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These flashcards provide essential vocabulary, clinical signs, and laboratory values related to fluid and electrolyte imbalances and acid-base disorders based on the medical-surgical nursing lecture.
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Volume
The total amount of fluid in the body.
Osmolality
The concentration of dissolved particles (solutes) per kg of water; normal serum range is 280−295mOsm/kg.
Composition
The specific concentrations of electrolytes within body fluids.
Acidity (pH)
The concentration of hydrogen ions (H+) in the body fluid.
Diffusion
The passive movement of electrolytes and particles from a higher to a lower concentration gradient requiring no energy.
Active Transport
The use of energy (ATP) to move electrolytes across a concentration gradient, often described as working 'uphill'.
-Digoxin inhibits this to keep K+ outside of cell
Filtration
The movement of fluid across capillary membranes resulting from differences in hydrostatic pressure. This pushes fluid into the interstitial
Osmosis
The movement of water across a semipermeable membrane from an area of low solute concentration to high solute concentration.
Isotonic Solutions
Fluids with an osmolality of 280−295mOsm/kg that result in no net water movement, allowing cells to maintain normal size. Examples include normal saline (0.9%NaCl) and Lactated Ringer's solution.
Hypotonic Solutions
Fluids with an osmolality less than 280mOsm/kg that cause water to move into cells, resulting in cell swelling. An example is 0.45% sodium chloride (half-normal saline) 0.33% NaCl, D5W (once metabolized)
Hypertonic Solutions
Fluids with an osmolality greater than 295mOsm/kg that cause water to move out of cells, leading to cell shrinkage. Examples include 3% sodium chloride (hypertonic saline) and D5NS (5% dextrose in normal saline).
Hypovolemia
An extracellular fluid volume deficit characterized by insufficient fluid, often caused by GI losses, renal losses, or hemorrhage.This condition can lead to decreased blood pressure, increased heart rate, and potential shock. Treatment typically involves fluid replacement and addressing the underlying cause.
Older Adults at HIGHEST risk due to decreased thirst reflex
Third Spacing
A pathological fluid shift that occurs when fluid moves from the intravascular compartment (the vascular space) into non-functional areas (such as body cavities including the abdomen, where it can accumulate in conditions like ascites, or within the bowel during an obstruction). This fluid becomes unavailable for normal physiological circulation and can lead to decreased effective circulating volume, contributing to various complications such as hypotension and shock.
Key Points:
-Third spacing often occurs after major surgery, trauma, or burns.
-Clinical manifestations may include abdominal distension, weight gain, hypotension despite apparent volume, and reduced urine output.
-Management typically involves addressing the underlying cause, optimizing fluid balance, and in some cases, draining the accumulated fluid if needed
Clinical Relevance:
-Helps in identifying patients at risk for hypovolemia despite normal total body fluid volume due to unavailable fluid in third spaces.
Hypovolemic Shock
A severe complication of fluid loss marked by a MAP < 70\,mmHg, tachycardia over 120bpm, urine output less than 0.5mL/kg/hrand altered mental status. It results from significant fluid volume deficit and requires immediate medical intervention to restore circulating volume.
-metabolic acidosis
Hypervolemia
Fluid volume excess in the extracellular compartment, commonly caused by heart failure, kidney disease, liver cirrhosis, hyperaldosteronism, prolonged corticosteroid therapy, SIADH, or rapid IV fluid administration.
This can lead to edema, hypertension, and complications such as pulmonary congestion or heart failure. Treatment focuses on fluid restriction, diuretics, and managing the underlying cause.
Key Labs:
Low HCT
Low Hgb
Low BUN
Low serum/urine osmolality
Low urine Na+
Pulmonary Edema
A severe complication of hypervolemia where fluid accumulates in the lung interstitium and alveoli, manifesting as pink-tinged frothy sputum and ascending crackles.
Hyponatremia
A serum sodium level less than 135mEq/L, representing a water excess relative to sodium and carrying a high risk of cerebral edema.
Causes:
- Excessive fluid intake or retention (e.g., heart failure, hepatic cirrhosis)
-Syndrome of inappropriate antidiuretic hormone secretion (SIADH)
-Renal losses due to diuretics or kidney disease
- Gastrointestinal losses (e.g., vomiting, diarrhea)
- Adrenal insufficiency
Manifestations:
- Nausea and vomiting
- Headache
- Altered mental status (confusion, lethargy)
- Muscle cramps and spasms
- Seizures or coma in severe cases
Nursing Management:
- Monitor serum sodium levels and assess for signs/symptoms.
- Implement fluid restriction as per healthcare provider orders.
- Administer hypertonic saline (e.g., 3% sodium chloride) cautiously under supervision if severe hyponatremia is present.
- Educate the patient about the importance of fluid management.
- Monitor neurological status closely to detect any signs of cerebral edema.
Hypernatremia
A serum sodium level greater than 145mEq/L, representing a water deficit relative to sodium and carrying a risk of neurological damage.
Causes:
Insufficient water intake (e.g., inability to access fluids, decreased thirst)
Excessive water loss (e.g., diabetes insipidus, prolonged diarrhea)
Increased sodium intake (e.g., hypertonic IV solutions, excessive salt intake)
Manifestations:
Increased thirst
Dry mucous membranes
Restlessness or irritability
Muscle twitching or spasms
Confusion or altered mental status
Seizures or coma in severe cases
Nursing Management:
Monitor serum sodium levels and vital signs regularly.
Ensure adequate fluid intake, offering fluids frequently as tolerated.
Administer hypotonic IV fluids (e.g., 0.45% NaCl) cautiously to correct sodium imbalance.
Educate the patient about the importance of adhering to fluid management protocols.
Osmotic Demyelination Syndrome (ODS)
A neurological condition caused by correcting hyponatremia too rapidly, exceeding the limit of 10−12mEq/L per 24 hours.
Hypokalemia
A serum potassium level less than 3.5mEq/L, typically showing flattened T waves and U waves on an ECG.
Causes:
Inadequate dietary intake (e.g., low potassium diet)
Excessive losses (e.g., gastrointestinal losses such as vomiting or diarrhea, renal losses from diuretics)
Shift of potassium into cells (e.g., due to insulin administration or metabolic alkalosis)
Manifestations:
Muscle weakness and cramps
Fatigue
Palpitations due to cardiac arrhythmias
Nausea and vomiting
Constipation
Nursing Management:
Monitor serum potassium levels and ECG changes regularly.
Administer potassium supplements orally or intravenously as prescribed, being cautious of the rate of infusion.
Educate the patient on potassium-rich foods (e.g., bananas, oranges, potatoes).
Monitor for signs of hypokalemia severity and potential complications, ensuring patient safety.
Hyperkalemia
A serum potassium level greater than 5.0mEq/L, characterized on an ECG by peaked, tented T waves and a widened QRS complex.
Causes:
Renal failure (decreased excretion)
Excessive potassium intake (e.g., supplements or potassium-rich foods)
Cell destruction (e.g., hemolysis, trauma, burns)
Shift of potassium from intracellular to extracellular space (e.g., acidosis, insulin deficiency)
Manifestations:
Muscle weakness
Fatigue
Palpitations or irregular heart rhythms
Nausea
Paresthesias (tingling sensations)
Nursing Management:
Monitor serum potassium levels and ECG changes closely.
Administer calcium gluconate for cardiac protection.
Administer insulin with glucose to shift potassium back into cells if indicated.
Monitor and treat underlying causes (e.g., renal dysfunction, medication review).
Educate the patient on potassium restriction and signs/symptoms of hyperkalemia.
Calcium Gluconate
The first-line medication for hyperkalemia when ECG changes are present, used to provide cardiac membrane protection.
Hypocalcemia
A serum calcium level less than 9mg/dL, often resulting in neuromuscular excitability like tetany and a prolonged QT interval.
Causes:
Vitamin D deficiency
Hypoparathyroidism
Chronic kidney disease
Magnesium deficiency
Excessive blood transfusions
Manifestations:
Muscle cramps and spasms
Numbness or tingling in the fingers and toes
Hyperreflexia
Seizures in severe cases
Positive Chvostek’s and Trousseau’s signs
Nursing Management:
Monitor serum calcium levels and ECG changes.
Administer calcium supplements orally or intravenously as prescribed.
Educate the patient about dietary sources of calcium (e.g., dairy products, leafy greens).
Monitor for signs of neuromuscular irritability and advise precautions to prevent injury due to muscle spasms.
Chvostek’s Sign
A clinical indicator of hypocalcemia involving a facial muscle twitch when the facial nerve (CNVII) is tapped.
Trousseau’s Sign
A carpal spasm induced by inflating a blood pressure cuff above the systolic pressure, indicating hypocalcemia.
Hypercalcemia
A serum calcium level greater than 10.5mg/dL, often summarized by the phrase 'Bones, Stones, Groans, Psychic Moans'.
Causes:
Primary hyperparathyroidism
Malignancies (e.g., metastasis to bone)
Vitamin D intoxication
Prolonged immobilization
Renal failure
Manifestations:
Bone pain and fractures
Renal calculi (kidney stones)
Abdominal pain and constipation (groans)
Neuropsychiatric symptoms (e.g., confusion, lethargy, depression)
Nursing Management:
Monitor serum calcium levels and hydration status.
Administer IV fluids to promote renal excretion of calcium.
Administer diuretics (e.g., furosemide) if prescribed to enhance calcium excretion.
Educate the patient on dietary modifications to limit calcium intake.
Monitor for and address complications, such as acute kidney injury or cardiac dysrhythmias.
Hypomagnesemia
A serum magnesium level less than 1.6mEq/L, which can cause refractory hypokalemia that cannot be corrected until magnesium is replaced.
Causes:
Inadequate dietary intake (e.g., low magnesium diet)
Excessive losses (e.g., gastrointestinal losses from vomiting or diarrhea, renal losses due to diuretics)
Alcoholism
Prolonged use of proton pump inhibitors
Manifestations:
Muscle weakness and cramps
Fatigue
Paresthesia (tingling sensations)
Cardiac arrhythmias
Seizures in severe cases
Nursing Management:
Monitor serum magnesium levels and ECG changes regularly.
Administer magnesium supplements orally or intravenously as prescribed, monitoring for signs of complications.
Educate the patient about dietary sources of magnesium (e.g., nuts, seeds, whole grains).
Monitor for signs of hypokalemia and treat appropriately, ensuring magnesium levels are corrected.
Hypermagnesemia
A serum magnesium level greater than 2.6mEq/L, where the loss of deep tendon reflexes (DTRs) serves as an early warning sign of toxicity.
Causes:
Renal failure (decreased excretion)
Excessive magnesium intake (e.g., magnesium-based antacids or supplements)
Tissues destruction (e.g., burns, sepsis)
Manifestations:
Loss of deep tendon reflexes
Muscle weakness
Fatigue
Nausea and vomiting
Respiratory depression
Cardiac arrhythmias
Nursing Management:
Monitor serum magnesium levels and vital signs closely.
Administer intravenous calcium gluconate for cardiac protection.
Provide dialysis if severe hypermagnesemia is present and renal function is compromised.
Educate the patient on limiting magnesium-rich foods and medications.
Refeeding Syndrome
A sudden drop in serum phosphorus levels when refeeding malnourished patients, potentially leading to cardiac and respiratory failure.
Kussmaul Respirations
Deep, rapid, and labored breathing used by the lungs to compensate for metabolic acidosis by eliminating CO2.
ROME Mnemonic
A memory aid for ABG interpretation meaning Respiratory Opposite (pH and CO2 move in opposite directions) and Metabolic Equal (pH and HCO3− move in the same direction).
Crystalloids
IV fluids containing water and electrolytes or glucose (e.g., 0.9%NaCl, Lactated Ringer's) that distribute throughout the extracellular fluid.
Colloids
Oncotic agents such as Albumin that stay within the vascular space to act as plasma expanders.
Extravasation
A complication where a vesicant medication (like calcium chloride) leaks into the tissue, potentially causing necrosis.
Intake Regulation
-regulated by the thirst mechanism
-social habits & routine influence intake
-average adult: ~2500mL/day to stay balanced
-solid foods contribute ~1000mL
-thirst is the final mechanism. Once someone feels thirsty then they are mildly dehydrated
Output Regulation
-Kidneys: major regulator (1500L/day)
-skin/insensible loss: ~600mL/day
-lungs: ~300mL/day
-GI tract: ~200mL/day
Daily wieghts needed for heat failure
—-1Kg of weight loss/gain= 1L of fluid
Extracellular Sub Compartments
Divided into three main compartments:
interstitial fluid (found between cells), (leads to edema when there is too much expansion)
plasma (contained within blood vessels), (what to expand during emergencies)
transcellular fluid (such as cerebrospinal fluid and synovial fluid). (think acsites and pleural effusion) These compartments are essential for nutrient transport, waste removal, and homeostasis.
Clinical Assessment Findings of Hypovolemia
Decreased blood pressure and elevated heart rate
Weak and thready pulse
Dry mucous membranes and skin turgor
Decreased urine output (often less than 0.5mL/kg/hr)
Cool, clammy skin
Altered mental status (e.g., confusion, lethargy)
Potential signs of shock (e.g., tachycardia, hypotension)
Nursing Interventions for Hypovolemia
Monitor vital signs closely, especially heart rate and blood pressure
Assess fluid intake and output
Administer IV fluids as ordered (e.g., isotonic solutions)
Perform frequent assessments of lab values (e.g., electrolytes, hematocrit)
Educate the patient on fluid intake and the importance of hydration
Monitor for signs of fluid overload once treatment begins
Nursing Actions for Hypovolemic Shock
- Administer IV fluids rapidly as ordered for volume resuscitation
Monitor vital signs closely, especially heart rate, blood pressure, and urine output
Assess for signs of fluid overload, such as edema or pulmonary congestion
Maintain an accurate intake and output record
Prepare for potential blood transfusions if indicated
Keep the patient warm to prevent hypothermia, and position them to optimize perfusion (e.g., supine with legs elevated)
Frequently reassess lab values, including electrolytes and hemoglobin/hematocrit levels.
Clinical Assessment Findings of Hypervolemia
Elevated blood pressure and heart rate
Bounding pulse and jugular venous distention
Edema (peripheral and/or pulmonary)
Weight gain over time (more than 1 kg in 24 hours)
Increased respiratory rate, potentially with difficulty breathing
Altered mental status as fluid overload progresses
Increased urine output initially, then may decrease as heart function declines
Nursing Interventions for Hypervolemia
Monitor vital signs closely, especially blood pressure and heart rate
Assess for signs of edema (peripheral and pulmonary)
Evaluate laboratory values, including electrolytes and hematocrit
Administer diuretics as ordered to promote fluid excretion
Restrict fluid intake as indicated by the healthcare provider
Educate the patient on the importance of weight monitoring and restriction protocols
Monitor and record input and output accurately
Regularly reassess respiratory status and manage any airway issues
Normal Serum Sodium Levels
A normal serum sodium level ranges from 135 to 145mEq/L and is crucial for maintaining fluid balance, nerve function, and muscle contraction.
Normal Serum Potassium Levels
A normal serum potassium level ranges from 3.5 to 5.0mEq/L and is essential for maintaining normal cell function, including the conduction of nerve impulses and muscle contractions.
Normal Serum Calcium Levels
A normal serum calcium level ranges from 8.5 to 10.5mg/dL and plays a significant role in bone health, blood clotting, and muscle contractions.
Normal Serum Magnesium Levels
A normal serum magnesium level ranges from 1.6 to 2.6mEq/L and is important for numerous biochemical reactions in the body, including energy production and muscle contraction.
Normal Serum Phosphorus Levels
A normal serum phosphorus level ranges from 2.5 to 4.5mg/dL and is vital for energy storage and release in the form of ATP, as well as bone and tooth mineralization.
Respiratory Acidosis
A condition where the pH of the blood decreases (acidosis) due to an increase in carbon dioxide (CO₂) levels resulting from inadequate ventilation.
Causes:
Chronic obstructive pulmonary disease (COPD)
Asthma exacerbations
Severe pneumonia
Neurological disorders affecting respiratory drive (e.g., stroke)
Chest wall deformities or respiratory muscle fatigue
Manifestations:
Headache
Confusion or lethargy
Shortness of breath
Rapid, shallow breathing
Dysrhythmias
Nursing Management:
Monitor respiratory status and ABGs (arterial blood gases).
Administer supplemental oxygen as needed.
Facilitate bronchodilator therapy as prescribed.
Encourage deep breathing exercises to improve ventilation.
Prepare for intubation if respiratory failure occurs.
Respiratory Alkalosis
A condition where the pH of the blood increases (alkalosis) due to a decrease in carbon dioxide (CO₂) levels as a result of hyperventilation.
Causes:
Anxiety or panic attacks
Hyperventilation syndrome
Fever
Salicylate overdose
Initial stages of pulmonary embolism
Manifestations:
Dizziness or lightheadedness
Tingling in fingers and toes (paresthesias)
Palpitations
Tetany or muscle cramps
Confusion
Nursing Management:
Monitor respiratory status and assess for signs of hyperventilation.
Provide reassurance and calm the patient.
Administer CO₂ rebreathing mask if necessary to restore CO₂ levels.
Encourage slower breathing techniques.
Metabolic Acidosis
A condition where the pH of the blood decreases (acidosis) due to a primary decrease in bicarbonate (HCO₃⁻) levels.
Causes:
Diabetic ketoacidosis
Renal failure
Lactic acidosis (e.g., sepsis, shock)
Loss of bicarbonate (e.g., diarrhea)
Ingestion of toxins (e.g., methanol, salicylates)
Manifestations:
Rapid, shallow breathing (Kussmaul respirations)
Confusion or lethargy
Nausea and vomiting
Coma in severe cases
Nursing Management:
Monitor vital signs and laboratory values (especially HCO₃⁻).
Administer sodium bicarbonate IV if indicated.
Identify and treat the underlying cause (e.g., insulin for diabetic ketoacidosis).
Supportive care and hydration.
Metabolic Alkalosis
A condition where the pH of the blood increases (alkalosis) due to an increase in bicarbonate (HCO₃⁻) levels or a loss of acids.
Causes:
Excessive use of diuretics
Vomiting or gastric suction
Excessive administration of bicarbonate
Hyperaldosteronism
Conn's syndrome
Manifestations:
Muscle twitching or cramps
Nausea and vomiting
Hypertension
Confusion or lethargy
Respiratory depression due to hypoventilation
Nursing Management:
Monitor vital signs and laboratory values (especially electrolytes and ABGs).
Administer IV fluids, electrolyte replacement, and medications as ordered.
Assess for signs of hypokalemia and manage as needed.
Educate the patient on avoiding excessive diuretic use.