electrolytes 1016

8/3/2019 Electrolytes 1016

http://slidepdf.com/reader/full/electrolytes-1016 1/90

•salts or minerals in body fluids

•contain electrically charged particles called ions

•principal source of osmotic forces which control volumeor location of fluid

Cations- positively charged; Na, K, Ca, Mg

Anions- negatively charged; CL, HCO3, PO4

ELECTROLYTES

Major electrolytesin ICF

Major electrolytes inECF



IONS An atom or a group of atoms that has an electric

charge. Positive ions, or cations, are formed by the lossof electrons; negative ions, or anions, are formed by the gain of electrons.

The American Heritage® Science Dictionary

Copyright © 2002. Published by Houghton Mifflin



Major extracellular

electrolytes Sodium

Chloride

Calcium



Major intracellular

electrolytes Potassium

phosphate

magnesium



ELECTROLYTES Na+: most abundant electrolyte in the body

K+: essential for normal membrane excitability for nerve impulse

Cl-: regulates osmotic pressure and assists in regulating acid-basebalance

Ca+: usually combined with phosphorus to form the mineral salts of bones and teeth, promotes nerve impulse and musclecontraction/relaxation

Mg+: plays role in carbohydrate and protein metabolism, storage anduse of intracellular energy and neural transmission. Important in thefunctioning of the heart, nerves, and muscles



Sodium Regulates ECF volume and dist.

Maintains blood volume

Transmits nerve impulses and contracting muscles



Chloride Major ECF anion

HCl production

Regulates acid base balance Buffer in O2- CO2 exchange in RBC



NaCl: “the leader” Na+ and Cl+ in Plasma

Inc. Osmolarity in interstitial fluid

Water moves out from cell

Water goes to plasma

Inc. in plasma/ blood volume



Calcium Muscle contraction and relaxation

Calcitriol, parathyroid hormone

Calcitonin



CalcitoninBone:

suppresses resorption of bone by inhibiting the

activity of osteoclasts, a cell type that "digests" bonematrix, releasing calcium and phosphorus into blood.

Kidney:

Calcium and phosphorus are prevented from being

lost in urine by reabsorption in the kidney tubules.Calcitonin inhibits tubular reabsorption of these twoions, leading to increased rates of their loss in urine



Phosphate Major ICF anion

Formation of bones and teeth (reciprocal rel. w/ Ca)

Metabolism



Calcitiol, Parathyroid hormone, Calcitonin

Dec. Ca in blood/ Inc. PO4

Release of Parathyroid hormone and calcitriol

Release of Ca from bones to ECF/ dec. absorp. Of PO4Inc. absorption of Ca in Intestines/ Excretion of PO4

Inc. Ca plasma level/ dec. in PO4

Calcitonin

Inc. deposition of Ca in Bones

Dec. Ca plasma level / Inc. PO4



Potassium Major ICF cation

Maintains ICF balance

Skeletal, cardiac, smooth muscle activity Regulates acid- base balance



Potassium RegulationICF ECF

Insulin AldosteroneTissue damage and acidosis



Mg Production of ATP

CHON and DNA synthesis

Nerve impulses and cardiac function regulation Intestinal absorption is increased w/ Vit D and PTH



MAJOR ELECTROLYTE IMBALANCES

Hyponatremia (sodium deficit < 130mEq/L)

Hypernatremia (sodium excess >145mEq/L)

Hypokalemia (potassium deficit <3.5mEq/L)

Hyperkalemia (potassium excess >5.1mEq/L)

Chloride imbalance (<98mEq/L or >107mEq/L)

Magnesium imbalance (<1.5mEq/L or >2.5mEq/L)



HypoNatremia Sodium deficiency

Serum level below 135 mEq/L (N: 135-145)

Results from excessive sodium loss or excessive watergain

Causes

Fluid loss Adrenal insufficiency

SIADH

Excessive water gain with deficient Na fluids



HypoNatremia S/s

Anorexia, N/V

Muscle cramps Altered LOC (lethargy, disorientation, Headache,

confusion, convulsion)

Labs

Serum Na less than 135 mEq/L Low urine Na & specific gravity – if cause is Na loss

High if the cause is SIADH



Nursing Management Maintain Fluid Balance

Monitor I & O

Weigh daily

Assess for s/s of fluid volume excess Administer Na supplements orally/NGT/parenterally

Infuse hypotonic solutions cautiously

Prevent injury

Assess neurologic (LOC, muscle twitching, seizures) and GIstatus (anorexia, NV, abdominal cramping)

Maintain seizure precautions

Monitor serum Na levels

Maintain water restriction if cause is fluid volume excess



Hypernatremia Sodium excess

Above serum Na level of 145 mEq/L

Causes: Water loss (diarrhea, fever, hyperventilation, Diabetes

insipidus)

Inadequate water replacement (elderly, cognitively

impaired, coma pts) Inability to swallow

Excessive intake of Na in any routes



HyperNatremia S/s

Thirst

Tented skin turgor

Edematous dry skin and sticky mucous membrane Elevated body temperature

Lethargy and restlessness

Peripheral and pulmonary edema

Labs Elevated serum Na >145 mEq/L

Serum osmolality > 295 mOsm/kg

Elevated urine specific gravity and urine osmolality



Nursing Management Maintain normal fluid balance

I&O accurately

Weigh daily

Increase OFI as appropriate

Use hypertonic sol’n cautiously

Monitor serum Na level

Protect from injury

Assess VS, Skin turgor, neurologic status and for thirst

Reposition frequently

Keep side rails up, bed in low position, call light within reach

Secure all invasive lines



HypoKalemia Potassium deficiency

Serum potassium < 3.5mEq/L

Causes: Inadequate dietary intake of potassium

Excessive loss Tx like amphotericin B, diuretics, coricosteroid therapy, IVT

without K replacement GI disorders (diarrhea, vomiting, fistula)

Diaphoresis & renal disorders

Metabolic alkalosis

Hyperaldosteronism



HypoKalemia S/s

Anorexia

N/V

Fatigue Muscle weakness, leg cramps or paresthesia

Cardiac arrthymias

Decrease bowel motility, ileus, abdominal distention

Labs Serum K+ <3.5 mEq/L

ECG : f lattened T wave, prominent U wave, depressed STsegment, prolonged PR interval



Nursing Management Encourage potassium rich foods

Administer potassium replacement orally (K durules)

Infuse parenteral potassium supplement. (diluted in atleast 100cc of solution, administered through infusionpump or side drip, monitor ECG)

Never administer potassium per IV push or IM

Monitor I&O, serum K Assess for abdominal distention

Prevent injury in client’s taking digitalis



HyperKalemia Potassium excess

Serum K+ >5.5 mEq/L

Causes:

Decreased renal excretion due to renal failure

Hypoaldosteronism

Acidosis Severe tissue damage (burns, massive infection)

Excessive intake of K supplement

Hemolysis



HyperKalemia S/s

Cardiac arrythmias

Muscle weakness, paresthesias, paralysis

Irritability and anxiety

Abdominal cramps with diarrhea

Labs

Serum K+ >5.5mEq/L ECG: tall tented T waves, prolonged PR interval and

QRS duration, absent P waves, and ST depression



Nursing Management Decrease intake of K+ rich foods Cation Exchange resins (e.g. kayexalate) Ca gluconate – antagonizes the effects in cardiac

conduction Parenteral NaH2CO3 – alkalinizes plasma and causes

temporary shift of K+ to cells Administration of D50-50 Hemodialysis

Assess s/s of hyperkalemia Assess ECG and serum K+ level Do not prolong use of torniquet in drawing blood Caution in use of salt substitutes and K+ sparing diuretics



HypoCalcemia Calcium deficiency Serum Ca of <8 mg/dL

Causes: Primary or surgical hypoparathyroidism due to

thyroidectomy Pancreatitis Inadequate Vit. D intake or synthesis Renal failure Drug therapy (e.g. aminoglycosides, corticosteroids,

caffeine) Insufficient Ca intake



HypoCalcemiaS/s

Tetany (tingling in fingers and circumoral area, musclespasms associated with pain in extremities and face)

Positive Trousseau sign Positive Chevostek sign

Carpopedal spasms

Hyperactive deep tendon reflexes due to neuromuscular

irritability Labs:

Serum Ca <8.5 mg/dL

ECG: prolonged QT interval



Nursing Management Increase Ca rich foods in the diet (e.g. dilis, etc)

Increase Vit. D rich foods intake

Regular exercise

Monitor serum Ca

Institute seizure precautions

Administer parenteral Ca. (caution: tissue necrosis if IV line – infiltrated)

Do not add Ca in solns with bicarbonate orphosphorus – can cause precipitation

Caution in the Ca administration in pts taking digitalis



HyperCalcemia Calcium excess

Serum Ca > 10.5 mg/dL

Causes:

Excessive calcium administration or intake

Movement of calcium from bones to serum

Decreased renal excretion due to renal failure

Drug therapy with thiazide diuretics

hyperparathyroidism



HyperCalcemia S/s

Anorexia, N/V

Constipation

Muscular weakness, incoordination ALOC (slurred speech, confusion, lethargy, coma)

Polyuria, polydypsia

Cardiac arrythmias

Hypoactive DTR Labs

Serum Ca >10.5 mg/dL

ECG: shortened QT interval, bradycardia and heart blocks



Nursing Management Teach importance of early ambulation to prevent calcium

loss during hospitalization

Participate in weight bearing exercises

Safety measures when there is mental confusion Assess for DHN, mental confusion, psychotic behavior

Encourage 3-4 quarts of fluid daily and dietary fiber

Parenteral saline solution to dilute serum Ca

Administer parenteral phosphate Administer furosemide

Treatment of underlying cause, calcitonin forhyperparathyroidism, corticosteroids for CA



HypoMagnesemia Magnesium deficiency

Serum Mg <1.5 mEq/L

Causes:

Poor nutrition

Alcoholism

GI and renal losses without replacement



HypoMagnesemia S/s

(+) Trousseau & Chevostek signs

Neuromuscular irritability

Insomia Mood changes

Cardiac arrythmias

Labs: Serum Mg < 1.5 mEq/L

ECG: f lattened T wave, prominent U wave, anddepressed ST segment



Nursing Management Discuss the misuse of diuretics and laxatives Dietary sources of Mg (nuts, whole grains, cornmeal,

bananas, etc)

Administer parenteral Mg in infusion pump Monitor for s/s of magnesium toxicity (hot, flushed skin,diaphoresis, anxiety or lethargy, hypotension, laryngealstridor)

Monitor ECG and pulse

Monitor Serum Mg levels Maintain on seizure precautions Institute safety measures for mental confusion Assess ability to swallow cause by dysphagia Monitor clients on digitalis (predisposes to toxicity)



HyperMagnesemia Mg excess

Serum Mg level > 2.5 mEq/L

Causes:

Renal failure

Overuse of Mg-containing antacids

Excessive Mg administration

Overuse of enemas or laxatives containing Mg

Severe dehydration, as in DKA



HyperMagnesemia S/s

Hot, flushed skin

Hypoactive reflexes

Hypotension, bradycardia Depressed respirations, lethargy, drowsiness, and absent

DTR

Cardiac arrythmias

Labs Serum Mg level >2.5 mEq/L

ECG: prolonged QT interval and AV blocks



Nursing Management Health teaching on antacid or cathartic use as well as OTC

drugs containing Mg Discontinue all parenteral or oral Mg

During respiratory or cardiac emergencies, collaborate withthe RT providing respiratory support Administer Ca gluconate to antagonize effect of Mg Prepare for hemodialysis as necessary Administer diuretics and 0.45% NSS – excretion of Mg

Monitor serum Mg level Monitor VS, CV status, Respiratory status, patellar reflexes,

LOC Institute safety precautions



HypoPhosphatemia Phosphorus deficiency

Serum Phosphorus < 2.5 mg/dL

Causes:

Overzealous intake or administration of CHO

TPN administration

Prolonged intense hyperventilation, alcohol withdrawal, DKA

Excess phosphorus binding antacids

Severe DHN, as occurs in DKA



HypoPhosphatemia S/s:

Irritability, apprehension, weakness, numbness,confusion, seizure, coma

Hypoxia leading to an increase RR and respiratory alkalosis

Muscle weakness, muscle pain

Bruising, bleeding due to platelet dysfunction

Increase susceptibility to infection Labs:

Serum Mg level <2.5 mEq/L

Increase urine Mg



Nursing Management Assess VS, s/s of apprehension, confusion, ALOC


Prevention of infection since may change granulocytes Introduce TPN gradually to prevent rapid shift of

phosphorus into the cells

Monitor serum level of Phosphorus (N: 2.5-4.5mEq/L)

Monitor possible complication of phosphorus – hypoCa



HyperPhosphatemia Phosphorus excess

Serum phosphorus > 4.5 mEq/L

Causes:

Renal failure

Chemotherapy for neoplastic disease

High phosphorus intake

Profound muscle necrosis



HyperPhosphatemia S/s

Soft tissue calcification

Tetany

Anorexia, N/V

Muscle weakness, hyperreflexia, tachycardia

Labs:

Serum phosphorus level >4.5 mEq/L Xray studies show skeletal changes with abnormal bone

development



Nursing Management Avoid foods high in phosphorus (hard cheese, cream,

nuts, whole grains, dried foods, dried vegetables)

Avoid phosphate containing substances (laxatives,enemas that contain phosphate)


Monitor serum phosphorus level



Hydrogen Ion and pHImportance:

Membrane integrity

Metabolic enzyme reactionsConcentration:

0.0000001 mg/L

pH = power of hydrogen

pH = -log [H+] = 10 -7 = pH 7.0



Hydrogen Ion and pH greater the H+ = more acidic = lower pH

lesser the H+

= more basic = higher pH

body fluid pH = 7.35 – 7.45 (narrow range)



pHH+

concentration



Regulation of Acid-Base Balance



BUFFERS

absorb excessive hydrogen (H+) (acid) or hydroxyl ion

(OH-) (base)

contains salts of either weak acids or weak bases thateither: combine with H+ when H+ increase in body fluids release H+ when H+ decrease in body fluids



1. PO4

3-

buffer system

Reaction:

HPO4

2-

+ H

+↔

H2PO4

-

monohydrogen hydrogen dihydrogen

phosphate ion ion phosphate ion



2. Proteins amino acid side chains

contains: Carboxyl group ( -COOH )

Amine group ( -NH2 )



Reaction:

-COO- + H+↔ -COOH

carboxyl hydrogen carboxyl

group ion group

-NH2 + H+↔ -NH 3

amine group hydrogen ammonium

ion group



3. Bicarbonate (HCO3

-

)Reaction:

CO2 + H2O↔

H2CO 3 ↔

H

+

+ HCO 3

-

Carbon water carbonic hydrogen bicarbonate

dioxide acid ion ion



responds rapidly to a change in pH and

function to bring the pH back to itsnormal range



powerful regulator of pH, but responds moreslowly than does the respiratory system

nephrons → secretion of H+ into the urine andreabsorption of bicarbonate → directly regulates pH



Nephrons are Microscopic Tubules That Form

the Urine

Insert fig 23-4



pH falls below 7.35

major effect: CNS malfunctions → can become comatose



pH increases above 7.45

major effect: hyperexcitability of thenervous system



Respiratory acidosis Respiratory alkalosis

Increased PCO2

Increased carbonic acid

Increased H+ = low pH

(<7.35)

Increased bicarbonate

Decreased PCO2

Decreased carbonic acid

Decreased H+ = high pH

(>7.45)

Decreased bicarbonate



RISK FACTORS

Acute lung condition thatimpair alveolar gasexchange (pneumonia,

edema, aspiration, near-drowning)

Chronic lung disease(asthma, emphysema)

Overdose of narcotics orsedatives

Brain injury that affects therespiratory center

MANIFESTATIONS

Breathlessness, restlessnessand apprehension

Increased PR and RR,gradually becomesdepressed

Headache, dizziness

Confusion, ↓ LOC

Convulsions Warm, flushed skin



Respiratory Acidosis

Hypoventilation

Hypercapnia (PaCO2 )

pH blood

Hyperventilation Renal buffering48-72 hours

Blow off CO2

Return the pHto normal

Hydrogen (H+)excretion

Bicarbonateretention

Return pH tonormal

C

o m p e n s a t i o n

When hypoventilation causes hypercapnia, blood pH falls. If this state persists, respiratory acidosis results.Compensatory mechanisms can be initiated to return the pH to normal.



RISK FACTORS

Hyperventilation due to:

Extreme anxiety

Elevated body temperature

Overventilation with amechanical ventilator

Hypoxia

Salicylate overdose

MANIFESTATIONS

Shortness of breath, chesttightness

Light-headedness,numbness, tingling of theextremities

Difficulty concentrating

Tremulousness, blurred vision



Respiratory Alkalosis

Hyperventilation

Hypercapnia (PaCO2 )

pH blood

Hypoventilation Renal buffering48-72 hours

Retain CO2

Return the pHto normal

Hydrogen (H+)retention

Bicarbonateexcretion

Return pH tonormal

C


When hyperventilation causes hypocapnia, the blood pH elevates. If this state persists, respiratory alkalosis results.Compensation by the lungs and kidneys will usually be initiated to return the pH to normal.



Metabolic acidosis Metabolic alkalosis

Increased H+ = low pH

(<7.35)

Decreased bicarbonate

Heavier breathing causes

decreased PCO2

Decreased H+ = high pH

(>7.45)

Increased bicarbonate

Lighter breathing causes

increased PCO2



RISK FACTORS

Conditions that ↑ nonvolatile

acids in the blood ( renal

impairment, DM,starvation )

Conditions that ↓ bicarbonate ( prolonged

diarrhea )Excessive infusion of

chloride-containing IV fluids ( NaCl )

MANIFESTATIONS

Kussmaul’s respirations

Lethargy, confusion

Headache

Weakness

Anorexia, nausea, vomitingand diarrhea

M b li A id i



Metabolic Acidosis

Loss of base or

Production of excess acid

serum pH

Hyperventilation Renal buffering

PaCO2

Serum pH

Hydrogen (H+)excretion

Bicarbonateretention

C


When base is lost or acid is produced excessively, the serum pH falls. If this state persists, metabolic acidosis results.

Compensatory mechanisms will usually be initiated to attempt to return the serum pH toward normal.

Serum pH



RISK FACTORSExcessive acid losses due to:

Vomiting

Gastric suction

Excessive use of K-losing diuretics

Excessive adrenal corticoidhormones due to:

Cushing’s syndrome

Hyperaldosteronism

Excessive bicarbonate intake from:

Antacids

Parenteral NaHCO3

MANIFESTATIONS Decreased RR and depth

Dizziness

Numbness and tingling of theextremities

Hypertonic muscles, tetany



Metabolic Alkalosis

Excess base or loss ofacid

serum pH

Hypoventilation Renal buffering

PaCO2

Serum pH

Hydrogen (H+)retention

Bicarbonateexcretion

C


When base is accumulated or acid is lost, the serum pH elevates. If this state persists, metabolic alkalosis results. Compensatory mechanismswill usually be initiated to attempt to return pH toward normal.

Serum pH



Arterial Blood Gases

performed to evaluate the client’s acid-base

balance and oxygenation

arterial blood – provides a truer reflection of gas exchange in the pulmonary system



Normal Values of ABGs

pH

PaO2

PaCO2

HCO3-

Base excess

O2 saturation

7.35 – 7.45

80 – 100 mmHg

35 – 45 mmHg

22 – 26 mEq/L

-2 to +2 mEq/L

95 – 98%



1. Look at the pH:

a. if pH less than 7.35 = acidosis

b. if pH greater than 7.45 = alkalosis

2. Look at the PaCO2:

a. if PaCO2

less than 35 = more CO2

exhaled

b. if PaCO2 greater than 45 = less CO2 exhaled



3. Assess the pH and PaCO2 relationship for apossible respiratory problem:

a. if pH less than 7.35 (acidosis) and PaCO2

isgreater than 45 mmHg, retained CO2 →

respiratory acidosis

b. if pH greater than 7.45 (alkalosis) and PaCO2 is less than 35 mmHg, lack of CO2 →

respiratory alkalosis



4. Look at the bicarbonate:

a. if HCO3 is less than 22 mEq/L = lower

bicarbonate levelb. if HCO3 is greater than 26 mEq/L = higherbicarbonate level



5. Assess pH, HCO3, and base excess (BE) values

for a possible metabolic problem:

a. if pH less than 7.35 (acidosis), HCO3 less than22 mEq/L and BE below -2mEq/L = low

bicarbonate levels = metabolic acidosis

b. if pH greater than 7.45 (alkalosis), HCO3

greater than 26 mEq/L and BE above +2mEq/L = high bicarbonate level =metabolic

alkalosis



6. Look for evidence of COMPENSATION:

a. Respiratory acidosis: pH < 7.35PaCO2 > 45 mmHgIf : HCO3 is greater than 26 mEq/L = kidneys maintaining

bicarbonate to minimize acidosis = RENALCOMPENSATION

b. Respiratory alkalosis: pH > 7.45PaCO2 < 35 mmHg

If : HCO3 is less than 22 mEq/L = kidneys excretingbicarbonate to minimize alkalosis = RENAL

COMPENSATION



c. Metabolic acidosis: pH < 7.35

HCO3 < 22 mEq/LIf : PaCO2 is less than 35 mmHg = CO2 being “blown off”

to minimize acidosis = RESPIRATORY COMPENSATION

d. Metabolic alkalosis: pH > 7.45

HCO3 > 26 mEq/L

If: PaCO2 is greater than 45 mmHg = CO2 being retainedto compensate for excess base = RESPIRATORY

COMPENSATION



1. pH 7.30

pCO2 55 mmHg

HCO3 25 mmHg

2. pH 7.49

pCO2 38 mmHg

HCO3 32 mmHg



3. pH 7.28

pCO2 42 mmHg

HCO3 19 mmHg

4. pH 7.51

pCO2 29 mmHg

HCO3 25 mmHg



5. pH 7.30

pCO2 38 mmHgHCO3 19 mmHg

6. pH 7.33

pCO2 33 mmHg

HCO3 19 mmHg

7. pH 7.35pCO2 29 mmHg

HCO3 19 mmHg



8. pH 7.28

pCO2 55 mmHgHCO3 26 mmHg

9. pH 7.32pCO2 55 mmHg

HCO3 31 mmHg

10. pH 7.35

pCO2 55 mmHg

HCO3 34 mmHg

electrolytes 1016

Documents