Fluid and Electrolyte Imbalance

COLLAGE OF HEALTH SCIENCE DEPARTMENT OF
NURSING
FOR 3rd YEAR BSc NURSE
Body Fluid and Electrolyte Imbalance
BY. Fentahun Minwuyelet(BSC, MSC IN AHN)

Senie, 2014 E.C
6/25/2022 BY. Fentahun Minwuyelet 1
Learning objectives
 On completion of this chapter, the learner will be
able to:
Describe the role of the kidneys, lungs, and
endocrine glands in regulating the body’s fluid
composition and volume.
 Identify the effects of aging on fluid and

electrolyte regulation.

Learning Objectives…
 Plan effective care of patients with the following
imbalances:
 Fluid volume deficit and fluid volume excess;
 Sodium deficit (hyponatremia)and sodium excess
(hypernatremia);
 Potassium deficit (hypokalemia) and potassium excess
(hyperkalemia).
 calcium , chlorine, phosphorous deficiency

Learning objectives cont…
 Describe the etiology, clinical manifestations,
management and nursing interventions for other
common electrolyte imbalances
 Explain the mechanisms of patients with ACID –
BASE imbalance based upon the formation of
acidosis and alkalosis
Metabolic acidosis
Metabolic alkalosis
Respiratory acidosis
Respiratory alkalosis

Brain storming questions
1. Where is your total body fluid primerly
distributed?
2. What are the constituents your body fluid?
3. Why fluid resuscitation is needed for

patients ?
4. Do you know imbalance between acid and

base affect our body hemodynamic?

Fundamental concepts
The human body functions when certain
conditions are kept with in a narrow range
of normal value.
These conditions include:-
Body temperature
Electrolytes
Blood PH
Blood volume

Continue…
 Body fluid contains:
water
Electrolytes
Non electrolytes (glucose, urine), and
other substances

Body fluid compartments
 Approximately 55-60%of a typical adult’s weight
consists of fluids.
 These fluids are distributed in to different
compartments:
1. Intracellular fluid(ICF) compartment
Is fluid with in the cells
Located mainly (primarily) in skeletal muscle mass
Contains approximately 2/3 (28L)of the total body
fluid
Constitute 45%of body weight
Body fluid…
2. Extra cellular fluid(ECF) compartment

Is fluid outside cells
Contains approximately 1/3(15L) of body fluid
Further divided in to
1) Intravascular space
2) Interstitial space
3) Trans-cellular space
Body fluid…
1. Intravascular space
Fluids are within the blood vessel
Contains plasma (3L of the average but 6L of
blood volume)
2. Interstitial space
Contains fluids that surrounds the cell
Comprises approximately 11-12L in adults
Example lymph

Body fluid…
3. Trans cellular space fluid
Comprises approximately 1L in adults
This fluid includes
CSF
Synovial fluid
Intra ocular
Pericardial fluid
Plural fluid

Body fluid…
 Factors that influence the amount of body fluid
include:
i. Age – younger has more fluid
ii. Gender- male has more fluid
iii. Body fat- thin has more fluid

FLUILD SHIFT
Is the term used to classify the distribution of
water. They are three types:
a. First space fluid shift
• normal distribution of fluid
b. Second spacing
• Is an excess accumulation of interstitial fluid
c. Third spacing
• Is losing of ECF in to spaces that do not have
contribution in the equilibrium of ICF and ECF.
• These are occurred during abnormality.

Body fluids …
Third spacing occurs in:
Ascites
Burns
Peritonitis
Bowl obstruction
Massive bleeding in to joint or body cavities

Body fluid…
S/S of third spacing.
ed urine out put
ed heart rate
ed BP
Edema
ed CVP
ed Body weight
Imbalances in fluid intake and out put

Functions of fluids
Water provides about 90-93% of the volume in the
extra cellular compartment. Its functions include:
Providing form for body structures
Acts as transport vehicle
Aids in the hydrolysis of food
Acts as medium and reactant for chemical
reactions
Acts as a lubricant
Cushions and acts as shock absorber

Gains and losses of body fluid (water)
 The sources of fluid gains

Absorption from GIT
Parenterally administered fluids
Metabolic oxidation of foods
Bathing in fresh water
 Routs of fluid losses
 Kidney (1ml/kg/hr in all age groups
 Insensible loss
» Skin
» Lungs
 Stool (GIT)
Gains and losses of body fluid (water) …
Average in take and out put of fluids in adults is the same
 Intake Out put
 Oral intake Urine-----1500ml
– As liquid -------------1300ml Stool------200ml
– In food ---------------1000ml Insensible
 Metabolic oxidation -----300ml Lung------300ml
Skin------600ml
 Total gain----------2600ml Total lose----2600ml

Regulation of body fluids
 Physiologic mechanisms assist in the regulation of
body fluids include:
I. Thirst level-primarily regulates intake
occurs when an increase in the extra cellular

osmolality causes osmoreceptors (nerve cells in
hypothalamus) to shrink.

Continue…
II. Renal concentrating mechanisms
 The kidney controls the concentration of most of
the constitutes in body fluid, including water and
electrolytes.
 This is mediated by the function of
 Osmo receptors
 Baro receptors
 Adrenal functions-Renin- angiotensin-
aldosterone system
 Release of atrial natriuretic peptide
Regulation of body fluids …
 Organs involved in the homeostasis of body fluid include:
Kidneys
Heart and blood vessels
Lungs
Posterior pituitary gland-store and release ADH
Adrenal gland(cortex)-secretes aldostrone which
increases sodium retention and potassium loss
Parathyroid gland-PTH(parathyroid hormone)
regulates calcium and phosphorus balance

Normal laboratory values used in evaluating
fluid and electrolyte status in adults
Serum test
Cations Reference range
 Sodium (Na+) -------------------------------135-145mEq/l
 Potassium (K+)-------------------------------3.5-5.5mEq/l
 Calcium (Ca2+)-------------------------------8.6-10mEq/l
 Magnesium (Mg2+---------------------------1.3-2.5mEq/l

Normal laboratory values…
Anions Referance range

 Chloride (Cl-)------------------------------------97-107mEq/l
 Bicarbonate (HCO3-)---------------------------20-30mEq/l
 Phosphate (PO43-)-------------------------------2.8-4.5mEq/l
 Osmolality----------------------------------------280-300mEq/l
 Blood urea nitrogen (BUN)--------------------5-20mg/dl

Non electrolytes
Creatinine ------------------F: 0.5-1.1mg/dl
M: 0.6-1.2mg/dl
BUN to creatinine ratio------------10:1-15:1
Hematocrite-----------------F: 35-47%
M: 42-52%
Glucose----------------------70-105mg/dl
Albumin-----------------------3.5-5.5g/dl

Urine tests
 Sodium(Na+)--------------------------------75-220mEq/l
 Potassium(K+)-------------------------------25-123mEq/l
 Chloride(Cl-)--------------------------------110-250mEq/l
 Specific gravity-----------------------------1.016-1.022
 Osmolality-----------------------------------250-900mOsml/kg H2O
 PH----------------------------------------------Random: 4.5-8.0

Laboratory Tests for Evaluating Renal
Function
Osmolality/ Osmolarity
 The most accurate measurement of the kidney’s
ability to dilute and concentrate urine
 Osmolality is expressed as milliosmoles per

kilogram of water (mOsm/kg) and
 Osmolarity expressed as milliosmoles per liter

of water (mOsm/L)

Formula for Serum Osmolality

Comparison of Serum and
Urine Osmolality

Urine specific gravity
 Measures the kidneys’ ability to excrete or conserve
water
 High density or too concentrated than water---

kidney is not functioning or not drink enough
water
 Is compared to the weight of distilled water, which

has a specific gravity of 1.000
 Normal value -- 1.010-1.025

BUN
Is made up of urea, an end product of metabolism of
protein
Increased with Decreased with:
 Decreased renal function  End-stage liver disease
 GI bleeding  A low-protein diet
 Dehydration  Starvation
 Increased protein intake  Any condition that
results in expanded fluid
 Fever volume (e.g., pregnancy)
 Sepsis, etc

Creatinine
 Is the end product of muscle metabolism
 A better indicator of renal function than BUN
because it does not vary with protein intake and
metabolic state
 Increase when renal function decreases
 Normal value in serum:
F: 0.5-1.1mg/dl
M: 0.6-1.2mg/dl
 Urine creatinine level = 2.5 to 8.2mmol/L
Glomerular Filtration Rate
Measures volume of blood cleared of endogenous
creatinine in 1 min
Sensitive indicator of renal disease used to

follow progression of renal disease.
Normal can range from 115 to 125 mL/min

(Porth & Matfin)

Hematocrit
 Measures the volume percentage of red blood
cells (erythrocytes) in whole blood
 Increase with dehydration and polycythemia
 Decrease with over hydration and anemia
 Normal Value:
 F: 35-47%
 M: 42-52%
Urinalysis
 Urine color
 Urine clarity and odor
 Urine pH and specific gravity
 Proteinuria, glycosuria, and ketonuria
 Microscopic examination of the urine sediment after
centrifugation to detect hematuria, pyuria, casts
(cylindruria), crystals (crystalluria), and bacteriuria
Urine Culture
 Determines whether bacteria are present in the urine, as
well as their strains and concentration
 Used to determine bacterial sensitivity to antibiotics

Summery
Test Purpose Normal
Values
Renal Concentration Tests
Specific Evaluates ability of kidneys to 1.010–1.025
gravity concentrate solutes
in urine.
Urine Measures the kidney’s 300–900
osmolality ability to dilute and concentrate mOsm/kg/24h,
urine 50–1200
mOsm/kg
random
Creatinine Measures volume of blood cleared sample
115-125 mL/min
clearance of endogenous creatinine in 1 min,
which provides an approximation of
6/25/2022
the glomerularBY. filtration rate
Fentahun Minwuyelet 40
Test Purpose Normal Values
Serum Tests
Creatinine level Measures effectiveness of renal .M: 06-1.2mg/dL
function .F: 05-1.1mg/dL
Urea nitrogen Serves as index of renal function 10-20 mg/dL
(blood urea
nitrogen [BUN])
BUN-to-  Evaluates hydration status. About 10:1
Creatinine ratio  An elevated ratio is seen in
hypovolemia;
 A normal ratio with an elevated
BUN and creatinine is seen with
intrinsic renal disease
Serum 280 to 300
Osmolality mOsm/kg
Fluid volume deficit (FVD)
(Hypovolemia)
 Occurs when loss of ECF volume exceeds the intake
of fluid.
 Occurs when water and electrolytes are lost in the
same proportion as they exist in normal body fluids,
 So that the ratio of serum electrolytes to water
remains the same.
 This should not be confused with dehydration b/c
water and electrolyte lost are not the same proportion.

Causes of FVD
Causes include: poor intake or loss
Inadequate fluid intake
Unconsciousness/coma or inability to express
thirst
Oral trauma or inability to swallow
Impaired thirst mechanism
Withholding of fluid for therapeutic reason

Causes…
Excessive fluid losses
 GI losses  Urine losses
Vomiting Diuretic therapy

Diarrhea Osmotic diuresis
GI suctioning (hyperglycemia)
Fistula drainage Salt wasting renal
disease
Causes…
 Skin losses (salt water)

Fever
Exposure to hot environment
Burns and wounds that remove skin
 Third space losses
Intestinal obstruction
Edema, ascites, burns (for the first several days)
 Other risk factors
Diabetic incipidus
Hemorrhage

Clinical manifestations of FVD
Acute weight loss (% body weight)
– Mild FVD: 2% loss
– Moderate FVD: 2-5%loss
– Severe FVD: 6% or more loss
Thirst, anorexia, nausea
Urine out put(oliguria)
Urine osmolality
Specific gravity

Clinical manifestation…
 Serum osmolality
Hematocrite
BUN
 Vascular volume
Tachycardia, weak thready pulse
Postural hypotention
Vein filling and vein refill time reduced
Hypotention and shock
 Volume in extra cellular space
Depressed fontanel
Sunken eyes and soft eyeballs

Clinical manifestation …
 Loss of ICF
Dry skin (skin turgor) and mucous membrane
Cracked and fissured tongue
Salivation and lacrimation loss
Neuromuscular weakness and cramps
Fatigue
 Increased body temperature
Cool clammy skin related to peripheral vasoconstriction

Diagnosis
Hx
Physical exam
ed BUN
ed BUN to creatnine ratio(>20:1)
ed hematocrite
Electrolyte changes may occur
Urine osmolality
ed as kidney attempt to conserve water
ed with DI

FVD: Medical Management
Goal  to provide fluids rapidly enough to attain

adequate tissue perfusion without compromising the
cardiovascular system
 The response by a patient with FVD for a patient

with normal renal function will be:
Increased urine output
Increase in blood pressure

Med mgt FVD cont’d…
Required solutions (Isotonic, Hypotonic, Hypertonic)
I. Isotonic fluid replacement:
Are IV fluids that have a similar concentration of
dissolved particles as blood
The fluid stays in the intravascular space and
osmosis does not cause fluid movement between
compartments.
Example: 0.9% NS , ringer’s lactate, DNS
Fluid challenge test --rate of administration
 Usually 100 to 200 mL of normal saline solution over
15 minutes
The most commonly used isotonic solutions

II. Hypotonic solution:
Have a lower concentration of dissolved solutes in
cells than blood:
It causes movement of water from the
intravascular space into the intracellular space.
 For this reason, hypotonic fluids are used to treat
cellular dehydration.
 (e.g., 0.45%NaCl) after the patient becomes normotensive

Hypotonic Saline Cont….
Hypotonic IV Solution Causing

Osmotic Movement of Fluid Into
Cell
III. Hypertonic Solutions
Have a higher concentration of dissolved particles
in cells than blood
It causes the osmotic movement of water out of the
cells and into the intravascular space to dilute the
solutes in the blood.
When hypertonic IV fluid is administered osmotic
movement of fluid out of a cell due to a higher
concentration of solutes in the bloodstream
compared to the cell.
Example: 3% Normal Saline (3% NaCl).

Hypertonic IV Solution Causing Osmotic

Fluid Movement Out of a Cell

Nursing Management
Nursing Diagnosis: Fluid Volume Deficit
Related factors
Active fluid loss, e.g., hemorrhage, vomiting,
diarrhea, burns, wounds, fistulas
Regulatory failure, e.g., adrenal disease,
recovery phase of ARF, diabetic ketoacidosis
(DKA), diabetes insipidus, systemic infections

Nursing Interventions FVD
Independent
 Monitor vital signs and CVP
 Note presence/degree of postural BP changes
 Observe for temperature elevations/fever
 Palpate peripheral pulses; note capillary refill, skin
color/temperature
 Assess mentation
 Monitor urinary output
Nursing Interventions FVD cont’d…
 Monitor urinary output
 Measure/estimate fluid losses from all sources, e.g.,
gastric losses, wound drainage, diaphoresis
 Weigh daily and compare with 24-hr fluid balance
 Mark/measure edematous areas, e.g., abdomen, limbs
 Encourage foods with high fluid content
 Turn frequently, massage skin, and protect bony
prominences

 Provide mouth care
 Bathe every other day using mild soap and apply
lotion as indicated
 Provide safety precautions as indicated, e.g., use of
side rails, bed in low position, frequent observation,
soft restraints (if required)
 Investigate & reports of sudden/sharp chest pain,
dyspnea, cyanosis, increased anxiety, restlessness
 Monitor for sudden/marked elevation of BP,
restlessness, moist cough, dyspnea, crackles, frothy
sputum
Collaborative
 Assist with identification/treatment of underlying
cause
 Monitor laboratory studies as indicated, e.g.,
electrolytes, glucose, pH/Pco2, coagulation studies
 Administer IV solutions as indicated
 Administer sodium bicarbonate, if indicated
 Provide tube feedings, including free water as
appropriate
Fluid Volume Excess (FVE)/
HYPERVOLEMIA
 Refers to an isotonic expansion of the ECF caused by

the abnormal retention of water and sodium in
approximately the same proportion in which they
exist in the total body fluid.
 It is always secondary to an increase in the total body

sodium content

Causes/ contributing factors FVE
 Excessive sodium and water in take
Dietary intake
Ingestion of medications containing sodium
 Inadequate renal losses
Renal disease (renal failure)
Increased corticosteroid level
Aldosterone
Glucocorticoids
 Congestive heart failure
 Liver cirrhosis
Clinical manifestations FVE
Acute weight gain (in excess of 5%)
Pitting edema of the extremities
Puffy eyelids
Pulmonary edema
Shortness of breathing (dyspnea)
Rales, wheezing
 Cough

Clinical Manifestation …
Tachycardia-full and bounding pulse

ed BP and CVP
Distended neck veins
ed Urinary out put

Diagnosis
 Hx.
Physical exam(antiropometric measurement)
 ed BUN
 Hematocrite may be ed
 ed Urine specific gravity (because of urine sodium level)
 ed Serum osmolality
 Chest X-ray reveals pulmonary congestion

FVE: Medical Management
Directed towards the underlining causes
I. Pharmacologic Therapy
Thiazide diuretics
Block sodium reabsorption in the distal tubule
Prescribed for mild to moderate hypervolemia
Loop diuretics
Cause a greater loss of both sodium and water
Prescribed for severe hypervolemia
FVE Medical Management Cont’d…
II. Hemodialysis or Peritoneal Dialysis
Used if pharmacologic and dietary

management cannot act effectively
Used to remove nitrogenous wastes and control

potassium and acid–base balance, and to remove
sodium and fluid.
Continuous renal replacement therapy

FVE Medical Management Cont’d…
III. Nutritional Therapy
Restriction of sodium 250mg of Na+/day
Foods high in sodium must be avoided
Lemon juice
Onions and garlic
Salt substitutes

Nursing Management FVE
Nursing Diagnosis: Fluid Volume Excess
Related Factors
Excess fluid or sodium intake
Compromised regulatory mechanism
Possible evidences
Signs/symptoms: weight gain, edema…

Nursing Management FVE Cont’d…
Independent
 Monitor vital signs, also CVP if available
 Auscultate lungs and heart sounds
 Assess for presence/location of edema formation
 Note presence of neck and peripheral vein distension,
along with pitting edema, dyspnea
 Maintain accurate Intake & Out put

 Give oral fluids with caution

 If fluids are restricted, set up a 24-hrs schedule for
fluid intake
 Monitor infusion rate of parenteral fluids closely
 Note decreased urinary output, positive fluid balance
(intake greater than output) on 24-hr calculations
 Weigh as indicated and alert for acute or sudden
weight gain

 Encourage coughing/deep-breathing exercises
 Maintain semi-Fowler’s position if dyspnea or ascites
is present
 Turn, reposition, and provide skin care at regular
intervals
 Encourage bedrest
 Schedule care to provide frequent rest periods
 Provide safety precautions as indicated, e.g., use of
side rails, bed in low position, frequent observation,
soft restraints (if required)
Collaborative
Assist with identification/treatment of underlying
cause
Monitor laboratory studies as indicated, e.g.,
electrolytes, BUN, ABGs
Provide balanced protein, low-sodium diet. Restrict
fluids as indicated
Administer diuretics
Replace potassium losses as indicated
Prepare for/assist with dialysis
Electrolyte imbalance
Electrolytes in body fluids are active

chemicals which contains:-
Cations , which carry positive charges,
Anions , which carry negative charges.

Electrolyte imbalance …
The major cations: The major anions:

– Chloride,
–Sodium
– Bicarbonate,
–Potassium
– Phosphate,
–Calcium – Sulfate and
–Magnesium and – Proteinate ions.
–Hydrogen ions.
6/25/2022
BY. Fentahun Minwuyelet
Functions of electrolytes include:-
Assist in regulating water balance ( Na+)
Participate in acid-base regulation (e.g. HCo-3
Na+, Cl)
Contribute to enzyme reaction (e.g. Mg 2+)
Plays an essential role in neuromuscular
function( e.g. k+, Ca2+, Na+)

People at risk for sever imbalances are:
Older clients
Clients with chronic renal or endocrine
disorder
Mentally impaired clients
Client who are taking medications that alter
fluid and electrolyte status.

Gains and losses of electrolytes
Gains
Through the GIT
Loss
Kidney
GIT  <10%
Skin  15-30 g/day with profuse sweating

Alterations in Sodium Balance
Sodium
The most abundant electrolyte in the ECF
Serum concentration 135 to 145 mEq/L (135—145
mmol/L)
Functions of Na+
 Is the primary determinant of ECF osmolality (90-95%
of osmolarity) and ECF volume
 It has a major role in controlling water distribution
throughout the body
 A loss or gain of sodium is usually accompanied by a
loss or gain of water
 For muscle contraction and the transmission of nerve
impulses
Sodium Deficit (Hyponatremia)
Serum sodium level that is below normal (less

than 135 mEq/L [135 mmol/L])
Related to loss of sodium containing fluids, water

excess in relation to the amount of sodium
(dilutional hyponatremia) or combination of both.

Cause of Hyponatremia
Excessive Sodium loss
 GI loss: Vomiting, diarrhea, draining wound,
fistulas, or diaphoresis
 Renal loss: Use of diuretics, particularly in
combination with a low-salt diet
Disease states
 Deficiency of aldosterone
 Hyperglycemia
 SIADH
 Heart failure
Cause Hyponatremia Cont’d…
Dilutional Hyponatremia
Water intoxication
Predisposing conditions:
Increased water intake (excessive hypotonic
IV fluids)
Head trauma and oat-cell lung tumor
Medications associated with water retention:
Oxytocin
Certain tranquilizers/anxiolytics like
diazepam, lorazepam, and oxazepam)
Cause Hyponatremia Cont’d…

C/Ms of Hyponatremia
Depend on the cause, magnitude, and speed with
which the deficit occurs
More severe symptoms and higher mortality rates--
acute decrease in serum sodium levels
May include:
Poor skin turgor
Dry mucosa
Decreased saliva production
Orthostatic fall in blood pressure
Nausea, and abdominal cramping
6/25/2022 By: Temamen Tesfaye 89
C/Ms Hyponatremia Cont’d…
Finger print edema with increased ICF
Neurologic changes-- probably related
to the cellular swelling and cerebral
edema
Altered mental status
Anorexia
Muscle cramps
Feeling of exhaustion
C/Ms Hyponatremia Cont’d…
 With serum sodium level drops below 115
mEq/L signs of increasing intracranial pressure:
 Lethargy
 Confusion
 Muscle twitching
 Hemiparesis
 Papilledema
 Seizures
Hyponatremia: Diagnosis
 History
 Physical examination
 Lab tests
Serum sodium: <135 mEq/L
Urine sodium:
<15 mEq/L – renal conservation of sodium
>20 mEq/L indicates SIADH
 Serum potassium
May be decreased
Hyponatremia: Dx Lab Cont’d…
 Serum chloride/bicarbonate
Decreased
 Serum osmolality
Commonly low
 Urine osmolality
Usually <100 mOsm/L unless SIADH present
Urine specific gravity
Decreased <1.010)
Increased >1.020) in SIADH
Hct: Depends on fluid balance
Medical Management of
Hyponatremia:
Rely on speed with which hyponatremia occurred
rather than relying only on the patient’s actual
serum sodium value
 Careful administration of sodium by PO,

NGT, parenteral route
 High sodium diets
 Lactated Ringer’s solution or isotonic saline

(0.9% sodium chloride)
Hyponatremia: Mgt…
 Serum sodium must not be increased by
greater than 12 mEq/L in 24 hours
 The usual daily sodium requirement in adults is
approximately 100 mEq, provided there are no
abnormal losses
 In SIADH patients:
 Hypertonic saline solution

 Lithium or demeclocycline which can
antagonize the osmotic effect of ADH on the
medullary collecting tubule
Hyponatremia: Mgt…
 Water restriction
 800 ml in 24 hours
 In a patient with normal or excess fluid

volume
 Far safer than sodium administration and is

usually effective
 Hypertonic sodium solution, such as 3% or

5% sodium chloride cautiously-- When
neurologic symptoms are present
Nursing Management Hyponatremia
Identify patients at risk for hyponatremia
For at risk patients the nurse monitors:
Fluid intake and output
Daily body weight
Be alert for GI changes and central nervous

system changes, such as lethargy, confusion,
muscle twitching, and seizures

Nurse Detecting and Controlling
Hyponatremia
Encourages foods and fluids with high
sodium content, like:
Milk
Meat
Eggs
Carrots
Beets
Fruit juices instead of plain water
Hyponatremia: Nursing Mgt…
 When administering fluids to patients with

cardiovascular disease
 Assessing for signs of circulatory overload (e.g.,

cough, dyspnea, puffy eyelids, dependent
edema, or weight gain in 24 hours)
 Auscultated lungs for crackles

Returning sodium level to normal
 Restriction of fluid intake --when the primary
problem is water retention
 Sodium administration to a patient with

normovolemia or hypervolemia
 In severe hyponatremia, it is generally recommended

that the serum sodium concentration be raised no
higher than 125 mEq/l with a hypertonic saline
solution

Nursing Alert: Highly hypertonic sodium solutions

(3% and 5% sodium chloride) should be
administered only in intensive care settings under
close observation, because only small volumes are
needed to elevate the serum sodium level from a
dangerously low value.

Sodium Excess (Hypernatremia)
Is a higher-than-normal serum sodium level
(exceeding 145 mEq/L [145 mmol/L]).
Can occur in patients with normal fluid volume or
in those with FVD or FVE
Cause
 Inadequate intake of water (unconscious or
cognitively impaired individuals)
 Diarrhea

Hypernatremia: Cause…
 Fluid deprivation
 Administration of hypertonic enteral feedings
without adequate water
 Greatly increased insensible water loss
 IV administration of hypertonic saline or
excessive use of sodium bicarbonate
 Diabetes insipidus, a deficiency of ADH
 Heat stroke
 Near-drowning in sea water (which contains a
sodium concentration of approximately 500
mEq/L)
C/Ms of Hypernatremia
C/Ms are primarily neurologic and are presumably
the consequence of cellular dehydration- water pulled
from the cells
 Restlessness and weakness in moderate
hypernatremia
 Disorientation, delusions, and hallucinations in
severe hypernatremia
 Behavioral changes in the elderly patient due to
dehydration
 Permanent brain damage can occur (especially in
children) in severe hypernatremia
 Thirst is a primary characteristic of hypernatremia
Hypernatremia: C/Ms…
Other signs include:
 A dry, swollen tongue and sticky mucous
membranes.
 Flushed skin, peripheral and pulmonary edema,

postural hypotension, and increased muscle tone
and deep tendon reflexes
 Body temperature may rise mildly but returns to

normal when the hypernatremia is corrected

Diagnosis of Hypernatremia
 History
 Physical examination
 Lab tests:
Serum sodium: exceeds 145 mEq/L (145
mmol/L)
Serum osmolality: exceeds 295 mOsm/kg
(295 mmol/L)
Urine sodium: Less than 50 mEq/L.
Urine chloride: Less than 50 mEq/L.
Hypernatremia Diagnosis….
Urine osmolality > 800mOsm/L
Urine specific gravity:
>1.015, if water deficit present
<1.010 when hypernatremia is due to polyuria
Hct: May be normal or elevated depending on

fluid status

Medical Management of Hypernatremia
A gradual lowering of the serum sodium level

by the infusion of:
 A hypotonic electrolyte solution (e.g. 0.3%

sodium chloride)
 Safer than D5W because it allows a gradual

reduction in the serum sodium level

Hypernatremia: Medical Mgt…
 An isotonic non-saline solution (e.g. dextrose 5%

in water [D5W])
 Indicated when water needs to be replaced

without sodium
 The solution of choice in severe

hyperglycemia with hypernatremia
 A rapid reduction in the serum sodium level may

cause dangerous cerebral edema

Hypernatremia: Medical Mgt…
 As a general rule, the serum sodium level is
reduced at a rate no faster than 0.5 to 1 mEq/L to
allow sufficient time for readjustment through
diffusion across fluid compartments.
 Desmopressin acetate (DDAVP) --to treat diabetes

insipidus if it is the cause of hypernatremia

Nursing Management of Hypernatremia
 Carefully monitoring fluid losses and gains in patients

at risk for hypernatremia
 Monitor BP
 Note respiratory rate, depth
 Assess for abnormal losses of water or low water
intake and for large gains of sodium
 Obtain a medication history
 Monitor for changes in behavior
 Evaluate level of consciousness and muscular
strength, tone, movement
Hypernatremia: Nursing Mgt…
 Maintain safety/seizure precautions, as indicated,
e.g., bed in low position, use of padded side rails
 Assess patient’s thirst, skin turgor, color,
temperature, and mucous membrane moisture.
 Provide/encourage meticulous skin care and
frequent repositioning.
 Provide frequent oral care. Avoid use of
mouthwash/rinse that contains alcohol.
 Monitor serum electrolytes, osmolality, and ABGs
as indicated.
Preventing Hypernatremia
 Offering fluids at regular intervals
 If fluid intake remains inadequate, consults with the
physician to plan an alternate route for intake
 If enteral feedings are used, sufficient water should
be administered to keep the serum sodium and BUN
within normal limits
 As a rule, the higher the osmolality of the enteral
feeding, the greater the need for water
supplementation
 Adequate water intake for patients with diabetes
insipidus, must be ensured.
Correcting Hypernatremia
Identification/treatment of underlying cause
Monitoring the patient’s response to the fluids
Monitor serum electrolytes, osmolality, and ABGs
as indicated
Increase PO/IV fluid intake, e.g., 5%
dextrose/water in presence of dehydration; 0.90%
of NaCl if extracellular deficit is present.
Restrict sodium intake and administer diuretics as
indicated.
Significance of Potassium
 Potassium is the major intracellular

electrolyte
 98% is found inside the cells
 2% is in the ECF, which is important in
neuromuscular function
 Potassium influences both skeletal and
cardiac muscle activity

Significance of Potassium…
The normal serum potassium concentration -
- 3.5 to 5.5 mEq/L
80% excreted daily by the kidneys; the other
20% is lost through the bowel and in sweat
As serum potassium levels increase, so does
the potassium level in the renal tubular cell

Potassium Deficit (Hypokalemia)
Is usually indicates an actual deficit in total
potassium stores (<3.5mEq/l)
Due to increased shift of potassium from
ECF to ICF or
Rarely from deficient dietary potassium
intake

Causes of Hypokalemia
 GI loss of potassium is probably
the most common cause which
could be caused by:
 Vomiting
 Gastric suction
 Diarrhea
 Prolonged intestinal suctioning,
recent ileostomy, and villous
adenoma
 Metabolic alkalosis
Hypokalemia Causes cont’d…
 Medications:
 Potassium-losing diuretics
 Thiazides (eg, chlorothiazide )
 Loop diuretics (e.g. furosemide)
 Corticosteroids, sodium penicillin,
carbenicillin, and amphotericin B
 Insulin
 Patients who are unable or unwilling to eat a
normal diet for a prolonged period
Clinical Manifestations -- Hypokalemia
Fatigue Paresthesias (numbness
Anorexia and tingling)
Nausea
Dysrhythmias, and
Vomiting
increased sensitivity to
Decreased bowel digitalis
motility
Muscle weakness Polyuria, nocturia
Leg cramps Glucose intolerance

Diagnosis of Hypokalemia
 History
 Physical examination
 Laboratory tests:
 Serum potassium: < 3.5 mEq/L
 Serum glucose: May be slightly elevated.
 Serum magnesium: Levels often decreased when
potassium deficit is present
 Plasma bicarbonate: >29 mEq/L.
 Urine osmolality: Decreased
 ABGs: pH and bicarbonate may be elevated (metabolic
alkalosis)
Diagnosis-- Hypokalemia Cont’d…
 A 24-hour urinary potassium excretion test
 Urinary potassium excretion exceeding 20

mEq/24h with hypokalemia suggests that renal
potassium loss
 Electrocardiographic (ECG) changes:
 Flat T waves, suggesting ischemia
 Depressed ST segments
 An elevated U wave is specific to hypokalemia

Dx Hypokalemia …

Medical Management of Hypokalemia:
 A diet containing sufficient potassium for at risk clients (50 to 100
mEq/day)
 Foods high in potassium include:
 fruits (bananas, and oranges),
 vegetables (like potatoes and tomatoes),
 legumes, whole grains, milk, meat, coffee, and tea

 Oral or IV replacement therapy
 Administration of 40 to 80 mEq/day of potassium is adequate in the

adult if there are no abnormal losses of potassium

Medical Management/Hypokalemia/
Cont’d….
Potassium salts
Potassium acetate
Potassium phosphate
Potassium chloride- except in sever deficiencies,
KCl is never given unless there is urine output of at
least 0.5ml/Kg body weight/hour
IV route--for patients with severe hypokalemia
IV rate administration should not exceed 10-
20meq/hour
Nursing Management of Hypokalemia
Independent
 Monitor heart rate/rhythm.
 Monitor respiratory rate, depth, effort
 Encourage cough/deep-breathing exercises
 Reposition frequently
 Assess level of consciousness and neuromuscular
function, e.g., strength, sensation, movement.
 Auscultate bowel sounds, noting decrease/absence
6/25/2022
or change. 126
Hypokalemia: Nsg mgt ….
 Maintain accurate record of urinary, gastric, and

wound losses
 Monitor rate of IV potassium administration and
check for side effects
 Review drug regimen for potassium-wasting drugs,
e.g., furosemide, hydrochlorothiazide
 Watch for signs of digitalis intoxication when used
 Observe for signs of metabolic alkalosis, e.g.,
hypoventilation, tachycardia, dysrhythmias, tetany,
changes in mentation
Hypokalemia Nsg Mgt…..
Collaborative:
cause
 Monitor laboratory studies, e.g.:
Serum potassium
ABGs
Serum chloride
 Administer oral and/or IV potassium

Preventing Hypokalemia
 Encouraging the patient at risk to eat foods rich in

potassium
 Sources of potassium: fruit and fruit juices (bananas,
citrus fruit), fresh and frozen vegetables, fresh meats
 Patient education for those taking laxatives or diuretics
 Careful monitoring of fluid intake and output is
necessary because 40 mEq of potassium is lost for
every liter of urine output
 ECG monitoring for changes
 ABG analysis for elevated bicarbonate and pH levels
Administering IV Potassium
 Potassium should be administered only after
adequate urine flow has been established
 A decrease in urine volume to less than 20 mL/h

for 2 consecutive hours is an indication to stop the
potassium infusion until the situation is evaluated
 IV potassium should not be administered faster

than 20 mEq/h or in concentrations greater than 30
to 40 mEq/L unless hypokalemia is severe

Administering IV Potassium Cont’d…
 When prepared for IV infusions, the fluid should be

agitated well to prevent bolus doses that can result
when the potassium concentrates at the bottom of
the IV container
 In administeration through a peripheral vein, the

rate of administration must be decreased to less than
60 mEq/L to avoid irritating the vein and causing a
burning sensation and sclerosis

Nursing Alert of Hypokalemia
 Oral potassium supplements can produce small

bowel lesions;
 Therefore , the patient must be assessed for and

cautioned about abdominal distention, pain, or GI
bleeding.

Potassium Excess (Hyperkalemia)
Hyperkalemia is an elevated blood level of the

electrolyte potassium above 5.5mEq/l.
Is usually more dangerous because cardiac arrest

is more frequently associated with high serum
potassium levels

Causes Pseudohyperkalemia
Use of a tight tourniquet
Marked leukocytosis or thrombocytosis
Drawing blood above a site where

potassium is infused
Blood awaiting for analysis

Cause of the actual hyperkalemia
 Excess potassium intake
 Excessive or rapid parenteral administration
 Drugs containing potassium like potassium

penicillin
 Potassium containing salt substitutes (KCL)

Hyperkalemia Cause cont’d…
Shift of potassium out of cells

 Acidosis
 Extensive tissue trauma as in burns, crushing
injuries, or severe infections
 Lysis of malignant cells after chemotherapy
Decreased renal excretion of potassium
 Hypoaldosteronism and Addison’s disease
 ACE inhibitors
 Potassium-sparing diuretics
Clinical Manifestations of Hyperkalemia
 Almost always present when the level is >8 mEq/L
 With a serum potassium level >6 mEq/L (6 mmol/L)
 Peaked, narrowT waves
 ST-segment depression
 A shortened QT interval and
 With continued rise in the serum potassium level there

will be:
 Prolonged PR interval followed by disappearance of the P
waves
 Prolongation of the QRS complex
Peaked, narrowT waves, ST-segment depression; A
shortened QT interval and Prolonged PR interval
and QRS, P-wave absent

Hyperkalemia: C/Ms…
GI manifestations, such as nausea, intermittent
intestinal colic, and diarrhea
With membrane depolarization that inactivates
many sodium channels:
 Smaller P waves and widening of the QRS
complex
 Skeletal muscle weakness and even paralysis,
related to a depolarization block in muscle
 Paralysis of respiratory and speech muscles

Diagnostic of Hyperkalemia
 History
 Physical examination
 Lab tests
Serum potassium: >5.5 mEq/L
Serum magnesium: Levels may be elevated if
renal failure is present
Renal function studies: May be altered,
indicating failure
ABG analysis may reveal metabolic acidosis
 ECG changes
Medical Management of
Hyperkalemia
In no-acute case:
 Restriction of dietary potassium
 Restriction of potassium-containing medications
 Eliminating the use of potassium-containing salt

substitutes in the patient taking a potassium-
conserving diuretic
 Administration of cation exchange resins (e.g.,

Kayexalate) either orally or by retention enema
Hyperkalemia
Emergency Pharmacologic Therapy
 IV administration of calcium gluconate (antagonizes
the effect of hyperkalemia on the heart)
Monitoring the blood pressure which can be caused
by rapid IV infusion of calcium gluconate
 IV administration of sodium bicarbonate to alkanize
the plasma and to antagonize the effect of hyperkalemia
on the heart
 Continuously ECG should be monitored during
administration

Hyperkalemia
Emergency Pharmacologic Therapy…
 IV administration of regular insulin and a
hypertonic dextrose solution which make
temporarily shift of K+ in to cells
 Beta-2 agonists (e.g., Albuterol) also move
potassium into the cells
 Actual removal of potassium by using cation
exchange resins,
 Peritoneal dialysis, hemodialysis

Nursing Management Hyperkalemia
 Identifying patients at risk for potassium excess

 Monitor heart rate/rhythm
 Monitor urinary output
 Assess level of consciousness, neuromuscular
function, e.g., movement, strength, sensation
 Encourage/assist with ROM exercises as tolerated
 Review drug regimen for medications
containing/affecting potassium excretion, e.g.,
penicillin G, spironolactone, hydrochlorothiazide
Hyperkalemia: Nsg Mgt…
 Identify/discontinue dietary sources of potassium,
e.g., tomatoes, broccoli, orange juice, bananas,
bran, chocolate, coffee, tea, eggs, dairy
products, dried fruits
 Administer medications as indicated, e.g.:
Diuretics, e.g., furosemide (Lasix);
IV glucose with insulin, sodium bicarbonate;
Calcium gluconate;
Sodium polystyrene sulfonate
B-Adrenergic agonist, e.g., albuterol
Hyperkalemia: Nsg Mgt…
 Monitor laboratory results, e.g., serum potassium,
ABGs, BUN/Cr, glucose
cause
 Infuse potassium-based medication/solutions
slowly.
 Provide fresh blood if transfusions required
 Prepare for/assist with dialysis (peritoneal or
hemodialysis)
Preventing Hyperkalemia
 Encouraging at risk patients to adhere to the
prescribed potassium restriction
 Potassium-rich foods to be avoided include

coffee, cocoa, tea, dried fruits, dried beans, and
wholegrain breads
 Encourage to take foods with minimal potassium

content include butter, margarine, cranberry juice,
ginger, hard candy, root beer, sugar, and honey

Alteration in calcium balance
More than 99% of the body’s calcium is located in
the skeletal system
Is a major component of bones and teeth.
The normal total serum calcium level is 8.5 to
10.5 mg/dL(2.1–2.6 mmol/L).
 It exists in plasma in three forms:
Ionized
Bound
Complexed

Alteration in calcium balance…
 Absorbed from foods in the presence of normal gastric

acidity and vitamin D.
 Excreted primarily in the feces, the remainder in
urine.
 The serum calcium level is controlled by PTH and
calcitonin.
 plays a major role in:
→Transmission of nerve impulses and helps to
regulate muscle contraction and relaxation.
→Activating enzymes
→Blood coagulation.
Calcium deficit (hypocalcemia)
• Serum calcium <8.5 mg/dL
Causes
– Hypoparathyroidism
– Malabsorption
– Pancreatitis
– Alkalosis
– vitamin D deficiency

Hypocalcaemia …
Generalized peritonitis
Massive transfusion of citrated blood
Chronic diarrhea
Decreased parathyroid hormone, and
Diuretic phase of renal failure

Clinical features
 Numbness, tingling of  Carpopedal spasms

fingers and toes  Irritability & anxiety
 positive Trousseau’s  Bronchospasm
sign  Impaired clotting time
 Chvostek’s sign  ↓ prothrombin
 Seizures  ECG:
 Hyperactive deep – prolonged QT interval
tendon reflexes and lengthened ST.
6/25/2022
152 BY. Fentahun Minwuyelet
Medical and Nursing managements
 Acute symptomatic hypocalcemia is life-threatening

and requires
IV administration of calcium gluconate,calcium
chloride, and calcium gluceptate.
Diluted in D5W and given as a slow IV bolus or
a slow IV infusion using a volumetric infusion
pump.
Observe the IV site for any evidence of
infiltration
Do not use a 0.9% sodium chloride /it increase
renal calcium loss/.
Continue…
Avoid Solutions containing phosphates or
bicarbonate because they will cause precipitation
when calcium is added.
Vitamin D therapy
Antacids such as- Aluminum hydroxide, calcium
acetate, or calcium carbonate
Increasing the dietary intake of calcium to at least
1,000 to 1,500 mg/dy

Calcium excess (hypercalcemia)
Serum calcium >10.5 mg/dL
Causes
Hyperparathyroidism
prolonged immobilization
overuse of calcium supplements
Thiazide diuretics
Vitamin D excess
Oliguric phase of renal failure
Corticosteroid therapy
Digoxin toxicity

Clinical features
∆ GI- constipation, anorexia, nausea and Vomiting
∆ GUT- polyuria and polydipsia, flank pain, calcium
stones
∆ CVS- Arrithymia & Bradicardia
∆ MSK- Muscular weakness, deep bone pain,
pathologic fractures
∆ CNS- lethargy
156
156 6/25/2022
Medical management
 Administering fluids to dilute serum calcium

0.9% sodium chloride solution
IV phosphate
 Promote calcium excretion by the kidneys
Furosemide (Lasix)
 Mobilizing the patient
 Restricting dietary calcium intake
 Administering Calcitonin
 Treatment of underlined diseases

Nursing management
Monitor for hypercalcemia in patients at
risk
Promote patient mobility
Encourage fluid intakes
Encourage adequate fiber in the diet
Safety precautions if mental symptoms of
hypercalcemia are present
Assess patient for signs and symptoms of
digitalis toxicity.
Alteration in Phosphorus balance
Significance of phosphorus
Essential to the function of:
– Muscle and red blood cells
– Formation of adenosine triphosphate (ATP)
– Maintenance of acid–base balance
The normal serum phosphorus level is 2.5 to
4.5 mg/dL (0.8–1.5 mmol/L)

Phosphorus deficit (hypophosphatemia)
Serum phosphorus <2.5 mg/dL
Causes/ contributing factors
– Re feeding after starvation, diabetic
ketoacidosis
– Intense hyperventilation
– poor dietary intake
– Vomiting, diarrhea
– Diuretic use
– Vitamin D deficiency
– Excess use of phosphorus binding antacids

Clinical features
Confusion
Paresthesias
Muscle weakness
Seizures
Bone pain and tenderness
Chest pain, tissue hypoxia and respiratory failure
Increased susceptibility to infection
Medical management
 Aggressive IV phosphorus if:
 serum phosphorus levels fall below 1 mg/dL
GI tract is not functioning
– The rate of phosphorus administration should
not exceed 10 mEq/h,
– The site should be carefully monitored for
tissue sloughing and necrosis
 Oral phosphorus replacement- In less acute situations
Phosphorous rich foods
Neutral Phos. capsules (250 mg
phosphorus/capsule)

Nursing Management
Identification of patients at risk

Gradual administration of parenteral nutrition
Encourage intake of phosphorus rich foods
Prevent infection
Monitor and document serum phosphorus levels,
and report when risk of hypophosphatemia is
evident

Phosphorus excess(hyperphosphatemia)
164
Serum phosphorus >4.5 mg/dL

 Causes
– Acute and chronic renal failure – Volume depletion
– Excessive intake of phosphorus – Leukemia/lympho
– Vitamin D excess ma treated with
cytotoxic agents
– Respiratory acidosis
– Increased tissue
– Hypoparathyroidism breakdown
6/25/2022
Clinical features
Tetany
Muscle weakness, hyporeflexia
Signs and symptoms of hypocalcemia
Anorexia, nausea and vomiting
Tissue calcification

Medical and Nursing Managements
Treatment of the underlying disorder

Phosphate-binding gels or antacids
Restriction of dietary phosphate
Dialysis
Patient teaching

Alteration in magnesium balance
Significance of magnesium
Most abundant intracellular cation./Next to
potassium/
Is activator for many intracellular enzyme systems
Important in neuromuscular function
An excess of magnesium diminishes the excitability
of the muscle cells, whereas a deficit increases
neuromuscular irritability and contractility.
Have a direct vasodilator effect on peripheral arteries
and arterioles.
167
6/25/2022 BY. Fentahun Minwuyelet
Magnesium deficit (hypomagnesemia
 it occurs when Serum magnesium <1.5 mg/dL
Causes
 GI suction & diarrhoea  Mal absorptive disorders
 Hyperparathyroidism  Re feeding after starvation
 Hyperaldosteronism
 Chronic laxative use
 Diuretic phase of renal
 Rapid administration of
failure
citrated blood
 Diabetic ketoacidosis

Hypomagnesaemia …
♣ C/M-
Neuromuscular irritability
Insomnia and mood changes
Vomiting & anorexia
Increased tendon reflexes

Medical and Nursing managements
Encouraging magnesium rich diet

IV administration of magnesium sulfate by an
infusion at a rate not to exceed 150 mg/min.
Determine the risk for hypomagnesemia and
observe for its signs and symptoms
Assess the presence of dysphagia before oral
administration of food and medication

Magnesium excess (hypermagnesemia)
♣ Occurred at Serum magnesium >2.7 mg/dL

Causes/ contributing factors
Oliguric phase of renal failure
Adrenal insufficiency
Excessive IV magnesium administration
Excessive use of antacids

Clinical features
Flushing & diaphoresis
Hypotension
Drowsiness
Hypoactive reflexes
Depressed respirations
Cardiac arrest and coma

Medical Management
Avoiding the administration of magnesium to
patients with renal failure
Careful monitoring seriously ill patients who
are receiving magnesium salts.
Ventilatory support
IV calcium gluconate10mL of a 10% solution
Hemodialysis
Loop diuretics
0.45% sodium chloride solution

Nursing Management
 Identify and assess patients at risk
 Monitors the vital signs
 Observes for decreased deep tendon reflexes
 Observe for changes in the level of consciousness
 Avoid magnisium containing medications in
patients with renal failure
 Patient teaching

Acid-Base Homeostasis

The homeostasis of CO2, O2, H+ & HCO-3
Depends on:
I. H+ production must be consistent, not excessive
II. CO2 loss from the body through breathing must

keep pace with H+ production
III. The ratio between H2CO3 and HCO-3 must be

maintained at 1:20 to maintain pH at 7.4

Metabolic acid and bicarbonate
production
 Acids are continuously produced as a byproduct of
metabolic processes
 Physiologically acids can be:
Non volatile/fixed
 Ex: Sulfuric, hydrochloric, phosphoric acids
 Buffered by body proteins or ECF buffers like
HCO-3, and then eliminated by the kidneys
Volatile: H2CO3
 Leaves the body through lungs
Carbon dioxide and Bicarbonate production
CO2 Production
Body metabolism results in the production of
approximately15,000 mmol CO2 each day
Transported in the circulation as:
1. Dissolved gas
2. Bicarbonate
3. Carbaminohemoglobin
HCO3 production
The small percentage of the gas CO2 reacts with
H2O to generate H2CO3, which is catalyzed by
carbonic anhydrase (largely present in RBCs, renal
tubules & other tissues in the body)
Production of Fixed Acids
 Fixed/non volatile acids and bases are produced from
metabolism of proteins and other substances
A. Sulfuric acid is produced from oxidation of sulfure-

containing amino-acids (Ex: methionine, cysteine)
B. Phosphoric acid is produced from oxidation of

phosphorus-containing amino acids (Ex: arginine
and lysine)
C. Lactic acid from incomplete oxidation of glucose
D. Ketoacids from incomplete oxidation of fats

Production of Base
Base primarily produced from metabolism of:
A. Amino acids like aspartate and glutamate
B. Organic anion like citrate, lactate, acetate
C. Consumption of vegetarian diet, which

contains large amount of organic anions

Regulatory mechanisms for acid-base
balance
I. Chemical buffer
II. Respiratory
III. Renal

Regulatory mechanisms for acid-base
balance…

I. Chemical Mechanisms (Buffers)
 Are the first line of defense against changes in H+
concentration
 Act as ‘H+ sponges’, buffers:

 Bind H+ when the concentration of H+ is too high
 Release H+ when concentration of H+ is too low
 Fluid buffers are composed of chemicals (e.g.
bicarbonate, phosphate) & proteins (e.g. albumin,
globulins, hemoglobin)

Chemical Buffer System…
The three buffer systems are:
1. The bicarbonate buffer system
 Uses H2CO3 as a weak acid and bicarbonate
salt (eg NaHCO3) as a weak base
 HCl + NaHCO3  H2CO3 + NaCl
 NaOH + H2CO3  NaHCO3 + H2O

2. Proteins buffer system (largest buffer
system)
 Are amphoteric (can function either as acid or
base)
 Albumin
 Plasma globulins

3. Trans cellular
H+/K+ exchange
buffer system

II. Respiratory Mechanism
Is the second line of defense against changes
Maintain a normal PH by excreting CO2 and

water

III. Renal Mechanism
 Is the third line of line of defense, strongest and it
takes longer (24-48hrs) to completely respond,
through:
Kidney movement of bicarbonate
 Reabsorption of HCO-3 and excretion of in H+
acidosis
 Retention of H+ & excretion of HCO-3 in
alkalosis of
Formation of acids
Formation of Ammonium
Renal Mechanism…
1. H+ elimination and HCO3- conservation
Through excreting excess H+ and
reabsorbing or regenerating HCO3-

Renal Mechanism…
2. Tubular Buffer System
When the pH of urine is <4.4 to 4.5, H+ secretion
ceases and to prevent damage to urinary tracts it is
excreted not as free H+ but buffered by
intratubular phosphate and ammonia buffer
systems
Once all the HCO3-has been reabsorbed and is no
longer available to combine H+, any excess H+
combines with HPO42- to form H2PO42-

Acid-Base Imbalances

1. Metabolic Acidosis
(Primary Base Bicarbonate [HCO3] Deficient)
 Is a clinical disturbance characterized by a

low pH (increased H+ concentration) less
than 7.35 and a low plasma bicarbonate
concentration less than 22mEq/l

Metabolic Acidosis Causes
Produced by:
A gain of hydrogen ion
A loss of bicarbonate
Can be:
Normal anion gap acidosis
High anion gap acidosis

Metabolic Acidosis
Causes of normal anion gap acidosis
 Result from anion loss or deficiency
 Direct loss of bicarbonate:
 Diarrhea
 Lower intestinal fistulas
 Ureterostomies
 Use of diuretics
 Under eliminations of H+ --Early renal insufficiency
 Excessive administration of chloride
 Administration of parenteral nutrition without
bicarbonate or bicarbonate-producing solutes (e.g.,
6/25/2022
lactate) BY. Fentahun Minwuyelet 196
Metabolic Acidosis Anion Gap Acidosis
 Results from excessive accumulation of fixed acid
 Occurs in:
 Ketoacidosis
 Lactic acidosis
 The late phase of salicylate poisoning
 Uremia
 Methanol or ethylene glycol toxicity– producing
glycolic acid

Metabolic Acidosis
Clinical Manifestations
 Anorexia, nausea, vomiting
 Head ache, lethargy, confusion
 Kussmaul respiration
 Peripheral vasodilatation & ed cardiac out
put
 Cold & clammy skin
 Decreased blood pressure
 Shock
Metabolic Acidosis
Assessment and Diagnostic Findings
History
Physical examination
Laboratory test
Arterial pH: <7.35
Bicarbonate (HCO3): <22 mEq/L
PaCO2: <35 mm Hg ( Componsantory).
Base excess: Negative
Anion gap: Higher than 14 mEq/L (high anion
gap) or range of 10–14 mEq/L (normal anion gap)
Metabolic Acidosis: Dx…
Serum potassium: Increased
Serum chloride: Increased
Plasma lactic acid: Elevated in lactic acidosis
Urine pH: Decreased, <4.5 (in absence of renal

disease)
ECG: Cardiac dysrhythmias (bradycardia) and

pattern changes associated with hyperkalemia,
e.g., tall T wave

Metabolic Acidosis
Medical Management
Treatment is directed at correcting the metabolic
defect
 If excessive intake of chloride--eliminating the
source of the chloride
 Adjusting potassium
 Monitor serum K+
 Rapid acting insulin to reverse drive K+ back
in to the cells
 NaHCo3 is administered IV
Metabolic Acidosis: Medical Mgt…
 Monitoring ECG changes

 Dialysis in patents with renal failure or toxic
reaction to drugs
 Alkalizing agents
 Fluids (NaCl solution) as required

 Antibiotics to treat source of infections & anti-
diarrheal to treat diarrhea induced bicarbonate
loss

Metabolic Acidosis
Nursing Management
Independent
 Monitor BP
 Assess LOC and note progressive changes in

neuromuscular status, e.g., Strength, tone,
movement
 Provide seizure/coma precautions, e.g., Bed in low

position, use of side rails, frequent observation
 Monitor heart rate/rhythm.

Metabolic Acidosis
Nursing Mgt…
 Observe for altered respiratory excursion, rate, and
depth
 Assess skin temperature, color, capillary refill
 Auscultate bowel sounds; measure abdominal girth
as indicated
 Monitor I&O closely and weigh daily
 Test/monitor urine pH
 Provide oral hygiene with sodium bicarbonate
washes
Metabolic Acidosis
Nursing Mgt…
 Administer medications as indicated, e.g.
 Sodium bicarbonate/lactate or saline IV
 Potassium chloride
 Phosphate
 Calcium
 Modify diet as indicated
 Low-protein, high-carbohydrate diet in presence
of renal failure
 American diabetes association (ADA) diet for the
person with diabetes
 Administer exchange resins and/or assist with
dialysis as indicated
Metabolic Acidosis
Nursing Mgt…
Collaborative

cause
 Monitor/graph serial ABGs
 Monitor serum electrolytes, e.g., Potassium
 Replace fluids, as indicated depending on

underlying etiology, e.g., D5W/saline solutions

2. Metabolic Alkalosis (Primary Base
Bicarbonate Excess)
 Is characterized by a blood PH above 7.45

and is compared by an HCO-3 level above
26mEq/L

Metabolic Alkalosis: Causes
 Increase of base component
 Oral ingestion of bases (antacids, milk alkali
syndrome)
 Parenteral base administration
 Decrease of acid component
 Prolonged vomiting, NG suctioning
 Potassium deficit
 Cushing’s syndrome (hypercortisolism)
 Thiazide diuretics
 Excessive retention of HCO-3
Metabolic Alkalosis:
Clinical manifestations
Alkalosis is primarily manifested by symptoms
related to decreased calcium ionization
Tingling of the fingers and toes
Dizziness
Hypertonic muscles
Ventricular disturbances
Decreased motility and paralytic ileus
Respiratory acidosis (Compensatory)
Atrial tachycardia
Assessment & Diagnostic Findings
History
Physical examination
Lab tests
Arterial pH: Increased, higher than 7.45.
Bicarbonate (HCO3): Increased, >26 mEq/L
(primary).
PaCO2: Slightly increased, >45 mm Hg
(compensatory).
Base excess: Increased
6/25/2022 Serum potassium: Decreased
BY. Fentahun Minwuyelet 210
Metabolic Alkalosis: Dx…
 Serum calcium: Usually decreased
 Serum chloride: Decreased, <98 mEq/L
 Urine chloride:
 <10 mEq/L suggests chloride-responsive
alkalosis
 >20 mEq/L suggest chloride resistance
 Urine pH: Increased, higher than 7.0.
 ECG: May show hypokalemic changes

Medical Management
Correcting the cause of the condition
Sufficient chloride supplementation for the
kidney to absorb sodium with chloride (allowing
the excretion of HCO-3).
Restoring normal fluid volume by administering
NaCl solution
KCl in patients with hypokalemia to replace both
K+ &Na+ losses

Medical Mgt…
Discontinuing thiazide diuretics & NG suctioning
Histamine-2 receptor antagonists e.g. cimetidine,

reduce the production of gastric HCl, thereby
decreasing the metabolic alkalosis associated with
gastric suction
Antiemetics may be administered to treat

underlying nausea &Vomiting
Monitoring input &out put

Nursing Management
Independent
 Record amount and source of output
 Monitor intake and daily weight
 Restrict oral intake of HCO-3 products
 Use intermittent/low suction during NG
suctioning
 Irrigate gastric tube with isotonic solutions rather
than water.
 Provide seizures/safety precautions as indicated
Nursing Mgt…
 Encourage intake of foods and fluids high in
potassium and possibly calcium
Canned grapefruit and apple juices
Bananas
Dried
Wheat
 Review medication regimen for use of diuretics,
such as thiazides, furosemide
 Instruct patient to avoid use of excessive
6/25/2022 amounts of sodium bicarbonate
BY. Fentahun Minwuyelet 215
Nursing Mgt…
Collaborative
 Assist with identification/treatment of
underlying disorder
 Monitor laboratory studies as indicated, e.g.,
ABGs/pH, serum electrolytes (especially
potassium), and BUN.
 Administer medications as indicated
 NaCl PO/Ringer’s solution IV unless C/I
 Potassium chloride
6/25/2022
 Ammonium chloride or arginine hydrochloride 216
Nursing Mgt…
 Avoid/limit use of sedatives or hypnotics.

 Encourage fluids IV/PO.
 Administer supplemental O2 as indicated
and respiratory treatments to improve
ventilation.
 Prepare patient for/assist with dialysis as

needed.

Respiratory Acidosis
(H2CO3 excess)
 Is a clinical disorder in which the PH is less
than 7.35 and the PaCO2 is greater than
42mmHg
 Always due to inadequate excretion of CO2

with inadequate ventilation(hypoventilation).
 Can be acute or chronic

Respiratory Acidosis:
Cause
Acute respiratory acidosis:
 Acute pulmonary edema
 Aspiration of foreign body
 Overdose of sedatives/barbiturate poisoning
 Smoke inhalation Breathing air with high CO2

content
 Acute laryngospasm
 Hemothorax/pneumothorax
Cause…
 Atelectasis
 Adult respiratory distress syndrome (ARDS)
 Anesthesia/surgery
 Mechanical ventilators
 Excessive CO2 intake (e.g., use of rebreathing

mask)
 Pickwickian syndrome

Cause…
Chronic respiratory acidosis
 Emphysema
 Asthma
 Bronchiectasis
 Neuromuscular disorders (such as Guillain-Barré
syndrome and myasthenia gravis)
 Botulism
 Spinal cord injuries

 Increased pulse, respiratory rate, and blood
pressure
 Mental cloudiness and feeling of fullness in the
head
 Ventricular fibrillation in anesthetized patients
especially if PaCO2 is higher than 60 mmHg
 Papilledema
 Cyanosis and Tachypnea
 Headache, confusion, depression,
hallucination, dizziness, stupor & coma,
tremors
Assessment and Diagnostic Findings
ABGs Evaluation:
PaO2: Normal or may be low and Oxygen

saturation (SaO2) decreased.
PaCO2: Increased, >45 mm Hg (primary acidosis).
Bicarbonate (HCO3): Normal or increased, >26

mEq/L (compensated/chronic stage)
Arterial pH: Decreased, <7.35

Respiratory Acidosis: Dx…
Serum Electrolytes:
Serum potassium: Typically increased.
Arterial pH may be within the lower limits of
normal, when compensation (renal retention of
bicarbonate) has fully occurred
Chest x-ray for determining any respiratory
disease
Drug screen if an overdose is suspected
ECG to identify any cardiac involvement as a
result of chronic obstructive pulmonary disease
Respiratory Acidosis: Medical management
Directed at improving ventilation

Pharmacologic agents as indicated
Bronchodilators to reduce bronchial
spasm
Antibiotics for respiratory infections
Thrombolytic or anticoagulants for
pulmonary emboli
Medical management
Pulmonary hygiene measures
Adequate hydration (2–3 L/day) ns
Supplemental oxygen
Mechanical ventilation
Semi-fowler’s position to facilitate
expansion of the chest wall

Nursing Management
Nursing Diagnosis: Gas Exchange, Impaired
May be related to:
Ventilation perfusion imbalance
Possibly evidenced by:
Dyspnea with exertion, tachypnea
Changes in mentation, irritability
Tachycardia
Hypoxia, hypercapnia

Nursing Interventions
Independent
Monitor respiratory rate, depth, and effort.
Auscultate breath sounds.
Note declining level of awareness/
consciousness.
Monitor heart rate/rhythm.
Note skin color, temperature, moisture.
Nursing Mgt….
Encourage/assist with deep-breathing
exercises and coughing
Place in semi-fowler’s position.
Restrict use of hypnotic sedatives or
tranquilizers.
Discuss cause of chronic condition (when
known) and appropriate interventions/self-
care activities
Nursing Mgt….
Collaborative
cause.
 Monitor/graph serial ABGs, pulse oximetry
readings; Hb, serum electrolyte levels.
 Administer oxygen as indicated
 Maintain hydration (IV/PO)/provide humidification.
 Chest physiotherapy, including postural drainage
and breathing exercises
Nursing Mgt….
 Administer IV solutions such as lactated Ringer’s
solution or 0.6 M solution of sodium lactate.
 Administer medications as indicated, e.g.
Sodium bicarbonate (NaHCO3)
Potassium chloride (KCl)
Bronchodilators
 Provide low-carbohydrate, high-fat diet if indicated
to reduce CO2 production and improves respiratory
muscle function and metabolic homeostasis.
Respiratory Alkalosis
(Primary Carbonic Acid Deficit)
 Is a clinical condition in which the PH is >7.45 &
PaCO2 is <35 mmHG due to hyperventilation
 Because respiratory alkalosis can occur suddenly,

compensatory decrease in HCO3- level may not
occur before respiratory correction has been
accomplished
 It may acute or chronic.

Respiratory Alkalosis:
Causes
Always caused due to hyperventilation
Extreme anxiety
Hypoxemia
Early phase of salicylate intoxication
Gram-negative bacteremia
Inappropriate ventilator settings that do
not match the patient’s requirements
 Lightheadedness
 S/S r/d to decreased calcium ionization:
 Inability to concentrate
 Numbness and tingling
 True Chvostek’s & Trousseau’s signs,
 Tetany
 Times loss of consciousness
 Tachycardia and ventricular and atrial
dysrhythmias
C/Ms…
Compensatory mechanisms include:
 Decreased respiratory rate (if the body is
able to respond to the drop in paCO2)
 Increased renal excretion of bicarbonate,
and retention of hydrogen

Respiratory Alkalosis….
Diagnosis
ABGs= PaCO2 < 35
Normal or decreased bicarbonate level.
PH level > 7.45
 Electrolytes= decrease in potassium, decreased

calcium,

Respiratory Alkalosis….
Medical Management
 If the cause is anxiety, the patient is instructed to
breathe more slowly to allow CO2 to accumulate or
to breathe into a closed system (such as a paper
bag).
 A sedative may be required to relieve
hyperventilation in very anxious patients.
 Treatment of other causes of respiratory alkalosis is
directed at correcting the underlying problem.

Fully , partial compensated and
uncompensated acid- base balance
• It is categorized based on the value ABG.
• The pH side from PH value=7.40 is important
to categorized alkalotic or acidosis for full
compensated ( see below).

Continue…
♥ When PaCO2 and HCO3 high but pH is Normal
instead of being acidic or basic, then the fully
compensatory mechanism is retained.
♥ When PaCO2 and HCO3 value high but pH is
abnormal , then it indicates partial compensation. It
means that the compensatory tried but failed to bring
the pH normal.
♥ If pH abnormal and if the value of either PaCO2 or
HCO3 abnormal (either of the two is normal), it
indicate that the system is uncompensated. This is
probably b/c of either respiratory or metabolic
acidosis.
Continue…..
• Questions to determine acidosis or alkalosis.
1. 1st . Is PH normal or Abnormal??
If normal fully compensated
2. 2nd . Is PH to acidosis or alkalosis side??
 If it is in acidosis side look PaCO2 and HCO3
3. 3rd . Based PCO2 or HCO3 determine the
metabolic or respiratory alkalosis or acidosis

Fig. PH Side inclination

Metabolic vs respiratory acid base
balance
PH PCO2 HCO3 Fully Partial uncompe Dx
compensated compensa nsated
te
7.41-45 incre incre fully m. alk
7.35-40 incre incre fully r. aci
>7.45 incr incre partial m.alka
<7.35 incre incre paritial R . acid
7.35-7.40 decr decr fully M-aci
7.41-7.45 decr decr Fully R-alkal
>7.45 decr Norma uncomp R-alkal
l/incre
<7.35 Normal/ decr uncom M-alka
incre

Summary
• ↑ pH ↓ H+
• ↑PH ↓ acidosis ↑ alkalosi
• ↑ HCO3 ↓ acidosis ↑ alkalosis
• ↑ PaCO2 ↓ alkalosis ↑ acidosis
• ↑ Acidity ↑ k+ ↓alkalosis


Fluid and Electrolyte Imbalance

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Fluid and Electrolyte Imbalance

Uploaded by

Copyright:

Available Formats

COLLAGE OF HEALTH SCIENCE DEPARTMENT OF

FOR 3rd YEAR BSc NURSE

Body Fluid and Electrolyte Imbalance

BY. Fentahun Minwuyelet(BSC, MSC IN AHN)

 Identify the effects of aging on fluid and

6/25/2022 BY. Fentahun Minwuyelet 4

6/25/2022 BY. Fentahun Minwuyelet 5

6/25/2022 BY. Fentahun Minwuyelet 6

2. What are the constituents your body fluid?

3. Why fluid resuscitation is needed for

4. Do you know imbalance between acid and

6/25/2022 BY. Fentahun Minwuyelet 8

6/25/2022 BY. Fentahun Minwuyelet 9

6/25/2022 BY. Fentahun Minwuyelet 10

2. Extra cellular fluid(ECF) compartment

6/25/2022 BY. Fentahun Minwuyelet 14

6/25/2022 BY. Fentahun Minwuyelet 15

6/25/2022 BY. Fentahun Minwuyelet 17

6/25/2022 BY. Fentahun Minwuyelet 18

Massive bleeding in to joint or body cavities

6/25/2022 BY. Fentahun Minwuyelet 19

6/25/2022 BY. Fentahun Minwuyelet 20

6/25/2022 BY. Fentahun Minwuyelet 21

 The sources of fluid gains

Average in take and out put of fluids in adults is the same

 Intake Out put

 Oral intake Urine-----1500ml

– As liquid -------------1300ml Stool------200ml

– In food ---------------1000ml Insensible

 Metabolic oxidation -----300ml Lung------300ml

 Total gain----------2600ml Total lose----2600ml

6/25/2022 BY. Fentahun Minwuyelet 23

I. Thirst level-primarily regulates intake

occurs when an increase in the extra cellular

6/25/2022 BY. Fentahun Minwuyelet 24

6/25/2022 BY. Fentahun Minwuyelet 26

 Sodium (Na+) -------------------------------135-145mEq/l

6/25/2022 BY. Fentahun Minwuyelet 27

Anions Referance range

6/25/2022 BY. Fentahun Minwuyelet 28

6/25/2022 BY. Fentahun Minwuyelet 29

6/25/2022 BY. Fentahun Minwuyelet 30

 Osmolality is expressed as milliosmoles per

 Osmolarity expressed as milliosmoles per liter

6/25/2022 BY. Fentahun Minwuyelet 31

6/25/2022 BY. Fentahun Minwuyelet 32

6/25/2022 BY. Fentahun Minwuyelet 33

 High density or too concentrated than water---

 Is compared to the weight of distilled water, which

 Normal value -- 1.010-1.025

6/25/2022 BY. Fentahun Minwuyelet 35

Sensitive indicator of renal disease used to

Normal can range from 115 to 125 mL/min

6/25/2022 BY. Fentahun Minwuyelet 37

 Increase with dehydration and polycythemia

 Decrease with over hydration and anemia

6/25/2022 BY. Fentahun Minwuyelet 39

6/25/2022 BY. Fentahun Minwuyelet 42

6/25/2022 BY. Fentahun Minwuyelet 43

Vomiting Diuretic therapy

 Skin losses (salt water)

6/25/2022 BY. Fentahun Minwuyelet 45

6/25/2022 BY. Fentahun Minwuyelet 46