A-fib rvr - Nursing Case Study

Pathophysiology

• Primary mechanism: Atrial fibrillation (A-Fib) is primarily caused by chaotic and irregular electrical impulses in the atria, the upper chambers of the heart. These irregular impulses cause the atria to fibrillate, or quiver, instead of beating normally.

• Secondary mechanism: Rapid ventricular response (RVR) in A-Fib refers to the fast and irregular conduction of these impulses from the atria to the ventricles, the heart's lower chambers. This results in uncoordinated contraction and reduced heart efficiency.

• Key complication: Inefficient heart pumping may lead to pooling and clotting of blood in the atria, increasing the risk of stroke. Additionally, long-term A-Fib RVR can weaken the heart muscle, leading to heart failure.

Patient Profile

Demographics:

67-year-old male, retired construction worker.

History:

• Key past medical history: Diagnosed with hypertension and hyperlipidemia.

• Current medications: Lisinopril 20mg daily, Atorvastatin 40mg daily

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Shortness of breath and palpitations.

• Key symptoms: Fatigue, irregular heartbeat, chest discomfort, lightheadedness.

• Vital signs: Blood pressure 160/90 mmHg, heart rate 135 bpm (irregular), respiratory rate 22 breaths per minute, oxygen saturation 93% on room air, temperature 37.2°C.

Section 1

Change in Patient Status:

The patient's condition starts to decline over the next few hours. His shortness of breath worsens and he becomes increasingly restless and agitated. His heart rate climbs to 160 bpm and his blood pressure drops to 125/80 mmHg. His oxygen saturation also decreases to 89% on room air, indicating increasing difficulty with oxygenation. Additionally, the patient complains of increasing chest discomfort, rating it an 8 on a scale of 10.

These new symptoms require urgent intervention and re-evaluation. The increasing heart rate and dropping blood pressure suggest a loss of cardiac output due to the rapid irregular heartbeats, which is also supported by the worsening oxygen saturation. The escalating chest pain may suggest myocardial ischemia due to the decreased efficiency of the heart. The patient's restlessness and agitation may be signs of reduced cerebral perfusion, again secondary to the loss of cardiac output. The team must act quickly to address the patient's deteriorating condition and prevent further complications such as stroke or heart failure.

Section 2

Response to Interventions:

The team immediately administers oxygen therapy, increasing the patient's oxygen saturation to 94%. An IV line is started and a bolus of normal saline is given to increase the intravascular volume and cardiac output. The patient is started on intravenous diltiazem, a calcium channel blocker, to slow down the heart rate and improve cardiac efficiency. Despite these interventions, the patient's heart rate remains at 160 bpm, and his blood pressure continues to drop, now at 110/70 mmHg. His chest pain persists, still at an 8/10, and he remains restless and agitated.

The team then decides to cardiovert the patient, which should help re-establish a regular heart rhythm and improve cardiac output. Sedation is given prior to the procedure for comfort. Post-cardioversion, the patient's heart rate drops to 110 bpm and his blood pressure rises to 130/85 mmHg. His oxygen saturation remains steady at 94%. The chest pain reduces to a 4/10, and the patient appears less agitated. However, the patient still exhibits signs of restlessness and becomes increasingly confused, suggesting ongoing cerebral perfusion issues. The team needs to monitor the patient closely and consider further diagnostic tests to identify possible causes of his confusion and determine the next steps in his care.

Section 3

New Diagnostic Results:

The team decides to perform a CT scan to rule out the possibility of a stroke, given the persistent confusion and restlessness. The results reveal a small ischemic stroke in the right middle cerebral artery territory, possibly due to an embolus from the atrial fibrillation. The INR is checked immediately and is found to be 1.0, indicating the patient is not therapeutically anticoagulated.

Additionally, a troponin level is checked due to the persistent chest pain, and comes back moderately elevated at 0.7 ng/mL, raising the concern for myocardial ischemia or infarction. The EKG is repeated and shows new T wave inversions in the inferior leads. This new information suggests that the patient's atrial fibrillation may have led to a clot formation in the atria, which embolized, causing both the stroke and possible myocardial infarction. These complications have significantly increased the complexity of the patient's condition, and the team must now address both the stroke and possible myocardial infarction in addition to managing the atrial fibrillation.

Section 4

The patient’s status continues to deteriorate despite the initial medical management. The patient becomes increasingly lethargic and complains of worsening chest pain. His blood pressure drops to 90/60 mmHg and his heart rate rises to 130 beats per minute. His respiratory rate is also elevated at 24 breaths per minute, and his oxygen saturation drops to 90% on room air. These findings suggest that the patient may be developing shock, possibly due to the myocardial infarction.

In response to these changes, the medical team initiates IV fluid resuscitation and administers supplemental oxygen. The patient is started on a heparin drip to address the inadequate anticoagulation and prevent further clot formation. Despite these interventions, the patient’s mentation continues to decline and he becomes increasingly unresponsive. In light of these findings, the team decides to intubate the patient to protect his airway and ensure adequate oxygen delivery. This decision further complicates the patient's condition, as it necessitates transfer to the intensive care unit (ICU) for ongoing management. It also raises new questions about the patient's prognosis and the potential need for long-term ventilatory support.

Section 5

As part of ongoing monitoring, the medical team orders a series of tests, including a complete blood count, basic metabolic panel, troponin levels, and another ECG. The patient's blood work reveals an elevated white blood cell count of 15,000/mm3, suggesting a possible infection. His potassium level is also elevated at 5.5 mEq/L. Troponin levels are significantly increased at 0.25 ng/mL, confirming the suspicion of myocardial infarction. The ECG shows persistent atrial fibrillation with a rapid ventricular response.

The patient's status continues to decline despite these interventions. His blood pressure remains low at 85/55 mmHg, his heart rate is still elevated at 135 beats per minute, and his oxygen saturation drops further to 88% despite being on supplemental oxygen. The patient becomes completely unresponsive and his Glasgow Coma Scale score drops to 7. This deteriorating condition raises concerns about the patient's cerebral perfusion and the possibility of impending multi-organ failure. The medical team decides to initiate vasopressor therapy, considering the patient's persistent hypotension and signs of shock. The choice of vasopressor and the decision to escalate care will depend on the patient's response to these interventions. The team also starts broad-spectrum antibiotics, given the patient's elevated white blood cell count and the potential risk of sepsis.