A patient with a history of Type 2 Diabetes and hypertension is diagnosed with diabetic ketoacidosis (DKA). The patient presents with increased respiratory rate, confusion, and muscle twitching. Laboratory results indicate metabolic acidosis with partial respiratory compensation and hyperkalemia. Which nursing intervention should be prioritized to address the patient's immediate clinical needs?

B) Initiate fluid resuscitation with isotonic saline

A) Administer sodium bicarbonate to correct acidosis

B) Initiate fluid resuscitation with isotonic saline

C) Administer calcium gluconate to stabilize cardiac membranes

D) Provide supplemental oxygen to improve oxygen saturation

A patient with a history of hypertension and Type 2 Diabetes is admitted with symptoms suggesting diabetic ketoacidosis (DKA) and has a blood glucose level of 320 mg/dL, a SpO2 of 88%, pH of 7.29, and potassium level of 6.0 mEq/L. What is the priority nursing intervention to address the patient's current condition?

C) Start fluid resuscitation with isotonic saline to improve renal perfusion

A) Administer sodium bicarbonate to correct the acidosis

B) Initiate insulin therapy to lower blood glucose levels

C) Start fluid resuscitation with isotonic saline to improve renal perfusion

D) Provide supplemental oxygen to improve oxygenation

A patient with worsening respiratory distress, despite supplemental oxygen, presents with SpO2 levels between 85-87%, pronounced wheezing, crackles at lung bases, and a recent ABG showing metabolic acidosis with a pH of 7.31. Which of the following interventions should the nurse prioritize to address the underlying issue and improve the patient's respiratory status?

C) Initiate non-invasive positive pressure ventilation (NIPPV).

A) Increase supplemental oxygen to 100% via non-rebreather mask.

B) Administer a loop diuretic to reduce pulmonary congestion.

C) Initiate non-invasive positive pressure ventilation (NIPPV).

D) Administer a bronchodilator to alleviate wheezing.

A patient with renal perfusion issues is experiencing worsening respiratory distress, SpO2 levels of 85-87%, and evidence of fluid overload despite ongoing treatment. The latest ABG shows a pH of 7.31, PaCO2 of 30 mmHg, and HCO3- of 18 mEq/L. Given these findings, what is the most appropriate initial nursing intervention to address the patient's respiratory status?

D) Initiate non-invasive ventilation support to enhance gas exchange and reduce respiratory effort

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

B) Prepare the patient for emergency intubation due to severe respiratory acidosis

C) Administer a diuretic to reduce pulmonary congestion and improve oxygenation

D) Initiate non-invasive ventilation support to enhance gas exchange and reduce respiratory effort

A patient receiving diuretic therapy with furosemide develops hypokalemia and fluctuating blood pressure. Which nursing intervention is most appropriate to address these complications?

B) Administer potassium supplements with food as prescribed and monitor the patient's blood pressure closely.

A) Encourage the patient to ambulate frequently to improve circulation.

B) Administer potassium supplements with food as prescribed and monitor the patient's blood pressure closely.

C) Increase the rate of intravenous fluids to rapidly correct fluid imbalances.

D) Tell the patient to limit fluid intake to prevent worsening fluid overload.

A patient receiving furosemide for fluid overload develops hypokalemia, with a potassium level of 2.9 mEq/L. Which intervention should the nurse prioritize to prevent complications associated with this electrolyte imbalance?

B) Administer potassium chloride as prescribed and monitor cardiac rhythm.

A) Increase the infusion rate of normal saline to correct hypokalemia.

B) Administer potassium chloride as prescribed and monitor cardiac rhythm.

C) Encourage the patient to consume high-potassium foods and reassess in 24 hours.

D) Continue diuretic therapy and monitor the patient's intake and output closely.

A patient with metabolic alkalosis is being treated with potassium chloride supplementation to address hypokalemia. Which of the following nursing interventions should be prioritized to monitor the effectiveness of the treatment and ensure patient safety?

C) Continuously monitor the patient's cardiac rhythm.

A) Monitor the patient's blood pressure every 4 hours.

B) Assess the patient's deep tendon reflexes regularly.

C) Continuously monitor the patient's cardiac rhythm.

D) Measure the patient's urine output every 2 hours.

A patient with metabolic alkalosis secondary to aggressive diuresis is exhibiting signs of hypokalemia and occasional premature ventricular contractions (PVCs). Which of the following nursing interventions is the most appropriate to address the underlying causes and prevent further complications?

B) Administer potassium chloride supplementation to correct hypokalemia.

A) Increase the patient's fluid intake to enhance renal excretion of bicarbonate.

B) Administer potassium chloride supplementation to correct hypokalemia.

C) Encourage the patient to perform deep breathing exercises to reduce respiratory rate.

D) Administer calcium gluconate to stabilize cardiac membranes.

A patient with persistent hypokalemia despite supplementation, metabolic alkalosis, and hemodynamic instability is being reassessed by the clinical team. What is the most appropriate nursing intervention to prioritize in this scenario?

B) Initiate a carefully calculated isotonic fluid bolus to address potential hypovolemia.

A) Administer a hypertonic saline solution to rapidly correct electrolyte imbalances.

B) Initiate a carefully calculated isotonic fluid bolus to address potential hypovolemia.

C) Increase the dose of diuretics to manage fluid overload and improve renal function.

D) Provide supplemental oxygen to address the elevated respiratory rate and agitation.

A patient is experiencing hypokalemia, metabolic alkalosis, and signs of hypovolemia after aggressive diuretic therapy. Which of the following interventions should the nurse prioritize to address the current clinical findings?

A) Administer an isotonic fluid bolus to correct hypovolemia and continue monitoring electrolyte levels.

B) Increase the rate of diuretic infusion to promote diuresis and manage electrolyte imbalances.

C) Encourage oral intake of potassium-rich foods to increase serum potassium levels.

D) Administer sodium bicarbonate to correct the metabolic alkalosis.

acid base - Nursing Case Study

Pathophysiology

• Primary mechanism: The bicarbonate buffer system maintains blood pH by balancing bicarbonate (HCO₃⁻) and carbonic acid (H₂CO₃). Kidneys regulate HCO₃⁻ reabsorption and secretion, while lungs control CO₂ (a component of H₂CO₃) exhalation, adjusting pH rapidly through respiratory rate changes.

• Secondary mechanism: Cellular respiration produces CO₂, which diffuses into blood and combines with water to form H₂CO₃. This dissociates into H⁺ and HCO₃⁻. An imbalance in H⁺ or HCO₃⁻ leads to acidosis or alkalosis, with respiratory or metabolic origins, affecting cellular function and enzyme activity.

• Key complication: In chronic kidney disease, impaired HCO₃⁻ reabsorption can result in metabolic acidosis, leading to compensatory hyperventilation and altered oxygen delivery, stressing cardiovascular and respiratory systems.

Patient Profile

Demographics:

45-year-old female, office worker

History:

• Key past medical history: Hypertension, Type 2 Diabetes

• Current medications: Metformin 500 mg BID, Lisinopril 10 mg daily

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Shortness of breath and fatigue

• Key symptoms: Nausea, confusion, muscle twitching

• Vital signs: Blood pressure 150/95 mmHg, heart rate 110 bpm, respiratory rate 24 breaths per minute, temperature 37.2°C, SpO2 88% on room air

Section 1

As the healthcare team conducts an initial assessment, they note the patient's increasing respiratory distress and low oxygen saturation levels. The patient's SpO2 of 88% on room air suggests significant hypoxemia. Auscultation reveals diminished breath sounds with scattered wheezes, indicating potential ventilation issues. The rapid respiratory rate of 24 breaths per minute reflects compensatory mechanisms in response to suspected metabolic acidosis. Given her history of hypertension and Type 2 Diabetes, the team considers the possibility of diabetic ketoacidosis (DKA) or lactic acidosis due to impaired renal function. The patient's confusion and muscle twitching could be attributed to electrolyte imbalances, possibly linked to acidosis.

Laboratory tests are promptly ordered, and the results provide critical insights: arterial blood gas (ABG) analysis shows a pH of 7.29, PaCO2 of 32 mmHg, and HCO3- of 16 mEq/L, confirming metabolic acidosis with partial respiratory compensation. Her blood glucose levels are elevated at 320 mg/dL, and ketones are present in the urine, suggesting DKA. Serum electrolytes reveal a potassium level of 6.0 mEq/L, indicating hyperkalemia, likely due to both acidosis and compromised renal function. The elevated BUN and creatinine levels further suggest acute kidney injury on top of chronic kidney disease, contributing to her current metabolic derangement.

The clinical team decides to initiate interventions aimed at correcting the acid-base imbalance and addressing the underlying causes. Fluid resuscitation with isotonic saline is started to improve renal perfusion and facilitate glucose clearance. Insulin therapy is also initiated to address hyperglycemia and promote intracellular potassium shift. Continuous cardiac monitoring is implemented due to the risk of cardiac arrhythmias from hyperkalemia. The patient is placed on supplemental oxygen to improve oxygenation, while preparations are made for potential advanced airway management if her respiratory status deteriorates. The team closely monitors her response to these interventions, ready to adjust the treatment plan as necessary.

Section 2

As the clinical team continues to monitor the patient, they observe a change in her status that raises concern. Despite the initiated interventions, the patient's respiratory distress worsens, manifesting as increased work of breathing and a respiratory rate climbing to 28 breaths per minute. Her SpO2 fluctuates between 85-87% even with supplemental oxygen, indicating a growing inefficiency in gas exchange. Auscultation now reveals more pronounced wheezing and the emergence of crackles at the lung bases, suggesting fluid overload potentially exacerbated by the aggressive fluid resuscitation required to address her renal perfusion issues.

New diagnostic results arrive, offering further insight into her condition. Repeat ABG analysis shows a pH of 7.31, PaCO2 of 30 mmHg, and HCO3- of 18 mEq/L, indicating a slight improvement in her metabolic acidosis but not resolving at the expected rate. Electrolyte panels confirm persistent hyperkalemia, with potassium levels still at 5.8 mEq/L, despite insulin therapy. Meanwhile, her renal function markers show no significant improvement, with BUN and creatinine levels remaining elevated. The developing pulmonary congestion, coupled with her declining respiratory status, suggests that acute pulmonary edema might be complicating her clinical picture, likely due to fluid resuscitation and underlying cardiac stress from her chronic hypertension.

The healthcare team must now employ critical reasoning to adjust the treatment strategy. They consider the initiation of diuretics to manage potential fluid overload and evaluate the need for non-invasive ventilation support to enhance oxygenation and reduce respiratory effort. The persistence of hyperkalemia prompts a reevaluation of her insulin therapy and consideration of additional measures, such as calcium gluconate for cardiac protection and sodium bicarbonate if warranted by further acid-base imbalances. The team remains vigilant, ready to escalate care, and closely monitors the patient for any signs of cardiac arrhythmias or further deterioration, ensuring timely intervention to prevent further complications.

Section 3

As the clinical team implements the adjusted treatment plan, they initiate diuretic therapy with furosemide to address the suspected fluid overload, watching closely for any changes in the patient's respiratory status and renal function. Concurrently, they introduce BiPAP (bilevel positive airway pressure) to alleviate the increased work of breathing and improve oxygenation. The respiratory therapist sets up the machine, and the patient is carefully monitored for tolerance and effectiveness of this non-invasive ventilation support. With these interventions, the team hopes to see an improvement in her oxygen saturation and a reduction in her respiratory distress.

However, despite these efforts, the patient exhibits a new complication: she begins to show signs of electrolyte imbalance, specifically hypokalemia. A repeat electrolyte panel shows her potassium level has dropped to 2.9 mEq/L, a significant shift from the previous hyperkalemic state. This sudden change raises concerns about overcorrection, likely a result of the combined effects of insulin therapy and diuretic use. The team quickly adjusts her treatment plan to address this new development, discontinuing further diuretic doses and considering potassium supplementation to stabilize her levels.

Additionally, the patient's blood pressure begins to fluctuate, with systolic readings ranging from 90 to 105 mmHg, possibly indicating a drop in effective circulating volume due to diuresis. The team reassesses her fluid status and evaluates the need for careful fluid management to prevent hypotension while still managing pulmonary congestion. They also continue to monitor for any cardiac arrhythmias, given her electrolyte shifts and underlying cardiac stress. Through these coordinated efforts, the team aims to stabilize the patient's condition, mitigate the risk of further complications, and guide her toward recovery.

Section 4

New Complications:

As the team continues to closely monitor the patient, a new complication arises: she begins to exhibit signs of metabolic alkalosis. This development is evidenced by an arterial blood gas (ABG) analysis showing a pH of 7.49 and a bicarbonate level of 30 mEq/L. The shift towards alkalosis is likely a consequence of the aggressive diuresis, which, in addition to causing hypokalemia, has led to excess bicarbonate retention. The patient's respiratory rate increases to 28 breaths per minute, and she reports feeling more anxious and light-headed, further complicating her clinical picture.

In response to this metabolic disturbance, the clinical team carefully reevaluates her treatment regimen. They decide to decrease the BiPAP pressure settings to reduce the risk of further respiratory compensation and assess the effectiveness of this adjustment through continuous monitoring of her arterial blood gases and electrolytes. Additionally, they initiate potassium chloride supplementation to address the hypokalemia, which may also help counteract the alkalosis by promoting renal bicarbonate excretion.

Despite these adjustments, the patient remains at risk for cardiac arrhythmias due to her altered electrolyte and acid-base status. The team intensifies cardiac monitoring, and an ECG is performed, revealing occasional premature ventricular contractions (PVCs), likely secondary to the electrolyte imbalances. This finding reinforces the importance of rapidly correcting the potassium levels while maintaining a delicate balance in fluid management. Through vigilant monitoring and timely interventions, the team aims to stabilize her metabolic status and prevent further complications, setting the stage for a potential improvement in her overall condition.

Section 5

As the clinical team continues to manage the patient's condition, they begin to notice a change in her status that requires immediate attention. Despite the potassium supplementation, the patient remains hypokalemic with a serum potassium level of 3.2 mEq/L. Her arterial blood gas analysis shows a persistent metabolic alkalosis, with a pH of 7.48 and a bicarbonate level of 29 mEq/L. Her respiratory rate remains elevated at 30 breaths per minute, and she is visibly more agitated, complaining of palpitations and a tingling sensation in her extremities.

The team performs a thorough physical assessment and notes that the patient's skin is cool and clammy, and her capillary refill time is prolonged. Her blood pressure has dropped to 90/58 mmHg, and her heart rate has increased to 112 beats per minute, indicating a possible hemodynamic instability. These findings suggest potential hypovolemia, likely exacerbated by the aggressive diuretic therapy.

Given these developments, the team decides to reassess the fluid management strategy. They consider initiating a carefully calculated isotonic fluid bolus to address the potential hypovolemia while continuing to correct the electrolyte imbalances. They also decide to closely monitor the patient’s renal function, as her urine output has decreased, raising concerns about acute kidney injury. The team remains vigilant, understanding that these interventions are crucial to stabilizing the patient's condition and preventing further deterioration. The goal is to achieve an equilibrium in her metabolic status, ensuring her safety and paving the way for recovery.