Week 2 Monika Electrolytes &fluids Flashcards
(40 cards)
The reference range for ; Calcium
• Chloride
• Magnesium
-Phosphorus
• Potassium
• Sodium
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
Electrolytes
• 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
Electrolyte imbalance is
an abnormality in the concentration of
electrolytes in the body.
Electrolytes
help to
regulate:
cardiac and neurological function
fluid balance
oxygen delivery
acid–base balance
Diffusion
Movement of mainly molecules
across a permeable membrane
from high to low concentration
• Simple diffusion is passive
Facilitated
diffusion
Uses carrier to move molecules
• Glucose cannot enter most cell
membranes without help of
insulin
Active
transport
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.
Sodium (Na)
• Plays a major role in
• ECF volume and concentration (osmolality)
• Generation and transmission of nerve impulses
• Muscle contractility
• Acid-base balance
Sodium (Na)
Normal Serum Sodium
: 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
Hypernatremia
Serum Sodium:
> 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
hypernatremia is
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.
Hypernatremia Causes
Excess sodium
intake
• High sodium diet
• Hypertonic IVF
• Fluid deprivation
• Heat Stroke
• DI
Hypernatremia
• Occurs in patients with:
• normal fluid volume
• FVD
• FVE
• Most affected are the very old, very
young, and cognitively impaired
Hyponatremia
Serum Sodium:
<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
Hyponatremia Common Causes:
• 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
Potassium
Normal Serum Potassium:
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
Hyperkalemia
Serum Potassium:
> 5 mEq/L
• Excessive serum potassium
Hyperkalemia Causes
• 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)
Hyperkalemia Clinical Manifestations
• 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
Hypokalemia
Serum Potassium:
<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)
Hypokalemia Clinical Manifestations
• 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
Nursing Implementation
• 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
Calcium
Normal Serum Calcium:
8.8 mg/dL-10.4 mg/dL
Functions
Formation of teeth and bone
Blood clotting
Transmission of nerve impulses
Myocardial contractions
Muscle contractions
Calcium
• 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