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Fluid and Electrolytic Imbalance

Prepared by: Tesfa D. (ANP)-2010


First Edition-2014

Objectives
At the end of this chapter, the learner be
able to:
Discuss the anatomy and physiology of
body fluids and electrolytes
Describe common fluid and electrolyte
changes, their causes and management
Identify common acid base imbalances
and their treatment
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Fluid volume imbalance


Hyper osmolar imbalance
Hypo osmolar imbalance
Isotonic volume deficit
Isotonic volume excess

Fluid volume deficit (hypovolemia)


Loss of ECF > intake of fluid
Electrolytes to water ratio is the same
Hypovolemia Vs Dehydration

Contd
Causes
Risk factors
Inadequate intake
Diabetes insipidus
Abn. fluid losses
Adrenal insuf
Third-space fluid
Osmotic diuresis
Hemorrhage
shifts
Coma

Contd
Clinical Manifestations
Skin-cool, clammy, decreased skin turgor
CVS-postural hypotension; a weak, rapid
heart rate; flattened neck veins;
GUS-oliguria; concentrated urine.
Mouth-dry mucus membrane.
Others-acute weight loss; thirst;
anorexia; nausea; lassitude; muscle
weakness; and cramps.
6

Contd
Assessment and diagnostic findings
Hx
PE
BUN
HCT
Urine specific gravity
Urine osmolality
Serum electrolyte
7

Contd
Medical Management
Mild to moderate (5-10%);
Oral fluid intake-small frequent sip
Frequent mouth care
Giving non-irritating fluid
Acute and severe (>15%);
IV route is required (1L/30min-1hr)
Isotonic electrolyte solutions
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Contd
Nursing Management
Monitoring;
Fluid intake and output.
Daily body weight.
Vital signs closely.
Skin and tongue turgor.

Fluid volume excess (hypervolemia)


An isotonic expansion of the ECF
Water to sodium proportion is the same

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Contd
Cause
Iatrogenic
Heart failure
Renal failure
Cirrhosis of the liver
Excessive sodium salts intake
Excessive administration of sodium
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Contd
Clinical Manifestations
Edema
Distended neck veins
Crackles, tachycardia; increased BP, PP,
and CVP
Increased weight, urine output
Shortness of breath
Wheezing.
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Contd
Assessment and Diagnostic Findings
BUN.
Hematocrit.
Serum osmolality.
Chest x-rays.

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Contd
Medical Management
Fluid restriction
Pharmacologic: diuretics
Hemodialysis/peritoneal dialysis
Nutritional

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Contd
Nursing Management
Measures intake and output
Assess breath sounds
Monitors the degree of edema
Maintaining semi-fowlers position
Frequent positioning
Teaching patient about edema

15

Electrolyte Imbalance
Sodium;
Primary determinant of ECF osmolality.
Most abundant electrolyte in ECF.
Controls water distribution.
Muscle contraction and transmission of
nerve impulses.
135 to 145 mEq/L (135145 mmol/L).
One millimol/kg, excreted by kidney.
Sodium deficit and excess.
16

Sodium deficit (hyponatremia)


Less than 135 mEq/L [135 mmol/L]).
Occurs when;

Low quantity of total body sodium


Normal total body sodium content
An excess of total body sodium

17

Contd
Causes
Sodium loss
Diuretics use
Low-salt diet
Adrenal insufficiency
Water intoxication

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Contd
Predisposing factors
SIADH
Hyperglycemia
Electrolyte-poor parenteral fluids
Use of tap-water enemas
Excessive parenteral administration of
dextrose and water solutions
Compulsive water drinking
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Contd
Clinical Manifestations
Poor skin turgor
Dry mucosa
Decreased saliva production
Orthostatic fall in blood pressure,
Nausea
Abdominal cramping
Altered mental status
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Contd
When the serum sodium level drops below

115 mEq/L (115 mmol/L);


lethargy
signs of
Confusion
increasing
muscle twitching
intracranial
focal weakness
pressure
Hemiparesis
papilledema
Seizures

21

Contd

Assessment and Diagnostic Findings


Serum sodium level
Serum osmolality
Urinary sodium content
Urine specific gravity

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Contd
Medical Management
Sodium replacement-12 mEq/L in 24 hrs
Diuretic-furosemide (Lasix)
Water restriction-800 mL in 24 hrs

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Contd
Nursing Management
Identification of patients at risk and
early detection and treatment
Monitor fluid intake/output and daily
body weights
Note abnormal losses of sodium or gains
of water and GI manifestations
Alert for central nervous system changes
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Sodium excess (hypernatremia)


Exceeding 145 mEq/L [145 mmol/L].
Occurs when;

Gain of sodium in excess of water


Loss of water in excess of sodium

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Contd
Causes
Fluid deprivation
High sodium intake
IV administration of hypertonic saline or
excessive use of sodium bicarbonate
Water loss
Diabetes insipidus
Heat stroke, near-drowning, e.t.c
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Contd
Clinical Manifestations
Moderate:-restlessness and weakness
Severe:- disorientation, delusions, and
hallucinations
Others:-Dry swollen tongue, Sticky
mucous membranes, Flushed skin,
Peripheral and pulmonary edema, Postural
hypotension, e.t.c
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Contd
Assessment and Diagnostic Findings
Serum sodium level
Serum osmolality
Urine specific gravity
Urine osmolality

What do you expect if the cause is DI?

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Contd
Medical Management
IV hypotonic electrolyte solution
0.3% sodium chloride-safer
Dextrose 5% in water [D5W])

Diuretics
Desmopressin acetate (DDAVP)

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Contd
Nursing Management
Fluid losses and gains are carefully
monitored
Assess for abnormal losses of water or
low water intake and for large gains of
sodium.
Obtain a medication history.
Monitors for changes in behavior.
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Contd
Prevention
Adequate fluid intake
Debilitated patients at regular
intervals.
Alternate route for intake.
Diabetes insipidus.

31

Potassium imbalance
98% is inside the cells, in SKM
3.5 to 5.5 mEq/L (3.55.5 mmol/L).
Daily requirement is 1mmol/kg.
Neuromuscular function
Sodium-potassium pump

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Potassium deficit (hypokalemia)


Less than 3.5mEq/L (3.5 mmol/L).
Hypokalemia may occur in patients with;

Normal potassium stores


Alkalosis
Hypokalemia is a common imbalance.

33

Contd

Causes
GI loss of potassium (most common)
Recent ileostomy
Villous adenoma
Alkalosis
Hyperaldosteronism
High-carbohydrate parenteral fluids
Magnesium depletion
34

Contd
Clinical Manifestations
Severe-death
Dysrhythmias, Muscle weakness
Leg cramps, Fatigue, VAN
Decreased bowel motility
Glucose intolerance
Paresthesias
Increased sensitivity to digitalis
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Contd
Assessment and diagnostic findings
ECG
Flat T waves and/or inverted T waves
Depressed ST segments
An elevated U wave
Urinary potassium

36

Contd
Medical Management
Potassium replacement (IV/Oral)
40 to 80 mEq/day-no risk of potassium loss
50 to 100 mEq/day-risky potassium loss

37

Contd
Nursing Management
Monitor for its early presence in patients
at risk
Monitoring of fluid intake and output
Monitor closely for signs of digitalis
toxicity

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Contd

Preventing hypokalemia
Encouraging the patient at risk to eat
foods rich in potassium, such as fruit and
fruit juices (bananas, citrus fruit), fresh
and frozen vegetables, fresh meats, and
processed foods. (when the diet allows).

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Potassium excess (hyperkalemia)


Greater than 5.5 mEq/L (5.5 mmol/L).
Pseudohyperkalemia-falsely high level

of potassium;

Use of a tight tourniquet around an


exercising extremity
Hemolysis of the sample before analysis.
Marked leukocytosis
Drawing blood above a site where
potassium is infusing
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Contd

Causes
Infection.
Decreased renal excretion of potassium.
Excessive intake of potassium in food
Hypoaldosteronism.
Addisons disease.
Acidosis.
Medications (in more than 60% )
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Contd
Clinical Manifestations
Disturbances in cardiac conduction
Ventricular dysrhythmias and cardiac
arrest
Skeletal muscle weakness and even
paralysis
GI manifestations
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Contd
Assessment and Diagnostic Findings
Serum potassium levels.
ECG changes.
Arterial blood gas analysis (metabolic
acidosis).

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Contd
Medical Management
Restriction of potassium source.
Cation exchange resins (eg, Kayexalate).
10-20 units of reg.insulin and 25-50g of
glucose.
10 ml of 10% calcium gluconate.
Dialysis.
Avoid exogenous potassium.
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Contd
Emergency pharmacologic therapy
IV calcium gluconate, sodium, regular
insulin and a hypertonic dextrose
solution.
Monitoring the blood pressure.
Extra caution is required if the patient
has been digitalized.
Beta-2 agonists
ECG monitoring during administration
45

Contd
Nursing Management
Monitor closely for signs of
hyperkalemia.
Avoid prolonged use of tourniquet and
exercise.
Blood sample should be delivered to the
laboratory as soon as possible.

46

Calcium imbalance
Calcium
>99% in the skeletal system
About 1% is rapidly exchangeable
Bounded, ionized, complexed
8.5 to 10.5 mg/dL (2.12.6 mmol/L)
Absorbed from foods
Excreted in the feces
Controlled by PTH and calcitonin
47

Contd
Function;

Transmitting nerve impulses


Regulate muscle contraction and
relaxation
Activating enzymes
Blood coagulation

48

Calcium deficit (hypocalcemia)


Less than 8.5 mg/dL

Causes
Primary hypoparathyroidism
Surgical hypoparathyroidism (more
common).
Massive dministration of citrated blood
(transient hypocalcemia).
Pancreatitis
Renal failure
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Contd
Clinical Manifestations
Tetany (most)
Spasms of muscles of the extremities
and face
Pain, seizure, hyperactive tendon
reflexes
+Ve Chvosteks and Trousseaus sign-late
ECG and mental status changes
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Contd
Assessment and Diagnostic Findings
Serum calcium
ABGA
Serum albumin

51

Contd
Medical Management
Calcium rich food (1,000 to 1,500
mg/day)
Parenteral calcium salts
Vitamin D therapy
Aluminum hydroxide, calcium acetate, or
calcium carbonate antacids.

52

Contd
Nursing Management
Observe for hypocalcemia in patients at
risk.
Seizure precautions.
Health education.

53

Calcium excess (hypercalcemia)


Greater than 8.5 mg/dL, >16 mg/dL
Hypercalcemic crisis- >17 mg/dL, 50% mortality

rate
Causes
Malignancies and hyperparathyroidism (most
common).
Immobility.
Thiazide diuretics.
Milk-alkali syndrome.
Vitamin A and D intoxication.
Lithium use.

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Contd
Clinical Manifestations
Muscle weakness
CNS presentation
VAN
Constipation
Cardiac standstill
Digitalis toxicity
Dehydration
Abdominal and bone pain
55

Contd
Assessment and Diagnostic Findings
The serum calcium level
ECG changes
PTH test

X-rays
The Sulkowitch urine test

56

Contd
Medical Management
General measures
Administering fluids to dilute serum
calcium and promote its excretion by
the kidneys.
Mobilizing the patient.
Restricting dietary calcium intake.
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Contd
Pharmacologic therapy
0.9% sodium chloride solution.
Administering IV phosphate.
Furosemide (Lasix)
Mithramycin
Bisphosphonates
Inorganic phosphate salts
Calcitonin (salmon)
Corticosteroids
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Contd
Nursing Management
Monitor the patients at risk.
Encourage hospitalized patient to move.
Encouraged fluid intake.
Adequate fiber diet.
Assess for signs and symptoms of
digitalis toxicity.
Cardiac rate and rhythm are monitored.
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Reading Assignment
Read about;
Magnesium Imbalances
Phosphorus Imbalances
Chloride Imbalances

60

Acid-Base Balance
Acid;

Higher concentration of hydrogen ions


Base;
Higher concentration of hydroxide
ions

61

Contd
pH;

Alkalinity or acidity of a substance.


Potential of hydrogen.
Measured on a scale 0-14.
Hydrogen ion concentration.
Normal Blood pH is 7.35 7.45.
pH decreases-acidity increases.
pH increases-acidity decreases.
62

Regulation of Acid - Base Balance


Buffer systems: bicarbonate and
carbonic acid, phosphates, serum
proteins and meth-hemoglobin
Respiratory system.
Renal system.

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Contd

Carbonic Acid-Bicarbonate Buffer System


Primary extracellular fluid buffer
system.
Maintains a ratio of 20 parts
bicarbonate to 1 part carbonic acid.
Uses the process of hydration of CO2
to break it down so it can be
neutralized.
64

Contd

Respiratory Regulation
Respiratory System regulates by
adjusting rate and depth of
respirations.
By increasing rate and depth more CO2
will be blown off.
By decreasing rate and depth CO2 will
be conserved.
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Contd

Renal Regulation
Works slower than respiratory
compensation.
Effects are more long lasting.
Primarily regulates amount of
bicarbonate absorbed or excreted.
Also regulates ammonia and
electrolytes which can effect acidbase.
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Acid-base Imbalance
Alkalosis

Respiratory
Metabolic
Acidosis
Respiratory
Metabolic

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Respiratory Alkalosis
Deficiency of carbon dioxide.
PCO2 below 31 mmHg.
Too much carbon dioxide is released.

Causes:
Hyperventilation
Hypoxemia
High altitudes
Salicylate overdose

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Contd
Clinical Manifestations
Numbness/tingling in extremities
Lightheadedness
Confusion/ agitation, vent. fibrillation
Heart palpitations, ventr. arrhythmias
Muscle cramping
Deep rapid respirations
pH high (>7.45)
pCO2 low (<35mmHg)
69

Contd
Management
Treat cause
Oxygen
Re-breathing CO2
Compensation kidneys will attempt to
compensate by excreting more
bicarbonate

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Contd

Nursing Care
Relieve anxiety
Sedation
Reassurance
Paper bag
Rest

71

Respiratory Acidosis
Excess acid (CO2)

Causes:
Hypoventilation
Anesthesia
Sedatives
COPD
Respiratory infections
Inadequate ventilatory management
Excessive CO2 production
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Contd
Clinical Manifestations
Decreased rate and depth of
respirations
Hypoxia
Hypotension
Hypercapnic encephalopathy
pH low (< 7.35)
PCO2 high (>45mmHg)
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Contd
Management
Treat cause
Ventilatory support
Pulmonary hygiene
Emotional support

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Metabolic Alkalosis
Excess of base

Causes
Gain of base
Loss of too much acid
Hypokalemia

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Contd
Clinical Manifestations
Shallow breathing, Cheyne-stokes resp
Nausea/vomiting/diarrhea
Confusion
Numbness / tingling
Hypocalcemia
Hypokalemia
pH high (> 7.45)
HCO3 high (>26)
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Contd
Management
Replace fluids and electrolytes.
Diamox (Acetazolamide) enhances
excretion of bicarbonate.
Proper functioning kidneys will excrete
excess bicarbonate with adequate
fluid volume and appropriate
potassium.
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Contd
Nursing Care
Monitor vital signs closely.
Monitor fluid status.
Safety measures ( change in level of
consciousness).
If nasogastric suction, irrigate with
NS, not water.

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Metabolic Acidosis
Acid excess or base deficit

Causes
Renal failure
Diabetic ketoacidosis
Lactic acidosis
Large amount drainage from ileostomy
tube
Malnutrition
Anaerobic tissue metabolism
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Contd
Clinical Manifestations
Nausea/ vomiting/ diarrhea
Kussmauls respirations
Fruity-smelling breathe
Hyperkalemia
Bradycardia
pH low (< 7.35)
HCO3 low (< 22)
80

Contd
Management
Treat cause
Administer bicarbonate in extreme
cases
Replace fluids and electrolytes
Safety

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The End!
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