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Fluids and Electrolytes

INTRODUCTION C. Body Compartment Volumes

 To maintain good health, a balance of fluids Normal values Premature Term
and electrolytes, acids and bases must be TBW Male: 80% 75%
normally regulated for metabolic processes Female:
to be in working state. ECF 45% 40%
ICF 35% 35%
 A cell, together with its environment in any
Blood Volume 90-100 ml/kg 85 ml/kg
part of the body, is primarily composed of
 neonates reach adult values by 2 yrs and
 Thus fluid and electrolyte balance must be are about half-way by 3 months
maintained to promote normal function.
 average values ~ 70 ml/100g of lean body
Potential and actual problems of fluid and
electrolytes happen in all health care
 percentage of water varies with tissue type,
settings, in every disorder and with a variety
A. lean tissues ~ 60-80%
of changes that affect homeostasis.
B. bone ~ 20-25%
 The nurse therefore needs to FULLY
C. fat ~ 10-15%
understand the physiology and
D. Tonicity of Body Fluids
pathophysiology of fluid and electrolyte
 Tonicity refers to the concentration
alterations so as to identify or anticipate of particles in a solution
and intervene appropriately.  The normal tonicity or osmolarity of
Fluids body fluids is 250-300 mOsm/L
 a solution of solvent and solute 1. Isotonic
Solvent  Same as plasma
2. Hypotonic
 a liquid substance where particles can be  have a lesser or lowers solute concentration
dissolved than plasma
3. Hypertonic
Solute  higher or greater concentration of solutes
 a substance, either dissolved or suspended
Common Intravenous Solutions
in a solution Solution Na Cl- K+ Ca Glu
Solution D5W 0 0 0 0 278
 a homogeneous mixture of 2 or more NaCl 0.9% 150 150 0 0 0
substances of dissimilar molecular structure NaCl 3.0% 513 513 0 0 0
 usually applied to solids in liquids but D4W/NaCL 0.18% 30 30 0 0 222
Hartmans 129 109 5 0 0
applies equally to gasses in liquids
Plasmalyte 140 98 5
Haemaccel 145 145 5.1 6.25 0
Body Fluids Mannitol20% 0 0 0 0 0
A. Function Dextran 70 154 154 0 0 0
1. Transporter of nutrients , wastes, Osmole
hormones, proteins and etc
2. Medium or milieu for metabolic  the weight in grams of a substance
processes producing an osmotic pressure of 22.4 atm. when
3. Body temperature regulation dissolved in 1.0 litre of solution
4. Lubricant of musculoskeletal joints  (gram molecular weight) / (no. of freely
5. Insulator and shock absorber
moving particles per molecule)
B. Body Fluid Compartments
Intrace Extracellular Transce
llular llular  the number of osmoles of solute per
Within Outside cells Containe kilogram of solvent
Cells d in Osmolarity
cavities  the number of osmoles of solute per litre of
55% or 42.5% or 1/3 TBW 2.5% solution
2/3 TBW Mole
Transport system of our body Not  that number of molecules contained in
readily 0.012 kg of C12, or,
by the
 the molecular weight of a substance in
grams = Avogadro's number
= 6.023 x 1023
Potassiu Sodium* CSF,
m* Bicarbonates Pleural
Phospha Chloride fluid,  the number of moles of solute per kilogram
tes Synovial of solvent
Magnesi Fluid and Molarity
um peritone  is the number of moles of solute per litre of
al fluid solution
epithelia The methods by which electrolytes and
l cells other solutes move across biologic membranes are
Intersti Intrava Bound Osmosis, Diffusion, Filtration and Active Transport.
tial scular Osmosis, diffusion and filtration are passive
Fluid Within processes, while Active transport is an active
surroun the process.
ding the blood
cells vessels 1. OSMOSIS
20%TB 1/3 of Bone  This is the movement of
W or ECF and water/liquid/solvent across a semi-
2/3 of Plasma Cartila permeable membrane from a lesser
ECF 7.5% ge concentration to a higher concentration
7.5%  Osmotic pressure is the power of a
Higher Dense solution to draw water across a semi-
protein Connec permeable membrane
content tive
 Colloid osmotic pressure (also called  Anti-diuretic hormone (ADH) is synthesized
oncotic pressure) is the osmotic pull by the hypothalamus and acts on the collecting ducts
exerted by plasma proteins of the nephron
 ADH increases rate of water reabsorption
2. DIFFUSION  The adrenal gland helps control F&E through
 “Brownian movement” or “downhill the secretion of ALOSTERONE- a hormone that
movement” promotes sodium retention and water retention in
 The movement of the distal nephron
particles/solutes/molecules from an  ATRIAL NATRIURETIC factor (ANF) is
area of higher concentration to an released by the atrial cells of the heart in response to
area of a lower concentration excess blood volume and increased wall stretching.
 This process is affected by: ANF promotes sodium excretion and inhibits thirst
a. The size of the molecules- larger size moves mechanism
slower than smaller size 3. Gastro-intestinal regulation
b. The concentration of solution- wide difference in  The GIT digests food and absorbs water
concentration has a faster rate of diffusion  The hormonal and enzymatic activities
c. The temperature- increase in temperature causes involved in digestion, combined with the passive and
increase rate of diffusion active transport of electrolyte, water and solutions,
 Facilitated Diffusion is a type of maintain the fluid balance in the body.
diffusion, which uses a carrier, but B. Fluid Intake
no energy is expended. One  Healthy adult ingests fluid as part of the
example is fructose and amino acid dietary intake.
transport process in the intestinal  90% of intake is from the ingested food and
cells. This type of diffusion is water
saturable.  10% of intake results from the products of
cellular metabolism
3. FILTRATION  Usual intake of adult is about 2, 500 ml per
 This is the movement of BOTH day
solute and solvent together across  The other sources of fluid intake are: IVF,
a membrane from an area of TPN, Blood products, and colloids
higher pressure to an area of lower C. Fluid Output
pressure  The average fluid losses amounts to 2, 500
 Hydrostatic pressure is the ml per day, counterbalancing the input.
pressure exerted by the fluids  The routes of fluid output are the following:
within the closed system in the  SENSIBLE LOSS- Urine, feces or GI losses,
walls of the container sweat
 INSENSIBLE LOSS- though the skin and
4. ACTIVE TRANSPORT lungs as water vapor
 Process where substances/solutes  URINE- is an ultra-filtrate of blood. The
move from an area of lower normal output is 1,500 ml/day or 30-50 ml per hour
concentration to an area of higher or 0.5-1 ml per kilogram per hour. Urine is formed
concentration with utilization of from the filtration process in the nephron
ENERGY  FECAL loss- usually amounts to about 200
 It is called an “uphill movement” ml in the stool
 Usually, a carrier is required. An  Insensible loss- occurs in the skin and lungs,
enzyme is utilized also. which are not noticeable and cannot be accurately
measured. Water vapor goes out of the lungs and
Types of Active Transport: skin.
a. Primarily Active Transport
 Energy is obtained directly Water Metabolism
from the breakdown of  Daily Balance: turnover ~ 2500 ml
ATP a. Intake
 One example is the i. drink ~ 1500 ml
Sodium-Potassium pump ii. food ~ 700 ml
b. Secondary Active Transport iii. metabolism ~ 300 ml
 Energy is derived b. Losses
secondarily from stored i. urine ~ 1500 ml
energy in the form of ionic ii. skin ~ 500 ml
concentration difference  insensible losses ~ 400 ml
between two sides of the  sweat ~ 100 ml
membrane. iii. lungs ~ 400 ml
 One example is the iv. faeces ~ 100 ml
Glucose-Sodium co- Minimum daily intake ~ 500 ml with a "normal" diet
transport; also the Minimum losses ~ 1500 ml/d
Sodium-Calcium counter- Losses are increased with;
transport a. increased ambient T
b. hyperthermia ~ 13% per °C
THE REGULATION OF BODY FLUID BALANCE c. decreased relative humidity
d. increased minute ventilation
To maintain homeostasis, many body e. increased MRO2
systems interact to ensure a balance of fluid intake Fluid Imbalances
and output. A balance of body fluids normally occurs FLUID VOLUME DEFICIT or HYPOVOLEMIA
when the fluid output is balanced by the fluid input
 Definition: This is the loss of extra cellular
A. Systemic Regulators of Body Fluids fluid volume that exceeds the intake of fluid.
The loss of water and electrolyte is in equal
1. Renal Regulation (RAS) proportion. It can be called in various terms-
 This system regulates sodium and water vascular, cellular or intracellular
balance in the ECF dehydration. But the preferred term is
 The formation of urine is the main hypovolemia.
mechanism  Dehydration refers to loss of WATER alone,
 Substance released to regulate water with increased solutes concentration and
balance is RENIN. Renin activates Angiotensinogen to sodium concentration
Angiotensin-I, A-I is enzymatically converted to Pathophysiology of Fluid Volume Deficit
Angiotensin-II ( a powerful vasoconstrictor)
 Etiologic conditions include:
a. Vomiting
2. Endocrine Regulation
b. Diarrhea
 The primary regulator of water intake is the c. Prolonged GI suctioning
thirst mechanism, controlled by the thirst center in d. Increased sweating
the hypothalamus (anterolateral wall of the third e. Inability to gain access to fluids
ventricle) f. Inadequate fluid intake
g. Massive third spacing  Etiologic conditions and Risks factors
 Congestive heart failure
 Risk factors are the following:  Renal failure
a. Diabetes Insipidus  Excessive fluid intake
b. Adrenal insufficiency  Impaired ability to excrete fluid as
c. Osmotic diuresis in renal disease
d. Hemorrhage  Cirrhosis of the liver
e. Coma  Consumption of excessive table
f. Third-spacing conditions like ascites, salts
pancreatitis and burns
 Administration of excessive IVF
 Abnormal fluid retention
 Factors  Excessive fluid
 inadequate fluids in the body  expansion of blood volume
 decreased blood volume  edema, increased neck vein
 decreased cellular hydration distention, tachycardia,
 cellular shrinkage hypertension.
 weight loss, decreased turgor, oliguria, The Nursing Process in Fluid Volume Excess
hypotension, weak pulse, etc. ASSESSMENT
Physical Examination
The Nursing Process in Fluid Volume Deficit 1. Increased weight gain
ASSESSMENT: 2. Increased urine output
Physical examination 3. Moist crackles in the lungs
4. Increased CVP
 Weight loss, tented skin
5. Distended neck veins
turgor, dry mucus
6. Wheezing
7. Dependent edema
 Hypotension
Subjective cue/s
 Tachycardia 1. Shortness of breath
 Cool skin, acute weight 2. Change in mental state
 Flat neck veins Laboratory findings
 Decreased CVP 1. BUN and Creatinine levels are LOW because
Subjective cues of dilution
 Thirst 2. Urine sodium and osmolality decreased
 Nausea, anorexia (urine becomes diluted)
 Muscle weakness and cramps 3. CXR may show pulmonary congestion
 Change in mental state NURSING DIAGNOSIS
o Fluid Volume excess
1. Elevated BUN due to depletion of fluids or • Administer diuretics as prescribed
decreased renal perfusion • Assist in hemodialysis
2. Hemoconcentration • Provide dietary restriction of
3. Possible Electrolyte imbalances: sodium and water
Hypokalemia, Hyperkalemia, Hyponatremia, NURSING MANAGEMENT
1. Continually assess the patient’s
4. Urine specific gravity is increased
condition by measuring intake and
(concentrated urine) above 1.020
output, daily weight monitoring, edema
assessment and breath sounds
• Fluid Volume deficit 2. Prevent Fluid Volume Excess by
PLANNING adhering to diet prescription of low salt-
• To restore body fluids foods.
IMPLEMENTATION 3. Detect and Control Fluid Volume Excess
ASSIST IN MEDICAL INTERVENTION by closely monitoring IVF therapy,
• Provide intravenous fluid as ordered administering medications, providing
• Provide fluid challenge test as ordered rest periods, placing in semi-fowler’s
NURSING MANAGEMENT position for lung expansion and
providing frequent skin care for the
1. Assess the ongoing status of the patient by doing
an accurate input and output monitoring 4. Teach patient about edema, ascites,
2. Monitor daily weights. Approximate weight loss 1 and fluid therapy. Advise elevation of
kilogram = 1liter! the extremities, restriction of fluids,
3. Monitor Vital signs, skin and tongue turgor, urinary necessity of paracentesis, dialysis and
concentration, mental function and peripheral diuretic therapy.
circulation 5. Instruct patient to avoid over-the-
counter medications without first
4. Prevent Fluid Volume Deficit from occurring by
checking with the health care provider
identifying risk patients and implement fluid because they may contain sodium
replacement therapy as needed promptly
5. Correct fluid Volume Deficit by offering ELECTROLYTES
fluids orally if tolerated, anti-emetics if with  Electrolytes are charged ions capable of
vomiting, and foods with adequate conducting electricity and are solutes found
electrolytes in all body compartments.
6. Maintain skin integrity 1. Sources of electrolytes
7. Provide frequent oral care  Foods and ingested fluids, medications; IVF
8. Teach patient to change position slowly to and TPN solutions
avoid sudden postural hypotension 2. Functions of Electrolytes
 Maintains fluid balance
FLUID VOLUME EXCESS: HYPERVOLEMIA  Regulates acid-base balance
 Refers to the isotonic expansion of the ECF  Needed for enzymatic secretion and
caused by the abnormal retention of water activation
and sodium  Needed for proper metabolism and effective
 There is excessive retention of water and processes of muscular contraction, nerve
electrolytes in equal proportion. Serum transmission
sodium concentration remains NORMAL 3. Types of Electrolytes
 CATIONS- positively charged ions; examples
Pathophysiology of Fluid Volume Excess are sodium, potassium, calcium
 ANIONS- negatively charged ions; examples compartment with a higher concentration
are chloride and phosphates] cell swelling
 The major ICF cation is potassium (K+); the  Water is pulled INTO the cell because of
major ICF anion is Phosphates decreased extracellular sodium level and
 The major ECF cation is Sodium (Na+); the increased intracellular concentration
major ECF anion is Chloride (Cl-) The Nursing Process in HYPONATREMIA
1. Electrolyte Distribution Sodium Deficit (Hyponatremia)
 ECF and ICF vary in their electrolyte ♦Clinical Manifestations
distribution and concentration
 Clinical manifestations of hyponatremia
 ICF has K+, PO4-, proteins, Mg+, Ca++ and
SO4- depend on the cause, magnitude, and
 ECF has Na+, Cl-, HCO3- rapidity of onset.
2. Electrolyte Excretion  Although nausea and abdominal
 These electrolytes are excessively cramping occur, most of the symptoms
eliminated by abnormal fluid losses are neuropsychiatric and are probably
 Routes can be thru urine, feces, vomiting, related to the cellular swelling and
surgical drainage, wound drainage and skin excretion cerebral edema associated with
3. Regulation of Electrolytes
a) Renal Regulation
 occurs by the process of glomerular  As the extracellular sodium level
filtration, tubular reabsorption and tubular secretion decreases, the cellular fluid becomes
b) Endocrine Regulation relatively more concentrated and ‘pulls”
 hormones play a role in this type of water into the cells.
regulation:  In general, those patients having acute
Aldosterone- promotes Na retention and K decline in serum sodium levels have
more severe symptoms and higher
ANF- promotes Na excretion
PTH- promotes Ca retention and PO4 excretion mortality rates than do those with more
Calcitonin- promotes Ca and PO4 excretion slowly developing hyponatremia.
c) GIT Regulation  Features of hyponatremia associated
 electrolytes are absorbed and secreted with sodium loss and water gain include
 some are excreted thru the stool anorexia, muscle cramps, and a feeling
THE CATIONS of exhaustion.
SODIUM  When the serum sodium level drops
 The most abundant cation in the ECF below 115 mEq/L (SI: 115 mmol/L), thee
 Normal range in the blood is 135-145 mEq/L ff signs of increasing intracranial
 A loss or gain of sodium is usually pressure occurs:
accompanied by a loss or gain of water.
o lethargy
 Major contributor of the plasma Osmolality
 Sources: Diet, medications, IVF. The o Confusion
minimum daily requirement is 2 grams o muscular twitching
 Imbalances- Hyponatremia= <135 mEq/L; o focal weakness
Hypernatremia= >145 mEq/L
o hemiparesis
 Functions:
1. Participates in the Na-K pump o papilledema
2. Assists in maintaining blood volume o convulsions
3. Assists in nerve transmission and muscle In summary:
contraction  Physical Examination
1. Altered mental status
4. Primary determinant of ECF concentration.
5. Controls water distribution throughout the 2. Vomiting
body. 3. Lethargy
4. Muscle twitching and convulsions
6. Primary regulator of ECF volume. (if sodium level is below 115
7. Sodium also functions in the establishment mEq/L)
of the electrochemical state necessary for 5. Focal weakness
muscle contraction and the transmission of  Subjective Cues
1. Nausea
nerve impulses.
2. Cramps
8. Regulations: skin, GIT, GUT, Aldosterone 3. Anorexia
increases Na retention in the kidney 4. Headache
 Laboratory findings
SODIUM DEFICIT: HYPONATREMIA 1. Serum sodium level is less than
 Refers to a Sodium serum level of less than 135 mEq/L
135 mEq/L. This may result from excessive 2. Decreased serum osmolality
sodium loss or excessive water gain. 3. Urine specific gravity is LOW if
Pathophysiology caused by sodium loss
 Etiologic Factors 4. In SIADH, urine sodium is high and
1. Fluid loss such as from Vomiting and specific gravity is HIGH
nasogastric suctioning NURSING DIAGNOSIS
2. Diarrhea  Altered cerebral perfusion
3. Sweating  Fluid volume Excess
4. Use of diuretics IMPLEMENTATION
 Other factors
1. Dilutional hyponatremia  Provide sodium replacement as ordered.
• Water intoxication, compulsive Isotonic saline is usually ordered.. Infuse the
water drinking where sodium level solution very cautiously. The serum sodium
is diluted with increased water must NOT be increased by greater than 12
intake mEq/L because of the danger of pontine
2. SIADH osmotic demyelination
• Excessive secretion of ADH causing  Administer lithium and demeclocycline in
water retention and dilutional SIADH
hyponatremia  Provide water restriction if with excess
 Hyponatremia hypotonicity of plasma NURSING MANAGEMENT
water from the intravascular space will
1. Provide continuous assessment by doing an
move out and go to the intracellular
accurate intake and output, daily weights,
mental status examination, urinary sodium 4. Flushed skin, postural hypotension
levels and GI manifestations. Maintain 5. Increased muscle tone and deep
seizure precaution reflexes
2. Detect and control Hyponatremia by 6. Peripheral and pulmonary edema
encouraging food intake with high sodium  Subjective Cues
content, monitoring patients on lithium 1. Delusions and hallucinations
therapy, monitoring input of fluids like IVF, 2. Extreme thirst
parenteral medication and feedings. 3. Behavioral changes
3. Return the Sodium level to Normal by  Laboratory findings
restricting water intake if the primary 1. Serum sodium level exceeds 145
problem is water retention. Administer mEq/L
sodium to normovolemic patient and 2. Serum osmolality exceeds 295
elevate the sodium slowly by using sodium mOsm/kg
chloride solution 3. Urine specific gravity and
 Serum Sodium level is higher than 145 IMPLEMENTATION
 There is a gain of sodium in excess of water 1. Administer hypotonic electrolyte solution
or a loss of water in excess of sodium. slowly as ordered
Pathophysiology: 2. Administer diuretics as ordered
 Etiologic factors 3. Desmopressin is prescribed for diabetes
1. Fluid deprivation insipidus
2. Water loss from Watery diarrhea, NURSING MANAGEMENT
fever, and hyperventilation 1. Continuously monitor the patient by
3. Administration of hypertonic assessing abnormal loses of water, noting
solution for the thirst and elevated body
4. Increased insensible water loss temperature and behavioral changes
5. Inadequate water replacement, 2. Prevent hypernatremia by offering fluids
inability to swallow regularly and plan with the physician
6. Seawater ingestion or excessive alternative routes if oral route is not
oral ingestion of salts possible. Ensure adequate water for patients
 Other factors with DI. Administer IVF therapy cautiously
1. Diabetes insipidus 3. Correct the Hypernatremia by monitoring
2. Heat stroke the patient’s response to the IVF
3. Near drowning in ocean replacement. Administer the hypotonic
4. Malfunction of dialysis solution very slowly to prevent sudden
 Increased sodium concentration cerebral edema.
4. Monitor serum sodium level.
 hypertonic plasma
5. Reposition client regularly, keep side-rails
 water will move out form the cell outside to up, the bed in low position and the call
the interstitial space bell/light within reach.
 CELLULAR SHRINKAGE 6. Provide teaching to avoid over-the counter
 then to the blood medications without consultation as they
 Water pulled from cells because of may contain sodium
increased extracellular sodium level and
decreased cellular fluid concentration POTASSIUM
The Nursing Process in HYPERNATREMIA  The most abundant cation in the ICF
A. Sodium Excess (Hypernatremia)  Potassium is the major intracellular
Clinical Manifestations electrolyte; in fact, 98% of the body’s
• primarily neurologic potassium is inside the cells.
• Presumably the consequence of cellular  The remaining 2% is in the ECF; it is this 2%
dehydration. that is all-important in neuromuscular
• Hypernatremia results in a relatively
concentrated ECF, causing water to be  Potassium is constantly moving in and out of
pulled from the cells. cells according to the body’s needs, under
the influence of the sodium-potassium
• Clinically, these changes may be manifested pump.
by:  Normal range in the blood is 3.5-5 mEq/L
o restlessness and weakness in  Normal renal function is necessary for
moderate hypernatremia maintenance of potassium balance, because
o disorientation, delusions, and 80-90% of the potassium is excreted daily
hallucinations in severe from the body by way of the kidneys. The
hypernatremia. other less than 20% is lost through the
• Dehydration (hypernatremia) is often bowel and sweat glands.
overlooked as the primary reason for  Major electrolyte maintaining ICF balance
behavioral changes in the elderly.  Sources- Diet, vegetables, fruits, IVF,
• If hypernatremia is severe, permanent brain medications
damage can occur (especially in children).  Functions:
Brain damage is apparently due to 1. Maintains ICF Osmolality
subarachnoid hemorrhages that result from
2. Important for nerve conduction and
brain contraction.
A primary characteristic of hypernatremia is muscle contraction
thirst. Thirst is so strong a defender of serum 3. Maintains acid-base balance
sodium levels in normal people that hypernatremia 4. Needed for metabolism of
never occurs unless the person is unconscious or is carbohydrates, fats and proteins
denied access to water; unfortunately, ill people may 5. Potassium influences both skeletal and
cardiac muscle activity.
have an impaired thirst mechanism. Other signs
a. For example, alterations in its
include dry, swollen tongue and sticky mucous concentration change
membranes. A mild elevation in body temperature myocardial irritability and
may occur, but on correction of the hypernatremia rhythm.
the body temperature should return to normal.  Regulations: renal secretion and excretion,
ASSESSMENT Aldosterone promotes renal excretion
 Physical Examination acidosis promotes K exchange for hydrogen
1. Restlessness, elevated body
temperature  Imbalances:
2. Disorientation  Hypokalemia= <3.5 mEq/L
3. Dry, swollen tongue and sticky  Hyperkalemia=> 5.0 mEq/L
mucous membrane, tented skin
 Condition when the serum concentration of monitor. To EMPHASIZE: Potassium should
potassium is less than 3.5 mEq/L NEVER be given IV bolus or IM!!
Pathophysiology 5. A concentration greater than 60 mEq/L is
 Etiology not advisable for peripheral veins.
1. Gastro-intestinal loss of potassium
such as diarrhea and fistula POTASSIUM EXCESS: HYPERKALEMIA
2. Vomiting and gastric suctioning
3. Metabolic alkalosis  Serum potassium greater than 5.5 mEq/L
4. Diaphoresis and renal disorders Pathophysiology
5. Ileostomy  Etiologic factors
 Other factor/s 1. Iatrogenic, excessive intake of
1. Hyperaldosteronism potassium
2. Heart failure 2. Renal failure- decreased renal
3. Nephrotic syndrome excretion of potassium
4. Use of potassium-losing diuretics 3. Hypoaldosteronism and Addison’s
5. Insulin therapy disease
6. Starvation 4. Improper use of potassium
7. Alcoholics and elderly supplements
• Decreased potassium in the body  Other factors
impaired nerve excitation and 1. Pseudohyperkalemia- tight
transmission signs/symptoms such as tourniquet and hemolysis of blood
weakness, cardiac dysrhythmias etc.. sample, marked leukocytosis
The Nursing Process in Hypokalemia 2. Transfusion of “old” banked blood
Potassium Deficit (Hypokalemia) 3. Acidosis
4. Severe tissue trauma
Clinical Manifestations
 Increased potassium in the body
 Potassium deficiency can result in  Causing irritability of the cardiac cells
widespread derangements in physiologic
 Possible arrhythmias!!
functions and especially nerve conduction.
The Nursing Process in
 Most important, severe hypokalemia can
result in death through cardiac or
respiratory arrest.
 Clinical signs rarely develop before the Potassium Excess (Hyperkalemia)
serum potassium level has fallen below 3 Clinical Manifestations
mEq/L (51: 3 mmol/L) unless the rate of fall  By far the most clinically important effect of
has been rapid. hyperkalemia is its effect on the
 Manifestations of hypokalemia include myocardium.
fatigue, anorexia, nausea, vomiting, muscle  Cardiac effects of an elevated serum
weakness, decreased bowel motility, potassium level are usually not significant
paresthesias, dysrhythmias, and increased below a concentration of 7 mEq/L (SI: 7
sensitivity to digitalis. mmol/L), but they are almost always
 If prolonged, hypokalemia can lead to present when the level is 8 mEq/L (SI: 8
impaired renal concentrating ability, causing mmol/L) or greater.
dilute urine, polyuria, nocturia, and  As the plasma potassium concentration is
polydipsia increased, disturbances in cardiac
ASSESSMENT conduction occur.
 Physical examination  The earliest changes, often occurring at a
1. Muscle weakness serum potassium level greater than 6 mEq/
2. Decreased bowel motility and L (SI: 6 mmol/L), are peaked narrow T waves
abdominal distention and a shortened QT interval.
3. Paresthesias  If the serum potassium level continues to
4. Dysrhythmias rise, the PR interval becomes prolonged and
5. Increased sensitivity to digitalis is followed by disappearance of the P waves.
 Subjective cues  Finally, there is decomposition and
1. Nausea , anorexia and vomiting prolongation of the QRS complex.
2. Fatigue, muscles cramps Ventricular dysrhythmias and cardiac arrest
3. Excessive thirst, if severe may occur at any point in this progression.
 Laboratory findings  Note that in Severe hyperkalemia causes
1. Serum potassium is less than 3.5 muscle weakness and even paralysis,
mEq/L related to a depolarization block in muscle.
2. ECG: FLAT “T” waves, or inverted T
 Similarly, ventricular conduction is slowed.
waves, depressed ST segment and
presence of the “U” wave and  Although hyperkalemia has marked effects
prolonged PR interval. on the peripheral neuromuscular system, it
3. Metabolic alkalosis has little effect on the central nervous
IMPLEMENTATION  Rapidly ascending muscular weakness
leading to flaccid quadriplegia has been
reported in patients with very high serum
1. Provide oral or IV replacement of potassium  Paralysis of respiratory muscles and those
2. Infuse parenteral potassium supplement. required for phonation can also occur.
Always dilute the K in the IVF solution and  Gastrointestinal manifestations, such as
administer with a pump. IVF with potassium nausea, intermit tent intestinal colic, and
should be given no faster than 10-20-mEq/ diarrhea, may occur in hyperkalemic
hour! patients.
3. NEVER administer K by IV bolus or IM
Physical Examination
1. Continuously monitor the patient by
1. Diarrhea
assessing the cardiac status, ECG
2. Skeletal muscle weakness
monitoring, and digitalis precaution
3. Abnormal cardiac rate
2. Prevent hypokalemia by encouraging the
Subjective Cues
patient to eat potassium rich foods like
1. Nausea
orange juice, bananas, cantaloupe, peaches,
2. Intestinal pain/colic
potatoes, dates and apricots.
3. Palpitations
3. Correct hypokalemia by administering
Laboratory Findings
prescribed IV potassium replacement. The
1. Peaked and narrow T waves
nurse must ensure that the kidney is
2. ST segment depression and shortened QT
functioning properly!
4. Administer IV potassium no faster than 20
3. Prolonged PR interval
mEq/hour and hook the patient on a cardiac
4. Prolonged QRS complex 2. Regulates serum Osmolality and blood
5. Disappearance of P wave volume
6. Serum potassium is higher than 5.5 mEq/L 3. Participates in the chloride shift
7. Acidosis 4. Acts as chemical buffer
IMPLEMENTATION  Regulations: Renal regulation by absorption
and excretion; GIT absorption
 Imbalances: Hypochloremia= < 95 mEq/L;
1. Monitor the patient’s cardiac status with
Hyperchloremia= >108 mEq/L
cardiac machine
2. Institute emergency therapy to lower
potassium level by:
a. Administering IV calcium  The major Anion of the ICF
gluconate- antagonizes action of K  Normal range is 2.5 to 4.5 mg/dL
on cardiac conduction  Sources: Diet, TPN, Bone reserves
b. Administering Insulin with dextrose-  Functions:
causes temporary shift of K into 1. Component of bones, muscles and nerve
cells tissues
c. Administering sodium bicarbonate- 2. Needed by the cells to generate ATP
alkalinizes plasma to cause 3. Needed for the metabolism of
temporary shift
carbohydrates, fats and proteins
d. Administering Beta-agonists
e. Administering Kayexalate (cation- 4. Component of DNA and RNA
exchange resin)-draws K+ into the Regulations: Renal glomerular filtration, endocrinal
bowel regulation by PTH-decreases PO4 in the
blood by kidney excretion
NURSING MANAGEMENT  Imbalances- Hypophosphatemia= <2.5
1. Provide continuous monitoring of cardiac mg/dL; Hyperphosphatemia >4.5 mg/dL
status, dysrhythmias, and potassium levels.
2. Assess for signs of muscular weakness, BICARBONATES
paresthesias, nausea  Present in both ICF and ECF
3. Evaluate and verify all HIGH serum K levels
 Regulates acid-base balance together with
4. Prevent hyperkalemia by encouraging high
risk patient to adhere to proper potassium
restriction  Normal range is 22-26 mEq/L
5. Correct hyperkalemia by administering  Sources: Diet; medications and metabolic
carefully prescribed drugs. Nurses must by-products of the cells.
ensure that clients receiving IVF with  Function: Component of the bicarbonate-
potassium must be always monitored and carbonic acid buffer system
that the potassium supplement is given  Regulation: Kidney production, absorption
correctly and secretion
6. Assist in hemodialysis if hyperkalemia  Imbalances: Metabolic acidosis= <22
cannot be corrected. mEq/L; Metabolic alkalosis= >26 mEq/
7. Provide client teaching. Advise patients at
risk to avoid eating potassium rich foods, ACID BASE BALANCE
and to use potassium salts sparingly.  Acids
8. Monitor patients for hypokalemia who are  substances that can donate or
receiving potassium-sparing diuretic release protons or hydrogen ions
(H+); examples are HCl, carbonic
acid, acetic acid.
CALCIUM  Bases or alkalis
 Majority of calcium is in the bones and teeth  substances that can accept protons
 Small amount may be found in the ECF and or hydrogen ions because they
ICF have low H+ concentration. The
 Normal serum range is 8.5 – 10.5 mg/dL major base in the body is
 Sources: milk and milk products; diet; IVF BICARBONATE (HCO3)
and medications  Carbon dioxide is considered to be acid or
 Functions: base depending on its chemical association
1. Needed for formation of bones and teeth  When assessing acid-base balance, carbon
2. For muscular contraction and relaxation dioxide is considered ACID because of its
3. For neuronal and cardiac function relationship with carbonic acid.
4. For enzymatic activation  Because carbonic acid cannot be routinely
measured, carbon dioxide is used.
5. For normal blood clotting
 pH- is the measurement of the degree of
 Regulations: acidity or alkalinity of a solution. This
1. GIT- absorbs Ca+ in the intestine; Vitamin D helps to reflects the relationship of hydrogen ion
increase absorption concentration in the solution.
2. Renal regulation- Ca+ is filtered in the glomerulus and  The higher the hydrogen ion concentration,
reabsorbed in the tubules: the acidic is the solution and pH is LOW
3. Endocrine regulation:  The lower the hydrogen concentration, the
Parathyroid hormone from the parathyroid glands is alkaline is the solution and the pH is HIGH
released when Ca+ level is low. PTH causes  Normal pH in the blood is between 7.35 to
release of calcium from bones and increased 7.45
retention of calcium by the kidney but PO4 is
 Sources of acids and bases are from:
Calcitonin from the thyroid gland is released when 1. ECF, ICF and body tissues
the calcium level is high. This causes excretion of 2. Foodstuff
both calcium and PO4 in the kidney and promoted 3. Metabolic products of cells like CO2, lactic
deposition of calcium in the bones. acids, and ammonia
 Imbalances- Hypocalcemia= <8.5 mg/dL;
Hypercalcemia= >10.5 mg/dL
THE ANIONS  Acids are constantly produced in the body
CHLORIDE  Because cellular processes need normal pH,
acids and bases must be balanced
 The major Anion of the ECF continuously
 Normal range is 95-108 mEq/L  CO2 and HCO3 are crucial in maintaining
 Sources: Diet, especially high salt foods, IVF the balance
(like NSS), HCl (in the stomach)  A ratio of HCO3 and Carbonic acid is
 Functions: maintained at 20:1
1. Major component of gastric juice
 Several body systems (like the respiratory,  Lean body has higher
renal and GIT) together with the chemical water content
buffers are actively involved in the normal
 The major ways in which balance is TEMPERATURE
maintained are the process of acid/base  Climate and heat and
secretion, production, excretion and humidity affect fluid
neutralization balance
 Buffers are present in all body fluids  Anorexia nervosa will lead
functioning mainly to prevent excessive to nutritional depletion
changes in the pH.  Stressful situations will
 Buffers either remove/accept H+ or increase metabolism,
release/donate H+ increase ADH causing
 The major chemical buffers are: water retention and
1. Carbonic acid-Bicarbonate Buffer (in the increased blood volume
ECF)  Chronic Alcohol
2. Phosphate buffer (in the ECF and ICF) consumption causes
3. Protein buffer (in the ICF) malnutrition
 The action of the chemical buffer is
immediate but limited  Trauma and burns release
K+ in the blood
 Cardiac dysfunction will
lead to edema and
 The respiratory center in the medulla is
 Carbon dioxide is the powerful MEDICATIONS AND SURGERY
stimulator of the respiratory center  Suctioning, diuretics and
 The lungs use CO2 to regulate H+ ion laxatives may cause
concentration imbalances
 Through the changes in the breathing
pattern, acid-base balance is achieved Acid Base Imbalances
within minutes
 Functions of the respiratory system in Metabolic Alkalosis
acid-base balance:  A base bicarbonate excess
1. CO2 + H2O H2CO3  A result of a loss of acid and the
2.↑ CO2activates medulla↑RRCO2 is  accumulation of bases
exhaled pH rises to normal  S/S - serum pH > 7.45, increased serum
 HCO3, serum K level less than 4,
3. ↑ HCO3depresses RRCO2 is
tetany, confusion and convulsions
retainedBicarbonate is neutralized pH drops to  Nursing Interventions - watch for s/s of
normal hypokalemia, LOC and seizure
THE KIDNEY Metabolic Acidosis
 Long term regulator of the acid-base  A base bicarbonate deficit
balance  Comes from too much acid from metabolism
 Slower to respond but more permanent and loss of bicarbonate
 Achieved by 3 interrelated processes  S/S - Serum pH <7.35, Increased K+ level,
1. Bicarbonate reabsorption in the DKA (Kussmaul’s Respirations), Shock,
stupor, coma
 Nursing Intervention - Give HCO3/Monitor
2. Bicarbonate formation K+ levels
3. Hydrogen ion excretion
 When excess H+ is present (acidic), pH Respiratory Alkalosis
fallskidney reabsorbs and generates  A deficit of carbonic acid caused by
Bicarbonate and excretes H+ hyperventilation
 S/S - decreased levels of CO2 and increased
 When H+ is low and HCO3 is high levels of pH, HCO3 near normal
(alkalotic). pH rises kidney excretes HCO3  Nursing Interventions - monitor for anxiety
and H+ is retained. and observe for signs and symptoms of
Normal Arterial Blood Gas Values
1. pH – 7.35-7.45 Respiratory Alkalosis
2. pO2 – 80-100 mmHg A carbonic acid excess
3. pCO2 – 35-45 mmHg Caused by an condition that interferes with the
4. Hco3 – 22-26 mEq/L release of CO2 from the lungs (sedatives, COPD,
narcotics etc.)
5. Base deficit/Excess – (+/-)2
S/S - serum pH < 7.35, increased serum CO2 levels>
6. O2 saturation – 98-100% 45 mm Hg, serum K increased, cyanosis
Nursing Interventions - Provide O2, Semifowlers
FACTORS AFFECTING BODY FLUIDS, position, seizure precautions
1. AGE Interpretation Arterial Blood Gases
 Infants have higher
proportion of body water  If acidosis the pH is down
than adults  If alkalosis the pH is up
 Water content of the body  The respiratory function indicator is the
decreases with age PCO2
 Infants have higher fluid  The metabolic function indicator is the
turn-over due to immature HCO3
kidney and rapid Step 1
respiratory rate  Look at the pH
 Is it up or down?
1. GENDER AND BODY SIZE  If it is up - it reflects alkalosis
 Women have higher body  If it is down - it reflects acidosis
fat content but lesser Step 2
water content
 Look at the PCO2
 Is it up or down?
 If it reflects an opposite response as the pH,
 then you know that the condition is a
respiratory imbalance
 If it does not reflect an opposite response as
the pH - move to step III
Step 3
 Look at the HCO3
 Does the HCO3 reflect a corresponding
 response with the pH
 If it does then the condition is a metabolic