Week 2 Monika Electrolytes &fluids Flashcards

1
Q

The reference range for ; Calcium
• Chloride
• Magnesium
-Phosphorus
• Potassium
• Sodium

A

Calcium 8.8 - 10.4 mg/dL
• Chloride 96 - 106 mEq/L
• Magnesium 1.8 - 2.6 mg/dL
• Phosphorus 2.7 - 4.5 mg/dL
• Potassium 3.5 - 5 mEq/L
• Sodium 135 - 145 mEq/L

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2
Q

Electrolytes

A

• Substances whose molecules dissociate into ions
when placed in water
• Cations: positively charged
• Anions: negatively charged
• Concentration of electrolytes is often expressed in
milliequivalents (mEq)/L
• Electrolyte concentrations differ depending on
fluid compartments
• Normal serum ranges can vary depending on
facility*
• Follow facility ranges

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3
Q

Electrolyte imbalance is

A

an abnormality in the concentration of
electrolytes in the body.

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4
Q

Electrolytes
help to
regulate:

A

cardiac and neurological function
fluid balance
oxygen delivery
acid–base balance

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5
Q

Diffusion

A

Movement of mainly molecules
across a permeable membrane
from high to low concentration
• Simple diffusion is passive

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6
Q

Facilitated
diffusion

A

Uses carrier to move molecules
• Glucose cannot enter most cell
membranes without help of
insulin

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7
Q

Active
transport

A

Process in which molecules
move against
concentration gradient
• External energy is required
for this process
• Example: sodium-potassium
pump
• ATP is used to move
sodium out of the cell and
potassium into the cell.

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8
Q

Sodium (Na)

A

• Plays a major role in
• ECF volume and concentration (osmolality)
• Generation and transmission of nerve impulses
• Muscle contractility
• Acid-base balance

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9
Q

Sodium (Na)
Normal Serum Sodium

A

: 135-145 mEq/L
Serum sodium level reflects the ratio of sodium to water
Major cation of ECF
Obtained from food/fluids in GI tract
Excreted through urine, sweat, feces
Kidneys primary regulator
Imbalances typically associated with equivalent changes in
osmolality

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10
Q

Hypernatremia
Serum Sodium:

A

> 145 mEq/L
• Excess serum sodium
• Elevated serum sodium occurring with water loss or
sodium gain
• Causes hyperosmolality leading to cellular
dehydration
• Primary protection is thirst from hypothalamus

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11
Q

hypernatremia is

A

hypernatremia is defined and named
after Na, it’s not really a sodium disorder, it is a
water disorder. Hypernatremia develops with a
loss of water not compensated for by adequate
ingestion of water or adequate generation of
electrolyte free water by the kidney. Also, gain of
Na can cause hypernatremia if the increased Na
load is not adequately matched with water
ingestion and generation of electrolyte free
water by the kidney. Hypernatremia is thus the
conjunction of too little water and/or too much
salt.

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12
Q

Hypernatremia Causes

A

Excess sodium
intake
• High sodium diet
• Hypertonic IVF
• Fluid deprivation
• Heat Stroke
• DI

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13
Q

Hypernatremia
• Occurs in patients with:

A

• normal fluid volume
• FVD
• FVE
• Most affected are the very old, very
young, and cognitively impaired

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14
Q

Hyponatremia
Serum Sodium:

A

<135 mEq/L
• Insufficient serum sodium
• Loss of more salt than water
• Inadequate Na intake
• Fasting, starvation, confusion
• Excess water intake
• fluid overload in surgical/sepsis patient

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15
Q

Hyponatremia Common Causes:

A

• Disease processes/symptoms
• SIADH, N/V/D, adrenal insufficiency
• Acute: Fluid overload in surgical/sepsis patient
• Chronic: outpatient, longer duration
• Exercise associated: extreme temperature,
excess water intake, prolonged exercise
• Medications
• anticonvulsants, SSRIs, or desmopressin
acetate

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16
Q

Potassium
Normal Serum Potassium:

A

3.5-5 mEq/L
• Major ICF cation
• Primary source is food
• Kidneys primary regulator (also GI tract and
sweat)
• Necessary for
• Transmission and conduction of nerve and smooth
muscle impulses
• Cellular growth
• Maintenance of cardiac rhythms
• Acid-base balance

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17
Q

Hyperkalemia
Serum Potassium:

A

> 5 mEq/L
• Excessive serum potassium

18
Q

Hyperkalemia Causes

A

• Excess intake
• Salt Substitutes
• Rapid parenteral administration
• Internal shift: K+ shifting out of cells
• Acidosis (DKA*)
• Rhabdomyolysis, severe burns, or crush injuries
• Retention
• Renal Injury or Disease
• ARBs (losartan), ACE inhibitors (Lisinopril), BB
(propranolol)

19
Q

Hyperkalemia Clinical Manifestations

A

• Increased cell excitability
• Changes in cardiac conduction (loss of P wave,
prolonged PR interval, widening of QRS)
• Tall, peaked T waves
• Heart block, ventricular fibrillation, cardiac arrest
• Muscle weakness
• Abdominal and/or leg cramps
• Diarrhea
• See Table 10-7

20
Q

Hypokalemia
Serum Potassium:

A

<3.5 mEq/L
• Low serum potassium caused by
• Increased loss of K+ via the kidneys
• Loop or thiazide diuretics
• GI tract losses
• Increased shift of K+ from ECF to ICF
• Magnesium deficiency
• Metabolic alkalosis
• Dietary K+ deficiency (anorexia, fasting)

21
Q

Hypokalemia Clinical Manifestations

A

• Hyperpolarization of cells impairs muscle
contraction
• Cardiac (ST segment depression, prolonged QRS,
Heart blocks, ventricular dysrhythmias)
• Skeletal muscle weakness (legs), cramps
• Weakness of respiratory muscles
• Decreased GI motility (constipation)
• Impaired regulation of arteriolar blood flow
• Hyperglycemia
• See Table 10-7

22
Q

Nursing Implementation

A

• Monitor:
• ECG for changes
• UOP before administering K+
• KCl supplements orally or IV
• Always dilute IV KCL
• NEVER give KCL via IV push or as a bolus
• Should not exceed 10 mEq/hr
• To prevent hyperkalemia and cardiac arrest

23
Q

Calcium
Normal Serum Calcium:

A

8.8 mg/dL-10.4 mg/dL
Functions
Formation of teeth and bone
Blood clotting
Transmission of nerve impulses
Myocardial contractions
Muscle contractions

24
Q

Calcium

A

• Obtained from ingested foods
• Vitamin D needed to absorb
• 99% is in bones
• Present in three forms: Ionized calcium is
biologically active
• Changes in pH
• Serum albumin affects total Ca levels

25
Q

Calcium
Balance controlled by

A

• Parathyroid hormone (PTH)
• production and release stimulated by low
serum calcium levels
• PTH increases bone resorption, increases GI
absorption of calcium, and increases renal
reabsorption of calcium
• Calcitonin
• produced by the thyroid gland
• stimulated by high serum calcium levels. It
opposes the action of PTH

26
Q

Hypocalcemia
Serum Calcium

A

<8.8 mg/dL
• Less Ca entering blood:
• Inadequate vitamin D, malnutrition (poor Ca
intake)
• Decreased production of PTH (hypothyroidism,
surgery)
• Chronic Renal Failure
• Excess Excretion
• Renal insufficiency
• Burns, Rhabdo
• Pancreatitis, Cirrhosis
• Diarrhea, laxative abuse
• Multiple blood transfusions

27
Q

Hypocalcemia Clinical Manifestations

A

• Tetany
• Positive Trousseau’s or Chvostek’s sign
• Laryngeal stridor
• Dysphagia
• Perioral Tingling
• Cardiac dysrhythmias
• See Table 10-8

28
Q

Hypercalcemia
Serum Calcium

A

> 10.5 mg/dL
High
serum
calcium
level
Hyperparathyroidism (2/3 of
cases)
Malignancy (1/3 of cases)
Rare
causes
Excessive intake
Prolonged immobilization
Excess Vitamin D

29
Q

Hypercalcemia Clinical Manifestations
• Neuro:

A

Fatigue, lethargy, muscle weakness, stupor, coma,
depressed reflexes, decreased memory, confusion,
personality changes, psychosis
• ECG changes
• Anorexia, nausea, vomiting
• Bone pain, fractures
• Flank pain from nephrolithiasis (renal calculi)
• Polyuria, dehydration
• See Table 10-

30
Q

Phosphate
Normal Serum Phosphate:

A

2.7 - 4.5 mg/dL
• Primary anion in ICF
• Most phosphorus located in bones & teeth
• Essential to function of muscle, red blood cells,
and nervous system
• Involved in
• acid-base buffering system
• ATP production
• cellular uptake of glucose
• metabolism of carbohydrates, proteins, and fats

31
Q

Phosphate

A

• Serum levels controlled by parathyroid hormone
• Maintenance requires adequate renal
functioning
• Reciprocal relationship with calcium
• high phosphate level tends to cause a low
calcium concentration in the serum
33

32
Q

Hyperphosphatemia
Serum Phosphate

A

> 4.5 mg/dL
High
serum
PO4 3-
caused
by
AKI or CKD
Chemotherapy
Hypoparathyroidism Increase phosphate
reabsorption
Tumor lysis, rhabdo
Excessive intake of
phosphate or vitamin D
Laxatives
Dairy products

33
Q

Hyperphosphatemia Clinical
Manifestations

A

Often asymptomatic unless Ca binds to PO43- (hypocalcemia)
Neuromuscular irritability
and tetany
(hypocalcemia)
Long term increase
results in calcified
deposits in soft tissue
such as:
Joints
Arteries
Skin
Kidneys
Corneas

34
Q

Hypophosphatemia
Serum Phosphate

A

< 2.7 mg/dL
Low serum PO43- caused by:
• Malnourishment/malabsorption
• Diarrhea
• ETOH abuse
• Use of phosphate-binding antacids
• Tums
• During parenteral nutrition with inadequate
replacement

35
Q

Hypophosphatemia Clinical
Manifestations

A

• Mild to moderate, often asymptomatic.
• CNS depression, confusion
• Muscle weakness and pain
• Cardiomyopathy
• Respiratory failure
• See Table 10-10

36
Q

Magnesium
Normal Serum Magnesium:

A

1.8 mg/dL-2.6 mg/dL
• Required for DNA & protein synthesis
• Necessary for sodium-potassium pump
• Important for normal cardiac function
• 50% to 60% contained in bone
• Absorbed in GI tract
• Excreted by kidneys & stool

37
Q

Hypermagnesemia Causes
Serum Magnesium

A

> 2.6 mg/dL
• High serum Mg caused by
• Increased intake or ingestion of products
containing magnesium when renal insufficiency or
failure is present
• Maalox, MOM
• Treatment of migraines or menstrual cramps
• Excess intravenous magnesium administration
• Tx of eclampsia
• Decreased output
• ESRD, AKI, adrenal insufficiency

38
Q

Hypermagnesemia Clinical Manifestations

A

• ECG changes
• Hypotension
• Lethargy / Somnolence
• N/V
• Impaired reflexes
• Respiratory and cardiac arrest
• See Table 10-9

39
Q

Hypomagnesemia
Serum Magnesium

A

< 1.8 mg/dL
• Low serum Mg caused by
• Prolonged fasting or starvation
• Chronic alcoholism
• Fluid loss from gastrointestinal tract
• Prolonged parenteral nutrition without
supplementation
• Diuretics
• Large blood transfusion

40
Q

Hypomagnesemia Clinical Manifestations

A

• Hyperactive deep tendon reflexes
• Muscle cramps
• Tremors
• Seizures
• Cardiac dysrhythmias
• Torsade de pointes, Vfib
• Corresponding hypocalcemia and hypokalemia
• See Table 10-9