Case Study
A rapid response event was initiated by the bedside nurse for sudden onset palpitations. Upon the prompt arrival of the rapid response team, the patient was found to be a 56-year-old male with a known history of hemorrhagic stroke status post tissue plasminogen activator (t-PA) a month prior with residual right-sided neurological deficits and tobacco abuse disorder. The patient was admitted to the hospital two days prior for management of infected decubitus ulcers. His symptoms had started 15 min before the rapid response was called, and he complained about palpitations and dizziness.
Vital Signs
Temperature: 98 °F, axillary
Blood pressure: 159/89 mmHg
Pulse: 160 beats per min (bpm) – narrow complex, irregular rhythm on telemetry ( Fig. 4.1 )
Respiratory rate: 22 breaths per min
Pulse oximetry: 95% oxygen saturation on room air
Focused Physical Exam
The patient was a middle-aged male in mild distress. Appropriate personal protective equipment was established, and the patient was examined. The patient was alert and oriented. He reported having an uncomfortable, fluttery feeling in his chest. He also complained of dizziness even while lying flat. However, he denied any overt chest pain. His cardiac exam showed tachycardia with an irregular rhythm. Jugular venous distension was not appreciated, and no peripheral edema was present. Lung and abdominal exams were benign.
Interventions
A cardiac monitor and pads were attached immediately. The monitor showed narrow complex tachycardia with irregularly spaced complexes and a rate variability between 140 to 180 beats per min. Stat electrocardiogram (EKG) was obtained, which was notable for the absence of p waves. The patient was given 5 mg intravenous (IV) metoprolol push which did not decrease the heart rate. The patient’s blood pressure fell to 110/83 mmHg, and a 500cc fluid bolus was initiated. He was given another 5 mg of IV metoprolol which again did not affect the heart rate. Then, 10 mg IV of diltiazem was given, which decreased the heart to a range of 120-130 beats per min. The patient was started on a continuous diltiazem drip and moved to the stepdown unit. Stat electrolyte panel, magnesium level, troponin level, and complete blood count were ordered, which were unremarkable. Given his recent history of hemorrhagic stroke, anticoagulation was not initiated.
Final Diagnosis
Atrial fibrillation with rapid ventricular response.
Atrial Fibrillation
Atrial fibrillation is the most common cardiac arrhythmia, which causes greater than 450,000 hospitalizations every year in the United States. It has also been associated with an estimated 158,000 deaths each year. It is a rapid, irregular heart rhythm produced by the rapid firing of a single focus in the atria, most commonly in the pulmonary veins. The short duration of action potential in the atrial muscle fibers and their short refractory period plays a key role in sustaining the extremely fast conduction rate seen in atrial fibrillation, which can cause atrial contraction rates as high as 400/min. The leads to the replacement of the coordinated conduction and contraction of the atria (represented by P waves on EKG) by the rapid, chaotic “fibrillation” of atrial musculature (seen as a wavy undulation of isoelectric axis or F waves – see Fig. 4.2 ). Atrial fibrillation is often classified based on the frequency and duration of arrhythmic episodes ( Table 4.1 ).
Category | Features |
---|---|
Paroxysmal/intermittent atrial fibrillation |
|
Persistent atrial fibrillation |
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Long-standing persistent atrial fibrillation |
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Permanent atrial fibrillation |
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“Lone” atrial fibrillation |
|
Despite the rapid firing of atria, the ventricular rate usually does not exceed 200 beats/min because of the “slow response” nature of atrioventricular (AV) nodal fibers, which serves as the rate-limiting step in cardiac conduction. The broad range of heart rate in rapid ventricular response lies between 90-170 beats per min unless special circumstances such as an accessory conduction pathway, catecholamine access, or hyperthyroidism are present. The most common presenting symptoms include palpitations, dizziness, lightheadedness, weakness, and fatigue. Symptoms of cardiac ischemia such as chest pain and dyspnea and symptoms of hemodynamic compromise such as syncope can present occasionally. However, patients with atrial fibrillation can be asymptomatic from an arrhythmia standpoint. This “occult” atrial fibrillation is usually discovered during the work-up of consequences of atrial fibrillation such as stroke and transient ischemic attack, where it is found to be the cause of cerebrovascular accident in about a quarter of the patients.
Table 4.2 lists the different associations and risk factors of atrial fibrillation. Atrial fibrillation has been associated with an increased risk of stroke, myocardial infarction, heart failure, systemic embolism, venous thromboembolism, and dementia. Systemic anticoagulation is initiated based on the patient’s risk of systemic embolism. The CHA 2 DS 2 -VASc score is often used to calculate this risk of systemic embolism ( Table 4.3 ).