used as areplacement 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 arehypertonic solutions and may partially meet bodyneeds for CHOs

- Dextran (commonly-used plasma expander) increasesplasma volume by increasing oncotic pressure. Maycause prolonged bleeding time and is CI in patientswith 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



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 aregenerally rotated every 72 hours

- For dextran and other plasma expanders, observe foranaphylactic reaction (apprehension, dyspnea,wheezing, tightness of chest, angioedema,itching, hives and hypotension). If this happens,

switch infusion to nonprotein solution and run at KVOrate, notify physician and monitor VS

- Pronounced and continued thirst despite administrationof fluids is not normal and should be reported (may

indicate DM or hypercalcemia)



* Patient/Family Education

- Include the signs and symptoms of water excess indischarge instructions

- With drug therapy, instruct patient and family regardingcorrect method of administration, correct dose, andtherapeutic and adverse effects

- Instruct to read labels for nutritional content

* For K restriction: avoid organ meats, fresh and driedfruits, and salt substitutes

- Skin assessment and care, positioning techniques forpatients with mobility restrictions



* Achievement of outcomes is successful in disturbances in fluidand electrolyte balance:

1 Maintains functional fluid volume level with adequate UO,VS within the patient’s normal limits, sp gr of urinewithin 1.003-1.035, moist mucous membranes, stableweight, Intake=output, elastic skin turgor, and no edema

2 States possible causes of imbalance and plan to preventrecurrence of imbalances

3 Reports a decrease or absence of symptoms causing

discomfort

Fluids and Electrolytes



Fluids and Electrolytes

Acid-base

balance

DRAWING ARTERIAL BLOOD GASES



DRAWING ARTERIAL BLOOD GASES

ALLEN’S TEST ARTERIAL PUNCTURE

NORMAL ACID-BASE BALANCE



Estimated HCO3 concentration after fullyoxygenated arterial blood has beenequilibrated with CO2 at a PCO2 of 40mmHg at 38C; eliminates the influence ofrespiration on the plasma HCO3concentration

22-26 mEq/LStandard HCO3

Partial pressure of CO2 in the arterialblood:

PCO2<35 mmHg = respiratory alkalosis

PCO2>45 mmHg = respiratory acidosis

35-45 mmHgPaCO2

Identifies whether there is acidemia oralkalemia:

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

Partial pressure of oxygen in arterialblood (decreases with age)

In adults < 60 years:

60-80 mmHg = mild hypoxemia

40-60 mmHg = moderate hypoxemia

< 40 mmHg = severe hypoxemia

80-100 HgPaO2

Definition and ImplicationsNormal ValueParameter



S C G O O C S C



BASIC REGULATION OF ACID-BASE BALANCE

CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3

The lungs help control acid-base balance by blowing off orretaining CO2. The kidneys help regulate acid-base balance by

excreting or retaining HCO3

TYPES OF ACID-BASE DISTURBANCES



Depression of the central

nervous system, asevidenced by disorientationfollowed by coma

Overexcitability of thenervous system; muscles

may go into a state of tetanyand convulsioons



EXPECTED DIRECTIONAL CHANGES WITH ACID-BASE IMBALANCES

HCO3 PCO2pHCONDITION



↑

↑

↑

↓

↓

↓

Normal

↓

↓

Normal

↑

↑

HCO3

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

PCO2pHCONDITION



Compensation



p

RESPIRATORY ACIDOSIS: CARBONIC ACID EXCESS

D t th i t t i th d ll d ti b t ti



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

Decrease in the rate of pulmonary ventilation

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

RESPIRATORY ACIDOSIS

Potassium moves out of the cells

HYPERKALEMIA

VENTRICULAR FIBRILLATION



NURSING MANAGEMENT OF RESPIRATORY ACIDOSIS

ASSESSMENT



* Health Hx: complaints of headache, confusion, lethargy,nausea, irritability, nausea, irritability, anxiety, dyspnea, and

blurred vision, preexisting conditions

* Physical Examination: lethargy to stupor to coma, tachycardia,hypertension, cardiac dysrhythmias, airway patency

NURSING DIAGNOSES include but are not limited to:

Diagnostic Title Possible Etiologic Factors1 Impaired gas exchange Hypoventilation

2 Disturbed thought processes Central nervous system depression

3 Anxiety Hypoxia, hospitalization

4 Risk for ineffective family Illness of a family member

coping5 Ineffective airway clearance Hypoventilation, secretions

6 Ineffective breathing pattern Hypoventilation, dyspnea

NURSING MANAGEMENT OF RESPIRATORY ACIDOSIS



EXPECTED PATIENT OUTCOMES include but are not limited to:

1 Will maintain airway patency and adequate breathing rate andrhythm will return of ABGs to patient’s normal level

2 Will be alert and oriented to time, place, and person, or to hisor her normal baseline level of consciousness

3 Will cope with anxiety

4 Will exhibit effective coping and awareness of effectivesupport systems

5 Will have secretions that are normal for self in amount and canbe raised

6 Will maintain adequate rate and depth of respirations using

pursed lip and other breathing techniques when necessary (asin the patient with COPD)

NURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSIS



INTERVENTIONS

1 Supporting effective gas exchange

- Provide a position of comfort to allow ease of respiration

- Obtain and monitor ABG results and VS. Refer accordingly

- Provide and monitor supplemental oxygen as ordered

- Turn the patient q2 and PRN

- Provide pulmonary hygiene PRN

- Maintain adequate hydration

- Provide comfort measures such as mouth care

- Assist with ADLs

- Instruct patient regarding coughing and deep breathing andmanagement of disease condition, especially COPD

2 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 withanxiety and stress

4 Enhancing coping mechanisms

- Provide support and information to family members about thepatient’s ongoing condition

- Reassure them that there is a physiologic cause for thepatient’s behavior





- Encourage questions and open communication

5 Promote airway clearance

- Implement regular breathing and coughing exercises

- Do suctioning as necessary

- Maintain good hydration

- Do chest physiotherapy as appropriate

6 Promoting an effective breathing pattern

- Maintain alveolar ventilation

- Teach the patient proper breathing techniques as well as panic

control breathing




EVALUATION. Achievement of outcomes is successful when the patient:

1a. Demonstrates improved ventilation and oxygenation

1b Has vital signs, ABGs, and cardiac rhythm within own normalrange

2 Returns to baseline LOC

3 Reports reduced anxiety

4 Family uses adequate coping mechanisms

5 Is able to raise secretions on own

6 Demonstrate effective breathing techniques

RESPIRATORY ALKALOSIS: CARBONIC ACID DEFICIT



Anxiety, hysteria, fever, hypoxia, pain, pulmonary disorders, lesions

affecting the respiratory center in the medulla, brain tumor,encephalitis, meningitis, hyperthyroidism, gram-negative sepsis

Hyperventilation: Excessive pulmonary ventilation

Decrease in hydrogen ion concentration

RESPIRATORY ALKALOSIS



NURSING MANAGEMENT OF RESPIRATORY ALKALOSIS

ASSESSMENT



* Health Hx: anxiety, shortness of breath, muscle cramps orweakness, palpitations, panic, dyspnea

* Physical Examination: light-headedness, confusion as a result ofcerebral hypoxia, hyperventilation, tachycardia or arrhythmia,

muscle weakness, (+) Chvostek’s sign or Trousseau’s sign

indicating a low ionized serum calcium level secondary tohyperventilation and alkalosis, hyperactive deep tendon

reflexes, unsteady gait, muscle spasms to tetany, agitation,psychosis, seizures in extreme cases, decreased potassiumlevels



1 Anxiety Stress, fear

2 Ineffective breathing pattern Hyperventilation, anxiety

3 Disturbed thought processes CNS excitability; irritability

4 Risk for injury Change in LOC, and potential for

seizures

NURSING MANAGEMENT OF RESPIRATORY ALKALOSIS




1 Will report decreased anxiety; verbalizes methods to cope withanxiety

2 Will return to normal respiratory rate and rhythm or at leastdecreased hyperventilation, with return to baseline ABGs

3 Will exhibit reorientation to person, place, and time as perpatient’s baseline

4 Will be free from injury

INTERVENTIONS

1 Allay anxiety

- Give antianxiety medications as ordered

- Have patient breath into a paper bag

- Teach relaxation techniques when initial anxiety attack isover




INTERVENTIONS

2 Promoting an Effective Breathing Pattern

- Encourage the patient to slow his or her RR

- Maintain a calm and comforting attitude

- Position the patient to promote maximal ease of inspiration

- Assist the patient with relaxation techniques

3 Coping with Disturbed Thought Processes

- Do frequent reorientation

- Encourage family to participate in 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






1 Reports reduction in anxiety levels

2a Demonstrates effective normal breathing patterns

2b Has ABG results within patient’s normal baseline

3 Returns to normal baseline LOC and orientation level

4 Remains free from injury; no seizure activity

METABOLIC ACIDOSIS: BICARBONATE DEFICIT



Increased acid production, uncontrolled diabetes mellitus,

alcoholism, starvation, renal acidosis, lactic acidosis, increased acidingestion, ethanol, salicylates, loss of bicarbonate, severe diarrhea,

intestinal fistulas, adrenal insufficiency, hypoparathyroidism

Excess organic acids are added to body fluids or

bicarbonate is lost

Decrease in bicarbonate concentration

METABOLIC ACIDOSIS



NURSING MANAGEMENT OF METABOLIC ACIDOSIS

ASSESSMENT



* Health Hx: anorexia, nausea, vomiting, abdominal pain,headache, thirst if the patient is dehydrated

* Physical Examination: confusion, hyperventilation, warm,flushed skin, bradycardia and other dysrhythmias, decreasing

LOC, nausea, vomiting, diarrhea, Kussmaul respirations, andacetone breath, especially if acidosis is due to ketoacidosis.Symptoms may progress to coma if untreated



1 Disturbed thought processes Secondary to CNS depression

2 Decreased cardiac output Dysrhythmias3 Risk for injury Secondary to altered mental state

4 Risk for imbalanced fluid Diarrhea, renal failure

volume

NURSING MANAGEMENT OF METABOLIC ACIDOSIS




1 Will return to usual baseline LOC

2 Will return to normal baseline parameters for vital signs withimproved CO and decreased or resolved dysrhythmias

3 Will remain in a safe, secure environment without injury

4 Will maintain fluid and electrolyte balance and stable renal

status

INTERVENTIONS


- Monitor LOC and reorient as necessary

- Monitor VS, esp. RRR, BP, and T

- Monitor ABGs to assess the effects of treatment

- Institute cardiac monitoring as ordered

NURSING MANAGEMENT OF PATIENT WITH METABOLIC ACIDOSIS



2 Supporting cardiac output

- Monitor VS, MIO, and fluid and electrolyte balance

- Institute cardiac monitoring to evaluate cardiac status

3 Promoting safety

- Provide a safe, secure and monitored environment

- Institute safety precautions

4 Promoting return of fluid and electrolyte balance

- Monitor MIO

- Administer medications per medical order






1 Exhibits baseline-level consciousness and orientation

2 Returns to normal baseline parameters for vital signs andCardiac Output with cardiac dysrhythmias resolved

3 Remains free from injury

4 Maintains fluid and electrolyte balance and stable renal function

METABOLIC ALKALOSIS: BICARBONATE EXCESS



Loss of stomach acid, gastric suctioning, persistent vomiting, excess

alkali intake, intestinal fistulas, hypokalemia, Cushing’s syndrome or aldosteronism, potassium-diuretic therapy

Excessive amounts of acid substance and

hydrogen ions are lost from the body or largeamounts of bicarbonate or lactate are added orally

or IV

Excess of base elements

METABOLIC ALKALOSIS



NURSING MANAGEMENT OF METABOLIC ALKALOSISASSESSMENT

* Health Hx: Prolonged vomiting or nasogastric suctioning,



g g g g,frequent self-induced vomiting, muscle weakness, light-headedness, ingestion of large amounts of licorice orantacids, use of diuretics, muscle cramping, twitching, or

tingling* Physical Examination: mental confusion, dizziness, changes in

LOC, hyperreflexia, tetany, dysrhthmias, seizurees, respiratoryfailure, positive Chvostek’s or Trosseau’s sign if the patient hasa low ionized serum calcium level, decreased hand grasps,generalized muscle weakness, decreased serum calcium orpotassium level, impaired concentration, seizures, ECG changes

consistent with hypokalemia



1 Disturbed thought processes CNS excitation

2 Decreased cardiac output Dysrhythmias and electrolyteimbalances

3 Risk for injury Muscle weakness, tetany, confusion and possibleseizures

4 Risk for imbalanced fluid Nasogastric drainage, diuretic therapy

volume fistula

NURSING MANAGEMENT OF METABOLIC ALKALOSIS




1 Will return to usual baseline LOC and orientation

2 Will return to normal baseline parameters for vital signs withimproved CO with resolution of electrolyte imbalances anddecreased or resolved cardiac dysrhythmias

3 Will remain in a safe, secure environment without injury

4 Will maintain fluid and electrolyte balance

INTERVENTIONS


- Monitor LOC and reorient as necessary

- Monitor VS, esp. RRR, BP, and T

- Monitor ABGs to assess the effects of treatment

- Institute cardiac monitoring as ordered

NURSING MANAGEMENT OF PATIENT WITH METABOLIC ALKALOSIS



2 Supporting cardiac output

- Monitor VS, MIO, and fluid and electrolyte balance

- Institute cardiac monitoring to evaluate cardiac status

3 Promoting safety

- Provide a safe, secure and monitored environment

- Institute safety precautions

4 Promoting return of fluid and electrolyte balance

- Monitor MIO

- Administer medications per medical order

NURSING MANAGEMENT OF PATIENT WITH METABOLIC



NURSING MANAGEMENT OF PATIENT WITH METABOLICALKALOSIS

EVALUATION. Achievement of outcomes is successful when thepatient:

1 Manifests mental status has returned to baseline

2 Is free from cardiac dysrhythmias

3 Remains free from injury

4 Maintains fluid balance at baseline level

CRITICAL THINKING EXERCISES



A 32-year-old administrative assistant comes to the urgent carecenter 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 is110/68 which she states “is about normal for me.” Her ABG

values are as follows:pH: 7.57

PaO2: 92

PaCO2: 41

HCO3: 36Describe her acid-base status, probable cause for the imbalance

and treatment

fluidsandelectrolytes-090305183533-phpapp01

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