hemodynamically unstable sepsis patient with cardiac dysrhythmia - Nursing Case Study

Pathophysiology

• Primary mechanism: Sepsis triggers systemic inflammatory response leading to vasodilation, increased capillary permeability, and microclot formation. This results in hypotension and impaired tissue perfusion, causing hemodynamic instability.

• Secondary mechanism: Sepsis-related myocardial depression and dysautonomia contribute to cardiac dysrhythmias. The hypoxia, acidosis, and electrolyte imbalances from poor tissue perfusion further exacerbate dysrhythmias.

• Key complication: The combination of hemodynamic instability and cardiac dysrhythmias increases the risk of cardiac arrest. Rapid recognition and prompt intervention are critical to improve patient outcomes.

Patient Profile

Demographics:

71-year-old male, retired construction worker

History:

• Key past medical history: Diagnosed with Type 2 diabetes, hypertension, and previously treated for a mild stroke

• Current medications: Metformin, Lisinopril, Aspirin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: High fever, chills, rapid heart rate, and confusion

• Key symptoms: Shortness of breath, extreme fatigue, palpitations, reduced urine output, cold and clammy skin

• Vital signs: Blood pressure 85/50 mmHg, heart rate 130 bpm, respiratory rate 22 breaths per minute, temperature 39.4°C, oxygen saturation 90% on room air

Section 1

Change in Patient Status:

The patient's condition continues to deteriorate. He is now experiencing severe abdominal pain and his level of consciousness is decreasing - he is only rousable to painful stimuli. His skin has a mottled appearance, indicating poor perfusion, and his extremities are cool to touch.

His vital signs have further declined: His blood pressure is now 78/40 mmHg, heart rate is 145 bpm, respiratory rate is 28 breaths per minute and his oxygen saturation has dropped to 86% on room air. His temperature has spiked to 40.2°C, indicating his body is still fighting the infection. The worsening tachycardia, hypotension, and decreased oxygen saturation suggest the sepsis is progressing to septic shock, and the patient is at high risk of multi-organ failure.

Clinical reasoning suggests the severe abdominal pain and altered mental status may indicate a new complication such as an intra-abdominal septic focus or decreased perfusion to the brain. The patient's decreased level of consciousness, coupled with the increased work of breathing and decreasing oxygen saturation, could suggest developing respiratory failure. Immediate interventions should focus on resuscitation to improve perfusion and consultation with critical care for possible intubation. The patient's declining condition necessitates urgent diagnostic investigations to ascertain the source of infection and guide antibiotic therapy.

Section 2

New Diagnostic Results:

Laboratory results show a white blood cell count of 22,000/uL, indicating an intense immune response. Lactic acid level is 5 mmol/L, showing evidence of tissue hypoperfusion. The blood cultures drawn earlier are still pending. An emergent CT scan of the abdomen reveals a perforated diverticulum with evidence of localized peritonitis. Blood gas analysis reveals a pH of 7.28, PaCO2 of 35 mmHg, PaO2 of 60 mmHg, and HCO3- of 14 mEq/L, indicating a primary metabolic acidosis with uncompensated respiratory alkalosis.

These findings suggest the source of the sepsis is the perforated diverticulum leading to peritonitis, which further complicates his hemodynamic instability. The metabolic acidosis could be due to lactic acidosis from poor tissue perfusion and the respiratory alkalosis could be a compensatory mechanism for the metabolic acidosis. The PaO2 also indicates moderate hypoxemia, further justifying the need for advanced respiratory support.

Given these results, the patient is at high risk of developing acute respiratory distress syndrome (ARDS) from sepsis and possible acute kidney injury (AKI) due to poor perfusion. These findings will guide the subsequent management of the patient, which will likely involve immediate surgical intervention for the perforated diverticulum, aggressive fluid resuscitation, broad-spectrum antibiotics, and possible vasopressor support to maintain adequate perfusion. The team also needs to consider the possibility of intubating the patient to secure his airway and improve oxygenation.

Section 3

New Complications:

The patient's condition continues to deteriorate despite the aggressive fluid resuscitation and broad-spectrum antibiotics. His blood pressure remains low at 85/50 mmHg, and heart rate is trending upwards at 120 beats per minute. He's becoming progressively more tachypneic with a respiratory rate of 30 breaths per minute. On examination, his skin appears mottled and cool to touch, indicating poor peripheral perfusion. Urine output has also decreased significantly to 20 mL/hr over the past two hours, raising concerns for potential acute kidney injury.

The latest arterial blood gas analysis reveals a worsening metabolic acidosis with pH of 7.21, PaCO2 of 38 mmHg, and HCO3- of 12 mEq/L. The lactate level has also risen to 6.3 mmol/L, indicating ongoing tissue hypoperfusion. This suggests that the patient's body is not responding adequately to the current resuscitative measures. At this point, the medical team must consider escalating care, which may include starting vasopressor support to maintain adequate blood pressure and organ perfusion. Given the worsening hypoxemia and tachypnea, intubation for mechanical ventilation may also be necessary to support the patient's respiratory status. The patient's worsening clinical picture underscores the need for immediate surgical intervention to address the underlying source of the sepsis.

Section 4

New Diagnostic Results:

Despite the initiation of vasopressor support, the patient's hemodynamic stability continues to falter. His blood pressure is now 80/45 mmHg and his heart rate has increased to 130 beats per minute. A repeat arterial blood gas test reveals further deterioration of the metabolic acidosis with a pH of 7.15, PaCO2 of 40 mmHg, and HCO3- of 10 mEq/L. The lactate level has now spiked to 7.6 mmol/L, demonstrating continued tissue hypoperfusion. A new set of blood cultures have been drawn and sent to the lab to identify possible pathogens.

Change in Patient Status:

The patient's consciousness level has also started to decline, with a Glasgow Coma Scale (GCS) now at 11/15, down from 14/15 just a few hours ago. His respiratory status has further declined with an increased respiratory rate of 35 breaths per minute and decreasing oxygen saturation levels despite supplemental oxygen. These signs indicate possible impending respiratory failure. The patient's decreased urine output persists, and his latest creatinine level has risen to 2.5 mg/dL from a baseline of 1.0 mg/dL, indicating acute kidney injury. The worsening renal function, along with the patient's deteriorating hemodynamics and respiratory status, calls for urgent reassessment of the current management plan.

Section 5

New Complications:

During a meticulous reassessment of the patient's condition, the nurse noticed that the patient's skin has become cold and clammy to touch, with a visible mottled appearance. This is indicative of worsening systemic hypoperfusion, suggesting that the septic shock is progressing. Furthermore, the patient's cardiac monitor started to show episodes of non-sustained ventricular tachycardia, a potential sign of myocardial ischemia or instability. This new cardiac dysrhythmia, along with his steadily declining blood pressure, raises concerns about the adequacy of the current vasopressor support and possible need for advanced cardiac support.

Response to Interventions:

The healthcare team decided to escalate the patient's care by initiating continuous renal replacement therapy (CRRT) to manage the acute kidney injury and metabolic disturbances. The patient was also intubated and mechanically ventilated to manage his deteriorating respiratory status. Despite these interventions, however, the patient's hemodynamic status remains precarious with a persistent hypotension (BP 75/40 mmHg) and tachycardia at 135 beats per minute. The team decided to add another vasopressor to provide additional support. The blood culture results are now eagerly awaited to guide targeted antibiotic therapy. The new findings and response to interventions underscore the gravity of the patient's condition and the need for a comprehensive, multidisciplinary approach to his care.