IV Therapy Notes

IV Complications

Infiltration

• Definition: Non-vesicant IV fluid or medication leaks into the subcutaneous tissue surrounding the catheter insertion site. This occurs when the catheter dislodges or perforates the vein wall.

• Causes: Improper insertion, dislodgement of catheter, friction from catheter movement, fragile veins (elderly, very young).

Signs

• Cool, pale skin at the insertion site and surrounding area due to compromised circulation and the temperature of the IV fluid.

• Swelling (edema) or puffiness around the site, often appearing blanched.

• Leakage at site of insertion.

• Slowed IV flow rate or complete cessation, despite a patent and open clamp, as fluid is no longer entering the vein efficiently.

• Absence of blood return in the IV tubing (though this can be unreliable).

• Discomfort or tenderness around the site.

Severity Grading (Infusion Nurses Society - INS Standard)

• Grade 0: No symptoms.

• Grade 1: Skin blanched, edema < 1 inch in any direction, cool to touch, with or without pain.

• Grade 2: Skin blanched, edema 1-6 inches in any direction, cool to touch, with or without pain.

• Grade 3: Skin blanched, translucent; gross edema > 6 inches in any direction; cool to touch; mild-moderate pain; possible numbness.

• Grade 4: Skin blanched, translucent, tight, leaking; pitting edema > 6 inches in any direction; skin discolored (bruised); deep indentation of tissue; circulatory impairment; moderate-severe pain; potential for skin breakdown.

Priority Interventions

1. STOP infusion IMMEDIATELY to prevent further fluid accumulation in the tissue.

2. Remove catheter from the affected extremity to prevent further leakage and allow the site to heal.

3. Elevate extremity above the heart to promote fluid reabsorption and reduce swelling.

4. Apply warm compress to the area to increase circulation and facilitate fluid dissipation. Avoid vigorous rubbing.

5. Document the infiltration grade, interventions, and patient response.

6. Insert new IV in the opposite extremity if continued IV therapy is needed, avoiding the compromised limb.

Extravasation (vesicants)

• Definition: Leakage of a vesicant solution (medication or fluid capable of causing blisters, tissue necrosis, or severe tissue damage) from the vein into the surrounding extravascular tissue. This is a more severe form of infiltration.

• Vesicants include: Many chemotherapy drugs (e.g., doxorubicin, vincristine), vasopressors (e.g., norepinephrine, dopamine, epinephrine), hyperosmolar solutions (e.g., D10W, TPN), some antibiotics (e.g., vancomycin), and contrast media.

Signs

• Pain, burning, or stinging at the insertion site, which may be immediate or delayed.

• Blistering (formation of vesicles containing fluid).

• Tissue necrosis (tissue death), which may manifest as darkening, hardening, or sloughing of the skin over time.

• Erythema (redness) and induration (hardening) of the tissue.

• Coolness or warmth depending on the vesicant.

• Edema (swelling) that progresses quickly.

Priority Interventions

1. STOP infusion IMMEDIATELY. Do not flush the line, as this can push more vesicant into the tissue.

2. Leave catheter IN for antidote administration. This allows for potential aspiration of residual drug from the catheter and direct injection of an antidote into the extravasated area.

3. Notify provider and pharmacy STAT.

4. Administer antidote per protocol. The choice of antidote is specific to the vesicant (e.g., phentolamine for adrenergic stimulators like norepinephrine, hyaluronidase for vinca alkaloids). If no specific antidote, sterile saline injection could be used to dilute the drug.

5. Remove catheter only after antidote administration and aspiration (if applicable).

6. Apply cool compress (for most vesicants, e.g., vasopressors, most chemo EXCEPT vinca alkaloids where warm compress is indicated) to vasoconstrict and limit spread.

7. Elevate extremity to promote venous return and reduce edema.

8. Document the extravasation site, size, appearance, patient symptoms, interventions, antidote, and photographic evidence if possible.

NCLEX Tip

• Don’t remove the IV until medication reversal (antidote) is given and/or any attempted aspiration of residual drug is completed, especially with vesicants where an antidote is available for direct injection into the compromised tissue.

Phlebitis

• Definition: Inflammation of the inner lining (intima) of a vein. It can be caused by mechanical irritation, chemical irritation, or bacterial infection.

• Causes:

  • Mechanical: Catheter movement, insertion in areas of joint flexion, large catheter chosen for a small vein.

  • Chemical: Irritating IV solutions (e.g., high osmolality, low pH medications, certain antibiotics), too rapid infusion.

  • Bacterial: Poor aseptic technique during insertion or dressing changes, contaminated equipment.

Signs

• Red, warm streak along the path of the vein, often accompanied by pain and tenderness.

• Palpable cord-like structure indicating inflamed, hardened vein.

• Pain at the insertion site and extending along the vein.

• Slight swelling or puffiness over the vein.

Severity Grading (Infusion Nurses Society - INS Standard)

• Grade 0: No symptoms.

• Grade 1: Erythema at access site with or without pain.

• Grade 2: Pain at access site with erythema and/or edema.

• Grade 3: Pain at access site with erythema, streak formation, and/or palpable cord.

• Grade 4: Pain at access site with erythema, streak formation, palpable cord >1 inch in length, and purulent drainage.

Interventions

• Remove IV catheter immediately to prevent further irritation or infection.

• Apply warm compress to the affected area to promote circulation, reduce pain, and decrease inflammation.

• Elevate the extremity to help reduce swelling.

• Document the phlebitis grade, site appearance, interventions performed, and patient’s response.

• Culture the catheter tip if purulent drainage is present or if infection is suspected.

• Insert a new IV in a different site, preferably in the opposite extremity.

Central Line Management

Priority Considerations

• Risk for air embolism is a critical complication. Air can enter the venous system during insertion, removal, or tubing changes, leading to an obstruction in the pulmonary circulation.

  • Signs of air embolism: Sudden onset of dyspnea, chest pain, hypotension, tachycardia, cyanosis, altered mental status, and a "mill wheel" murmur heard over the precordium.

• Always clamp prior to cap change or tubing disconnection to prevent air entry into the catheter and venous system. If catheter has multiple lumens, clamp all unused lumens.

• If suspected embolus, position patient in Trendelenburg on LEFT side. This position helps trap air in the right ventricle, preventing it from entering the pulmonary artery and allowing it to dissipate gradually. Administer oxygen and notify provider immediately.

• Monitor for signs of sepsis (e.g., temperature increase, chills, malaise), as central lines are direct access points to the bloodstream and carry a higher risk of infection than peripheral IVs. Other signs include elevated WBC, hypotension, and increased heart rate. Maintain strict aseptic technique for insertion and site care.

PCA Pump Safety

Assessment Focus

• Risk for respiratory depression is highest with opioid PCA administration, especially within the first 24 hours or with initial bolus doses. Opioids suppress the central nervous system respiratory drive.

• Conduct sedation scale assessment (e.g., Pasero Opioid-Induced Sedation Scale - POSS) before noting changes in respiratory rate (RR). Sedation is often an early indicator of impending respiratory depression.

  • POSS Scale: S = sleep, easy to arouse; 1 = awake and alert; 2 = slightly drowsy, easily aroused; 3 = frequently drowsy, arousable, drifts off to sleep during conversation (UNACCEPTABLE sedation level, frequently precedes significant respiratory depression); 4 = somnolent, minimal or no response to verbal/physical stimulation (UNACCEPTABLE, requires immediate intervention).

Teaching Points

• Only the patient should push the button for medication delivery (not family or nurses), ensuring that the medication is administered only when the patient perceives a need, thus reducing the risk of overdose and respiratory depression. This is known as "patient-controlled" analgesia for a reason. Family members or nurses pressing the button could lead to over-sedation if the patient is already drowsy or asleep.

IV Fluids — Contraindications

Basics

• Isotonic solutions (e.g., 0.9% Normal Saline (NS), Lactated Ringer's (LR), D5W (in body)): Same osmolality as body fluids. Used for volume expansion, hydration.

  • DO USE: Hypovolemia, hemorrhage, burns, DKA (after initial bolus), surgery.

  • DO NOT USE (Contraindication): Patients with conditions causing fluid overload (e.g., heart failure, renal failure, liver cirrhosis) as it can exacerbate edema. Caution with D5W in head injury patients as it can cause cerebral edema.

• Hypotonic solutions (e.g., 0.45% NS, 0.33% NS, D2.5W): Lower osmolality than body fluids. Shift fluid from ECF to ICF, causing cells to swell.

  • DO USE: Hypernatremia, severe cellular dehydration (e.g., DKA after initial NS & before insulin for intracellular rehydration), gastric fluid loss.

  • DO NOT USE (Contraindication): Increased intracranial pressure (ICP) as it can worsen cerebral edema, burns, trauma, or third-space fluid shifts due to risk of hypovolemia.

• Hypertonic solutions (e.g., 3% NaCl, D5NS, D5LR, D10W, D50W): Higher osmolality than body fluids. Shift fluid from ICF to ECF, causing cells to shrink.

  • DO USE: Severe symptomatic hyponatremia, cerebral edema (to pull fluid from brain cells), shock (as temporary plasma expander).

  • DO NOT USE (Contraindication): Dehydrated patients (risk of further dehydration), DKA (unless severe hyponatremia), heart or renal disease (risk of fluid overload and pulmonary edema). Administer slowly and with caution, often via central line due to risk of phlebitis/extravasation.

Key Points

• Hypotonic solutions lower serum sodium, causing water to move into cells (intracellular) due to osmotic gradient, leading to cell swelling (e.g., brain cells, potentially causing cerebral edema).

• Hypertonic solutions increase serum sodium, causing water to move out of cells (from intracellular to extracellular space) due to osmotic gradient, leading to cell shrinkage. This effect can be used therapeutically (e.g., to reduce cerebral edema) but also carries risks like cellular dehydration or fluid overload if not carefully monitored.

Electrolytes — In-Depth

Hyponatremia ($Na^+$ < 135 mEq/L)

Assessment Signs

• Neurological (due to cerebral edema):

  • Headache

  • Confusion, lethargy

  • Seizures if severe (often $Na^+$ < 120 mEq/L)

  • Coma (in extreme cases)

• Musculoskeletal: Muscle cramps, weakness.

• Cardiovascular:

  • Tachycardia (if hypovolemic hyponatremia)

  • Hypotension (if hypovolemic hyponatremia)

  • Bounding pulses and hypertension (if hypervolemic hyponatremia)

• Gastrointestinal: Nausea, vomiting.

Treatment Interventions

• Hypertonic saline (3% NaCl or 5% NaCl) if neurological signs/symptoms (s/s) are present (e.g., seizures, coma). Administer slowly and in small volumes, typically in an ICU setting with frequent neurological checks.

• Fluid restriction for euvolemic and hypervolemic hyponatremia to limit further hemodilution.

• Monitor sodium levels with slow correction (no more than 8-12 mEq/L in 24 hours) to avoid central pontine myelinolysis (osmotic demyelination syndrome), a severe neurological complication caused by rapid shifts in osmolarity leading to brain cell damage.

• Loop diuretics (e.g., furosemide) for hypervolemic hyponatremia.

• Vasopressin receptor antagonists (e.g., conivaptan, tolvaptan) for euvolemic hyponatremia.

Hypernatremia ($Na^+$ > 145 mEq/L)

Risk Factors

• Dehydration: Insufficient water intake or excessive water loss (e.g., severe vomiting, diarrhea, burns, excessive sweating without adequate fluid replacement).

• Diabetes insipidus: Deficiency of ADH (central DI) or renal insensitivity to ADH (nephrogenic DI), leading to excessive water excretion.

• Fever with increased insensible water loss.

• Watery diarrhea (loss of more water than sodium).

• Hyperaldosteronism (increased sodium reabsorption).

• Administration of excessive hypertonic saline or sodium bicarbonate.

Signs

• Thirst (primary symptom).

• Neurological:

  • Irritability, restlessness, agitation leading to seizures and coma.

  • Lethargy (especially in severe cases).

  • Disorientation.

• Musculoskeletal: Muscle twitching, profound weakness due to cell shrinkage.

• Skin and mucous membranes: Dry, flushed skin; dry sticky oral mucous membranes; decreased skin turgor.

Interventions

• Hypotonic fluids (0.45% NS, D5W) to gradually lower serum sodium and rehydrate cells. Administer orally if patient can tolerate.

• Slow correction of sodium levels (no more than 8-12 mEq/L in 24 hours) to minimize brain swelling risk (cerebral edema) which can occur if serum osmolarity rapidly decreases, causing water to rush into brain cells.

• Strict monitoring of fluid intake and output (I&O), daily weights, and neurological status.

• Treat underlying cause: e.g., Aquadrate (DDAVP) for central diabetes insipidus.

Hypokalemia ($K^+$ < 3.5 mEq/L)

Causes

• Diuretics (loop/thiazides): Furosemide, hydrochlorothiazide increase potassium excretion.

• Vomiting and NG suction: Loss of potassium-rich gastric fluids.

• Severe diarrhea: Loss of potassium from the intestines.

• Cushing's syndrome: Excess mineralocorticoids increase K+ excretion.

• Alkalosis: Drives potassium from ECF into ICF.

• Insulin administration: Shifts potassium into cells (useful in hyperkalemia).

• Corticosteroids.

Danger

• Life-threatening dysrhythmias: Potassium is crucial for cardiac electrical activity.

  • ECG changes: Prominent U waves, flattened or inverted T waves, ST segment depression, prolonged PR interval. These changes increase the risk of ventricular fibrillation and asystole.

• Muscle weakness and cramps, decreased deep tendon reflexes (DTRs).

• Ileus (decreased bowel motility) due to smooth muscle weakness.

• Overall muscle weakness leading to respiratory compromise.

Treatment Interventions

• Dietary potassium replacement for mild cases (e.g., oranges, bananas, potatoes, spinach).

• Oral potassium supplements (e.g., K-Dur, Micro-K) for moderate cases.

• IV potassium chloride (KCl) replacement for severe or symptomatic hypokalemia.

  • NEVER IV push K+: Rapid administration can cause fatal cardiac arrest. Always dilute.

  • Dilute and give via pump: Typically administered at a rate no faster than 10 mEq/hr via a peripheral line. For central lines or severe cases, higher rates (up to 20 mEq/hr) may be used in an ICU with continuous ECG monitoring.

  • Monitor ECG continuously during IV K+ administration to detect dysrhythmias.

  • Assess IV site frequently as KCl is highly irritating to veins and can cause phlebitis or infiltration.

  • Concurrent magnesium replacement may be necessary as hypomagnesemia can worsen hypokalemia or make it resistant to treatment.

Hyperkalemia ($K^+$ > 5.0 mEq/L)

Assessment Signs

• Cardiovascular (MOST DANGEROUS):

  • Peaked, narrow T waves (early sign)

  • Prolonged PR interval

  • Widened QRS complex

  • Loss of P waves

  • Progression to sine wave pattern, ventricular fibrillation, or asystole.

• Neuromuscular:

  • Muscle weakness, flaccid paralysis (starts in lower extremities and ascends).

  • Paresthesias (tingling or numbness) of fingers, toes, circumoral region.

• Gastrointestinal: Nausea, vomiting, diarrhea, hyperactive bowel sounds.

Risk Factors

• Renal failure: Kidneys cannot excrete potassium effectively.

• Potassium-sparing diuretics: Spironolactone, triamterene.

• ACE inhibitors and ARBs: Reduce aldosterone secretion, leading to K+ retention.

• Massive tissue injury: Burns, trauma, rhabdomyolysis release intracellular K+ into ECF.

• Acidosis: Shifts K+ out of cells.

• Adrenal insufficiency.

• Excessive oral or IV potassium intake.

Pharmacological Interventions (Acute management for severe hyperkalemia)

1. Calcium gluconate (or calcium chloride): Provides cardiac protection by stabilizing the myocardial cell membrane, reducing the risk of dysrhythmias. Does not lower serum K+. Administer IV.

2. Insulin (regular insulin) + D50W (dextrose 50% in water): Insulin shifts K+ into cells. Dextrose is given concurrently to prevent hypoglycemia from the insulin.

3. Sodium bicarbonate: Can shift K+ into cells, especially in metabolic acidosis.

4. Albuterol (beta-2 agonists): Administered via nebulizer, can temporarily shift potassium into cells.

5. Kayexalate (Sodium Polystyrene Sulfonate): Oral or rectal administration. Binds with potassium in the GI tract for removal from the body (takes hours to work, not for acute emergency).

6. Loop diuretics (e.g., Furosemide): Promotes renal excretion of potassium if renal function is adequate.

7. Dialysis (Hemodialysis): The most effective and fastest way to remove potassium from the body, typically used in renal failure or severe, refractory hyperkalemia.

Hypocalcemia ($Ca^{++}$ < 8.5 mg/dL or < 4.5 mEq/L ionized)

Assessment Signs

• Neuromuscular excitability:

  • Trousseau’s sign: Carpal spasm induced by inflating a blood pressure cuff above systolic pressure for 2-3 minutes.

  • Chvostek’s sign: Facial muscle twitching when the facial nerve (just below the temple) is tapped.

  • Tetany: Involuntary muscle contractions and spasms.

  • Laryngospasm: Spasm of the vocal cords, causing airway obstruction (emergency condition, can lead to respiratory arrest).

  • Seizures.

  • Paresthesias (tingling around mouth, fingers, toes).

• Cardiovascular: Prolonged QT interval on ECG, dysrhythmias.

• Gastrointestinal: Hyperactive bowel sounds, abdominal cramping.

Causes

• Hypoparathyroidism: Decreased PTH (parathyroid hormone) leads to decreased calcium absorption and increased renal excretion.

• Pancreatitis (acute): Saponification (fat necrosis) consumes calcium.

• Chronic kidney disease: Impaired vitamin D activation, phosphate retention.

• Vitamin D deficiency.

• Alkalosis.

• Massive blood transfusions: Citrate in transfused blood binds with calcium.

• Hypomagnesemia: Often co-existent and can impair PTH secretion.

Intervention

• IV calcium gluconate (preferred for peripheral administration) or calcium chloride (for central line or severe, acute cases) for symptomatic hypocalcemia. Administer slowly to avoid cardiac effects (bradycardia, hypotension).

• Seizure precautions: Ensure padded side rails, suction equipment readily available due to the risk of seizures.

• Monitor airway patency due to risk of laryngospasm. Keep tracheostomy tray and intubation supplies nearby for severe cases.

• Oral calcium and vitamin D supplements for chronic management.

• Dietary teaching: Encourage calcium-rich foods.

Note

• Calcium $(Ca^{++})$ and Magnesium $(Mg^{++})$ often move in the same direction in the body. If one is low, the other may also be low. Hypomagnesemia can directly cause hypocalcemia by impairing PTH release and action.

Hypermagnesemia ($Mg^{++}$ > 2.1 mg/dL)

Risk Factors

• Renal failure: Impaired magnesium excretion by the kidneys (most common cause).

• Excessive magnesium sulfate administration (common in OB patients for preeclampsia/eclampsia management, tocolysis).

• Overuse of magnesium-containing antacids or laxatives (e.g., Milk of Magnesia, Maalox).

• Adrenal insufficiency.

Assessment Signs

• Neuromuscular depression (primary concern):

  • Decreased deep tendon reflexes (DTRs) (early sign, patellar reflex diminishes first) progressing to absent DTRs.

  • Muscle weakness, lethargy, drowsiness.

  • Paralysis (in severe cases).

• Cardiovascular:

  • Hypotension, bradycardia.

  • ECG changes: Prolonged PR interval, widened QRS complex, prolonged QT interval.

  • Cardiac arrest (in severe cases).

• Respiratory:

  • Respiratory depression due to muscle weakness affecting diaphragm and intercostal muscles.

• Gastrointestinal: Nausea, vomiting.

Antidote

• IV calcium gluconate (10%) acts as an antagonist to magnesium's effects on cardiac and neuromuscular function. It does not reduce serum magnesium levels but provides emergent symptomatic relief.

• Loop diuretics (e.g., furosemide) with IV fluids (e.g., 0.9% NS) to promote renal excretion of magnesium in patients with adequate renal function.

• Dialysis for severe cases or in patients with renal failure.

ABG Interpretation

ROME Strategy (Respiratory Opposite, Metabolic Equal)

• Respiratory Acidosis: pH and PaCO₂ move in opposite directions. (If pH is low, PaCO₂ is high).

• Metabolic Acidosis: pH and HCO₃ move in the same direction. (If pH is low, HCO₃ is low).

• Respiratory Alkalosis: pH and PaCO₂ move in opposite directions. (If pH is high, PaCO₂ is low).

• Metabolic Alkalosis: pH and HCO₃ move in the same direction. (If pH is high, HCO₃ is high).

Normal Values:

• pH: 7.35 - 7.45

• PaCO₂ (partial pressure of carbon dioxide): 35 - 45 mmHg (respiratory component)

• HCO₃⁻ (bicarbonate): 22 - 26 mEq/L (metabolic component)

• PaO₂ (partial pressure of oxygen): 80 - 100 mmHg

Respiratory Acidosis

• Cause: Hypoventilation, leading to retention of CO₂, which combines with water to form carbonic acid, lowering pH. $CO2 + H2O \rightleftharpoons H2CO3 \rightleftharpoons H^+ + HCO_3^-$

• Common Causes:

  • COPD exacerbation, asthma attacks: Airway obstruction leads to impaired gas exchange.

  • Overdose (e.g., sedatives, opioids): Depresses respiratory drive.

  • Severe pneumonia, pulmonary edema: Impairs alveolar-capillary gas exchange.

  • Neuromuscular diseases: Guillain-Barré, myasthenia gravis, spinal cord injury affecting respiratory muscles.

  • Airway obstruction (e.g., foreign body, aspiration).

  • Hypoventilation from mechanical ventilation settings.

• Interventions:

  • Encourage ventilation through deep breathing techniques, coughing, and incentive spirometry.

  • Administer Naloxone if opioid-induced respiratory depression is suspected.

  • Bronchodilators for obstructive airway diseases.

  • Mechanical ventilation or BiPAP/CPAP support if severe.

  • Position patient to facilitate breathing (e.g., semi-Fowler's).

Respiratory Alkalosis

• Cause: Hyperventilation, leading to excessive blowing off of CO₂, which reduces carbonic acid, raising pH.

• Common Triggers:

  • Anxiety, panic attacks: Increased respiratory rate (tachypnea).

  • Pain: Physiological response to discomfort.

  • Hypoxemia: Stimulates respiratory drive (e.g., high altitude, early pulmonary embolism).

  • Fever, sepsis.

  • Mechanical ventilation: Settings may be too high.

  • Salicylate toxicity (early phase).

• Interventions:

  • Promote slow, deep breathing techniques (e.g., coaching the patient, using a paper bag for short periods under direct supervision to re-breathe CO₂ if appropriate and the cause is anxiety-related and not hypoxemia).

  • Treat underlying anxiety or pain with appropriate anxiolytics or analgesics.

  • Adjust mechanical ventilation settings.

Metabolic Acidosis

• Cause: Acid build-up or bicarbonate loss, lowering pH and HCO₃⁻.

• Common Causes:

  • Diabetic Ketoacidosis (DKA): Accumulation of ketoacids.

  • Lactic acidosis: Due to severe hypoxemia, shock, sepsis.

  • Renal failure: Inability to excrete acids or reabsorb bicarbonate.

  • Diarrhea (severe): Loss of bicarbonate from intestines.

  • Salicylate overdose (late phase).

• Interventions:

  • Treat the underlying cause:

    • Insulin for DKA.

    • Fluid resuscitation and vasopressors for shock/sepsis.

    • Renal dialysis for renal failure.

    • Antidiarrheals for severe diarrhea.

  • Administer bicarbonate for severe cases (pH < 7.1 or rapidly dropping), but caution is needed as it can worsen CO₂ retention if ventilation is impaired.

Metabolic Alkalosis

• Cause: Loss of acid or bicarbonate retention, raising pH and HCO₃⁻.

• Common Causes:

  • Vomiting (prolonged) or NG suction (excessive): Loss of gastric acid.

  • Loop or thiazide diuretics: Lead to volume depletion and increased H+ excretion, HCO₃⁻ retention.

  • Hypokalemia: Shifts H+ into cells, moving HCO₃⁻ out.

  • Cushing's syndrome, hyperaldosteronism.

  • Excessive antacid intake or bicarbonate administration.

• Interventions:

  • Administer anti-emetics to control vomiting.

  • Replace electrolytes (e.g., $K^+$ and $Cl^-$) as chloride depletion can perpetuate alkalosis.

  • Administer IV fluids (e.g., 0.9% NS) to expand ECF volume and promote renal excretion of bicarbonate.

  • Discontinue causative agents (e.g., diuretics, laxatives).

  • Administer carbonic anhydrase inhibitors (e.g., acetazolamide) to promote renal bicarbonate excretion in severe cases.

Diuretics — Priority Assessment

• Monitor Blood Pressure (BP): Diuretics reduce fluid volume, which can lead to hypotension. Orthostatic hypotension is a particular concern.

• Monitor Potassium levels ($K^+$): Diuretics can significantly alter potassium balance depending on their type (loop and thiazide diuretics cause hypokalemia; potassium-sparing diuretics cause hyperkalemia).

• Perform Daily weights: Best indicator of fluid balance. A rapid weight change ($\approx 1$ kg or $2.2$ lbs) often correlates with a liter of fluid gain or loss.

• Track Input & Output (I&O): Essential to evaluate diuretic effectiveness and fluid balance. Decreased urine output despite diuretic administration could indicate renal impairment or severe dehydration.

• Assess for signs of dehydration/fluid overload: Skin turgor, mucous membranes, lung sounds (crackles for overload), edema.

• Monitor renal function tests (BUN, creatinine): Diuretics can impact kidney function.

Diuretic Types

• Loop Diuretics (e.g., furosemide (Lasix), bumetanide (Bumex)):

  • Mechanism: Inhibit reabsorption of sodium, chloride, and potassium in the thick ascending loop of Henle, leading to significant diuresis.

  • Risk: Hypokalemia (due to increased K+ excretion), hyponatremia, hypomagnesemia, hypochloremia, dehydration, ototoxicity (especially with rapid IV push), hypotension.

  • Nursing consideration: Administer in the morning to prevent nocturia, monitor electrolytes closely.

• Thiazide Diuretics (e.g., hydrochlorothiazide (HCTZ)):

  • Mechanism: Inhibit sodium and chloride reabsorption in the distal convoluted tubule. Less potent than loop diuretics.

  • Risk: Hypokalemia, hyponatremia, hypomagnesemia, hypercalcemia (unique to thiazides, as they decrease calcium excretion), hyperglycemia, hyperuricemia, dehydration, hypotension.

  • Nursing consideration: Often used for hypertension, similar electrolyte monitoring to loop diuretics.

• Potassium-sparing Diuretics (e.g., spironolactone (Aldactone), triamterene, amiloride):

  • Mechanism: Work in the collecting duct. Spironolactone is an aldosterone antagonist. Triamterene and amiloride directly block sodium channels.

  • Risk: Hyperkalemia (especially when used with ACE inhibitors, ARBs, or K+ supplements), gynecomastia (with spironolactone), dehydration, hypotension.

  • Nursing consideration: Avoid potassium supplements and foods high in potassium. Monitor K+ levels very closely.

• Osmotic Diuretics (e.g., mannitol):

  • Mechanism: Increase the osmolality of the glomerular filtrate, pulling water from the extracellular space into the renal tubules, leading to rapid diuresis.

  • Risk: Fluid and electrolyte imbalances, pulmonary edema (if fluid shifts too quickly into vasculature).

  • Nursing consideration: Used primarily to reduce intracranial pressure and intraocular pressure. Administer with an inline filter due to crystallization.

Documentation + Reporting

• Chart only what you observe or do: Focus on factual, objective information. Direct quotes from the patient can be included but should be clearly identified as such.

• Avoid subjective opinions, speculation, or judgment: Documentation must be objective and factual. For example, instead of "patient was annoying," write "patient repeatedly called for nurse with non-urgent requests." Instead of "patient was faking pain," write "patient reports pain as 8/10 on a 0-10 scale, yet is observed laughing and watching TV."

• Reminder: If it isn’t documented, it didn’t happen. This is a crucial legal principle. Thorough and accurate documentation protects the nurse, ensures continuity of care, and can be vital in legal proceedings.

• Ensure legible handwriting if not electronic.

• Timeliness of documentation is important; chart as soon as possible after an event.

• Correcting errors: Draw a single line through the error, write "error" and initial/date. Never erase or use correction fluid.

SBAR Communication Standard

• S: Situation: Concisely state the immediate problem or concern (e.g., "I'm calling about Mr. Smith in room 302, he's experiencing sudden onset of shortness of breath").

  • What is the current problem?

• B: Background: Provide pertinent patient history related to the current situation (e.g., "He's a 78-year-old post-op CABG patient day 2, with a history of COPD. His baseline oxygen saturation is 92% on 2L NC").

  • What is the relevant clinical context?

• A: Assessment: State your assessment findings of the patient's condition (e.g., "His oxygen saturation has dropped to 85% on 2L NC, respiratory rate is 28 and labored, lung sounds have new crackles bilaterally, and he appears anxious").

  • What do you think is happening? (Your clinical judgment).

• R: Recommendation: Clearly state what you think needs to be done or what you are requesting (e.g., "I recommend increasing his oxygen to 4L NC, obtaining a stat chest X-ray, and I'd like an order for a diuretic").

  • What do you need/want from the provider?

This standardized communication tool promotes clear, concise, and effective information exchange among healthcare professionals, reducing errors and improving patient safety.

Therapeutic Communication

Do’s

• Listen actively and empathetically: Pay full attention to the patient's verbal and non-verbal cues.

• Ask open-ended questions: Encourage the patient to elaborate, fostering a deeper understanding of their feelings and concerns (e.g., "Tell me more about how you're feeling," or "What are your concerns about your upcoming surgery?").

• Acknowledge patient feelings: Validate their emotions and experiences (e.g., "It sounds like you're feeling very frustrated right now," or "I can see why you would be worried").

• Provide your presence: Offer a comforting, non-judgmental presence through active listening, eye contact, and appropriate touch (if culturally acceptable and appropriate).

• Use silence appropriately: Allows the patient time to think and express themselves without feeling rushed.

• Clarify and paraphrase: Ensure mutual understanding (e.g., "So, what I hear you saying is…").

Avoid** (Non-therapeutic Communication)

• Saying "Don’t worry," "Everything will be fine," or "You shouldn’t feel that way": These are clichés, false reassurances, or dismissive statements that invalidate the patient's feelings and can block further communication.

• Asking "Why" questions: Can sound accusatory, judgmental, or put the patient on the defensive, leading to resistance (e.g., instead of "Why didn't you take your medication?", try "Can you tell me about the reasons that made it difficult to take your medication?").

• Giving unsolicited advice or telling the patient what to do: Disempowers the patient and implies the nurse knows best. Instead, help them explore their options.

• Changing the subject abruptly: Indicates disinterest or discomfort with the patient's topic, shutting down communication.

• Minimizing feelings: (e.g., "It's just a little pain").

• Using professional jargon: Can alienate the patient.

• Falsely reassuring.

• Moralizing or expressing approval/disapproval.

Lateral Violence

Definition

• Bullying or hostile, aggressive, and disruptive behavior among nursing staff at the same or similar levels in a hierarchical structure. It can be overt (e.g., verbal abuse, unfair assignments) or covert (e.g., eye-rolling, social isolation, withholding information). Also known as horizontal violence or nurse-to-nurse bullying.

Key Manifestations

• Verbal abuse: Sarcasm, criticism, gossiping, spreading rumors.

• Non-verbal behaviors: Eye-rolling, sighing, ignoring, ostracism.

• Withholding information or professional support.

• Sabotage: Setting up a colleague for failure.

• Exclusion or social isolation.

• Unfair assignments or workload distribution.

Prevention Strategies

• Encourage reporting of issues: Create a safe environment where staff feel empowered to report lateral violence without fear of retaliation. Implement clear reporting mechanisms and disciplinary actions.

• Foster teamwork and collaboration: Promote a positive work environment through team-building activities, shared goals, and recognition of collective achievements.

• Promote a just culture: Emphasize accountability while also promoting learning from errors without blame, focusing on systemic issues rather than individual fault. This helps build trust.

• Early conflict resolution techniques: Provide education and training on conflict resolution, communication skills, and assertiveness for all staff.

• Leadership accountability: Leaders must model respectful behavior, actively address incidents, and enforce policies against lateral violence.

• Education on recognizing and addressing bullying behaviors.

Dosage Calculations

Formula for Flow Rate (mL/hr)

• $\text{mL/hr} = \frac{\text{Total Volume (mL)}}{\text{Time (hr)}}$

Example Calculation

• If 1000 mL of fluid is to be administered over 8 hours:

  • $\text{mL/hr} = \frac{1000 \text{ mL}}{8 \text{ hr}} = 125 \text{ mL/hr}$

Formula for Drip Rate (gtt/min) - for gravity infusions

• $\text{gtt/min} = \frac{\text{Volume (mL)} \times \text{Drip Factor (gtt/mL)}}{\text{Time (min)}}$

Example Calculation - Drip Rate

• If 1000 mL is to be infused over 8 hours, and the tubing has a drip factor of 15 gtt/mL:

  • First, convert hours to minutes: $8 \text{ hr} \times 60 \text{ min/hr} = 480 \text{ min}$

  • Then, calculate gtt/min: $\text{gtt/min} = \frac{1000 \text{ mL} \times 15 \text{ gtt/mL}}{480 \text{ min}} = \frac{15000}{480} \approx 31.25 \text{ gtt/min}$

  • Round to the nearest whole number for practical administration: $\approx 31 \text{ gtt/min}$

Conclusion

• This comprehensive study guide provides a detailed breakdown of IV therapy, central line management, medication safety, fluid and electrolyte balance, ABG interpretation, diuretic pharmacology, and essential professional nursing skills like communication and documentation. The expanded information, including specific assessment findings, detailed interventions, underlying causes, and practical examples, aims to enable thorough preparation and enhance understanding for examinations and clinical practice.