Body fluids are organized into compartments: intracellular fluid (inside cells), extracellular fluid (outside cells) - which itself is divided into interstitial fluid (between cells) and the intravascular compartment (blood plasma).

Rationale for correct answer:

2. Intravascular fluid: Plasma is the liquid portion of blood that remains when cells are removed; it occupies the vascular (intravascular) compartment and carries proteins, clotting factors, electrolytes, nutrients, and hormones.

Rationale for incorrect answers:

1. Interstitial fluid: Interstitial fluid is the ECF that surrounds cells (fluid in tissue spaces). It is outside the blood vessels; plasma is inside the blood vessels.

3. Intracellular fluid: Intracellular fluid is the fluid inside cells (largest compartment). Plasma is extracellular and intravascular, not intracellular.

4. 40% of total body fluid: Rough approximations: total body water ≈ 60% of body weight; intracellular ≈ 2/3 of TBW, extracellular ≈ 1/3. Plasma is only a portion of the ECF (about ~5% of body weight, roughly 20–25% of the ECF), not 40% of TBW.

Take home points

• Plasma = intravascular (the fluid inside blood vessels); interstitial fluid = ECF outside vessels; intracellular = inside cells.
• Remember relative volumes: intracellular ≈ two-thirds of TBW, extracellular ≈ one-third; plasma is only a small fraction of TBW but is critical for perfusion and transport.

Transport across cell membranes occurs by several mechanisms. Some move solvent (water) and some move solutes (ions, molecules). Understanding the difference between passive processes (no ATP) and active processes (require ATP), and between movement of water versus movement of dissolved particles, is essential for predicting how cells respond to changes in their environment

Rationale for correct answer:

1. Osmosis is the passive movement of water (solvent) across a semipermeable membrane from an area of lower solute concentration (higher water concentration) to an area of higher solute concentration (lower water concentration) until equilibrium is reached.

Rationale for incorrect answers:

2. Diffusion is the passive movement of solute particles from an area of higher concentration to an area of lower concentration (down their concentration gradient). It refers to solute movement, not solvent movement specifically.

3. Active transport moves substances against their concentration gradient and requires energy (ATP) - e.g., the Na⁺/K⁺ pump. It’s not the passive movement of water from low to high solute concentration.

4. Filtration is movement of fluid and solutes across a membrane driven by hydrostatic pressure (for example, blood pressure forcing plasma across glomerular membranes). It’s pressure-driven, not osmosis.

Take home points

• Osmosis = water moves toward the higher solute concentration across a semipermeable membrane.
• Distinguish osmosis (water) from diffusion (solute) and from pressure-driven filtration or energy-dependent active transport.

Electrolytes are distributed differently between compartments and each has a “major” role: sodium predominates in the extracellular fluid and potassium predominates intracellularly. These distributions are essential for resting membrane potential, nerve and muscle function, and cardiac conduction.

Rationale for correct answer:

3. The major cation of intracellular fluid: Potassium (K⁺) is the principal positive ion inside cells and is crucial for maintaining resting membrane potential, muscle contraction, and cardiac rhythm.

Rationale for incorrect answers:

1. The chief electrolyte of extracellular fluid: Sodium (Na⁺) is the chief extracellular electrolyte/cation, not potassium.

2. The most abundant electrolyte in the body: Potassium is the major intracellular cation and, by total body content (because the intracellular compartment is large), potassium is present in large amounts

4. The chief extracellular anion: Chloride (Cl⁻) is the chief extracellular anion; potassium is a cation and is primarily intracellular.

Take home points

• Potassium is the principal intracellular cation- vital for resting membrane potential, skeletal and cardiac muscle function.
• Potassium balance is tightly regulated by the kidneys and by shifts (insulin, acid–base changes); small serum changes can produce large effect.

Accurate assessment of a patient’s fluid status is critical for safe nursing care (managing IV fluids, diuretics, heart failure, dehydration). Clinicians use multiple data points (intake/output, exam findings, labs), but some measures are more sensitive and reproducible than others.

Rationale for correct answer:

4. Daily weights (same scale, same time of day, same clothing/blanket conditions) are the most reliable and objective method to detect small changes in total body water - roughly 1 kg (2.2 lb) ≈ 1 L of fluid change.

Rationale for incorrect answers:

1. Intake and output: I&O monitoring is important, but it’s subject to recording errors, misses insensible losses (sweat, respiration), and doesn’t account for fluid shifts between compartments. It’s helpful trend data but less precise than weight.

2. Skin turgor: Skin turgor can be affected by age, nutrition, and skin elasticity; it’s a supportive physical sign but insensitive for small changes in total body fluid.

3. Complete blood count: Hematocrit/hemoglobin can reflect hemoconcentration or hemodilution but are influenced by bleeding, anemia, transfusion, and other factors; they’re not the best single indicator of fluid balance.

Take home points

• Use daily weights as the primary objective measure of fluid status; weigh at the same time each day, on the same scale, with consistent clothing/linens for accuracy.
• Combine daily weights with I&O, vital signs, exam findings, and labs for full clinical context - but trust the daily weight for detecting true net fluid gain/loss.

Calcium is essential for cardiac contractility and conduction, neuromuscular excitability, and bone metabolism. Severe hypocalcemia can produce life-threatening cardiac effects (prolonged QT, arrhythmias, decreased contractility) in addition to neuromuscular signs such as tetany and paresthesias.

Rationale for correct answer:

2. Cardiac: Calcium is critical to myocardial contraction and electrical conduction. Hypocalcemia may prolong the QT interval and predispose to dangerous arrhythmias or impaired contractility; therefore continuous cardiac monitoring and rapid correction (when indicated) are top priorities.

Rationale for incorrect answers:

1. Renal: The kidneys participate in calcium balance (via reabsorption and vitamin D activation), but immediate nursing interventions for hypocalcemia are less often renal-directed. Renal issues are important for long-term calcium management but are not the highest acute priority.

3. Gastrointestinal: GI symptoms (nausea, abdominal cramps) can occur with electrolyte disturbances, but they are not the most urgent systems to monitor for acute hypocalcemic complications.

4. Neuromuscular: Hypocalcemia commonly causes paresthesias, muscle cramps, tetany, and positive Chvostek/Trousseau signs. These are important and potentially severe (e.g., laryngospasm), but cardiac complications take precedent because they are immediately life-threatening.

Take home points

Always place a patient with significant hypocalcemia on continuous cardiac monitoring and watch for QT prolongation and arrhythmias.

Treat symptomatic/severe hypocalcemia promptly:

• IV calcium per protocols
• Correct contributing factors (low magnesium, vit D deficiency)
• Monitor IV sites and vital signs during calcium administration.

After several days without food or fluids, an older adult is at high risk for hypovolemia (dehydration). Age-related blunted thirst, comorbidities, and medications make them especially vulnerable. Classic findings reflect reduced circulating volume and compensatory sympathetic responses.

Rationale for correct answer:

2. Weak, rapid pulse: Tachycardia is a compensatory response to low stroke volume; the pulse feels weak (thready) due to reduced preload.

Rationale for incorrect answers:

1. Increased blood pressure: With decreased intravascular volume, BP typically falls (or shows orthostatic drops). Hypertension would not be expected unless there’s another cause.

3. Moist mucous membranes: Dehydration causes dry, sticky mucous membranes and often a coated tongue.

4. Jugular vein distention: Hypovolemia produces flat/collapsed neck veins; JVD suggests fluid overload or right-sided heart issues, not dehydration.

Take home points:

In dehydration, expect:

• Tachycardia
• hypotension/orthostasis
• dry mucosa
• poor skin turgor
• concentrated urine (often with ↑ BUN/Cr ratio and ↑ serum osmolality).

Prolonged nasogastric suction removes fluid and electrolytes, often causing actual fluid volume deficit and dry mucous membranes.

Rationale for correct answer:

1. Deficient Fluid Volume: Negative I&O over 2 days with GI suction results in actual hypovolemia.

3. Impaired Oral Mucous Membranes: NPO/NG suction commonly cause dry, irritated oral mucosa.

Rationale for incorrect answers:

2. Risk for Deficient Fluid Volume: “Risk for” is used when a problem hasn’t occurred yet; here the deficit is present.

4. Impaired Gas Exchange: No evidence of oxygenation/ventilation issues provided.

5. Decreased Cardiac Output: Could occur with severe hypovolemia, but no VS or perfusion findings provided.

Take home points

• Use actual vs risk correctly: negative I&O from NG suction = Deficient Fluid Volume (not “Risk for”).
• NG suction commonly causes dry oral mucosa; include oral care and humidification in the plan.

Hypokalemia, defined as a serum potassium level below 3.5 mEq/L, can result from excessive potassium loss (e.g., diuretics, GI losses) or inadequate intake. Treatment focuses on replacing potassium and addressing the underlying cause.

Rationale for correct answer:

4. “I will stop using my salt substitute.” Most salt substitutes are made with potassium chloride, which can actually help correct hypokalemia. Stopping the use of salt substitutes would decrease potassium intake and worsen hypokalemia.

Rationale for incorrect answers:

1. “I will use avocado in my salads.” Avocados are rich in potassium and are an appropriate dietary choice for someone with hypokalemia. This statement reflects correct understanding of incorporating potassium-rich foods.

2. “I will be sure to check my heart rate before I take my digoxin.” Hypokalemia increases sensitivity to digoxin, putting the client at risk for digoxin toxicity, which manifests as bradycardia, nausea, and visual disturbances. Checking the heart rate before taking digoxin is an essential safety practice.

3. “I will take my potassium in the morning after eating breakfast.” Potassium supplements can irritate the gastrointestinal tract, so they should be taken with food or after meals to reduce GI upset. Taking them in the morning after breakfast is appropriate.

Take home points

• Hypokalemia can be corrected through both dietary intake (bananas, oranges, avocados, potatoes) and supplements.
• Clients on digoxin should be carefully monitored because hypokalemia increases the risk of digoxin toxicity.

Sodium is the primary extracellular electrolyte and a major determinant of serum osmolality and fluid distribution between body compartments. Changes in sodium (either high or low) most commonly affect the central nervous system because shifts in osmolality cause neuronal swelling or shrinkage.

Rationale for correct answer:

2. Mental confusion: Sodium disturbances (both hyponatremia and hypernatremia) cause changes in neuronal cell volume and cerebral function, so altered mental status/confusion is a hallmark sign.

Rationale for incorrect answers:

1. Hyperreflexia: More typically associated with disorders that increase neuromuscular excitability (for example, hypocalcemia or hypomagnesemia). It is not a classic or specific sign of sodium imbalance.

3. Irregular pulse: Cardiac rhythm disturbances are most classically linked to potassium abnormalities (hyper- or hypokalemia). Sodium imbalance is less likely to present primarily as an irregular pulse.

4. Muscle weakness: Can occur with several electrolyte problems (notably potassium disorders). Severe hypernatremia may cause weakness, but muscle weakness is a less specific/typical sign of sodium imbalance than CNS changes like confusion.

Take home points:

• Altered mental status is the most sensitive and common clinical clue to a clinically significant sodium imbalance.
• Always check serum sodium and assess volume status when an older patient presents with new-onset confusion.
• Correct sodium disturbances carefully to avoid rapid shifts.
• Risk of central pontine myelinolysis with overly rapid correction of chronic hyponatremia.

Excess Fluid Volume (fluid overload) occurs when there is too much fluid in the intravascular and/or interstitial spaces. Common causes include excessive IV fluid administration, heart failure, renal failure, and conditions that increase fluid retention.

Rationale for correct answer:

3. Excessive IV infusion: Administering IV fluids too rapidly or in inappropriate amounts is a common iatrogenic cause of fluid volume excess, especially in patients with impaired cardiac or renal function who cannot handle the added load.

Rationale for incorrect answers:

1. Increased need for fluids secondary to fever: Fever increases insensible losses and fluid need; if anything, fever predisposes to deficit, not excess.

2. Abnormal fluid loss from vomiting: Vomiting causes fluid loss and dehydration, not excess volume.

4. Decreased fluid intake secondary to depression: Decreased intake produces deficit, not excess.

Take home points

• The most preventable cause of excess fluid volume in hospitalized patients is excessive IV infusion (rate or volume).
• Always verify orders, titrate carefully, and consider patient comorbidities (HF, renal failure).
• Monitor for early signs of fluid overload: daily weights, I&O, peripheral edema, crackles on lung auscultation, increased JVD, rising BP - intervene early to prevent pulmonary edema.

In acid-base pattern recognition use ROME: Respiratory Opposite (pH and PaCO₂ move opposite), Metabolic Equal (pH and HCO₃⁻ move together). Respiratory acidosis = low pH, high PaCO₂ (with normal/high HCO₃⁻ if compensation).

Rationale for correct answer:

2. pH 7.32; PaCO₂ 46; HCO₃⁻ 24: Respiratory acidosis (acute): low pH with elevated PaCO₂; HCO₃⁻ normal (no or minimal compensation).

Rationale for incorrect answers:

1. pH 7.54; PaCO₂ 28; HCO₃⁻ 22: Respiratory alkalosis (high pH, low PaCO₂).

3. pH 7.31; PaCO₂ 35; HCO₃⁻ 20: Metabolic acidosis: low pH with low HCO₃⁻; PaCO₂ not elevated.

4. pH 7.50; PaCO₂ 37; HCO₃⁻ 28: Metabolic alkalosis: high pH with elevated HCO₃⁻ and near-normal PaCO₂.

Take home points:

• Respiratory acidosis = ↓pH with ↑PaCO₂; think hypoventilation.
• Use ROME: Respiratory (Opposite), Metabolic (Equal); check pH first, then PaCO₂/HCO₃⁻ to classify and assess compensation.

Arterial blood gas interpretation uses three key values: pH (acidemia vs alkalemia), PaCO₂ (respiratory component- high CO₂- respiratory acidosis), and HCO₃⁻ (metabolic component- low HCO₃⁻ -metabolic acidosis).

Rationale for correct answer:

2. Respiratory acidosis: The pH is acidic and PaCO₂ is markedly elevated (58 mmHg - hypoventilation), indicating a primary respiratory acidosis. The HCO₃⁻ is elevated, reflecting renal (metabolic) compensation.

Rationale for incorrect answers:

1. Metabolic acidosis: In metabolic acidosis you would expect low HCO₃⁻ (not high). Here HCO₃⁻ is elevated, so metabolic acidosis is not the primary problem.

3. Metabolic alkalosis: Would present with an elevated pH and elevated HCO₃⁻. Here pH is low, so not metabolic alkalosis.

4. Respiratory alkalosis: Would present with low PaCO₂ and alkalemia (high pH). This ABG shows the opposite (high PaCO₂ and acidemia), so it’s not respiratory alkalosis.

Take home points:

• Interpret ABGs in order: pH → PaCO₂ → HCO₃⁻. If pH is acidotic and PaCO₂ is high, the primary process is respiratory acidosis.
• Respiratory acidosis results from hypoventilation (e.g., COPD exacerbation, respiratory depression from drugs, neuromuscular failure).
• Treatment focuses on improving ventilation and addressing the underlying cause; monitor for compensation and oxygenation.

Arterial blood gas (ABG) interpretation is a core nursing skill for assessing acid-base balance.

Rationale for correct answer:

3. Metabolic acidosis: Low pH (acidemia) with low HCO₃⁻ = metabolic acidosis. PaCO₂ is normal, so there’s no respiratory compensation yet.

Rationale for incorrect answers:

1. Respiratory acidosis: Would show low pH with high PaCO₂. Here PaCO₂ is normal, so not respiratory acidosis.

2. Respiratory alkalosis: Would show high pH with low PaCO₂. Here the pH is low and HCO₃⁻ is abnormal, so not respiratory alkalosis.

4. Metabolic alkalosis: Would show high pH and high HCO₃⁻, which is the opposite of this ABG.

Take home points

• Always check whether PaCO₂ and HCO₃⁻ are moving in the same or opposite direction as the pH to identify the primary disturbance.

Acid-base balance is maintained mainly by the lungs (regulate carbonic acid via CO₂ exhalation) and the kidneys (regulate bicarbonate via HCO₃⁻ reabsorption/production).

Rationale for correct answer:

2. Lungs: The lungs control CO₂ elimination (CO₂ + H₂O ↔ H₂CO₃). Impaired ventilation or lung damage prevents effective removal of CO₂, altering the carbonic acid component and causing respiratory acid–base disturbances.

Rationale for incorrect answers:

1. Kidneys regulate the metabolic component (bicarbonate HCO₃⁻) and excrete or retain H⁺ and HCO₃⁻; they do not directly control CO₂ (carbonic acid) removal.

3. Adrenal glands influence electrolyte and volume status (aldosterone) and can indirectly affect acid–base balance, but they are not the primary controllers of carbonic acid/CO₂.

4. Blood vessels transport gases and acids but do not control CO₂ elimination; impaired vasculature alone would not be described as inability to control carbonic acid supply.

Take home points

• The lungs regulate the respiratory/CO₂ (carbonic acid) component of acid–base balance; impaired ventilation → respiratory acidosis (CO₂ retention) or alkalosis (hyperventilation).
• When ABGs show an abnormal CO₂ (PaCO₂) causing pH changes, think lung (respiratory) pathology first; when HCO₃⁻ is primary abnormality, think kidney (metabolic) causes.

Infiltration occurs when IV fluid leaks from the vein into the surrounding tissues. It produces local changes at the site (temperature, color, swelling, pain, flow changes) that help you distinguish it from other IV complications (phlebitis, infection, occlusion).

Rationale for correct answer:

4. The site is pale, cool, swollen, and painful: Infiltration typically causes pallor, coolness at the site (because fluid is in tissue, not in blood flow), swelling, and sometimes pain or discomfort.

Rationale for incorrect answers:

1. In the past hour, only 50 mL of fluid has infused: Slow or reduced infusion rate is nonspecific - could indicate an occlusion, a kinking of the tubing, an air or pressure issue, or infiltration, but by itself it is not the most characteristic sign of infiltration.

2. The insertion site is red, hot, and swollen: Redness and warmth are classic for phlebitis (inflammation of the vein) or local infection, not infiltration. Phlebitis tends to be tender along the course of the vein.

3. The patient’s temperature has risen to 101°F (38.3°C). A fever suggests systemic infection or catheter-related bacteremia - a serious sign but not the characteristic local finding of infiltration.

Take-home points

Inspect and palpate IV sites frequently; look for pallor, coolness, swelling, and pain - these are classic for infiltration.

If infiltration is suspected:

• stop the infusion
• remove the cannula
• elevate the extremity
• follow facility protocol for management and documentation (and notify provider if vesicant or large volume).

In hypovolemia and electrolyte loss (especially potassium) from GI losses, first actions should stabilize circulation and create access for rapid treatment and labs.

Rationale for correct answer:

1. Start an IV: Establishes access for rapid fluid resuscitation and lab draws, addressing immediate circulation risk and enabling antiemetics/electrolytes to be given IV.

Rationale for incorrect answers:

2. Review the results of serum electrolytes: Results aren’t available yet; delaying access/treatment for labs risks worsening hypovolemia. Draw labs after IV access is obtained.

3. Offer the woman foods high in sodium and potassium: Not appropriate in an actively vomiting, lethargic patient; risk of aspiration and likely intolerance. Electrolytes should be replaced parenterally initially.

4. Administer an antiemetic: Helpful, but you need IV access to give it promptly and fluids are the higher priority for stabilization.

Take home points

• In hypovolemia, think ABCs → IV access → fluids → labs/meds.
• GI losses often cause volume depletion and electrolyte deficits; correct both, but stabilize circulation first.

Magnesium is an important intracellular cation involved in neuromuscular function, cardiac conduction, and many enzymatic reactions. Hypomagnesemia commonly results from inadequate intake, gastrointestinal losses (vomiting, diarrhea, prolonged nasogastric suction), malabsorption, chronic alcoholism, and some critical illnesses (including pancreatitis).

Rationale for correct answer:

2. A client with pancreatitis: Both acute and chronic pancreatitis are associated with magnesium depletion (malabsorption in chronic disease; saponification of cations in necrotic fat in acute pancreatitis), so patients with pancreatitis are at risk for hypomagnesemia.

4. A client with excessive nasogastric drainage: Prolonged NG suctioning or other GI losses (vomiting, diarrhea) can cause significant magnesium depletion.

5. A client with chronic alcoholism: Chronic alcohol use is one of the most common causes of hypomagnesemia because of poor intake, GI losses, and increased renal excretion.

Rationale for incorrect answers:

1. A client with renal failure: Not typically associated with hypomagnesemia. Renal failure usually decreases magnesium excretion and therefore predisposes to hypermagnesemia, not hypomagnesemia, unless the patient has other complicating factors.

3. A client taking magnesium-containing antacids: Magnesium-containing antacids tend to increase magnesium load (and can cause hypermagnesemia, especially if renal function is impaired). They are not a classic cause of hypomagnesemia.

Take home points:

• Recognize common risk settings for hypomagnesemia.
• Suspect low magnesium when neuromuscular irritability, refractory hypokalemia, or cardiac arrhythmias occur.
• Monitor electrolytes (Mg²⁺, K⁺, Ca²⁺), ECG, and replace magnesium per protocol.

Adequate hydration supports renal function, tissue perfusion, and homeostasis. Nurses play a key role in promoting fluid intake, especially for clients at risk of dehydration. The most effective interventions are practical, patient-centered strategies that increase actual fluid consumption, rather than abstract teaching.

Rationale for correct answer:

2. Keeping fluids readily available for the patient: Accessibility is the most effective measure because it promotes actual drinking behavior. Fluids placed within reach make adherence easier.

Rationale for incorrect answers:

1.Explaining the mechanisms involved in transporting fluids: This provides knowledge but doesn’t directly improve fluid intake. Education alone may not translate into behavior.

3. Emphasizing long-term outcomes: Future benefits may not motivate immediate intake. Patients are more likely to respond to short-term, practical actions.

4. Planning to offer most fluids in the evening: Ineffective and potentially problematic. Concentrating fluids late in the day increases nocturia and risk of disturbed sleep/falls, especially in older adults.

Take home points

• The best nursing interventions are often the simplest: keep fluids within reach, offer them frequently, and individualize to patient preference.
• Avoid strategies that increase nighttime urination (like giving most fluids in the evening), especially for older patients at fall risk.

Central venous catheters come in several types (nontunneled short-term CVCs, tunneled CVCs, implanted ports, PICCs, femoral lines) and are used for central venous access for fluids, medications, hemodynamic monitoring, and blood draws.

Rationale for correct answer:

4.A chest radiograph is required to confirm placement: After placement via the internal jugular or subclavian approach, a chest x-ray is required to confirm the catheter tip position (usually at the lower SVC) and to rule out immediate complications such as pneumothorax.

Rationale for incorrect answers:

1. This catheter usually remains in place for 2 to 3 months: Nontunneled percutaneous central lines are short‑term (usually days to a few weeks). Longer-term central access (months) is achieved with tunneled catheters or implanted ports/PICCs.

2. The catheter is introduced via the basilic or cephalic veins in the antecubital space: Basilic/cephalic antecubital veins are used for peripheral IVs or PICC insertion. Nontunneled CVCs are typically inserted into central veins (internal jugular, subclavian, or sometimes femoral).

3. Nursing responsibility includes accessing the catheter with an angled needle: Accessing with an angled (Huber) needle is how implanted ports are accessed. Nontunneled CVCs have external lumens and are accessed directly.

Take-home points

• After percutaneous central line placement, always confirm tip location and exclude pneumothorax with a chest x-ray before using the line.
• Know which device you’re dealing with: different insertion sites, expected dwell times, and access/maintenance procedures.

The lungs regulate the respiratory component of acid–base balance by changing CO₂ elimination. Hyperventilation lowers PaCO₂ and causes a respiratory alkalosis; hypoventilation raises PaCO₂ and causes respiratory acidosis.

Rationale for correct answer:

2. Respiratory alkalosis (carbonic acid deficit): Respiratory alkalosis results from excessive ventilation (blowing off CO₂). Slowing the breathing rate raises PaCO₂ toward normal and helps correct the alkalosis (for example, in anxiety-driven hyperventilation).

Rationale for incorrect answers:

1. Respiratory acidosis (carbonic acid excess): This condition is caused by CO₂ retention (hypoventilation). Asking the patient to breathe more slowly would further increase PaCO₂ and worsen the acidosis.

3. Metabolic acidosis (bicarbonate deficit): In metabolic acidosis the body compensates by increasing ventilation to blow off CO₂ (Kussmaul respirations when severe). Instructing slower breathing would reduce compensation and worsen acidemia.

4. Metabolic alkalosis (bicarbonate excess): Although retaining CO₂ (by breathing more slowly) can provide some respiratory compensation for metabolic alkalosis, this is not the typical or primary nursing intervention to treat metabolic alkalosis. T

Take home points

• Slow, controlled breathing is an effective immediate intervention for respiratory alkalosis caused by hyperventilation (e.g., panic/anxiety).
• For metabolic disturbances, encourage or treat the underlying cause - respiratory pattern changes are compensatory, not primary treatment.

Hyperkalemia (high serum potassium) can cause life-threatening cardiac arrhythmias. Dietary management means avoiding high-potassium foods and potassium-containing salt substitutes, and reviewing medications that raise potassium.

Rationale for correct answer:

3. Bananas and apricots (especially dried apricots), oranges, potatoes, tomatoes, beans, and certain dairy and dried fruits are among the highest dietary sources of potassium and are commonly recommended to limit in hyperkalemia.

Rationale for incorrect answers:

1. Carrots and squash: These contain potassium but are generally moderate sources compared with fruits like bananas and many dried fruits. They are not the classic foods singled out as the highest-risk items.

2. Canned soups and potato chips: These are typically high in sodium, not the highest potassium sources. They may be unhealthy for other reasons (HTN, fluid retention) but are not the prototypical high-K foods to avoid first.

4. Whole-grain cereals and milk: Milk contains potassium (moderate amount) and some cereals contain potassium, but these are generally not as concentrated as bananas/dried fruits/potatoes.

Take home points

• Teach patients at risk for hyperkalemia to avoid obvious high-potassium foods and to not use potassium-based salt substitutes.
• Review medications and kidney function as part of hyperkalemia prevention.
• Always advise checking serum K and ECG if symptoms (weakness, palpitations) occur - and refer to a dietitian for individualized meal planning.

When initiating IV therapy in an emergency or multisystem trauma, choose a site that allows rapid, reliable access (large, proximal veins) in an unaffected extremity.

Rationale for correct answer:

1. Left antecubital: The antecubital fossa contains large superficial veins (e.g., median cubital, cephalic) that are easy to cannulate and allow rapid infusion - ideal in trauma when fast fluid/medication administration may be needed.

Rationale for incorrect answers:

2. Dorsal aspect of either foot: Foot veins are generally avoided in adults unless no upper-extremity sites are available (higher risk of thrombosis and slower flow). In trauma, you prefer a proximal upper-extremity site first.

3. Right hand: The right arm has a cast; avoid inserting an IV into or distal to a cast because of impaired circulation, risk of infection, and difficulty assessing the site.

4. Left forearm: The left forearm could be used, but the antecubital site provides larger, more proximal veins appropriate for rapid resuscitation- making the left antecubital more appropriate in a multisystem trauma situation.

Take home points

• For emergency IV access in trauma, pick a large, proximal vein in an uninjured limb (antecubital fossa is excellent for rapid infusion).
• Avoid IV insertion through or distal to casts, injured limbs, or areas of poor circulation; reserve foot veins for when no suitable arm veins exist.

Nursing care for IV therapy focuses on maintaining patency and safety (correct rate, preventing infection and infiltration, accurate delivery of ordered fluids/medications).

Rationale for correct answer:

4. Monitoring the flow rate at least every hour: Regular monitoring ensures the ordered infusion rate is being delivered, helps detect occlusions, infiltration, or pump failures early, and allows timely corrective action.

Rationale for incorrect answers:

1. Changing the IV catheter and entry site daily: Routine daily removal/reinsertion is unnecessary and may increase patient discomfort and infection risk.

2. Changing the tubing every 8 hours: Tubing change intervals are set by facility/infection-control guidelines and are usually less frequent than every 8 hours for standard continuous infusions.

3. Increasing the rate to catch up if the correct amount has not been infused at the end of the shift: You should not speed an infusion without a new order- that risks fluid overload or incorrect medication dosing. Instead, notify the provider and document reasons for the delay.

Take home points

• Routinely assess the IV site and infusion (flow rate, pump alarms, tubing, site condition) - hourly checks are a safe, practical standard in many settings.
• Never alter an infusion rate to "catch up" without provider authorization; follow facility protocols for catheter/tubing changes and for troubleshooting delayed/occluded infusions.

Transfusion reactions are most likely to occur early in the transfusion (especially within the first 15 minutes). Nursing practice is to obtain baseline vitals, begin the transfusion slowly for the first few minutes, and reassess the patient shortly after starting so that acute reactions are identified and treated immediately.

Rationale for correct answer:

1. 15 minutes after the infusion is started: Most acute hemolytic and allergic transfusion reactions occur within the first 15 minutes. Standard practice is baseline vitals then start transfusion slowly then reassess the patient (vitals, symptoms) at 15 minutes.

Rationale for incorrect answers:

2. After the blood is all infused: Waiting until the end risks missing a severe early reaction; if a reaction occurs during the transfusion it can be life-threatening and requires immediate action.

3. Every hour: Hourly checks may be done after the initial period in some settings, but they are not sufficient to catch the most dangerous early reactions.

4. Every 15 minutes: Although frequent monitoring is good, the exam-focused, high-yield timing is the initial 15-minute check (and then regularly per protocol).

Take home points

Always obtain baseline vitals before a transfusion and reassess the patient about 15 minutes after starting - this is when acute reactions most commonly appear.

If a transfusion reaction is suspected:

• stop the transfusion immediately
• keep the IV patent with normal saline (new tubing)
• notify the provider and blood bank
• return the blood product per policy
• obtain required specimens (blood/urine) and documentation.

When an infusion pump is set correctly but the actual infusion is slower than ordered, the problem is usually mechanical (tubing, clamps, kinks, position) or related to the catheter/vein (infiltration, occlusion). A systematic site-to-device check prevents delays and complications.

Rationale for correct answer:

1.Infiltration at VAD site; If the catheter tip or cannula has dislodged from the vein and fluid is going into the tissue, effective intravascular flow is reduced and the pump may deliver more slowly (or meet backpressure).

2. Patient lying on tubing: External compression of the tubing (patient lying on it) creates partial or complete occlusion and will slow or stop flow.

4. Tubing kinked in bedrails: A kink in the tubing increases resistance or occludes the line and will slow or stop flow.

Rationale for incorrect answers:

3. Roller clamp wide open: If the roller clamp is wide open, it would increase flow (unless something else is blocking the line). A wide-open clamp is not a cause of slowing.

5. Circulatory overload is a patient physiologic condition (too much fluid in the circulation) and would not mechanically cause the pump to run slow.

Take home points

If a pump is set correctly but infusion is slow, do a quick systematic check:

• inspect the site (for infiltration)
• follow the tubing (kinks, clamps, compression)
• check connections and pump alarms before touching infusion rates.

Local signs at a vascular access device (VAD) site - pain, redness, swelling, warmth - suggest phlebitis, infiltration, or local infection. The nurse’s first action must protect the patient from further harm by stopping the source of the problem and preventing additional infusion into a compromised tissue/vein.

Rationale for correct answer:

4. Discontinue the IV infusion: If the site shows signs of a complication, stop the infusion immediately to prevent further tissue injury or introduction of infected/irritating fluid.

Rationale for incorrect answers:

1. Apply a warm, moist compress: This is an appropriate treatment for phlebitis (after stopping the infusion) because it helps decrease inflammation and discomfort, but it is not the first action. You must first stop the infusion.

2. Aspirate the infusing fluid from the VAD: Aspirating the line is not the immediate priority and is not a standard first step for suspected phlebitis or local infection. Removing the IV and stopping the infusion comes first.

3. Report the situation to the health care provider: Reporting is important, but only after you’ve secured the patient (stopped the infusion and removed the catheter if indicated). Immediate safety actions come before notification.

Take-home points

• When a VAD site looks inflamed or painful, stop the infusion first - patient safety and preventing further harm are the priority.
• After stopping the infusion, follow protocol: remove the catheter if indicated, apply appropriate local measures

Accurate intake and output (I&O) measurement depends on standardized rules for counting foods and liquids that change volume (e.g., ice). Because ice is solid water and melts, most institutions require converting ice-chip volume to the equivalent liquid volume for accurate fluid balance.

Rationale for correct answer:

2.One-half of the volume: The usual convention is to record ice chips as 50% of their measured volume because they occupy more space as solid ice than as liquid water once melted (and because some may be lost as condensation or melting).

Rationale for incorrect answers:

1.Two-thirds of the volume: This is not the standard conversion used in clinical practice.

3. One-quarter of the volume: This underestimates intake and is not the standard conversion.

4. Two times the volume: This would grossly overestimate fluid intake.

Take-home points

• Use facility policy, but the common rule is: record ice chips as one-half of the measured volume when doing I&O.
• Be consistent: measure and document I&O the same way each shift.

Read ABGs in the order: pH → PaCO₂ → HCO₃⁻. If pH is acidotic (<7.35) determine whether the respiratory (PaCO₂) or metabolic (HCO₃⁻) component explains the change. Also note whether compensation is present (the opposing system moves toward correction).

Rationale for correct answer:

3. Respiratory acidosis: pH is low and PaCO₂ is elevated (CO₂ retention- carbonic acid excess). HCO₃⁻ is normal, suggesting an acute (or early) respiratory acidosis without renal compensation.

Rationale for incorrect answers:

1.Metabolic acidosis: Metabolic acidosis would show decreased HCO₃⁻ (usually <22). Here HCO₃⁻ is normal (24).

2. Metabolic alkalosis: That would be alkalemia (pH >7.45) with increased HCO₃⁻.

4. Respiratory alkalosis: Respiratory alkalosis would have low PaCO₂ and high pH.

Take home points

• pH ↓ with PaCO₂ ↑ = respiratory acidosis (impaired ventilation/CO₂ retention).
• Normal HCO₃⁻ with an abnormal PaCO₂ suggests acute respiratory disturbance; kidneys haven’t yet compensated.

IV potassium can rapidly alter serum K⁺ and cardiac conduction; it is contraindicated if renal excretion is inadequate or if serum K⁺ is already high. Nursing pre-checks focus on confirming need and safety (serum level, urine output, IV patency, ECG when indicated).

Rationale for correct answer:

1.Urine output: Adequate urine output (commonly ≥30 mL/hr in adults, or ~0.5 mL/kg/hr) is essential because kidneys excrete potassium; impaired output increases risk of hyperkalemia.

4. Serum potassium laboratory value in EHR: Always check the most recent serum K⁺ before administering IV K⁺ to avoid giving potassium to someone already hyperkalemic.

Rationale for incorrect answers:

2. ABGs assess gas exchange/acid–base status, not directly required before giving routine IV potassium. ABGs are not a standard pre-check for potassium administration.

3. Fullness of neck veins: Jugular venous distention relates to fluid volume/venous pressure, not directly to potassium handling; it’s not a standard pre-assessment for IV potassium.

5. Level of consciousness: Altered LOC can be important clinically, but it’s not a standard prerequisite assessment specifically for safely hanging K⁺. (Cardiac rhythm/ECG is the important additional check if potassium is elevated or if the patient is symptomatic.)

Take-home points

• Always verify a recent serum K⁺ and ensure the patient has adequate urine output before starting IV potassium.
• IV potassium must never be given IV push; infuse per protocol/rate limits, monitor ECG for dysrhythmias, and recheck labs as ordered.

Calculate infusion rate as: total volume ÷ total time= mL per hour. Use the infusion pump to program that rate and recheck calculations.

Order: 500 mL 0.9% NaCl IV over 4 hours.

500 mL ÷ 4 hr = 125 mL/hr.

Correct answer: 125 mL/hr

Take home points

• Use volume ÷ time to calculate mL/hr and program the pump accordingly.
• Always double-check calculations, verify the order and the pump setting, ensure IV patency