A patient with type 2 diabetes presents with hyperglycemia, metabolic acidosis, and an increased anion gap. Considering the possibility of diabetic ketoacidosis (DKA), which nursing intervention is most appropriate to prioritize?

B) Initiate insulin therapy to lower blood glucose levels

A) Administer sodium bicarbonate to correct the acidosis

B) Initiate insulin therapy to lower blood glucose levels

C) Provide supplemental oxygen to improve oxygen saturation

D) Administer potassium supplements to prevent hypokalemia

A patient with type 2 diabetes is admitted with metabolic acidosis, respiratory compensation, and an increased anion gap. Her blood glucose is 320 mg/dL, and ketones are present in the urine. Which nursing intervention is the most important to prioritize in managing her condition?

B) Initiate insulin therapy to address the hyperglycemia and reverse ketoacidosis.

A) Administer supplemental oxygen to improve oxygen saturation.

B) Initiate insulin therapy to address the hyperglycemia and reverse ketoacidosis.

C) Provide intravenous fluids to correct dehydration and electrolyte imbalances.

D) Administer sodium bicarbonate to immediately correct the acidosis.

A patient with diabetic ketoacidosis (DKA) is showing signs of decreased perfusion and lethargy despite insulin therapy and initial fluid resuscitation. Which nursing intervention is most appropriate to address the current hemodynamic instability?

B) Administer a bolus of isotonic saline.

A) Increase the rate of insulin infusion.

B) Administer a bolus of isotonic saline.

C) Start a continuous infusion of sodium bicarbonate.

D) Increase supplemental oxygen to maintain saturation above 95%.

A patient with diabetic ketoacidosis (DKA) is being treated with insulin therapy and aggressive fluid resuscitation. Despite initial improvements, she begins to exhibit signs of declining perfusion and lethargy, with a blood pressure drop and an elevated respiratory rate. Which of the following interventions should the nurse prioritize to address the current clinical findings?

B) Administer additional isotonic saline to improve her hemodynamic status.

A) Increase the rate of insulin infusion to further lower blood glucose levels.

B) Administer additional isotonic saline to improve her hemodynamic status.

C) Provide a high-carbohydrate snack to prevent further hypoglycemia.

D) Administer sodium bicarbonate to rapidly correct metabolic acidosis.

A patient receiving fluid resuscitation and insulin therapy for diabetic ketoacidosis is experiencing decreased urine output and elevated creatinine levels, indicating possible acute kidney injury (AKI). Her potassium level is 5.2 mEq/L. Which intervention should the nurse prioritize to address the patient's current clinical status?

D) Collaborate with the healthcare team to adjust the insulin therapy to optimize potassium levels.

A) Increase the rate of fluid resuscitation to improve renal perfusion.

B) Administer a potassium-wasting diuretic to decrease serum potassium levels.

C) Prepare the patient for hemodialysis to address electrolyte imbalance and renal function.

D) Collaborate with the healthcare team to adjust the insulin therapy to optimize potassium levels.

A patient with acute kidney injury (AKI) and declining oxygen saturation presents with elevated serum potassium and intermittent confusion. Which nursing intervention should be prioritized to address her immediate clinical needs?

A) Administer calcium gluconate to stabilize cardiac membranes and prevent hyperkalemia-induced arrhythmias.

B) Increase the rate of fluid resuscitation to improve renal perfusion and enhance urine output.

C) Administer bronchodilator therapy to improve respiratory status and oxygenation.

D) Prepare the patient for emergent dialysis to rapidly reduce serum potassium levels and manage fluid balance.

A patient with acute kidney injury is exhibiting signs of pulmonary edema and a mixed acid-base disorder. Which of the following interventions should the nurse prioritize to address the patient's respiratory status?

C) Start non-invasive ventilation

A) Initiate high-flow oxygen therapy

B) Administer a diuretic to reduce fluid overload

C) Start non-invasive ventilation

D) Administer sodium bicarbonate to correct acidosis

A patient with acute kidney injury and pulmonary edema is experiencing decreased oxygen saturation and increased respiratory rate. The healthcare team is implementing non-invasive ventilation to support respiratory status. Which intervention should the nurse prioritize to address the patient's fluid and electrolyte imbalance?

B) Initiate renal replacement therapy to manage fluid overload.

A) Administer diuretics to promote fluid excretion.

B) Initiate renal replacement therapy to manage fluid overload.

C) Restrict fluid intake to 500 mL per day.

D) Administer intravenous potassium to correct the electrolyte imbalance.

A patient with acute kidney injury and metabolic acidosis is undergoing continuous venovenous hemofiltration (CVVH). Despite therapy, the patient remains intermittently confused with a fluctuating Glasgow Coma Scale score. What is the most appropriate nursing intervention to address the patient's neurological status?

D) Perform frequent neurological assessments and report changes.

A) Administer a sedative to reduce confusion.

B) Monitor blood glucose levels regularly.

C) Increase the CVVH rate to enhance clearance.

D) Perform frequent neurological assessments and report changes.

A patient with acute kidney injury is receiving continuous venovenous hemofiltration (CVVH) for management of hyperkalemia and metabolic acidosis. Which nursing intervention is most critical to monitor for potential complications associated with CVVH?

C) Assessing electrolyte levels and adjusting replacement fluids as ordered

A) Monitoring blood pressure every 4 hours

B) Checking the hemofiltration machine settings every shift

C) Assessing electrolyte levels and adjusting replacement fluids as ordered

D) Measuring urine output hourly to assess renal recovery

Acid base balances - Nursing Case Study

Pathophysiology

• Primary mechanism: Respiratory Regulation - The respiratory system maintains acid-base balance by controlling carbon dioxide (CO2) levels. Increased CO2 from hypoventilation leads to respiratory acidosis, while decreased CO2 from hyperventilation results in respiratory alkalosis.

• Secondary mechanism: Renal Compensation - The kidneys regulate bicarbonate (HCO3-) levels and excrete hydrogen ions (H+) to maintain pH balance. In metabolic acidosis, the kidneys increase H+ excretion and HCO3- reabsorption; in metabolic alkalosis, they do the opposite.

• Key complication: Buffer Systems - Rapid but temporary pH adjustments are mediated by buffer systems like bicarbonate, phosphate, and proteins, which neutralize excess acids or bases in the blood, providing immediate but short-term stabilization until respiratory and renal mechanisms take over.

Patient Profile

Demographics:

45-year-old female, office manager

History:

• Key past medical history: Hypertension, type 2 diabetes, history of recurrent urinary tract infections

• Current medications: Metformin 500 mg twice daily, Lisinopril 10 mg once daily, Hydrochlorothiazide 25 mg once daily

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Shortness of breath and fatigue

• Key symptoms: Nausea, headache, muscle twitching, confusion

• Vital signs: Blood pressure 145/90 mmHg, heart rate 102 bpm, respiratory rate 28 breaths per minute, temperature 98.6°F, oxygen saturation 92% on room air

Section 1

As the healthcare team continues to assess the patient, new diagnostic results provide critical insights into her condition. Arterial blood gas analysis reveals a pH of 7.32, partial pressure of carbon dioxide (PaCO2) at 30 mmHg, and bicarbonate (HCO3-) level at 18 mEq/L, indicating a state of metabolic acidosis with partial respiratory compensation. Her serum electrolytes show a sodium level of 138 mEq/L, potassium at 4.0 mEq/L, and a notably elevated blood glucose level of 320 mg/dL. The anion gap is increased, suggesting the presence of an underlying metabolic condition contributing to her acid-base imbalance.

These findings prompt further investigation into the potential causes of her metabolic acidosis. Given her history of type 2 diabetes and current hyperglycemia, the possibility of diabetic ketoacidosis (DKA) becomes a primary concern. The presence of ketones in the urine supports this hypothesis, pointing towards the accumulation of ketoacids as a contributing factor to her acid-base disturbance. Additionally, her elevated respiratory rate and decreased oxygen saturation suggest that her respiratory system is actively trying to compensate for the metabolic acidosis by expelling more CO2, although this compensation appears inadequate given her ongoing symptoms of confusion and muscle twitching.

The clinical team must now consider interventions aimed at addressing the underlying cause of the metabolic acidosis while supporting her respiratory function. This necessitates careful management of her blood glucose levels and consideration of initiating insulin therapy to reverse the ketoacidosis. Monitoring her electrolyte levels, particularly potassium, becomes crucial as insulin therapy may lead to hypokalemia. The team will also need to assess her fluid status to correct any dehydration, which is common in DKA, and provide supplemental oxygen to improve her oxygen saturation. These interventions, along with continuous monitoring of her vital signs and laboratory values, are essential to stabilize her condition and prevent further complications.

Section 2

As the healthcare team implements interventions to address the patient's metabolic acidosis and underlying diabetic ketoacidosis, they closely monitor her response to treatment. Initial insulin therapy is commenced cautiously, with regular checks on her blood glucose and electrolyte levels. Within several hours, there is a noticeable decrease in her blood glucose level, which drops to 250 mg/dL. However, as anticipated, her serum potassium level begins to decline, reaching 3.5 mEq/L, indicating the need for potassium supplementation to prevent hypokalemia. Despite these adjustments, her respiratory rate remains elevated at 28 breaths per minute, and oxygen saturation hovers around 91% on room air, prompting the team to administer supplemental oxygen via nasal cannula.

During a routine reassessment, the patient begins to exhibit new complications. Her blood pressure, initially stable, drops to 92/60 mmHg, and she becomes increasingly lethargic, with a Glasgow Coma Scale score declining to 13. These changes suggest worsening perfusion and possible progression to shock-like symptoms, likely due to the severe dehydration associated with DKA. The team promptly initiates an aggressive fluid resuscitation protocol with isotonic saline to improve her hemodynamic status and enhance tissue perfusion.

Continuous monitoring reveals that her arterial blood gas parameters have shown slight improvement, with a pH rising to 7.35, but her bicarbonate remains low at 19 mEq/L, indicating that full metabolic correction has not yet been achieved. Her anion gap, though reduced, is still elevated, underscoring the need for ongoing management. This evolving clinical picture challenges the team to refine their therapeutic strategies, emphasizing the importance of vigilant monitoring, fluid balance optimization, and electrolyte management as they work to stabilize her condition and prevent further deterioration.

Section 3

As the healthcare team continues to monitor the patient, there is a new development in her clinical status that requires immediate attention. Despite the ongoing fluid resuscitation and insulin therapy, the patient's urine output has significantly decreased, with only 20 mL over the past hour, suggesting the onset of acute kidney injury (AKI). This decrease in urine output, coupled with rising creatinine levels now at 2.1 mg/dL, highlights the risk of renal hypoperfusion and the need for further evaluation and intervention. Concurrently, her serum potassium level, previously supplemented, shows a rebound to 5.2 mEq/L, necessitating careful titration to avoid hyperkalemia, especially given her compromised renal function.

The patient's respiratory status continues to be a concern. Her respiratory rate remains elevated, and oxygen saturation has decreased slightly to 89% despite supplemental oxygen, indicating potential respiratory compromise or a developing pulmonary complication. A repeat chest X-ray is ordered to rule out pulmonary edema or an infection that could be contributing to her declining oxygenation. Meanwhile, her mental status fluctuates, with intermittent confusion and disorientation, suggesting potential cerebral hypoperfusion or metabolic disturbances impacting her neurological function.

In response to these emerging complications, the healthcare team revisits their management plan, emphasizing the need for a multidisciplinary approach. Nephrology consultation is sought to address the renal challenges, while respiratory therapy is engaged to optimize her ventilation and oxygenation strategies. The team also considers the possibility of advanced hemodynamic monitoring to better assess her fluid status and guide further interventions. As they strive to stabilize her condition, they remain vigilant for any additional signs of deterioration, ready to adjust their therapeutic strategies to meet her evolving needs.

Section 4

The healthcare team reconvenes as new diagnostic results bring additional clarity and urgency to the patient's evolving condition. The repeat chest X-ray reveals bilateral infiltrates, suggesting the development of pulmonary edema, likely secondary to fluid overload in the context of acute kidney injury. This finding correlates with her decreased oxygen saturation and elevated respiratory rate, signaling compromised pulmonary function. The team must now balance the need for fluid resuscitation with the risk of exacerbating pulmonary congestion, prompting a more tailored approach to her fluid management.

Laboratory results show a further increase in creatinine to 2.5 mg/dL, confirming the progression of acute kidney injury. Electrolyte analysis indicates a worsening acid-base imbalance, with her arterial blood gas revealing a mixed acid-base disorder characterized by metabolic acidosis with a pH of 7.29 and respiratory alkalosis due to hyperventilation. The serum bicarbonate level has decreased to 18 mEq/L, further complicating her acid-base status. The patient's serum potassium remains elevated at 5.4 mEq/L, necessitating cautious use of potassium-lowering therapies while monitoring renal function closely.

In light of these developments, the team intensifies their collaborative efforts, implementing non-invasive ventilation to support her respiratory status and considering the initiation of renal replacement therapy to manage her fluid and electrolyte imbalances. They continue to monitor her mental status closely, aware that her intermittent confusion may be exacerbated by both cerebral hypoperfusion and the systemic effects of her acid-base disturbance. As they refine their treatment strategies, they remain poised to address any emerging complications swiftly, maintaining a vigilant and adaptive approach to her care.

Section 5

The healthcare team decides to initiate a trial of non-invasive ventilation to support the patient's respiratory function and address the metabolic acidosis. Over the next few hours, her oxygen saturation improves to 92%, and her respiratory rate stabilizes at 22 breaths per minute. However, the team notes that she remains intermittently confused, with a Glasgow Coma Scale score fluctuating between 13 and 14, indicating mild alterations in her mental status. This prompts a reassessment of her neurological status and consideration of the potential cerebral effects of her acid-base imbalance.

New diagnostic results from a follow-up arterial blood gas reveal a slight improvement in her pH, which is now 7.31, and a bicarbonate level of 20 mEq/L, suggesting a partial compensation. Despite these encouraging changes, her serum potassium has risen slightly to 5.6 mEq/L, necessitating more aggressive management to prevent cardiac complications. The team decides to initiate renal replacement therapy, specifically continuous venovenous hemofiltration (CVVH), to enhance clearance of potassium and metabolic acids, and to better control her fluid status.

As the renal replacement therapy progresses, the patient's urine output remains negligible, confirming the severity of her acute kidney injury. Her blood pressure remains stable at 110/68 mmHg, but the team remains vigilant for signs of hemodynamic instability, particularly given the risk of fluid shifts with CVVH. To mitigate potential complications, they adjust her electrolyte management carefully, focusing on maintaining a delicate balance between correcting her hyperkalemia and avoiding further disruption of her acid-base homeostasis. Through these targeted interventions, the healthcare team hopes to stabilize her condition, while continuously evaluating her response and readiness for potential escalation of care if necessary.