Transcript LPN-C - Faculty Sites

LPN-C
Unit Three
Fluids and Electrolytes
Why are fluids and electrolytes
important for the nurse to
understand?

Fluids and electrolytes are essential to
identifying and defining the problem
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What is the relationship to the disease process
What intervention is appropriate
How will the intervention affect the patient
Safety management of infusion therapy
 What is the IV infusion order
 Why was it ordered
◦ Continual assessment and evaluation of
patient progress, status of labs, response to
treatment

Electrolyte imbalances can occur suddenly
◦ Must be able to assess changes
◦ Intervene appropriately and in a timely manner
◦ Frequent review of lab values, diagnostic tests,
medications, IV fluid orders

Homeostasis = a dynamic process
involving a continuous series of selfregulating adjustments to maintain a
balance of the internal environment
◦ Preserved through the intake and output of
water
◦ Water is the primary chemical component
within the body, and an individual can perceive
a need for it
Fluids
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Water
Individuals with lean tissue mass have a higher
percentage of body water than those with more
fat
The average adult female holds 52% of water by
weight
The average adult male holds 63% of water by
weight
Water serves as a vehicle for the delivery of
electrolytes and nutrients to body cells
Water serves as a vehicle for the excretion of
waste products
Water is a medium for biochemical reactions
Water contributes to temperature regulation
Water cushions organs and joints
Water Intake

The need for water is signaled through
the mechanism of thirst
◦ Osmotic pressure from extracellular fluids
◦ Thirst center in the hypothalamus

Percentages of daily water intake
◦ 60% water from drinking
◦ 30% water from moist foods
◦ 10% water from metabolism processes
Water Output
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There are 4 avenues for daily water loss
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Lungs
Skin
Urine
Feces
The route of water loss depends on
◦ Temperature
 When the temperature outside is high, water loss
via the skin and lungs increases
◦ Humidity
◦ Physical exercise
Water Balance
Urine output increases when water intake
increases
 Urine volume decreases when water
intake decreases, or when the body loses
excessive water
 Water balance occurs when water intake
equals water output
 Regulation of water balance

◦ Neurosecretions of the hypothalamus
(antidiuretic hormone, or ADH/vasopressin)
◦ Mineralocorticoid secreted from the adrenal
cortex (Aldosterone)
Antidiuretic Hormone (ADH)
ADH is produced by the hypothalamus
 Regulates water output by regulating
extracellular fluid osmolarity
 Acts directly on the collecting ducts and
tubules of the nephrons in the kidneys to
bring about water reabsorption

ADH
↓
Secreted by the posterior lobe of the
pituitary gland
↓
Regulates water retention and excretion
ADH (cont’d)
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Hypertonic extracellular fluid –
Excess sodium or decreased blood
volume
↓
Release of ADH
↓
Sensation of thirst and conservation of
water in the body through reabsorption
ADH (cont’d)
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Hypotonic extracellular fluid –
Increased blood volume
↓
Pituitary signaled to inhibit the release of
ADH
↓
Stimulates the excretion of urine
↓
Increases the concentration of
extracellular fluid
ADH (cont’d)

Release of ADH can be influenced by
drugs
◦ Increase of ADH
 Nicotine
 Morphine
 Barbiturates
◦ Inhibition of ADH
 Alcohol

Malfunctions of the ADH system
◦ Diabetes insipidus
◦ Syndrome of inappropriate ADH (SIADH)
Diabetes Insipidus --
Pituitary gland is unable to secrete ADH
 Not common (only 1 in 25,000 affected)
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◦ Head trauma
◦ Surgery to the region of the pituitary and/or
hypothalamus
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Urine is excessive and diluted
◦ Polyuria (urine output of 3-18 L/day)
◦ Polydipsia
Hallmark signs include urine specific
gravity at ≤ 1.005 and urine osmolality at
<200/kg
 Treated with synthetic vasopressin PO or
intranasal (desmopressin or DDAVP)
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Syndrome of Inappropriate ADH (SIADH) -Continued secretion of ADH
 Urine is concentrated and diminished
 Hyponatremia (<135 mEq/L)
 Increased urine sodium concentration (>20
mEq/L)
 Hypotonicity
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◦ Plasma osmolality at <280/kg
Water retention with increased extracellular
fluid
 Closely monitor for weight change, fluid
imbalance, restlessness, CHF, convulsions
 Treated with Lasix to maintain urine output
and block secretion of ADH
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SIADH (cont’d) -Most common cause is idiopathic
 Other causes include
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◦ Problems with the brain or head
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Trauma, hemorrhage
Tumor, abscess
Hydrocephalus, encephalitis
Meningitis
◦ Medications
 Antibiotics, oral hypoglycemics, thiazide diuretics
◦ Stroke
◦ Respiratory issues
 Asthma, COPD, pneumonia
 Neonatal hypoxia
 Lung cancer, tuberculosis
Aldosterone
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Regulates extracellular fluid volume
◦ Maintains water balance through sodium
reabsorption in the nephrons
◦ Causes sodium retention (and subsequent
water retention) if renal blood flow decreased
Decrease in sodium level or extracellular
fluid volume
↓
Secretion of Aldosterone
↓
Kidney reabsorption of water and sodium
↓
Increase in extracellular fluid
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Water Distribution
The total volume of water in the body is
distributed among two large
compartments, which are separated by a
selectively permeable cell membrane
◦ Intracellular compartment
◦ Extracellular compartment
Nurses must understand the differences
between these two compartments, and
know how various illnesses and diseases
can bring about imbalances
 Intracellular fluid is fluid that is contained
within the cells of the body, and comprises
2/3 of the body’s total fluids
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Water Distribution (cont’d)
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Extracellular fluid is found outside the cells
◦ Comprises 1/3 of total body fluids
◦ High in oxygen and carbon dioxide
◦ Contains essential substances
 Glucose for energy supply
 Amino acids and fatty acids for growth, repair, and
health maintenance
 Sodium, calcium, chloride, and bicarbonate
◦ Transports cholesterol, urea, lactate, creatinine,
and sulfates
◦ Constant movement within the systemic
circulation
◦ Main function is to maintain cell membrane
permeability and to serve as a vehicle for
movement of life-sustaining substances
Extracellular Fluid

The extracellular fluid compartment is
subdivided in three components
◦ Intravascular = contained within the blood
vessels
◦ Interstitial = the solution that exists in the
small spaces and gaps between body
structures, cells, and tissues
◦ Transcellular = smallest amount of solution;
includes mucus, ocular fluid, sweat, secretions
of the genitourinary system, cerebral spinal
fluid, pleural solution, pericardial fluid, and
peritoneal secretions; separated from other
fluid by the epithelial lining or other
membranes
Extracellular Fluid (cont’d)

The maintenance of the proportional
distribution of the extracellular fluid
among these three spaces depends on a
variety of factors
◦ Protein content of the blood
 Albumin pulls fluid toward itself
◦ Integrity of the vascular endothelium
◦ Hydrostatic pressure inside the vessels
 Tends to force fluid out of the vessels
Composition of Body Fluids
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Solvent = able to hold substances and act
to dissolve them
◦ Water is a solvent, and is the main constituent
of all body fluids
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Solute = a substance that is dissolved in
the solvent; two major categories
◦ Electrolytes
◦ Nonelectrolytes

Solution = the combination of a solvent
and a solute
Electrolytes
Electrolytes
Electrolytes comprise 95% of the body’s
solute molecules
 Electrolytes are chemicals that carry an
electric charge (ions)
 Ions converts a solution into a product
capable of conducting electricity
 Anions = ions with a negative charge
 Cations = ions with a positive charge
 Electrolytes are expressed in
milliequivalents per liter (mEq/L)
 Electrolytes are crucial to the distribution
and movement of water
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Electrolytes (cont’d)
Electrolytes are needed for the
maintenance of acid-base balance
 Electrolytes are needed to carry out
cellular reactions
 Electrolytes are necessary for the
transmission of electrochemical impulses
in muscles and nerve fibers
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Major Anions
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Bicarbonate (HCO3)
◦ Most present in the extracellular fluid at
24mEq/L
◦ Helps in acid-base balance
Major Anions (cont’d)
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Chloride (Cl-)
◦ Most present in the extracellular fluid at
105mEq/L
◦ Aids in fluid balance and osmotic pressure
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Phosphate (PO4)
◦ Most present in the intracellular fluid at
149mEq/L
◦ Aids in energy storage
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Sulfate (SO4)
◦ Most present in the intracellular fluid at
variable amounts
◦ Assists in protein metabolism
Major Cations
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Sodium (Na+)
◦ Most present in the extracellular fluid at
142mEq/L
◦ Assists with fluid balance and osmotic pressure
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Calcium (Ca+)
◦ Most present in the intracellular fluid at variable
amounts
◦ Responsible for bone growth and assists in
blood clotting
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Magnesium (Mg+)
◦ Most present in the intracellular fluid at
123mEq/L
◦ Assists in enzyme production
Major Cations (cont’d)
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Potassium (K+)
◦ Most present in the intracellular fluid at
100mEq/L
◦ Responsible for neuromuscular excitability
◦ Helps with acid-base balance
Fluid and Electrolyte Movement
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Passive transport = noncarrier-mediated
transportation
◦ Movement of solutes through membranes
without the expenditure of energy
◦ Types of passive transport –
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Passive diffusion
Facilitated diffusion
Filtration
Osmosis
Active transport = the use of energy to
move molecules
◦ Moves substances against the concentration
gradient from low to high concentration areas
Passive Transport
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Passive diffusion = the process in which
ions, water, and lipid-soluble molecules
move randomly in all directions from an
area of high concentration to an area of
lower concentration through pores in the
membrane resulting in even distribution of
particles in the fluid
◦ Particles must be
small enough to pass
through the pores in
the membrane
Passive Transport (cont’d)

Passive diffusion (cont’d) –
◦ If molecules become more populous in one
area of the solution compared to another, a
concentration difference or concentration
gradient results, and the particles will
redistribute themselves until they reach a state
of equilibrium
◦ An example of this is a metabolic activity that
consumes oxygen
 Causes the diffusion of oxygen from high to lower
concentration in the alveoli
 Reduces the concentration of oxygen in the
bloodstream
 Allows oxygen to be replenished
Passive Transport (cont’d)

Facilitated diffusion = diffusion across a
membrane that is enhanced by a transport
protein in the membrane
◦ The transport protein is specific to the
substance that is being transported
◦ Glucose is transported in this way
Passive Transport (cont’d)

Filtration = pressure causes water, ions,
and molecules to move from an area of
higher pressure to an area of lower
pressure
◦ Movement is one-directional
◦ The size of the openings in the membrane
determine the size of the particle that can be
filtered
◦ Examples include the heart, nephrons in the
kidney
Passive Transport (cont’d)
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Osmosis = the passage of water through a
semi-permeable membrane in cells and
capillaries; water flows from a dilute
solution to a more concentrated solution;
once the concentration of solutes are
equal on each side of the membrane, the
flow of water stops and the solutions are
isosmotic to each other
◦ Water molecules are very small
◦ A membrane that is semi-permeable is more
permeable to water due to its size
Passive Transport (cont’d)

Osmosis (cont’d) –
◦ An isotonic solution is one in which the salt
concentration on either side of the membrane
is the same
◦ A hypertonic solution is one in which the salt
concentration in the solution is higher, causing
water to leave the cell
◦ A hypotonic solution is one in which the salt
concentration in the solution is lower, causing
water to enter the cell
◦ Osmotic pressure is the amount of hydrostatic
pressure needed to draw water across the
membrane
Passive Transport (cont’d)

Osmosis (cont’d) –
◦ A solution with higher osmotic pressure
compared to another solution is hypertonic
with respect to the other
◦ If one solution has a lower osmotic pressure
compared to another solution, it is hypotonic
with respect to the other
◦ If two solutions have the same osmotic
pressure, they are isotonic with respect to each
other
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Tonicity refers to the osmotic pressure, or
tension, of a solution (impacts cell
shrinking or swelling)
Osmolality
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Osmolality refers to the concentration of a
solute per kilogram of solvent
◦ Measured in weight (kilograms)
◦ Determination of the total number of particles
present in blood, urine, or other fluids
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Osmolality is affected by hydration
◦ Increases with dehydration
◦ Decreases with overhydration
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Types of osmolality tests
◦ Urine (tests concentrating ability of the kidney)
◦ Plasma (used to test electrolyte imbalances)
◦ Stool (used to diagnose the cause of diarrhea)
Osmolarity
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Osmolarity refers to the concentration of a
solute per liter of solution
◦ Measured in volume (liters) and expressed in
milliosmols of solute per liter of solution
(mOsm/L)
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Serum osmolarity = 290 – 300 mOsm/L
◦ Refers to the concentration of particles, like
sodium, in plasma

Estimated serum osmolarity is 2 times the
serum sodium level
◦ Sodium is the major solute in plasma
◦ If the sodium level is 145 mEq/L, estimated
serum osmolarity would be 290 mOsm/L
Osmolarity of IV Solutions
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Isotonic solutions
◦ 250 – 375 mOsm/L
◦ Have the same osmolarity as normal plasma,
so no osmotic pressure difference is created
◦ No fluid movement (fluids stay in the
extracellular fluid)
◦ Useful in hemorrhagic conditions because
isotonic solutions expand vascular volume
quickly and replace extracellular fluid losses
◦ Intracellular and extracellular fluid are isotonic,
so red blood cells maintain their concave
shape
Osmolarity of IV Solutions (cont’d)

Isotonic solutions per IV
◦ 0.9% NaCl (Normal saline – NS)
 Sodium and chloride in water has the same
osmolarity as normal plasma
 No calories or free water (water without solute in it)
◦ Ringer’s solution
 Contains sodium, potassium, and calcium
 No dextrose, magnesium, or bicarbonate
 No calories or free water
◦ Lactated Ringer’s solution (LR)
 Contains sodium, chloride, potassium, calcium, and
lactate in concentration similar to normal plasma
 No dextrose, magnesium
 No free water
Osmolarity of IV Solutions (cont’d)

Hypotonic solutions
◦ <259 mOsm/L
◦ Lower osmolarity than normal plasma
◦ Water moves out of the vessels into the
dehydrated cell
 Decreased vascular volume
 Increased cell water
◦ Useful in preventing and treating cellular
dehydration by providing free water to cells
◦ Never used in acute brain injuries
 Cerebral cells are very sensitive to free water
 Absorbed quickly and leads to cerebral edema
◦ Hypotonic extracellular fluid (ion concentration
is decreased) causes cells to burst
Osmolarity of IV Solutions (cont’d)

Hypotonic solutions per IV
◦ 5% dextrose in water (D5W)
 Isotonic in the bag, but hypotonic in the body
 Dextrose is rapidly metabolized once infused
 Leaves free water to shift by osmosis from the vessels into
the cells
 For each liter of D5W, 2/3 enters the cells, and 1/3
remains in the extracellular space
◦ 0.45% saline (1/2 NS) and
0.224% saline (1/4 NS)
 Provide free water and small amounts of sodium and
chloride to the cells
 Half of each liter moves into the cells, and half
remains in the extracellular space
Osmolarity of IV Solutions (cont’d)

Hypotonic solutions per IV (cont’d) -◦ 5% dextrose in 0.45% saline (D5 ½ NS) and
5% dextrose in 0.225% saline (D5 ¼ NS)
 Hypertonic in the bag, but hypotonic in the body
 Composed of hypotonic saline solutions
 Amount of dextrose does not meet daily nutritional
requirements, but is enough to help prevent ketosis
and starvation
Osmolarity of IV Solutions (cont’d)

Hypertonic solutions
◦ ≤ 375 mOsm/L
◦ Higher osmolarity than plasma
◦ Water moves out of the edematous cell into
the vessels
 Increased vascular volume
 Decreased cell water
◦ Hypertonic extracellular fluid (ion
concentration is increased) causes cells to
shrink (crenation)
Osmolarity of IV Solutions (cont’d)

Hypertonic solutions per IV
◦ Carefully controlled to avoid vascular volume
overload and cell dehydration
◦ Used to pull excess fluid from the cells and to
promote osmotic diuresis
◦ Types of hypertonic IV solutions
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3% saline
5% saline
10% dextrose
50% dextrose
◦ IV pump should always be used to control
infusion of hypertonic solutions
◦ Frequent monitoring of vital signs, I&O, lung
sounds, LOC, and serum sodium levels to avoid
hypernatremia and vascular volume overload
Active Transport

Active transport is necessary to get
potassium ions into the cells
◦ Diffusion can not occur because the
concentration of potassium is highest in the
cells
Active transport is necessary anytime
there is a concentration differential where
a substance must move from lower to
higher concentration
 Adenosine triphosphate (ATP) provides the
energy for active transport

Active Transport (cont’d)

Sodium-potassium pump
◦ Most important pump in the body
◦ Carrier transports sodium out of the cell and
pumps potassium into the cell
◦ Maintains higher level of potassium in the
intracellular fluid
◦ Essential for neuron and muscle membranes
 Electrical polarity must be maintained for neurons to
generate and conduct electrical impulses
Quick Reference for
Electrolyte Imbalances
Sodium (Na+) helps to balance fluid levels in the
body and facilitates neuromuscular functioning
Potassium (K+) helps to regulate neuromuscular
functioning and osmotic pressure
Calcium (Ca+) affects neuromuscular performance
and contributes to skeletal growth and blood
coagulation
Magnesium (Mg+) influences muscle contraction
and intracellular activity
Chloride (Cl-) regulates blood pressure
Hydrogen phosphate (HPO4) impacts metabolism
and regulates acid-base balance and calcium
levels
Bicarbonate (HCO3) assists in the regulation of pH
levels in the blood
Sodium

Sodium is a major cation in the
extracellular fluid
◦ Contains 99% of all of the body’s sodium

Sodium is responsible for water balance
and determination of plasma osmolality
◦ The osmolality of both extracellular fluid and
intracellular fluid are isotonic
Sodium remains in the extracellular space
because it is pumped out of the cells by
the sodium-potassium pump
 The normal range of sodium =
135 – 145 mEq/L

Hyponatremia
Sodium level <135mEq/L
Indicates there is a greater concentration
of water than of sodium, which is a
hypervolemic state
 Clients at highest risk for hyponatremia
are the very young, the elderly, and women
 Causes of hyponatremia –
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◦ Abnormal loss of GI secretions
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Vomiting, diarrhea
Suction drainage
Fistulas
Excessive tap water enemas
◦ Excessive sweating
◦ Excessive water consumption
◦ Burns
Hyponatremia (cont’d)

Causes of hyponatremia (cont’d) –
◦ Disease states that add to increased
extracellular fluid volume
 CHF
 SIADH
 Prolonged use of hypotonic intravenous therapy

Signs and symptoms (related to the shift of
water into the cells) –
◦ Cardiovascular
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Bounding pulse
Tachycardia
Hypotension if extracellular fluid volume is decreased
Hypertension if extracellular fluid volume is increased
◦ Gastrointestinal
 Vomiting
 Diarrhea
Hyponatremia (cont’d)

Signs and symptoms (cont’d) –
◦ Integumentary
 Decreased extracellular fluid volume = pale, dry skin;
dry mucus membranes
 Increased extracellular fluid volume = edema, weight
gain
◦ Renal
 Thirst
 Renal failure
◦ Neuromuscular
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Weakness
Headache
Confusion
Seizures
Nursing interventions –
◦ Assess vital signs
Hyponatremia (cont’d)

Nursing interventions (cont’d) –
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◦
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Diagnostics –
◦
◦
◦
◦
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Assess mental status; monitor CNS symptoms
Monitor ADH levels
Monitor labs, electrolytes
Monitor GI losses; perform accurate I&O
Obtain daily weight
Plasma level <135mEq/L
Serum osmolality <270mOsm/kg
Serum chloride may be decreased
Decreased BUN and hematocrit
Treatment –
◦ Intravenous administration of saline solution
◦ Diet therapy
Hyponatremia (cont’d)

Treatment (cont’d) –
◦ If client with hyponatremia is hypovolemic,
treat with NS or LR to correct the extracellular
fluid volume deficit
◦ If client with hyponatremia is hypervolemic,
administer Mannitol
◦ Replace sodium slowly
 Too rapid of a correction in sodium further
compromises the patient’s condition
 Hypernatremia may result in brain shrinking
Hypernatremia
Elderly clients at risk due to age-related
decline in thirst sensitivity
 As sodium increases, water is lost

◦ Water shifts out of cells to establish osmotic
equilibrium, causing the brain cells to shrink

Brain cells are very sensitive to changes in
sodium levels
Elevated sodium
↓
Hypertonicity (stimulates thirst and release
of ADH)
↓
Body takes in water, which is retained via
ADH mechanism
Hypernatremia (cont’d)

Causes of hypernatremia –
◦ Decreased fluid intake
◦ Increased insensible loss of water
 Watery diarrhea
 Osmotic diarrhea (i.e. enteral tube feedings)
◦ High sodium diet
◦ Infusion of sodium-containing fluids
◦ Administration of hypertonic IV solution (i.e.
sodium bicarbonate or 3% saline)
◦ Diabetes insipidus
 Defect in ADH secretion that may cause sodium
retention and increased secretion of dilute urine
◦ Head trauma
◦ High glucose levels
 Osmotic diuresis
Hypernatremia (cont’d)

Causes of hypernatremia (cont’d) –
◦ Over-the-counter medications with high sodium
content
 Alka-Seltzer
 Cough syrups
 Aspirin
◦ Other medications
 Prednisone
 Certain antibiotics

Signs and symptoms –
◦ Neurological
 Progressive lethargy, coma
 Intracranial bleeding due to brain tissue shrinkage
◦ Gastrointestinal
 Watery diarrhea
 Nausea
Hypernatremia (cont’d)

Signs and symptoms (cont’d) –
◦ Cardiovascular
 Tachycardia
 Hypertension
 Decreased cardiac contractility
◦ Integumentary
 Dry, sticky mucus membranes
 Rough, dry tongue
 Flushed skin
◦ Renal
 Thirst
 Increased urine output
◦ Neuromuscular
 Twitching, tremors, seizures, hyperreflexia
 Agitation, CNS irritability
 Coma
Hypernatremia (cont’d)

Diagnostics –
◦
◦
◦
◦
◦

Sodium plasma level >145mEq/L
May see an increase in urine output
Chloride level may be elevated
Serum osmolality >290mOsm/kg
Increased BUN, hematocrit
Nursing interventions –
◦ Assess mental status
◦ Monitor for CNS changes
◦ Assess vital signs; assess blood pressure with
bounding pulses if client is hypervolemic
◦ Monitor labs
◦ Obtain accurate I&O, daily weight
◦ Maintain client on seizure precautions
◦ Provide a safe environment
Hypernatremia (cont’d)

Treatment –
◦ Administer 0.9% NS at a rate to correct
hypernatremia but avoid cerebral edema
 Correction usually occurs within 36-72 hours
◦ Once volume deficit is restored, administer
fluids with D5W
◦ Administer hypotonic intravenous fluids if there
is fluid loss
◦ Administer isotonic IV fluid if there is fluid and
sodium loss
◦ Restrict sodium intake
◦ Decrease sodium level slowly as too rapid of a
correction may further compromise the
patient’s condition
 Hyponatremia may result in brain swelling
Potassium
Normal serum potassium level =
3.5 – 5.5 mEq/L
 Potassium is a major cation in the
intracellular fluid
 Small changes in potassium level have
profound effects
 Potassium’s role in acid-base balance –

◦ In alkalotic states, hydrogen moves out of cells
to correct high pH; potassium moves in to cells
to maintain an electrically stable state
◦ In acidosis, the reverse of the above actions
occurs
Potassium (cont’d)

Function of potassium
◦ Intracellular
 Controls cellular metabolism
 Functions in the regulation of protein/glycogen
synthesis
◦ Extracellular
 Maintains action potential in muscles and neuron
cells
 Assists in controlling cardiac rate and rhythm,
conduction of nerve impulses, skeletal muscle
contraction, and function of smooth muscle and
endocrine tissues

The body cannot store potassium
◦ Daily intake of 40 mEq required
Potassium (cont’d)
The sodium-potassium pump controls the
concentration of potassium by removing
three 3 sodium ions from the cell for every
2 potassium ions that return to the cell
 The kidneys eliminate 90% of potassium
 The remaining potassium is eliminated
through stool and perspiration
 An increased level of aldosterone
stimulates and increases excretion of
potassium

Hypokalemia
Serum potassium level <3.5mEq/L
 Hypokalemia may lead to cardiac and
respiratory arrest if not corrected quickly
 Causes of hypokalemia –

◦ Alkalosis
 Potassium migrates into the cells as hydrogen ions
move out to correct high pH
◦
◦
◦
◦
◦
Water intoxication (dilutes serum potassium)
Potassium-wasting diuretics
Excessive loss in GI tract
Hemodialysis
NPO status without sufficient IV replacement
therapy
◦ Malnutrition
Hypokalemia (cont’d)

Hypokalemia enhances the effects of
digoxin
◦ Toxicity may occur at therapeutic levels

Signs and symptoms –
◦ Cardiovascular






Weak, thready pulse
Pedal pulses that are difficult to palpate
PVCs
Heart block
Orthostatic hypotension
ECG changes
 S-T segment depression
 Flattened T wave
 Appearance of a U wave
◦ Polyuria
Hypokalemia (cont’d)

Signs and symptoms (cont’d) –
◦ Respiratory
 Decreased breath sounds
 Shallow respirations
 Dyspnea
◦ Gastrointestinal





Abdominal distention
Hypoactive bowel sounds
Nausea/vomiting
Constipation
Paralytic ileus
◦ Neurological
 Anxiety
 Confusion
 Lethargy, coma
Hypokalemia (cont’d)

Signs and symptoms (cont’d) –
◦ Neuromuscular
 Decreased deep tendon reflexes
 Muscle weakness/weak hand grasps
 Leg cramps

Nursing interventions –
◦
◦
◦
◦
◦
◦
◦
◦
Monitor vital signs
Monitor serum potassium levels
Assess heart rate and rhythm
Assess ECG changes
Assess respiratory rate, depth, and pattern
Protect patient from injury
Monitor I&O
Monitor for signs of metabolic alkalosis

Hypokalemia (cont’d)
Nursing interventions (cont’d) –
◦ Administer potassium supplements as ordered
◦ Assess mental status

Treated with oral or intravenous potassium
replacement
◦ Never administer potassium by IV push or IM as
this can lead to fatal arrhythmias
◦ Always use an IV pump for parenteral
potassium administration
◦ Observe infusion site frequently for infiltration,
phlebitis
◦ Always verify the dosage of potassium in the
intravenous solution before hanging
◦ Ensure the diluent is dextrose-free to prevent
release of insulin
Hypokalemia (cont’d)

Treatment (cont’d) –
◦ Do not exceed safe administration rate
 Potassium infusion per peripheral IV should not be
infused more quickly than 20mEq/hour
 Potassium infusion per central line should not be
infused in concentrations greater than 40mEq
◦ If more than 20mEq/hour given, perform
continuous ECG monitoring and check serum
potassium levels every 4 – 6 hours until normal
Hyperkalemia
Serum potassium level >5.0mEq/L
 Potassium moves from the extracellular
fluid to the intracellular fluid
 The myocardium is most sensitive to an
increase in potassium levels
 Changes in the T wave (tall, peaked, or
tented) provides the earliest indication that
the patient has a high serum potassium
level
 Causes of hyperkalemia –

◦
◦
◦
◦
Rapid infusion of IV potassium
Renal failure
Adrenal insufficiency
Acidosis
Hyperkalemia (cont’d)

Causes of hyperkalemia (cont’d) –
◦ Addison’s disease
 Decreased aldosterone leads to sodium depletion
and potassium retention
◦ Medications
 Potassium-sparing diuretics
 Ace inhibitors
◦ GI bleed
◦ Trauma or ischemia
 Massive cell damage
 Burns

Signs and symptoms –
◦ Neuromuscular
 Muscle twitching
 Paralysis of the arms and legs
Hyperkalemia (cont’d)

Signs and symptoms (cont’d) –
◦ Cardiovascular
 Slow, irregular heart rate
 Decreased blood pressure
 ECG changes
◦ Gastrointestinal




Hypermotility/diarrhea
Nausea
Abdominal cramping
Hyperactive bowel sounds
◦ Respiratory
 Unaffected until serum potassium level is extremely
high
 Respiratory failure due to muscle weakness
Hyperkalemia (cont’d)

Nursing interventions –
◦ Monitor potassium levels
◦ Monitor for ECG changes
◦ Monitor I&O
 Adequate renal function is important for the
excretion of potassium
◦ Assess for signs of metabolic acidosis
◦ Monitor ABGs
 Hyperkalemia frequently seen with acidotic state,
though it often resolves when pH is corrected
◦ Monitor labs
 If dehydration is causing hyperkalemia, hematocrit,
hemoglobin, and sodium should be elevated
 If condition is associated with renal failure, creatinine
and BUN levels should be affected
Hyperkalemia (cont’d)

Treatment –
◦ Discontinue oral and/or IV potassium
◦ Promote potassium excretion
 Increase urine output
 Administer potassium-excreting diuretics, like lasix
◦ Administer Kayexalate orally or per rectum
 Exchanges sodium for potassium in the GI tract and
excretes potassium in the stool
◦ Administer insulin and dextrose to shift
potassium from the extracellular fluid to the
intracellular fluid
◦ Dialysis if hyperkalemia is severe
◦ Administer calcium gluconate IV
 Does not promote potassium loss, but decreases
myocardial irritability
Hyperkalemia (cont’d)

Treatment (cont’d) –
◦ Administer sodium bicarbonate
 Makes cells more alkaline, which shifts potassium
back into the cells
Calcium
Calcium is a major cation in the body’s
extracellular fluid
 Calcium is stored in the hard bones
 Calcium concentration is maintained by
the calcium pump, which moves calcium in
and out of cells
 Normal serum calcium levels =
8.5 – 10.5 mg/dL
 Changes in serum protein (especially
albumin) causes changes in calcium level
because calcium binds to protein
 An increase in calcium causes a decrease
in phosphorus

Calcium (cont’d)

Parathyroid hormone
◦ Responsible for the transfer of calcium from
bone to plasma
◦ Aids in intestinal absorption
◦ Enhances renal calcium reabsorption
Calcium, along with phosphorus, enhances
bone strength and durability
 Calcium helps to maintain cell membrane
structure, function, and permeability
 Calcium affects activation, excitation, and
contraction of cardiac and skeletal muscle
 Calcium helps to activate specific steps in
blood coagulation

Calcium (cont’d)
Calcium assists in the regulation of the
acid-base balance
 Calcium plays a major role in nerve
impulse transmission because it
determines the speed of ionic refluxes
through nerve membranes

Hypocalcemia
Calcium level < 8.5mg/dL
 The most common cause of hypocalcemia
is inadequate secretion of parathyroid
hormone caused by hypoparathyroidism
 Other causes –

◦
◦
◦
◦

Diarrhea
Wound exudate
Acute pancreatitis
Vitamin D deficiency
Signs and symptoms –
◦ Cardiovascular
 Decreased blood pressure
 ECG changes with prolonged QT interval
 Cardiac arrest
Hypocalcemia (cont’d)

Signs and symptoms (cont’d) –
◦ Respiratory
 Laryngospasm
◦ Renal failure
◦ Gastrointestinal
 Hyperactive bowel sounds
 Diarrhea
 Intestinal cramps
◦ Musculoskeletal
 Muscle cramps of the face and/or extremities
 Bone fractures due to demineralization and/or
osteoporosis
◦ Neurological
 Increased irritability, mental changes
 Seizures
Hypocalcemia (cont’d)

Signs and symptoms (cont’d) –
◦ Neuromuscular
 Paresthesias/numbness and tingling in the hands
and feet
 Hyperactive deep tendon reflexes
 Tetany
 Positive Trousseau’s sign
 Positive Chvostek’s sign
◦ Other signs and symptoms of hypocalcemia





Dry, brittle nails
Dry hair
Bone pain
Increased bruising
Nursing interventions –
◦ Seizure precautions
Hypocalcemia (cont’d)

Nursing interventions (cont’d) –
◦
◦
◦
◦
◦

Assess for Trousseau’s and Chvostek’s signs
Assess vital signs, bowel sounds
Provide foods high in calcium
Monitor calcium labs, ECG
Assess for musculoskeletal injury
Treatment –
◦ Administer calcium gluconate orally or by IV
◦ Intravenous calcium is 10% calcium gluconate
administered by slow IV push
 Rapid administration can result in bradycardia or
cardiac arrest
 Monitor IV site
 Monitor for signs and symptoms of hypercalcemia
Hypercalcemia
Hypercalcemia results from excessive
release of calcium from the bones
 Causes

◦ Metastatic cancer
◦ Hyperparathyroidism
◦ Hyperthyroidism
 Excessive bone reabsorption
◦
◦
◦
◦
◦
Thiazide diuretics
Excessive calcium intake
Immobility
Vitamin D intoxication
Hypophosphatemia
Hypercalcemia (cont’d)
Symptoms appear when serum calcium
level >12mg/dL
 Signs and symptoms –

◦ Cardiovascular





Hypertension
Decreased S-T segments
Shortened QT interval
Heart block
Cardiac arrest
◦ Gastrointestinal
 Hypoactive bowel sounds
 Constipation
 Nausea/vomiting
Hypercalcemia (cont’d)

Signs and symptoms (cont’d) –
◦ Renal
 Polyuria
 Polydipsia
 Renal calculi
◦ Musculoskeletal
 Bone fractures/thinning
 Deep bone pain
 Decreased muscle tone
◦ Neuromuscular




Depressed neuromuscular excitability
Decreased deep tendon reflexes
Impaired memory
Lethargy, confusion, coma
Hypercalcemia (cont’d)

Nursing interventions –
◦
◦
◦
◦
◦
◦
◦
◦

Monitor calcium and phosphorus levels
ECG monitoring
Strict I&O; strain urine
Monitor neurological status
Assess heart rate and blood pressure
Assess vital signs, daily weight
Assess level of consciousness
Assess bowel sounds
Treatment –
◦ Administer 0.9% NS to dilute serum calcium
and promote renal excretion
 Hydration at 3,000 – 4,000 mL/day
Hypercalcemia (cont’d)

Treatment (cont’d) –
◦ Administer phosphate orally or per enema
◦ Administer loop diuretics (Lasix) to enhance
calcium excretion and prevent fluid overload
during saline administration
◦ Administer corticosteroids to inhibit calcium
absorption in the intestine and increase urinary
excretion of calcium
◦ Administer calcium binders
◦ Administer dialysis
◦ Discontinue oral or intravenous calciumcontaining drugs (i.e. antacids)
Magnesium
Normal magnesium levels =
1.4 – 2.1 mEq/L
 Uses for magnesium

◦ Enzyme action (needed in at least 300
reactions)
◦ Regulation of neuromuscular activity
◦ Skeletal muscle relaxation following
contraction
◦ Powers the sodium/potassium pump
◦ Necessary for maintaining normal heart rhythm
◦ Relaxes the lung muscles responsible for
opening the airways
Hypomagnesemia
Magnesium level <1.4mEq/L
The most common cause for
hypomagnesemia is alcoholism
 Other causes –


◦ Altered absorption
◦ Increased renal loss
◦ Prolonged IV therapy without a magnesium
supplement due to magnesium moving into the
cells
◦ Vomiting
◦ Diarrhea

Vitamin D intoxication
Hypomagnesemia (cont’d)

Signs and symptoms (detectable when
levels drop below 1 mEq/L) –
◦
◦
◦
◦
◦
◦
◦
◦
◦
◦
Muscle twitching, tremors
Hyperreactive reflexes
Laryngeal stridor
Cardiac dysrhythmias
 Supraventricular tachycardia (SVT)
 Premature ventricular contractions (PVCs)
 Ventricular fibrillation
Increased susceptibility to digoxin toxicity
Mood changes
Nausea/vomiting
Diarrhea
Positive Chvostek’s sign
Similar to s/s associated with hypocalcemia
Hypomagnesemia (cont’d)

Treatment –
◦ Oral replacement of magnesium
◦ Continuous IV infusion of magnesium chloride
 Rapid infusion may result in respiratory or cardiac
arrest, flushing and sweating

Diagnostics –
◦
◦
◦
◦
Decreased serum levels of magnesium
Increased renal excretion of magnesium
Increase in serum calcium
Blood gases indicate respiratory or metabolic
acidosis
Hypermagnesemia
Magnesium level >2.1mEq/L
 The most common cause of
hypermagnesemia is renal failure
 Other causes –

◦ Hyperparathyroidism
◦ Hyperthyroidism
◦ Ingestion of medications high in magnesium

Requires emergency treatment
◦ IV calcium gluconate 10%
◦ IV diuretics
Hypermagnesemia (cont’d)

Signs and symptoms –
◦
◦
◦
◦
◦
◦
Flushing
Sense of skin warmth
Hypoactive deep tendon reflexes
Depressed respirations
Hypotension
Cardiac involvement
 Bradycardia
 Heart block
 Cardiac arrest
◦ Increased susceptibility to digoxin toxicity
◦ Nausea/vomiting
◦ Seizures
Phosphorus
Normal phosphorus levels =
2.5 – 4.5 mg/dL
 Uses for phosphorus –

◦ Metabolism of proteins and fats
◦ Formation of adenosine triphosphate
◦ Formation of red blood cell enzymes that aid in
oxygen delivery
80% of phosphorus in the body is
contained in the bones and teeth
 20% of phosphorus is found in the
intracellular fluid
 Phosphorus has an inverse effect on
calcium levels (an increase in one will
cause a decrease in the other)

Hypophosphatemia
Serum phosphate level <2.5mg/dL
 Causes –

◦ Administration of TPN in the absence of a
phosphorus malabsorption syndrome
◦ Alcohol withdrawal
◦ Vomiting
◦ Chronic diarrhea
◦ Aluminum-containing antacids
◦ Diuretics
◦ Corticosteroids
◦ Treatment of diabetic ketoacidosis (insulincontaining dextrose causes phosphorus to
move into the cells)
Hypophosphatemia (cont’d)

Signs and symptoms –
◦ Anemia due to increased RBC fragility resulting
from low adenosine triphosphate (ATP) levels
◦ Bruising due to platelet dysfunction
◦ Slurred speech
◦ Confusion, coma
◦ Tremors, tetany, seizures
◦ Numbness and tingling of the extremities
◦ Muscle weakness, paresthesias
◦ Chest pain, dysrhythmias due to decreased
oxygen availability
◦ Increased rate and depth of breathing due to
hypoxemia
◦ Hypoactive bowel sounds
◦ Vomiting
Hypophosphatemia (cont’d)

Treatment –
◦ Oral phosphate supplements for mild
deficiency
◦ IV phosphorus for severe deficiency; watch for
hypocalcemia and/or hyperphosphatemia
◦ May be added to TPN
◦ Hypotension may occur if administered too
quickly
◦ Watch infusion site for infiltration
Hyperphosphatemia
Phosphate level >4.5mg/dL
 Phosphate shifts into the extracellular fluid
 Primary cause is renal disease
 Signs and symptoms –

◦ Tetany
◦ Mental changes
Sudden hyperphosphatemia (such as in IV
administration of phosphates) may result
in hypocalcemia
 Treated by promoting phosphorus excretion

◦ Aluminum-containing antacids bind
phosphates in the GI tract
Chloride
Normal chloride levels in the body =
95 – 108 mEq/L
 The primary role of chloride is the
regulation of serum osmolarity fluid
balance
 Chloride is a major anion in extracellular
fluid
 Chloride has a reciprocal relationship with
bicarbonate (HCO3)
 Chloride binds with other cations (NaCl,
HCL, KCL)

Chloride (cont’d)

Chloride plays an important role in acidbase balance
◦ Chloride shift = an ionic exchange that occurs
within the red blood cells
◦ Maintains a 1:20 ratio of carbonic acid and
bicarbonate that is essential for pH balance in
plasma
Hypochloremia
Chloride level <95mEq/L
 Results from vomiting/diarrhea or
prolonged use of D5W intravenous solution
 Signs and symptoms –

◦ Increased muscle excitability
◦ Tetany
◦ Decreased respirations
Hyperchloremia
Chloride level >106mEq/L
 Results from severe dehydration or head
trauma
 Signs and symptoms –

◦
◦
◦
◦
◦
Drowsiness, lethargy
Headache
Weakness
Tremors
Cardiac dysrhythmias
Acid-Base
Balance
What is the Acid-Base Balance?
In order for homeostasis to be maintained,
an equalization must exist between the
acidity and alkalinity of body fluids
 This equalization is known as the acid-base
balance
 The acid-base balance is measured using
arterial blood gases (ABGs)
 The greater the concentration of hydrogen
ions, the more acidic a solution becomes

◦ pH is the concentration of hydrogen (H)
◦ The greater the concentration of H, the lower
the number of pH
Normal ABG Values
pH = acid/base
7.35 – 7.45
PO2 = partial pressure of oxygen
80 mmHg – 100 mmHg
SaO2 = oxygen saturation
93% – 100%
PCO2 = partial pressure of carbon dioxide
35 mmHg – 45 mmHg
HCO3 = bicarbonate
22mEq/L – 26mEq/L
pH = Potential of Hydrogen

The narrow range of pH balance is
accomplished by H+ ion balance
◦ HCO3 is regulated by the kidneys
◦ PCO2 is regulated by the lungs

pH of body fluids
◦
◦
◦
◦
◦
◦

Extracellular fluid = 7.35 - 7.45
Intracellular fluid = 6.9 - 7.2
Urine = 6.0
Gastric secretions = 1.0 - 2.0
Intestinal secretions = 6.6 - 7.6
Bile = 5.0 - 6.0
pH is always the product of two
components: respiratory and metabolic
Acidosis/Alkalosis
Acidosis = pH below 7.35
 Alkalosis = pH above 7.45
 Respiratory alkalosis = PCO2 <35
 Respiratory acidosis = PCO2 >45
 Metabolic acidosis = HCO3 <22mEq/L
 Metabolic alkalosis = HCO3 >26mEq/L

Respiratory Acidosis

Occurs in response to hypoventilation
◦
◦
◦
◦
◦
◦
◦
Respiratory depression
Inadequate chest expansion
Airway obstruction
Interference with alveolar-capillary exchange
COPD
Sedative or barbiturate overdose
Pneumonia
pH decreases while PCO2 increases
 Respiratory distress
 Change in level of consciousness
 Treated by opening airway passages

Respiratory Acidosis (cont’d)
Nursing assessment –
 Cardiovascular
◦ Hypotension
◦ ECG shows peaked T waves, prolonged PR
intervals, and widened QRS complexes
◦ Peripheral vasodilation with warm, flushed skin
◦ Thready, weak pulse
◦ Tachycardia

Respiratory
◦ Dyspnea
◦ Hypoventilation
◦ Hypoxia
Respiratory Acidosis (cont’d)
Nursing assessment (cont’d)

CNS
◦
◦
◦
◦
◦
◦
Headache
Muscle twitching
Seizures
Altered mental status
Decrease in LOC
Drowsiness
Diagnostic findings - pH <7.35
 PCO2 >45 mmHg
 Hyperkalemia
Respiratory Acidosis (cont’d)
Compensation (how the body compensates
for respiratory acidosis) –
 Rate and depth of respirations increased in
order to blow off CO2
 Kidneys eliminate hydrogen ions and retain
bicarbonate
 HCO3 rises when the body is compensating
for acidosis
 HCO3 increase raises pH
Treatment –
 Treat the underlying cause
 Improve ventilation (may need a ventilator)
 Assess respiratory depth and rate
Respiratory Acidosis (cont’d)
Treatment (cont’d)
 Pulmonary hygiene
◦ Clear respiratory tract of mucus
Provide adequate fluids to liquefy
secretions
 Low flow oxygen for carbon dioxide
retention in patients with chronic
respiratory acidosis
 Position patient to facilitate best lung
expansion
 Assess apical pulse, color of skin, nail
beds, mucus membranes, LOC
 Assess for tachycardia or arrhythmias

Respiratory Acidosis (cont’d)
Treatment (cont’d)
 Monitor arterial blood gases, potassium
 Administer medications
◦ Bronchodilators
◦ Antibiotics
◦ Mucomyst to decrease viscosity of pulmonary
secretions
Oral hygiene
 Provide a calm atmosphere
 Keep siderails up and call light within
reach
 Orient patient frequently if needed

Respiratory Acidosis (cont’d)
Satisfactory Outcomes - ABGs improved to patient’s baseline
 Decreased anxiety
 Improved breathing with less effort
 Freedom from injury
 No cardiac arrhythmias
 Improved LOC
 Normal respiratory rate and depth
Respiratory Alkalosis

Occurs in response to hyperventilation
◦ Stress
◦ Fever
◦ Pain
pH increases while PCO2 decreases
 Caused by infection, incorrect ventilator
settings, respiratory center stimulation as
a result of fever, salicylate intoxication
 Signs and symptoms include headache,
dizziness, paresthesias, neuromuscular
irritability

Respiratory Alkalosis (cont’d)
Nursing assessment –
 Cardiovascular
◦ Increased myocardial irritability
◦ Increased heart rate

Respiratory
◦ Rapid, shallow breathing
◦ Chest tightness

CNS
◦
◦
◦
◦
Dizziness, light-headedness, blurred vision
Difficulty concentrating, anxiety, panic
Numbness and tingling in the extremities
Hyperactive reflexes, tetany, convulsions
Respiratory Alkalosis (cont’d)
Diagnostic findings - pH >7.45
 PCO2 <35 mmHg
 Hypokalemia
 Hypocalcemia
Compensation –
 Kidneys conserve hydrogen and excrete
bicarbonate
 Low HCO3 levels indicates that the body is
attempting to compensate
Respiratory Alkalosis (cont’d)
Treatment –
 Treat the cause of the condition
 Assist patient to breathe more slowly
 Use rebreather mask or paper bag
 Administer oxygen if patient is hypoxic
 Administer anxiolytics if needed
 Provide emotional support
 Monitor patient’s vital signs
 Monitor patient’s arterial blood gases
 Protect patient from injury
Respiratory Alkalosis (cont’d)
Satisfactory Outcomes - Patient will have a decreased respiratory
rate
 Patient will have absence of numbness or
tingling in the extremities
 Normal (or baseline) ABGs
 Patient will experience diminished anxiety
 Patient will be free from injury
Metabolic Imbalance
Bicarbonate (HCO3) is a direct reflection
of the renal system’s ability to compensate
for pH changes
 Normal HCO3 range is 22 – 26 mEq/L
 HCO3 level <22 indicates acidosis
 HCO3 level >26 indicates alkalosis
 Base Excess is an indication of the amount
of HCO3 available in the extracellular fluid
 Normal base excess range is -3.0 to +3.0
 A value >3.0 indicates metabolic alkalosis
 A value <3.0 indicates metabolic acidosis

Metabolic Acidosis
Causes - Kidney failure
 Diabetic ketoacidosis
 Hyperthyroidism
 Trauma, shock
 Increased exercise
 Severe infection, fever
 Starvation
 Malnutrition
 Chronic diarrhea
Metabolic Acidosis (cont’d)
Nursing assessment –
 Cardiovascular
◦
◦
◦
◦

Peripheral vasodilation
Hypotension
Dysrhythmias
Cold, clammy skin
Respiratory
◦ Deep, rapid breathing (Kussmaul’s respirations)

CNS
◦ Drowsiness/lethargy that progresses to coma
◦ Headache, confusion
◦ Weakness
Metabolic Acidosis (cont’d)
Nursing assessment (cont’d)
 Gastrointestinal
◦ Nausea/vomiting
◦ Diarrhea
◦ Abdominal pain
Diagnostic findings - pH <7.35
 HCO3 <22
 Hyperkalemia
Metabolic Acidosis (cont’d)
Compensation (how the body compensates
for metabolic acidosis) –
 Lungs eliminate carbon dioxide
 Kidneys conserve bicarbonate
Treatment –
 Treat the underlying cause
 Provide hydration
 Monitor arterial blood gases
 Monitor I&O and weight
 Assess vital signs
 Assess respiratory rate and depth
Metabolic Acidosis (cont’d)
Treatment (cont’d)
 Assess level of consciousness
 Monitor GI function
 Administer ECG
 May need to administer alkalotic IV
solution
◦ NaHCO3
◦ Must be administered cautiously due to
possibility of metabolic alkalosis and
hypokalemia
Metabolic Acidosis (cont’d)
Satisfactory Outcomes - Patient will be free from injury
 Patient will experience no dysrhythmias
 Normalized ABGs
 Patient will have no fluid deficits
 LOC returns to normal
 Relief of GI symptoms
Metabolic Alkalosis

Occurs with loss of hydrogen ions
◦ Vomiting
◦ NG suction
Occurs with increase in HCO3 due to
ingestion of bicarbonate-based antacids
Nursing assessment –
 Cardiovascular

◦ Tachycardia, dysrhythmias
◦ Hypertension

Respiratory
◦ Hypoventilation
◦ Respiratory failure
Metabolic Alkalosis (cont’d)
Nursing assessment (cont’d)

CNS
◦
◦
◦
◦
◦
◦
◦
◦
Dizziness
Irritability
Tremors
Muscle cramps
Hyperreflexia
Paresthesias of the fingers and toes
Tetany
Seizures
Metabolic Alkalosis (cont’d)
Diagnostic findings - pH >7.45
 HCO3 >26
 Hypokalemia
 Hypocalcemia (pH increases calcium
binding)
Compensation –
 Lungs retain carbon dioxide
 Kidneys conserve hydrogen and excrete
bicarbonate
 PCO2 increases with compensation
Metabolic Alkalosis (cont’d)
Treatment –
 Treat underlying cause
 Assess level of consciousness
 Assess vital signs
 Assess respiratory rate and depth
 Administer potassium supplement if
needed
 Administer ranitidine or famotidine to
decrease secretion of hydrogen from GI
drainage
 Assess I&O
 Assess arterial blood gases
 Assess ECG findings
Metabolic Alkalosis (cont’d)
Satisfactory Outcomes - Hypertension corrected
 Electrolytes within normal range
 Normalized ABGs
 Normal ECG
Buffer System

Bicarbonate –
◦ Linked to both the respiratory and renal
systems
◦ Normal bicarbonate (HCO3) to carbonic acid
(H2CO3) ratio is 20:1
◦ Ratio changes if pH is increased or decreased
◦ Once compensation occurs, the ratio stabilizes

Respiratory –
◦ The lungs control the respiratory carbonic acid
buffer system, but fatigue quickly
◦ Respiratory rate and depth adjusted in
response to carbon dioxide in the extracellular
fluid; quick reaction time
Buffer System (cont’d)

Renal –
◦ The kidneys control the metabolic buffer
NaHCO3 (sodium bicarbonate)
◦ Excretes acidic or alkaline urine
◦ Reaction is slow (hours to days)
◦ More effective than the respiratory buffer
system
Review of Simple
Acid-Base Disturbances --
pH <7.35 = acidosis
 pH >7.45 = alkalosis
 Abnormal PCO2 = respiratory
 Abnormal HCO3 = metabolic
 If the patient is acidotic with a PCO2
>45mmHg, the problem is respiratory
 If the pt is acidotic with an HCO3
<22mEq/L, the problem is metabolic
 If the patient is alkalotic with a PCO2
<35mmHg , the problem is respiratory
 If the patient is alkalotic with an HCO3
>26mEq/L, the problem is metabolic

Review of Compensation -If both HCO3 and PCO2 are above or below
their normal ranges and are shifting in the
same direction, the patient’s buffering
system is functioning and trying to bring
the acid-base balance back to normal
 Respiratory Acidosis –

◦ pH <7.35
◦ PCO2 >45
◦ HCO3 elevated with compensation (kidneys
eliminate hydrogen and retain bicarbonate)

Respiratory Alkalosis –
◦ PCO2 <35
◦ HCO3 decreased with compensation (kidneys
conserve hydrogen and excrete bicarbonate)