Acute kidney injury and dialysis questions test fluid balance, electrolyte emergencies, and access-site safety in one package. The NCLEX expects you to classify AKI as prerenal, intrarenal, or postrenal from the clinical picture, track the phases from oliguria through diuresis to recovery, and treat hyperkalemia as the lethal complication it is. Dialysis content centers on hemodialysis access protection — the fistula arm is off-limits to blood pressure cuffs, venipuncture, and IV lines — and on recognizing complications like disequilibrium syndrome and peritonitis. These questions reward nurses who connect a lab value to an immediate action rather than a routine one.
Quick Study Tips
Classify AKI first: perfusion problem, kidney damage, or obstruction.
Oliguria is under 400 mL/day — trend output, not single readings.
Hyperkalemia sequence: calcium gluconate, insulin/dextrose, then removal.
Thrill and bruit every shift; nothing by cuff, needle, or IV in the fistula arm.
Cloudy peritoneal dialysis effluent means peritonitis until proven otherwise.
Practice Quiz: Acute Kidney Injury & Dialysis NCLEX Questions
Answer these exam-style questions to test your knowledge. Detailed rationales are shown after each answer.
Prerenal AKI results from decreased renal perfusion — hypovolemia, heart failure, sepsis — and the kidney itself is undamaged, so restoring perfusion reverses it. Intrarenal AKI reflects direct parenchymal damage from nephrotoxins (aminoglycosides, contrast dye, NSAIDs), prolonged ischemia, or rhabdomyolysis. Postrenal AKI comes from obstruction below the kidneys — an enlarged prostate, stones, or a blocked catheter — and the priority is relieving the obstruction, sometimes as simply as flushing or replacing a kinked Foley. The NCLEX tests classification through BUN-to-creatinine ratios and history clues: a ratio above 20:1 suggests prerenal, while a recent CT with contrast or a new aminoglycoside points intrarenal. Oliguria (urine output under 400 mL/day) is the hallmark early finding, and daily weights plus strict intake and output guide every decision.
Hyperkalemia: The Lethal Complication
Potassium rises when the kidneys fail, and hyperkalemia is the most dangerous electrolyte emergency in AKI because it causes fatal dysrhythmias. Watch for peaked T waves, widened QRS complexes, muscle weakness, and paresthesias. The treatment sequence is tested in order: IV calcium gluconate first to stabilize the cardiac membrane (it does not lower potassium), then insulin with dextrose and possibly sodium bicarbonate to shift potassium into cells, then potassium-removing agents or dialysis to eliminate it. Dietary teaching restricts high-potassium foods — bananas, oranges, potatoes, tomatoes — and salt substitutes, which are potassium chloride. A client in the diuretic phase flips the risk: massive urine output can cause hypokalemia, hypotension, and dehydration, so fluid and electrolyte replacement becomes the priority instead.
Hemodialysis and Peritoneal Dialysis Safety
For hemodialysis, the arteriovenous fistula or graft is a lifeline: palpate for a thrill and auscultate for a bruit every shift, and never take blood pressure, draw blood, or start an IV in that arm. Post-dialysis, monitor for hypotension from rapid fluid removal and for disequilibrium syndrome — headache, nausea, confusion from rapid shifts in urea and osmolality — which is managed by slowing or stopping the treatment. Hold morning antihypertensives before dialysis as ordered to prevent intradialytic hypotension. For peritoneal dialysis, the outflow should be clear and pale yellow; cloudy effluent signals peritonitis, the most serious complication, and requires culture and antibiotics. Weigh the client daily, compare dialysate outflow to inflow (outflow should exceed inflow), and keep the exchange sterile throughout. Dietary teaching for chronic kidney disease restricts potassium, phosphorus, and sodium, with protein adjusted to the treatment plan.
Review each question with its correct answer and a rationale for every choice.
1. A client on metoclopramide reports restlessness and involuntary tongue movements. The nurse should…
A. Give the next dose with foodGiving metoclopramide with food does not mitigate or prevent the development of extrapyramidal symptoms, such as restlessness and involuntary tongue movements, which are neurological side effects. Food primarily affects gastric absorption and can sometimes reduce gastrointestinal upset, but it does not alter the drug's dopamine receptor blocking action in the central nervous system that leads to these adverse effects. Therefore, this action does not address the underlying cause of the client's symptoms and is an inappropriate intervention for neurological complications.
B. Encourage fluids and reassess in an hourEncouraging fluids and reassessing in an hour does not address the immediate and potentially serious nature of the client's symptoms, which are indicative of a drug-induced neurological reaction. Restlessness and involuntary tongue movements, particularly in the context of metoclopramide use, suggest extrapyramidal symptoms, specifically akathisia (restlessness) and tardive dyskinesia-like movements (involuntary tongue movements). These symptoms require immediate medical evaluation, as they can worsen or become permanent if the offending drug is continued, and merely increasing fluids will not resolve them.
C. Hold the drug and notify the providerRestlessness (akathisia) and involuntary tongue movements are classic signs of extrapyramidal symptoms (EPS), specifically tardive dyskinesia or acute dystonic reactions, which are serious adverse effects of metoclopramide due to its dopamine receptor blocking properties in the central nervous system. Continuing the drug can worsen these symptoms or even make them irreversible. Therefore, the nurse's priority is to immediately hold the medication to prevent further neurological damage and promptly notify the healthcare provider for assessment and potential intervention, such as prescribing an anticholinergic medication to counteract the EPS.
D. Document as an expected effectDocumenting restlessness and involuntary tongue movements as an expected effect of metoclopramide is inaccurate and potentially dangerous. While metoclopramide is known to cause extrapyramidal symptoms, these are serious adverse drug reactions, not benign or "expected" side effects that can be ignored. Failure to recognize and act upon these symptoms can lead to significant patient harm, including permanent neurological dysfunction like tardive dyskinesia, and is a breach of nursing responsibility to ensure patient safety and advocate for appropriate medical intervention.
Correct answer: C. Option A: Giving metoclopramide with food does not mitigate or prevent the development of extrapyramidal symptoms, such as restlessness and involuntary tongue movements, which are neurological side effects. Food primarily affects gastric absorption and can sometimes reduce gastrointestinal upset, but it does not alter the drug's dopamine receptor blocking action in the central nervous system that leads to these adverse effects. Therefore, this action does not address the underlying cause of the client's symptoms and is an inappropriate intervention for neurological complications.
Option B: Encouraging fluids and reassessing in an hour does not address the immediate and potentially serious nature of the client's symptoms, which are indicative of a drug-induced neurological reaction. Restlessness and involuntary tongue movements, particularly in the context of metoclopramide use, suggest extrapyramidal symptoms, specifically akathisia (restlessness) and tardive dyskinesia-like movements (involuntary tongue movements). These symptoms require immediate medical evaluation, as they can worsen or become permanent if the offending drug is continued, and merely increasing fluids will not resolve them.
Option C: Restlessness (akathisia) and involuntary tongue movements are classic signs of extrapyramidal symptoms (EPS), specifically tardive dyskinesia or acute dystonic reactions, which are serious adverse effects of metoclopramide due to its dopamine receptor blocking properties in the central nervous system. Continuing the drug can worsen these symptoms or even make them irreversible. Therefore, the nurse's priority is to immediately hold the medication to prevent further neurological damage and promptly notify the healthcare provider for assessment and potential intervention, such as prescribing an anticholinergic medication to counteract the EPS.
Option D: Documenting restlessness and involuntary tongue movements as an expected effect of metoclopramide is inaccurate and potentially dangerous. While metoclopramide is known to cause extrapyramidal symptoms, these are serious adverse drug reactions, not benign or "expected" side effects that can be ignored. Failure to recognize and act upon these symptoms can lead to significant patient harm, including permanent neurological dysfunction like tardive dyskinesia, and is a breach of nursing responsibility to ensure patient safety and advocate for appropriate medical intervention.
A. Metabolic acidosisMetabolic acidosis is characterized by a low pH, a low bicarbonate (HCO₃⁻) level (typically below 22 mEq/L), and a normal or compensatory decrease in PaCO₂. In this scenario, while the pH is low (acidic), the bicarbonate level is within the normal range (22-26 mEq/L), indicating that the primary problem is not a deficit of bicarbonate. Therefore, the imbalance is not primarily metabolic in origin, making this option incorrect.
B. Respiratory acidosisRespiratory acidosis is diagnosed by a low pH (acidemia) and an elevated partial pressure of carbon dioxide (PaCO₂), typically above 45 mmHg, which reflects inadequate alveolar ventilation and CO₂ retention. The given ABG values show a pH of 7.28 (acidic) and a PaCO₂ of 62 mmHg (significantly elevated), directly correlating with respiratory acid buildup in the blood. The HCO₃⁻ of 26 mEq/L is within the normal range, indicating that the kidneys have not yet had sufficient time to compensate or are not the primary cause of the acidosis, thus confirming a primary respiratory issue.
C. Respiratory alkalosisRespiratory alkalosis occurs when there is a high pH (alkalemia) and a low PaCO₂ (below 35 mmHg), which results from hyperventilation causing excessive CO₂ elimination. The provided ABG values demonstrate a low pH (acidic) and a high PaCO₂ (acidic), directly contradicting the definition of respiratory alkalosis. This client is retaining CO₂, not blowing it off, making this option inconsistent with the clinical picture.
D. Metabolic alkalosisMetabolic alkalosis is characterized by a high pH (alkalemia) and an elevated bicarbonate (HCO₃⁻) level (above 26 mEq/L), often accompanied by a compensatory increase in PaCO₂. In this client's ABG, the pH is low (acidic), not high, and the bicarbonate level is within the normal range. These findings rule out metabolic alkalosis as the primary acid-base disturbance.
Correct answer: B. Option A: Metabolic acidosis is characterized by a low pH, a low bicarbonate (HCO₃⁻) level (typically below 22 mEq/L), and a normal or compensatory decrease in PaCO₂. In this scenario, while the pH is low (acidic), the bicarbonate level is within the normal range (22-26 mEq/L), indicating that the primary problem is not a deficit of bicarbonate. Therefore, the imbalance is not primarily metabolic in origin, making this option incorrect.
Option B: Respiratory acidosis is diagnosed by a low pH (acidemia) and an elevated partial pressure of carbon dioxide (PaCO₂), typically above 45 mmHg, which reflects inadequate alveolar ventilation and CO₂ retention. The given ABG values show a pH of 7.28 (acidic) and a PaCO₂ of 62 mmHg (significantly elevated), directly correlating with respiratory acid buildup in the blood. The HCO₃⁻ of 26 mEq/L is within the normal range, indicating that the kidneys have not yet had sufficient time to compensate or are not the primary cause of the acidosis, thus confirming a primary respiratory issue.
Option C: Respiratory alkalosis occurs when there is a high pH (alkalemia) and a low PaCO₂ (below 35 mmHg), which results from hyperventilation causing excessive CO₂ elimination. The provided ABG values demonstrate a low pH (acidic) and a high PaCO₂ (acidic), directly contradicting the definition of respiratory alkalosis. This client is retaining CO₂, not blowing it off, making this option inconsistent with the clinical picture.
Option D: Metabolic alkalosis is characterized by a high pH (alkalemia) and an elevated bicarbonate (HCO₃⁻) level (above 26 mEq/L), often accompanied by a compensatory increase in PaCO₂. In this client's ABG, the pH is low (acidic), not high, and the bicarbonate level is within the normal range. These findings rule out metabolic alkalosis as the primary acid-base disturbance.
3. Three days of vomiting and NG suction. Which ABG does the nurse expect?
A. pH 7.50, HCO₃⁻ 32The prolonged vomiting and nasogastric (NG) suction lead to a significant loss of hydrochloric acid (HCl) from the stomach. The kidneys compensate by retaining bicarbonate and excreting hydrogen ions, resulting in an excess of bicarbonate in the blood. A pH of 7.50 indicates alkalosis, and a bicarbonate (HCO₃⁻) level of 32 mEq/L (normal range 22-26 mEq/L) is elevated, confirming a metabolic component. This clinical picture is consistent with metabolic alkalosis, which is the expected acid-base imbalance in a client experiencing significant gastric fluid loss.
B. pH 7.30, HCO₃⁻ 16A pH of 7.30 indicates acidosis, and a bicarbonate (HCO₃⁻) level of 16 mEq/L (below the normal range of 22-26 mEq/L) signifies metabolic acidosis. While severe dehydration from vomiting could potentially lead to lactic acidosis, the primary and most immediate acid-base disturbance resulting from the direct loss of stomach acid is alkalosis, not acidosis. Therefore, this option represents an acid-base imbalance contrary to what is expected from gastric fluid loss.
C. pH 7.31, PaCO₂ 58A pH of 7.31 indicates acidosis. A PaCO₂ of 58 mmHg (normal range 35-45 mmHg) is elevated, indicating respiratory acidosis. Respiratory acidosis results from hypoventilation and retention of carbon dioxide. Vomiting and NG suction primarily affect metabolic balance through loss of gastric contents, not directly impairing respiratory function to this extent, making this acid-base disturbance inconsistent with the primary pathophysiology described.
D. pH 7.49, PaCO₂ 28A pH of 7.49 indicates alkalosis, and a PaCO₂ of 28 mmHg (below the normal range of 35-45 mmHg) indicates respiratory alkalosis. Respiratory alkalosis is caused by hyperventilation, leading to excessive expulsion of carbon dioxide. While a patient with severe metabolic alkalosis might hyperventilate slightly as a compensatory mechanism (though primary compensation is typically hypoventilation to retain CO2 in metabolic alkalosis), the primary disturbance from vomiting and NG suction is metabolic, not respiratory alkalosis.
Correct answer: A. Option A: The prolonged vomiting and nasogastric (NG) suction lead to a significant loss of hydrochloric acid (HCl) from the stomach. The kidneys compensate by retaining bicarbonate and excreting hydrogen ions, resulting in an excess of bicarbonate in the blood. A pH of 7.50 indicates alkalosis, and a bicarbonate (HCO₃⁻) level of 32 mEq/L (normal range 22-26 mEq/L) is elevated, confirming a metabolic component. This clinical picture is consistent with metabolic alkalosis, which is the expected acid-base imbalance in a client experiencing significant gastric fluid loss.
Option B: A pH of 7.30 indicates acidosis, and a bicarbonate (HCO₃⁻) level of 16 mEq/L (below the normal range of 22-26 mEq/L) signifies metabolic acidosis. While severe dehydration from vomiting could potentially lead to lactic acidosis, the primary and most immediate acid-base disturbance resulting from the direct loss of stomach acid is alkalosis, not acidosis. Therefore, this option represents an acid-base imbalance contrary to what is expected from gastric fluid loss.
Option C: A pH of 7.31 indicates acidosis. A PaCO₂ of 58 mmHg (normal range 35-45 mmHg) is elevated, indicating respiratory acidosis. Respiratory acidosis results from hypoventilation and retention of carbon dioxide. Vomiting and NG suction primarily affect metabolic balance through loss of gastric contents, not directly impairing respiratory function to this extent, making this acid-base disturbance inconsistent with the primary pathophysiology described.
Option D: A pH of 7.49 indicates alkalosis, and a PaCO₂ of 28 mmHg (below the normal range of 35-45 mmHg) indicates respiratory alkalosis. Respiratory alkalosis is caused by hyperventilation, leading to excessive expulsion of carbon dioxide. While a patient with severe metabolic alkalosis might hyperventilate slightly as a compensatory mechanism (though primary compensation is typically hypoventilation to retain CO2 in metabolic alkalosis), the primary disturbance from vomiting and NG suction is metabolic, not respiratory alkalosis.
4. Which client does the nurse assess FIRST on an acute GI unit?
A. Diverticulitis, temp 100.8°FA client with diverticulitis and a temperature of 100.8°F (38.2°C) presents with signs of inflammation and infection, which are expected findings for this condition. While requiring ongoing assessment and management with antibiotics and pain control, this temperature is considered a low-grade fever and does not indicate immediate, life-threatening instability compared to other options. The nurse would monitor for worsening signs like increasing abdominal pain, higher fever, or signs of perforation, but this client is not the highest priority.
B. Upper GI bleed, HR 122 and BP 86/50A client with an upper GI bleed exhibiting a heart rate of 122 bpm and blood pressure of 86/50 mmHg is showing classic signs of hypovolemic shock due to significant blood loss. The compensatory tachycardia (HR 122) and profound hypotension (BP 86/50) indicate inadequate tissue perfusion and organ hypoperfusion, which is a life-threatening emergency requiring immediate intervention. The nurse must prioritize this client to stabilize circulation, initiate fluid resuscitation, potentially prepare for blood transfusions, and identify the source of bleeding to prevent irreversible organ damage or death.
C. Post-op cholecystectomy, pain 6/10A post-operative cholecystectomy client reporting pain of 6/10 requires nursing intervention for pain management, as adequate pain control is crucial for recovery, deep breathing, and ambulation, preventing complications like atelectasis or DVT. While a pain level of 6/10 is significant and warrants attention, it is an expected post-surgical finding and is not immediately life-threatening. The nurse would administer prescribed analgesics and reassess, but this situation does not pose the same acute threat to life as active hypovolemic shock.
D. Appendicitis, NPO awaiting surgeryA client with appendicitis who is NPO and awaiting surgery is in an appropriate and stable state given their diagnosis. The NPO status is a necessary precaution to prevent aspiration during anesthesia, and awaiting surgery is the standard course of treatment for appendicitis. While appendicitis can rupture if not treated, this client is currently being managed appropriately and does not exhibit immediate signs of deterioration or life-threatening complications that would supersede the critically unstable client in hypovolemic shock.
Correct answer: B. Option A: A client with diverticulitis and a temperature of 100.8°F (38.2°C) presents with signs of inflammation and infection, which are expected findings for this condition. While requiring ongoing assessment and management with antibiotics and pain control, this temperature is considered a low-grade fever and does not indicate immediate, life-threatening instability compared to other options. The nurse would monitor for worsening signs like increasing abdominal pain, higher fever, or signs of perforation, but this client is not the highest priority.
Option B: A client with an upper GI bleed exhibiting a heart rate of 122 bpm and blood pressure of 86/50 mmHg is showing classic signs of hypovolemic shock due to significant blood loss. The compensatory tachycardia (HR 122) and profound hypotension (BP 86/50) indicate inadequate tissue perfusion and organ hypoperfusion, which is a life-threatening emergency requiring immediate intervention. The nurse must prioritize this client to stabilize circulation, initiate fluid resuscitation, potentially prepare for blood transfusions, and identify the source of bleeding to prevent irreversible organ damage or death.
Option C: A post-operative cholecystectomy client reporting pain of 6/10 requires nursing intervention for pain management, as adequate pain control is crucial for recovery, deep breathing, and ambulation, preventing complications like atelectasis or DVT. While a pain level of 6/10 is significant and warrants attention, it is an expected post-surgical finding and is not immediately life-threatening. The nurse would administer prescribed analgesics and reassess, but this situation does not pose the same acute threat to life as active hypovolemic shock.
Option D: A client with appendicitis who is NPO and awaiting surgery is in an appropriate and stable state given their diagnosis. The NPO status is a necessary precaution to prevent aspiration during anesthesia, and awaiting surgery is the standard course of treatment for appendicitis. While appendicitis can rupture if not treated, this client is currently being managed appropriately and does not exhibit immediate signs of deterioration or life-threatening complications that would supersede the critically unstable client in hypovolemic shock.
5. A client with GERD is started on pantoprazole. Which statement shows the teaching worked?
A. “I’ll take it 30 min before breakfast.”This statement demonstrates correct understanding because proton pump inhibitors (PPIs) like pantoprazole are most effective when taken 30-60 minutes before the first meal of the day. This timing allows the medication to be absorbed and reach the parietal cells in the stomach before the proton pumps are maximally activated by food intake, thus inhibiting acid secretion most efficiently. By blocking these pumps early, pantoprazole effectively reduces stomach acid production, which is crucial for managing GERD symptoms and allowing esophageal healing.
B. “I’ll take it with an antacid.”Taking pantoprazole with an antacid is not the optimal way to administer this medication and does not show proper understanding. While antacids provide immediate relief by neutralizing existing stomach acid, pantoprazole works by irreversibly blocking the proton pumps that produce acid, a process that takes time. Combining them unnecessarily or relying on the antacid to enhance PPI action is incorrect; the PPI needs to be absorbed and begin its action independently to provide long-term acid suppression.
C. “I’ll take it right after meals.”Taking pantoprazole right after meals is an incorrect statement regarding its administration and indicates a lack of understanding. PPIs like pantoprazole are designed to be taken *before* meals, specifically 30-60 minutes prior to eating. Administering it after a meal significantly reduces its effectiveness because the proton pumps are already highly active, and the medication will not have sufficient time to inhibit them before acid production surges in response to food.
D. “I’ll stop it once heartburn goes away.”This statement is incorrect and demonstrates a dangerous misunderstanding of GERD management and PPI therapy. Stopping pantoprazole abruptly once heartburn subsides can lead to a rebound effect, where acid production increases significantly, worsening GERD symptoms and potentially causing esophageal damage. PPIs are often prescribed for a specific duration or as maintenance therapy to ensure sustained acid suppression and promote healing of the esophageal lining, requiring a healthcare provider's guidance for discontinuation.
Correct answer: A. Option A: This statement demonstrates correct understanding because proton pump inhibitors (PPIs) like pantoprazole are most effective when taken 30-60 minutes before the first meal of the day. This timing allows the medication to be absorbed and reach the parietal cells in the stomach before the proton pumps are maximally activated by food intake, thus inhibiting acid secretion most efficiently. By blocking these pumps early, pantoprazole effectively reduces stomach acid production, which is crucial for managing GERD symptoms and allowing esophageal healing.
Option B: Taking pantoprazole with an antacid is not the optimal way to administer this medication and does not show proper understanding. While antacids provide immediate relief by neutralizing existing stomach acid, pantoprazole works by irreversibly blocking the proton pumps that produce acid, a process that takes time. Combining them unnecessarily or relying on the antacid to enhance PPI action is incorrect; the PPI needs to be absorbed and begin its action independently to provide long-term acid suppression.
Option C: Taking pantoprazole right after meals is an incorrect statement regarding its administration and indicates a lack of understanding. PPIs like pantoprazole are designed to be taken *before* meals, specifically 30-60 minutes prior to eating. Administering it after a meal significantly reduces its effectiveness because the proton pumps are already highly active, and the medication will not have sufficient time to inhibit them before acid production surges in response to food.
Option D: This statement is incorrect and demonstrates a dangerous misunderstanding of GERD management and PPI therapy. Stopping pantoprazole abruptly once heartburn subsides can lead to a rebound effect, where acid production increases significantly, worsening GERD symptoms and potentially causing esophageal damage. PPIs are often prescribed for a specific duration or as maintenance therapy to ensure sustained acid suppression and promote healing of the esophageal lining, requiring a healthcare provider's guidance for discontinuation.
6. Which home medication should a client recovering from acute kidney injury be taught to avoid?
A. AcetaminophenAcetaminophen is hepatically metabolized and is preferred for pain in kidney disease at recommended doses.
B. IbuprofenCorrect. NSAIDs constrict the afferent arteriole, reduce renal perfusion and are a common cause of kidney injury.
C. Docusate sodiumStool softeners are not nephrotoxic.
D. LoratadineSecond-generation antihistamines are not nephrotoxic at usual doses.
Correct answer: B. NSAIDs, IV contrast and aminoglycosides are the classic nephrotoxins to avoid after acute kidney injury.
7. Which assessment most reliably measures a client's fluid status in acute kidney injury?
A. Daily weight at the same time on the same scaleCorrect. A one-kilogram change equals roughly one liter of fluid, making daily weight the most reliable measure.
B. Skin turgor over the sternumSkin turgor is a late and unreliable indicator, particularly in older adults.
C. The client's report of thirstThirst is subjective and blunted in many clients with kidney disease.
D. Blood pressure once per shiftBlood pressure is affected by medications, pain and position and changes late.
Correct answer: A. Daily weights on the same scale at the same time are the gold-standard bedside measure of fluid balance.
8. A client with cirrhosis has an INR of 2.4 and is not receiving any anticoagulant. Which nursing action is the priority?
A. Hold all oral intakeWithholding food does not address bleeding risk and worsens nutritional status in cirrhosis.
B. Use a soft toothbrush, avoid IM injections and hold pressure after venipunctureCorrect. The failing liver cannot synthesize clotting factors, so bleeding precautions are the priority intervention.
C. Keep the client on bed rest with the head of bed flatBed rest does not prevent bleeding, and lying flat worsens dyspnea in a client with ascites.
D. Request a heparin infusion for clot preventionAnticoagulation would compound an already prolonged INR and increase hemorrhage risk.
Correct answer: B. A prolonged INR in cirrhosis reflects impaired clotting factor synthesis. Institute bleeding precautions rather than adding anticoagulation.
9. A client with acute kidney injury develops crackles, jugular vein distention and dyspnea. Which action should the nurse take first?
A. Increase IV fluids to improve kidney perfusionAdditional fluid would worsen pulmonary congestion in a client who cannot excrete it.
B. Raise the head of the bed and apply oxygenCorrect. These are signs of fluid overload; positioning and oxygen immediately support oxygenation while the provider is notified.
C. Encourage oral fluidsOral fluids add to the volume the failing kidney cannot remove.
D. Obtain a urine cultureA culture investigates infection and does not relieve the respiratory distress.
Correct answer: B. Fluid overload with pulmonary congestion is treated by improving oxygenation first, then removing volume — never by adding fluid.
10. A client with oliguric acute kidney injury has a potassium of 6.3 mEq/L with peaked T waves. Which prescription should the nurse question?
A. IV insulin with dextroseInsulin with dextrose shifts potassium into cells and is appropriate emergency therapy.
B. Oral sodium polystyrene sulfonateSodium polystyrene sulfonate binds potassium in the gut and removes it from the body.
C. Lactated Ringer's at 125 mL/hrCorrect. Lactated Ringer's contains potassium and would worsen hyperkalemia in an oliguric client.
D. Continuous cardiac monitoringCardiac monitoring is essential because hyperkalemia causes lethal dysrhythmias.
Correct answer: C. In hyperkalemic acute kidney injury, avoid potassium-containing fluids such as lactated Ringer's; shift and remove potassium instead.