Fluid and Electrolytes

Balance & Imbalances Part 2

Common Disturbances in
Fluid & Electrolyte Balance
 Fluid Imbalances
◼ If fluid homeostasis is disturbed by
pathophysiologic processes or other
factors ( such as medications),
imbalances may result:
Two major categories:
1. Imbalances of ECF volume ( saline
imbalances)
2. Imbalances of body fluid concentration
( water imbalance)
 Common Disturbances in
Fluid & Electrolyte Balance
◼ Isotonic imbalances /Volume imbalances

◼ Osmolar imbalances /Hypo & Hypertonic

imbalances

◼ Compositional Changes:
Isotonic imbalances
◼ Hypovolemia (water depletion)
◼ Hypervolemia (water excess)
Osmotic imbalances
◼ Hyponatremia (decrease sodium)
◼ Hypernatremia (increase sodium)
Compositional imbalances

◼ Hypokalemia (decrease K+)

◼ Hyperkalemia (↑K+)
◼ Hypochloremia (↓Cl-)
◼ Hyperchloremia (↑Cl-)
◼ Hypocalcemia (↓Ca++)
◼ Hypercalcemia (↑Ca++)
◼ Hypophosphatemia (↓Phosphate)
◼ Hyperphosphatemia (↑phosphate)
◼ Hypomegnesemia (↓mg2+)
◼ Hypermagnesemia (↑mg2+)
Isotonic imbalances

◼ Hypovolemia or VOLUME DEFICIT

◼ Hypovolemia is a state of decreased

blood volume; more specifically,
decrease in volume of blood plasma.
Symptoms of hypovolemia may include cold
hands and feet, light headedness, infrequent
urination, increased heart rate, and weakness.
 Isotonic imbalances
Extra cellular Fluid volume deficit or
Hypovolemia or VOLUME DEFICIT

CAUSES OF ECF VOLUME DEFICIT:

◼ GI losses,
Vomiting; GI suction, diarrhea, pancreatic
/biliary fistula’s drainage,: bleeding
◼ Skin losses,
Diaphoresis(excess perspiration),extensive
burn,fever.
CAUSES of Hypovolemia Cont’d

◼ Renal Loss (Polyuria)

Renal disease (salt-wasting nephritis);
Diuretic excess; diabetic glycosuria;
Addison’s disease; Hypo-aldosteronosim,
mannitol therapy; high protein
elimentation.
 Hypovolemia:Clinical Features

▪ Weakness, fatigue,Anorexia, thirsty dry

mucous membranes.
▪ postural hypotension, tachycardia,, dizziness.
▪ poor skin & tongue turgor, confusion,,
lethargy, oliguria (< 30 ml/hr), weak pulse,
sunken eyeball, dry conjunctiva.
▪ slow vein filling (>3-5 second), falling venous
return & CVP ( central venous pressure), flat
jugular vein.
Hypovolemia:Clinical Features Cont’d

▪ rapid weight loss

▪ Longitudinal furrows in the tongue
▪ Infants have a sunken fontanelle
with extracellular volume deficit

▪ (2% loss = mild deficit, 5% loss =

moderate,8% loss = severe deficit
 Hypovolemia

LABORATORY FINDINGS:
📫 Elevated hematocrit (HCT >50% )
📫 Urine specific gravity above 1.030
📫 Normal serum Na+(usually)
📫 Increased serum protein ,elevated BUN >
25 (N=10)
📫 Urine osmolarity >450 m Osm/kg
(N 50-200 mOsm/kg)
Pathophysiology of Hypovolemia

Due to low blood pressure the

aldosterone and ADH work to absorb
water from nephron but due to
deficiency of fluid, marked reduction
occur in central venous pressure,
cardiac out put and inadequate
perfusion of most organs so the most
serious problems arises which is
circulatory shock and neurological
dysfunction.
Hypervolemia
Hypervolemia or fluid overload, is the
medical condition where there is
buildup of too much blood plasma
which leads to increased blood
volume.
 Hypervolemia causes
◼ Heart problems
◼ Causes of hypervolemia can vary, Hyperaldosteronism
and some may include the Kidney failure
following: Liver failure
Lung problems
Blood transfusion reaction Nephritis (kidney inflammation)
Chronic liver disease
Congestive heart failure Secondary
Cushing's syndrome Nephropathy
Glomerulonephritis Preeclampsia
Acute Pregnancy
Focal or embolic Surgery / operation complications
Membranoproliferati
Postinfectious
Post-streptococcal
 Isotonic imbalance (Cont’d)
📋 Extra cellular Fluid volume excess or
Hypervolemia:

CAUSES OF ECF VOLUME EXCESS:

◼ Congestive heart failure
◼ Chronic renal failure, cirrhosis of the liver
◼ increased aldosterone & steroid levels (cushing
syndrome)
◼ excess sodium intake or rapid infusion of IV
saline----saline excess
◼ Starvation (hypoalbiuminia)
◼ Glucocorticoids therapy
 Hypervolemia: Clinical Features
📫 Jugular vein distension
📫 Elevated blood pressure; full bounding pulse
elevated CVP
📫 Dyspnea, orthopnea
📫 Slow emptying of veins (>3-5 sec)
📫 edema (peripheral & periorbital)
📫 Ascities, pleural effusion, APE
📫 polyuria, crackles in lungs
📫 Rapid weight gain
📫 Infants who develops hypervolemia have
bulging fontanelle
 Hypervolemia:Clinical Features

●LABORATORY FINDINGS:
📫 Decreased hematocrit (< 38% )
📫 Normal serum Na+ level
📫 Low serum proteins
📫 Decreased BUN (< 10) b/c of
hemodilution
📫 Low urinary Na+ (< 10 mEq/2 hr)
 Pathophysiology of Hypervolemia
◼ This fluid, primarily salt and water, builds up in
various locations in the body and leads to an
increase in weight, swelling in the legs and arms
(peripheral edema), and/or fluid in the abdomen
(ascites).
◼ Eventually, the fluid enters the air spaces in the
lungs, reduces the amount of oxygen that can
enter the blood, and causes shortness of breath
(dyspnea).
◼ Fluid can also collect in the lungs when lying down
at night and can make night time breathing and
sleeping difficult.
Normal values of Na and K

◼ Sodium: normal adult: 135-145 mEq/L,

responsible for water movement.
◼ Potassium norm: 3.5-5.0 mEq/L
 Hyponatremia
◼ A serum concentration below the lower limit
of normal ( too little sodium in the blood).
Hyponatremia:
(Na<135Eq/L,<280mos/kg)
◼ Loss of sodium in excess of water---it
is relatively too dilute.
 Hyponatremia (cont’d)

◼ Gain of relatively more water than salt will

cause hyponatremia.
Dilutional hyponatremia;
- Decreased ability to excrete free water
- Effective circulating volume depletion(CHF,
nephrotic syndrome or cirrhosis)
- Excessive use of diuretics , IV
administration of hypotonic fluids & tap
water enemas, Renal failure
- SIADH
 Osmolar Imbalances:
Hypoosmolarity Imbalance
◼ Depletional hyponatremia;
-Prolonged diuretic therapy with low- salt
diet.
▪ Excessive GI losses; NG suctioning;
irrigation of NG tube with tap water;
Replacement of lost body fluids (from
diaphoresis, hemorrhage or third space
transduction) with only water.
▪ Salt losing renal failure, adrenal
deficiency & excess water intake
Pathophysiology of Hyponatremia

◼ Sign & Symptoms are caused by swelling of

neurons as result of decreased osmolality of
the ECF.( cerebral edema).
◼ ECF becomes too dilute----ICF is more
concentrated.
◼ Water moves into cells by osmosis.
Hyponatremia:Clinical Features

◼ SIGN & SYMPTOMS

Neurological dysfunction induced by
hyponatremia
◼ Serum Na+ < 125mEq/L ; Anorexia
,impaired taste & muscle cramps
◼ Serum Na+ =115-120mEq/L; headache,
personality changes,weakness, lethargy,
nausea,vomiting & abdominal cramps
◼ Serum Na+ <115mEq/L; seizures, coma,
diminished reflexes
Hyponatremia:Clinical Features
• LABORATORY FINDINGS:
- serum osmolarity <280m Osm/kg
- serum Na+ level < 135mEq/l
- urine specific gravity < 1.004
- Urine Na+ is low < 10 mEq/L
Osmolar Imbalances:
Hyperosmolarity Imbalance
◼ Hypernatremia; (Na+ > 145mEq/L)
◼ INSUFFICIENT WATER INTAKE;
- Unable to perceive or respond to thirst (comatose)
- NPO without sufficient IV maintenance
◼ EXCESSIVE WATER LOSS;
- diaphoresis,burns, hyperventilation, watery
diarrhea,diabetes inspidus.head trauma
neurosergery, brain neoplasm,osmotic diuresis
◼ SODIUM GAIN;
- sea water drowning, excessive use of sodium salt
,hypertonic saline or sodium bicarbonate
Hypernatremia

◼An electrolyte disturbance that is defined by an

elevated sodium level in the ECF or Plasma
Causes:
◼ Dehydration.
◼ Ingestion of large amounts of salt solution
◼ Increased aldosterone secretion
◼ Water deprivation.
◼ Excessive sodium in diet.
◼ Hyper tonicity of ECF, which pull water out of
body cells into ECF, causing cellular dehydration
Hypernatremia:Clinical
Features

◼ SIGN & SYMPTOMS;

◼ Neurologic
◼ Lethargy, weakness, irritability, seizures,
coma
◼ Thirst, elevated body temperature, flushed
skin, dry & sticky mucous membrane, red
tongue
◼ LABORATORY FINDINGS;
◼ SERUM Na+> 145mEq/L
◼ Serum osmolarity > 295m Osm/kg
Pathophysiology of Hypernatremia

Usually, hypernatremia results from dehydration For

example, people may lose body fluids and become
dehydrated from drinking too little, vomiting,
diarrhea, diuretic use, or excessive sweating.
◼ People with diabetes mellitus and high blood sugar
may have excessive urine volumes, causing
dehydration.
◼ Diabetes insipidus (which causes excessive urine
volume without high blood sugar
◼ kidney disorders can also cause dehydration.
◼ Hypernatremia is most common among older people.
◼ Hypernatremia typically causes thirst
Hypoakalemia

Hypokalemia: <3.5 K
Refers to the condition in which the concentration
of potassium in the ECF is decreased.
 CAUSES OF HYPOKALEMIA
◼ Decreased Dietary Intake of K+
◼ Seriously ill or patient NPO several days without
K+ supplement added to IV infusion
◼ Starvation, alcoholism
◼ GIT Loss
◼ Excessive Vomiting, diarrhea, NG suction, chronic
laxative abuse,fistulas
◼ Renal Loss:
◼ Diuretic drugs (Lasix), renal disesses,diabetic
acidosis, healing stage of severe burns,
hyper-aldosteronism, cushing’s syndrome,
swallowing chewing tobacco (licorice ingestion)
◼ Heavily perspiring, Metabolic alkalosis, treatment
of DKA with insulin and glucose
 HYPOKALEMIA: CLINICAL
MANIFESTATION

◼ CNS & NMS

Early symptoms are vague: fatigue, “not feeling
well”,Paresthesias, diminished deep tendon
reflexes,generalized muscle weakness
◼ Respiratory:
Week respiratory muscles, shallow respirations
◼ GIT
Decreased bowel motility: anorexia, nausea,
vomiting,
◼ CVS
Postural hypotension, dysrhythmias, ECG changes
( flat T wave and depressed ST segments)
◼ Renal:
Polyuria, nocturia
Pathophysiology of Hypokalemia

◼ As ECF potassium concentration falls, more

K+ move from the ICF to the ECF.
◼ With the loss of these cation from the
cytoplasm cell become hyperpolarize a nerve
and muscle cells are less excitable this is
reflected in muscle weakness, loss of muscle
tone, depressed reflexes and irregular
electrical activity of the heart.
Hyperkalemia

◼ Hyperkalemia is an elevated potassium level in

ECF. >5.6 k
CAUSES OF HYPERKALEMIA

◼ Inadequate Excretion:
Renal failure, adrenal insufficiency, addison’s
disease, K+ sparing diuretics
◼ Shift of K+ out of Cells into ECF:
Metabolic acidosis(in renal failure), tissue
damage(extensive burn, crushing injury,
internal hemorrhage)
◼ Excessive Intake:
Rapid IV infusion of K+ containing solution,
transfusion of aged blood
◼ Blood cell lysis; Poor venipuncture technique
HYPERKALEMIA:CLINICAL
MANIFESTATION
◼ Neuromuscular:
Vague muscle weakness progressing to flaccid
paralysis in legs & later in trunk and arm,
paresthesias of face, tongue, feet & hands
◼ GIT:
nausea, intestinal colic, diarrhea
◼ Renal:
Oliguria progressing to anuria
◼ CVS:
Dysrhythmias, bradycardia,complete heart block &
ventricular fibrillation, ECG changes(high, peaked
T waves;(K+>6mEq/L) prolonged PR interval, widen
QRS
◼ Lab findings: Serum K+ level>5.5mEq/L
Pathophysiology of Hyperkalemia

◼ Increased extracellular potassium levels result in

depolarization of the membrane potentials of cells.
◼ This depolarization opens some voltage-gated
sodium channels, but not enough to generate an
action potential.
◼ After a short while, the open sodium channels
inactivate and become refractory, increasing the
threshold to generate an action potential.
◼ This leads to the impairment of neuromuscular,
cardiac, and gastrointestinal organ systems.
◼ Of most concern is the impairment of cardiac
conduction which can result in ventricular
fibrillation or asystole.
ECG changes in K+ Imbalances
 Movement and Regulation
of Calcium

◼ Stored in bone, plasma and body cells

(Cation)
▪ 90% in bones
▪ 1% in ECF
▪ In plasma, binds with albumin
▪ Necessary for bone and teeth formation, blood
clotting, hormone secretion, cell membrane
integrity, cardiac conduction, transmission of
nerve impulses, and muscle contraction
▪ Normal level – 4.5-5.5
▪ Regulated by bone resorption
Regulation of Phosphate
◼ Buffer anion found mainly in ICF
▪ Assists in acid-base balance
▪ Inversely proportional to calcium
▪ Helps maintain healthy bones and teeth, neuromuscular
activity, and CHO metabolism
▪ Absorbed through GI tract
▪ Normal level 2.5-4.5
▪ Regulated by dietary intake, renal excretion, intestinal
absorption and PTH
 Regulation of Magnesium and
Chloride.

◼ Cation
▪ Normal 1.5-2.5
▪ Regulated by dietary, renal and PTH
◼ Major anion in ECF
▪ Normal level – 95-108
▪ Follows sodium
▪ Regulated by dietary intake and the kidneys
Hypocalcemia
Serum Calcium <4. 5 mEq/l

◼ PTH deficit , Hypoparathyroidism

◼ Abnormal metabolism of Vitamin D
In adequate intake , lack of exposure to
sunlight or malabsorptive disease
◼ Alcoholic liver diseases
◼ Chronic renal failure
◼ Hypomagnesemia
◼ Drugs
CLINICAL MANIFESTATION

◼ CVS: ECG changes, dysrhythmias

◼ Neuromuscular: Paresthesias, hyperactive
reflexes, tetany
◼ NS: Altered mood, confusion
◼ GIT: Diarrhea & loose stool
◼ Brittle nails
Hypercalcemia
Serum Calcium > 10. 5 mEq/l
◼ HyperParathyroidism
◼ Chronic renal failure
◼ Vitamine D malabsorption
◼ Malignancies
◼ S&S
◼ Hhypertension ECG changes, heart block
◼ Generalized muscular weakness,
decrease tendon reflexes
◼ Altered state of consciousness
◼ Formation of bone cyst( bone resorption)
Hypo-phosphatemia: < 2.5 mEq/L

◼ Decrease intake/ intestinal absorption

◼ Shift from ECF into cell / bone
◼ Increased urinary losses
◼ S&S
◼ Hematological: RBCs, WBCs & platelets
dysfunction
◼ Muscle weakness
◼ Respiratory acidosis
◼ Long term skeletal effects
Hyper-phosphatemia: > 5.5 mEq/L

◼ Decreased Renal phosphate excretion

◼ Redistribution from ICF to ECF
◼ Increased intake / intestinal absorption