afib - Nursing Case Study

Pathophysiology

• Primary mechanism: Afib results from aberrant electrical impulses, usually within the pulmonary veins, causing rapid and irregular atrial contractions. This disrupts normal sinus rhythm, leading to ineffective atrial pumping and irregular ventricular rate.

• Secondary mechanism: The irregular atrial contractions cause blood to pool and stagnate, increasing the risk of clot formation within the atria (thromboembolism).

• Key complication: If a thrombus dislodges, it can cause occlusion in the cerebral vasculature leading to stroke, or in the coronary arteries leading to myocardial infarction. Also, long-term rapid ventricular response can result in tachycardia-induced cardiomyopathy.

Patient Profile

Demographics:

72-year-old male, retired construction worker

History:

• Key past medical history: Diabetes type II, Hypertension, Hyperlipidemia, previous stroke

• Current medications: Metformin, Lisinopril, Atorvastatin, Warfarin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Rapid heart rate, shortness of breath, fatigue

• Key symptoms: Irregular heartbeat, dizziness, fainting spells, chest discomfort, anxiety

• Vital signs: Blood pressure 190/100 mmHg, Pulse 140 bpm irregular, Respiratory rate 22 breaths per minute, Temperature 98.6 F, Oxygen saturation 88% on room air.

Section 1

Change in Patient Status:

Following initial assessment, the patient was placed on supplemental oxygen, and rate control measures were initiated. Despite these interventions, the patient's symptoms continued to worsen. He became increasingly tachypneic, with a respiratory rate of 28 breaths per minute, and his oxygen saturation dropped to 84% on 2 liters of oxygen. He also complained of increasing chest discomfort and fatigue. His blood pressure became labile, fluctuating between 180/110 mmHg and 150/90 mmHg. His heart rate remained irregular and high, ranging between 130-150 beats per minute.

New Complications:

The patient's worsening respiratory status, coupled with his unstable hemodynamics, suggested the development of a possible complication, such as tachycardia-induced cardiomyopathy or a thromboembolic event. The medical team was particularly concerned about the risk of a myocardial infarction given the patient's history of hyperlipidemia and hypertension, in addition to his new-onset chest discomfort. A 12-lead ECG showed new ST segment changes suggestive of ischemia. Troponin levels were ordered, and the initial result came back above the reference range at 0.12 ng/mL (reference <0.04 ng/mL), indicating possible myocardial injury. An urgent cardiology consult was requested, and the patient was prepared for potential transfer to the cardiac catheterization lab.

Section 2

Change in Patient Status:

Despite the efforts of the healthcare team, the patient's condition continued to deteriorate. His tachypnea worsened, with his respiratory rate spiking to 35 breaths per minute, and his oxygen saturation fell further to 78% on 4 liters of oxygen. His blood pressure remained unstable, ranging now between 200/120 mmHg and 160/100 mmHg. His heart rate continued to fluctuate irregularly, now peaking at 170 beats per minute. The patient began to exhibit signs of altered mental status, demonstrating confusion and exhibiting restlessness. His skin became cool and clammy, suggesting a possible decrease in cardiac output.

New Diagnostic Results:

In response to the patient's deteriorating condition, further investigations were initiated. An urgent echocardiogram was performed and revealed a new reduction in ejection fraction to 30% (reference >55%), indicative of heart failure. His troponin levels were repeated, which escalated to 0.35 ng/mL, suggesting ongoing myocardial injury. An arterial blood gas showed a respiratory acidosis with a pH of 7.28 (reference 7.35-7.45), PaCO2 of 55 mmHg (reference 35-45 mmHg), and a PaO2 of 55 mmHg (reference >75 mmHg), indicating severe hypoxemia and inadequate ventilation. These new findings led the medical team to suspect a possible acute coronary syndrome superimposed on his atrial fibrillation, exacerbating his hemodynamic instability. The critical nature of his condition necessitated immediate escalation of care.

Section 3

Response to Interventions:

Despite aggressive therapeutic strategies, the patient's condition remained critical. The healthcare team elected to intubate him due to worsening respiratory distress and impending respiratory failure, following which he was placed on mechanical ventilation. His ventilator settings were adjusted to target a PaO2 >60 mmHg and a PaCO2 <50 mmHg. He was also started on a nitroglycerin drip to reduce myocardial oxygen demand and alleviate the coronary artery spasm, in addition to a titrated beta-blocker to control his heart rate and blood pressure. However, his blood pressure and heart rate remained labile, and he continued to exhibit signs of end-organ damage, including tachypnea, altered mental status, and cool, clammy skin.

New Complications:

Within hours of intubation, the patient became more unstable. He developed a fever of 38.9 degrees Celsius, suggestive of a possible infection. Blood cultures were drawn immediately, and empiric broad-spectrum antibiotics were initiated. A chest x-ray revealed new bilateral infiltrates, raising concern for possible ventilator-associated pneumonia or acute respiratory distress syndrome. His renal function also deteriorated, with a sudden rise in serum creatinine to 2.5 mg/dL (reference 0.7-1.2 mg/dL) and a decrease in urine output to less than 0.5 mL/kg/hr, suggesting acute kidney injury. This new constellation of complications added further complexity to his clinical picture, necessitating an even higher level of critical thinking and clinical judgement from the healthcare team.

Section 4

Change in Patient Status and Response to Interventions:

Despite prompt initiation of empiric antibiotics, the patient's fever persisted with spiking temperatures up to 39.5 degrees Celsius. His blood pressure further dipped to 90/50 mmHg, and his heart rate increased to 130 beats per minute, signifying ongoing sepsis. The healthcare team initiated aggressive fluid resuscitation with 30 ml/kg of crystalloid solution and escalated his vasopressor support with norepinephrine to maintain a mean arterial pressure greater than 65 mmHg. An urgent nephrology consult was sought in view of his deteriorating renal function and oliguria, prompting the start of continuous renal replacement therapy (CRRT).

New Diagnostic Results:

The blood culture results came back 48 hours later, revealing gram-negative bacilli identified as Pseudomonas aeruginosa, a common cause of ventilator-associated pneumonia. The patient's antibiotic regimen was promptly de-escalated to a targeted therapy of piperacillin-tazobactam based on the susceptibility pattern. Furthermore, a transthoracic echocardiogram showed new-onset severe left ventricular systolic dysfunction with an ejection fraction of 30% (reference 55-70%), suggestive of myocardial damage from the prolonged tachycardia and sepsis. These findings necessitated a careful balance of the patient's hemodynamics, respiratory, and renal function, requiring meticulous titration of his medications and a high level of clinical acumen from the healthcare team.

Section 5

Change in Patient Status and New Complications:

Over the next 24 hours, the patient's condition continued to deteriorate. Despite aggressive fluid resuscitation and vasopressor support, his blood pressure remained hypotensive at 85/45 mmHg and the heart rate was persistently high at 135 beats per minute. His respiratory status also worsened, requiring an increase in ventilator support. The patient's oxygen saturation dropped to 88% on FiO2 of 70%. His arterial blood gas showed a pH of 7.28 (reference 7.35-7.45), PaCO2 of 48 mmHg (reference 35-45 mmHg), PaO2 of 55 mmHg (reference 75-100 mmHg), and HCO3 of 20 mEq/L (reference 22-28 mEq/L), indicative of combined metabolic and respiratory acidosis.

New Diagnostic Results:

Due to the worsening hemodynamics and respiratory status, a repeat transthoracic echocardiogram was done, which revealed a further decrease in ejection fraction to 25%, confirming a progression of the myocardial dysfunction. His chest x-ray showed worsening bilateral infiltrates suggestive of acute respiratory distress syndrome (ARDS). Additionally, his serum lactate levels increased to 5 mmol/L (reference <2.0 mmol/L) and procalcitonin to 15 ng/mL (reference <0.5 ng/mL), further indicating worsening sepsis and possible multiorgan dysfunction. At this point, the healthcare team was faced with the critical challenge of treating the patient's severe sepsis, myocardial dysfunction, and ARDS, all while managing his renal failure with ongoing CRRT. This complexity required a high level of clinical reasoning and decision making.