A 72-year-old patient with critical aortic stenosis and reduced ejection fraction is admitted to the ICU. The patient shows signs of respiratory acidosis and heart failure exacerbation. As the nurse prepares to implement the care plan, which intervention should be prioritized to address the patient's immediate needs?

C) Initiate non-invasive positive pressure ventilation (NIPPV) to improve oxygenation and reduce work of breathing.

A) Administer intravenous diuretics to reduce fluid overload and relieve pulmonary congestion.

B) Prepare the patient for emergency aortic valve replacement surgery to correct the stenosis.

C) Initiate non-invasive positive pressure ventilation (NIPPV) to improve oxygenation and reduce work of breathing.

D) Administer inotropic agents to enhance cardiac contractility and improve cardiac output.

A 68-year-old patient with critical aortic stenosis, severe systolic heart failure, and moderate pulmonary hypertension is admitted to the ICU. The patient exhibits signs of respiratory distress and elevated cardiac biomarkers. As the ICU nurse, what is the most appropriate initial nursing intervention to address the patient's respiratory status?

B) Initiate non-invasive positive pressure ventilation (NIPPV) to improve oxygenation and reduce work of breathing.

A) Administer intravenous diuretics to reduce preload and pulmonary congestion.

B) Initiate non-invasive positive pressure ventilation (NIPPV) to improve oxygenation and reduce work of breathing.

C) Increase the oxygen flow rate on the nasal cannula to achieve a higher FiO2.

D) Prepare the patient for immediate intubation and mechanical ventilation.

A patient in the ICU is exhibiting signs of acute decompensation with profound hypotension, tachycardia, respiratory distress, and decreased urine output. The laboratory findings include elevated creatinine and lactate levels. As the ICU nurse, what is the most critical action to prioritize while awaiting the multidisciplinary team's assessment?

B) Prepare for intubation and mechanical ventilation to improve oxygenation.

A) Administer a rapid infusion of normal saline to address the hypotension.

B) Prepare for intubation and mechanical ventilation to improve oxygenation.

C) Initiate continuous renal replacement therapy (CRRT) to address acute kidney injury.

D) Begin inotropic support with medications like dobutamine to improve cardiac output.

Upon observing the patient's deterioration in the ICU, which nursing intervention should be prioritized to address the signs of cardiogenic shock and inadequate tissue perfusion?

C) Initiate vasopressor support to stabilize blood pressure and improve organ perfusion.

A) Administer a bolus of intravenous fluids to increase blood pressure and tissue perfusion.

B) Prepare the patient for immediate intubation and mechanical ventilation to manage respiratory failure.

C) Initiate vasopressor support to stabilize blood pressure and improve organ perfusion.

D) Increase the frequency of neurologic assessments to monitor for further changes in mental status.

A patient with severe aortic stenosis and congestive heart failure is experiencing rapid decompensation. Considering the clinical scenario, which nursing intervention is the highest priority to address the patient's current condition?

D) Collaborate with the healthcare team to initiate intra-aortic balloon pump support.

A) Administer diuretics to reduce pulmonary congestion.

B) Initiate non-invasive positive pressure ventilation to improve oxygenation.

C) Prepare for immediate transfer to the cardiac catheterization lab for aortic valve intervention.

D) Collaborate with the healthcare team to initiate intra-aortic balloon pump support.

In managing a patient with severe aortic stenosis and acute decompensated heart failure, which nursing intervention is most critical to prioritize in the immediate management of the patient's deteriorating condition?

C) Initiating mechanical ventilation to address respiratory failure.

A) Administering diuretics to manage pulmonary congestion.

B) Preparing the patient for emergent aortic valve replacement surgery.

C) Initiating mechanical ventilation to address respiratory failure.

D) Administering vasopressors to improve hemodynamic stability.

A 62-year-old male patient in the ICU is experiencing acute kidney injury (AKI) secondary to low cardiac output and systemic hypoperfusion. The medical team is considering continuous renal replacement therapy (CRRT) due to fluid overload and a serum creatinine level of 2.8 mg/dL. His blood pressure is 85/50 mmHg despite inotropic support, and he exhibits signs of poor peripheral perfusion. Which nursing intervention is the highest priority to support the patient's hemodynamic status and organ perfusion?

A) Initiate CRRT immediately to manage fluid overload and support renal function.

C) Increase the dose of inotropic medications to improve cardiac output.

D) Administer a bolus of intravenous fluids to increase blood pressure.

A patient in the ICU has developed acute kidney injury (AKI) following the initiation of mechanical ventilation and shows signs of fluid overload and respiratory acidosis. The medical team is considering the initiation of continuous renal replacement therapy (CRRT). As a nurse involved in the care of this patient, what is the most critical assessment to prioritize before starting CRRT?

C) Assess the patient's coagulation status and prepare for potential anticoagulation management with CRRT.

A) Evaluate the patient's current electrolyte levels, particularly potassium and calcium.

B) Review the patient's medication list for nephrotoxic drugs.

C) Assess the patient's coagulation status and prepare for potential anticoagulation management with CRRT.

D) Monitor the patient's nutritional status and potential need for parenteral nutrition during CRRT.

A patient undergoing continuous renal replacement therapy (CRRT) for fluid overload and hemodynamic instability has just been assessed with a Glasgow Coma Scale (GCS) score of 10 and severe respiratory acidosis. Considering the current clinical scenario, which nursing action is most crucial to prioritize at this time?

B) Prepare for urgent intubation to manage the patient's respiratory acidosis.

A) Increase the inotropic support to maintain hemodynamic stability.

B) Prepare for urgent intubation to manage the patient's respiratory acidosis.

C) Initiate the intra-aortic balloon pump (IABP) to improve cardiac output.

D) Administer a bolus of intravenous fluids to increase central venous pressure.

In the context of the patient's current hemodynamic instability and respiratory acidosis, which nursing intervention is most critical to prioritize before initiating continuous renal replacement therapy (CRRT) and intra-aortic balloon pump (IABP) insertion?

C) Initiating vasopressor support to stabilize blood pressure and improve cerebral perfusion.

A) Administering a bolus of isotonic saline to increase intravascular volume.

B) Adjusting ventilator settings to improve oxygenation and reduce respiratory acidosis.

C) Initiating vasopressor support to stabilize blood pressure and improve cerebral perfusion.

D) Performing frequent neurological assessments to monitor for further changes in mental status.

Aortic sténoses - Nursing Case Study

Pathophysiology

• Primary mechanism: Aortic stenosis is primarily caused by progressive calcification and fibrosis of the aortic valve cusps, leading to a narrowing of the valve opening. This restricts blood flow from the left ventricle to the aorta, causing increased left ventricular pressure and hypertrophy as the heart works harder to pump blood.

• Secondary mechanism: As the left ventricular hypertrophy progresses, the myocardial oxygen demand increases, while coronary artery perfusion decreases due to elevated intramyocardial pressure. This imbalance can lead to myocardial ischemia and angina, even in the absence of coronary artery disease.

• Key complication: Severe aortic stenosis can result in heart failure due to the inability of the hypertrophied left ventricle to maintain adequate cardiac output. Additionally, the increased pressure can lead to pulmonary congestion, contributing to dyspnea and decreased exercise tolerance.

Patient Profile

Demographics:

78-year-old male, retired construction worker

History:

• Key past medical history: Severe aortic stenosis diagnosed 3 years ago, coronary artery disease, chronic obstructive pulmonary disease, type 2 diabetes mellitus

• Current medications: Aspirin, lisinopril, metformin, furosemide, atorvastatin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Severe shortness of breath and chest pain

• Key symptoms: Fatigue, dizziness, syncope, palpitations, difficulty breathing especially when lying flat, swollen ankles

• Vital signs: Blood pressure 85/60 mmHg, heart rate 110 bpm, respiratory rate 28 breaths/min, oxygen saturation 88% on room air, temperature 37.2°C (99°F)

Section 1

New Diagnostic Results:

Following the initial assessment, the patient was immediately transferred to the intensive care unit for further evaluation and monitoring. A comprehensive echocardiogram was conducted, revealing critical aortic stenosis with an aortic valve area of 0.5 cm² and a mean gradient of 60 mmHg, indicating severe obstruction. The left ventricular ejection fraction was noted to be significantly reduced at 35%, pointing towards systolic heart failure. Additionally, the presence of moderate pulmonary hypertension was detected, likely secondary to left-sided heart failure and chronic lung disease.

Laboratory tests showed elevated cardiac biomarkers, with troponin levels at 0.8 ng/mL, suggestive of ongoing myocardial injury, possibly exacerbated by the concurrent coronary artery disease. The patient's BNP level was markedly elevated at 1500 pg/mL, indicative of heart failure exacerbation. Arterial blood gas analysis demonstrated respiratory acidosis with a pH of 7.32, PaCO2 of 55 mmHg, and PaO2 of 60 mmHg, corroborating the clinical picture of worsening respiratory distress. These findings necessitated immediate collaborative discussions among the cardiology, pulmonology, and cardiothoracic teams to strategize the optimal approach to management, considering the high surgical risk posed by the patient’s complex medical history.

Section 2

Change in Patient Status:

Despite the intensive monitoring and implementation of initial medical management strategies, the patient's condition began to deteriorate swiftly. Approximately 12 hours after admission to the ICU, the patient exhibited signs of acute decompensation. He developed profound hypotension, with blood pressure readings plummeting to 80/50 mmHg, accompanied by a heart rate of 120 beats per minute, indicating potential cardiogenic shock. The patient's respiratory distress intensified, necessitating increased oxygen support, and he was placed on a non-rebreather mask delivering 100% oxygen. However, his oxygen saturation persistently hovered around 85%, prompting concerns about inadequate tissue perfusion and worsening hypoxemia.

Concurrently, the patient's urine output dropped to less than 20 mL/hour, raising alarms about impending acute kidney injury. Further laboratory work revealed a rising creatinine level, now at 2.1 mg/dL, from a baseline of 1.2 mg/dL, and a lactate level of 4.5 mmol/L, suggesting systemic hypoperfusion and anaerobic metabolism. Additionally, his mental status began to decline, with episodes of confusion and agitation, likely secondary to hypoxia and reduced cerebral perfusion. These developments required the rapid convening of the ICU team, cardiologists, and nephrologists to reassess the treatment plan, considering the potential need for urgent surgical intervention or the initiation of mechanical circulatory support. This change in status underscored the precariousness of the patient's condition and the urgency for decisive, multidisciplinary decision-making.

Section 3

In light of the patient's rapidly deteriorating condition, a comprehensive reassessment was promptly conducted. On examination, the patient was found to be diaphoretic and cyanotic, with peripheral pulses weak and thready, indicating significant hemodynamic instability. Auscultation of the chest revealed diminished breath sounds bilaterally with crackles, suggesting pulmonary edema secondary to left ventricular failure. The presence of a harsh systolic ejection murmur was noted, consistent with the underlying severe aortic stenosis. Jugular venous distention was evident, pointing towards congestive heart failure exacerbation. Neurologically, the patient's Glasgow Coma Scale (GCS) score had decreased to 10, reflecting his altered mental status.

To further elucidate the cause of the acute decompensation, the healthcare team prioritized urgent diagnostic imaging and laboratory tests. An echocardiogram revealed critically reduced left ventricular ejection fraction at 25%, with severe concentric left ventricular hypertrophy and a peak gradient across the aortic valve of 70 mmHg, confirming severe aortic stenosis with significant obstruction of blood flow. A chest X-ray demonstrated bilateral pulmonary congestion and cardiomegaly. Arterial blood gas analysis showed severe respiratory acidosis with a pH of 7.25, PaCO2 of 60 mmHg, and PaO2 of 55 mmHg, corroborating the findings of respiratory compromise. The markedly elevated lactate level persisted, now at 5.8 mmol/L, further indicating systemic hypoperfusion.

Despite aggressive fluid resuscitation and inotropic support, the patient’s condition continued to decline, necessitating the initiation of mechanical ventilation to manage the worsening respiratory failure. The ICU team, in consultation with cardiology, deliberated on the possibility of proceeding with aortic valve replacement surgery or implementing mechanical circulatory support, such as an intra-aortic balloon pump, to stabilize the patient. This decision was complicated by the risk of potential perioperative complications, given the patient's hemodynamic fragility and deteriorating multi-organ function. The urgency of these interventions underscored the critical need for precise clinical judgment and a coordinated, multidisciplinary approach to optimize the patient's chances of recovery.

Section 4

As the ICU team continued to monitor the patient's condition closely, a new complication emerged that further challenged the clinical team’s ability to stabilize him. Within hours of initiating mechanical ventilation, the patient developed acute kidney injury, evidenced by rapidly rising serum creatinine levels, now at 2.8 mg/dL from a baseline of 1.2 mg/dL, and a significant drop in urine output to less than 0.3 mL/kg/hr. This renal compromise, likely secondary to persistent low cardiac output and systemic hypoperfusion, compounded the difficulty in managing fluid balance, particularly in the context of existing pulmonary edema. Blood urea nitrogen also increased to 45 mg/dL, signaling the severity of the renal impairment.

The patient's hemodynamic status remained precarious, with blood pressure readings dropping to 85/50 mmHg despite inotropic support. Heart rate remained tachycardic at 120 beats per minute, and the patient continued to exhibit signs of poor peripheral perfusion, including mottled skin and cold extremities. In addition, repeat arterial blood gases indicated worsening respiratory acidosis with a pH of 7.20, suggesting that despite mechanical ventilation, the patient's respiratory status was not improving as anticipated. These findings prompted the team to consider renal replacement therapy in the form of continuous renal replacement therapy (CRRT) to manage fluid overload and support renal function.

The onset of acute kidney injury and ongoing respiratory failure necessitated a reevaluation of the treatment plan. The critical care and cardiology teams convened to discuss the feasibility and timing of advanced interventions, such as the insertion of an intra-aortic balloon pump to enhance coronary perfusion and reduce cardiac workload. The multidisciplinary team was tasked with weighing the risks and benefits of each potential intervention, considering the patient's deteriorating multi-organ function and the likelihood of recovery. This complex scenario demanded advanced clinical reasoning and careful coordination to prioritize interventions that could offer the greatest potential benefit in the face of rapidly evolving complications.

Section 5

As the team prepared to initiate continuous renal replacement therapy (CRRT), a new complication arose that further complicated the clinical picture. The patient suddenly developed altered mental status, becoming increasingly agitated and disoriented. Neurological assessment revealed a Glasgow Coma Scale (GCS) score of 10, with the patient responding only to painful stimuli, opening eyes to speech, and using inappropriate words. This acute change prompted an urgent CT scan of the head, which fortunately ruled out any intracranial hemorrhage or ischemic stroke. However, the findings were consistent with cerebral hypoperfusion, likely a consequence of the ongoing hemodynamic instability and systemic hypoperfusion.

In parallel, the patient's hemodynamic parameters continued to decline. Despite aggressive titration of inotropes, the blood pressure further decreased to 80/45 mmHg, and the heart rate escalated to 130 beats per minute. The central venous pressure remained low at 3 mmHg, indicating possible inadequate intravascular volume despite the risk of pulmonary congestion. The nursing team observed that the patient's respiratory effort had increased, with the ventilator displaying frequent high-pressure alarms due to reduced lung compliance from worsening pulmonary edema. The arterial blood gas now revealed a pH of 7.18, PaCO2 of 60 mmHg, and PaO2 of 55 mmHg, highlighting severe respiratory acidosis and hypoxemia.

Faced with these critical issues, the multidisciplinary team prioritized the initiation of CRRT to address the fluid overload and correct electrolyte imbalances, while simultaneously preparing for the insertion of an intra-aortic balloon pump (IABP) to support cardiac function. The decision to proceed with IABP was not taken lightly, given the potential complications, but it was deemed necessary to stabilize the cardiovascular status and improve perfusion. This plan required meticulous coordination among the critical care nurses, nephrologists, and cardiologists to manage the delicate balance between hemodynamic support and renal protection, all while closely monitoring the potential for further deterioration in the patient’s neurological and respiratory status.