NCM 310 LEC – Care of Clients with Problems in Oxygenation, Fluid and Electrolytes,

Infectious, Inflammatory and Immunologic Response, Cellular Aberrations, Acute and

Chronic

HOMEOSTASIS Functions of Electrolytes

⮚ Assisting in regulating water balance
- Derived from the Greek word meaning “to ⮚ Regulating and maintaining acid-base
stay the same” balance
- Homeostasis is the body’s tendency to ⮚ Contributing to enzyme reactions essential
maintain a state of physiological balance in for neuromuscular activity
the presence of constantly changing Body Fluid Distribution
- Intracellular Fluid (ICF 40%)
conditions
● K+
- Homeostasis depends on multiple factors
● Mg 2+
both the external and internal environments ● PO42-
- the normal volume, composition, distribution - Extracellular Fluid (ECF 20%)
and pH of body fluids reflects a state of ● Na+
homeostasis ● Cl_
● HCO3-
Body Fluid Composition ● Interstitial Fluid (15%)
⮚ Water - is located in the spaces between
Functions of Water most of the cells of the body
❖ Provides a medium for the ● Intravascular Fluid/Plasma (5%)
transport and exchange of - is contained within the arteries,
nutrients and other substances veins and capillaries
❖ Provides a medium for metabolic ● Transcellular Fluid (1-2%)
reactions within cells - Includes urine, digestive
❖ Assists in regulating body secretions and perspiration, as
temperature through the well as cerebrospinal, pleural,
evaporation of perspiration synovial, intraocular, gonadal and
❖ Provides form for body structure pericardial fluids
and acts as a shock absorber Normal Values
How do we maintain normal fluid balance?
Electrolyte Trick Normal

Sodium (Na+) ODD Numbers: 135 135-145 mEq/L

Chloride (Cl-) Swimming Pool 95-105 mEq/L

95-105 F

Bicarbonate (HCO3-) Carbonation Soda 12 23-29 MEq/L

per pack x2

Calcium (Ca2+) Call 911 9-11 mg/dl

Potassium (K+) 3-5 bananas 3-5 mEq/L

Phosphate (PO42-) PO42- 2.5-4.5 mg/dl

Magnesium (Mg2+) Magnifying glass 1.5-2.5 mg/dl

1.5-2.5x
➢ Electrolytes
● Electro - electricity Serum osmolality 280-300 mOsm/kg

● lytes - dissolve
● Electrolytes are substances that Types of Membranes
dissociate in solution to form ● Cell membranes
charged particles called ions - separate interstitial fluid from
Electrolytes carry electrical charges intracellular fluid
● Capillary membrane
- separate plasma from interstitial
fluid
● Epithelial membrane
- separate transcellular fluid form
from interstitial fluid and plasma.
These membranes include the
mucosa of the stomach, intestines,
and gallbladder, the pleural,
peritoneal and synovial
 membranes;and the tubules of the Tonicity of IV Fluids
kidney ● Hypertonic
Body Fluid Movement - 5% Saline
● Osmosis - 3% Saline
- The process by which water moves across - 5% dextrose in 0.9 Saline (D5NS)
a selectively permeable membrane from an - 5% dextrose in LR (D5LR)
area of lower solute concentration to an area - 10% dextrose in water (D10W)
of higher solute concentration ● Isotonic
● No energy needed - 0.9% sodium chloride (NS)
- Lactated Ringers (LR)
- 5% Dextrose in Water
● Hypotonic
- 0.45% saline
- 0.33 saline
- 0.225 Saline
- 5% Dextrose in Water (D5W)
Note: 5% Dextrose in Water starts as ISOTONIC and
then changes to HYPOTONIC
● Diffusion
- the process by which solute
Osmolarity and Osmolality molecules move from an area of
● Osmolarity high solute concentration to an
- refers to the quantity of solutes per area of low solute concentration to
litre of solution (by volume) become evenly distributed
- it is reported in milliosmoles per litre - No energy needed
(m0sm/L)
● Osmolality
- refers to the quantity of solutes per
kilogram of water (by weight)
- it is reported in milliosmoles per
kilogram (m)sm/kg)
Osmotic Pressure and Tonicity
● Osmotic Pressure
● The power of a solution to draw water across
a membrane Types
● Tonicity ❖ Simple Diffusion - occurs by
● The ability of all solutes to cause an osmotic the random movement of
driving force that promotes water movement particles through a solutions
from one compartment to another ❖ Facilitated Diffusion - aka
● Effective osmoles: sodium, mannitol, carrier-mediated diffusion,
glucose, sorbitol allows large water-soluble
The Effect of Tonicity on Cells molecules, such as glucose
● Isotonic Solutions and amino acids, to diffuse
- the same concentration of solutes across cell membranes
as plasma
- Cells will neither shrink nor swell
● Hypertonic Solutions
- have greater concentration of
solutes than plasma
- Water is drawn out of a cell
causing it to shrink
● Hypotonic Solutions
- have a lower solute concentration
than plasma
- water moves into the cells,
causing them to swell and rupture
(haemolyse)
● Filtration
- the process by which water and
dissolved substances (solutes)
move from an area of high
hydrostatic pressure to an area of
low hydrostatic pressure
- This usually occurs across
capillary membranes. Hydrostatic
pressure is created by the
pumping action of the heart and
gravity against the capillary wall
 - Filtration occurs in the glomerulus
of the kidneys, as well as at the
arterial end of capillaries

Clinical Tip
❖ The thirst mechanism declines with
ageing: Risk of dehydration and
● Active Transport hyperosmolarity
- allows molecules to move across ❖ People with an altered level of
cell membranes and epithelial consciousness or who are unable to
membranes against a respond to thirst are also at risk
concentration gradient ● Kidneys
- This movement requires energy - In adults, about 170 L of plasma
(adenosine triphosphate, or ATP) are filtered through the glomeruli
and a carrier mechanism every day
- by selectively reabsorbing water
and electrolytes, the kidneys
maintain the volume and
osmolality of body fluids
- about 99% of the glomerular
filtrate is reabsorbed, and only
about 1500 mL of urine is
produced over a 24-hour period

● Renin-Angiotensin-Aldosterone system

Body Fluid Regulation

Regulatory Mechanisms
● Thirst
- is the primary regulator of water
intake
- Plays an important role in
maintaining fluid balance and
preventing

- The renin-angiotensin-aldosterone-system.
Decreased blood volume and renal perfusion
set off a channel of reactions, leading to
release of aldosterone from the adrenal
cortex. Increased levels of aldosterone
regulate serum K+ and Na+ blood pressure
 and water balance through effects on the
Assessment Fluid Deficit
kidney tubules
● Antidiuretic hormone Blood Pressure Decreased systolic, Postural
Hypotension

Heart Rate Increased

Pulse amplitude Decreased

Respirations Normal

Jugular Vein Flat

Edema Rare

Skin turgor Loose, poor turgor

Urine Output Low, concentrated

Urine-specific gravity High

Loss
Weight 2%-5%: mild FVD
6%-9%: moderate FVD
>10%: Severe

● Atrial Natriuretic Peptide

Distention of Atrial Muscle Cells: Release of ANP
↓ Diagnostic Findings
ANP: Inhibition of renin and aldosterone secretion
↓ ↑ HCT and HgB Decreased plasma volume
Sodium wasting and diuresis, vasodilation
↑ Serum and urine Due to kidney’s attempt to
HYPOVOLEMIA osmolality and specific conserve water
gravity
- Fluid Volume Deficit, or hypovolemia, occurs
when loss of ECF volume exceeds the intake
of fluid ↓ Urine sodium Due to secretion of
aldosterone
- It occurs when water and electrolytes are
lost in the same proportion as they exist in
↑ BUN and creatinine A volume-depleted patient
normal body fluids; thus, the ratio of serum
has a BUN elevated out of
electrolytes to water remains the same proportion to the serum
- FVD may occur alone or in combination with creatinine (ratio greater
other imbalances than 20:1)
- Unless other imbalances are present
concurrently, serum electrolyte
concentrations remain essentially
unchanged
Pathophysiology
Loss of body fluids + decreased fluid intake
(Vomiting, Diarrhea, Fistulas, Fever, Excess Sweating,
Burns, Blood Loss, GI Suction, Third Space fluid shifts)
↓
Prolonged period of inadequate intake
(Anorexia, Nausea, Inability to gain access to fluid)
 ● Oral fluids
Serum Electrolyte Changes ● ice chips
● Foods that are or become liquid at room
Hypokalemia occurs with GI and renal losses
temp
Hyperkalemia occurs with adrenal insufficiency
● Parenteral fluids
● tube feeding
Hyponatremia occurs with increased thirst and ADH
● IV medications
release ● Catheter or tube irrigants
Fluid Output
Hypernatremia results from increased insensible losses ● Urinary output
and diabetes insipidus ● Vomitus and Liquid feces
● Tube drainage
● Wound and fistula drainage
Hydration Acute or Severe When patient is Analyzing Intake and Output
(Hypotensive Normotensive I&O measurements are totaled at the end of the shift
Patients) (q8 to 12 hrs), and the totals are recorded in a client’s
chart
● Mild: Oral ● Isotonic ● Hypotonic ↓
Route Solutions: Solution: for Compare the total 24-hour fluid output measurement
expands renal with the total 24-hour fluid intake measurement and
plasma excretion of
volume metabolic compare both to previous measurements
wastes ↓
Clients whose output substantially exceeds intake are
Monitoring at risk for fluid volume deficit, whereas clients whose
- I&O intake substantially exceeds output are at risk for fluid
- Weight volume excess
- Vital signs ↓
- Central venous pressure When there is a significant discrepancy between intake
- level of consciousness and output or when fluid intake or output is inadequate
- breath sounds Nursing Diagnosis and Interventions
- skin color ● Deficient Fluid Volume
Fluid Challenge - Assess v/s, CVP and peripheral
● Typical fluid challenge test involves pulse vol. at least q4hrs
administering 100 to 200 mL of normal saline - Weigh daily under standard
solution over 15 minutes conditions
● The goal is to provide fluids rapidly enough - Administer and monitor intake of
to attain adequate tissue perfusion without oral fluids as prescribed
compromising the cardiovascular system. - Administer IV as prescribed using
The response by a patient with FVD but an electronic infusion pump
normal renal function is increased urine ● Ineffective Tissue Perfusion
output and an increase in blood pressure - Monitor in level of consciousness
and central venous pressure and mental status
Central Venous Pressure - Monitor serum urea and creatinine
● CVP is a hemodynamic monitoring method and cardiac enzymes, reporting
for monitoring for evaluating fluid volume elevated levels to the physician
status - Turn at least every 2 hours.
- it measures mean right atrial provide good skin care and
pressure by means of a catheter monitor evidence of skin or tissue
- The CVP catheter is inserted by a breakdown
doctor into the antecubital, internal ● Risk for Injury
jugular or subclavian vein. - Institute safety precautions,
● Normal CVP range is 2 to 5mmHg keeping bed in low position, using
❖ Low CVP - inadequate venous side rails, slowly raising the person
return from fluid deficit and from supine to sitting or sitting to
hypovolemia or peripheral standing position
vasodilation - Teach patient and family how to
❖ High CVP - fluid overload, cardiac, reduce orthostatic hypotension
problems that decrease cardiac
contractility or pulmonary HYPERVOLEMIA
disorders that increase pulmonary - Fluid Volume Excess (FVE) results when
vascular resistance both water and sodium are retained in the
Fluid Balance Monitoring body
● Monitor I and O every 8 hours. Normal urine - Fluid volume excess may be caused by fluid
output is 30mL/hr overload (excess water and sodium intake)
● Daily Body Weight or by impairment of the mechanisms that
● Monitor Vital signs maintain homeostasis
● Monitor for skin and tongue turgor - If FVE, both water and sodium are gained in
● Monitor Mental Function about same proportions as normally exists in
Fluid Intake extracellular fluid
 - The total body sodium content is increased,
which in turn causes an increase in total Medications: Diuretics
body water
- Because the increase in sodium and water is - 3Ds: Diuresis, Decrease BP, Dehydrate
isotonic, the serum sodium and osmolality
remain normal and the excess fluid remains
Loop diuretics act in Thiazide-type Potassium-sparing
in the extracellular space ascending loop of diuretics act on the diuretics affect the
Conditions that Causes Fluid Volume Excess Henle distal convoluted distal nephron
- Heart failure tubule
- Adrenal gland disorders
- Excessive intake of sodium containing foods - Furosemide (Lasix) - Chlorothiazide - Spironolactone
- Ethacrynic Acid - Hydrochlorothiazide
- Cirrhosis of liver
- Corticosteroid administration
- Drugs that cause sodium retention
- Renal failure
- Stress conditions causing the release of
ADH and aldosterone
Assessment Fluid Deficit Fluid Excess

Blood Pressure Decreased systolic, Increased

Postural
Hypotension

Heart Rate Increased Increased

Pulse amplitude Decreased Increased

Nursing Diagnosis and Interventions

Respirations Normal Moist crackles,
wheezes ● Excess Fluid Volume
- Assess v/s, heart sounds, CVP
Jugular Vein Flat Distended and volume of peripheral arteries
- Assess for the presence and
Edema Rare Dependent extent of edema, particularly in the
lower extremities, the back, and
Skin turgor Loose, poor turgor Tout sacral and periorbital areas
- Assess urine output hourly.
Urine Output Low, concentrated May be low or maintain accurate intake and
normal output records
- Obtain daily weights at the same
Urine-specific High Low time of day, using approximately
gravity
the same clothing and balanced
scales (Weight gain of 2 kgs is
Loss Gain
Weight 2%-5%: mild FVD equivalent to 2 L of fluid gain)
6%-9%: moderate
FVD
>10%: Severe

Diagnostic Findings
Serum electrolytes and Serum sodium and
serum osmolality osmolality usually remain
within normal limits

Serum Hct and HgB often are decreased due to

plasma dilution from
excess extracellular fluid

Additional tests of renal may be ordered to help

and liver functions (such as determine the cause of fluid
serum urea and creatinine volume excess if its unclear
and liver enzymes)

Medical Management
● Fluid Management
- Fluid intake may be restricted in a
person who has fluid volume ● Risk of Impaired Skin Integrity
excess - Frequently assess skin,
● Dietary Management particularly in pressure areas and
- A sodium-restricted diet is often over bony prominences
prescribed - Reposition the person at least
every 2 hours
 - Provide an egg-crate mattress or - Multiple electrolytes roughly the same
alternating pressure mattress, foot concentration as your plasma (except for
cradle, heel protectors and other Mg), provide 9cal/L
divides to reduce pressure on - Used in treatment of hypovolemia, burns,
tissue fluid lost as bile or diarrhea, and acute blood
loss
PARENTERAL FLUIDS - Not given to patient with lactic acidosis
Fluid and Electrolyte Therapy - Not given to patients with a pH of >7.5
● IV fluid and electrolyte therapy are - Not given to patient with kidney injury,
necessary to treat many different fluid and hyperkalemia, liver dysfunction
electrolyte imbalances
● Many patients need maintenance IV fluid
therapy when they cannot take oral fluids
● Other patients need corrective or
replacement therapy for losses that are
ongoing or have already occurred
Tonicity of IV Fluids
● Hypertonic - 170cal/L and free water to aid in renal
- 5% Saline excretion of solutes
- 3% Saline - Used in hypernatremia, fluid loss and
- 5% dextrose in 0.9 Saline (D5NS) dehydration
- 5% dextrose in LR (D5LR) - Should not be used in early post operative
- 10% dextrose in water (D10W) period (ADH is increased) • Contraindicated
● Isotonic in head injuries - ↑ICP
- 0.9% sodium chloride (NS) - Not used for fluid resuscitation because it
- Lactated Ringers (LR) can cause hyperglycemia
- 5% Dextrose in Water - May cause peripheral circulatory collapse,
● Hypotonic anuria in patients with sodium deficiency,
- 0.45% saline and increased blood fluid loss; for extended
- 0.33 saline period may cause hypokalemia
- 0.225 Saline - Converts to hypotonic solution in the body
- 5% Dextrose in Water (D5W) Hypotonic Solutions
Note: 5% Dextrose in Water starts as ISOTONIC and ● A hypotonic solution has a lower
then changes to HYPOTONIC osmolality when compared to
Classification of Parenteral Fluids plasma.
Isotonic Solutions ● Infusing a hypotonic solution
● An isotonic solution has an dilutes ECF, lowering serum
osmolality similar to plasma. osmolality. Osmosis then produces
● Because of this similarity, giving a movement of water from ECF to
an isotonic solution expands only interstitial spaces and cells,
ECF and the fluid does not move causing cells to swell.
into cells

- Provides Na+, Cl- and free water

- Used to treat hypertonic dehydration, Na+
and Cl- depletion and gastric fluid loss
- Expands ECF volume; used in hypovolemic
- Not for third-space fluid shifts or increased
states, resuscitative efforts, shock, diabetic
intracranial pressure
ketoacidosis (UHRSDK)
- Administer cautiously: may cause
- Can cause fluid volume excess and cardiovascular collapse and ↑ ICP
hyperchloremic acidosis if used in excessive Hypertonic Solutions
volumes. (CFVECHLO) ● Has a higher osmolality than
- Not a desirable routine solution plasma. higher osmotic pressure
- Only solution given with blood draws water out of the cells into
ECF.
● Those receiving hypertonic
solutions need frequent monitoring
of BP, lung sounds, and serum
sodium levels because of the risk
for intravascular fluid volume
excess

- Tonicity the same as plasma

 - Used to increase ECF volume, decrease
cellular swelling
- Used only in critical situations to treat
hyponatremia
- Give slowly and cautiously because it can
cause intravascular volume overload and Functions of Sodium
pulmonary edema ● Is the primary regulator of the volume,
osmolality and distribution of ECF
● It is also important for maintaining
neuromuscular activity
How sodium affects water distribution between
fluid compartments

- Assists in removing intracellular fluid excess

- Highly hypertonic solution used to treat
symptomatic hyponatremia
- Administer slowly and cautiously because it
can cause intravascular volume overload
and pulmonary edema
Colloid Solution
● Colloid solutions contain large
molecules that increase oncotic Hyponatremia
pressure and pull fluid into the ● Hyponatraemia is a serum sodium
blood vessels. level of less than 135 mEq/L.
● Because this action restores blood ● Hyponatraemia usually results
volume, colloids are also called from a loss of sodium from the
volume expanders or plasma body, but it may also be caused by
expanders. water gains that dilute ECF.
● Colloids include human plasma
products (albumin, fresh frozen
plasma, blood) and semisynthetic
solutions (dextran, starches)

Causes of Hyponatremia: 4D1N

● Diuretics
● Diarrhea
● Dehydration ( Impaired Aldosterone and
cortisol production, Excessive Sweating)
● Drains (NGT suction)
● Neurological Conditions: stroke, cerebral
hemorrhage
Clinical Manifestations:
SALT LOSS
● Stupor/Coma
● Anorexia, nausea vomiting
● Lethargy
SODIUM IMBALANCES ● Tendon reflexes decreased
Sodium ● Limb weakness
● Sodium is the most plentiful electrolyte in ● Orthostatic hypotension
ECF, with normal serum sodium levels ● Seizure, headaches
ranging from 135 to 145 mEq/L ● Stomach cramps
●
With Decreased ECF With Normal or Increased
 Two Regulatory Mechanism that protect the body
ECF
from Hypernatremia
excess sodium in ECF stimulates the release of ADH
• Postural Hypotension • Weight gain, ↑ BP, ↑CVP
• ↓ BP so more water is retained by the kidneys
• ↓Jugular venous filling ↓
• ↑ pulse, thread the thirst mechanism is stimulated to increase the
• Cold, clammy skin
intake of water
Causes of Hypernatremia: 7Ds
Diagnostic Findings ● Diuresis
● Diarrhea
Serum sodium and osmolality • Decreased in hyponatremia
● Diabetes Insipidus
● Dehydration
24-hour urine specimen • Is obtained to evaluate sodium
excretion ● Diseases of Kidney
● Doctors and nurses (Iatrogenic)

Medical Management Clinical Manifestations

FRIED
With Decreased ECF Normal or Excess ECF
● Fever, Flushed Skin
● Restless, Really Agitated and Thirsty
• Sodium-containing fluids (oral, • Loop Diuretics: isotonic
NGT, IV) diuresis
● Increased Fluid Retention
• To replace both water and • No to Thiazide Diuretics ● Edema, Extremely confused
sodium: ● Decreased Urine Output, Dry mouth and skin
• Isotonic Ringer’s or Isotonic
Saline Solution
Diagnostic Findings
Serum sodium levels • are greater than 145 mEq/L in
hypernatraemia
Nursing Management
● Risk for Imbalanced Fluid Volume Serum osmolality • is greater than 295 mOsm/kg
- Use an intravenous flow control in hypernatraemia
device to administer hypertonic
saline (3% and 5% NaCl) Water deprivation test • may be conducted to identify
solutions; carefully monitor flow diabetes insipidus.

rate and response. Medical Management

- If fluids are restricted, explain the ● Is oral or intravenous water replacement
reason for the restriction, the ● Hypotonic intravenous fluids such as 5%
amount of fluid allowed and how to dextrose in water
calculate fluid intake. ● Diuretics may also be given to increase
● Risk of ineffective cerebral tissue perfusion sodium excretion
- Assess for neurological changes, Nursing Management
such as lethargy, altered level of ● Risk for Injury
consciousness, confusion and - Monitor and maintain fluid
convulsions replacement to within the
- Assess for neurological changes, prescribed limits
such as lethargy, altered level of - Monitor serum sodium levels and
consciousness, confusion and osmolality; report rapid changes to
convulsions the attending doctor.
- Assess muscle strength and tone - Monitor neurological function,
and deep tendon reflexes. including mental status, level of
Hypernatremia consciousness and other
● Hypernatraemia is a serum manifestations such as headache,
sodium level greater than 145 nausea, vomiting, elevated blood
mEq/L. pressure and decreased pulse rate
● It may develop when sodium is - Institute safety precautions as
gained in excess of water or when necessary: keep the bed in its
water is lost in excess of sodium. lowest position, side rails up and
● Either fluid volume deficit or fluid padded, and an airway at the
volume excess often accompanies bedside.
hypernatraemia
Practice Questions
A patient with a sodium level of 178 is ordered
to be started on 0.45% Saline. What is the most
IMPORTANT nursing intervention for this patient?
A. Maintain patent IV
B. Give rapidly to ensure fluids levels are shifted
properly
C. Clarify doctor’s order because 0.45% saline is
contraindicated in hypernatremia
D. Give slowly and watch for signs and symptoms
of cerebral edema
You have completed diet teaching with a patient
who has hypernatremia. Which statement by the
patient causes concern?
A. “I will buy fresh vegetables and fruits.”
B. “I will avoid eating canned foods.”
C. “I’m glad I can still eat sandwiches with
bologna.”
D. “I will avoid cooking with butter.”

A patient with Cushing’s Syndrome has been

experiencing an infection and has a fever of 102’F.
On assessment, you find the patient to be
Hypokalemia
confused, restless, has dry mucous membranes,
●is an abnormally low serum
and flushed skin. Which finding below correlates
potassium (less than 3.5 mEq/L)
with the presentation of this patient?
● Results from excess potassium
A. Sodium level of 144
loss
B. Sodium level of 115
Causes of Hypokalemia: BADLOAD
C. Sodium level of 170
● Barter Conn’s syndrome
D. Sodium level of 135
(hyperaldosteronism)
● Alkalosis
POTASSIUM IMBALANCES ● Drugs
Potassium ● Laxative abuse, Losses via vomiting &
● The primary intracellular cation, plays a vital gastric suction
role in cell metabolism and cardiac and ● Overdose of Insulin
neuromuscular function ● Acute Glucose Load (Dm-Osmotic Diuresis)
● Normal Value: 3.5-5 mEq/L ● Diarrhea, Drainage
Drugs causing Hypokalemia: BAD FIT
● Beta-2 Agonists (Epinephrine, Albuterol,
Salmeterol)
● Amphotericin B
● Digoxin
● Furosemide
● Insulin
● Thiazides
Clinical Manifestations: Low and Slow
Heart Muscular GI

Functions of Potassium • Arrhythmias • Decreased Deep • Decreased motility

• ECG Changes: Tendon Reflexes • Constipation
● Involved in cardiac and neuromuscular flattened/ inverted T • Muscle cramps • Abdominal
function waves, development • Flaccid paralysis Distention
● Regulates intracellular osmolality and of U waves, • Paralytic Ileus
depressed ST
promoting cell growth segment
● Required by glycogen to be deposited in
muscle and liver cells
● Plays a role in acid base balance
 -
Monitor skeletal muscle strength
and tone, which are affected by
moderate hypokalemia
- Monitor respiratory rate, depth and
effort; heart rate and rhythm; and
blood pressure at rest and
following activity.
● Risk for Imbalanced Fluid Volume
- Maintain accurate intake and
output records. Gastrointestinal
fluid losses can lead to significant
potassium losses.
Diagnostic Findings - Monitor bowel sounds and
abdominal distension
Serum potassium (K+) • Mild :3.0 to 3.5 mEq/L,
Moderate: h 2.5 to 3.0 mEq/L Hyperkalemia
• Severe: less than 2.5 mEq/L ● Hyperkalemia is an abnormally
high serum potassium level
Arterial blood gases (ABGs) • are measured to determine (greater than 5 mEq/L).
acid–base status. An increased ● Hyperkalemia can result from
pH (alkalosis) often is
associated with hypokalemia. inadequate excretion of
potassium, excessively high intake
Renal function studies • such as serum urea and of potassium, or a shift of
creatinine,may be ordered to potassium from the intracellular to
evaluate for potential causes or the extracellular space.
effects of hypokalemia
Causes of Hyperkalemia: MACHINE
ECG recordings • are obtained to evaluate the
● Medications: ACE Inhibitors, NSAIDs,
effects of hypokalemia on the potassium sparing diuretics
cardiac conduction system. ● Acidosis, metabolic and respiratory
● Cellular destruction (burns or traumatic
injury)
● Hypoaldosteronism (Addison’s), Hemolysis
● Intake (excessive)
● Nephrons (renal failure)
● Excretion Impaired

Clinical Manifestations: Tight and Contracted

Heart GI Tract Neuromuscular

• ST elevation and • Diarrhea • Paralysis

Peaked T Waves • Hyperactive Bowel • Increased DTR
Pharmacologic Management • Severe: VFIb or Sounds
Cardiac Standstill
• Hypotension,
Bradycardia

Clinical Tip:
● Do NOT administered as IV push
● Do not administer undiluted
Nursing Management
● Decreased Cardiac Output
- Monitor serum potassium levels,
particularly in the person at risk of
hypokalemia).
- Monitor vital signs, including
orthostatic vitals and peripheral
pulses.
- Monitor the person taking digitalis Diagnostic FIndings
for toxicity. Monitor response to Serum Electrolyte • serum potassium level greater
antiarrhythmic drugs than 5.0 mEq/L
● Activity Intolerance
 - Maintain accurate intake and
Arterial blood gases (ABGs) • are measured to determine if
acidosis is present. output records. Report an
imbalance of 24-hour totals and/or
ECG • to evaluate the effects of urine output less than 30 mL/hour.
hyperkalemia on cardiac - Monitor the person receiving
conduction and rhythm
sodium bicarbonate for fluid
volume excess
Practice Questions
Pharmacologic/Medical Management A patient has a potassium level of 9.0. Which
Mnemonic: C BIG K DIE nursing intervention is priority?
If you see a big K, the patient could die A. Prepare the patient for dialysis and place the
patient on a cardiac monitor
Calcium gluconate • is given intravenously to B. Administer Spironolactone
counter the effects of
hyperkalemia on the cardiac C. Place patient on a potassium restricted diet
conduction system D. Administer a laxative

Insulin + 50g of glucose • promote potassium uptake by Tall peaked T-waves, flat P-waves, prolonged PR
the cells shifting potassium out intervals and widened QRS complexes can be
of ECF
present in which of the following conditions?
ß2-agonist such as salbutamol • temporarily push potassium
A. Hypokalemia
into the cells B. Hyperkalemia
C. Hypokalemia
Sodium bicarbonate • may be given to treat acidosis D. Hyperkalemia

Kayxelate (Sodium polystyrene • a resin that binds potassium in A patient with nasogastric suctioning is
sulfonate) the GI tract, may be experiencing diarrhea. The patient is ordered a
administered orally or rectally
morning dose of Lasix 20mg IV. Patient’s
potassium level is 3.0. What is your next nursing
Potassium wasting diuretics are given to promote potassium
excretion
intervention?
A. Hold the dose of Lasix and notify the doctor for
further orders
Nursing Management B. Administered the Lasix and notify the doctor for
● Risk of decreased cardiac output further orders
- Closely monitor the response to C. Turn off the nasogastric suctioning and
intravenous calcium gluconate, administered a laxative
particularly in people taking D. No intervention is need the potassium level is
digitalis within normal range
- Monitor the ECG pattern for
development of peaked, narrow T CALCIUM IMBALANCES
waves, prolongation of the PR
interval, depression of the ST
segment, widened QRS interval
and loss of the P wave.
- Notify the physician of changes.
Progressive ECG changes from a
peaked T wave to loss of the P
wave and widening of the QRS
complex indicate an increasing
risk of arrhythmias and cardiac
arrest.
● Risk of activity of intolerance
- Monitor skeletal muscle strength
and tone. Increasing weakness,
muscle paralysis or progression of
affected muscles to affect the
upper extremities or trunk can
indicate increasing serum
potassium levels.
- Monitor respiratory rate and depth.
Regularly assess lung sounds.
- Assist with self-care activities as
needed. Increasing muscle
weakness can lead to fatigue and
affect the ability to meet self-care
needs
● Risk for Imbalanced Fluid Volume
- Closely monitor serum potassium,
serum urea and creatinine
Mechanisms that Regulate Calcium Balance ●
The systemic effects of
● Hormones: Parathyroid Hormone, calcitonin hypocalcemia are caused by
and calcitriol decreased levels of ionized
● Acid Base Balance calcium in extracellular fluid
● Plasma Protein Levels Causes of Hypocalcemia: PBPK IDEA
Hormones
Parathyroidectomy • hypoparathyroidism
Parathyroid Hormone & Calcitonin or neck surgery
Calcitriol
Blood Transfusion • Citrate combines with
• ↑Serum calcium, • ↓Serum calcium, calcium
↓bone calcium ↑bone calcium
Pancreatitis • Breakdown of
lipids→Calcium combine
with Lipids→soaps

Kidney Injury • hyperphostatemia→↓

serum Calcium

Inadequate Vitamin • Less exposure to the sun

D consumption

Drugs • Loop diuretics, calcitonin,

phenobarbital, phosphate
enemas, drugs that lower
magnesium) cisplatin and
gentamicin

Electrolyte Changes • Hypomagnesemia,

Hyperphosphatemia

Alcohol Abuse • Alcohol can decrease the

absorption of calcium via
the intestine, or it can have
effects on the pancreas
and vitamin D metabolism

Clinical Manifestations
● Calcium has a stabilizing or sedative effect
on neuromuscular transmission.
● Low Calcium levels facilitate sodium
transport, as the normal inhibition by
Calcium of sodium movement through
Hypocalcemia voltage gated sodium channels is lost
● Hypocalcemia is a total serum ● ↓Calcium level – increased neuromuscular
calcium level of less than 9 mg/dL. excitability
● Hypocalcemia can result from
decreased total body calcium
stores or low levels of extracellular
calcium with normal amounts of
calcium stored in bone.
Clinical Manifestations: Excited
Numbness and tingling • Increased neural
around the mouth and excitability
in the feet

Tetany • cause bronchial

muscle spasms and
visceral muscle spasms
→ airway
obstruction→respiratory
arrest

Chvostek sign • contraction of the

(C-cheek smile when facial muscles produced
touched) by tapping the facial
nerve in front of the ear

Trousseau sign • carpal spasm induced

(T-Twerking arm with by inflating a blood
BP cuff on) pressure cuff on the
upper arm to above
systolic blood pressure
for 2 to 5 minutes

Seizures • Increased irritability of

the CNS and PNS

Mental changes • Depression, impaired

memory, confusion,
delirium, hallucinations

Cardiovascular • Bradycardia,
symptoms ventricular
arrhythmias→cardiac
arrest

ECG changes • Prolongation of the ST

segment, QT
prolongation, torsades
de pointes

Chronic hypocalcemia • Hyperactive bowel Diagnostic Findings

sounds, dry and brittle Total serum calcium • the amount of ionized
hair and nails and (active) calcium
abnormal clotting available, is usually
estimated

Serum albumin • affects serum calcium

result

Serum phosphate • hyperphosphatemia

can lead to
hypocalcemia

Serum Magnesium • normal magnesium

levels must be restored
to correct the
hypocalcaemia

Parathyroid hormone • to identify the possible

(PTH) diagnosis of
hyperparathyroidism

ECG • to evaluate the effects

 Hypercalcemia
of hypocalcemia on the ● Hypercalcemia (serum calcium value greater
heart than 10.4 mg/dL [2.6 mmol/L])
Medical Management Causes of Hypercalcemia: Hyper and Mali
Promised Rena to not consume Vitamin A and D
Intravenous Calcium • Calcium Chloride-
provides more ionized
Calcium but more Hyperparathyroidism • Increased PTH causes
irritating resorption of calcium
• Calcium Gluconate from the bones

Nursing Intervention • Watch out for Malignancies • develop as a result of

infiltration bone destruction by the
• Use cautiously for tumor or due to
patients using hormone-like
Digitalis-derived substances produced
medications by the tumor itself
• Don’t use .9 Nacl –
increases Calcium Prolonged immobility • increased resorption
excretion via kidney and lack of of bone with calcium
• Don’t use with weight-bearing activity release into
phosphates and extracellular fluids
bicarbonates- causes
precipitation Renal failure, • Interfere with
• May cause postural Medications (lithium and elimination of calcium
hypotension during IV thiazide diuretics) by the kidneys
infusion
Vitamin A and D • This vitamins
intoxication enhances Calcium
absorption
Clinical Manifestations:
● High levels of calcium block sodium
movement through voltage-gated sodium
channels causing reduced depolarization
and impaired action potential.
● ↑Calcium level – decreased neuromuscular
excitability
Clinical Manifestations: ↓ Neuromuscular
Nutritional Management Excitability
Neuromuscular • Muscular weakness,
fatigue
• Decreased DTR

Behavioral • Personality changes

• Altered mental status
• Decreasing level of
consciousness

Gastrointestinal • Abdominal pain

• Constipation
• Anorexia, n&V
Nursing Management
Cardiovascular • Arrhythmias
● Report changes such as respiratory stridor
• Shortened ST
(a high-pitched, harsh inspiratory sound
segment, shortened QT
indicative of upper airway obstruction), or
interval
increased respiratory rate or effort, to the
• Hypertension
physician. These changes may indicate
laryngeal spasm due to tetany
● Monitor cardiovascular status, including Renal • Polyuria
heart rate and rhythm, blood pressure and • Thirst
peripheral pulses. Hypocalcaemia decreases
myocardial contractility, causing reduced
cardiac output and hypotension
● Continuously monitor ECG in the person
receiving intravenous calcium preparations,
especially if the person also is taking digitalis
 intravenous • Calcium binds to
administration of phosphate,thus
sodium phosphate or decreasing serum
potassium phosphate. calcium levels

Glucocorticoids which compete with

(cortisone), vitamin D, and a
low-calcium diet may be
prescribed to decrease
Complications: PepPan KidCal gastrointestinal
absorption of calcium
Peptic Ulcer Disease • ↑ gastric acid
secretion
Nursing Management
● Monitor cardiac rate and rhythm, treating
Pancreatitis • Calcium deposits in
and/or reporting arrhythmias as indicated.
the pancreas
● Prepare for possible cardiac arrest; keep
emergency resuscitation equipment readily
Kidney stones • Calcium precipitates available.
out of the urine ● Observe manifestations of digitalis toxicity,
including vision changes, anorexia, and
Hypercalcemic crisis • Acute rise of changes in heart rate and rhythm. Monitor
calcium→Cardiac arrest serum digitalis levels
● Promote fluid intake (oral and/or
intravenous) to keep the person well
Diagnostic Findings hydrated and maintain dilute urine.
Serum electrolytes • show a total serum Encourage fluids such as prune or cranberry
calcium greater than juice to help maintain acidic urine.
11.0 mg/dL. ● If excess bone resorption has occurred, use
caution when turning, positioning,
transferring or ambulating
Serum PTH levels • are measured to
identify or rule out
hyperparathyroidism as MAGNESIUM IMBALANCES
the cause of Magnesium
hypercalcaemia. ● The normal serum concentration of
magnesium ranges from 1.8 to 2.6 mg/dL
(1.5 to 2.5 mEq/L).
ECG changes • shortened QT interval,
● Magnesium is vital to many intracellular
shortened an depressed
processes, including enzyme reactions and
ST segment and
synthesis of proteins and nucleic acids.
widened T wave.
● Magnesium exerts a sedative effect on the
Bradycardia or heart
neuromuscular junction, decreasing
block
acetylcholine release.

Bone density scans • may be done to

monitor bone resorption
and the effects of
treatment measures on
mineralization of bone.

Medical Management
Isotonic saline • used because sodium
excretion is
accompanied by Functions of Magnesium
calcium excretion. ● Transferring and storing energy
● Regulation of parathyroid hormone
Intravenous Fluid with • promote elimination of ● Metabolizes carbohydrates, lipids and
Loop Diuretics excess calcium. proteins
● Regulates blood pressure
Calcitonin • which promotes the
uptake of calcium into
bones

bisphosphonates • which promotes the

(pamidronate and uptake of calcium into
etidronate) bones
 Urine magnesium • To identify cause of
magnesium depletion

Hypomagnesemia
● Is a magnesium level of less than 1.6 mg/dL.
● It is a common problem, particularly in the
critically ill person.
Causes of Hypomagnesemia: LOWMAG
● Limited intake of magnesium (starvation)
● Other electrolyte issues (hypokalemia and
hypocalcemia), Others: Parenteral Nutrition
● Wasting Magnesium via Kidneys: Kidney Medical Management
disease Medications: aminoglycosides, ● Mild: Diet, Magnesium salts
cyclosporine, cisplatin, diuretics, digitalis, ● PN: Magnesium in IV Solution
and amphotericin ● Magnesium Sulfate: IV or IM
● Malabsorption Issues intestinal resection or ● Magnesium Sulfate Toxicity: BURP
inflammatory bowel disease - Blood pressure decreased
● Alcohol Intake , Administration of citrated - Urine Output decreased
Blood - Respirations < 12
● Glycemic Issues (Osmotic Diuresis in DKA, - Patellar reflex absent
Insulin Therapy), GI losses ( NGT suction,
diarrhea and fistula)
Clinical Manifestations:
● Magnesium exerts a sedative effect on the
neuromuscular junction, decreasing Antidote:
acetylcholine release Calcium Gluconate 1g
● MAGNESIUM MELLOWS THE MUSCLES IV over 3 minutes
Clinical Manifestations: CRAZY & WILD
Neuromuscular • Muscle Weakness,
tremors
• Tetany, Seizures
• Chvostek and
Trousseau sign

Gastrointestinal • Dysphagia
• Anorexia, Nausea and
Nursing Management
Vomiting, diarrhea
● Monitor serum electrolytes, including
magnesium, potassium and calcium.
Cardiovascular • Tachycardia ● Screen for dysphagia
• Arrhythmias ● Monitor gastrointestinal function, including
• Hypertension bowel sounds and abdominal distension
● Initiate cardiac monitoring, reporting and
CNS • Mood and personality treating (as indicated) ECG changes and
changes arrhythmias
• Paraesthesias ● In the person receiving digitalis, monitor for
digitalis toxicity.
Diagnostic Findings ● Assess deep tendon reflexes frequently
Serum Magnesium • diagnoses during intravenous magnesium infusions and
hypomagnesemia prior to each intramuscular dose.
● Maintain a quiet, darkened environment.
Institute seizure precautions
ECG • Prolonged QRS,
depressed ST segment,
torsades de pointes,
Vfib, SVT
Hypermagnesemia
● is a serum magnesium level greater than 2.6 Pacemaker • To maintain adequate
mg/dL. cardiac output.
Causes of Hypermagnesemia: MAG
● Magnesium containing antacids or laxatives Nursing Management
(Maalox), Magnesium overdose ● Monitor vital signs, noting hypotension and
● Aging shallow respirations.
● Glomerular infiltration insufficiency ● Observe DTRs and changes in the level of
Clinical Manifestations: Calm and Quiet consciousness.
Neuromuscular • Weakness ● Withhold magnesium containing medications
• Decreased DTR and patients are cautioned to inform doctor
before taking OTC medications
GI • Nausea and vomiting

Cardiovascular • Hypotension, flushing,

feeling of warmth
• Bradycardia,
Arrhythmias
• Cardiac Arrest

CNS • Respiratory
depression
• Coma

Diagnostic Findings
Serum magnesium • Greater than 3.0
mg/dL

Serum Potassium and • Increased

Calcium

ECG • Prolonged PR interval,

tall T waves, widened
QRS, prolonged QT
intervals, AV block

Medical Management
● Withheld medications containing Magnesium
● Renal failure patients- hemodialysis
● Normal renal function patients: Loop
diuretics, Normal saline or LR
Calcium Gluconate IV • administered
intravenously to reverse
the neuromuscular and
cardiac effects of
hypermagnesemia

Mechanical Ventilation • to support respiratory

function
 most common cause of hypophosphatemia.
PHOSPHORUS IMBALANCES
Causes of Hypophosphatemia : Low
“PHOSPHATE”
● Pharmacy
- Aluminum based or magnesium
based antacids (bind with
phosphate)
- Lack of Vitamin D
● Hyperparathyroidism
- Increases PTH secretion, inhibits
reabsorption by kidneys
● Oncogenic malacia
- Kidney start to waste phosphate
● Syndrome of Refeeding
- In protein-calorie malnutrition,
Phosphorus Release of insulin
● Normal Phosphorus Level: 2.5 to 4.5 mg/dL ● Pulmonary issues
- Respiratory Alkalosis- enhances
Functions of Phosphate in the Body phosphorus uptake by the muscles
● the production of ATP ● Hyperglycemia
● the fuel that supports muscle contraction - Ketoacidosis- osmotic diuresis
● nerve cell transmission and electrolyte waste phosphate
transport ● Alcoholism
● vital for red blood cell function and oxygen - affects both the intake and
delivery to tissues absorption of phosphate.
● Vital for nervous system and muscle function ● Thermal Burns
● metabolism of fats, carbohydrates and - phosphate extracellular to
protein intracellular
● assists in maintaining acid–base balance. ● Electrolyte Imbalance
- Hypercalcemia, hypokalemia,
hypomagnesemia

Clinical Manifestations: ↓oxygenation, ↓ATP

synthesis
Central nervous system: • irritability,
apprehension,
weakness,
paraesthesias, lack of
coordination, confusion,
seizures and coma

Haematological: • Hemolytic anemia

(excessive red blood
cell destruction)

Musculoskeletal: • Decreased ATP

• muscle weakness •
acute rhabdomyolysis
(muscle cell
breakdown)- ARF
(myoglobin’s toxic effect
on kidneys)

Respiratory: • chest muscle

weakness →respiratory
failure

Cardiovascular: • decreased myocardial

- parathyroid hormone, calcitonin and vitamin
contractility
D --also influence phosphate levels
• decreased
oxygenation of the heart
Hypophosphatemia
muscle: chest pain and
● Hypophosphatemia is a serum phosphorus
arrhythmias
of less than 2.5 mg/dL
● Low serum phosphate levels may indicate a
total body deficit of phosphate or a shift of Gastrointestinal: • anorexia
phosphate into the intracellular space, the
 Clinical Manifestations: “Low Calcium”
• dysphagia ● Chvostek sign
● Trousseau sign
N&V • ↓ bowel sounds ● Muscle spasm
• possible ileus ● Circumoral and peripheral paresthesias
● Tetany
● Soft Tissue Calcification
Diagnostic Findings
Serum phosphorus level • Less than 2.5 mg/dL Diagnostic Findings
Serum phosphorus level • exceeds 4.5 mg/dL
PTH level • Increased in patients
with
Serum calcium level • used for diagnosing
hyperparathyroidism
the primary disorder
and assessing the
Serum Magnesium • Decreased due to effects of treatments
kidney excretion
X-rays • may show skeletal
Alkaline phosphatase • Increased with changes with abnormal
osteoblastic activity bone development.

X-ray Rickets, osteomalacia PTH levels • are decreased in

hypoparathyroidism
Medical Management
● Mild: Phosphorus Rich Diet BUN and creatinine • are used to assess
- Milk and milk products, organ levels renal function.
meats,nuts, fish poultry
● Oral phosphate supplement
Medical Management
● Severe: Intravenous phosphate (sodium
● Treatment of underlying disorder
phosphate or potassium phosphate)
● Eliminate:Phosphate containing drugs and
- < 1 mg/dL serum phosphorus
Rich foods
- Should not exceed 10 mEq/hr
● Agents that bind phosphate (Calcitriol): Oral:
Rocatrol, Parenteral: paricatol
Nursing Management
● Amphojel (oral antacid)- effective but Can
● Avoid rapid administration of parenteral
cause bone and CNS toxicity
nutrition
● Loop diuretics, saline Solution, Dialysis
● Encourage diet rich in phosphorus in
● Surgery- removal of large calcium and
patients wild mild deficit
phosphorus deposits
● Patients with documented
hypophosphatemia watch out for infection

Hyperphosphatemia
● Hyperphosphatemia is a serum phosphate
level greater than 4.5 mg/dL.
● As with other electrolyte imbalances, it may
be the result of impaired phosphate
excretion, excess intake or a shift of
phosphate from the intracellular space into
extracellular fluids.

Causes of Hyperphosphatemia: PHOSHI

● Phosphate-containing solutions (fleet
enemas)
● Hypoparathyroidism
- decreased PTH- inhibits
phosphate reabsorption Nursing Management
● Overuse of Vitamin D ● If a low phosphorus diet is prescribed, the
- Causes increased absorption of patient is instructed to avoid phosphorus-rich
phosphate foods, such as hard cheeses, cream, nuts,
● Syndrome of Tumor Lysis meats, wholegrain cereals, dried fruits, dried
- Chemotherapy, trauma vegetables, kidneys, sardines, sweetbreads,
● Heat stroke , hypothermia and foods made with milk.
● Insufficiency of the Kidneys ● Avoid phosphate-containing laxatives and
- Acute or Chronic KD • Primary enemas.
cause of impaired phosphate ● Educates the patient about recognizing the
excretion signs of impending hypocalcemia and
monitoring for changes in urine output.
 severe vomiting and diarrhea), Cystic
CHLORIDE IMBALANCES Fibrosis
● Hyponatremia
Chloride ● Addison’s Disease, Administration of
● the major anion of the ECF, is found more in chloride deficient IV solutions
interstitial and lymph fluid compartments ● Medications (diuretics “thiazides”)
than in blood ● pH Imbalances (metabolic alkalosis)
● also contained in gastric and pancreatic
juices, sweat, bile, and saliva Clinical Manifestations: OVERLAPPING ↓Na↓K↑pH
● Normal Range 95 -105 mEq/L CNS • Agitation
• Irritability
Functions of Chloride in the Body • Seizures
● Chloride is a halogen (non ionized form of
halide) that combines with alkali metals to
form salts in the body, such as sodium Cardiovascular • Dysrhythmias
chloride and potassium chloride • Hypotension
● Circulates primarily with sodium and water
and helps maintain cellular integrity by Neuromuscular • Tremors
maintaining a balance between intracellular • Muscle Cramps
and extracellular fluids in the body • Hyperactive Deep
● Helps control osmotic pressure Tendon Reflexes
● Essential for maintaining acid-base balance • Tetany
● Enzyme activator
● Buffer in the exchange of oxygen and carbon Respi • Slow shallow
dioxide in the body (“Chloride shift”) respirations
● With Magnesium and Calcium, Chloride
helps to maintain nerve transmission and
normal muscle contraction and relaxation
● The kidneys eliminate or retain chloride
mainly as sodium chloride to regulate
acid-base levels
● May also assist the liver in clearing the
waste products
● Found in significant amounts in sweat

Relationships

Diagnostic Findings
Na, K, Cl • decreased

ABGs • ↑pH, metabolic

alkalosis

Urine chloride level • decreased

Hypochloremia
● Hypochloremia is a serum chloride level Medical Management
below 97 mEq/L (97 mmol/L). ● Normal saline (0.9% sodium chloride) or half
strength saline (0.45% sodium chloride)
Causes of Hypochloremia: CHAMP solution
● Chloride Loss (GI tube drainage, gastric - to replace the chloride.
suctioning, gastric surgery, burns, fever
 ● If the patient is receiving a diuretic (loop,
osmotic, or thiazide), it may be discontinued
or another diuretic prescribed.
● Ammonium chloride
- to treat metabolic alkalosis
Nursing Management
● I&O
● Monitor patient’s level of consciousness,
muscle strength and movement
● Vital signs are monitored, and respiratory
assessment is carried out frequently.
● Educate the patient about foods with high
chloride content, which include tomato juice,
bananas, dates, eggs, cheese, milk, salty
broth, canned vegetables, and processed
meats
Hyperchloremia
● Hyperchloremia exists when the serum level
of chloride exceeds 105 mEq/L (105
mmol/L).
● Hypernatremia, bicarbonate loss, and
metabolic acidosis can occur with high
chloride levels.
Causes of Hyperchloremia
● Iatrogenically induced hyperchloremic
metabolic acidosis (o.9 NaCl, .45%NaCl or
LR)
● Loss of bicarbonate ions Diagnostic Findings
● Head trauma, increased perspiration, excess ● ↑serum Cl
adrenocortical hormone production, and ● ↑ Na
decreased glomerular filtration ● ↑serum K
Clinical Manifestations ● ↓ serum pH
● ↓ serum bicarbonate
CNS • Decline in mental ● ↑urinary chloride
status
Medical Management
Neuromuscular • Lethargy ● Hypotonic IV solutions may be given to
• Weakness restore balance
• Coma ● Lactated Ringer solution
- to convert lactate to bicarbonate in
Respi • Tachypnea the liver which increases the
• Deep rapid bicarbonate level and corrects the
respirations acidosis
● IV sodium bicarbonate may be given to
increase bicarbonate levels
Cardiovascular • ↓Cardiac output ● Diuretics may be given to eliminate chloride
• Tachycardia ● Sodium, chloride, and fluids are restricted.
• Pitting edema
• dysrhythmias Nursing Management
● Monitoring vital signs, arterial blood gas
values, and I&O
● The nurse educates the patient about the
diet that should be followed to manage
hyperchloremia and maintain adequate
hydration
 ACID BASE IMBALANCES Systems that Maintain pH
Buffers Seconds - minutes
Homeostasis
● Homeostasis and optimal cellular function
require maintenance of the hydrogen ion Respiratory System Minutes - Hours
(H+) concentration of body fluids within a
relatively narrow range. Renal System Slowest - strongest
● Normal Range: 7.35- 7.45
● Hydrogen ions determine the relative acidity
of body fluids Buffers
● Acids release protons & hydrogen ions ● prevent major changes in pH by removing or
- HCl → H+ + HCl- releasing hydrogen ions
- H2CO3→ H+ + HCO3 ● Body is too BasicRelease Hydrogen ions
● Bases (or alkalis) accept protons & ● Body is too Acidic- Bind to hydrogen ions
hydrogen ions Major Buffer Systems
- HCO3 + H+→ H2CO3 ● bicarbonate–carbonic acid buffer system
● phosphate buffer system
● protein buffers
Bicarbonate-Carbonic Acid Buffer System

Carbonic Acid + base Produce normal

( weak acid) Hydrogen pH
ions

Bicarbonates + acid Remove Normal

(weak base) hydrogen pH
ions

Normal pH level: 7.35-7.45

Metabolic processes in the body continuously produce

acids
Volatile Acids Nonvolatile Acids

• can be eliminated from • must be metabolized

the body as a gas or excreted from the
• Ex: Carbonic Acid body in fluid
• Ex Lactic acid,
hydrochloric acid,
phosphoric acid and
sulfuric acid
The Respiratory System Effects of Acid-Base Imbalances on Serum
Electrolytes
acidosis ↑ rate and ↓carbonic pH normal
depth of acid level
respiration

alkalosis ↓ rate and Carbon pH normal

depth of dioxide is
respiration retained
● Compensatory Changes occur within
minutes– less effective overtime.
Serum PaCO2
● exerted by dissolved carbon dioxide in the
blood reflects the respiratory component of
acid–base regulation and balance

The Renal System

Acidosis excrete H+ pH normal

retain HCO3

Alkalosis retain H+ pH normal

excrete HCO3
● Compensatory Changes takes LONGER –
MORE EFFECTIVE long-term mechanism
Serum HCO3
● reflects the renal regulation of acid–base
balance • called the metabolic component of
arterial blood gasses

Acid-Base Imbalances
Metabolic Acidosis

Acid-Base Imbalances
Metabolic

Respiratory

Primary/Simple • are due to one cause

Mixed • occur from

combinations of
respiratory and
metabolic disturbances Cause
● Excess Nonvolatile acids; Bicarbonate
deficiency
Compensation
● Rate and depth of respirations decrease,
retaining CO2
Effect on ABGs
● ↓pH, ↓HCO3 - , ↓PaCO2
Pathophysiology Cause
● Bicarbonate Excess
↑ Acid ↓ Acid ↑ ↑ Chloride Compensation
Production secretio Bicarbonate ● Rate and Depth of Respirations decrease,
n Loss retaining Carbon dioxide
Effect on ABGs
• Lactic • Renal • Diarrhea, • Sodium ● ↑pH, ↑HCO3 - , ↑PaCO2
acidosis failure ileostomy chloride IV
• Ketoacidosis drainage, solutions Pathophysiology
r/t diabetes, intestinal • Renal
starvation or fistulas Tubular ↑ Acid Loss or Excretion ↑Bicarbonates
alcoholism acidosis
• Salicylate • Carbonic • Vomiting • Alkali ingestion
toxicity anhydrase • Gastric suction (bicarbonate of soda)
inhibitors • Excess bicarbonate
administration

Medical Management
Respiratory Acidosis
Metabolic Acidosis • Alkalinizing solutions
• Sodium bicarbonate
(Oral and IV)
• Lactate, citrate,
acetate

Ketoacidosis • intravenous insulin

and fluid replacement

Alcoholic ketoacidosis • saline solutions and

glucose

lactic acidosis • focuses on correcting

the underlying problem

Metabolic Alkalosis

Cause
● Retained CO2, and excess carbonic acid
Compensation
● Kidneys conserve bicarbonates to restores
carbonic acid : bicarbonate ratio of 1:20
Effect on ABGs
● ↑pH, ↓PaCO2 - , ↓HCO3 -

Pathophysiology
Acute Respiratory Chronic Respiratory
Acidosis Acidosis

• Acute respiratory • Chronic respiratory

conditions (pulmonary conditions (COPD)
 Cause
edema, pneumonia, • Stroke ● Loss of CO2, and deficient carbonic acid
acute asthma) Compensation
• Narcotic analgesics ● • Kidneys excrete bicarbonate and conserve
H+ to restore carbonic acid : bicarbonate
Consideration for Practice: ration
Carefully monitor neurological and respiratory Effect on ABGs
status in the person with chronic respiratory status in ● ↑pH, ↓PaCO2 - , ↓HCO3 -
the person with chronic respiratory acidosis who is
receiving oxygen therapy. Immediately report a Pathophysiology
decreasing LOC or depressed respirations. Anxiety induced hyperventilation

Fever

Early salicylate intoxication

Hyperventilation with mechanical ventilator

Chronic Respiratory Acidosis

● Weakness
● Dull Headache
● Sleep Disturbances with daytime sleepiness
● Impaired Memory
● Personality Changes

Medical Management
● Acute respiratory failure usually requires Medical Management
treatment in the emergency department or ● A sedative or anti-anxiety agent may be
intensive care unit. necessary to relieve anxiety and restore a
● Bronchodilator drugs may be administered to normal breathing pattern
open the airways and antibiotics prescribed ● Instruct the person to breathe more slowly
to treat respiratory infections. and having the person breathe into a paper
● If excess narcotics or anesthetic has caused bag or rebreather mask.
acute respiratory acidosis, drugs to reverse ● If excessive ventilation by a mechanical
their effects (such as naloxone) may be ventilator is the cause of respiratory
given. alkalosis, ventilator settings are adjusted to
● The person with severe respiratory acidosis reduce the respiratory rate and tidal volume
and hypoxaemia may require intubation and as indicated.
mechanical ventilation ● When hypoxia is the underlying cause of
Respiratory Alkalosis hyperventilation, oxygen is administered.

Arterial Blood Gases (ABGs)

● Arterial blood is used because it reflects
acid–base balance throughout the entire
body better than venous blood.
● Arterial blood also provides information
about the effectiveness of the lungs in
oxygenating blood.
● Elements
- pH
- PaCO2
- PaO2
- bicarbonate level
 Normal Values

pH A 7.35 - 7.45 B

PaCO2 A 35 - 45 B

HCO3 A 22 - 26 B

Other ABG Components Normal

PaO2 80 - 100 mmHg

BE -3 to +3

How to interpret ABGs: TIC TAO METHOD

1. Look at the pH
2. Look at the PaCO2
3. Look at the HCO3
4. Look for compensation
- Uncompensated
- Partially Compensated
- Fully Compensated

Uncompensated: • pCO2 and HCO3 is normal

Partially Compensated: • Nothing is Normal

Compensated: • pH is normal