By Jhessa Reyes

"FLUIDS AND ELECTROLYTES" ○ Interstitial Space

➢ Is dependent upon dynamic processes that ▪ 12L of fluids surrounds the
are crucial for life and homeostasis. cells.
○ Transcellular Space
POSITIVE AND NEGATIVE FEEDBACK ▪ The smallest division of ECF,
and contains 1L of fluids in
body cavities (CSF,
Pericardium, Intraocular,
Pleural, Sweat/Tears, Digestive
Secretions)

"FLUIDS"
➢ 60% of Adult's body weight consists of fluid
(water and electrolytes)
➢ Skin, Muscle, and Blood contains the highest NORMAL INTAKE AND OUTPUT
amount of water. • Daily intake. An adult human at rest takes
appropriately 2,500 ml of fluid daily.
FACTORS AFFECTING AMOUNT OF BODY • Levels of intake. Approximate levels of
FLUID intake include fluids 1, 200 ml, foods
• Body fat (thin > obese) 1, 000 ml, and metabolic products 30 ml.
• Gender (male > female) • Daily output. Daily output should
• Age (young > older) approximately equal in intake.
• Normal output. Normal output occurs as
urine, breathing, perspiration, feces, and
in minimal amounts of vaginal secretions.
• ICF and ECF normally shifts between each
other to maintain EQUILIBRIUM
• DISEQUILIBRIUM happens if there’s:
❖ A LOSS OF FLUID from the body
❖ THIRD SPACE FLUID SHIFT
- Fluid shifts into a space that
doesn't contribute to
2 BODY FLUID COMPARTMENTS equilibrium
❖ Intracellular Space (ICF) - fluids in the - Fluid shift from
cells and approximately 2/3 of body fluids is INTRAVASCULAR into
in ICF and primarily located at skeletal INTERSTITIAL (edema) and
system. into TRANSCELLULAR space
❖ Extracellular Space (ECF) - fluids outside - Manifestations:
the cells, approximately 1/3 of the body □ Increased heart rate
fluids are in ECF. □ Increased body weight
ECF is divided into 3: □ Decreased blood pressure
○ Intravascular Space □ Decreased central venous
▪ 6L blood ( 3L is made up of pressure
plasma, and 3L is made up of □ Edema
erythrocytes, leukocytes, and □ I&O imbalances
thrombocytes in adult.

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OVERVIEW OF FLUID AND ELECTROLYTES

"ELECTROLYTES" 2. DIFFUSION - Solute moves from area of

➢ Active chemicals either positively HIGHER to LOWER concentration.
(CATIONS) or NEGATIVELY (ANIONS) 3. FILTRATION - Intravascular to Interstitial
charged Shift Hydrostatic Pressure
➢ Measured in mEq/L - 180L of plasma is being filtered by
➢ Most accessible medium of measuring kidney every 24 hours
electrolyte concentration: plasma 4. ACTIVE TRANSPORT - energy must be
expended to allow movement against a
MAJOR ELECTROLYTES IN THE BODY concentration gradient.
N.V. (Serum)
-

Sodium - 135 - 145 mEq/L

,

ROUTES OF GAINS AND LOSSES

Potassium - 3.5 - 5 mEq/L • Input: Oral (eating and drinking), Parenteral
Calcium - 4.5 - 5.5 mEq/L and Enteral administration of fluids
Magnesium - 1.5 - 2.5 mEq/L • Output
Phosphorus - 2.5- 4.5 mg/L ▫ Kidneys - 1mL/kg/hr or 1 1/2 L of urine
Chlorine - 96 - 106 mEq/L every day
▫ Skin - Sensible perspiration
FLUID SHIFTING (0-1L/hour); Insensible perspiration
• Hydrostatic Pressure - pressure exerted by (600mL/day through evaporation
fluid on blood vessel wall ▫ Lungs - Insensible (400mL/day) water
• Osmotic Pressure - pressure exerted by vapor loss; increase loss in DRY
plasma cells climate/ R.R.
▫ GIT - 100-200mL/day

AVERAGE DAILY I&O

Intake Output
Oral Liquids 1,300mL Urine 1500 ml
H2O in Flood 1000mL Stool 200 ml
H2O produced by Lungs 300 ml
metabolism 300mL Skin 600 ml

Total - 2600 mL Total 2600 ml 2600 ml

❖ (+) Penrose drain = 50 mL

REGULATION OF BODY FLUID ❖ (+) IFC = 1.2L
COMPARTMENTS ❖ (+) NGT, Oral feeding = 800mL
❖ BT = 250 cc/bag x 2
1. OSMOSIS - Fluid moves from LOWER to ❖ (+) IVF = @1000cc (start of shift) and @
HIGHER solute concentration. 100cc (end of shift)
❖ (+) Colostomy = 300mL
Related terms: ❖ Suctioned oral secretions = 50 mL
❖ Osmolality - Solute concentration
❖ Tonicity - ability of solute to cause osmosis
LAB TEST FOR FLUID STATUS
(Hypertonic/ increase tonicity osmoles;; Na,
• Serum Osmolality (mOsm/kg ) and
Mannitol and Glucose)
Osmolarity (mOsm/L)
❖ Osmotic Pressure - concentration of solute
- Plasma sodium concentration
that is needed to stop osmosis
- Normal value: 275-300
❖ Oncotic Pressure - osmotic pressure
• Urine Osmolality (mOsm/kg) and
exerted by proteins
Osmolarity (mOsm/L)
❖ Osmotic Diuresis - increase urine output,
- Most reliable indicator of urine
caused by excretion of hypertonic osmoles concentration
- Normal Value: 250-900

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OVERVIEW OF FLUID AND ELECTROLYTES
• Urine Specific Gravity - CORTISOL produced in ADRENAL
- Measures kidney's ability to conserve MEDULLA when
and excrete water secreted/administered in large
- Normal Value: 1.010 - 1.025 quantities can also cause sodium and
- Inversely proportional to Urine Output water retention
• Blood Urea Nitrogen (BUN) • Parathyroid Glands - Calcium and phosphate
- End product of metabolism of protein balance
by the liver - Increases serum calcium by bone
- Made up of urea resorption and absorption in the
- Normal value: 10-20 mg/dl intestine
- INCREASES with: Increased protein
intake, IG bleeding and dehydration and FLUID REGULATION MECHANISMS
decreased renal function. • The thirst center. The thirst center in
- DECREASES with: liver disease, the hypothalamus stimulates or inhibits
decreased protein intake/starvation, the desire for a person to drink.
fluid overload • Antidiuretic hormone. ADH regulates the
- Inversely proportional to renal function amount of water the kidney tubules
• Serum Creatinine absorb and is released in response to low
- End product of muscle metabolism blood volume or in response to an increase
- Better indicator of renal function in concentration of sodium and other
because it is not affected by protein solutes in the intravascular fluids.
intake/metabolic state • The RAA system. The RAA system
- Normal value: 0.7-1.4 mg/dL controls fluid volume, in which when the
• Hematocrit blood volume decreases, blood flow to the
- Percentage of RBC vs WHOLE BLOOD renal juxtaglomerular apparatus is
- Normal value: Males: 42-52%; Females: reduced, thereby activating the RAA
35-47% system.
- HIGH in: dehydration/polycythemia • Atrial natriuretic peptide. The heart also
- LOW in: overhydration/anemia plays a role in correcting overload
imbalances, by releasing ANP from the
HOMEOSTATIC MECHANISMS right atrium.
• Kidney - regulates ECF, electrolytes
(selective retention and excretion) and pH OTHER MECHANISMS:
(retaining H ions) 1. Baroreceptors
- excretion of metabolic wastes and 2. RAAS
toxins 3. Osmoreceptors
- responds to ADH and aldosterone 4. ADH + Thirst
- thus, renal failure causes multiple fluid 5. Release of ANP/ANF by atrial cardiac
and electrolyte imbalances cells
• Heart and Blood Vessels - blood being
pumped by the heart circulates through the
blood vessels and being filtered in the kidney
for excretion
• Lung - regulation of pH
- medium of insensible fluid loss
• Pituitary - stores ADH secreted by the
hypothalamus
• Adrenal Glands - secretion of
ALDOSTERONE at the ADRENAL CORTEX
which promotes sodium and water retention,
and potassium excretion

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FLUID VOLUME DISTURBANCES

"HYPOVOLEMIA/FLUID 4. Assess alteration in mentation/sensorium

(confusion, agitation, slowed responses).
VOLUME DEFICIT" 5. Assess color and amount of urine. Report
➢ ECF loss > fluid intake urine output less than 30 ml/hr for two (2)
➢ Water and electrolytes are lost in the consecutive hours.
SAME PROPORTION (fluid volume 6. Monitor and document temperature.
decreases but water and electrolyte ratio 7. Monitor fluid status in relation to dietary
is STILL THE SAME) intake.
➢ Different from DEHYDRATION (loss of 8. Note the presence of nausea, vomiting, and
water alone, causing increased serum fever.
sodium) 9. Auscultate and document heart sounds; note
➢ Occurs rapidly when coupled with rate, rhythm, or other abnormal findings.
decreased fluid intake 10. Monitor serum electrolytes and urine
osmolality, and report abnormal values.
CAUSES/RISK FACTORS 11. Ascertain whether the patient has any
❖ FLUID LOSS related heart problem before initiating
○ Diabetes insipidus parenteral therapy.
○ Adrenal insufficiency 12. Weigh daily with the same scale, and
○ Osmotic diuresis preferably at the same time of day.
○ Hemorrhage 13. Identify the possible cause of the fluid
○ Third-space fluid shifting disturbance or imbalance.
❖ DECREASED FLUID INTAKE 14. Monitor active fluid loss from wound
○ Comatose drainage, tubes, diarrhea, bleeding, and
vomiting; maintain accurate input and output
SIGNS AND SYMPTOMS record.
• Decreased BP/Orthostatic Hypotension 15. During treatment, monitor closely for signs
• Acute weight loss of circulatory overload (headache, flushed
• Decreased skin turgor skin, tachycardia, venous distention,
• Oliguria/Concentrated urine elevated central venous pressure [CVP],
• Rapid but weak pulse shortness of breath, increased BP,
• Decreased CVP tachypnea, cough).
• Cool and clammy skin 16. Monitor and document hemodynamic status,
• Thirst and anorexia including CVP, pulmonary artery pressure
(PAP), and pulmonary capillary wedge
ASSESSMENT AND DIAGNOSTIC pressure (PCWP) if available in the hospital
FINDINGS: setting.
• Health history and physical examination 17. Monitor for the existence of factors
• Increased Hematocrit causing deficient fluid volume (e.g.,
• Increased Urine Specific Gravity gastrointestinal losses, difficulty
• Hyper (adrenal insufficiency) and Hypo maintaining oral intake, fever, uncontrolled
(GI and renal losses) kalemia type II diabetes mellitus, diuretic therapy).
• Hyper (DI) and Hypo (Osmotic Diuresis)
natremia MANAGEMENT
• Oral fluid replacement for mild losses
NURSING ASSESSMENT • IV route is required for acute and severe
1. Monitor and document vital signs, cases
especially BP and HR. - Fluid of choice for hypotensive
2. Assess skin turgor and oral mucous patients: ISOTONIC SOLUTION
membranes for signs of dehydration. (PNSS/PLRS)
3. Monitor BP for orthostatic changes - As soon as BP normalizes, HYPOTONIC
(changes seen when changing from supine SOLUTIONS follow
to standing position). Monitor HR for
orthostatic changes.

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FLUID VOLUME DISTURBANCES
• Accurate assessment (I&O, wt, v/s, CVP, • Increased Heart Rate
LOC and breath sounds and skin color) to • Increased Blood pressure
determine need to slow therapy to prevent • Increased pulse pressure
overload • Increased CVP
- I&O is monitored q8h • Increased weight
- Daily weight (loss of .5kg = loss of .5L)
- Assess for orthostatic hypotension ASSESSMENT AND DIAGNOSTIC FINDINGS
(decreased systolic pressure by • Decreased BUN
15mmHg from lying to sitting position) • Decreased Hematocrit
- Check for skin turgor (forehead, • Decreased Serum Sodium/Osmolality
sternum and inner thigh)
- Assess the oral cavity and tongue MANAGEMENT
(small and with multiple longitudinal • Management is directed at the cause
furrow • Symptomatic treatment
- Assess LOC • Administer DIURETICS as prescribed
• FLUID CHALLENGE TEST – for patients - decreases reabsorption of sodium
with U.O., to determine presence of Acute - Thiazide diuretics – given for mild
Tubular Necrosis (ATN caused by prolonged cases
FVD - Loop – for severe cases (S/E:
- Amount of fluids are given at specific decreased
rates/intervals while patients - potassium and magnesium levels)
hemodynamic response is monitored • Hemodialysis/Peritoneal Dialysis
(V/S/, LOC, CVP, U.O., Breath sounds) - removal of water, sodium and
- For patients with ATN, still U.O., and nitrogenous wastes
for patients with normal renal - to control potassium levels and acid-
function, U.O. base balance
• Shock – 25% loss of intravascular fluid • Nutritional Therapy
• FVD prevention measures by identifying and - Dietary restriction of sodium/Low
controlling risk sodium diet of 250mg/day (normal
• OFI depending on patient’s likes and dislikes average intake: 6-15 g of salt)
and type of fluid patient has lost - Advise the patient to read food and
• Oral rehydration solution can be given beverage labels
- Provide patient the option of consuming
"HYPERVOLEMIA/FLUID salt substitutes (usually contains
potassium)
VOLUME EXCESS" - Consume distilled water (local water
➢ Isotonic expansion of ECF caused by supply may contain high volumes of
abnormal retention of water and sodium in sodium)
the same proportions • I&O monitoring q8h
➢ Always caused by increased sodium in the • Daily weight
body • Assess breath sounds and degree of edema
(limb
CAUSES • circumference)
• Fluid overload (excessive • Hypervolemia prevention measures: avoid
intake/administration of Na-containing OTCs without medical advice
fluid) • Promote bed rest (favors diuresis)
• Decreased function of the homeostatic • Monitor patient’s response to diuretics
mechanisms (renal, heart and liver failure) • Semi-fowler’s position for patients with
dyspnea
SIGNS AND SYMPTOMS • Turn q2h (edematous skin is especially prone
• Edema to breakdown)
• Distended neck vein • Provide patient health teachings
• Crackles and shortness of breath

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FLUID VOLUME DISTURBANCES

"EDEMA"
➢ Caused by increased hydrostatic pressure/
increased ECF volume
➢ Can be localized/generalized(anasarca)
➢ Usually affects dependent areas
(Periorbital region, Ankle, Sacrum and
Scrotum)
➢ Pitting edema – pit forms after finger-
press
➢ Pulmonary Edema - Increased fluid in
alveoli and pulmonary interstitium
➢ Ascites - fluids that accumulate in the
peritoneal cavity caused by nephritic
syndrome, cirrhosis and some malignant
tumors

SIGNS AND SYMPTOMS

• Shortness of breath
• Pressure sensation
• Abdominal bloating

MANAGEMENT
• DIURETICS
• Extremity elevation
• Elastic compression stockings
• Paracentesis (for ascites)
• Dialysis

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ELECTROLYTES IMBALANCES

"SODIUM IMBALANCES" LABORATORY AND DIAGNOSTIC FINDINGS

• Serum sodium = less than 135 mEq/L
SODIUM - the most abundant electrolyte in ECF • Decreased serum osmolality
ranges from 135 – 145 mEq/L regulated by ADH, • Decreased urine specific gravity (1.002 -
thirst, RAAS 1.004)

FUNCTIONS OF SODIUM MANAGEMENT

• primary determinant of ECF Osmolality • Sodium replacement
• major role in controlling water distribution ○ Careful administration pf sodium
throughout the body P.O., or parenterally
• primary regulator of ECF volume • For patient's with SIADH:
• establishes electrochemical state necessary ○ Hypertonic saline solution
for muscle contraction and transmission of ○ Diuretic therapy (Furosemide)
nerve impulses ○ Lithium or Demeclocycline
• Water restriction

"SODIUM DEFICIT ❖ If edema exists alone, sodium is

(HYPONATREMIA)" restricted; if edema and hyponatremia
➢ refers to a serum sodium level that is occur together, both sodium and water
below normal (less than 135 mEq/L) are restricted.

CAUSES/RISK FACTORS NURSING MANAGEMENT

• vomiting, diarrhea, fistulas ✓ Identify patients at risk of hyponatremia
• sweating so that they can be monitored.
• use of diuretics ✓ Monitor I&O, daily weight
• adrenal insufficiency ✓ Note abnormal losses of sodium or gains
• low-salt diet of water as well as GI manifestations; Be
• SIADH particularly alert for CNS manifestations
• Excessive intake of Hypotonic solution (IV, ✓ Monitor serum sodium level closely, may
• NGT, Enema) include urine sodium & specific gravity
• Psychogenic Polydipsia ✓ Encourage foods & fluids with high

❖ Dilutional Hyponatremia (Water "SODIUM EXCESS

Intoxication) - Increased ECF volume and a
normal or increased total body sodium (HYPERNATREMIA)"
➢ refers to a higher-than-normal serum
SIGNS AND SYMPTOMS sodium level (exceeding 145 mEq/L)
• poor skin turgor ➢ refers to a higher-than-normal serum
• dry mucosa, ↓ saliva production sodium level (exceeding 145 mEq/L)
• orthostatic hypotension
• nausea, anorexia, abdominal cramping RISK FACTORS
• muscle cramps, feeling of exhaustion, apathy • Fluid Deprivation in patients who can’t
• Neurologic signs and symptoms: perceive, respond to or communicate their
thirst
○ Altered LOC/mental status ○ Unconscious patients
○ Status epilepticus ○ Very old or very young
○ Coma, obtundation ○ Cognitively impaired
○ Increased ICP • Administration of hypertonic enteral
feedings without adequate water
supplements
• Watery diarrhea
• Increased insensible water loss

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 ELECTROLYTES IMBALANCES
• Diabetes Insipidus "POTASSIUM DEFICIT
• Heat stroke
• Near-drowning in seawater
(HYPOKALEMIA)"
• IV administration of hypertonic saline ➢ Below-normal serum potassium
solution concentration; indicates an actual deficit
SIGNS AND SYMPTOMS in total K+ stores
1. Restlessness, weakness
2. Confusion, disorientation, delusions, CAUSES
hallucination • GI losses (most common causes)
3. Permanent brain damage in severe ○ Vomiting, diarrhea
Hypernatremia ○ GI suctioning
4. Thirst ○ Recent ileostomy
5. Dry, swollen tongue ○ Villous adenoma
6. Sticky mucous membranes • Use of diuretics (Thiazides & Loop
7. Flushed skin diuretics); corticosteroids
8. Peripheral & pulmonary edema • Metabolic Alkalosis
9. Increased muscle tone & DTR • Hyperaldosteronism
• Insulin Hypersecretion; TPN
LABORATORY AND DIAGNOSTIC FINDINGS • Poor intake of foods rich in K+
• Serum sodium = greater than 145 mEq/L • Bulimia nervosa
• Increased specific gravity and Osmolality • Magnesium depletion

MANAGEMENT SIGNS AND SYMPTOMS

Infusion of hypotonic solution (0.3 % NaCl) or • Fatigue, muscle weakness, leg cramps
isotonic non-saline solution (D5W) • Anorexia, N/V, ↓ peristalsis
Diuretics • Paresthesia
Desmopressin acetate (DDAVP) • Dysrhythmias, ↑digitalis sensitivity
• Polyuria, nocturia
NURSING MANAGEMENT • Excessive thirst
1. Assess for abnormal losses of water or • Glucose intolerance
decreased water intake & for large gains of • ↓ muscle strength & tendon reflexes
sodium • Respiratory or Cardiac arrest
2. Take note of patient’s thirst or increased body
temperature and evaluate it in relation to other LABORATOY AND DIAGNOSTIC FINDINGS
S/Sx • Serum K+ = ↓ 3.5 mEq/L
3. Monitor for neurologic S/Sx of Hypernatremia; • ECG = flat T wave or inverted T wave;
Monitor serum sodium levels Depressed ST segments; elevated U
4. Offer fluids at regular intervals, particularly waves
debilitated or unconscious patients • ABG = Metabolic Alkalosis
5. Provide access to water in patients with
diabetes insipidus to ensure adequate water in MANAGEMENT
❖ Prevention of Hypokalemia

"POTASSIUM ○ Encourage patient to eat foods rich

IMBALANCES" in potassium
➢ major intracellular electrolyte influences ○ Careful monitoring of I&O
➢ both skeletal & cardiac muscle activity ○ Monitor ECG for changes; monitor
➢ moves in & out of the cells under the ABG for increased HCO3 - & pH
➢ influence of Na+ - K+ pump levels
➢ ranges from 3.5 – 5 mEq/L
➢ Kidneys do not conserve K+; Aldosterone
↑ K+ excretion

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ELECTROLYTES IMBALANCES
❖ Replacement of Potassium LABORATORY AND DIAGNOSTIC FINDINGS
○ Increased intake of potassium in the • Serum K+ = ↑ 5 mEq/L
daily diet • ECG changes
○ Oral potassium supplements ○ Shortened QT interval
○ IV potassium therapy: ○ ST segment depression
▪ Potassium Chloride (KCl) ○ Peak, narrow T waves
□ Never administer by IV • ABG – Metabolic Acidosis
push or IM to avoid
MANAGEMENT
replacing K+ too rapidly
• Obtain ECG stat to detect changes; Monitor
□ Monitor ECG during
serum K+ levels (Obtain blood sample from a
potassium replacement
vein w/o IV infusing a K+ containing solution)
• Restriction of dietary K+ & K+ containing
"POTASSIUM EXCESS medications in non-acute situations
(HYPERKALEMIA)" • Administer the following medications as
➢ Greater-than-normal serum K+ ordered:
concentration ✓ Diuretics
➢ Although less common than hypokalemia, it ✓ Calcium Gluconate
is usually more dangerous because cardiac ✓ Sodium Bicarbonate
arrest is more frequently associated with ✓ Glucose & Insulin
↑ serum K+ levels ✓ Sorbitol
➢ Often related to IATROGENIC ✓ Beta-2 Agonists (Albuterol)
(treatment – induced) causes • Prepare & assist patient who will undergo
Dialysis
CAUSES • Treated with Kayexalate
• Decreased renal excretion of K+ • Metabolic Acidosis
• Hypoaldosteronism (Addison’s Disease) • Addison’s Disease
• Medications: KCl, heparin, ACE inhibitors • Metabolic Alkalosis
(Captopril), NSAIDs, K+ sparing diuretics • Dialysis is one of the treatment options
• Improper/ excessive use of potassium • Cushing’s Disease
supplements • Prolonged use of diuretics
• Administration of Aged (Stored) blood • Total Parenteral Nutrition causes
• Metabolic Acidosis • More Cardiotoxic
• Extensive tissue trauma • Too tight TQ application; Familial
• Burns
• Crushing injuries "CALCIUM IMBALANCES"
• Severe infections CALCIUM - a major component of bones & teeth
• Chemotherapy (lysis of malignant cells) - ranges from 8.6 – 10.2 mg/dL or 4.5 – 5.5
mEq/L
SIGNS AND SYMPTOMS - regulated by Calcitonin & parathyroid
• GI manifestations: hormone (PTH)
• Nausea, diarrhea, intermittent intestinal - 99% is found in the skeletal system; 1 % is
colic located outside the bone which circulates in
• Muscle weakness & paralysis the serum
• Respiratory & speech muscle paralysis
• Ventricular Dysrhythmias 3 FORMS OF CALCIUM IN PLASMA
• Cardiac arrest 1. Ionized calcium
2. Bound calcium
3. Complexed calcium

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ELECTROLYTES IMBALANCES
FUNCTIONS OF SERUM CALCIUM LABORATORY AND DIAGNOSTIC FINDINGS
• major role in transmitting nerve impulses • Serum Calcium = less than 8.6 mg/dL or 4.5
• regulates muscle contraction & mEq/L
• relaxation • Increased serum phosphorus & decreased
• activates enzymes that stimulate many serum magnesium levels
essential chemical reactions in the body • ECG: prolonged QT interval (Torsades de
• plays a role in blood coagulation pointes)

MANAGEMENT
"CALCIUM DEFICIT
• For acute symptomatic hypocalcemia:
(HYPPOCALCEMIA)" ✓ IV administration of Calcium (i.e.
Calcium Gluconate; calcium chloride;
➢ lower-than-normal serum concentration of calcium gluceptate)
calcium ✓ Administer as a slow IV bolus or a slow
➢ less than 8.6 mg/dL or 4.5 mEq/L IV infusion; diluted in D5W
• Oral calcium supplements with Vitamin D to
RISK FACTORS increase calcium absorption in GIT
• Primary & Surgical Hypoparathyroidism • If the cause is hyperphosphatemia;
• Massive administration of citrated blood Aluminum hydroxide, calcium acetate or
(i.e. exchange transfusion in newborn; calcium carbonate antacids may be given
massive hemorrhage & shock) • Increase dietary intake of calcium – at least
• Pancreatitis 1000 – 1500 mg/day
• Renal Failure • Foods rich in calcium (milk & dairy products;
• Inadequate Vit. D intake green leafy vegetables; sardines, salmon or
• Magnesium Deficiency fresh oysters)
• Low serum albumin levels • Monitor patient’s BP during calcium
• Alkalosis replacement & keep in bed to avoid postural
• Alcohol abuse; Smoking hypotension
• Aminoglycosides, caffeine, • Health Teachings:
corticosteroids, phosphates, isoniazid & ✓ Importance of weight bearing
loop diuretics exercises in decreasing bone loss
✓ Avoidance of alcohol, caffeine and
SIGNS AND SYMPTOMS smoking
• Tetany; hyperactive DTR; tingling ✓ Intake of foods rich in calcium and
sensations (tips of fingers, around the vitamin D supplementation
mouth, feet)
• Pain as a result of spasms "CALCIUM EXCESS
• Trousseau’s sign
• Chvostek’s sign
(HYPERCALCEMIA)"
➢ Excess calcium concentration in the plasma
• Seizures
➢ A dangerous imbalance when severe; 50 %
• Mental Changes: depression, impaired
mortality rate if not treated promptly
memory, confusion, delirium, hallucinations
• Resp: Dyspnea, laryngospasm
RISK FACTORS
• Hyperactive bowel sounds, dry & brittle
• Malignancies (tumors can produce
hair/nails, abnormal clotting
Hypercalcemia by a variety of mechanisms)
• Hyperparathyroidism
• Immobilization, prolonged bed rest (e.g. pts.
with severe or multiple fracture or SCI;
comatose pts.)
• Use of Thiazide diuretics

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 ELECTROLYTES IMBALANCES
• Milk – Alkali syndrome (pts. with PUD • Monitor serum calcium levels; assess for
treated for a long period with milk & S/Sx of Hypercalcemia
• antacids) • Provide adequate fiber in the diet to
• Vitamin A & D intoxication decrease the tendency of constipation
• Hypophosphatemia • Safety precautions are implemented when
neurologic S/Sx are present
SIGNS AND SYMPTOMS • Monitor ECG of the patient to detect for
1. Muscle weakness, incoordination possible arrhythmias
2. Anorexia, nausea/vomiting, constipation,
abdominal distention, paralytic ileus
3. Polyuria, DHN, severe thirst
"MAGNESIUM IMBALANCE"
4. Peptic ulcer disease MAGNESIUM - the most abundant intracellular
5. Confusion, impaired memory, slurred cation after potassium
speech, lethargy, coma NORMAL RANGE: 1.5 - 2.5 mEq/L (1.8 - 3 mg/dL)
6. Cardiac arrest
FUNCTIONS
LABORATORY AND DIAGNOSTIC FINDINGS • Acts as an activator for many intracellular
1. Serum calcium = greater than 10.2 mg/dL or 5.5 enzyme systems
mEq/L • Plays a role in both CHO & CHON metabolism
2. PTH levels: • Acts directly on the myoneural junction
- increased in hyperparathyroidism affecting neuromuscular irritability &
- decreased in malignancy contractility
3. ECG: shortened QT interval & ST segment; PR • Exerts effects on CV system, acting
interval is sometimes prolonged peripherally to produce vasodilation
4. Sulkowitch urine test – analyze the amount of
calcium in urine "MAGNESIUM DEFICIT
(HYPOMAGNESEMIA)"
MANAGEMENT
➢ below normal serum magnesium concentration
• Identify & treat the underlying cause (e.g.
Chemotherapy for malignancy, partial
SPECIFIC CAUSES
parathyroidectomy for
1. GI losses of Magnesium
hyperparathyroidism)
a. Nasogastric suction
• Administer IV fluids to dilute serum
b. Diarrhea Fistulas
calcium & promote its excretion by the
2. Alcohol withdrawal
kidneys: NSS (0.9 % NaCl); Furosemide
3. Tube feedings or TPN
(Lasix) is given in conjunction with NSS
4. Diabetic Ketoacidosis
• Administer the following medications as
5. Medications: Aminoglycosides, cyclosporine,
ordered:
cisplatin, diuretics, digitalis amphotericin
✓ IV phosphorus
6. Others: Sepsis, burns, hypothermia
✓ Calcitonin
SIGNS AND SYMPTOMS
NURSING MANAGEMENT
• Hyperexcitability with muscle weakness,
• Prevention of Hypercalcemia:
tremors & athetoid movement (Slow,
✓ Monitor patients who are at risk
involuntary twisting, writhing)
✓ Increase patient mobility if tolerable
• Tetany, seizures
and avoid prolonged bed rest; provide
• Laryngeal stridor (laryngospasm)
ROM exercises, unless
• (+) Trousseau’s and Chvostek’s sign
contraindicated
• Increased sensitivity to digitalis
✓ Encourage fluids esp. those
• Apathy, depression, apprehension, extreme
containing sodium unless
agitation, ataxia, dizziness, confusion
contraindicated (sodium favors
calcium excretion)

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ELECTROLYTES IMBALANCES
DIAGNOSTIC FINDINGS SIGNS AND SYMPTOMS
• Magnesium level = less than 1.5 mEq/L 1. Mild Hypermagnesemia; Acute phase
• Decreased serum calcium levels a. Depression of CNS & PNS
• ECG: prolonged PR & QT interval, widening b. Hypotension
QRS, ST segment depression; Torsades de c. Nausea & vomiting, diarrhea
pointes d. Weakness
e. Facial flushing & sensations of
MANAGEMENT warmth
1. Mild deficiencies can be corrected by diet 2. Severe hypermagnesemia
alone: Magnesium-rich foods a. Lethargy, dysarthria, drowsiness
a. Green leafy vegetables b. Loss of DTR, muscle weakness,
b. Nuts, seeds, legumes paralysis
c. Whole grains c. Respiratory depression
d. Seafoods d. Coma, heart block & cardiac arrest
e. Peanut butter, cocoa
2. For moderate-severe deficiencies: DIAGNOSTIC FINDINGS
a. Magnesium salts (Oxide or Gluconate - • Serum Magnesium = greater than 2.5
to replace continuous excessive losses) mEq/L
b. IV administration of Magnesium (Mg • Increased serum calcium & potassium
SO4) • ECG: Prolonged PR interval, tall T waves,
widened QRS, prolonged QT interval
NURSING MANAGEMENT
1. Monitor for pts. at risk for hypomagnesemia MANAGEMENT
and observe for its S/Sx 1. Hypermagnesemia can be prevented by
2. Patients receiving digitalis are monitored avoiding administration of magnesium to
closely because a deficit of Mg+ can pts. with renal failure and carefully
predispose the pt. to digitalis toxicity monitoring seriously ill pts. who are
3. Institute safety precautions if confusion is receiving magnesium salts.
observed; seizure precautions if 2. Discontinue/Withhold all parenteral & oral
hypomagnesemia is severe magnesium salts
4. Health teachings: 3. In emergencies (i.e. respiratory
✓ Encourage foods rich in Magnesium depression or heart block), ventilatory
✓ Avoidance of alcohol support and IV calcium Gluconate are
✓ Avoid abuse of diuretics or laxatives indicated
4. In pts. with renal failure, hemodialysis
"MAGNESIUM EXCESS with magnesium-free dialysate can reduce
serum magnesium to a safe level within
(HYPERMAGNESEMIA)" hours
➢ Above the normal serum concentration of 5. Loop diuretics (Furosemide) & NaCl or LR’s
Magnesium IV solution to increase Magnesium
➢ A rare electrolyte abnormality because the excretion in pts. with adequate renal
kidneys are efficient in excreting Magnesium function

SPECIFIC CAUSES NURSING MANAGEMENT

1. Renal Failure (most common) 1. Monitor V/S especially BP and RR,
2. Untreated DKA neuromuscular reflexes and LOC
3. Excessive Magnesium administration (e.g. 2. Advise the pt to consult the doctor
pts. with Eclampsia, hypomagnesemia) before taking OTCs
4. Excessive use of antacids, laxatives (milk of
magnesia) & medications that decrease GI
motility (opioids, Anticholinergics)

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ELECTROLYTES IMBALANCES

"PHOSPHORUS DIAGNOSTIC FINDINGS

1. Serum phosphorus = less than 2.5 mg/dL
IMBALANCES" or < 1.8 mEq/L decreased magnesium &
potassium, increased PTH
FUNCTIONS 2. X-ray = skeletal changes of osteomalacia
1. Essential to the function of muscle and blood or rickets
cells especially RBCs
2. Formation of ATP and 2,3 MANAGEMENT
diphosphoglycerate 1. Serum phosphate levels should be
3. Maintenance of acid-base balance monitored closely and correction initiated
4. Affects functions of nervous system before deficits become severe
5. Metabolism of CHO, CHON & fat 2. Adequate amounts of phosphorus should
6. Provides structural support to bones & teeth be added to parenteral and enteral
feeding solutions
"PHOSPHORUS DEFICIT 3. Severe Hypophosphatemia is dangerous
and requires prompt attention –
(HYPOPHOSPHATEMIA)" Aggressive IV phosphorus (Sodium or
potassium phosphate) correction is limited
PHOPHORUS DEFICIENCY - an abnormally low
to pts. Whose serum phosphorus levels is
content of phosphorus in lean tissues that may
less than 1 mg/dL and whose GIT is not
exist in the absence of Hypophosphatemia
functioning
4. For less acute situations (mild to
SPECIFIC CAUSES
moderate cases) – oral phosphorus
1. Administration of calories to pts. with
replacement is usually adequate
severe protein-calorie malnutrition (e.g.
a. Neutra-Phos capsules (250 mg
anorexia nervosa, alcoholism, elderly
Phosphorus/capsule)
debilitated pts.)
b. Fleet’s Phosphosoda (815 mg
2. Chronic alcoholism
Phosphorus/5 ml)
3. Low magnesium & potassium levels,
5. Health teachings:
hyperparathyroidism (Inc. Ca+)
a. Prevention of Infection
4. Respiratory alkalosis
b. Foods rich in phosphorus
5. Excessive renal loss of phosphorus (e.g.
✓ Milk & milk products
Acute volume expansion, osmotic diuresis,
✓ Organ meats, poultry
use of carbonic anhydrase inhibitors)
✓ Nuts, whole grains
6. Use of antacids containing magnesium,
✓ Fish
calcium or aluminum and phosphate binding
agents
7. Chronic diarrhea, potassium restriction "PHOSPHORUS EXCESS
8. Vitamin D deficiency (HYPERPHOSPHATEMIA)"
SIGNS AND SYMPTOMS SPECIAL CAUSES
1. 2,3-diphoshpoglycerate deficiency 1. Renal Failure (most common)
• Tissue hypoxia/anoxia 2. Increased intake, decreased output or a
• Increased RR, Respiratory alkalosis shift from ICF to ECF of phosphorus
• Pale skin and conjunctiva 3. Chemotherapy for CA
2. ATP deficiency 4. Hypoparathyroidism
• Muscle damage – Acute Rhabdomyolysis 5. Metabolic or Respiratory Acidosis
• Muscle weakness, muscle pain 6. Acute Hemolysis
• Weakness of Respiratory muscles 7. High phosphate intake or absorption
3. Insulin Resistance – Hyperglycemia
4. Bruising, bleeding
5. Infection
6. Neurologic: Irritability, fatigue,
apprehension, numbness, Paresthesia,
dysarthria, dysphagia, diplopia, confusion,

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ELECTROLYTES IMBALANCES
SIGNS AND SYMPTOMS FUNCTIONS
1. Tetany • Assist in determining osmotic pressure
2. Anorexia, nausea & vomiting together with sodium
3. bone & joint pain • Maintains acid-base balance
4. muscle weakness, hyperreflexia • Works as a buffer in the exchange of O2 &
5. tachycardia CO2 in RBC’s
6. oft tissue calcification (↓ U.O., impaired
vision, palpitations) "CHLORIDE DEFICIT
(HYPOCHLOREMIA)"
DIAGNOSTIC FINDINGS
➢ Below the normal serum concentration of
1. Serum phosphorus = greater than 4.5
chloride.
mg/dL or 2.6 mEq/L
2. decreased serum calcium & PTH levels
CAUSES
3. X – ray – skeletal changes with abnormal
• GI losses of chloride
bone
○ GI tube drainage
4. development
○ Severe vomiting
5. Increased BUN & creatinine in Renal
○ Diarrhea
Failure
• Administration of chloride-deficient
formulas
MANAGEMENT
• Low sodium intake; decreased sodium levels
• Administer the following medications as
• Metabolic alkalosis
ordered:
• Prolonged therapy with IV dextrose
a. Vitamin D preparations (Calcitriol)
• Diuretic therapy
b. Calcium-based antacids
• Burns
c. Phosphate binding agents
d. Loop diuretics (Furosemide)
SIGNS AND SYMPTOMS
e. Saline solution for volume repletion
• Similar with hyponatremia, hypokalemia, &
• Prepare the pt. for the following
metabolic alkalosis
procedures if indicated:
• Hyperexcitability of muscles, hyperactive
✓ Dialysis
DTR, tetany, weakness, twitching & muscle
✓ Surgery for removal of large
cramps
calcium-phosphorus deposits
• Cardiac dysrhythmias
• Health teachings:
• Seizures & coma (severe hyponatremia)
✓ Avoid foods rich in phosphorus
✓ Avoid phosphate containing
DIAGNOSTIC FINDINGS
substances (laxatives, enemas)
• Serum chloride = less than 96 mEq/L
✓ Recognize signs & symptoms of
• Decreased serum sodium & potassium levels
hypocalcemia & monitor U.O.
• ABG = metabolic alkalosis (↑ pH)
• Urine chloride level is decreased
"CHLORIDE IMBALANCES"
MANAGEMENT
CHLORIDE - major anion of the ECF
• Identify & correct the underlying cause of
- found more in interstitial/lymphatic
Hypochloremia & the contributing
fluid compartments than in blood
electrolyte & acid-base imbalance.
- also contained in gastric &
• NSS (0.9 % NaCl) or half-strength saline
pancreatic juices, sweat, bile & saliva
(0.45% NaCl) is administered by IV to
- Normal range: 96 – 106 mEq/L
replace chloride.
- Primarily obtained from the diet as
• Patient receiving a diuretic (loop, Thiazide,
table salt (NaCl)
osmotic) should discontinue the medication
- Chloride is directly proportional to
or change to another diuretic
sodium & inversely proportional to
HCO3

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 ELECTROLYTES IMBALANCES
• Encourage foods high in chloride • IV sodium bicarbonate
✓ tomato juice, bananas • Diuretics
✓ eggs, cheese, milk • Sodium, chloride & fluids are restricted
✓ salty broth, canned vegetables, & • Monitor VS, ABGs & I&O
processed meats • Assess respiratory, neurologic and cardiac
• Instruct patient to avoid free water (water status of patient
without electrolytes) – causes pt. to excrete • Health Teachings:
large amounts of chloride ✓ Avoidance of foods rich in sodium &
• Monitor the patient’s I&O, ABGs & serum chloride
electrolyte levels, as well as LOC & muscle ✓ Maintenance of adequate hydration
strength & movement • Correct the underlying cause of
• Assessment of VS & respiratory status is Hyperchloremia & restore F&E and acid-base
carried out frequently. balance
• Administer Ammonium chloride as ordered to • IV therapy is initiated to correct imbalances:
treat metabolic alkalosis ✓ Hypotonic IV solution
✓ Lactated Ringer’s solution
"CHLORIDE EXCESS • IV sodium bicarbonate
• Diuretics
(HYPERCHLOREMIA)" • Sodium, chloride & fluids are restricted
➢ it exists when the serum level of chloride • Monitor VS, ABGs & I&O
exceeds 106 mEq/L • Assess respiratory, neurologic and cardiac
➢ hypernatremia, HCO3 loss & metabolic acidosis status of patient
can occur with high chloride levels • Health Teachings:
✓ Avoidance of foods rich in sodium &
CAUSES chloride
• Loss of HCO3- ions via the kidney or GIT (most ✓ Maintenance of adequate hydration
common)
• Head trauma
• Excess ACTH production
• Decreased GFR

SIGNS AND SYMPTOMS

• Similar with metabolic acidosis, hypervolemia &
hypernatremia
• Tachypnea, hyperventilation
• Weakness, lethargy
• Diminished cognitive ability
• hypertension
• Dysrhythmias, Coma

DIAGNOSTIC FINDINGS
• Serum chloride level = greater than 106 mEq/L
• Increased serum sodium levels
• ABG: Metabolic acidosis (↓ pH) & ↓ HCO3-
levels

MANAGEMENT
• Correct the underlying cause of Hyperchloremia
& restore F&E and acid-base balance
• IV therapy is initiated to correct imbalances:
✓ Hypotonic IV solution
✓ Lactated Ringer’s solution

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ACID BASE IMBALANCES

"ACID-BASE IMBALANCES" - regulation of carbon dioxide level, a gas

pH - a calculation based on the percentage of that combines with water to form
hydrogen ions in a solution as well as the amount carbonic acid (increased level causes
of acids and bases. decreased pH)
- CO2 levels in the blood is reflected by
ACID - consist of molecules that can give up or PaCO2 with a normal value of
donate hydrogen ions to other molecules. 35-45mmHg.
Example: Carbonic acid (H2CO3 ) – is an
acid that occurs naturally in the body RESPIRATION/RESPIRATORY MECHANISM
Decreased pH/Acidosis Increased pH
ACIDOSIS - greater concentration of H+, blood ↓ ↓
pH is below 7.35, occurs when acids accumulate Increased RR and depth Decreased RR and
↓ depth
or bases are lost.
CO2 excretion from the ↓
lungs CO2 retained in the
BASE - consist of molecules that can accept
↓ lungs
hydrogen ions Increased pH ↓
Example: Bicarbonate (HCO 3) is a base Decreased pH
agent

ALKALOSIS - lower concentration of H+, blood

III. KIDNEYS/RENAL MECHANISM - Regulates
pH higher than 7.45, occurs when bicarbonate
the bicarbonate level which reflects the
accumulates or acids are lost.
metabolic component of acid base balance.
- Normal level of bicarbonate is
REGULATING ACIDS AND BASES/
22-26 mEq/L
COMPENSATORY MECHANISMS
I. BUFFER SYSTEM (takes seconds) - A A. ACIDOSIS B. ALKALOSIS
buffer is a substance that can act as a Excess H Ions Excess HCO3
chemical sponge, either soaking up or ↓ ↓
Enters Tubules Enters tubules
releasing hydrogen ions so that the pH
↓ ↓
remains relatively stable Combines with Buffers Lack H, can't form H2CO3
Main Chemical Buffers: ↓ ↓
A. CARBONIC ACID-BICARBONATE Excreted via urine Combined with Na or K
↓
buffer system Excreted via urine
- The clinically most important
buffer; If this buffer is stable,
SYSTEMIC EFFECTS
the other buffer systems are
stable ACIDOSIS ALKALOSIS
↓ ↓
- Two types of carbonate in body CNS DEPRESSANT CNS STIMULANT
fluids: (Disorientation to Coma) (Overexcitability)
Carbonic Acid (H2CO3) ↓ ↓
Bicarbonate (HCO3) Cerebral vasodilation Cerebral Vasoconstriction
↓ ↓
B. PHOSPHATE buffer system Increased capillary Cerebral Ischemia
C. PROTEIN buffer system permeability ↓
↓ Cerebral Hypoxia
Intravascular to interstitial ↓
II. RESPIRATION/RESPIRATORY Cerebral Tissue injury
shift
MECHANISM (takes minutes) - serves as ↓ ↓
the second line of defense against acid- Cerebral edema IICP
↓
base balance and causes temporary IICP
↓ Peripheral Vasodilation
adjustment ↓
Peripheral Vasoconstriction
↓ Decreased BP
Increased BP

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ACID BASE IMBALANCES
CELLULAR COMPENSATION EXAMPLE OF ABG INTERPRETATION

ACIDOSIS (↑H) ALKALOSIS (↓ H)

ACID NORMAL BASE
H+ PaCO2 = 49 mmHg pH = 7.46
HCO3 = 29 mEq/L
K+ H+
= PARTIALLY COMPENSATED METABOLIC
ALKALOSIS
K+

↑ ↓K+ ACID NORMAL BASE

Hyperkalemia Hypokalemia pH = 7.27
paCo2 = 52 mmHg
HCO3 = 16 mEq/L
DIAGNOSING IMBALANCES
= SEVERE ACIDOSIS
ABG Analysis - is a diagnostic test in which
sample of blood obtained from an arterial
puncture can be used to assess the ACID NORMAL BASE
effectiveness of breathing and overall acid-base pH = 7.59
balance PaCo2 = 29 mmHg
- Radial, brachial or femoral arteries HCO3 + 39 mEq/L
are used = SEVERE ALKALOSIS
- Also measures partial pressure of
oxygen dissolved in arterial blood
ACID NORMAL BASE
(PaO2) with a normal value of 80-100
pH = 7.39
mmHg and arterial oxygen saturation
PaCO2 = 39 mmHg
(Sa O2), with a normal value of
HCO3 = 26 mEq/L
95-100%.
= NORMAL ABG READING

ACID NORMAL BASE

HCO3 = 25 mEq/L pH = 7.59

PaO2 = 89 mmHg PaCO2 = 26 mmHg
= UNCOMPENSATED RESPIRATORY
ALKALOSIS

ACID NORMAL BASE

PaCO2 = 49 mmHg pH = 7.44 HCO3 = 29 mEq/L

= FULLY COMPENSATED METABOLIC

ALKALOSIS

"RESPIRATORY ACIDOSIS
"ABG INTERPRETATION" (CARBONIC ACID EXCESS)"
NORMAL VALUES CAUSES
ACID NORMAL BASE • Damage to respiratory center in medulla &
pH 7.34 and Lower 7.35-7.45 7.46 and Higher pons
• Depression of respiratory center by drugs
PaCO2 46 and higher 45-35 34 and lower
(narcotics)
HCO3 21 and lower 22-26 27 and higher
• Obstruction of pulmonary passages
PaO2 79 lower 80-100 101 higher • Loss of lung surface for ventilation
• Weakness of respiratory muscles
• Intubated patient who are under ventilated

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ACID BASE IMBALANCES
EFFECTS "RESPIRATORY ALKALOSIS
• Rapid, shallow breathing
• Visual and behavioral disturbances +
(CARBONIC ACID
Headache DEFICIT)"
• Changes in the level of consciousness
• HYPERKALEMIA CAUSES
1. Hyperventilation syndrome (anxiety,
DIAGNOSTIC TESTS hysteria, fever, hypoxia)
• ABG analysis 2. Pulmonary disorders
• Serum Electrolytes 3. Lesions in the respiratory center
• ECG 4. 4Excess assisted ventilation
• Xray
EFFECTS
MANAGEMENT • Light headedness
• Chest physiotherapy • Inability to concentrate
• Administer bronchodilators • Coma
• Avoid sedatives or narcotics • Paresthesia
• IVF for hydration and facilitating removal • Blurred vision
of thick pulmonary secretions • HYPOKALEMIA
• Assess for presence of bowel sounds and
gastric distention DIAGNOSTIC TESTS
• Encourage pursed-lip breathing • ABG Analysis
• Give oxygen inhalation cautiously • Serum Electrolytes
• ECG

MANAGEMENT
• Monitor hypokalemia
• Administer calcium gluconate for tetany
• Monitor assisted ventilation
• Maintain renal function
• Encourage patient to breath slowly or
rebreathe CO2 into a paper bag.
• Sedatives and tranquilizers should be
administered as prescribed

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ACID BASE IMBALANCES

"METABOLIC ACIDOSIS "METABOLIC ALKALOSIS

(BICARBONATE DEFICIT)" (BICARBONATE EXCESS)"
CAUSES CAUSES
1. Increased acid production (ketoacidosis, 1. Loss of stomach acid (gastric suctioning,
uremic acidosis, lactic acidosis) persistent vomiting, pyloric stenosis)
2. Decreased acid secretion 2. Bicarbonate retention (excess use of
3. Increased acid ingestion (salicylates, antacid)
ethanol) 3. Loss of potassium
4. Loss of bicarbonate (diarrhea, fistula)
EFFECTS
EFFECTS • Depressed respirations/Hypoventilation
• Hyperventilation • Altered LOC: Confusion
• Kussmaul’s respiration • Muscle twitching
• Weakness • Tetany, convulsion
• Hyperkalemia • Hypokalemia
• Cerebrovascular dilation: Headache,
confusion, drowsiness, and altered LOC DIAGNOSTIC TESTS
(Disorientation, coma) • ABG
• Serum electrolytes
DIAGNOSTIC TESTS • ECG
• ABG (dec. pH)
• Serum electrolytes (Inc. K,Cl,PO4) MANAGEMENT
• ECG 1. Sodium chloride or ammonium chloride oral
• Serum Anion Gap -- used to identify the or IV
cause of metab. ACIDOSIS by estimating 2. Carbonic Anhydrase Inhibitor (Diamox)
the level of unmeasured ANIONS (PO4, 3. Maintain good respiratory function
SO4, Albumin, etc...) 4. Maintain potassium level through diet or
drugs
#Measured ANIONS: Cl & HCO3 5. Protect patient from injury.
6. Maintain calm, quiet environment.
MANAGEMENT
1. Treat the underlying cause
2. Sodium bicarbonate IV
3. Maintain good respiratory function
4. Fluid replacement
5. Monitor I&O, vital signs
6. Protect patient from injury
7. Give insulin as ordered

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