Castillo, Lucky Anthony M.

Hypovolemia
Terms
 Fluid Volume Deficit, or hypovolemia, occurs when loss of Extracellular Fluids volume exceeds the
intake of fluid.
 It occurs when water and electrolytes are lost in the same proportion as they exist in normal body fluids;
thus, the ratio of serum electrolytes to water remains the same.
 FVD and Dehydration are different: Dehydration are loss of water but FVD can occur in any
imbalances.
Pathophysiology
FVD results from loss of body fluids and occurs more rapidly when coupled with decreased fluid intake.
FVD can also develop with a prolonged period of inadequate intake. Causes of FVD include abnormal fluid
losses, such as those resulting from vomiting, diarrhea, GI suctioning, and sweating; decreased intake, as in
nausea or lack of access to fluids; and third-space fluid shifts, or the movement of fluid from the vascular
system to other body spaces (e.g., with edema formation in burns, ascites with liver dysfunction). Additional
causes include diabetes insipidus (a decreased ability to concentrate urine owing to a defect in the kidney
tubules that interferes with water reabsorption), adrenal insufficiency, osmotic diuresis, hemorrhage, and coma.
Contributing Factors or Causes
 Loss of water and electrolytes, as in vomiting, diarrhea, fistulas, fever, excess sweating, burns, blood
loss. Gastrointestinal suction, anorexia, decreased fluid intake, etc.
 Diabetes Insipidus- is an uncommon condition in which the kidneys are unable to prevent the excretion
of water. It is caused by problems with a chemical called vasopressin (AVP), which is also known as
antidiuretic hormone (ADH).

3 types of Fluid loss

External Fluid Loss Internal Fluid Loss Inadequate Vascular
Volume
 Trauma  Hemorrhage  Value of blood in
 Surgery  Burns circulatory system,
 Vomiting  Ascites essentially blood
 Diarrhea  Peritonitis plasma.
 Diabetes Insipidus  Dehydration
Effects of FVD to the Body system

Hypovolemic shock results from depletion of intravascular volume, whether by extracellular fluid loss
or blood loss. The body compensates with increased sympathetic tone resulting in increased heart rate,
increased cardiac contractility, and peripheral vasoconstriction. The first changes in vital signs seen in
hypovolemic shock include an increase in diastolic blood pressure with narrowed pulse pressure. As volume
status continues to decrease, systolic blood pressure drops. As a result, oxygen delivery to vital organs is unable
to meet oxygen demand. Cells switch from aerobic metabolism to anaerobic metabolism, resulting in lactic
acidosis. As sympathetic drive increases, blood flow is diverted from other organs to preserve blood flow to the
heart and brain. This propagates tissue ischemia and worsens lactic acidosis.
Signs and Symptoms
Vital Signs Temperature: Low temperature
Respiratory Rate: Normal to increased Respiratory rate
Heart Rate: Tachycardia
Blood Pressure: Low Blood Pressure
Urine Output: Decreased urine output
General appearance Thirsty, General Weakness, Weight loss.
Neurologic Status Unconsciousness (lack of responsiveness), dizziness and confusion.
Skin and Nail beds Sweating or Moist skin, pallor, cold clammy skin, capillary filling
time prolonged and decreased skin turgor.
Hair, skull, face Pale face
Eyes Sunken eyes
Thorax and Lungs Increased chest activity due to rapid breathing
Abdomen Abdominal pain and swelling
Muscle, bones, joints Muscle cramps and joint pain
Others Low central venous pressure- (Normal: 2 to 6 mm Hg) a low CVP
(less than 2 mm Hg) indicates reduced right ventricular preload.

Laboratory and Diagnostic Procedures

 Blood testing- Evaluating fluid volume status include BUN and its relation to serum creatinine
concentration.

*Normal BUN to serum creatinine concentration ratio is 10:1. A volume-depleted patient has a BUN
elevated out of proportion to the serum creatinine (ratio greater than (20:1). Serum electrolyte changes
(reduced).

*Blood Urea Nitrogen- A blood urea nitrogen (BUN) test measures the amount of nitrogen in your blood
that comes from the waste product urea. Urea is made when protein is broken down in your body. Urea
is made in the liver and passed out of your body in the urine. A BUN test is done to see how well your
kidneys are working.

*A serum creatinine test measures the level of creatinine in your blood and provides an estimate of how
well your kidneys filter (Glomerular filtration rate).

 Health history and Physical examination- Information about the patient’s allergies, illnesses,
surgeries, immunizations, and results of physical exams in Head-to-Toe Assessment.

 Urinalysis- Urine specific gravity, osmolality and measure amount of urine for possible decreased urine
output.

Laboratory indications
 Increased Hemoglobin and Hematocrit level
Hemoglobin and Hematocrit increase in values in hypovolemic patients because the plasma volume does
not increase to achieve a normal state.

 Increased serum and urine osmolality and specific gravity

- An osmolality urine test is performed to measure the concentration of particles in urine.
-If a patient is hypovolemic the concentration of chemicals in your blood (serum osmolality) increases.
 - Increase in specific gravity means increased concentration of solutes in the urine.

 Decreased urine sodium

Decreased urine sodium level may be a sign of Adrenal glands releasing too much hormone or there are
not enough fluids in the body.

 Increased BUN and creatinine

Increased BUN and creatinine levels may mean that your kidneys are not working as they should like
Glomerular filtration rate or amount of BUN production.

Management
Medical
 Patient’s maintenance requirements and other factors that can influence fluid needs.
Example:
-Not severe, Oral route is preferrable to maintain fluid requirements.
-Acute or Severe fluid loss, IV route is required. Isotonic electrolyte solutions (e.g., lactated Ringer solution,
0.9% sodium chloride).
-For Hypotensive patient with FVD, 0.45% sodium chloride) is often used to provide both electrolytes and
water for renal excretion of metabolic wastes.
Nursing Management
Accurate and frequent assessments of I&O, weight, vital signs and Head-to-Toe Physical Assessment like, level
of consciousness, breath sounds, Abdomen, muscles and joints and skin color are monitored to determine when
therapy should be slowed to avoid volume overload and central venous pressure to assess volume status.
*Monitoring electrolytes and acid/base status in patients in hypovolemic shock is of utmost importance.

Hypovolemic shock Nursing Management

Hypovolemic shock is a life-threatening condition that results when you lose more than 20 percent (one-
fifth) of your body’s blood or fluid supply. This severe fluid loss makes it impossible for the heart to pump a
sufficient amount of blood to your body. Hypovolemic shock can lead to organ failure.
- estimated blood loss of 500 mL is considered hemorrhage.
Assessment
 History
For patients with hemorrhagic shock, a history of trauma or recent surgery is present.
 Vital Signs

 Physical Assessment
Physical findings suggestive of volume depletion include dry mucous membranes, decreased skin
turgor, and low jugular venous distention. Tachycardia and hypotension can be seen along with
decreased urinary output. Patients in shock can appear cold, clammy, and cyanotic
  Cause of fluid loss
For hypovolemic shock due to fluid losses, history and physical should attempt to identify possible GI,
renal, skin, or third-spacing as a cause of extracellular fluid loss.

Causes of hypovolemic shock can be related to volume depletion, electrolyte imbalances, or acid-base
disorders that accompany hypovolemic shock.

 Mild and Severe Symptoms

Patients with volume depletion may complain of thirst, muscle cramps, and/or orthostatic hypotension.
Severe hypovolemic shock can result in mesenteric and coronary ischemia that can cause abdominal or
chest pain. Agitation, lethargy, or confusion may result from brain malperfusion.

Nursing Goal for Management

 Maintain fluid volume at a functional level.
 Report understanding of the causative factors of fluid volume deficit.
 Maintain normal blood pressure, temperature, and pulse.
 Maintain elastic skin turgor, most tongue and mucous membranes, and orientation to person, place, and
time.

Nursing management
 Monitor Vital Signs
 If the patient is hemorrhaging, efforts are made to stop the bleeding.
 If it is Diarrhea or Vomiting- medication while identifying and treating the cause.
 Fluid and Blood Replacement (lactated Ringer’s solution or 0.9% sodium chloride solution).
 If hypovolemia is primarily due to blood loss- 3 mL of crystalloid solution for each milliliter of
estimated blood loss. (3:1 rule).
 Colloid solutions (e.g., albumin 5% or 25%) may also be used.
 Blood- 1:1:1: ratio, meaning units of plasma, platelets, and packed red blood cells.
 Trendelenburg position for redistribution of fluid.

Evaluation
 Monitor Vital Signs and Physical Assessment
 Assess and document degree of deficit and current sources of fluid intake.
 Assess and document I&O, fluid balance, changes in weight, presence of edema, urine specific gravity,
and vital signs.
 Document results of diagnostic studies.
Corral, Warren James G.

Hypervolemia
Refers to an Isotonic Expansion of the Extracellular Fluid caused by the Abnormal retention of water and
sodium in approximately the same proportion in which they normally exist in the extracellular fluid.

Pathophysiology
Fluid overload or diminished homeostatic mechanism responsible for regulating fluid balance.

Contributing Factors:
1. Hearth Failure
 Heart Failure Is A Condition In Which The Heart Cannot Pump Enough Blood To Meet The
Body's Needs. When The Heart's Blood Pumping Ability Decreases, The Kidneys Cannot Work
As They Should, Which Leads To An Excess Of Fluid In The Body.
2. Kidney Injury
 Healthy Kidneys Take Out Extra Fluid (Liquid) From Your Blood. When Your Kidneys Are Not
Working As Well As They Should, They Cannot Take Out Enough Fluid
3. Cirrhosis Of The Liver
 Expanded Extracellular Fluid Volume Due To The Inability Of The Kidneys To Excrete Solute-
Free Water Proportionate To The Amount Of Free Water Ingested
 It Is Caused By The Affected Liver Sending Signals To The Kidney To Retain Excess Salt And
Water. Which Accumulates In The Tissues, Increasing The Volume.
 The Liver’s Inability To Produce Enough Of The Protein Albumin Which Is The Main Protein In
The Blood That Maintains Stable Blood Volume.
4. Consumption Of Sodium
5. Excessive Administration Of Sodium Containing Fluid

Signs And Symptoms

1. Edema (Dependent/Pitting) – Is A Common Manifestation Of Fve. Edema Can Occur As A Result Of
Increased Capillary Fluid Pressure, Decreased Capillary Oncotic Pressure, Or Increased Interstitial
Oncotic Pressure, Causing Expansion Of The Interstitial Fluid Compartment
2. Distended Neck Veins - Is When The Increased Pressure Of The Superior Vena Cava Causes The
Jugular Vein To Bulge, Making It Most Visible On The Right Side Of A Person's Neck (Central Venous
Pressure) Described As A Sign Of Failure Of The Right Ventricle. Impaired Right Ventricular Function
3. Crackles – Abnormal Lung Sound
4. Weight Gain
5. Tight Smooth Shiny Skin – Because Of The Edema
6. Cool And Pale Skin – Decrease Blood Flow
7. Ascites - Is A Type Of Edema In Which Fluid Accumulates In The Peritoneal Cavity
8. Pleural Effusion - Is The Build-Up Of Excess Fluid Between The Layers Of The Pleura Outside The
Lungs
9. Pericardial Effusion - Buildup Of Extra Fluid In The Space Around The Heart. If Too Much Fluid
Builds Up, It Can Put Pressure On The Heart. This Can Prevent It From Pumping Normally.

Diagnostic Procedures
1. Bun Test - Measures The Amount Of Urea Nitrogen, A Waste Product Of Protein Metabolism, In The
Blood. Urea Is Formed By The Liver And Carried By The Blood To The Kidneys For Excretion.
Because Urea Is Cleared From The Bloodstream By The Kidneys, A Test Measuring How Much Urea
Nitrogen Remains In The Blood Can Be Used As A Test Of Renal Function.
2. Hematocrit Level - Causes Decreased Hemoglobin Concentration
 (Both Of These Values May Be Decreased Because Of Plasma Dilutation, Low Protein Intake, And
Anemia.
3. Xray – Can Reveal Pulmonary Congestion.

Medical Management
A. Medical Management
1. Diuretics – It Is Prescribed When Dietary Restriction Of Sodium Aline Is Insufficient To Reduced
Edema Caused By Inhibiting The Reabsorption Of Sodium And Water By The Kidneys.
(The Choice Of Diuretic Is Based On The Severity Of The Hypervolemic State, Degree Of
Impairment Of Renal Function, And The Potency Of The Diuretics.
- Thiazide Diuretics (Hydrochlorothiazide/Microzide)
- (Block Sodium Reabsorption In The Distal Tubule. 5-10%
- Loop Diuretics (Furosemide/Lasix, Torsemide/Demadex)
- (Can Cause A Greater Loss Of Both Sodium And Water Because They Block Sodium
Reabsorption In The Ascending Limb Of Henle Loop 20-30%
2. Electrolyte Imbalance Result From Side Effects Of Diuretics
Hypokalemia – Potassium supplements
Hyperkalemia – Spironolactone/Aldactone
B. Dialysis
- If Pharmacologic Agent Cannot Act Efficiently
- Remove Nitrogenous Wastes And Control Potassium And Acid-Base Balance
- Remove Sodium And Fluid

Hemodialysis
Pre-Procedure:
1. Weight – Determines Amount Of Fluid To Be Removed During Dialysis
2. Vital Signs - Bp For Hypo And Hypertension, Temp For Sepsis, Respiration For Fluid Overload
3. Potassium Level – Determines Potassium Level In Dialysate
4. Assess Fistula
5. Assess Circulation In Distal Portion Of Extermity
6. Auscultate For Thrill
7. No Iv Of Blood Draws In That Arm
8. No Bp In Arm

During:
1. Watch For Hypotension,
2. Muscle Cramps
3. Nausea
4. Vomiting
5. Headache
6. Itching

Post:
1. Monitor Bp – Report Hypo And Hypertension
2. Watch For Bleeding
3. Check Weight And Compare – Weight Loss Should Be Close To Fluid Removal Goal Set During
Treatment
4. Document Unusual Findings
5. Assess Site For Bruit, Thrill, Exudate, Signs Of Infection, Bleeding
6. Give Missed Medication, If Indicated.
 C. Nutritional Therapy
- Restriction Of Sodium 250mg Per Day Depending On Patient’s Need
- High Chon Diet

Nursing Management:
1. Measure I&O – To Identify Excessive Fluid Retention
2. Measure Weight Daily
3. Auscultate Breath Sounds – Assess At Regular Intervals In At-Risk Patients Particularly If Parenteral
Fluids Are Being Given.
4. Monitor Degree Of Edema – Most In Dependent Parts Of The Body, Feet, Ankles, Sacral In Ambulatory
Patients.
5. Assess For Pitting Edema – By Pressing A Finger Into The Affected Part, Creating A Pit Or Indentation
That Is Evaluated On A Scale Of 1 To 4
6. Assess For Peripheral Edema – By Measuring The Circumference Of The Extremity With A Tape
Marked In Mm.

Preventing Hypervolemia
1. Avoid OTC medication – Because They May Contain Sodium.
2. Prescribed Diet
3. Water Softeners

Detecting And Controlling Hypervolemia

1. Promote Rest – Bed Rest Favors Diuresis Of Fluid. The Mechanism Is Related To Diminished Venous
Pooling And The Subsequent Increase In Effective Circulating Blood Volume And Renal Perfusion
2. Restricting Sodium Intake - Because Most Patients With Fve Require Diuretics, The Patient’s Response
To These Agents Is Monitored.
3. Monitoring Parenteral Fluid Therapy – The Rate Of Parenteral Fluids And The Patient’s Response To
These Fluids Are Also Closely Monitored
4. Administering Appropriate Medications
5. Semi-Fowlers When Dyspnea Or Orthopnea Is Present – Promote Lung Expansion
6. Repositioned At Regular Intervals – Because Edematous Tissue Is More Prone To Skin Breakdown
Than Normal Tissue.
7. Documenting Fluid I&O And Body Weight

A. Effects To Cardiovalscular System

- Excess Fluid In Blood Stream – Raises The Blood Pressure And Force Heart To Work Harder
- Excess Fluid That Can Speed Up Heart Rate, Harm Your Heart Muscle And Increase The Size
Of The Heart
- Increased Central Venous Pressure – Extra Fluid Increases Venous Return (Jugular Vein Appear
Distended)
- CVP: Blood Pressure In The Vena Cava, Reflects The Amount Of Blood Returning To The
Heart And The Ability Of The Heart To Pump The Blood Back Into The Arterial System

B. Effects To Respiratory System

- Extra Fluid Entering The Lungs And Reduces Ability To Breathe Normally Leading To
Shortness Of Breath
- Pulmonary Edema – Fluid Accumulation In The Lungs, Which Collects In Air Sacs Making It
Difficult To Breath (Folwer’s)
- Dyspnea
- Orthopnea
- Productive Breath Sounds
C. Effects To Neuromuscular
- Confusion
- Muscle Weakness

D. Effects To Renal System

- Due To Heart Failure, It Is Unable To Pump Enough Blood And Supply Oxygen To Support
Other Organs In The Body. Kidney May Not Get Enough Blood Learing To Body Retains Salt
And Water To Attempt To Boost Blood Volume. Cause Fluid To Build Up Throughout The
Body And Can Lead To Heart Failure
- S/S: Weight Gain, Swollen Ankles/Feet, Sob

E. Effects To Integumentary System

- Skin Breakdown
- Edema

F. Effects To Gastrointestinal System

- Weight Gain
- Ascites – Because Of Not Able To Rid Of The Fluid In The Body Causes The Fluid To Build Up
In The Abdomen
- Anorexia
- Nausea
- Vomiting
Dizon, Jaylawrence Victor V.
Hypokalemia
A. Description
Hypokalemia is when the serum potassium level is below 3.5 mEq/L (3.5 mmol/L) usually indicates a
deficit in total potassium stores. The normal range for Potassium is 3.5 - 5.0 mEq/L
B. Risk factors
You can lose great amounts of potassium through urinating, sweating, or during bowel movements.
Inadequate potassium intake and low magnesium levels can result in hypokalemia. Malnutrition, people with
heart conditions also have a higher risk for complications. Medical conditions such as congestive heart failure,
arrhythmias, or history of heart attacks. Hypokalemia can be life threatening, the nurse needs to monitor for its
early presence in patients at risk. Fatigue, anorexia, muscle weakness, decreased bowel motility, paresthesias,
and dysrhythmias are common signs and symptoms.
C. Pathophysiology

Your kidneys control your body’s potassium levels, allowing for excess potassium to leave the body through
urine or sweat. Potassium-losing diuretics, such as the thiazides and loop diuretics, can induce hypokalemia.
Other medications that can lead to hypokalemia include corticosteroids, sodium penicillin, and amphotericin B.
GI loss of potassium is another common cause of potassium depletion. Vomiting and gastric suction frequently
lead to hypokalemia, because potassium is lost when gastric fluid is lost and because potassium is lost through
the kidneys in response to metabolic alkalosis.

D. Signs and Symptoms

Potassium deficiency can result in widespread derangements in physiologic function. Severe
hypokalemia can cause death through cardiac or respiratory arrest. Clinical signs develop when the potassium
level decreases to less than 3 mEq/L (3 mmol/L). Fatigue, anorexia, nausea and vomiting, muscle weakness,
polyuria, decreased bowel motility, paresthesias, leg cramps, decreased BP, hypoactive reflexes, and
dysrhythmias such as ventricular fibrillation and asystole.
E. Diagnostic procedure
In hypokalemia, the serum potassium concentration is less than the lower limit of normal.
Electrocardiographic (ECG) changes can include flat T waves or inverted T waves or both, suggesting ischemia,
and depressed ST segments, and an elevated U wave is specific to hypokalemia. The source of the potassium
loss is usually evident from a careful history. However, if the cause of the loss is unclear, a 24-hour urinary
potassium excretion test can be performed to distinguish between renal and extrarenal loss. Urinary potassium
excretion exceeding 20 mEq/day with hypokalemia suggests that renal potassium loss is the cause.
F. Management
a. Medical management
If hypokalemia cannot be prevented by conventional measures such as increased intake in the daily diet
or by oral potassium supplements for deficiencies, then it is treated cautiously with IV replacement therapy.
Potassium loss must be corrected daily; administration of 40 to 80 mEq/day of potassium is adequate in the
adult if there are no abnormal losses of potassium. For patients who are at risk for hypokalemia, a diet
containing sufficient potassium should be provided. Dietary intake of potassium in the average adult is 50 to
100 mEq/day.
b. Surgical management
Generally, hypokalemia is a medical, not a surgical, condition. Surgical intervention is required only
with certain etiologies, such as the following: Renal artery stenosis. Adrenal adenoma.
c. Nursing management
Because hypokalemia can be life threatening, the nurse needs to monitor for its early presence in
patients at risk. Fatigue, anorexia, muscle weakness, decreased bowel motility, paresthesias, and dysrhythmias
are signals that warrant assessing the serum potassium concentration. Prevention may involve encouraging the
patient at risk to eat foods rich in potassium (when the diet allows). Consumption of foods high in potassium
should be encouraged; examples include bananas, melon, citrus fruits, 855 fresh and frozen vegetables (avoid
canned vegetables), lean meats, milk, and whole grains. If the hypokalemia is caused by abuse of laxatives or
diuretics, patient education may help alleviate the problem. Part of the health history and assessment should be
directed at identifying problems that are amenable to prevention through education. Careful monitoring of fluid
I&O is necessary, because 40 mEq of potassium is lost for every liter of urine output. In correcting
hypokalemia, the oral route is ideal to treat mild to moderate hypokalemia because oral potassium supplements
are absorbed well.
Safety alert: Oral potassium supplements can produce small bowel lesions; therefore, the patient must be
assessed for and cautioned about abdominal distention, pain, or GI bleeding.
Potassium should be given only after adequate urine output has been established. A decrease in urine volume to
less than 20 mL per hour for 2 consecutive hours is an indication to stop the potassium infusion and notify the
primary provider. Potassium is primarily excreted by the kidneys; when oliguria occurs, potassium
administration can cause the serum potassium concentration to rise dangerously.
Safety alert: Potassium is never given by IV push or intramuscularly to avoid replacing potassium too quickly.
IV potassium must be given using an infusion pump. Each health care facility has its own policy for the
administration of potassium, which must be consulted. Administration of IV potassium is done with extreme
caution using an infusion pump with the patient monitored by continuous ECG.
Diaz, Normie A.
Hyperkalemia
A. Description
Hyperkalemia (serum potassium level greater than 5mEq/L/ 5mmol/L) it is more dangerous because
cardiac arrest is more frequently associated with high serum potassium level.
B. Risk factors
 Decreases in renin
 Decreases in aldosterone
 Renal failure
 Medication

C. Pathophysiology

D. Signs and Symptoms

 Muscle weakness, tachycardia-bradycardia, dysrhythmias, flaccid paralysis, parenthesias,

intestinal colic, cramps, abdominal distention, irritability, anxiety.
 ECG: tall tented T waves, prolonged PR interval and QRS duration, absent P waves, ST
depression.

E. Diagnostic Procedure.
1. Laboratory tests/ Serum Potassium Levels
2. ECG

F. Management
a. Medical Management
1. Obtain ECG immediately.
 2. Repeat Serum potassium level should be obtained from a vein without an IV infusing a
potassium containing solution.
3. Restriction of dietary potassium.
4. Eliminate the use of potassium containing salt substances.

Emergency Pharmacologic Therapy

If serum potassium levels are dangerously elevated, it maybe necessary to:
1. Monitor blood pressure
2. Administer Calcium Gluconate
3. ECG should be monitored during administration.
4. IV administration of sodium bicabornate may be necessary.
5. IV administration of regular insulin and a hypertonic dextrose solution.
6. Beta2- agonists

G. Nursing Management
 Identify and closely monitored for signs of hyperkalemia.
 Monitor I&O
 Observes for signs of muscle weakness and dysrhythmias
 Monitor serum potassium levels.
Cainglet, Shannen Marie V.
Hypernatremia
Hypernatremia is a serum sodium level higher than 145 mEq/L (145 mmol/L). It can be caused by a gain of
sodium in excess of water or by loss of water in excess of sodium. It can occur in patients with normal fluid
volume or in those with FVD or FVE. With a water loss, the patient loses more water than sodium; as a result,
the serum sodium concentration increases and the increased concentration pulls fluid out of the cell. This is both
an extracellular and in extracellular and an intracellular FVD. In sodium excess, the patient ingests or retains
more sodium than water.
Risk Factors
- Fluid deprivation in patients who cannot respond to thirst.
- Hypertonic tube feedings without adequate water supplements.
- Diabetes insipidus
- Heatstroke
- Hyperventilation
- Watery diarrhea
- Burns and diaphoresis
- Excess corticosteroid, sodium bicarbonate and sodium chloride administration.
- Saltwater near-drowning victims.
Pathophysiology
Signs and symptoms
- Thirst
- Elevated body temperature
- Swollen dry tongue and sticky mucous membranes
- Hallucinations
- Lethargy, restlessness
- Irritability
- Simple partial or tonic-clonic seizures
- Pulmonary edema
- Hyperreflexia, twitching
- Nausea, vomiting, anorexia
- Increase pulse rate and blood pressure
Labs indicate: increase serum sodium, decrease urine sodium, increase specific gravity and osmolality and
decease CVP.
Diagnostic procedure
Hypernatremia is often diagnosed through blood tests. Urine tests can also be used to identify high levels of
sodium along with urine concentration. Both blood and urine tests are fast, minimally invasive tests that require
no preparation. The serum sodium level exceeds 145 mEq/L (1455 mmol/L) and the serum osmolality exceeds
300 mOsm/kg (300 mmol/L). The urine specific gravity and urine osmolality are increased as the kidneys
attempt to conserve water (provided the water loss is from a route other than the kidneys.
Medical management
- Treatment for hypernatremia consists of a gradual lowering of the serum sodium level by the infusion of
a hypotonic electrolyte solution (e.g., 0.3% sodium chloride) or an isotonic non-saline solution (D5W).
D5W is indicated when water needs to be replaced without sodium.
- To reduce the risk of cerebral edema, Clinicians consider a hypotonic sodium solution to be safer than
D5W because it allows a gradual reduction in the serum sodium level. It is a solution of choice in severe
hyperglycemia with hypernatremia.
- Diuretics may be prescribed also to treat the sodium gain.
- Desmopressin acetate (DDAVP), a synthetic antidiuretic hormone, may be prescribed to treat diabetes
insipidus if it is the cause of hypernatremia.
Nursing management
- The nurse should assess for abnormal losses of water or low water intake and for large gains of sodium
as might occur with ingestion of OTC medications that have high risk of sodium content (e.g., Alka-
Seltzer).
- The nurse obtains medication history, because some prescription have high sodium content.
- The nurse notes the patient’s thirst or elevated body temperature and evaluates it in relation to other
clinical signs.
- The nurse monitors for changes in behavior, such as restlessness, disorientation and lethargy.
Preventing hypernatremia
- The nurse attempts to prevent hypernatremia by providing fluids at regular intervals, particularly in
debilitated or unconscious patients who are unable to perceive or respond to thirst.
 - If fluid intake still inadequate, the nurse will consults with the physician to plan for alternative route for
intake either enteral or parenteral route.
- For patients with diabetes insipidus, adequate water intake must be ensured.
Correcting hypernatremia
- When parenteral fluids are necessary for managing hypernatremia, the nurse monitors the patient’s
response to the fluids by reviewing the serial serum sodium levels and by observing for changes in
neurologic signs.
Diet (low sodium diet)
- Avoid foods with high sodium content.
- Use low sodium foods alternatives instead.
De Guzman, Ericca B.

Hyponatremia

A. Description
- Hypo: “under/beneath”
- Natr: Na is a prefix for Sodium, Sodium is an electrolyte, and it helps regulate the amount of water
that's in and around your cells.
- Emia: “blood”
- Refers to the serum sodium concentration that is less than 135 mEq/L (135 mmol/L)
- Acute Hyponatremia is commonly the result of a fluid overload in a surgical patient.
- Chronic hyponatremia is seen more frequently in patients outside the hospital setting, it has a
longer duration, and has less serious neurological sequelae
- Exercised-associated hyponatremia is another type of hyponatremia. It is more frequently found in
women and those of smaller stature. It can occur during extreme temperatures, because of excessive
fluid intake before exercise, or prolonged exercise that results in a decrease in serum sodium

B. Risk factors
 Age
o Older adults may have more contributing factors for hyponatremia, including age-related
changes, taking certain medications and a greater likelihood of developing a chronic disease
that alters the body's sodium balance.

 Certain drugs
o Medications that increase your risk of hyponatremia include thiazide diuretics as well as
some antidepressants and pain medications. In addition, the recreational drug Ecstasy has
been linked to fatal cases of hyponatremia.

 Conditions that decrease your body's water excretion.

o Medical conditions that may increase your risk of hyponatremia include kidney disease,
syndrome of inappropriate anti-diuretic hormone (SIADH) and heart failure, among others.

 Intensive physical activities.

o People who drink too much water while taking part in marathons, ultramarathons, triathlons
and other long-distance, high-intensity activities are at an increased risk of hyponatremia.
C. Pathophysiology

D. Signs and Symptoms

Poor skin turgor, dry mucosa, headache, decreased saliva production, orthostatic fall in blood pressure,
nausea, vomiting, and abdominal cramping.

Neurologic changes, including altered mental status, status epilepticus, and coma.

In general, patients with an acute decrease in serum sodium levels have more cerebral edema and higher
mortality rates than do those with more slowly developing hyponatremia. Acute decreases in sodium,
developing in less than 48 hours, may be associated with brain herniation and compression of midbrain
structures. Chronic decreases in sodium, developing over 48 hours or more, can occur in status
epilepticus and other neurologic conditions.

When the serum sodium level decreases to less than 115 mEq/L (115 mmol/L), signs of increasing
intracranial pressure, such as lethargy, confusion, muscle twitching, focal weakness, hemiparesis,
papilledema, seizures, and death, may occur.

Laboratory indicates
- Decrease in serum and urine sodium
- Decrease in urine specific gravity and osmolarity

E. Diagnostic procedure (discuss especially nursing responsibilities – preparation etc)

In hypernatremia, the serum sodium level exceeds 145 mEq/L (145 mmol/L) and the serum osmolality
exceeds 300 mOsm/kg (300 mmol/L). The urine specific gravity and urine osmolality are increased as
the kidneys attempt to conserve water (provided the water loss is from a route other than the kidneys).
Patients with nephrogenic or central diabetes insipidus have hypernatremia and produce a dilute urine
with a urine osmolality less than 250 mOsm/kg
F. Management
a. Medical management
- The key to treating hyponatremia is an assessment that focuses on the clinical symptoms
of the patient and signs of hyponatremia (including laboratory values). As a general rule,
treating the underlying the condition is essential.

- In general, hyponatremia is treated with fluid restriction (in the setting of euvolemia),
isotonic saline (in hypovolemia), and diuresis (in hypervolemia). A combination of these
therapies may be needed based on the presentation. Hypertonic saline is used to treat
severe symptomatic hyponatremia.

- Sodium Replacement is the most common treatment for hyponatremia.

b. Surgical management (discuss especially the nursing responsibilities of pre op and post -op)
- Post-operative hyponatremia requires careful fluid balance. Start close fluid monitoring,
catheterizing if necessary; this is particularly important during the intraoperative and
post-operative period.
- Intravenous fluids (such as 0.9% sodium chloride) are generally advised over enteral
hydration for the hyponatremic patient, as they will provide a greater control to the serum
electrolyte levels. Monitor renal function and electrolyte levels regularly, as potential
derangement may occur during any fluid redistribution during your management.
- If the cause is unknown or evidence of prolonged and marked hyponatremia, urine
osmolality and sodium concentration should be measured to inform additional diagnosis.

c. Nursing management
o Nurse needs to identify and monitor patients at risk for hyponatremia
o Nurse should assess for abnormal losses of water or low water intake and for large gains of
sodium.
o Nurse should strictly monitors I&O as well as daily body weight.
o Nurse needs to get a thorough history to identify if the patient is a performance athlete
o Nurse should monitor serum electrolytes levels.
o Assess for location of Edema formation.
o Administer oral fluid with caution.
o Nurse monitors the patient closely for changes in behavior, such as restlessness,
disorientation, and lethargy.
o Provide balance protein and low sodium diet
o Document I&O accurately.
Calderon, Paulyn Faith D.

Hypermagnesemia

Magnesium (Mg++) is an abundant intracellular cation. It acts as an activator for many intracellular enzyme
systems and plays a role in both carbohydrate and protein metabolism. The normal serum magnesium level is
1.3 to 2.3 mg/dL (0.62 to 0.95 mmol/L). Half is stored in the bones and half is stored in the cells wherein it is
the seconds most common positive ion next to Potassium. 1% is in the extracellular space where it is divided
into the intravascular and interstitial space. 20% of Magnesium in the extracellular space about 0.2% of total
Magnesium in the body is bound to proteins like albumin and 80% (0.8 Mg in the body) is filtered in the
kidneys.

Functions of Magnesium
1. Magnesium acts directly on the myoneural junction, variations in the serum level affect neuromuscular
irritability and contractility. For example, an excess of magnesium diminishes the excitability of the
muscle cells, whereas a deficit increases neuromuscular irritability and contractility.
2. Magnesium affects the cardiovascular system, acting peripherally to produce vasodilation and decreased
peripheral resistance.
3. Cell regulation like the transferring and storing of energy.
4. Regulation of the parathyroid hormone (plays a role in calcium levels).
5. Metabolizes carbohydrates, lipids, and proteins.
6. Regulates blood pressure.

A. Description (Calderon)
-NORMAL RANGE: 1.3-2.1 mEq/L
-Serum level higher than 3.0 mg/dL is a rare electrolyte abnormality because the kidneys efficiently excrete
magnesium.
-A serum magnesium level can appear falsely elevated if blood specimens if drawn from extremity with a
torniquet that was applied too tightly.
- Seldom develop in the presence of normal renal function.
-May occur as a result of Mg replacement
-Careful monitoring is imperative

B. Risk Factors(Calderon)
1. Oliguric Phase of Kidney Injury
- Oliguric Phase: Reduction in urine output less than 400 mL/day
-Due to kidney injury, the process that keeps the levels of Magnesium in body doesn’t work properly.
-Unable to get rid of excess Magnesium, therefore, more susceptible to build of Magnesium in the blood
(Hypermagnesemia).
-Urine output also decreases.
2. Adrenal Insufficiency
-In adrenal insufficiency, the glands do not produce adequate amount of steroid hormones and there has an
impaired production of aldosterone.
-Steroids help control metabolism, inflammation, immune functions, salt and water balance.
-Aldosterone regulates salt and blood pressure and water in the body.

ADDISON’S DISEASE
-It is an example of adrenal insufficiency which is an endocrine disorder.
-Doesn’t produce enough steroid hormones.
-Hypocortisolism
-Signs and Symptoms: Hyperpigmentation, fever, syncope, weakness, weight loss, nausea and
vomiting, hypoglycemia, abdominal pain
Explanation:
-The Magnesium helps the body to RELAX, it inhibits the Adrenocorticotropic Hormone(ACTH), wherein
adrenal glands would not release the stress hormone (Cortisol).
-Too much Magnesium: RELAXES even more
Decrease Cortisol even more
Vasodilation

3. IV magnesium Administration
-Too much IV Magnesium Administration can result in Hypermagnesemia.
-Magnesium Sulfate is used to prevent seizures in pregnant women with pre-eclampsia. -Careful
monitoring is needed.

4. Diabetic Ketoacidosis
` -A condition wherein it starts breaking down fat at a rate that is too much fast.
-This condition is when the cells do not get enough glucose need for energy and the body begins to burn
fat which produces KETONES.
-Then, Magnesium release in cells because it cannot be excreted due to profound fluid volume depletion
resulting Oliguria.

5. Hypothyroidism
-Normal Range of PTH: 10-55 pg/mL
-In hypothyroidism, there is a low levels of PTH, specifically less than 10 pg/mL and it is a condition
wherein the thyroid gland does not produce enough crucial hormones and it affect metabolism, mental
functions, and bowel movements.

- PTH regulates Calcium and Phosphorus.

- Under normal circumstances, Magnesium inhibits the PTH. Now, too much magnesium will inhibit
more the PTH, then, PTH doesn’t release Calcium resulting hypocalcemia.
- Low PTH level in hypothyroidism ---- inhibitor effect of magnesium
 - Relationship of Magnesium and Calcium: Magnesium and Calcium work in hand together to support
bone health and bodily functions. Magnesium is needed for Calcium absorption but it suppresses PTH
and stimulated Calcitonin that helps deposit Calcium into the bones.

C. Pathophysiology

a) Procedure
A health care professional will take a blood sample from a vein in the arm, using a small needle. After
the needle is inserted, a small amount of blood will be collected into a test tube or vial. Patient may feel a
little sting when the needle goes in or out. This usually takes less than five minutes.

b) Nursing Responsibilities
1) Monitor vital signs.
2) Assess signs and symptoms of hypermagnesemia.
3) Monitor and assess for following risks such as bleeding at the site, infection, hematoma, and
fainting or lightheadedness.

Electrocardiogram
- Determine heart rhythm and rate changes related to Hypermagnesemia

ECG findings may include:

- Prolonged PR interval; Tall T waves; Widened QRS, Prolonged QT, AV Block
 A. Preparation
- Explain the procedure.
- Informed Consent
- Assess vital signs.
- Assess the client's chest for areas of irritation, skin breakdown, or excessive hair growth that may
interfere with the electrode placement.
- Keep the chest area dry.
- If the client has a pacemaker, nurse can perform an ECG with or without a magnet, according to
the physician's orders. Be sure to note the presence of a pacemaker and the use of a magnet on the
strip.
- Ensure empty bladder.

B. Nursing Responsibilities
- Instruct patient to resume regular diet and activities.
- Inform the patient that the study will be interpreted by the physician.

D. Management

A. Medical Management(Calderon)
a) Avoidance of administration of Mg and Mg rich foods.
b) Ventilatory support and 10-20mL of 10% Calcium Gluconate administered over 10 mins
- For Emergency such as Respiratory depression or defective cardiac conduction.
- Neuromuscular and cardiac function become antegonized by Calcium.
- Note for bradycardia, hypotension, headache, and diarrhea

1. Loop Diuretics- Furosemide with NaCl or Lactated Ringers IV Solution

- ”Water pills”
- It increases the excretion of Sodium and water by kidneys
- It helps patient to urinate when kidneys are not working properly.
- Side effects: Increase urination, thirst, muscle cramps, itchiness, weakness, dizziness
2. Hemodialysis with a magnesium-free dialysate

a) Nursing Management
1) Monitor vital signs and laboratory values.
2) Note hypotension and shallow respirations.
3) Observe for deep tendon reflex.
DTR: 0 No response
1+ Slightly but definitely present response
2+ Brisk Response – NORMAL
3+ Very Brisk Response
4+ Tap elicits a repeating reflex

4) Do no administer medications that contain Mg to the patients with kidney injury or compromised
renal function.
5) Instruct patients with kidney injury that they are cautioned to check with their primary physician
before taking OTC medications.
6) Take caution when preparing and administering Mg-containing fluids parenterally.
7) Note for Magnesium Sulfate Toxicity: Absent DTR; RR less than 12 cpm; Shortness of Breath
 8) Discourage food intake high in Magnesium. Foods rich in Mg are the ff:

Pnemonics: Always Get Plenty Of Food Containing Large Numbers Of Magnesium

- Avocado
- Green Leafy Vegetables
- Peanut
- Oatmeal
- Fish
- Legumes
- Nuts
- Oranges
- Milk
Dela Ysla, Angelica Grace D.
Hypomagnesemia
Hypomagnesemia refers to a below-normal serum magnesium concentration (1.3 mg/dL [0.62 mmol/L]) and is
frequently associated with hypokalemia and hypocalcemia.
Contributing factors:
1. Chronic alcoholism
- by malnutrition or electrolyte disturbances which leads to a loss of Mg in the tissues and increase in
urine output.
2. Hyperparathyroidism
- Leads to an increase in Calcium which may lead to hypercalcemia therefore delivering more Calcium
to the loop of Henle; ensuring the increase in Calcium reabsorption therefore diminishes Mg
reabsorption.
3. Hyperaldosteronism
- Refers to too much aldosterone produced by the adrenal glands; Aldosterone increases clearance and
excretion of Magnesium and Potassium through urinary excretion.
4. Diuretic phase of acute kidney injury
- In this phase, the kidneys try to heal and increase urine output resulting in renal Mg loss therefore
unable to reabsorb Magnesium.
5. Malabsorption disorders
- Impaired gastrointestinal absorption especially involving the small intestine like Celiac and Crohn’s
disease can lead to Magnesium malabsorption.
6. Diabetic ketoacidosis
- Insulin therapy reduces renal Mg absorption resulting in urinary Magnesium wasting.
7. Refeeding after starvation
- Refeeding syndrome is for patients who were previously malnourished and is fed with carbohydrate
loads which leads to poor intake of Magnesium.
8. Parenteral nutrition
- Patients receiving total parenteral nutrition may not get enough Mg especially those with problems in
gastrointestinal disorders leading to Magnesium malabsorption.
9. Chronic laxative use, diarrhea
- Extreme fluid loss like these two can lead to malabsorption of electrolytes like Magnesium.
10. Acute myocardial infarction and heart failure
- Loop and Thiazide diuretics therapy for fluid removal in patients with heart failure; makes lumen less
positively charged and diminishes Magnesium’s electrochemical gradient therefore more Mg stays in the
lumen and gets excreted.
11. Certain pharmacologic agents (such as gentamicin, cisplatin, and cyclosporine)
- Cisplatin induces hypomagnesemia through its renal toxicity possibly by a direct injury to mechanisms
of magnesium reabsorption in the ascending limb of the loop of Henle as well as the distal tubule.
Gentamicin leads to tubular dysfunction and substantial wasting of electrolytes like Hypomagnesemia.
Proton pump inhibitors like cyclosporine can leads to impaired magnesium absorption therefore leading
to hypomagnesemia.
Clinical manifestations
Some clinical manifestations of hypomagnesemia are due directly to the low serum magnesium level; others are
due to secondary changes in potassium and calcium metabolism. Symptoms do not usually occur until the
serum magnesium level has dropped to less than 1.8 mEq/L (0.75 mmol/L).
 Neuromuscular irritability
 Positive Trousseau sign and Chvostek sign (may occur as part of accompanying hypocalcemia)
A. Chvostek sign: a contraction of the facial muscles elicited in response to light tap over the facial nerve in
front of the ear.
B. Trousseau sign: a carpopedal spasm induced by inflating a blood pressure cuff above systolic blood
pressure
 Insomnia and mood changes
 Anorexia and vomiting
 Increased tendon reflexes
 Increased BP
 ECG: PVCs, flat or inverted T waves, depressed ST segment, prolonged PR interval, widened QRS, and
predisposing to cardiac dysrhythmias, such as premature ventricular contractions, supraventricular
tachycardia, torsades de pointes, and ventricular fibrillation.
*Torsades de pointes – abnormal heart rhythm that can lead to sudden cardiac death.
 Increased susceptibility to digitalis toxicity is associated with low serum magnesium levels. Patients
receiving digoxin are also likely to be receiving diuretic therapy, predisposing them to renal loss of
magnesium.
 Hypocalcemia can be worsened by isolated treatment of hypomagnesemia with intravenous magnesium
sulfate because sulfate binds ionized calcium

Magnesium is similar to calcium in two aspects:

1. It is the ionized fraction of magnesium that is primarily involved in neuromuscular activity and other
physiologic processes.
2. Magnesium levels should be evaluated in combination with albumin levels. Because about 30% of
magnesium is protein bound, principally to albumin, a decreased serum albumin level can reduce the
measured total magnesium concentration; however, it does not reduce the ionized plasma magnesium
concentration.
*In the neuromuscular junction there’s a voltage gate Calcium channel on the presynaptic neurons which let
calcium in which causes neurons to release neurotransmitters that cause muscle contractions. Magnesium
inhibits calcium influx for stability without Magnesium, Calcium easily enters and causes more muscle
contractions.
Pathophysiology

Assessment and Diagnostic Findings

Hypomagnesemia is diagnosed based on a physical exam, symptoms, medical history, and a blood test.
Hypomagnesemia is diagnosed by measurement of serum magnesium concentration through a total serum
magnesium test either by measuring Magnesium in the blood or a 24hr urine collection. On laboratory analysis,
the serum magnesium level is less than 1.3 mg/dL (0.62 mmol/L). Urine magnesium may help identify the
cause of magnesium depletion, and levels are measured after a loading dose of magnesium sulfate is given.

Patient preparation (Magnesium blood test)

- There is no food, fluid, activity, or medication restrictions unless by medical direction.
Nursing Interventions:
- Monitor symptoms such as tetany, weakness, dizziness, tremors, hyperactivity, nausea, vomiting, and
convulsions occur at decreased concentrations which may indicate hypomagnesemia.
- Monitor for ECG changes
- Monitor for respiratory paralysis, decreased reflexes, and cardiac arrest occur at grossly elevated
levels. Which may indicate hypermagnesemia
- Notify health care provider for any critical findings and related symptoms.
Magnesium deficiency is also suspected even when serum magnesium concentration is normal in patients with
unexplained hypocalcemia or refractory hypokalemia.
Additional diagnostic techniques such as nuclear magnetic resonance spectroscopy and the ion-selective
electrode are sensitive and direct means of measuring ionized serum magnesium levels.
Medical Management
Mild magnesium deficiency can be corrected by diet alone. Principal dietary sources of magnesium include
green leafy vegetables, nuts, seeds, legumes, whole grains, seafood, peanut butter, and cocoa.

If necessary, magnesium salts can be given orally in an oxide or gluconate form to replace continuous losses.
Patients who are receiving parenteral nutrition require magnesium in the IV solution. Overt symptoms of
hypomagnesemia (severe cases) are treated with parenteral administration of magnesium because a bolus dose
of magnesium sulfate given too rapidly can produce alterations in cardiac conduction leading to heart block or
asystole.
Always Get Plenty Of Foods Containing Large Numbers Of Magnesium
 Avocado
 Green Leafy Vegetables
 Peanuts
 Oatmeal
 Fish
 Cauliflower
 Legumes
 Nuts
 Milk
Nursing management
 The nurse should be aware of patients at risk for hypomagnesemia and observe them for its signs and
symptoms.
 Patients receiving digitalis are monitored closely, because a deficit of magnesium can predispose them
to digitalis toxicity.
 If hypomagnesemia is severe, seizure precautions are implemented. (side-rails up)
 Because difficulty in swallowing (dysphagia) may occur in those with magnesium depletion, these
patients should be screened for dysphagia.
 A patient with serious signs and symptoms such as ventricular dysrhythmias may require I.V.
magnesium sulfate given slowly with careful monitoring. Monitor the patient for signs of
 hypermagnesemia, which can occur with magnesium administration. Calcium gluconate must be readily
available to treat hypermagnesemia.
 Assess patients for complications associated with a low magnesium level. Magnesium toxicity can
depress or cause the loss of deep tendon reflexes, so routinely assess for this warning sign.
 Vital signs must be assessed frequently during magnesium administration to detect changes in cardiac
rate or rhythm, hypotension, and respiratory distress. (for magnesium sulfate toxicity)
 Monitoring urine output is essential before, during, and after magnesium administration; the physician is
notified if urine volume decreases to less than 100 mL over 4 hours. (for magnesium sulfate toxicity)
 Patient education plays a major role in treating magnesium deficit. The patient is educated about sources
of magnesium-rich foods, including green vegetables, nuts, legumes, bananas, and oranges.
 Educate the patient about diet and medications, and about signs and symptoms that should be reported
immediately, such as chest discomfort. If appropriate, offer resources for treating chronic alcohol abuse.
 Calderon, Paulyn Faith D.
Hypercalcemia
- It is a cation.
- Calcium located in skeletal system- 99%
- About 1% of skeletal calcium is rapidly exchangeable with blood calcium.
- Major component of bones and teeth.
- Calcium exists in plasma in three forms:

1. Ionized - 50% of the serum Calcium exists in a physiologically active ionized calcium that is important
for neuromuscular activity and blood coagulation.
- NORMAL: 4.5-5.1 mg/dL (1.1 - 1.3 mmol/L)
2. Bound- Less than half of the plasma calcium is bound to serum proteins, primarily albumin.
3. Complex- The remainder is combined with nonprotein anions: Phosphate, Citrate, and Carbonate
- Serum calcium levels is controlled by PTH and CALCITONIN.
- Calcium is absorbed from foods in the presence of normal gastric acidity and vitamin D.
- Calcium is excreted primarily in the feces, with the remainder in excreted in the urine.
- Functions and roles:
1. Transmit nerve impulses
2. Helps regulate muscle contraction, including cardiac muscle
3. Activate enzymes that stimulate many essential chemical reactions in the body
4. Plays a role in blood coagulation
- Ionized serum calcium decreases → PTH glands secrete PTH → Increases Ca reabsorption from
GI Tract and renal tubule → Released Ca from bone → Increases calcium ion concentration
- When Calcium releases excessively → Thyroid gland secretes Calcitonin → Inhibits Ca
reabsorption → Decreases Calcium ion concentration

A. Description
-Hypercalcemia is a condition in which the calcium level in your blood is above normal. Too much calcium in
your blood can weaken your bones, create kidney stones, and interfere with how your heart and brain work.
- Normal Range: 9.0-10.5 mg/dL
- Hypercalcemia: >10.5 mg/dL
- It is a dangerous imbalance when severe.
- It has a mortality rate as high of 50% if NOT TREATED promptly.
-
B. Risk Factors
1. Hyperparathyroidism
- Most common cause of hypercalcemia.
- PTH is is overproduce due to benign malignant growth within the parathyroid gland.
- NORMAL PTH Level: 10-55 pg/mL
- Hyperparathyroidism- Calcium levels >10.5 mg/ dL and >55 pg/mL

2. Malignant Neoplastic disease

- Malignant neoplasm is a cancerous tumor, an abnormal growth uncontrolled and spread to other
parts of the body.
- Some cancer cells produce a protein similar to PTH called PTHrP (PTH related protein) that
increases Calcium levels abnormally.

3. Overuse of calcium supplements and Vitamin D excess

 - Too much use of Calcium and Vitamin D excess stimulates GI tract to absorb more Calcium.
- Vitamin D (Calcitriol) is responsible for absorption of Calcium in small intestine and increases
reabsorption of Calcium in kidney.

4. Oliguric Phase of Renal Failure

- Oliguric Phase: Reduction in urine output less than 400 mL/day
- Due to renal failure, calcium cannot be excreted properly and retains.

5. Acidosis
- Damages protein binding -> Increase free Calcium levels
- It lowers the amount of albumin created in the body levels to muscle loss “muscle wasting”.
- It is renal calcium wasting.
- Hypercalcemia was attributable to metabolic acidosis increasing Calcium efflux while renal
failure decreases the capacity to excrete Calcium.

6. Corticosteroid therapy
- Chronic hypercalcemia can be an important complication of steroid abuse.

7. Thiazide Diuretic Use

- It increases reabsorption of Calcium and decreases urine Calcium levels resulting increases in
Calcium in blood.

8. Increase Parathyroid Hormone

- PTH triggers:
1. Bones release Calcium in blood
2. Kidneys excretes less Calcium and activates Vit. D which is vital for Calcium absorption
3. Digestive tract to absorb more Calcium

9. Digoxin Toxicity
- Hypercalcemia aggravates Digoxin positive inotropic effect.
C. Pathophysiology
D. Signs and Symptoms
1. Muscular Weakness and deep bone pain- Excess Calcium was leached from bones which weakens
them, causing pain and weakness.
2. Constipation; Anorexia; Nausea and Vomiting - Decrease GI motility
3. Polyuria and Polydipsia - Kidneys work hard to filter excess Calcium
4. Dehydration- Low amount of fluid in blood because of accumulation of high Calcium levels
5. Hypoactive deep tendon reflexes 1+ or 0
DTR: 0 No response
1+ Slightly but definitely present response
2+ Brisk Response - NORMAL
3+ Very Brisk Response
4+ Tap elicits a repeating reflex
6. Lethargy- Hypercalcemia suppresses CNS.
7. Flank pain- Discomfort in upper abdomen or back and side.
8. Calcium stones-Urine contains too much Calcium, crystals might form in kidneys and overtime, form
into kidney stones.
9. Hypertension-Increases Vascular resistance from renal dysfunction and direct vasoconstriction
10. ECG:
- Shortened ST Segment and QT interval
- Bradycardia
- Heart Blocks

E. Diagnostic Procedures
1. Calcium Blood Test
a) Preparation
- Instruct the patient to stop the following medications/supplements: lithium, thiazide diuretics
,antacids containing calcium, vitamin D supplements, calcium supplements.
- Instruct patient not to consume large amount of foods or drinks that contain calcium because it can
increase the levels of calcium in your blood and affect test results.
b) Procedure
- To perform the test, the healthcare provider will draw a blood sample from your arm.
- A needle will be inserted into a vein in the arm, and a small amount of blood will be collected
into a tube. The blood draw should take less than five minutes.
- Patient may feel a slight pinch when the needle enters your arm.

c) Nursing Responsibilities
- Observe patient for the signs and symptoms of hyper or hypocalcemia.
- Assess for health history of the patient.
- Monitor and assess for following risks such as bleeding at the site, infection, hematoma, and
fainting or lightheadedness.

2. Electrocardiogram
 - To determine cardiovascular changes that may include a variety of dysrhythmias (heart blocks,
bradycardia) and shortening of QT interval and ST segment. PR interval is sometimes
prolonged.

a) Preparation
i. Explain and consent
ii. Assess the client's medical record for information regarding the needs for an ECG.
iii. Assess the client's heart rate, heart sounds, and blood pressure.
iv. Assess the client's chest for areas of irritation, skin breakdown, or excessive hair growth that may
interfere with the electrode placement.
v. Keep the chest area dry.
vi. If the client has a pacemaker, nurse can perform an ECG with or without a magnet, according to
the physician's orders. Be sure to note the presence of a pacemaker and the use of a magnet on the
strip.
vii. Ensure empty bladder.

b) Nursing Responsibilities
- Instruct patient to resume regular diet and activities.
- Inform the patient that the study will be interpreted by the physician.

3.PTH Test
- Identify hyperparathyroidism , to find the cause of abnormal calcium levels, or to check the status of
chronic kidney disease. PTH controls calcium and phosphorus levels in the blood.
- To differentiate between primary hyperthyroidism and malignancy as a cause of
hypercalcemia.
- PTH levels increased
- Primary or secondary hyperthyroidism
- Suppressed in malignancy
- NORMAL VALUES: 10-55 pg/mL. Normal value ranges may vary slightly among different
laboratories. -Note: pg/mL = picograms per milliliter

a) Preparation
- Fasting (except water) is required for 10 to 12 hours before the test.
- Tell patient when the needle is inserted to draw blood, patient may feel moderate pain or feel only a
prick or stinging sensation. Afterward, there may be some throbbing.

b) Procedure
- Blood is drawn from a vein, usually from the inside of the elbow or the back of the hand.
- The puncture site is cleaned with antiseptic, and a tourniquet is placed around the upper arm to
apply pressure and restrict blood flow through the vein. This causes veins below the tourniquet to
fill with blood.
- A needle is inserted into the vein, and the blood is collected in an air-tight vial or a syringe.
- The tourniquet is then removed to restore circulation.
- After blood has been collected the needle is removed, and the puncture site is covered to stop any
bleeding.

c) Nursing Responsibilities
 - There is very little chance of a problem from having blood sample taken from a vein. Patient
may get a small bruise at the site.
- Keep pressure on the site for several minutes because it can lower the chance of bruising.
- In rare cases, the vein may become swollen after the blood sample is taken. This problem is
called phlebitis. A warm compress can be used several times a day to treat this.
- Assess for the following risk:
 Excessive bleeding
 Fainting or feeling lightheaded
 Hematoma
 Infection

F. Management

a) Medical Management
i. Administer 0.9% Sodium Chloride solution.
- Major Cation of ECF
- It controls water distribution, fluid and electrolyte imbalance.
- Appropriate volume repletion with isotonic NaCl Solution is an effective short treatment
for hypercalcemia.
- Once volume is restored, simultaneous administration of loop diuretics blocks Sodium and
Calcium reabsorption in TALH (Thick Ascending Loop of Henle).

ii. Administer Furosemide with saline solution.

- Water Pills
- Increases renal calcium excretion.
- Avoid Thiazide Diuretics because it increases Calcium reabsorption
- Side Effects: Increase Urination, Thirst, Muscle Cramps, Weakness, Dizziness, Diarrhea

iii. Phosphate Therapy: Via Oral, NGT, IV, Rectal

- Inorganic Phosphate Salts- Oral or NGT (Phospho-Soda or Neutro Phos), rectally (as
retention enemas)
- It is used with extreme caution because it can cause: Severe Calcification in various
tissues, Hypotension, Tetany, Acute Kidney Injury
- Note: Increase Calcium - Decrease Phosphate
Increase Phosphate -Decrease Calcium
iv. Calcium Reabsorption Inhibitors:
1. Calcitonin (Miacalcin) via IM because patients with hypercalcemia have poor perfusion of
subcutaneous tissue.
2. It control Calcium in the blood.
3. It decreases Serum Calcium concentration by increasing renal Calcium excretion.
4. Side Effects: Nausea and Vomiting, Diarrhea, Abdominal Pain, Flushing, Dizziness,
Headache, Taste disturbance

v. Corticosteroids
1. It lessens intestinal Calcium reabsorption
2. It may be used to decrease bone turnover and tubular reabsorption for patients with
Sarcoidosis, Myelomas, Lymphomas, and Leukemias; Patients with solid tumors are
less responsive.
 3. PREDNISONE- First Choice in hypercalcemia caused by Vit D; It influences bone
metabolism by uncoupling bone formation and bone resorption.
4. Side Effects: Confusion, Excitement, Restlessness, Headache, Vomiting, Thinning skin

vi. Biphosphonates:
1. Inhibit osteoclast activity.
2. Quickly decreases Calcium levels
3. Pamidronate Disodium (Aredia)
4. Ibandronate sodium (Boniva)
5. SIDE EFFECTS: IV forms can cause fever, transient leukopenia, eye inflammation, nephrotic
syndrome, and jaw osteonecrosis

vii. Mithramycin
1. Cytotoxic Antibiotic
2. It inhibits bone resorption, thus lowers the serum calcium level.
3. Rapidly controlled the hypercalcemia
4. This control was temporary and intermittent administration of the antibiotic that was required.
5. SIDE EFFECTS: Thrombocytopenia, Nephrotoxicity, Rebound Hypercalcemia when
discontinued, Hepatotoxicity

b) Surgical Management
Therapeutic aims include decreasing the serum calcium level and reversing the process causing
the hypercalcemia. Treating the UNDERLYING CAUSE is essential.

1. Parathyroidectomy
- General anesthesia with endotracheal intubation; local anesthesia is possible with confident
preoperative localization.
- An incision is made at the base of the neck and is about two to four inches long. Using
magnifying lenses, the surgeon locates the parathyroid glands and the abnormal or excess
one(s) are removed.
- Position: Neck slightly hyperextended by placing a bolster between the scapulae
9) Pre-Op
1. For one week prior to surgery you should not be taking any aspirin, baby aspirin, advil,
ibuprofen, vitamin E, Plavix or any medication that can increase bleeding or decrease clot
formation. If patient are on Coumadin or other blood thinners, this will need to be stopped by
your internist or medical physician prescribing the blood thinner, approximately 4-5 days
before surgery.
2. Vitamin D (Ergocalciferol, calcitriol): If patient’s Vitamin D levels are low before surgery,
patient will be given a supplement to take.
3. NPO 6 hours prior surgery.

10) Post-Op
1. Common medications may be needed after surgery:
a) Monitor vital signs and laboratory values especially calcium levels.
b) Pain medication
c) Calcium (TUMS): After parathyroid surgery, all patients are discharged home with
calcium supplementation. Parathyroid glands regulate calcium levels in the blood.
 d) After surgery, patient may require a different form of Vitamin D (calcitriol) because your
parathyroid glands may produce a low amount of parathyroid hormone, which will
make your calcium levels low. This is not always necessary in all patients.
e) Instruct patient that he/she can resume a normal diet after surgery as tolerated.
Sometimes there can be nausea after anesthesia, but this is usually temporary. Patient is
not limited in what he/she can eat, but it is best to avoid foods that are difficult for you to
swallow or digest.
f) Avoid strenuous activity like heavy lifting and vigorous exercise for about 1 week
after surgery. Elevate the head when laying down by sleeping on 2 pillows. After
one week you can resume your normal routine.
g) Educate patient about possible changes in voice, including hoarseness, which
generally improves within the first month after your surgery.

c) Nursing Management
i. Monitor vital signs.
1. Increase BP and decrease HR are signs of hypercalcemia.
ii. Increase patient mobility. Monitor for DTR.
DTR: 0 No response
1+ Slightly but definitely present response
2+ Brisk Response – NORMAL
3+ Very Brisk Response
4+ Tap elicits a repeating reflex
iii. Encourage fluid intake. (2.8 to 3.8 L or 3-4 quarts) of fluid daily.
iv. Fluids containing sodium should be indicated unless contraindicated.
v. Adequate fiber in diet is encouraged to offset the tendency of constipation.
vi. Assess for symptoms of digitalis toxicity.
1. Confusion
2. Irregular Pulse; Palpitations
3. Loss of Appetite
4. Nausea and Vomiting
5. Diarrhea
6. Vision changes including blind spots, blurred vision, changes in how color look or seeing
spots (Unusual)
vii. Monitor for abnormal cardiac rates and rhythm.
viii. Safety precautions are implemented, as necessary, when altered mental status is present. Inform
the patient’s family that these mental changes are reversible with treatment.
ix. Instruct patient to decrease calcium rich foods and decrease intake of Thiazides, calcium
supplement, and Vitamin D.

Pnemonics: Young Sally’s Calcium Serum Continues To Randomly Mess Up

- Yogurt
- Sardines
- Cheese
- Spinach
- Colored Greens
- Tofu
- Rhubarb
- Milk
Catana, Erroll D.

Hypocalcemia

- It is a cation.
- Calcium located in skeletal system- 99%
- About 1% of skeletal calcium is rapidly exchangeable with blood calcium.
- Major component of bones and teeth.
- Calcium exists in plasma in three forms:
1. Ionized - 50% of the serum Calcium exists in a physiologically active ionized calcium that is
important for neuromuscular activity and blood coagulation.
 NORMAL: 4.5-5.1 mg/dL (1.1 - 1.3 mmol/L)
2. Bound- Less than half of the plasma calcium is bound to serum proteins, primarily albumin.
3. Complex- The remainder is combined with nonprotein anions: Phosphate, Citrate, and Carbonate
 Serum calcium levels is controlled by PTH and CALCITONIN.
 Calcium is absorbed from foods in the presence of normal gastric acidity and vitamin D.
 Calcium is excreted primarily in the feces, with the remainder in excreted in the urine.

Functions and roles:

1. Transmit nerve impulses
2. Helps regulate muscle contraction, including cardiac muscle
3. Activate enzymes that stimulate many essential chemical reactions in the body
4. Plays a role in blood coagulation
- Ionized serum calcium decreases
- PTH glands secrete PTH
- Increases Ca reabsorption from GI Tract and renal tubule
- Released Ca from bone
- Increases calcium ion concentration
- When Calcium releases excessively
- Thyroid gland secretes Calcitonin
- Inhibits Ca reabsorption
- Decreases Calcium ion concentration

A. Description
In hypocalcemia, the calcium level in blood is too low.
- serum calcium value lower than 8.6 mg/dL [2.15 mmol/L] or an ionized calcium <4.2 mg/dl.

B. Risk Factors:
• People who have had parathyroidectomy
• Older adults (especially women)
• People with lactose intolerance
• Alcoholic people
• Hypoparathyroidism and pseudohypoparathyroidism.
C. PATHOPHYSIOLOGY

D. SIGNS/ SYMPTOMS:

- (+)Trousseau sign- is a carpal spasm that occurs by inflating a BP cuff on the upper arm to
20mmHg greater than systolic pressure for 2-5 mins.
- (+) Chvostek sign- is the contraction of the facial muscle that is produced by tapping the facial
nerve in front of the ear.
 Tetany
 Numbness
 Seizures
 Irritability
 Anxiety
 Paresthesia
 Confusion
 Decrease BP
 ECG: prolonged QT interval and lengthened ST.

E. DIAGNOSTIC PROCEDURE:
Physical Examination
1. Trousseau sign
2. Chvostek sign

1. Calcium Blood Test

a. Preparation:
1. Educate patient about food, fluid, activity, or medication restrictions unless by
medical direction.
2. Explain to the patient that may feel a slight pinch when the needle enters the arm.

b. Nursing Responsibilities:
1. Monitor vital signs.
2. Assess signs and symptoms of hypocalcemia.
3. Monitor and assess for following risks such as bleeding at the site, infection, hematoma, and
fainting or lightheadedness.
2.Electrocardiogram
1. Explain the procedure to the patient.
2. Informed Consent.
3. Assess vital signs.
 4. Assess the client's chest for areas of irritation, skin breakdown, or excessive hair growth that may
interfere with the electrode placement.
5. Keep the chest area clean and dry.
6. Place the patient in semi recumbent position.
7. Patient must be completely relaxed.

Nursing Responsibilities
- Inform patient no special preparation is needed.
- Encourage the patient to cooperate.
- Inform the patient that the study will be interpreted by the physician.

F. MANAGEMENT
Medical Management
 IV Calcium
- intermittent IV boluses for severe symptomatic (total serum Ca< 7.5mg/dl or <1.9
mmol/L) or ionized Ca < 4 mg/dl or 1 mmol/L
 Symptomatic hypocalcemia is an emergency
- Administer 1g Calcium Chloride or Ca Gluconate (1000 mg of elemental calcium/10ml)
IV over 10 mins.
 Refractory hypocalcemia: continuous infusion of elemental calcium. Note: Avoid ringer lactate
when infusing calcium preparations
 Vitamin D supplementation
 Correct hypomagnesemia, if present

Nursing Management
o Assess IV site for patency. Don’t administer Calcium if there is a risk for leakage into the tissues.
o May be given by slow IV push (dilute with normal saline for injection prior to administration.
o Frequently monitor serum calcium levels and response to therapy. o Administer oral calcium
preparations 1-1.5 hours after meals and at bedtime. o Give calcium tablets with full glass of water.
o Diet high in calcium:
• Food High in calcium- leafy green, sardines, dairy, cheese, milk, broccoli and tofu
• Administer Medicine-calcium acetate , IV calcium with Vitamin D
• Safety-Risk for fall, fractures and bleeding
• Teach-
Take: calcium boosters
Avoid: calcium depletors, laxatives, loop diuretics