A patient with acute myocardial infarction has deteriorated into ventricular fibrillation. After initiating cardiopulmonary resuscitation (CPR) and defibrillation, which intervention should the nurse prioritize to enhance the patient's chances of survival and address the underlying cause?

B) Prepare for immediate thrombolytic therapy

A) Administer intravenous amiodarone

B) Prepare for immediate thrombolytic therapy

C) Initiate a continuous dopamine infusion

D) Establish a central venous access

A patient with suspected acute myocardial infarction has deteriorated into ventricular fibrillation and requires immediate intervention. After initiating CPR, what is the most appropriate next step in the management of this patient according to ACLS guidelines?

C) Deliver an unsynchronized shock with a defibrillator

A) Administer 1 mg of epinephrine IV/IO every 3-5 minutes

B) Perform synchronized cardioversion immediately

C) Deliver an unsynchronized shock with a defibrillator

D) Administer 300 mg of amiodarone IV push

A patient who recently experienced cardiac arrest has been stabilized with CPR and defibrillation, but now presents with wide-complex tachycardia, hypotension, and deteriorating renal function. The medical team is considering mechanical circulatory support to optimize hemodynamics. As the nurse, what is the most appropriate immediate action to assist in stabilizing the patient's condition?

B) Prepare and initiate an intra-aortic balloon pump (IABP) as ordered.

A) Administer a rapid infusion of intravenous fluids to address hypotension.

B) Prepare and initiate an intra-aortic balloon pump (IABP) as ordered.

C) Increase the dose of amiodarone to further stabilize the cardiac rhythm.

D) Administer a vasopressor such as norepinephrine to improve blood pressure.

A patient has just been resuscitated from cardiac arrest and presents with wide-complex tachycardia, hypotension, and deteriorating renal function. The healthcare team is considering multiple interventions to stabilize the patient's condition. As the nurse, which intervention should be prioritized to address the patient's immediate hemodynamic instability while minimizing further complications?

B) Initiate an infusion of norepinephrine to improve blood pressure and perfusion

A) Administer an additional bolus of amiodarone to stabilize the cardiac rhythm

B) Initiate an infusion of norepinephrine to improve blood pressure and perfusion

C) Prepare for emergent intubation to secure the airway and improve oxygenation

D) Arrange for immediate insertion of an intra-aortic balloon pump for mechanical support

A patient in critical condition presents with severe metabolic acidosis, reduced ejection fraction, and signs of right-sided heart failure. Laboratory findings show elevated liver enzymes and a decreased platelet count. After initiating low-dose norepinephrine and preparing for intra-aortic balloon pump insertion, which nursing intervention is the priority to optimize the patient's outcomes?

D) Evaluate urine output hourly to assess renal perfusion and function.

A) Administer sodium bicarbonate to correct metabolic acidosis.

B) Monitor for signs of bleeding due to low platelet count and potential DIC.

C) Assess for changes in mental status to evaluate cerebral perfusion.

D) Evaluate urine output hourly to assess renal perfusion and function.

A critically ill patient with severe metabolic acidosis, reduced ejection fraction, and signs of multi-organ dysfunction is being managed in the ICU. The team has initiated low-dose norepinephrine for hypotension and is preparing for an intra-aortic balloon pump insertion. Which nursing intervention is most crucial to prioritize in this scenario?

D) Regularly assess peripheral perfusion and urine output to determine the adequacy of hemodynamic support.

A) Monitor for signs of improved liver function to assess the effectiveness of cardiac support.

B) Evaluate for decreased acidosis by checking serial arterial blood gas analyses.

C) Assess for signs of worsening coagulopathy and monitor platelet counts closely.

D) Regularly assess peripheral perfusion and urine output to determine the adequacy of hemodynamic support.

A patient with heart failure and suspected disseminated intravascular coagulation (DIC) is on vasopressor support and has been intubated due to respiratory distress. The team needs to address the coagulation issues while considering the patient's cardiac and respiratory status. Which nursing intervention is most appropriate to prioritize in this situation?

A) Administer low-dose heparin infusion to prevent thrombotic complications while closely monitoring coagulation parameters.

B) Initiate a fluid restriction protocol to manage pulmonary edema and reduce cardiac workload.

C) Collaborate with the team to increase vasopressor support to improve cardiac output and tissue perfusion.

D) Prepare to administer blood products, such as platelets and fresh frozen plasma, to address coagulopathy and bleeding risk.

A patient with severe cardiac dysfunction and suspected pulmonary edema is showing signs of disseminated intravascular coagulation (DIC) with an increased prothrombin time (PT), activated partial thromboplastin time (aPTT), and thrombocytopenia. Considering the patient's condition and the risk of hemodynamic instability, what is the most appropriate nursing intervention to prioritize?

D) Implement mechanical ventilation settings to minimize further respiratory distress.

A) Administer intravenous furosemide to manage pulmonary congestion.

B) Initiate a low-dose heparin infusion to address the risk of thrombotic events.

C) Prepare for immediate transfusion of fresh frozen plasma to correct coagulopathy.

D) Implement mechanical ventilation settings to minimize further respiratory distress.

A patient with cardiogenic shock secondary to reduced left ventricular ejection fraction is experiencing acute kidney injury and disseminated intravascular coagulation (DIC). Despite maximum vasopressor support, the patient's blood pressure remains low. What is the most appropriate nursing intervention to prioritize at this time?

C) Prepare for the insertion of an intra-aortic balloon pump to enhance cardiac output.

A) Increase the dose of vasopressors to further support blood pressure.

B) Initiate renal replacement therapy to address acute kidney injury.

C) Prepare for the insertion of an intra-aortic balloon pump to enhance cardiac output.

D) Administer cryoprecipitate to correct coagulation abnormalities.

A 68-year-old patient with severe cardiogenic shock and acute kidney injury (AKI) is being managed in the ICU. Despite maximal vasopressor support, the patient's blood pressure is 85/50 mmHg with a heart rate of 140 beats per minute. The echocardiogram shows an ejection fraction of 15% and significant right ventricular dysfunction. The patient has decreased urine output and rising creatinine levels, indicating worsening renal function. Considering the patient's current condition, which intervention should the nurse prioritize to address the hemodynamic instability and prevent further renal deterioration?

C) Prepare for the insertion of an intra-aortic balloon pump to support cardiac output

A) Administer a bolus of intravenous fluids to improve renal perfusion

B) Initiate continuous renal replacement therapy to manage fluid overload and electrolyte imbalances

C) Prepare for the insertion of an intra-aortic balloon pump to support cardiac output

D) Administer cryoprecipitate to correct coagulopathy and improve hemodynamic stability

Myocardial infarction - Nursing Case Study

Pathophysiology

• Primary mechanism: Atherosclerotic plaque rupture in coronary arteries leads to thrombus formation, obstructing blood flow and causing ischemia in myocardial tissue. This results in the deprivation of oxygen and nutrients, leading to cell injury and death (necrosis) if not promptly resolved.

• Secondary mechanism: The ischemic cascade is triggered, involving the loss of ATP production due to impaired oxidative phosphorylation. This disrupts ionic homeostasis, causing calcium overload in cells, which further exacerbates cell injury and contributes to arrhythmias.

• Key complication: Without timely reperfusion, extensive myocardial necrosis can occur, resulting in impaired cardiac contractility and potential heart failure. Additionally, electrical instability can lead to life-threatening arrhythmias like ventricular fibrillation.

Patient Profile

Demographics:

62-year-old male, retired construction worker

History:

• Key past medical history: Hypertension, type 2 diabetes mellitus, hyperlipidemia, previous myocardial infarction 5 years ago

• Current medications: Metformin, Lisinopril, Atorvastatin, Aspirin, Metoprolol

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Severe chest pain radiating to the left arm and jaw

• Key symptoms: Shortness of breath, diaphoresis, nausea, dizziness

• Vital signs: Blood pressure 90/60 mmHg, heart rate 110 bpm, respiratory rate 28 breaths per minute, oxygen saturation 88% on room air, temperature 37.8°C

Section 1

As the healthcare team initiates the initial assessment, the patient's condition begins to further deteriorate. Despite the supplemental oxygen provided, his oxygen saturation stubbornly remains at 88%, indicating significant respiratory compromise. On auscultation, crackles are audible at the lung bases, suggesting pulmonary congestion, likely secondary to acute left ventricular failure. Jugular venous distention is noted, further supporting the presence of heart failure. The patient exhibits pronounced pallor and remains diaphoretic, with a weak, thready pulse. His blood pressure has dropped to 85/55 mmHg, while his heart rate slightly increases to 115 bpm, signifying a state of cardiogenic shock.

Laboratory results reveal elevated cardiac biomarkers; troponin I levels are significantly raised at 15 ng/mL, indicating substantial myocardial injury. The complete blood count shows mild leukocytosis, and a comprehensive metabolic panel reveals worsening renal function with a creatinine level of 2.1 mg/dL, reflecting acute kidney injury likely due to hypoperfusion. An arterial blood gas analysis indicates metabolic acidosis with a pH of 7.32 and a partial pressure of carbon dioxide (PaCO2) of 30 mmHg, alongside a bicarbonate level of 18 mmol/L, suggesting compensatory respiratory alkalosis.

As the team deliberates the next steps, the patient suddenly becomes unresponsive. The monitor displays ventricular tachycardia, quickly degenerating into ventricular fibrillation. Immediate cardiopulmonary resuscitation (CPR) is initiated, and the defibrillator is charged. This acute deterioration forces the team to prioritize rapid defibrillation and advanced cardiac life support (ACLS) protocols, while simultaneously considering the urgent need for reperfusion therapy to address the underlying myocardial infarction and prevent further complications.

Section 2

As the team continues with CPR and prepares for immediate defibrillation, the patient's condition remains critical. After two cycles of CPR and a single defibrillation shock, the patient regains a pulse, but his rhythm reverts to a wide-complex tachycardia. The team administers a bolus of amiodarone, hoping to stabilize the rhythm, while considering the need for intubation due to his compromised respiratory status. An urgent consultation with the interventional cardiology team is made to discuss the feasibility of an emergent percutaneous coronary intervention (PCI), given the likelihood of an occluded coronary artery contributing to the myocardial infarction and subsequent cardiac arrest.

Simultaneously, the patient's renal function continues to deteriorate, with a repeat creatinine measurement now at 2.5 mg/dL. This exacerbates concerns about potential fluid overload and the delicate balance required to manage the heart failure without worsening the acute kidney injury. The team is faced with the challenge of optimizing hemodynamics, considering both inotropic support to improve cardiac output and careful fluid management to avoid further pulmonary congestion.

Despite these efforts, new complications arise as the patient develops significant hypotension, with blood pressure dropping further to 78/50 mmHg, raising the possibility of multi-organ failure. The team quickly deliberates the need for mechanical circulatory support, such as an intra-aortic balloon pump, to stabilize the patient's hemodynamics while addressing the urgent need for reperfusion. This complex scenario necessitates advanced clinical judgment to prioritize interventions that will maximize the patient's chance of recovery, all while monitoring for potential complications from both the interventions and the underlying conditions.

Section 3

As the team continues to manage the patient's critical condition, they receive new diagnostic results from the laboratory and imaging studies that further complicate the clinical picture. The patient's arterial blood gas analysis reveals severe metabolic acidosis with a pH of 7.22, a bicarbonate level of 16 mEq/L, and a base deficit of -12, indicating significant tissue hypoxia and the need for urgent correction of acid-base imbalances. Concurrently, an echocardiogram performed at the bedside shows a severely reduced ejection fraction of 25%, with marked left ventricular hypokinesis and signs of right ventricular dysfunction, suggesting the possibility of right-sided heart failure contributing to the hypotension and multi-organ strain.

In addition to these findings, the patient's liver enzymes are markedly elevated, with AST and ALT levels over 300 IU/L, raising concerns about hepatic congestion and potential ischemic hepatitis secondary to low cardiac output. The team also notes a drop in platelet count to 90,000/µL, which could be indicative of early disseminated intravascular coagulation (DIC) or a response to the acute inflammatory state. These results necessitate a re-evaluation of the current treatment strategy, emphasizing the importance of hemodynamic stabilization and careful titration of medications, while also considering potential complications like bleeding risk due to the evolving coagulopathy.

Faced with this complex clinical scenario, the healthcare team re-assesses the balance between pharmacologic interventions and mechanical support. The decision is made to initiate low-dose vasopressor support with norepinephrine to address the refractory hypotension, while closely monitoring for signs of worsening organ perfusion. Meanwhile, preparations are underway for the placement of an intra-aortic balloon pump, aiming to optimize coronary perfusion and reduce cardiac workload. Throughout this process, the team remains vigilant for any new developments, recognizing that the patient's path to recovery will require ongoing critical thinking and dynamic adjustment of the treatment plan in response to his rapidly changing clinical status.

Section 4

As the team implements the new treatment strategy, they monitor the patient's response to the vasopressor support and initiate preparations for the intra-aortic balloon pump. Within the first hour, the patient's mean arterial pressure shows a slight improvement, rising to 65 mmHg, and there is a marginal increase in urine output, suggesting some stabilization of renal function. However, the team remains cautious, aware that these improvements could be transient. Despite the initial positive signs, the patient begins to exhibit signs of respiratory distress, with an increased respiratory rate climbing to 30 breaths per minute and a drop in oxygen saturation to 88% on a non-rebreather mask. This prompts an urgent reassessment of his respiratory status.

A repeat arterial blood gas analysis reveals worsening hypoxemia, with a PaO2 of 55 mmHg and a persistent metabolic acidosis, now with a pH of 7.18. The team suspects the development of pulmonary edema secondary to the severely compromised cardiac function and right-sided heart failure, exacerbated by aggressive fluid resuscitation attempts earlier in the course of the treatment. Chest X-ray confirms bilateral infiltrates consistent with pulmonary congestion. Considering these findings, the team decides to intubate the patient and initiate mechanical ventilation to ensure adequate oxygenation and reduce the work of breathing, recognizing the risk of further hemodynamic instability with positive pressure ventilation.

In the midst of these challenges, the patient's coagulation profile becomes a critical concern. The laboratory reports an increased prothrombin time (PT) and activated partial thromboplastin time (aPTT), alongside a further drop in platelet count to 75,000/µL, confirming the suspicion of evolving disseminated intravascular coagulation (DIC). This complicates the administration of anticoagulants, vital for preventing thrombotic events given the reduced ejection fraction and potential for stasis. The team must now balance the bleeding risk against the need for anticoagulation, considering options such as low-dose heparin infusion under strict monitoring or alternative therapies. This delicate balance underscores the need for meticulous clinical judgment as the team navigates the multifaceted challenges in stabilizing the patient’s condition.

Section 5

As the team continues to manage the patient’s complex condition, they closely monitor his response to mechanical ventilation and the ongoing vasopressor support. However, within a few hours, new complications arise. The patient's hemodynamic status takes a concerning turn, with his blood pressure dropping to 85/50 mmHg despite maximum vasopressor doses. This hypotensive episode is accompanied by a significant tachycardia, with heart rates spiking to 140 beats per minute. Recognizing the potential for cardiogenic shock, the team conducts an urgent bedside echocardiogram, which reveals a marked reduction in left ventricular ejection fraction, now estimated at 15%, and signs of significant right ventricular dysfunction. This finding correlates with the patient’s deteriorating clinical status and prompts immediate consideration of additional circulatory support options, including the imminent initiation of the intra-aortic balloon pump.

In parallel, the patient's renal function shows a sharp decline, with serum creatinine rising to 3.8 mg/dL and blood urea nitrogen increasing to 78 mg/dL, indicating acute kidney injury likely precipitated by ongoing hypoperfusion and potential nephrotoxic effects from therapeutic interventions. Urine output has decreased to less than 20 mL/hour, underscoring the severity of renal compromise. This prompts the nephrology consult team to evaluate the need for renal replacement therapy, balancing the risks of fluid shifts against the necessity to manage volume overload and prevent further metabolic derangements. The team remains vigilant for signs of worsening electrolyte imbalances, particularly hyperkalemia, which could further destabilize the patient’s cardiac rhythm.

Concurrently, the patient's coagulation abnormalities continue to evolve, with further decreases in fibrinogen levels and an increase in D-dimer, reinforcing the diagnosis of disseminated intravascular coagulation. This ongoing coagulopathy necessitates a careful reassessment of the anticoagulation strategy, as the risk of catastrophic bleeding events must be weighed against the need to mitigate thromboembolic complications in the setting of severely impaired cardiac function and immobility. The team deliberates potential interventions, such as administering cryoprecipitate to address the low fibrinogen, while cautiously continuing low-dose anticoagulation under rigorous monitoring. The complexity of the patient's condition necessitates constant reevaluation and adjustment of the treatment plan, as the team endeavors to stabilize him amidst the multifaceted clinical challenges.