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🔹 Section 1: Fluid Imbalances
Why do fluid and electrolyte imbalances occur in most patients with major illness or injury?
Illness disrupts the normal homeostatic mechanism.
What can directly cause fluid and electrolyte imbalances?
Illness or disease and therapeutic measures (IV fluid replacement, medications)
How are fluid and electrolyte imbalances commonly classified?
Deficits or excesses
Can more than one imbalance occur at the same time?
Yes. Example: prolonged NG suction → loss of Na+, K+, H+, Cl- → deficiency of Na+ & K+, fluid volume deficit, and metabolic alkalosis from loss of HCl.
What is ECF volume deficit (hypovolemia)?
Abnormal loss of normal body fluids, inadequate intake, or plasma-to-interstitial fluid shift.
What are some causes of hypovolemia?
Vomiting, diarrhea, hemorrhage, diuresis, burns, 3rd spacing, secondary to disease processes (ex. diabetes insipidus), high-intensity training/exercise.
What is diabetes insipidus?
A rare disorder where the body makes too much urine (up to 20 quarts/day) due to decreased ability to concentrate urine caused by ADH deficit or nephron resistance.
What are the symptoms of diabetes insipidus?
Polyuria (frequent urination) and polydipsia (constant thirst).
What are some other causes of diabetes insipidus?
Adrenal insufficiency, osmotic diuresis, hemorrhage, or coma.
What are clinical manifestations of hypovolemia?
Restlessness, drowsiness, lethargy, confusion, postural hypotension, tachycardia, tachypnea, weakness, dizziness, thirst, weight loss, pale skin, seizures, coma, decreased skin turgor, capillary refill, urine output (later signs).
What should be checked in older adults for signs of hypovolemia?
Mucous membranes, lips, and eyes.
What is the treatment for hypovolemia?
Replace water and electrolytes with balanced IV solutions.
What is ECF volume excess (hypervolemia)?
Excessive intake of fluids, abnormal retention of fluids, or interstitial-to-plasma fluid shift.
What are causes of hypervolemia?
Excessive intake of fluids, abnormal retention of fluids (heart failure, renal failure), shift of interstitial fluid into plasma, inadequate renal/kidney excretion.
What are clinical manifestations of hypervolemia?
Headache, confusion, lethargy, peripheral edema, jugular venous distention, bounding pulse, hypertension, dyspnea, crackles, pulmonary edema, muscle spasms, weight gain, seizures, coma.
What is the treatment for hypervolemia?
Remove fluid without changing electrolyte composition or osmolality of ECF; diuretics and fluid restriction are primary therapy; sodium restriction may be indicated; if ascites/pleural effusion present, perform abdominal paracentesis or thoracentesis.
What should nurses monitor for both hypovolemia and hypervolemia? (5 things)
1.) I&O (oral, IV, enteral, irrigants; urine, perspiration, drainage, vomit, diarrhea)
2.) Daily weights (same time, same clothes, same scale). 1 kg (2.2 lbs) = 1 L fluid retained
3.) Vital signs
4.) LOC (level of consciousness)
5.) Pupillary response & extremity movement
What urine specific gravity indicates concentrated urine?
Readings of greater than 1.025 indicate concentrated urine (>1.025)
What urine specific gravity indicates dilute urine?
less than 1.010 indicate dilute urine (<1.010)
What cardiovascular changes are seen in fluid imbalances?
BP, pulse force, jugular venous distention
What is a sign of orthostatic hypotension in fluid volume deficit?
Orthostatic hypotension
How does ECF excess (Hypervolemia) affect respiratory status?
Causes pulmonary congestion/edema (↑ hydrostatic pressure → fluid in alveoli → SOB, crackles)
How does ECF deficit (Hypovolemia) affect respiratory status?
Causes tachypnea (↓ perfusion → hypoxia)
How does ECF excess (Hypervolemia) affect neurologic function?
Causes cerebral edema (Too much fluid → can cause cerebral edema (swelling in the brain)
How does ECF deficit (Hypovolemia) affect neurologic function?
Causes reduced cerebral tissue perfusion (Too little fluid → can cause reduced cerebral tissue perfusion (less blood and oxygen reaching the brain)
What is the normal range for serum sodium (Na⁺)?
135-145 mEq/L.
What type of ion is sodium?
The main cation of ECF (positive ion).
What are the major functions of sodium?
Controls water distribution in the body, regulated by ADH, thirst, RAAS, muscle contraction, transmission of nerve impulses, maintains Na⁺/K⁺ pump, maintains water balance & neuromuscular activity, promotes acid-base balance.
Where does most sodium come from?
Dietary intake.
How is sodium regulated?
By the kidneys (primary regulator of fluid volume, osmolality, and ECF distribution).
How much salt should be consumed daily?
2-4 grams/day.
What problems occur with sodium imbalance?
Cerebral dehydration, seizures, and/or coma.
What can abnormal sodium levels reflect?
Primary water imbalance, primary sodium imbalance, or a combination of both.
M.H., a 62-year-old female, admitted with confusion and lethargy.
History: diarrhea for a week, drank lots of water to prevent dehydration.
What caused M.H.’s sodium level to fall?
Excessive diarrhea caused fluid and sodium loss. Replacing fluid with plain water → dilutional hyponatremia (sodium loss > water loss).
What is hyponatremia?
Hyponatremia is defined as sodium (Na⁺) levels less than 135 mEq/L.
What primarily causes hyponatremia?
An imbalance of water rather than sodium.
What are some clinical manifestations of hyponatremia?
Poor skin turgor, dry mucosa, headache, nausea/vomiting, cramping, altered mental status, seizures, coma, cellular swelling, and cerebral edema.
What are some causes of hyponatremia related to loss of sodium-rich body fluids?
Diaphoresis, draining wounds, diarrhea, vomiting, and trauma with blood loss.
What are some causes of hyponatremia related to water excess?
Inappropriate use of sodium-free/hypotonic IV fluids, psychiatric excessive water intake, and SIADH (abnormal water retention leading to dilutional hyponatremia).
How is hyponatremia caused by water excess treated?
Fluid restriction.
What is the treatment for severe hyponatremia (seizures)?
Small amount of IV hypertonic saline solution (3% NaCl) with close monitoring.
How is hyponatremia caused by abnormal fluid loss treated?
Fluid replacement with sodium-containing solutions.
What drug therapy may be used in hyponatremia?
Vasopressin (ADH) blockers. [Conivaptan (Vaprisol) and Tolvaptan (Samsca)]
What is Conivaptan (Vaprisol) used for in hyponatremia?
It increases urine output without loss of Na⁺ & K⁺ (not for water-loss hyponatremia).
What is Tolvaptan (Samsca) used for in hyponatremia?
It is used for hyponatremia in heart failure, liver cirrhosis, and SIADH.
What is hypernatremia?
Hypernatremia is defined as sodium (Na⁺) levels greater than 145 mEq/L.
What causes hypernatremia?
Hypernatremia can be caused by a gain of sodium in excess of water or a loss of water in excess of sodium.
What is the most common cause of hypernatremia?
The most common cause of hypernatremia is fluid deprivation in patients unable to respond to thirst.
What are the clinical manifestations of hypernatremia related to cellular dehydration?
Clinical manifestations include thirst and a swollen dry tongue.
What neurological symptoms can occur with hypernatremia?
Neurological symptoms of hypernatremia can include lethargy, irritability, impaired level of consciousness, hallucinations, seizures, and coma.
What is the primary goal of hypernatremia treatment?
Treat the underlying cause.
How is primary water deficit treated in hypernatremia?
Replace fluids orally or IV with isotonic or hypotonic fluids (0.45% saline preferred; 5% dextrose in water may also be used).
How is excess sodium treated in hypernatremia?
Dilute with sodium-free IV fluids (5% dextrose in water) and promote excretion with diuretics.
What should be closely monitored in hypernatremia?
Neuro status (baseline and ongoing), serum sodium levels, fluid gains/losses.
Why must sodium correction be done carefully in hypernatremia?
Quick reduction can cause rapid water shift back into cells → cerebral edema and neurologic complications. Risk is greatest if hypernatremia developed over several days.
What is the normal range for potassium?
3.5-5.0 mEq/L.
What type of ion is potassium?
Major ICF cation (98% intracellular).
What are the functions of potassium?
Influences skeletal & cardiac muscle activity, maintains resting membrane potential, required for glycogen deposition, and plays a role in acid-base balance.
What is the intracellular concentration of potassium?
~140 mEq/L.
What is the extracellular concentration of potassium?
3.5-5.0 mEq/L.
How is potassium distributed between ICF & ECF?
Maintained by Na⁺/K⁺ pump (K⁺ in, Na⁺ out).
What are dietary sources of potassium?
Fruits, vegetables (bananas, oranges), salt substitutes, stored blood, PO/IV potassium medications.
How is potassium regulated in the body?
By the kidneys (90% of daily intake excreted; rest lost in stool/sweat).
What is the relationship between sodium & potassium reabsorption in the kidneys?
Inverse relationship (Na⁺ retention → K⁺ loss).
What EKG change is associated with potassium imbalance?
Peaked T-wave.
What was the hypokalemia case study?
T.M., 76-year-old male with HTN & type 2 diabetes. Doubled his furosemide (Lasix, potassium-wasting diuretic) for 2 weeks due to 'feeling puffy.' Admitted with confusion & lethargy.
What caused T.M.'s hypokalemia?
Increased diuresis → increased renal excretion of water & potassium.
What caused T.M.'s elevated hematocrit (Hct 56%)?
Fluid loss → hemoconcentration → false elevation.
What are the causes of hypokalemia?
Increased loss of K⁺ via kidneys or GI tract.
What are GI causes of hypokalemia?
Diarrhea, laxative abuse, vomiting, ileostomy drainage.
What are renal causes of hypokalemia?
Diuretics, increased aldosterone, low magnesium.
What causes increased shift of potassium from ECF to ICF?
Insulin therapy with DKA, β-adrenergic stimulation, alkalosis.
What deficiency can cause hypokalemia?
Magnesium deficiency.
What are clinical manifestations of hypokalemia?
Cardiac arrhythmias, skeletal muscle weakness, respiratory muscle weakness, decreased GI motility, impaired regulation of arteriolar blood flow, hyperglycemia.
What are ECG effects of hypokalemia?
Flattened T wave, U wave appears, peaked P waves, prolonged QRS, increased incidence of lethal ventricular dysrhythmias.
What did assessment of T.M. show?
Poor skin turgor, leg cramps, HR 135 & irregular, RR 26, BP 110/58.
What are priority nursing actions for hypokalemia?
Replacement therapy (PO or IV KCl), Monitor serum K⁺ levels, Monitor vital signs (place on telemetry), Watch for dysrhythmias (potential complication)
How is IV potassium (KCl) administered?
Dilute IV KCl; never IV push or bolus, Should not exceed 10 mEq/hr, Use infusion pump, Invert IV bag for even distribution, Assess IV site hourly, Use central line if rapid correction needed, Oral K⁺ given if able to tolerate
When is KCl not given?
If urine output <0.5 mL/kg/hr (risk of hyperkalemia).
What is the maximum IV concentration for potassium?
Preferred 40 mEq/L (up to 80 mEq/L in severe cases with cardiac monitoring).
What teaching is important for discharge after hypokalemia?
Recognize/report signs of hypokalemia, Increase dietary potassium if on Lasix, Foods high in potassium (bananas, oranges, spinach, potatoes, etc.), Salt substitutes contain 50-60 mEq/tsp of potassium, Take medication as prescribed (do not adjust dose), Consult MD before making medication changes.
What are the causes of hyperkalemia?
Impaired renal excretion (most common in renal failure), Shift from ICF → ECF (acidosis, massive cell destruction, trauma, burns, exercise), Rapid administration of KCl, Medications: ACE inhibitors, K⁺-sparing diuretics (spironolactone, amiloride), aldosterone receptor blockers, Adrenal insufficiency → ↓ aldosterone → K⁺ retention, β-blockers, digoxin-like drugs → impair K⁺ entry into cells.
What are the manifestations of hyperkalemia?
Muscle cramps, Abdominal distention, diarrhea, cramping, Muscle weakness (legs → respiratory), Cardiac dysrhythmias.
What are ECG effects of hyperkalemia?
Flattened P waves, widened QRS, Shortened QT interval, Narrow, peaked T waves, Ventricular fibrillation or cardiac standstill may occur.
What is a key nursing management action for hyperkalemia regarding potassium intake?
Eliminate oral/parenteral K⁺ intake
What is a method to increase elimination of potassium in hyperkalemia?
Diuretics, dialysis, or Kayexalate
How can potassium be forced from the extracellular fluid to the intracellular fluid in hyperkalemia?
IV insulin + glucose, sodium bicarbonate if acidotic
What is used to reverse membrane effects in hyperkalemia?
IV calcium gluconate
What monitoring should be done immediately for a patient with hyperkalemia?
Place patient on EKG monitoring
What should patients with hyperkalemia be educated about?
Diet & potassium-containing medications
What is Kayexalate (sodium polystyrene sulfonate)?
A resin that binds K⁺ in exchange for Na⁺ and is excreted in feces (risk: intestinal necrosis → FDA removed brand)
What are patients with hyperkalemia at risk for?
Activity intolerance & injury (muscle weakness) and cardiac dysrhythmias
What is the normal range for magnesium?
1.5-2.5 mEq/L.
What type of ion is magnesium?
Abundant ICF cation (2nd most abundant).
What role does magnesium play in carbohydrate and protein metabolism?
It is involved in carbohydrate and protein metabolism.
How does magnesium help maintain calcium and potassium balance?
It helps maintain calcium and potassium balance.
Why is magnesium necessary for the sodium-potassium pump function?
It is necessary for sodium-potassium pump function.
What effect does excess magnesium have on muscle cells?
Excess magnesium decreases excitability of muscle cells (sedative effect).
What effect does a deficit of magnesium have on neuromuscular activity?
Deficit increases neuromuscular irritability and contractility.