cardiac arrest - Nursing Case Study

Pathophysiology

• Primary mechanism: Electrical Dysfunction - Cardiac arrest often stems from arrhythmias such as ventricular fibrillation, where chaotic electrical activity prevents effective heart contractions, halting blood circulation.

• Secondary mechanism: Ischemia - Reduced blood flow due to coronary artery blockage can deprive heart tissue of oxygen, impairing electrical impulses and contractility, potentially leading to cardiac arrest.

• Key complication: Global Ischemia - The cessation of effective heart pumping results in widespread oxygen deprivation, risking irreversible organ damage if circulation isn't rapidly restored.

Patient Profile

Demographics:

58-year-old male, construction worker

History:

• Key past medical history: Hypertension, Type 2 Diabetes, Hyperlipidemia

• Current medications: Lisinopril, Metformin, Atorvastatin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Sudden collapse at work with loss of consciousness

• Key symptoms: Chest pain prior to collapse, shortness of breath, dizziness, and palpitations

• Vital signs: Blood pressure 85/60 mmHg, heart rate 120 bpm, respiratory rate 28 breaths/min, oxygen saturation 88% on room air, temperature 98.6°F (37°C)

Section 1

New Diagnostic Results:

Following the initial resuscitation efforts, the patient was transferred to the emergency department for further evaluation and stabilization. An immediate electrocardiogram (ECG) was performed, revealing ST-segment elevation in the inferior leads, indicating a probable acute inferior myocardial infarction. This correlates with the patient's pre-arrest symptoms of chest pain and palpitations. Blood tests, including cardiac biomarkers, were drawn, and initial results showed elevated troponin levels, confirming myocardial injury. The patient's blood glucose was measured at 185 mg/dL, reflecting inadequate control of his Type 2 Diabetes, which may have contributed to his current cardiac event.

In addition to the laboratory findings, a chest X-ray was performed to assess for any potential complications such as pulmonary edema, which can often accompany myocardial infarction. The X-ray showed mild pulmonary congestion, suggesting early signs of heart failure, possibly due to the compromised cardiac function from the infarction. Furthermore, the patient's blood pressure remained low at 90/58 mmHg despite fluid resuscitation, and his oxygen saturation improved to 91% with supplemental oxygen, indicating ongoing hemodynamic instability and a need for urgent intervention to restore coronary perfusion.

These diagnostic results necessitate a nuanced clinical approach, balancing the need for reperfusion therapy such as percutaneous coronary intervention (PCI) with the management of his hemodynamic status. The healthcare team must consider the patient's history of hypertension, diabetes, and hyperlipidemia, as these factors increase the complexity of his care. The findings highlight the importance of promptly addressing the myocardial infarction to prevent further complications such as cardiogenic shock or multi-organ failure, which could significantly impact the patient's prognosis and recovery.

Section 2

Change in Patient Status:

As the medical team prepared to initiate reperfusion therapy, the patient's condition began to deteriorate. His blood pressure continued to drop, now reading at 82/50 mmHg, despite the administration of intravenous fluids and vasopressor support. The patient exhibited signs of altered mental status, becoming increasingly lethargic and confused, which raised concerns about cerebral perfusion. His heart rate increased to 130 beats per minute, indicative of a compensatory response to hypotension but also raising the risk of further myocardial oxygen demand, potentially worsening the ischemic injury.

Simultaneously, the patient's respiratory status showed signs of compromise. Although his oxygen saturation initially improved with supplemental oxygen, it began to decline again, now recorded at 88%. Auscultation revealed crackles in both lung bases, suggesting worsening pulmonary congestion and possible flash pulmonary edema, a complication often seen in acute heart failure exacerbations. The patient's respiratory rate increased to 28 breaths per minute, indicating respiratory distress and the need for escalation of respiratory support.

Given these developments, the healthcare team was confronted with the critical decision of prioritizing interventions that would stabilize the patient hemodynamically while preparing for urgent PCI. The necessity to optimize cardiac output and ensure adequate oxygen delivery to vital organs became paramount. The team considered the potential need for advanced circulatory support, such as intra-aortic balloon pump (IABP) insertion, to bridge the patient to more definitive treatment. Additionally, the consideration of diuretics to manage fluid overload was weighed against the risk of further compromising blood pressure. This complex situation underscored the importance of dynamic clinical reasoning and the need to frequently reassess and adapt the treatment plan as the patient's status evolved.

Section 3

As the medical team continued to monitor the patient closely, new diagnostic results provided further insight into the complexities of his condition. An urgent arterial blood gas analysis revealed a mixed metabolic and respiratory acidosis, with a pH of 7.28, pCO2 of 55 mmHg, and HCO3 of 18 mEq/L. This finding indicated inadequate ventilation and possible respiratory failure, compounded by the metabolic demands of ongoing ischemia. Concurrently, laboratory tests showed elevated lactate levels at 5.2 mmol/L, reflecting tissue hypoperfusion and highlighting the urgency to optimize circulatory support.

The echocardiogram performed at the bedside revealed severely reduced left ventricular ejection fraction at 25%, consistent with acute heart failure and cardiogenic shock. These findings underscored the critical need for immediate intervention to support cardiac function and improve tissue perfusion. The team discussed the potential benefits of inserting an intra-aortic balloon pump (IABP) to decrease afterload and enhance coronary perfusion, considering the patient's hypotension and high myocardial oxygen demand.

As the team deliberated on the course of action, the patient's renal function began to decline, evidenced by a rising creatinine level from 1.2 to 2.1 mg/dL, suggesting acute kidney injury secondary to poor perfusion. This development further complicated the decision-making process regarding diuretic use for pulmonary congestion. The case now necessitated a delicate balancing act between managing hemodynamic instability, addressing respiratory compromise, and protecting renal function, all while ensuring timely preparation for potential percutaneous coronary intervention. The unfolding situation highlighted the need for a coordinated, multidisciplinary approach to stabilize the patient and prevent further complications.

Section 4

As the medical team proceeded with the plan to insert an intra-aortic balloon pump (IABP), the patient's condition presented new complications that required immediate attention. Despite efforts to stabilize the respiratory status, the patient began exhibiting signs of acute respiratory distress; his oxygen saturation dropped to 84% on high-flow oxygen, and he became increasingly tachypneic, with a respiratory rate climbing to 32 breaths per minute. Auscultation revealed diffuse crackles throughout the lung fields, indicating worsening pulmonary edema. This respiratory compromise necessitated the prompt initiation of non-invasive positive pressure ventilation (NIPPV) to improve oxygenation and decrease the work of breathing, while the team considered the potential need for intubation if his condition did not improve.

Simultaneously, the patient’s hemodynamic status remained precarious. Blood pressure readings fluctuated, with systolic pressures barely reaching 90 mmHg despite the administration of inotropic support. The decision to proceed with IABP insertion was reaffirmed, aiming to provide mechanical assistance to improve coronary perfusion and reduce cardiac workload. Meanwhile, the renal function continued to decline, with the latest creatinine level rising to 2.5 mg/dL and urine output decreasing significantly to less than 20 mL/hour over the past three hours. This oliguria suggested worsening acute kidney injury, further complicating fluid management strategies.

In light of these developments, the team recognized the critical need for a multidisciplinary approach to simultaneously address the cardiac, respiratory, and renal challenges. They coordinated closely with nephrology to discuss the feasibility of renal replacement therapy should the renal function continue to deteriorate despite optimization of hemodynamics. The critical care team remained vigilant in monitoring the patient’s response to the NIPPV and IABP, preparing for potential escalation of care in the form of mechanical ventilation and advanced cardiac interventions. This collaborative effort underscored the complexity of managing a patient with multifaceted organ failure and emphasized the importance of timely and coordinated interventions to stabilize the patient’s condition and prevent further deterioration.

Section 5

As the team continued to manage the patient's critical condition, new diagnostic results provided further insights into the underlying complications. A repeat chest X-ray revealed worsening pulmonary congestion, confirming the severity of pulmonary edema. The non-invasive positive pressure ventilation (NIPPV) was achieving some improvement in oxygenation, with the patient’s oxygen saturation rising to 90%, but his work of breathing remained high. Arterial blood gas analysis showed a pH of 7.28, PaCO2 of 58 mmHg, and HCO3 of 24 mEq/L, indicating a respiratory acidosis with partial metabolic compensation. These findings suggested that despite partial stabilization, the patient’s respiratory compromise was significant and could necessitate intubation if not rapidly resolved.

Concurrently, the laboratory results returned with an elevated troponin level of 0.45 ng/mL, indicative of ongoing myocardial stress and potential ischemia, perhaps exacerbated by the low cardiac output state. The inotropic support was adjusted to optimize cardiac function, and the intra-aortic balloon pump (IABP) was successfully inserted, aiming to enhance coronary perfusion and reduce afterload. The interdisciplinary team, including cardiology and critical care specialists, evaluated the patient’s hemodynamic response post-IABP insertion. Initial readings showed a slight improvement, with systolic blood pressure stabilizing around 95 mmHg, offering a glimmer of hope in the hemodynamic stabilization process.

However, the renal function continued to pose a challenge. The latest laboratory tests showed further increases in blood urea nitrogen and serum creatinine, with levels escalating to 80 mg/dL and 3.2 mg/dL, respectively. The nephrology team was consulted, and discussions were initiated regarding the timing and modality of renal replacement therapy. The team considered continuous renal replacement therapy (CRRT) to manage the acute kidney injury, given its potential benefits in hemodynamic stability and fluid management. This decision-making process required careful clinical reasoning to balance the benefits of immediate intervention against the risks of further hemodynamic compromise. As the team prepared for potential CRRT initiation, they remained vigilant, understanding that the patient's journey was far from over and that meticulous coordination would be crucial in navigating the complex interplay of cardiac, pulmonary, and renal challenges.