pulseless electrical activity - Nursing Case Study

Pathophysiology

• Primary mechanism: Pulseless Electrical Activity (PEA) arises when the heart's electrical activity remains intact, but the mechanical pumping function fails. This discrepancy occurs due to significant decreases in heart muscle responsiveness or cardiovascular system resistance.

• Secondary mechanism: The underlying causes of PEA are commonly remembered as the H's and T's: Hypovolemia, Hypoxia, Hydrogen ion (acidosis), Hypo/hyperkalemia, Hypothermia, Thrombosis (pulmonary and coronary), Tamponade (cardiac), Tension pneumothorax, and Trauma. These conditions disrupt the electrical-mechanical coupling in the heart, leading to ineffective contractions.

• Key complication: PEA often results in inadequate circulation of blood, leading to cardiac arrest. Despite the presence of organized electrical activity, the absence of a pulse causes a life-threatening situation that requires immediate intervention.

Patient Profile

Demographics:

62-year-old male, retired construction worker

History:

• Key past medical history: Hypertension, Type 2 Diabetes, previous myocardial infarction

• Current medications: Aspirin, Metformin, Lisinopril

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Sudden onset of shortness of breath and chest discomfort

• Key symptoms: Fatigue, dizziness, cold and sweaty skin

• Vital signs: Blood pressure 90/60 mmHg, pulse not palpable, respiratory rate 22/min, temperature 98.6°F, oxygen saturation 88% on room air

Section 1

Change in Patient Status:

Over the next couple of hours, the patient's condition began to deteriorate. His shortness of breath and chest discomfort worsened, and he became increasingly lethargic. His skin was cool, pale, and clammy. His oxygen saturation dropped to 82% despite receiving oxygen supplementation. An ECG showed normal sinus rhythm, however, no pulse could be detected which confirmed the diagnosis of PEA.

New Diagnostic Results:

Blood tests revealed severe metabolic acidosis, with an arterial blood gas showing a pH of 7.10 and a bicarbonate level of 15 mEq/L. This finding suggests that the patient's Pulseless Electrical Activity might be secondary to severe acidemia, one of the H's in the H's and T's of PEA. The patient's potassium level was also elevated at 6.5 mEq/L, which could be a factor contributing to the patient's PEA. His glucose level was 350 mg/dL suggesting poor control of his diabetes. A chest X-ray suggested no signs of tension pneumothorax or cardiac tamponade.

These findings indicate a critical situation and the need for immediate intervention. The healthcare team would need to address the underlying causes (acidosis and hyperkalemia) to restore effective contractions and circulation. This situation requires the rapid application of clinical reasoning skills to manage the patient's deteriorating condition, and highlights the interconnected nature of the patient's comorbidities and their impact on his current health crisis.

Section 2

Response to Interventions:

The healthcare team initiated aggressive treatment to address the acidosis and hyperkalemia. They administered sodium bicarbonate to correct the metabolic acidosis but the patient’s pH only marginally improved to 7.15. The team also started the patient on insulin and dextrose to reduce the elevated potassium levels and to manage his hyperglycemia. Despite these interventions, the patient’s potassium level remained at 6.3 mEq/L, still significantly higher than normal.

Simultaneously, attempts were made to support the patient's respiratory status. He was placed on a non-rebreather mask with 100% oxygen, which raised his oxygen saturation to 88%. However, this was still insufficient and the patient required intubation and mechanical ventilation to maintain effective oxygenation. Despite these aggressive interventions, the patient's overall condition remained critical, with persistent PEA and a dangerously low blood pressure of 80/50 mmHg.

The healthcare team was confronted with a complex clinical picture and required to utilize their clinical reasoning skills to plan the next steps in patient management. The patient’s ongoing acidosis, hyperkalemia, poor glycemic control, and deteriorating respiratory and hemodynamic status painted a grim picture. The team had to consider additional potential complications, such as acute kidney injury or sepsis, and decide on the most appropriate course of action.

Section 3

New Complications:

Despite the team's efforts, the patient's condition began to deteriorate further. His blood pressure dropped to a dangerously low level of 70/40 mmHg and his heart rate accelerated to 120 beats per minute. His oxygen saturation, despite being on mechanical ventilation, also dropped to a concerning 82%. Additionally, the patient's urine output started to decrease, dropping to less than 30 mL/hr, suggesting the onset of acute kidney injury.

New lab results added to the team's concerns. The patient's serum creatinine level increased to 2.5 mg/dL from a baseline of 0.9 mg/dL, and his blood urea nitrogen (BUN) level rose to 40 mg/dL. The patient's persistent hyperkalemia, worsening acidosis, and new onset of renal dysfunction pointed towards a potential diagnosis of sepsis. The team decided to initiate broad-spectrum antibiotics and fluid resuscitation while awaiting the results of blood cultures. The situation was dire, and the team continued to utilize their clinical reasoning skills to manage the patient's rapidly evolving condition.

Section 4

Change in Patient Status:

The patient’s status continued to decline despite aggressive interventions. His blood pressure further dropped to 65/35 mmHg and his heart rate escalated to 130 beats per minute. The oxygen saturation remained at a low 80% even with the adjustments to the ventilator settings. His urine output continued to decrease, now less than 20 mL/hr. The patient became increasingly unresponsive, and his Glasgow Coma Scale (GCS) dropped to 8 from an initial 15 upon admission.

In response to the worsening condition, the team decided to administer vasoactive medications in an attempt to increase the patient's blood pressure and to optimize tissue perfusion. An arterial line was placed to closely monitor the patient's blood pressure and a central venous catheter was inserted for the administration of vasoactive drugs. The team also consulted a nephrologist considering the possibility of initiating renal replacement therapy due to the patient's progressive renal dysfunction. The team knew they needed to act rapidly to reverse the patient's deteriorating condition.

Section 5

New Diagnostic Results:

Upon further examination, the patient's lab results revealed an increase in serum potassium levels to 6.0 mEq/L from an initial 4.2 mEq/L and a rise in creatinine levels to 2.5 mg/dl from 1.2 mg/dl upon admission, indicating worsening renal function. Blood gas analysis showed a metabolic acidosis with a pH of 7.25, a pCO2 of 35 mmHg, and a bicarbonate level of 18 mEq/L, all indicative of a systemic problem.

The patient's chest X-ray demonstrated diffuse bilateral infiltrates, raising the possibility of acute respiratory distress syndrome (ARDS). The electrocardiogram (ECG) showed peaked T-waves and a widened QRS complex, suggesting hyperkalemia. These findings prompted the team to reconsider their clinical approach, recognising the vital need to address the patient's worsening renal function and electrolyte imbalance.