FLUIDS AND ELECTROLYTES: BALANCE AND DISTURBANCE

Fluid and electrolyte balance is

essential to your body’s
homeostasis.
Body Fluids

Refers to body water in which electrolytes are

dissolved.

Been described as “a sea within”

Water is the largest single constituent of the body,

representing 45% - 75% of the body weight
Body Fluids

FACTORS THAT INFLUENCE

AMOUNT OF BODY
FLUIDS
• Age
• Gender
• Body fat
 Functions of Body Fluids

Transport nutrients to the cells and carries waste products away

from the cells.

Maintains blood volume.

Regulates body temperature.

Serves as aqueous medium for cellular metabolism.

 Functions of Body Fluids

Assists in digestion of food through hydrolysis.

Acts as solvents in which solutes are available

for cell function.

Serves as medium for the excretion of waste

products.
Body fluids are •1. Intracellular fluid
distributed in compartment (ICF)
the body in two •Fluid inside the cells
compartments: •Contains 2/3 of body
fluids
•Located primarily in
skeletal muscle mass
Body fluids are •2. Extracellular (ECF)
distributed in •Outside the cell
the body in two •Contains 1/3 of body
fluids
compartments:
•maintains blood volume
and serves as the
transport system to and
from the cells
Body fluids are •ECF subdivided
distributed in further into:
the body in two •Interstitial fluid
compartments: •Intravascular fluid
•Transcellular
 I. Intravascular
Body fluids are • Fluid within blood vessels
distributed in • Contains plasma (3 L out
of the average 6 L blood
the body in two volume)

compartments:
II. Interstitial
• Fluids that surrounds the
cells (11 to 12 L)
• Ex: lymph
 III. Transcellular
Body fluids are • 1-3% of body weight
distributed in • Approximately 1-2 L
• Cerebrospinal fluid, pericardial fluid,
the body in two synovial fluid, pleural fluids
compartments: • Sweat
• Digestive secretions
 • There is a continuous exchange of
Note: fluid between the fluid
compartment, of these spaces,
only the plasma is directly
influenced by the intake or
elimination of fluid from the body.
• third-space fluid shift or “third
spacing” where there is a loss of
ECF into a space that does not
contribute to the equilibrium
between ICF and ECF.
 “Third spacing” occurs in:

• ascites
• burns
Note: • peritonitis
• bowel obstruction
• massive bleeding into a joint or
body cavity.
 Chemical compounds in
solution that have the ability
to conduct an electrical
current.
ELECTROLYTES

They break into ions:

Cations carry • Sodium – primary cation in
positive charges; the ECF; important in
regulating fluid volume
Anions carry • Chloride – primary anion
negative charges in the ECF
• Potassium – primary
cation in the ICF
• Phosphates and sulfates –
primary anions in the ICF
 Promote promote neuromuscular irritability

General Maintain maintain body fluid volume and osmolality.

Functions of
electrolytes: Distribute distribute body water between compartments

Regulate regulate acid-base balance

•Movements of Water and
Electrolytes
•PASSIVE TRANSPORT
•Diffusion
•Osmosis
•Filtration
•2. ACTIVE TRANSPORT
 Passive transport
• a.Diffusion
Movements of • movement of particles from an area of
higher to lower concentration within
Water and one compartment.
Electrolytes • occurs through the random movement
of ions and molecules.
• particles will distribute themselves
evenly.
• an example is the exchange of O2 and
CO2 between the pulmonary
capillaries and alveoli.
 Passive transport
Movements of • b. Osmosis
Water and • movement of fluid from an area
of lower concentration to
Electrolytes higher concentration across the
semi-permeable membrane.
• normal serum osmolality is 280-
300mOsm/kg.
• osmolality of ECF and ICF is
always equal.
Movements of •Important terms:
Water and •Tonicity
•is the ability of all the
Electrolytes solutes to cause an
osmotic driving force
that promotes water
movement from one
compartment to another
• Osmolality
• reflects the concentration of fluid that affects the
movement of water between fluid compartments by
osmosis.
• Also measures the ability of a solution to create
osmotic pressure and affect movement of water.
(mOsm/kg)

• Osmolarity
• reflects the concentration of solutions. (mOsm/L)
• Oncotic pressure
• is the osmotic pressure exerted by proteins (ex.
albumin)

• Osmotic diuresis
• occurs when the urine output increases due to the
excretion of substances such as glucose, mannitol, or
contrast agents in the urine.
 Passive transport
Movements of • c. Filtration
Water and • is the process by which
water and diffusible
Electrolytes substances move together
in response to fluid
pressure. This process is
active in capillary beds.
• an example is the passage of
water and electrolytes from the
arterial capillary bed to the
interstitial fluid.
• Hydrostatic pressure
• blood entering the capillaries does so at
a pressure greater that the interstitial
pressure, so fluid and solutes move out
of capillaries. At the venous end of the
capillary bed, hydrostatic pressure is
less than the interstitial pressure and
fluid and waste products move back
into capillaries.
 2. Active transport
Movements
of Water •movement of ions from
an area of lesser to
and greater concentration
Electrolytes with an ion pump.
•(Na –K pump)
Concentration of Fluids

•Isotonic
•Hypotonic
•Hypertonic
 • Isotonic
• Exerts the same osmotic
pressure as that found in
Concentration plasma. Osmolarity is 240-
340mOsm/L.
of Fluids • Hypotonic
• Exerts less osmotic pressure than
that of blood plasma. Osmolarity is
less than 240 mOsm/L
• Hypertonic
• Exerts a higher osmotic
pressure than that of blood
plasma. Osmolarity is more
than 340mOsm/L.
 •Kidneys
•Daily urine volume: 1 to 2 L
REGULATION OF •Normal output should be 1
BODY FLUIDS mL/kg/hr
AND •Skin
ELECTROLYTES •Insensible water loss
through the skin: 600 mL
REGULATION OF •Adrenal glands
BODY FLUIDS •The adrenal glands
AND secrete aldosterone.
ELECTROLYTES
REGULATION OF •Aldosterone:
BODY FLUIDS •Retains sodium and
AND water.
ELECTROLYTES
•Excretes potassium
at the same time.
sodium and potassium have
an inverse relationship.
REGULATION OF BODY FLUIDS AND
ELECTROLYTES
Aldosterone:
• Retains sodium and water.
• Excretes potassium at the same time.
• Builds up vascular volume, which makes the BP

to increase
Remember, more vascular volume means more
blood pressure.
REGULATION OF BODY FLUIDS AND
ELECTROLYTES
Lungs
•The lungs regulate fluid by releasing water as
vapor with every exhalation. Every time you
exhale, water is lost
•Gastrointestinal tract
•Usual loss is around 100 to 200 mL
REGULATION OF BODY FLUIDS AND
ELECTROLYTES
•Cardiovascular system
•Pumps and carries fluids and other good stuff
throughout the body, to the vital organs,
especially to the kidneys
REGULATION OF BODY FLUIDS AND
ELECTROLYTES
Pituitary gland
•antidiuretic
hormone (ADH),
which causes
retention of
water.
REGULATION OF BODY FLUIDS AND
ELECTROLYTES
Parathyroid glands
•The parathyroid glands secrete parathyroid
hormone (PTH).
REGULATION OF BODY FLUIDS AND
ELECTROLYTES
Parathyroid glands
•The parathyroid glands secrete parathyroid
hormone (PTH).
•This causes an increase in serum calcium by
pulling it from the bones and placing the
calcium in the blood.
REGULATION OF BODY FLUIDS AND
ELECTROLYTES
Thyroid gland
The thyroid gland releases thyroid hormones.
• Providing energy
• Increasing pulse rate
• Increasing cardiac output
• Increasing renal perfusion
• Increasing diuresis
• Ridding of excess fluid
REGULATION OF BODY FLUIDS AND
ELECTROLYTES
Hypothalamus
•thirst response
•AGE matters
REGULATION OF BODY FLUIDS AND
ELECTROLYTES
Small intestine
•absorbs 85% to 95% of fluid from ingested food
•delivers it into the vascular system
REGULATION OF BODY FLUIDS AND
ELECTROLYTES
Lymphatic system
•moves water and protein back into the vascular
space
How do we lose fluid?

We lose fluid by 2 ways:

1. Sensible
2. Insensible
How do we lose fluid?
1. Sensible fluid loss:
✓loss that is SEEN
✓urine, sweat, and feces.
✓Kidneys--800 to 1500 mL/day
✓NGT
How do we lose fluid?
2. Insensible fluid loss:
loss that is NOT SEEN
• Occurs through the intestinal tract, lungs, and

skin.
•Skin—water evaporation
•Lungs- approximately 500 mL/day
•GI-100 to 200 mL/day
Abnormal fluid loss
Abnormal fluid loss results from a physiologic
imbalances.
Examples include:
✓Fever or an increased room temperature
✓Severe burns
✓Hemorrhage
✓Emesis
Abnormal fluid loss
Abnormal fluid loss results from a physiologic
imbalances.
✓Fistulas
✓Secretions
✓Wound exudates
✓Paracentesis
✓Thoracentesis
✓Diaphoresis
DEHYDRATION
The 2 types of dehydration are:
1. Mild dehydration:
2% loss of body weight, which equals 1 to 2 L of
body fluid.
2. Marked dehydration:
5% loss of body weight, which equals 3 to 5 L of
body fluid.
How do we measure electrolytes?
• 1.mg/dL (deciliter)
• measures the weight of the particle in a certain amount of
volume.
• 2. mEq/L
• milliequivalent is one-thousandth of an equivalent
• the amount of a substance that will react with a certain number of
hydrogen ions. This is measured per liter of fluid. Simply put, this is
atomic weight.
How do we measure electrolytes?
3. mmol/L (millimoles/liter)
• millimole is one-thousandth of a mole per liter of
fluid.
• Basically, this measurement offers an in-depth analysis
of the electrolyte being evaluated.
Where do electrolytes live in the body?
Electrolytes can be found all over the body.
1.Potassium: found inside the cell; the most
plentiful electrolyte in the body.
2.Magnesium: found inside the cell; second most
plentiful electrolyte in the body.
3.Sodium: numero uno electrolyte in the
extracellular fluid.
Where do electrolytes live in the body?
Electrolytes can be found all over the body.
4.Phosphorus: found inside the cell and in the
bones.
5.Calcium: found mainly in bones and teeth;
some floats around in the blood as well.
6.Chloride: found inside the cell, the blood, and
the fluid between cells.
Hormones
Hormones help keep electrolytes within normal
range.
1. Insulin
•moves potassium from the blood to the inside of
the cell, causing the serum K to drop.
Hormones
Hormones help keep electrolytes within normal
range.
2. Parathyroid hormone (PTH)
•moves calcium from the bone into the blood
when serum calcium levels are low.
•causes the serum calcium to increase.
Hormones
Hormones help keep electrolytes within normal
range.
3. Calcitonin:
moves calcium into the bones as needed.
When the serum calcium is too high, calcitonin
increases and moves calcium from the blood into
the bone.
This causes serum calcium to decrease.
How do we get rid of excesselectrolytes?
Excess electrolytes are excreted by:
• Urine, feces, and sweat.
• Aldosterone:
• causes sodium and water retention while causing
potassium excretion through the urine.
• PTH:
• increases urine excretion of phosphorus and
decreases urine excretion of calcium.
What causes decreased oral electrolyte intake?
•Anorexia
•Feeling weak
•Shortness of breath
•GI upset
•Income
•Fad dieting (low in potassium)
Abnormal electrolyte losses
•Vomiting
•Nasogastric (NG) suction
•Intestinal suction
•Drainage
Abnormal electrolyte losses
•Paracentesis
•Diarrhea
•Diuretics
•Kidney trauma, illness,
CASE IN POINT
A common nursing order is “nothing by mouth”
(NPO).
What causes electrolyte excess in the blood?
•Kidney trauma, illness, or disease
•Massive blood transfusions
•Tumors
•Crushing injuries
•Chemotherapy
Substances that can alter fluid balance
1. Plasma protein.
2. Glucose.
Substances that can alter fluid balance
1. Plasma protein
Plasma protein holds on to fluid in the vascular
space.
Albumin – AKA as Colloids
CASE IN POINT
•If a client is badly burned, malnourished
(decreased protein intake), or has a disease
where the liver is not making adequate amounts
of albumin, problems can occur.
• Adequate albumin needed to hold fluid in the

vessels may not exist; therefore, the fluid may

leak out of the vessels into the tissues and cause
shock.
Substances that can alter fluid balance
2. Glucose
•The vascular space likes the particle-to-water
ratio to be equal.
CASE IN POINT
•When the blood sugar is very high, as in
diabetics, the blood has too many glucose
particles compared to water in the vascular
space. This causes particle-induced diuresis
(PID), sometimes called osmotic diuresis.
HYPERVOLEMIA
AND
HYPOVOLEMIA
✓Fluid volume deficit
✓Fluid volume excess
Fluid volume deficit
Fluid volume deficit (FVD) results when fluid loss
exceeds fluid intake.
sodium and water are lost in equal amounts
from the vascular space.
•Also called hypovolemia or isotonic
dehydration.
*Not the same as dehydration.
What causes it?
•Decreased intake or poor appetite
•Drugs that affect fluids and electrolytes
•Diuresis
•Forgetting to drink and eat
•Poor response to fluid changes
•Vomiting
What causes it?
•Diarrhea
•GI suction
•Diuretics
•Impaired swallowing
•Tube feedings
•Fever
What causes it?
•Laxatives
•Hemorrhage
•Third spacing
Signs and symptoms
•Acute weight loss
•Decreased skin turgor (tenting occurs)
•Postural hypotension (orthostatic hypotension)
•Increased urine specific gravity
Signs and symptoms
•Weak, rapid pulse
•Cool extremities
•Dry mucous membranes
•Decreased BP
Signs and symptoms
•Decreased peripheral pulses
•Oliguria
•Decreased vascularity in the neck and hands
•Decreased central venous pressure
•Increased respiratory rate
Diagnostic tests and treatments
Laboratory testing for FVD include:
• serum electrolytes
• Hct
• Urine specific gravity
Treatment measures:
✓oral or IV fluid replacement
✓if is due to hemorrhage or blood loss---blood
products
Complications
✓Shock.
✓Poor organ perfusion, leading to acute tubular
necrosis and renal failure.
✓Multiorgan dysfunction due to poor perfusion.
✓Decreased cardiac output.
Fluid volume excess
fluid volume excess (FVE) results when fluid
intake exceeds fluid loss.
•Excessive retention of water and sodium in the
extracellular fluid (ECF).
• Also called hypervolemia or isotonic

overhydration.
Causes
•Renal failure
•CHF
•Cushing syndrome
•Excessive sodium: from IV normal saline or
lactated ringers(iatrogenic)or foods
•Blood product administration
•Increased ADH
Causes
•Medications
•Liver disease
•Hyperaldosteronism
•Burn treatment
Signs and symptoms
•Jugular vein distension ( JVD)
•Bounding pulse, tachycardia
•Abnormal breath sounds
•Polyuria
•Decreased urine specific gravity
•Dyspnea and tachypnea
•Increased BP
Signs and symptoms
•Increased central venous pressure (CVP)
•Edema
•Productive cough
•Weight gain
Diagnostic tests and treatments
Tests:
•Serum Electrolytes
•BUN and Creatinine
•Chest x-ray:
• If the heart is enlarged, as can be seen with an x-
ray, this could mean congestive heart failure.
Diagnostic tests and treatments
Treatments:
•Treat the cause
•Loop diuretics: Furosemide (Lasix)
•Potassium-Sparing Diuretics: Spironolactone
(Aldactone)
•Dietary Sodium Restrictions
Complications

•CHF
•pulmonary edema
In fluid volume deficit and fluid volume excess,
the osmolarity and serum sodium are not
affected as the client loses fluid and sodium
proportionately.
SODIUM
Sodium imbalances
The following apply to the electrolyte sodium:
• Chief electrolyte in ECF.
• Assists with generation and transmission of

nerve impulses.
• An essential electrolyte of the sodium–

potassium pump in the cell membrane.

Sodium imbalances
Food sources: bacon, ham, sausage, catsup,
mustard, relishes, processed cheese, canned
vegetables, bread, cereals, snack foods.
Excess sodium is excreted by kidneys.
Excretion of sodium retains potassium.
Normal adult sodium level is 135 to 145 mEq/L.
Helps maintain the volume of body fluids.
• Sodium is the only electrolyte that is affected by
water.
• Sodium level decreases when there is too much
water in the body.
• Conversely, sodium level increases with less
water in the body.
Renin–angiotensin system

•ECF (vascular volume) decreased → Renin

produced by the kidneys →Angiotensin I
converted to angiotensin II →Aldosterone
secreted → Sodium and water retained.
•If sodium and water are retained or lost
equally then there will be no change in
serum sodium.
Hyponatremia
Serum sodium less than 135 mEq/L.
Hyponatremia is:
• Not enough sodium in the ECF (vascular space).
• Possibly, there is too much water diluting the
blood which makes serum sodium go down.
• Anytime there is a sodium problem there is a
fluid problem as well.
Hyponatremia classification according to ECF
volume level
• HYPOVOLEMIC HYPONATREMIA
• HYPERVOLEMIC HYPONATREMIA
• ISOVOLUMIC HYPONATREMIA
Causes
• Excessive administration of D5W
• Diuretics
• Wound drainage
• Psychogenic polydipsia
• Decreased aldosterone
• Low-sodium diet
Causes
• Syndrome of inappropriate antidiuretic hormone
(SIADH)
• Vomiting and sweating
• Replacing fluids with water only
• Muscle weakness
Signs and symptoms
• Decreased deep tendon reflexes (DTRs)
• Diarrhea
• Respiratory problems
Diagnostic tests and treatments

• Tests:
• hyponatremia is serum electrolytes
• Treatment:
• Depends on the cause
• 0.9% normal saline IV
• 3% Saline
Diagnostic tests and treatments
• Watch for FVE
• Increased dietary Sodium
• If appropriate, discontinue drugs/treatments
that could be causing sodium loss.
COMPLICATIONS
• Seizures and brain damage are the major
complications associated with hyponatremia.
• Also, consider what caused the hyponatremia
when determining what could harm your
patient.
Hypernatremia
• serum sodium greater than 145 mEq/L
• similar to dehydration:
• there is too much sodium and not enough water in
the body.
Causes
• Anything that causes an increased “water” loss
or excessive sodium intake can cause
hypernatremia.
Causes
• Administration of IV normal saline without
proper water replacement
• Hyperventilation
• Watery diarrhea
• Hyperaldosteronism
• Renal failure
Causes
• Heat stroke
• NPO status
• Infection
• Diabetes insipidus
• Tachycardia
Signs and symptoms
• Dry, sticky mucous membranes
• Thirst
• Changes in level of consciousness (LOC)
• Decreased heart contractility
• Seizure
• Muscle twitching
Signs and symptoms
• Muscle weakness
• Decreased DTRs
Diagnostic tests and treatments
• Tests:
• serum electrolytes
• Treatment:
individualized/specific depending on the cause.
• Restrict all forms of sodium: Foods can have
excess sodium as well as drugs and IV fluids.
COMPLICATIONS
• As with hyponatremia, seizures and brain
damage are the major complications associated
with hypernatremia.
POTASSIUM
Potassium imbalances
• Makes skeletal and cardiac muscle work
correctly.
• Major electrolyte in the intracellular fluid.
• Potassium and sodium are inversely related
(when one is up, the other is down).
• Plays a vital role in the transmission of electrical
impulses.
Potassium imbalances
• Food sources: peaches, bananas, figs, dates,
apricots, oranges, melons, raisins, prunes,
broccoli, potatoes, meat, dairy products.
• Excreted by the kidneys.
• Stomach contains large amount of potassium.
• Normal potassium level: 3.5 mEq/L to 5.0 mEq/L
Hypokalemia
• serum potassium below 3.5 mEq/L
• Paralytic ileus can occur from severe hypokalemia.
• Abdominal distension
• muscle cramps
• muscle weakness
Causes
• Diuretics
• Steroids
• GI suction
• Vomiting
• Diarrhea
• NPO status; poor oral intake
• Age
Causes
• Cushing syndrome
• Kidney disease
• Alkalosis
• IV insulin
Signs and symptoms
• Muscular weakness, cramps, flaccid paralysis
• Hyporeflexia
• Life–threatening arrhythmias
• Slow or difficult respirations
• Weak, irregular pulse
Signs and symptoms
• Decreased bowel sounds
• Decreased LOC
Diagnostic tests and treatments
Tests:
• serum electrolytes
• EKG (shows flattened T wave, depressed ST
segment, and a U-wave)
Diagnostic tests and treatments
Treatments:
• determine the cause
• High potassium diet
• IV or oral potassium chloride
• check for proper kidney function or good urine
output.
• A good rule to remember when administering IV K
is not to exceed 20 mEq/hour.
Diagnostic tests and treatments
• Clients taking a cardiac glycoside with a diuretic
should be monitored closely for hypokalemia,
which can potentiate the cardiac glycoside and
cause toxicity
• switched to a potassium-sparing diuretic
COMPLICATIONS
• life-threatening arrhythmias
• arrhythmias  decreased cardiac output 
resulting in hypotension.
• Respiratory depression may also occur.
Hyperkalemia
• serum potassium greater than 5.0 mEq/L.
• In severe hyperkalemia, ascending flaccid
paralysis of the arms and legs may be seen;
• this paralysis moves distal to proximal.
Causes
• Renal failure
• IV potassium chloride overload
• Burns or crushing injuries
• Tight tourniquets
• Hemolysis of blood sample
• Incorrect blood draws
Causes
• Salt substitutes
• Potassium-sparing diuretics
• Blood transfusions
• ACE inhibitors
• Tissue damage
• Acidosis
Causes
• Adrenal insufficiency (Addison’s disease)
• Chemotherapy
Signs and symptoms
• Begins with (1)muscle twitching associated with
tingling and burning; (2)progresses to
numbness, especially around mouth;
(3)proceeds to weakness and flaccid paralysis
• Excess potassium interferes with skeletal and
smooth muscle contraction, nerve impulse
conduction, acid–base balance, enzyme action,
and cell membrane function
Signs and symptoms
• Diarrhea
• Smooth muscles of the intestines hyper contract, resulting
in increased motility
• Dysfunctional nerve impulse conduction and smooth
muscle contraction
Signs and symptoms
• Cardiac arrhythmia;
• bradycardia; EKG changes: peaked T-wave, flat or
no P-wave, wide QRS complex; ectopic beats on
EKG leading to complete heart block, asystole,
ventricular tachycardia, or ventricular fibrillation
Diagnostic tests and treatments
Tests:
• serum electrolytes
• ECG will also be assessed
Diagnostic tests and treatments
Treatments:
• depends on the primary cause.
• IV insulin in conjunction with 10–50% glucose IV (IV

insulin will lower the serum K by pushing it into the

cell.
• Administration of sodium polystyrene sulfonate
(Kayexalate) with 70% sorbitol
• Kayexalate---serum sodium as hypernatremia can
occur.
Diagnostic tests and treatments

• Diuretics to increase renal excretion of K.

• 10% calcium gluconate IV (to decrease myocardial
irritability).
• Hemodialysis
• Peritoneal dialysis
• Limit high potassium foods.
• Limit drugs which could cause retention of K
(aldactone).
Complications
• monitor clients for dehydration, neurological
changes, and life-threatening arrhythmias.
CALCIUM
Calcium imbalances
• Acts like a sedative on muscles.
• Most abundant electrolyte in the body.
• Has an inverse relationship to phosphorus.
• Necessary for nerve impulse transmission,

blood clotting, muscle contraction, and

relaxation.
• Needed for vitamin B12 absorption.
Calcium imbalances
Promotes strong bones and teeth.
Who needs extra calcium?
• Children, pregnant women, lactating women.
Food sources: milk, cheese, dried beans.
Must have vitamin D present to utilize calcium.
Calcium imbalances
If blood levels of calcium decrease, the body takes
calcium from the bones and teeth. (to build the blood
level back up)
Parathyroid hormone (PTH) increases serum calcium
by pulling it from the bones and putting it in the blood.
Calcitonin decreases serum calcium by driving the
blood calcium back into the bones.
Normal calcium: 9.0 to 10.5 mg/dL
Hypocalcemia
• serum calcium level drops below 9.0 mg/dL.
• When calcium is decreased, think “not sedated.”
Causes
• Decreased calcium intake
• Kidney illness
• Decreased vitamin D
• Diarrhea
• Pancreatitis
Causes
• Hyperphosphatemia
• Thyroidectomy
• Medications (calcium binders)
Signs and symptoms
• Muscle cramps
• Tetany
• Convulsions
• Arrhythmias
• Positive Chvostek’s sign
• Positive Trousseau’s sign
Signs and symptoms
• Laryngeal spasm
• Hyperactive DTRs
• Cardiac changes: decreased pulse, prolonged ST
interval, prolonged QT interval, decreased
myocardial contractility
• Calcium regulates depolarization in the cardiac
cells. If calcium is decreased, depolarization is
impaired
Signs and symptoms
• Respiratory arrest
• LOC changes
• Increased gastric activity
Diagnostic tests and treatments
Tests:
• assess the electrolytes
• ECG may be performed
Diagnostic tests and treatments
• dependent on the cause
• IV calcium
• heart monitor
• Vitamin D therapy
• Increase dietary calcium
Complications
• Seizures, laryngospasm, respiratory arrest, and
arrhythmias
Hypercalcemia
• serum calcium level that exceeds 10.5 mg/dL.
• If there is increased Ca in the blood, think that
the muscles will be “sedated”
Causes
• Decreased DTRs
• Muscle weakness
• Renal calculi
• Pathological fractures
• Central nervous system (CNS) depression:
lethargy, coma, confusion
Signs and symptoms
• Early cardiac changes: increased P-wave;
decreased ST interval; wide T-wave; increased
BP
• Late cardiac changes: decreased pulse moving to
cardiac arrest
• Respiratory arrest
• Decreased bowel sounds
Signs and Symptoms
• Increased urine output
• Increased clotting times
• Kidney stones
Diagnostic tests and treatments
Tests:
• assess the serum electrolytes.
• ECG
• X-ray
• UTZ
• Urinalysis
Diagnostic tests and treatments
Treatment:
• dependent on the cause
• Normal Saline IV
• Excess calcium: think SEDATED
• IV phosphate
Complication
• Respiratory depression and arrhythmias
CHLORINE
HYPERCHLOREMIA
•Excess Chloride in the ECF
•Serum Cl level: greater than 106 mEq/L
•Hyperchloremia is associated with
hypernatremia
•Inverse relationship with bicarbonate
•HYPERCHLOREMIC METABOLIC ACIDOSIS
Causes
•Excessive Cl intake
•Renal Tubular Necrosis
•DHN
•Excessive reabsorption of Cl from GI tract
•Excessive intake of NaCl with water loss
•Hypernatremia
Assessment Findings
•Lethargy
•Drowsiness
•Weakness
•Dyspnea
•Tachypnea
•Headache
Diagnostic Findings and Treatments
•Serum Cl (electrolyte)
•Serum Na (electrolyte)
•Fluid administration
•Restricted Na and Cl intake
PHOSPHORUS
Phosphorus imbalances
•Promotes the function of muscle, red blood cells
(RBCs), and the nervous system.
•Assists with carbohydrate, protein, and fat
metabolism.
•Food sources: beef, pork, dried peas/beans,
instant pudding.
Phosphorus imbalances
•Has an inverse relationship with calcium.
•Regulated by the parathyroid hormone.
•Normal phosphorus is 3.0 to 4.5 mg/dL.
•Remember that phosphorus and calcium have an
inverse relationship!
Hypophosphatemia
•serum phosphate that is below 3.0 mg/dL.
Causes
•Hypophosphatemia looks just like
hypercalcemia.
Signs and symptoms
•Hypophosphatemia looks just like
hypercalcemia.
Diagnostic tests and treatments
Tests:
•Serum electrolytes
•X-ray
Diagnostic tests and treatments
Treatment:
•Supplemental Phosphorus
•IV phosphorus is given when phosphorus drips
below 1 mg/dL and when the GI tract is
functioning properly
•Additional treatments depend on the underlying
cause.
Complication
•respiratory depression and arrhythmias
Hyperphosphatemia
•serum phosphate level that is above 4.5 mg/dL.
Causes
•Hyperphosphatemia looks just like
hypocalcemia.
Signs and symptoms
•Hyperphosphatemia looks just like
hypocalcemia.
Diagnostic test and treatments
Tests:
•check electrolyte levels.
•X-ray
Diagnostic test and treatments
Treatment:
•underlying cause must be treated
•Administer of vitamin D preparations such as
calcitrol (rocaltrol)
•Administration of phosphate-binding gels
•Restriction of dietary phosphorus
•Possibly dialysis
Complications
•Seizures, laryngospasm, respiratory arrest, and
arrhythmias
MAGNESIUM
Magnesium imbalances
Present in heart, bone, nerves, and muscle
tissues.
Second most important intracellular ion.
Assists with metabolism of carbohydrates and
proteins.
Helps maintain electrical activity in nerves and
muscle.
Magnesium imbalances
Also acts like a sedative on muscle.
Food sources: vegetables, nuts, fish, whole grains,
peas, beans.
Magnesium levels are controlled by the kidneys
(excreted by kidneys).
Normal magnesium: 1.3 to 2.1 mEq/L.
Magnesium imbalances
Can cause vasodilatation.
The majority of magnesium comes from our
dietary intake.
Hypomagnesemia
•serum magnesium level below 1.3 mEq/L.
Causes
•Diarrhea
•Diuretics
•Decreased intake
•Chronic alcoholism
•Medications
•Decreased magnesium levels increase nerve
impulses. Think: NOT SEDATED.
Signs and symptoms
•Increased neuromuscular irritability
•Seizure
•Hyperactive DTRs
•Laryngeal stridor
Signs and symptoms
•Positive Chvostek’s and Trousseau’s signs
•Cardiac changes: arrhythmias; peaked T-waves;
depressed ST segment; ventricular tachycardia;
ventricular fibrillation; irregular heartbeat
•The heart is a smooth muscle. If there is not
enough magnesium to sedate it, impaired nerve
conduction and muscle spasms can occur
Signs and symptoms
•Dysphagia
•Decreased GI motility
•Changes in LOC
Diagnostic tests and treatments
Tests:
•assess the serum electrolytes.
•Urinalysis
•ECG
•New diagnostic tests include nuclear magnetic
resonance spectroscopy and ion-selective
electrode tests
Diagnostic tests and treatments
Treatment:
•underlying cause must be identified and treated.
• Increased dietary magnesium
•Magnesium salts
•Magnesium sulfate IV
Complications
•Laryngospasm.
• Aspiration due to dysphagia.
• Arrhythmias.
Hypermagnesemia
•serum magnesium level above 2.1 mEq/L.
•Remember magnesium acts like a sedative.
“THINK SEDATED” with hypermagnesemia.
Causes
•Renal failure
•Increased oral or IV intake
•Antacids
Signs and symptoms
•BP decreases
•Facial warmth and flushing
•Drowsiness to comatose state depending on
severity of imbalance
•Decreased DTRs
Signs and symptoms
•Generalized weakness
•Decreased respirations to respiratory arrest
depending on severity of imbalance
•Cardiac changes: decreased pulse, prolonged PR,
wide QRS, cardiac arrest
Diagnostic tests and treatments
Tests:
•serum electrolytes
•ECG
Diagnostic tests and treatments
Treatments:
• depends on the primary cause
• Decrease magnesium salt administration
• If in an emergency situation, respiratory support may be
needed
• Hemodialysis with magnesium free dialysate
• Loop diuretics
• 0.45% saline solution and/or IV calcium gluconate to help
balance the magnesium levels.
Complications
•arrest, cardiac arrest, and hypotension.
A client presents to the emergency department
(ED) with tachycardia, elevated blood pressure,
and seizures. Further assessment reveals a history
of chronic alcoholism, causing the nurse to
suspect:
a. Magnesium deficit.
b. Sodium deficit.
c. Potassium excess.
d. Calcium excess.
Respiratory acidosis
 • An acid–base imbalance that
occurs when the pH is
decreased, partial pressure of
carbon dioxide (PCO2) is
increased—greater than 45
Respiratory mm Hg.
acidosis • When you hypoventilate…?
• Carbon dioxide builds up in the
blood: Hypercapnia--buildup of
carbon dioxide in the blood to
levels greater than 45 mm Hg.
 respiratory acidosis: “breathing”

Decreased alveolar ventilation: carbon

Causes dioxide retention

Anytime poor gas exchange exists, CO2

builds up in the bloodà Respiratory
acidosis
 Respiratory arrest

Some drugs (narcotics, sedatives hypnotics,

anesthesia, ecstasy)

Causes Sleep apnea

Excessive alcohol

Surgical incisions (especially abdominal), broken

ribs
 Collapsed lung (pneumothorax, hemothorax)

Weak respiratory muscles (myasthenia gravis, Guillain–

Barré syndrome)

Airway obstruction (poor cough mechanism, laryngeal

spasm)
Causes
Brain trauma (specifically medulla)

High-flow O2 in chronic lung disease

Severe respiratory distress syndrome

 •Vary depending on the
initial cause:
•Neurological changes:
headache, confusion,
Signs and blurred vision, lethargy
symptoms coma,
•Papilledema
•Hyperkalemia
•Decreased muscle tone;
decreased DTRs
•Acute respiratory acidosis
causes hyperkalemia. With
chronic respiratory acidosis, the
K+ may be normal as the
kidneys have time to readjust
and get the K+ back into the
normal range.
 Signs and symptoms

• Vary depending on the initial cause:

• Neurological changes: headache,
confusion, blurred vision, lethargy
coma,
• Papilledema
• Hyperkalemia
• Decreased muscle tone; decreased DTRs
Signs and symptoms

Restlessness;
Hypotension Arrhythmias
tachycardia

Cardiac
Acidic urine Warm skin
arrest
 Diagnostic tests and treatments

• Treat the cause.

• Airway clearance: possible intubation.
• Administer drugs to open up the
airways and thin out secretions so
they can be coughed up.
• Increase fluids to liquefy secretions so
they can be coughed up more easily.
• Oxygen therapy.
 • Respiratory therapy: breathing
treatments.
• Elevate head of bed (HOB) for
Diagnostic lung expansion.
• Monitor ABGs.
tests and • Monitor for electrolyte
imbalances.
treatments • Monitor pulse oximetry.
• Administration of Pulmocare:
a tube feeding sometimes
used to decrease CO2
retention.
 MORE ON OXYGEN THERAPY
Diagnostic
tests and • low-dose oxygen-- chronic lung
treatments conditions
• high dose oxygen– acute lung
conditions
 •pH
•Less than 7.35
•PaCO2
•Greater than 45 mm Hg
What do the •PaO2
ABGs look •Less than 80 mm Hg
like? •HCO3
•Normal until kidney
compensation starts;
then will start to rise
above 26 mEq/L
What can • Respiratory arrest.
• Arrhythmias: leading to
harm my cardiac arrest and shock.
client? Severe decrease in LOC.
 • The name “respiratory” tips you off
to the fact that a lung problem
exists
• Since it is a lung problem, the
Recap of problem chemical is the acid carbon
dioxide
respiratory • Acidosis from a lung problem is
due to irregular breathing.
acidosis Perhaps the client is
hypoventilating— breathing
only 2 to 4 times a minute,
causing retention of carbon
dioxide (CO2).
 • Maybe the client has stopped
breathing altogether—
possibly not exhaling carbon
Recap of dioxide (CO2) at all. The
client retains all of this
respiratory carbon dioxide (CO2), which
acidosis causes a buildup of acid in
the body
• This buildup of acid causes
the pH to decrease.
Respiratory Alkalosis
Respiratory alkalosis

• an acid–base imbalance where the PaCO2 is less

than 35 mm Hg and the pH is greater than 7.45.
• Decrease PaCO2 in the blood: excessive
exhalation—hyperventilation.
• When the lungs are impaired, the kidneys
compensate with their own chemicals—
bicarbonate and H+.
• The kidneys will retain H+ because this is acid.
Respiratory alkalosis

• The kidneys will excrete bicarbonate because

this is base/alkalotic.
• This excretion of the base will help raise acid
levels and restore the body to a normal pH.
• Respiratory alkalosis means that the client has lost
excessive CO2 (acid), thus making the client
alkalotic.
• Hypocapnia: occurs when the CO2 is low
Causes

•High altitudes • Hysteria; anxiety

•Anemia • High mechanical ventilator

setting
•Hypoxia
• Aspirin overdose
•Labor and delivery • Fever
measures! • Sepsis
Signs and symptoms
•Hyperventilation
•Light-headedness, dizziness fainting
•Rapid pulse
•Hypokalemia
•Arrhythmias
• Hypocapnia stimulates the autonomic nervous
system, which cause anxiety, changes in
respiration, tingling, and sweating.
• Calcium acts like a sedative. Hypocapnia
decreases serum calcium so the muscles may get
tight. This can lead to tetany and seizures!
Why do you breathe into the brown
bag when you are hyperventilating?
 Diagnostic tests and treatments

Treat the cause. Monitor vital signs, Monitor electrolytes. Administer antianxiety
especially respirations. medications as ordered.
 • Place on
mechanical
ventilator to
control
respiratory rate
Diagnostic tests and in severe cases.
treatments • Monitor ABGs.
• Calm the client.
• Have client breathe into
paper bag or rebreather
mask to encourage CO2
retention.
 • pH
• Greater than 7.45 (alkalosis
makes pH go up)
• PaCO2
• Less than 35 mm Hg
What do the ABGs (because it is being exhaled)
look like? • PaO2
• Greater than 100 mm Hg
• HCO3
• Normal until kidney
compensation starts; then
will be less than 22 mEq/L
Complications

Life-threatening arrhythmias. Seizures.

Recap of respiratory alkalosis

• The name “respiratory” tips you off to the fact that a lung
problem exists
• Since it is a lung problem, the problem chemical is the acid
carbon dioxide (CO2)
• Excessive exhalation causes PaCO2 to decrease in the
blood. Acid is lost.
• When the lungs are impaired, the kidneys compensate with
their own chemicals—bicarbonate and H+. The kidneys will
retain H+ because this is acid.
Recap of respiratory alkalosis

• We want to keep acid since the body is

losing acid from the excessive exhalation.
•The kidneys will excrete bicarbonate—a
base—in order to create a more acidic
environment and return the pH to normal
•Respiratory alkalosis means that the client
has lost excessive CO2 (acid), thus making
the client alkalotic
Metabolic
Acidosis
Metabolic acidosis

•An acid–base imbalance where the pH is

less than 7.35 and the bicarbonate level is
less than 22 mEq/L.
• Acid (H+ ions) builds up in the body, or too
much bicarbonate has been lost from the
body.
Metabolic acidosis

• The less bicarb you have in the body, the more acid
you will be.
• Kidneys: Metabolic disorders
• Bicarbonate and H+
• The decrease in the alkaline substances (bases) causes
a build up of acids in the body, causing acidosis.
• Lungs: compensate in just a few minutes
Causes

• increased acid production (ex: DKA where ketones (acids)

increase in the body which decreases bicarbonate)
• Diabetic ketoacidosis, malnutrition, starvation
• Lactic acidosis
• Shock
• decreased acid excretion (ex: renal failure where there is
high amount of waste left in the body which causes the acids
to increase and bicarb can’t control imbalance)
• Kidney illness
Causes

•loss of too much bicarb (diarrhea)

•Gastrointestinal (GI) illness: diarrhea
•Drugs: Diamox, Aldactone
•Aspirin overdose
 if renal failure is the initial
cause, you will see signs and
symptoms related to renal
failure;
Signs and
symptoms
if diabetic, ketoacidosis is the
initial cause
 Hyperkalemia

Signs and Arrhythmias

symptoms Increased respiratory rate

Headache, decreased LOC, coma

Signs and symptoms

• Muscle twitching and burning, oral numbness,

weakness, flaccid paralysis (severe
hyperkalemia)
• A Kussmaul’s respiration is an increase in rate
and depth of respiration.
• When Kussmaul’s respirations are present, CO2
is being blown off in increased amounts.
Diagnostic tests and treatments

1 2 3 4 5
Monitor ABGs. Treat the Monitor and Monitor and Monitor and
cause. manage manage manage
hyperkalemia. arrhythmias. hypercalcemia.
Diagnostic tests and treatments

Administer Administer sodium bicarbonate IV to decrease acidity of blood.

Monitor Monitor LOC closely.

Administer Administer lactated Ringers (LR) given IV to increase base level.

Institute Institute seizure precautions (brain doesn’t like it when the pH is messed up).
What do the ABGs look like?

• pH
• Less than 7.35
• PaCO2
• Will decrease to less than 35 mm Hg as it is blown off
• PaO2
• Normal
• HCO3
• Less than 22 mEq/L
Sodium bicarbonate:
• should be used only as a quick, temporary fix for
increased acid levels and should be given
according to specific ABG values rather than
generously as we used to do in the past during
code situations.
Complications

Life-threatening
arrhythmias.

Cardiac arrest.
Recap of metabolic acidosis

• The problem is with the kidneys, not the lungs.

• Bicarbonate (base) and H+ (acid) are associated
with the kidneys.
• Metabolic acidosis can be caused by loss of
bicarbonate through diarrhea, and renal
insufficiency.
Recap of metabolic acidosis

•The decrease in the alkaline substances (bases)

causes a buildup of acids in the body. It can also
be caused by diseases that increase acid levels
(OFA)
•The lungs compensate increasing respiratory
rate and depth to blow off CO2 and increase pH.
This is called a Kussmaul’s respiration.
Metabolic alkalosis
Metabolic alkalosis

•an acid–base imbalance where the pH is

greater than 7.45 and the bicarbonate
level is greater than 26 mEq/L.
•There is an excess of base in the body
and a loss of acid.
•Basically, pH is increased and
bicarbonate is increased.
 Metabolic alkalosis

Metabolic: kidneys, which The lungs compensate by This compensates for the
involve bicarbonate and H+. retaining CO2 by means of alkalosis and helps the pH go
hypoventilation. down into normal range.
 Vomiting; bulimia; nasogastric (NG)
tube suctioning
Excess antacid ingestion

Blood transfusions
Causes
Sodium bicarbonate

Thiazide and loop diuretics

 Baking soda

Hypokalemia

Activation of renin–angiotensin system

Causes Steroids

Dialysis

Licorice
 Decreased
Arrhythmias, flattened
respirations,
T-wave
hypoventilation

Tightening of muscles,
Signs and Hypokalemia
tetany, LOC changes,
seizures, tingling in
symptoms fingers and toes

Hepatic
LOC changes
encephalopathy
 pH
Greater than 7.45
PaCO2
What do Normal; increases with compensation
the ABGs PaO2
look like?
Remains the same
HCO3
− Greater than 26 mEq/L
 Treating the cause of the acid–base imbalance (antiemetics
Treating for vomiting, etc.).

Monitoring Monitoring ABGs for further complications.

Diagnostic
tests and Treating Treating arrhythmias.
treatments
Stopping Stopping client bicarbonate intake.

Monitoring Monitoring potassium levels and correcting hypokalemia.

 Monitoring Monitoring respirations and LOC.

Assessing Assessing for hypotension.

Diagnostic
Treating Treating dehydration if present.
tests and
treatments Assessing Assessing DTRs.

Administering Administering
(increases H+).
ammonium chloride IV in severe cases to increase acidity

Administering Administering acetazolamide (Diamox) to increase excretion of bicarbonate

through the kidneys.
Complications

Metabolic alkalosis can cause the

following life- threatening illnesses:
•Arrhythmias.
•Cardiac arrest.
•Seizures.
 The problem is with the
Recap of kidneys, not the lungs
metabolic
alkalosis
Bicarbonate (base) and
H+ (acid) are associated
with the kidneys
 Metabolic alkalosis can be caused by
increased bicarbonate through
diuretic therapy, prolonged
nasogastric suctioning, and excessive
Recap of vomiting, resulting in ↑ pH levels
metabolic
alkalosis
The lungs compensate by retaining
CO2 by means of hypoventilation.
This compensates for the alkalosis
Metabolic alkalosis is
the most common acid–
base imbalance.

It accounts for 50% of

all acid–base
disturbances.
SUMMARY

• The respiratory and renal systems can be both

the cause and “cure” for pH imbalances.
• Remember that the lungs control carbon dioxide
levels and the kidneys control bicarbonate levels.
• By monitoring your client’s carbon dioxide,
bicarbonate, and pH levels you can successfully
prevent and treat any acid–base imbalances.
SUMMARY

•Acidosis:
•Think hyperkalemia and hypercalcemia.
•Alkalosis:
•Think hypokalemia and hypocalcemia.
END
Urinary System Disorder
and Management
Kidney and Nephron Anatomy
What is the role of the kidneys?

• In short, to filter the blood. The kidneys produce urine with

the assistance of the nephron. The urine contains waste and
excessive water/minerals we don’t need. The kidneys want to
maintain a fine balance of water and electrolytes in the body
and remove excessive waste.
• You have two kidneys (right and left).
• The right kidney sits lower than the left kidney. WHY? To help accommodate
the large size of the liver, which sits right above the right kidney.
• The kidneys receive fresh blood from the heart via the renal artery, and drains
filtered blood back to the heart via the renal vein.
• The nephron is the functional part of the kidney….meaning it is where urine is
produced.
• Each kidney contains MILLIONS of nephrons which are found in the renal
cortex and renal medulla of the kidney.
• The nephron consists of the following parts:
• Renal Corpuscle (function is to FILTER the blood and create filtrate)
• Glomerulus
• Bowman ’s capsule
• Renal Tubule (function is to REABSORB and SECRETE substances IN or
OUT of the filtrate with the assistance of the peritubular capillaries)
• Proximal Convoluted Tubule
• Loop of Henle
• Distal Convoluted Tubule
• Collecting Tubule
Basic Parts of the
Kidney:
• Renal Capsule: outer layer of the kidney that gives the kidney its shape
and protects the kidney from infections that may occur from surrounding
organs.
If you slice the kidney in half you will see:
• Renal cortex: outside layer that contains the renal corpuscles (glomerulus
and bowman’s capsule which primary functions are to FILTER the urine)
and renal tubules EXCEPT the loop of HENLE ( it is found in the renal
medulla).
• Renal medulla: inside layer (found within the renal pyramids) which is very
hypertonic “salty”. These conditions help maintain water and salt balance
in our body with the help of the nephron, specifically the Loop of Henle.
• Renal artery: takes fresh oxygenated blood that came from the heart to the
kidney to be filtered. It further branches off around the renal columns into the
renal cortex into arterioles (afferent/efferent) then peritubular capillaries.
• Renal vein: take filtered blood back to the heart to be re-oxygenated and
pumped to the body. It comes from the efferent arterioles.
• Renal pyramids: found within the renal medulla which contains the loop of
henle and parts of the collecting tubule.
• Renal papilla: pointed projection of the renal pyramid that project into
the minor calyx and major calyx
• Minor and Major calyx along with the renal pelvis, ureters,
bladder, and urethra play a role in draining out the urine that
has left the nephron.
• Nephrons: the functional part of the kidneys that filters the
blood (renal corpuscle), reabsorbs minerals/water and secretes
waste (renal tubule), and produces the substance called urine
which will drain down into the ureters, be stored in the
bladder, and voided out via the urethra.
Individual role of each part of the nephron:

How does the nephron receive its blood supply?

• From the AFFERENT ARTERIOLE…the afferent arteriole
sends blood to the first part of the nephron called the
Glomerulus.
• Glomerulus: It is a collection of
circular capillaries that have extremely
high pressure which help perform
ULTRAFILTRATION. During this
process the blood will be filtered and
FILTRATE will be created (which is a
liquid consisting of the collection of
fluid and particles that came from the
blood). These substances will “drip”
down into a capsule that surrounds
the glomerulus called BOWMAN’S
CAPSULE (collects the filtrate).
What drips down?

• Water
• Ions: sodium, chloride, calcium, potassium, magnesium, phosphate,
bicarbonate
• Amino acids
• Glucose
• Creatinine
• Urea
****not filtered blood cells or proteins
• Then the newly filtered blood exits via the EFFERENT
arterioles which will go on and form the peritubular capillaries
that will surround the nephrons. The peritubular capillaries on
the loop of henle are known as the vasa recta.
• The peritubular capillaries will play a role in carrying the
reabsorbed nutrients from the filtrate back into the body’s
system to the renal vein and secreting substances (urea, ions)
and drugs found in the blood into the tubules at certain points.
• Side Note….why do we called it RE-absorption rather the just absorption? The
substances filtered from the glomerulus where already ABSORBED at some point in the
GI tract via specialized cells which took the nutrients into the blood stream (most of this
happens in the small intestine). Then the substances traveled through the body via the
heart and made their way to the kidneys via the renal artery to be FILTERED out.
Therefore, our body will RE-ABSORB these nutrients based on what our body needs
(because we already absorbed them once from the food we ate). Then the left overs
will be excreted in the urine.
• The created filtrate then flows through the proximal convoluted tubule (PCT) and this
tubule reabsorbs MOST of the parts of the filtrate that we need to survive which just
came from the Bowman’s capsule.
• Then the filtrate enters into the Loop of Henle ( remember it is found down in the renal
medulla). The loop of henle has a descending limb and ascending limb. Its goal is
to concentrate the urine and it will accomplish this with the renal medulla. The renal
medulla’s interstitial fluid is very hypertonic. This helps reabsorb water from the filtrate
to maintain the body’s water and salt balance.
• The descending limb is ONLY PERMABLE TO WATER…while the ascending limb is ONLY
PERMABLE TO IONS.
• The filtrate then enters in the distal convoluted tubule where more substances are
reabsorbed and secreted. Then it travels to the collecting tubule where the filtrate is
brushed up with the final touches of reabsorption. Then the filtrate leaves the
collecting tubule as urine which again flows through the renal papilla, minor/major
calyx, renal pelvis, ureters, bladder, and urethra.
Acute Glomerulonephritis
Poststreptococcal
What is acute glomerulonephritis
(poststreptococcal)?

• It is the inflammation of the filtering structure of the

nephron (what is the filtering structure of the nephron?
Glomerulus) that causes permeability to protein and red blood
cells due to previous strep infection. Therefore, protein and
red blood cells will be present in the urine.
Facts about Acute Glomerulonephritis

• It tends to present 14 days after a strep infection of the throat or skin (impetigo).
• It mainly affects the pediatric population ages 2-10.
• It is not caused from the strep bacteria attacking the glomerulus but the
immune system’s response to the bacteria by creating antigen-antibody
complexes, which inflames the glomerulus. This is why you see it AFTER a
strep infection
• Glomerulonephritis is an umbrella term for various types of kidney disorders
where there is injury to the glomerulus and they can be nephritic or nephrotic.
• Poststreptococcal glomerulonephritis is a type of NEPHRITIC SYNDROME meaning
there is the leakage of BOTH red blood cells and a mild amount of protein from the
inflamed glomerulus.
• Contrasting: Nephrotic Syndrome (which we will discuss in the next lecture) is an inflamed
glomerulus that is leaking massive amount of proteins into the filtrate (NOT red blood cells)
What is the nephron?

• the functional unit of the kidney that filters the blood

(specifically the glomerulus with the assistance of Bowman’s
capsule) and reabsorbs and secretes substances taken from
the filtrate/blood with the help of the renal tubule and
peritubular capillaries .
Role of Glomerulus

• (this is what is damaged in acute glomerulonephritis): it filters

the blood and removes ions, water, waste EXCEPT proteins
and bloods cells (they are too big to pass through)
What is happening in Poststreptococcal
Glomerulonephritis?

• The glomerulus becomes inflamed due to a recent infection

from a group of bacteria called streptococcus.
• The bacteria itself doesn’t cause the inflammation to the
glomerulus but the immune system which has created immune
complexes. These complexes become stuck in the glomeruli
which leads to inflammation and permeability of PROTEINS
(albumin) and RED BLOOD CELLS.
MAJOR CAUSES

• Hematuria: patient will present with cola colored or tea colored urine
• Proteinuria (mild): this can lead to low amounts of protein found in the blood
• What happens when there is a low amount of protein the blood? Swelling in the
interstitial tissue…hence EDEMA. The swelling mainly presents in the face/eyes and
will be mild.
• Fluid overload: at risk for heart failure, renal failure, and respiratory distress due to
congestion of fluid in lungs (retaining salt and water), hypertension
• Decrease glomerular filtration rate (GFR): What is GFR? It is the flow rate of filtered
fluids through the kidneys, specifically the glomerulus.
• Low Urine Output: Oliguria (watch potassium levels…hyperkalemia…the potassium will
start to build-up in the blood because the kidney’s filtration rate has decreased)
• Hypertension: WHY? decreased filtration rate of the kidneys, increased blood volume,
and retaining sodium
Signs and Symptoms of Acute
Glomerulonephritis

• Hypertension
• ASO antistreptolysin titer positive (test used to diagnose strep infections)
• Decreased GFR (low urine output)
• Swelling in face/eyes (edema)…mild
• Tea-colored urine (cola colored)…from hematuria
• Recent strep infection
• Elevated BUN and creatinine
• Proteinuria (mild)
Nursing Interventions for Acute
Glomerulonephritis

• Monitor fluid status VERY closely: patient may be prescribed

diuretics (if renal function is normal)
• Daily weights (weight gain is the earliest sign of fluid retention):
use same standing scale every day. Try to avoid bed scale if
possible…standing scales are the best.
• Strict calculation of intake and output (at risk for low urinary
output if renal failure presents)
• Since the disorder mainly affects the pediatric population
remember these patients should void 1mL/kg/hr.
Nursing Interventions for Acute
Glomerulonephritis

• How much should a patient who is 30 lbs void? 13.6 mL/hr

• If Oliguric (low urinary output) watch for hyperkalemia WHY? When the
GFR is decreased, potassium is not excreted properly which leads to
hyperkalemia
• Assess color of urine…is the urine starting to look normal?
• Assess swelling status in face/around the eyes and extremities (mainly in
the face/around the eyes and it is worst in the mornings)
• Monitor lung sounds for crackles…signs of pulmonary edema
• Monitor BUN and Creatinine levels ….renal failure
Nursing Interventions for Acute
Glomerulonephritis

• Monitor vital signs ESPECIALLY blood pressure (may experience hypertension…it can
become severely elevated and this can lead to hypertensive encephalopathy)
• Bedrest until recovered: due to hypertension
• Sodium restriction along with fluid restriction diet (helps with edema and hypertension)
and if oliguria is present restrict potassium-rich foods until recovered
• Administering diuretics and antihypertensives or antibiotics to treat presenting strep
infection (if needed…not always ordered) per MD order
• Education: importance of seeking treatment for infections of the skin or throat…strep
infection can reoccur
Renal Calculi
(Kidney
Stones)
What are kidney stones?

• Hard insoluble crystallized minerals and

salts that have formed out of the filtrate
produced by the nephron.
• Remember the nephron is the functional
unit of the kidney that filters the blood
and reabsorbs/secretes mineral, water,
and waste, which is urine. Learn more
about the nephron’s structure and
function.
Where can kidneys stones be located?

• Inside the kidney

• Ureters (top, middle, or bottom of ureter before entering
bladder)
• Bladder
Types of Kidney Stones

• *Calcium Oxalate: most common type of kidney stone, and

they tend to form in acidic urine. This type of stone is
composed of calcium and oxalate, and forms when there is a
high concentration of calcium or oxalate in the filtrate.
What can increase the amount of calcium in the
filtrate?

• Hypercalcemia/uria: taking excessive amounts of calcium

supplements, eating too much salt (increases the amount of
calcium in the urine), renal tubule problems within the nephron,
consuming too much animal protein (increases the amount of
calcium in the urine)
• Hyperparathyroidism: the parathyroid is responsible for secreting
PTH (parathyroid hormone) which causes the bones to release
calcium into the blood…overactive parathyroid gland increases
calcium levels.
What can increase the amount of oxalate in the
filtrate?

• High intake of foods with oxalates (see nursing interventions to see

the foods high in oxalate)
• GI disorders like ulcerative colitis and Crohn’s disease due to
malabsorption of fats. Normally, calcium and oxalates bind
together in the gut, therefore, oxalate is excreted in the stool.
However, when a GI disorder like ulcerative colitis is present there
is a problem with digesting fats. So, fats bind with calcium…leaving
oxalates behind. The leads to the build-up of oxalate in the urine.
Types of Kidney Stones

• Uric Acid: forms when there is too much uric acid in the
urine (acidic urine)
What can cause high amounts of uric acid in the
urine?

• Eating a diet high in purine or animal protein. These substances are

broken down into uric acid and if too much of these products are
consumed it can make the urine more acidic. Remember the
glomerulus of the nephron is responsible for filtering the blood and
removing uric acid.
• Dehydration: urine becomes acidic and the filtrate contains low
amounts of water…allowing uric acid to crystallize.
• Gout: patients with Gout have high amount of uric acid in the body
• Metabolic problems like diabetes, especially Type 2 Diabetes
Types of Kidney Stones

• Cystine: forms where there is too much of the amino acid

cysteine in the urine. This is rare and tends to run in families.
Types of Kidney Stones

• Struvite: this type of stone is also rare and usually forms due
to chronic urinary tract infections (UTIs).
Types of Kidney Stones

• Calcium phosphate: forms in alkaline urine and can be happen

when renal tubule issues are present
How does kidney stone formation happen?

• Remember the nephron, specifically the glomerulus, filters the

blood and all minerals/water/waste are removed from the
blood and leak down into Bowman’s Capsule (these
substances include nearly everything expect proteins and
blood cells).
 Causes of Kidney Stones
“Crystal”

• Consuming high amounts of oxalates, purine, animals protein, salt (eating too much salt keeps the body from
reabsorbing calcium in the urine), and taking excessive amounts of calcium supplements with Vitamin D (calcium
oxalate, uric acids type stones)
• Recurrent UTIs (struvite stones)
• hYpocitraturia, hYpercalemia/uria, hYperparathyroidism
• Hypocitraturia: Citrate plays a role in stopping the formation of calcium salt crystals (specifically calcium oxalate and calcium
phosphate binding). Therefore, citrate binds with calcium and stops it from binding with oxalate or phosphate. Furthermore, it
keeps the urine alkaline and prevents it from becoming too acidic….hence preventing uric acid or cystine stones to form since
these stones form in acidic urine.

• Structural blockage or stasis of the urine (prostate problems, strictures, deformities)

• Too much uric acid (gout, dehydration, high diet in purine/animal proteins)
• Absorption problems: gut doesn’t absorb fats as with ulcerative colitis or crohn’s diseae…fats bind with calcium and
leaves oxalates behind, Acquired (family history)
• Low activity: immobile patients tend to have an increased amount of minerals and salts compared to people who are
physically active and the urine stays stagnant in the kidney…hence increase risk of kidney stone formation.
Signs and Symptoms of Renal Calculi

• Renal colic: stone in the renal pelvis…dull,

deep aching in the flank or costovertebral
area
• Ureteral colic: stone residing in
the ureter and as it moves it can
cause…….intense, sharp, radiating, wavelike
pain to the genitalia (scrotum, vaginal area)
• The patient may feel like they need to void but
a small amount is voided.
• Can have blood in the urine due to stone
scraping the ureter (hematuria)
Nausea and vomiting (due to the intense pain)
• Signs and symptoms of infection: fever,
cloudy, odorous urine
• Urinary retention: especially if stone is
stuck in neck of bladder…this makes it
extremely hard to completely pass all
the urine in the bladder…(note the
location of the neck of the bladder)

• Asymptomatic: until stone moves

within the kidneys and to the ureters
Complications of Renal Stone

• Obstruction: stones blocks the flow of urine. The urine can back up and causes
hydrostatic pressure (hence increase water pressure) within the kidney. This
will increase pressure in Bowman’s Capsule which will decrease the amount of
blood the kidneys can filter.
• Hydronephrosis or Hydroureteronephrosis: due to the back up of urine which
causes swelling and dilation in various parts of the kidneys (renal pelvis,
minor/major calyx and ureters)…depending on where the stone is located. The
end result is the loss of function to the kidney.
• Damage to the nephrons…hence renal failure
• Infection
How is Renal Calculi Diagnosed?

• KUB (x-ray of the kidneys, ureters, and bladder)

• IVP (intravenous pyelogram): a special dye, which is iodine-based, is given
through the patient’s IV. Then x-ray images will be taken to assess the kidneys,
bladder, ureters, and urethra.
• Nurse’s Role:
• Make sure patient isn’t allergic to iodine or shellfish, pregnant or might be, nursing a baby, impaired
renal function or taking metformin/Glucophage.

• Ultrasound or CT scan
• Urine tests:
• U/A assess for crystals, infection
• 24 hour urine to measure concentrate of ions (calcium, sodium etc.), waste products in
urine (uric acid, creatinine), citrate, pH, kidney function
• Nurse’s Role
• Keep specimen cold by keeping it on ice for the whole 24 hours…if not kept cold this can alter the test
results.
Nursing Interventions for Renal Calculi

**most patients will pass the stone and the nurse’s job is to
keep the patient’s pain controlled, give fluids, strain urine, and
monitor for complications.
Nursing Interventions for Renal Calculi

• Control pain (very, very painful)…pain doesn’t go away until it is passed or removed. Patient needs around-the-clock
pain medications rather than PRN medications (where the patient has to request it). This will help keep pain
medication blood levels constant and hopefully help control the pain. The physician may order NSAIDs to help
control the inflammation which can help the stone pass if it is stuck within inflamed areas.
• Maintain oral fluids (3-4 L per day) unless contraindicated:
• WHY? It is very important in helping the stone pass. Fluid intake increases the pressure which can help move the kidney stone.
In addition, it keeps the urine diluted because remember stones are more likely to form in concentrated urine. It also keeps
flushing the kidneys to prevent stagnant urine within the urinary system…decreasing the risk of infection.
• Closely monitor I/Os (intake and output)
• WHY? The patient will be consuming a lot of fluids and the nurse needs to make sure the kidneys are putting out enough fluid
based on the intake. If the fluid output is low, renal function may be impaired, an obstruction may be present or other
complications like hydronephrosis,etc.
• Monitor for signs and symptoms of UTI
• Strain urine and ASSESS very closely for stones (VERY IMPORTANT): Then notify the physician who will give you
an order to send it to the lab. This is crucial so the physician can determine what type of stone is causing the
problem and appropriate treatment can be ordered.
• Keep patient as mobile as possible and try to avoid supine position for long periods of time. Remember immobility is
one of the causes of kidney stone formation…if urine stays stagnant it can allow crystallization. Keeping the patient
mobile helps the stone pass. If the patient is immobile, turn the patient more frequently.
Prevention Education (can reoccur):

• Keep hydrated (prevents concentrated urine) 2L per day

• Take medication as prescribed: MD may order the following as
preventive measures in preventing kidney stone formation based
on the type of stone the patient is susceptible to:
• Allopurinol: decreases uric acid levels (used in gout)…uric acid
stones
• “HCTZ” hydrochlorothiazide: decreases the amount of calcium in
the urine…calcium type stones
Prevention Education (can reoccur):

• Limiting calcium intake not recommended due to osteoporosis risk, unless patient has metabolic
problems or a problem with the nephrons of the kidney. Instead, limiting medication forms of
calcium supplements and vitamin D.
• Limiting animal proteins (high amount of protein increases the amount of calcium in the urine and
increases uric acid levels)
• Limit sodium to 2-3 g per day….sodium decreases the reabsorption of calcium which will leave
more calcium in the urine (watch hidden sodium foods like canned food, soda drinks, sandwich
meats, processed foods)
• Avoid foods high in purine: organ meats, beer, pork, red meats, seafood (scallops, anchovies,
sardines) (uric acid stones)
• Avoid high oxalate foods: spinach, cabbage, rhubarb, tomatoes, beets, nuts, chocolate, wheat
bran, strawberries, tea (calcium oxalate stones)
• How to stain urine and why it is important and to keep stone so it can be analyzed
 Treatments for Renal Stones

• Extracoporeal shock wave

lithotripsy (ESWL): NONINVASIVE:
shockwaves are created to penetrate
though the skin and body tissue.
Shockwaves will hit the stone and
break it down into grains of sand like
particles which can be passed out.
Several treatments may be required
depending on stone size. Stent may be
placed to facilitate the passage of the
fragments…not for large stones
Nurse’s Role for Extracoporeal shock wave
lithotripsy (ESWL)

• Maintain fluid intake to facilitate stone fragment removal

• Keep patient mobile
• Control pain
• May have bleeding in urine
• Strain urine and send stone to lab
 Treatments for Renal Stones

• Percutaneous Nephrolithotomy: INVASIVE: used when the stone is

large or can’t use ESWL. The kidney stone is removed by a urologist
and doesn’t have to be passed by the patient as with EWSL.
• An incision is made on the back where the kidney is and an
nephroscope is used to remove the stone. Sometimes lithotripsy is used
to break up the stone.
• A nephrostomy tube may be placed to drain urine until healed (this is a
catheter placed in the renal pelvis to drain urine)
Nurse’s Role for Percutaneous Nephrolithotomy

• Maintain fluid intake of 3-4 liters

• Maintain nephrostomy: it drains kidney and stone fragments,
empty the bag regularly, keep site secure so tube doesn’t
move, and monitor for infection
• Strain urine and send stones to lab
 Treatments for Renal Stones

• Ureteroscopy: no incision made…scope is inserted through the urinary

system from urethra to the kidneys…can remove the stone or break it up with
a laser or lithotripsy…stent may be placed to allow fragments to pass
Nurse’s Role
• Maintain fluid intake to facilitate stone fragment removal
• Keep patient mobile
• Control pain
• May have bleeding in urine
• Strain urine and send stone to lab
Urinary System Disorder and
Management