Fluid & Electrolytes Lab Values
Fluid & Electrolytes Lab Values
Sodium (Na+): 136 - 145 mEq/L
Potassium (K+): 3.5 - 5.0 mEq/L
Magnesium (Mg++): 1.3 - 2.1 mEq/L
Hemoglobin (Hgb)
Carries oxygen to the body, tissue, organs.
Male: 14 - 18 g/dL
Female: 12 - 16 g/dL
Hematocrit (Hct)
Percentage of blood made up of RBCs.
Male: 42 - 52%
Female: 37 - 47%
Blood Urea Nitrogen (BUN)
10 - 20 mg/dL
Tells us about kidneys.
Creatinine
Accurate test to test kidney function.
Male: 0.6 - 1.2 mg/dL
Female: 0.5 - 1.1 mg/dL
Therapeutic = 1.0 mg/dL
High Cr = renal failure/injury
Kidneys
Critical for fluid & electrolyte balance.
Fluid Balance
Water volume in the body can be intracellular or extracellular.
Intracellular = water inside cells
Extracellular = outside cells
Interstitial = space between cells, not in blood
Plasma = serum
Electrolytes can affect fluid balance, and fluid balance can affect electrolytes.
Plasma volume = a small proportion of total water volume.
Adequate plasma volume maintains blood pressure and tissue perfusion
Perfusion
Delivery of blood to the capillary bed of an organ or tissue
Ischemia
Reduction in blood supply to any tissue or organ, causing a shortage of oxygen
Fluid balance = fluid intake – fluid output
Urine output = fluid volume status
Water Loss
Kidney is the most important and most sensitive water loss route because it is regulated and adjustable.
Kidney Functions
Endocrine functions
Metabolic waste excretion
Control of solutes and fluids where kidney filters extra electrolytes &/or fluids
Blood pressure control
Drug metabolism
Acid/base balance and excretion
Kidneys = sensitive to fluid volume
Dehydrated = kidneys puts out less water = concentrated urine
Hormones Regulating Fluid and Electrolyte Balance
Aldosterone
Anti-diuretic hormone (ADH)
Natriuretic peptides (ANP & BNP)
Aldosterone
Reabsorbs sodium & water in kidneys.
The RAAS system is triggered by decreased tissue perfusion to the kidneys
Leads to the retention of water and sodium & increases blood volume and blood pressure
Critical for BP & fluid volume
How to know if you have low perfusion:
Low BP = low perfusion
Low blood volume; if the blood volume is too low = bad perfusion
Ischemia = low blood oxygen
Poor perfusion = kidneys sendse a drop in bp —> release of renin —> angiotensin —> angio 1 —> A.C.E —> angio 2 = causes vasoconstriction (which increases blood pressure) —> stimulates aldosterone secretion (from the adrenal gland) —> leading to aldosterone promoting the reabsorption of sodium and water to the kidneys, further increasing blood volume & BP.
Anti-diuretic Hormone (ADH)
Aldosterone holds onto reabsorbed sodium andwater in the kidneys while ADH is only go ing to reabsorb water (DOES NOT REABSORB SODIUM)
ADH is NOT triggered by the kidneys
triggered by the change in blood osmolarity
when solute concentration increases our osmolarity increases our blood becomes more concetratede bc of a decrease in blood volume
will trigger the pituitary gland to release ADH
ADH goes to kidneys and tells the kidneys to let them reabsorb water
*once water has been reabsorbed its going to increase blood volume while also decreasing the osmolarity back to its normal range.
Natriuretic Peptides (BNP, ANP)
Hormones released from the heart in states of fluid volume overload (when the heart stretches it causes the release of hormones).
Helps decrease fluid volume
ANP released from atria, BNP released from ventricles
Lead to vasodilation = results in decreased BP
Natriuresis (sodium excretion)
Diuresis (water excretion)
BNP is tested in the hospital frequently to check for lfuid volume overload which is usually realted to heart failure.
with too much fluid/volume we want to get rid of mit and also vasodilate so there is less pressure.
we vasodilate, natriuresis (get rid of sodium) & diuresis (get rid & increase urine production) = will help decrease BP & manage the excess fluid volume.
Fluid Volume Overload
Edema, tight, weeping, no skin turgor
Hypertension
Tachycardia (bounding pulse)
Weight gain
Crackles, cough
Decrease in H&H, diluted
Hyponatremia
JVD
Clear, normal increase in urine
Fluid Volume Deficit
Increase thirst
Tachycardia (thready pulse)
Dry mouth & skin, tenting
Hypotension
Dizziness (from lack of perfusion)
Increase in H&H, concentrated
Hypernatremia
Decrease in urine, concentrated
oliguria
Electrolyte Imbalance
Intake: food/diet
Output: kidney excretion or reabsorption
Cause: Change in fluid intake/output
Actual loss of electrolytes or retention
Risk factors:
Elderly
Chronic kidney disease
Endocrine disorders
Drugs that alter fluid/electrolyte balance
ex. diuretics
Sodium (Na+)
136-145 mEq/L
Important for nerve conduction
EXTRACELLULAR (found outside the cell)
responsible for:
Muscle contraction
Cardiac muscle contraction
Nerve impulses (big effect on CNS)
Water distribution (helps maintain plasma volume and BP)
Intake: diet/food
Output: kidney excretion or reabsorption
Regulated by:
ADH
RAAS
Natriuretic peptides
Thirst mechanism
Hyponatremia
< 136 mEq/L
Etiology:
Low sodium
Deficient sodium intake
Loss of body fluids (wound drainage w/ burn victims = must drink electrolytes)
Water Gain: Hypervolemia (gain of too much fluid; the body becomes fluid volume overloaded and the blood gts diluted down)
H&H decreases
S/S:
CNS: Confusion, Seizure, Coma & death
Muscular: Weakness, Decreased reflexes
GI: Nausea & vomiting, Diarrhea
Treatment:
Sodium loss: Hypertonic IV fluids, Nutritional therapy
Water gain: Fluid restriction, Diuretics/dialysis
Hypernatremia
> 145 mEq/L
Etiology:
Sodium gain: Excessive sodium intake can be caused by Kidney failure
Water loss: Hypovolemia (dehydration)
Hgb increases (blood volume becomes more concentrated)
Pts usually on NPO or tube feedings
S/S:
CNS: Confusion, Agitation, Lethargy / coma
Muscular: Twitching progressing to weakness, Decreased reflexes
GI: Constipation
Treatment:
Sodium gain: Nutritional therapy, Diuretics/dialysis
Water loss: Ensure adequate water intake, Isotonic or hypotonic IV fluids
Dietary Sources of Sodium
Most Americans consume too much sodium
Salty Six (foods that can add high levels of sodium):
Breads & Rolls
Pizza
Sandwiches
Cold Cuts & Cured Meats
Soup
Burritos & Tacos
Potassium
3.5-5.0 mEq/L
Intracellular (most inside the cell) cation responsible for:
Muscle contraction
Cardiac muscle contraction
Critical = can cause dysrhythmias
Nerve impulses
Regulation of acid-base balance
Intake: diet
Output: kidney excretion or reabsorption
Sodium is affected by fluid volume status, not potassium or magnesium since its intracellular
Hypokalemia
< 3.5 mEq/L
Etiology:
Deficient intake (not enough potassium in diet)
Loss of body fluids (ex. vomiting or diarrhea)
Medications (diuretics, insulin)
Hypomagnesemia (potassium needs magnesium)
Can cause hypokalemia, but no the other way around
S/S:
Cardiac: dysrhythmias / tachyarrhythmias & shallow respirations
CNS: lethargy and confusion
Muscular: weakness, paralysis, shallow respirations
GI: nausea, vomiting, constipation, paralytic ileus (when stool becomes paralyzed and doesn’t move through bowel)
Watch out for cardiac changes in pts w/ potassium balances high/low
Treatment:
Correct cause (give tablets or IV solution of potassium)
Potassium replacement (need HCP order & can use throughout stay as long as it’s appropriate)
Nutritional therapy
Cardiac and respiratory monitoring
Hyperkalemia
> 5.0 mEq/L
Etiology:
Excessive intake
Kidney failure
Tissue/crush injury
When this happens, potassium is released into the plasma causing hyperkalemia
S/S:
Cardiac: dysrhythmias / bradycardia
CNS: irritability and anxiety
Muscular: twitching, progresses to weakness, paralysis
GI: diarrhea, increased bowel sounds
Treatment:
Correct cause
Diuretics/ dialysis
Sodium polystyrene sulfonate (Kayexalate)
Potassium exits
Insulin / glucose
Give together if higher dose of insulin not for DM
Nutritional therapy
Cardiac monitoring
High Potassium Foods
Fruits
Vegetables
Others: Breakfast Drinks, Ensure/Boost, Coconut Milk, Molasses, Salt Substitute (made from potassium, beware if low sodium & potassium)
Administration of Intravenous Potassium
Give carefully!
Hyperkalemia can cause fatal cardiac dysrhythmias
NEVER give IV push > 5.0
Give slowly, no faster than 10mEq/hr
ALWAYS use a pump (no drip rate)
Can be irritating to the veins
Magnesium
1.3-2.1 mEq/L
Intracellular cation responsible for:
Muscle contraction
Cardiac muscle contraction
Carbohydrate metabolism
Absorption of potassium
Intake: diet
Output: kidney excretion or reabsorption
Hypomagnesemia
(< 1.3 mEq/L)
Etiology:
Deficient intake
Malnutrition
Alcohol abuse
Loss of body fluids
GI diseases
Medications
S/S:
Cardiac: Dysrhythmias
CNS: Agitation, Confusion
Muscular: Increased reflexes, Numbness & tingling
GI: Constipation, Paralytic ileus
Treatment:
Magnesium replacement
Check and replace calcium and potassium
Nutritional therapy
Cardiac monitoring
Hypermagnesemia
> 2.1 mEq/L = helps you relax (to remember sx)
Etiology:
Excessive intake
Magnesium containing antacids/laxatives
Kidney failure
S/S:
Cardiac: Bradycardia, hypotension
CNS: Lethargy & drowsiness, Coma
Muscular: Decreased reflexes, Muscle weakness
GI: diarrhea
Treatment:
Diuretics
Dialysis
Nutritional counseling
Cardiac monitoring
Summary of Nursing Care
Monitor:
Labs
Vital signs
Cardiac rhythm
I&O
Weight
Administer medications properly
Educate:
Medications
Diet
Follow up with HCP
Signs and symptoms to report
Prioritization
Airway
Breathing
Circulation
Safety
Pain
Assess
Intervention
Reassessment