Alterations in Fluids and Electrolytes and Acid- base balance

Fluid Volume
 55% of female body composed of water
 65% of male body composed of water
 The extracellular and intracellular fluids = separated by the capillary wall and
cell membrane.

Fluid Intake and Output

INTAKE: 2, 500 mL/day OUTPUT: 2, 500 mL/day
 Metabolism (400mL) Feces (100mL)
 Food (500 mL) Breathing (400 mL)
 Drinking (1, 500 mL) Skin (500 mL)
Urine (1, 500 mL)

Fluid and Electrolyte regulation

 OSMOSIS- movement of water(H2O) from an area of higher concentration to an

area of lower concentration.

 DIFFUSION- movement of molecules from higher concentration to an area of

lower concentration.

 FILTRATION- water dissolved substances cross a membrane as a result of

hydrostatic pressure ( is the pressure exerted in to the vessel walls by a fluid)- the
higher the fluid the higher the pressure

 Renal System
 Endocrine System
 Natriuretic Peptide Hormones (Nph)
 Renin- Angiotensin Mechanism
 Respiratory System
 Insensible Losses (Skin, Diarrhea, Emesis)

Indicators of fluid status

 BLOOD UREA NITROGEN (BUN)- 8-21 mg/dL
 CREATININE - 0.5- 1.2 mg/dL
 SPECIFIC GRAVITY- 1.005-1.030
 URINE OSMOLALITY- 275- 295 Mosm/kg
 HEMOGLOBIN
 M= 14-17.3
 F= 11.7-15.5 G/Dl
 HEMATOCRIT
 M= 42-52
 F= 36=48
Fluid volume Imbalances

Hypervolemia
refers to increasing blood volume and also called fluid overload. A condition in which
the liquid portion of the blood (plasma) is too high. Hypervolemia is an excess of
isotonic fluid (water and sodium) in the extracellular compartment.

CAUSES:
 Increased water and sodium retention
 Use of corticosteroids
 Increased fluid intake
 Diminished homeostatic mechanisms:
 Heart failure
 Cirrhosis
 Hepatitis
 Kidney failure
 Nephrotic syndrome
 High-salt diet

Laboratory Findings:
Decreased in:
 Serum osmolality
 Hematocrit
 Blood urea nitrogen (b u n) level
 Serum sodium and potassium level
 Urinary specific gravity
 Albumin

Clinical manifestations

CARDIOVASCULAR RESPIRATORY SYSTEM:

SYSTEM:  Increased rate and depth of
respiration. (shallow respiration)
Tachycardia  Dyspnea
Hypertension’  Crackles on auscultation
Distended neck and hand
veins
Increased CVP
Dysrhythmias
NEUROMUSCULAR SYSTEM: RENAL SYSTEM:
 Altered level of consciousness  Increased urine output if kidneys can
 Headache compensate; decreased urine output if
 Visual disturbances kidney damage is the cause
 Skeletal muscle weakness
 Paresthesias
 GASTROINTESTINAL SYSTEM:
 Increased motility
 Diarrhea
 Liver enlargement
 Ascites
 Increased body weight

MEDICAL MANAGEMENT UNTREATED HYPERVOLEMIA CAN

 Fluid restriction CAUSE SEVERAL
 Discontinue iv fluids COMPLICATIONS
 Diuretics ( thiazide diuretics &  Pericarditis, or swelling of the
loop diuretics) heart tissues
 Digoxin (heart failure)
 Heart failure
 Morphine and nitroglycerin
(pulmonary edema)  Delayed wound healing
 Potassium supplements in case of  Tissue breakdown
hypokalemia
 Decreased bowel function
Nursing Management:SYSTEM:
INTEGUMENTARY
Pitting
Collecting
edema health history
 Physical assessment
 Pale, cool skin
 Reviewing laboratory data
 Monitoring body weight
 Calculating i & o
 Monitor electrolyte level
 Watch for distended veins in the hands or neck
 Abg results: changes in acid -
 base balance
 Grading edema
 Abdominal girth- ascites.
 Provide oral hygiene and skin
 care
 Use infusion pump for administering medication to prevent fluid overload
 Assess for bounding peripheral pulses and s3-signs of fluid overload.
 Elevate edematous extremities,
 and handle with care
 Used antiembolic stockings or bandages, as ordered

Fluid Volume Deficit

- Fluid volume deficit (FVD) or hypovolemia is a state or condition where the
fluid output exceeds the fluid intake. It occurs when the body loses both water
and electrolytes from the ECF in similar proportions. Common sources of fluid loss
are the gastrointestinal tract, polyuria, and increased perspiration.

- Risk factors for FVD are as follows: vomiting, diarrhea, GI suctioning, sweating,
decreased intake, nausea, inability to gain access to fluids, adrenal insufficiency,
osmotic diuresis, hemorrhage, coma, third-space fluid shifts, burns, ascites,
and liver dysfunction.

- Fluid volume deficit may be an acute or chronic condition managed in the hospital,
outpatient center, or home setting.

Causes:
 Abnormal losses through the skin,  Diuresis
GI tract, or kidneys.  Abnormal drainage
 Decrease in intake of fluid (e.g.,  Inadequate fluid intake
inability to intake fluid due to oral  Increased metabolic rate (e.g.,
trauma) fever, infection)
 Bleeding
 Movement of fluid into third
space.
 Diarrhea

Signs and Symptoms:

 Alterations in mental state  Dry mucous membranes, sunken
 Patient complaints of weakness and eyeballs
thirst that may or may not be  Weak pulse, tachycardia
accompanied by tachycardia or  Decreased skin turgor
weak pulse  Decreased blood pressure,
 Weight loss (depending on the hemoconcentration
severity of fluid volume deficit)  Postural hypotension
 Concentrated urine, decreased urine
output

Nursing Management:

ASSESSMENT
1. Monitor fluid intake and output. Measurement of the client’s intake and output is
first measured by the nurse and evaluated for at least at 8-hour intervals is the first
step to assessing the presence of hypovolemia.

2. Closely monitor the client’s vital signs. Weak, rapid pulse and postural hypotension
should alert the nurse.

3. Monitor skin turgor on a regular basis. Turgor refers to the elastic property of the
skin. Pinching the skin of a normal healthy person will immediately return to its
normal position when released.

4. Monitor urinary concentration. The concentration of urine is measure by the urine

specific gravity.

5. Monitoring mental function. Clients with severe depletion of fluid volume have a
poormental function as a result of decreased cerebral perfusion. Decreased peripheral
perfusion may result in cold extremities. Low central venous pressure is indicative of
hypovolemia in clients with normal cardiopulmonary function.

INTERVENTIONS
6. Prevent further fluid depletion. The nurse must implement measures to minimize
or prevent further fluid losses.
7. Fluid replacement. As mentioned above, oral fluids should
be administered to the client to help correct fluid loss.

Hyponatremia
Hypo: “under/beneath” Natr: prefix for Sodium Emia: blood
Meaning: Low sodium in blood Normal Range: 135-145 mmol/L
Hyponatremia: <135 mmol/L
Severe Hyponatremia: <120 mmol/L

Pathophysiology:
Osmolality/Osmolarity:
 Osmolality: number of osmoles of
solute in kg of solvent
 Osmolarity: number of osmoles in solute in litre of solution
 About concentration of solutes
(dissolved substances) in the blood.
 It controls the distribution of fluid in the body.
Role of Na+: electrolyte that helps regulate the water inside the cell
outside the cell. (H2O and Na+ loves each other)
- Cell Swells

Causes:
1. More water coming in
2. Less water going out
3. Less sodium coming in
4. More sodium going out
Mnemonic for Causes:
Remember “No Na+”
Na+ excretion is increased with renal problems like NG suction, vomiting,
diuretic therapy, sweating, diabetes, insipidus, decrease aldosterone secretion
and waste in sodium
Overload of fluid, (CHF, hypotonic fluid, solutions and liver failure)
Na+ intake is low this could either be through a low salt diet or NPO status
Antidiuretic hormone is oversecreted (SIADH) and adrenal insufficiency

Types:
Dilutional/Euvolemic Hyponatremia:
 H2O in the body increases but sodium stays the same.
Hypovolemic Hyponatremia:
 Sodium becomes diluted.
 patient becomes
 No edema
 dehydrated
 Causes: SIADH (Syndrome of Inappropriate Antidiuretic Hormones). ADH:
 They have a loss of blood volume (decrease in
retains water in the body
sodium and a decrease in water)
 Causes: Vomiting, diarrhea, burns, excessive
sweating, diuretic therapy
One way that sodium can be lost through kidneys is through the use of medications
such as diuretics which includes aldosterone and cortisol. Loop diuretics, thiazide,
Potassium sparing diuretics all act to prevent sodium reabsorption. And as a result, all
these medications can lead to hyponatremia.

Hypervolemic Hyponatremia:

 H20 and Na+ both increase in the body -> fluid volume overload.
 Swelling
 Causes: CHF, Kidney failure, excessive infusion of saline, liver failure.

Signs and Symptoms:

Seizure, Stupor
Abdominal Cramping or attitude changes
Lethargic
Tendon reflexes diminished and trouble concentrating
Loss of urine and appetite
Orthostatic hypertension, overactive bowel sounds
Shallow respirations
Spasms of muscles

Nursing Management:
- Watch cardiac status, respiratory status,neuro, renal and GI status
- Hypovolemic Hyponatremia: administer IV sodium solution to restore balance of
fluid and sodium
(3% saline: hypertonic solution)
Is really hard on veins
close monitoring -> fluid volume overload
(give slowly)

Hypervolemic Hyponatremia:
 restrict more fluid intake
 In some cases, doctors may order diuretics to excrete extra fluids in the body but
conserve sodium
 renal failure= dialysis

SIADH: restrict fluids and usually treated with an antidiuretic hormone antagonist
  DECLOMYCIN (tetracyclines): do not give with food (dairy and antacids)
 LITHIUM: check/monitor lithium drug levels

Hypernatremia
Hyper: “excessive” Natr: prefix for
Sodium Emia: “blood”

Meaning: Excessive sodium in blood Normal Na+ level:

135-145 mmol/L (>145=hypernatremia)

Pathophysiology:

The basic mechanisms of hypernatremia are water deficit and excess solute.
Total body water loss relative to solute loss is the most common reason for
developing hypernatremia. Hypernatremia is usually associated with hypovolemia,
which can occur in conditions that cause combined water and solute loss, where
water loss is greater than sodium loss, or free water loss. Sodium is important to
maintain extracellular fluid (ECF) volume. Changes in the ECF volume provide
feedback to maintain total sodium content by increasing or decreasing sodium
excretion in the urine. When serum sodium increases, the plasma osmolality increases
which triggers the thirst response and ADH secretion, leading to renal water
conservation and concentrated urine.

Role of Na+: electrolyte that helps regulate the water inside the cell outside the cell. (H2O
and Na+ loves each other) - Cell shrinks

Signs And Symptoms:

Fever, flushed skin

Restlessness, really agitated
Increased fluid retention
Edema, extremely confused
Causes:
Decreased urinary output, dry mouth and skin
Hypercortisolism (Cushing syndrome) (overproduction of aldosterone -> retaining lots of salt Na+),
Hyperventilation
Increased Na+ intake (eating a lot of salt or IV route)
GI feeding without adequate H2O supplement
Hypertonic Solutions (ex: 3% saline)
Sodium Excretion decreased (ex. Corticosteroids)
Aldosterone problems (increased reabsorption of sodium)
Loss of fluids (dehydrated) with fever or sweating
Thirst impairment
Nursing Interventions

-Nursing
RestrictManagement:
Na+ Intake: (Bacon, butter, canned foods, cheese, hotdogs, lunch meats,
processed foods, table salt)
- Patient Safety: confused & agitated
- MD may order an isotonic or hypotonic IV Solution (0.45% saline): give this slowly
(hydrating cell) @ risk for cerebral edema
- Educate about diet and about signs and
symptoms of increased sodium level
 Hypokalemia and Hyperkalemia
Hypokalemia and hyperkalemia are common electrolyte disorders caused by
changes in potassium intake, altered excretion, or transcellular shifts.

Normal potassium level: 3.5-5 mEq/L

Hyperkalemia

Potassium level: >5.5mEq/l

 Typically results in no symptoms
 Occasionally when severe it results in:
 Muscle pain
 Muscle weakness or numbness
 Irritability and anxiety
 Palpitations
 Dysrhythmias (irregular heart rhythm)
 Decrease Blood pressure
 Abdominal cramping and diarrhea
 Decrease urine output
 Hyperventilation - compensatory response to Metabolic acidosis

CAUSES:
 High amount of K+ supplement
 Kidney failure
 Hypoaldosteronism
 Rhabdomyolysis
SEVERITY IS DIVIDED INTO:

MEDICATIONS THAT CAUSE  Mild (5.5-5.9 mEq/L)

 Moderate (6.0-6.4 mEq/L
HIGH K+:  Severe (>6.5 mEq/L)
 Spironolactone
 NSAIDs
 ACE inhibitors

Pathophysiology:
 Normal homeostatic mechanisms serve to precisely maintain the serum potassium level
within a narrow range. The primary mechanisms for maintaining this balance are the
buffering of extracellular potassium against a large intracellular potassium pool (via the
sodium-potassium pump) and urinary excretion of potassium.

Nursing Management:

 Kayexalate is sometimes ordered and given PO or via enema. This drug promotes GI
sodium absorption which causes potassium excretion.
 Doctor may order potassium wasting drugs like Lasix or Hydrochlorothiazide
 Administer a hypertonic solution of glucose and regular insulin to pull the potassium
into the cell

Hypokalemia
 Monitor cardiac, respiratory, neuromuscular, renal, and GI status
 Stop IV potassium if running and hold any PO potassium supplements
Potassium level:
 Initiate <3.5mEq/L
potassium restricted diet and remember foods that are high in
Mildly potassium
low levels do not typically cause symptoms Results in:
 Prepare
Musclepatient for ready for dialysis. Most patient are renal patients who
weakness
get dialysis
 Myalgia regularly and will have high potassium.
 Tremor
 Muscle cramps
 Decrease intestinal motility
 Constipation
 Abnormal heart rhythm (often too slow)
 Cardiac arrest
 Flaccid paralysis
 Hyporeflexia

CAUSES: MEDICATIONS THAT CAUSE

 Vomiting LOW K+:
 Diarrhea
 Furosemide
 Steroids
 Dialysis
 Diabetes insipidus
 Hyperaldosteronism
 Hypo magnesium
 Not enough intake
Hypokalemia- when blood’s potassium levels are too low. Potassium is an important
 electrolyte for nerve and muscle cell functioning, especially for muscle cells in the
heart.
- generally defined as a serum potassium level of less than 3.5 mEq/L (3.5 mmol/L).
Moderate hypokalemia is a serum level of 2.5-3.0 mEq/L, and
Severe hypokalemia is a level of less than 2.5 mEq/L.

 May result from:

inadequate potassium intake, increased potassium excretion, or a shift of
potassium from the extracellular to the intracellular space.

Pathophysiology:
Potassium, the most abundant intracellular cation, is essential for the life of
an organism. Potassium homeostasis is integral to normal cellular function,
particularly of nerve and muscle cells, and is tightly regulated by specific ion-
exchange pumps, primarily by cellular, membrane-bound, sodium-potassium
adenosine triphosphatase (ATPase) pumps.

 Renal factors in potassium homeostasis:

Kidneys adapt to acute and chronic alterations in potassium intake. When potassium
intake is chronically high, potassium excretion likewise is increased. In the absence of
potassium intake, however, obligatory renal losses are 10-15 mEq/day. Thus, chronic losses
occur in the absence of any ingested potassium.

 Potassium distribution
Potassium is predominantly an intracellular cation; therefore, serum potassium levels can be a
very poor indicator of total body stores. Because potassium moves easily across cell membranes,
serum potassium levels reflect movement of potassium between intracellular and extracellular
fluid compartments, as well as total body potassium homeostasis.
-Several factors regulate the distribution of potassium between the intracellular and
extracellular space, as follows:
 Glycoregulatory hormones: (1) Insulin (2) glucagon
 Adrenergic stimuli: (1) Beta-adrenergic stimuli (2) alpha-adrenergic
 pH: (1) Alkalosis (2) acidosis Pathogenic mechanisms

Hypokalemia can occur via the following pathogenetic mechanisms:

 Deficient intake
 Increased excretion
 A shift from the extracellular to the intracellular space

Nursing Management:
  IV Potassium for levels less 2.5 (NEVER EVER GIVE POTASSIUM via IV
push or by IM or subq routes)
 Give according to the bag instruction don’t increase the rate
 Don’t give LASIX, demadex , or thiazides or Digoxin

Hypercalcemia
 Watch heart rhythm, respiratory status, neuro, GI, urinary output and renal status
 Watch other electrolytes like Magnesium, watch glucose, sodium, and calcium
- is a condition in whichallthe
gocalcium level inand
hand-in-hand the play
blooda role
is above normal.
in cell transport
- is usually a result of overactive parathyroid glands.
 Administer oral Supplements for potassium with doctor’s order: usually for
levels 2.5- 3.5…give with food can cause GI upset
CAUSES
 Hyperparathyroidism
 Lung diseases and cancers
 Medication side effects
 Dietary supplements and over-the-counter medications
 Dehydration

Pathophysiology:
 Calcium concentration is regulated by plasma membrane calcium receptor, PTH
and its receptor, calcitonin and its receptor, and by the actions of vitamin D on
kidneys, bone, and intestines. PTH mobilizes calcium directly by enhancing
bone resorption, and indirectly, by stimulating one alpha-hydroxylase which
increases vitamin D3 production, in turn, leading to increased absorption of
calcium from the gut and increased bone resorption. Primary
hyperparathyroidism is due to a solitary adenoma or diffuse hyperplasia of the
gland. In this condition, there is an abnormal set point in the relation between
calcium and PTH levels and calcium-independent PTH secretion. Familial
hypocalciuric hypercalcemia is inherited autosomal dominant pattern and is due
to an inactivating mutation in the calcium- sensing receptor gene.
Granulomatous lesions cause ectopic vitamin D production.
 Transient neonatal hypercalcemia can rarely be seen in infants born to
mothers with hypoparathyroidism.

Nursing Management:
 Mild cases
Mild cases may not need immediate treatment. Treatment of hypercalcemia
depends on what is causing the disorder and how severe it is. Often the doctor may
tell you calcium levels can be lowered if you:
Drink more water
Switch to a non-thiazide diuretic or blood pressure medicine
Stop calcium-rich antacid tablets
Stop calcium supplements
Moderate to severe cases
Calcitonin
Intravenous fluids
Corticosteroids
Loop diuretic medications
Intravenous bisphosphonates
Dialysis

Hypocalcemia
is a lowered blood calcium level that occurs to some extent in all newborns before they begin sucking well.
 Early hypocalcemia happens in the first 2 to 3 days of a baby's life. It is more likely to go away.
 Late hypocalcemia starts in the first week or weeks after birth and is less likely to go away.

CAUSES
 Prematurity
 Maternal diabetes or hyperparathyroidism
 Perinatal asphyxia

Pathophysiology:
Hypocalcemia manifests as central nervous system (CNS) irritability and
poor muscular contractility. Low calcium levels decrease the threshold of excitation
of neurons, causing them to have repetitive responses to a single stimulus. Because
neuronal excitability occurs in sensory and motor nerves, hypocalcemia produces a
wide range of peripheral and CNS effects, including paresthesia, tetany (i.e.,
contraction of hands, arms, feet, larynx, bronchioles), seizures, and even psychiatric
changes in children.

Nursing Management:
Hypocalcemia may get better without treatment, especially if there are no
symptoms. Early hypocalcemia most often goes away in a few days.
Babies with late hypocalcemia may have calcium supplements in their
feedings or in an IV.

Many hypocalcemia cases are also easily treated with a dietary change.
Taking calcium, vitamin D, or magnesium supplements, or eating foods
with these can help treat it.

Hypermagnesemia
— Refers to an excess amount of magnesium in the bloodstream.

CAUSES
 Magnesium containing antacids and laxatives
 Glomerular filtration insufficiency (<30mL/min) renal failure.
 Tumor lysis syndrome

Pathophysiology:
 Renal function plays a crucial role in the metabolism of magnesium. Of note, only
approximately 10% of filtered magnesium is absorbed in the proximal tubule, whereas
most of the filtered magnesium gets passively reabsorbed in the ascending limb of the
loop of Henle. This factor is essential for the pathophysiology of kidney-related
hypermagnesemia as along the loop of Henle, not only the volume of the filtrate gets
reduced, but also the osmolarity decreases significantly (-66%), and consequently the
solutes become less concentrated. Furthermore, this explains the high resorbent
capacity of the kidney, which generally maintains magnesium equilibrium until the
creatinine clearance falls below 20 ml/min. Thus, an increase in plasma magnesium
levels is practically impossible to achieve with diet alone in conditions of perfect
renal health. However, the odds of hypermagnesemia can increase by taking mega-
doses of magnesium. The pathophysiology of hypermagnesemia related to excess
laxative use is different. In this case, the huge amount of magnesium given through
the digestive tract can lead to overwhelming the excretory mechanism, especially in
 cases with underlying
Magnesium works assubclinical renal calcium
a physiologic failure. blocker. Increased levels
determine substantial electrophysiological and hemodynamic effects. Moreover,
the potential concomitance of hyperkalemia increases the risk of cardiac
arrhythmias and cardiac arrest. The neurologic manifestations are the result of
the inhibition ofacetylcholine release from the neuromuscular endplate due to
increased extracellular magnesium levels.

Nursing Management:
 Monitor cardiac, respiratory, neuro system, renal status. Put patient on
cardiac monitor (watch for EKG changes)
 Ensure safety due to lethargic/drowsiness
 Administer diuretics that waste magnesium (if patient is not in renal
failure) such as Loop and Thiazide diuretics
 An intravenous (IV) calcium supply
 People with renal dysfunction or those who have had a severe
magnesium overdose may require dialysis
 Hypomagnesemia
 is a condition in which the amount of magnesium in the blood is lower than normal
 is a common entity occurring in up to 12 percent of hospitalized patients

CAUSES
 Alcohol use
 Chronic diarrhea
 Excessive urination (polyuria), such as in uncontrolled diabetes and during recovery from acute kidney
failure
 Kidney tubule disorders
 Malnutrition
 Medicines including amphotericin, cisplatin, cyclosporine, diuretics, proton
pump inhibitors, and aminoglycoside antibiotics

Pathophysiology:
 Magnesium is a co-factor in many biochemical reactions. Magnesium has a
direct effect on various other electrolytes, including sodium,calcium, and
potassium. As described above, low levels of magnesium can occur secondary to
renal and gastrointestinal losses.
 Magnesium homeostasis involves the kidney (primarily through the
proximal tubule, the thick ascending loop of Henle, and the distal tubule),
small bowel (primarily through the jejunum and ileum), and bone.
Hypomagnesemia occurs when something, whether a drug or a disease
condition, alters the homeostasis of magnesium.
 Magnesium deficiency also can cause hypocalcemia, as the two are inter-related.
Decreased magnesium causes impaired magnesium-dependent adenyl cyclase
generation of cyclic adenosine monophosphate (cAMP), which decreases the release
of parathyroid hormone (PTH). In turn, calcium levels are decreased as well, as PTH
regulates calcium levels.

 Magnesium also affects the electrical activity of the myocardium and vascular
tone, which is why patients with hypomagnesemia are at risk for cardiac arrhythmias.

Nursing Management:
 Monitor cardiac, GI, respiratory, neuro status. Place on a cardiac monitor
 May administer potassium supplements due to
 hypokalemia
 Administering calcium supplements (oral calcium supplements w/ Vitamin-D or
10% Calcium Gluconate)
 Administer Magnesium Sulfate IV route. Monitor Mg+ level closely because
patient can become magnesium toxic
 Place patient in seizure precautions
 Oral forms of Magnesium may cause diarrhea which can increase magnesium
loss so watch out for this
 Watch other electrolyte levels like calcium and potassium