Scenario: This electrocardiogram (ECG) was obtained by paramedics from a 52-year-old man with chest heaviness, chest “fluttering,” and shortness of breath (SOB) for several hours after moving heavy items into his car. The patient stated that for the past week, he has been using pillows at night to sleep because of SOB when he lays flat. His medical history includes hypertension, type 1 diabetes, hyperlipidemia, and obstructive sleep apnea (OSA). He was obese, with a body mass index (weight in kilograms divided by height in meters squared) of 38. Current medications included amlodipine, long-acting insulin, and simvastatin. To treat his sleep apnea, he was prescribed continuous positive airway pressure for night use, but he said that he does not use it consistently and recalls not using it for several weeks. Pertinent vital signs and assessment included blood pressure, 158/94 mm Hg; heart rate, 103/min; temperature, 97.8 °F (36.6 °C); respiratory rate, 22/min; oxygen saturation by pulse oximetry, 94%; slight edema in the lower limbs, which he has had for the past few weeks; and decreased breath sounds in the lung bases on auscultation.Sinus tachycardia with trigeminal premature atrial contractions (PACs) and a nonspecific ventricular conduction delay.Such contractions (PACs) are triggered by atrial ectopic myocardial cells originating outside the sinoatrial node. They are characterized by early depolarization, a taller T wave before the early beat followed by what appears to be a pause. Importantly, the latter feature is not a pause of conduction but rather a compensatory pause as the sinus node resets. In general, PACs are benign, do not require treatment, and are most often triggered by stress, caffeine, fatigue, alcohol, and/or tobacco. However, increased frequency can be associated with structural heart changes including coronary artery disease, left ventricular hypertrophy (LVH), hypertension, heart failure, and valvular heart disease. Some patients may complain of symptoms such as a feeling of fluttering in their chest, their heart skipping a beat, or palpitations. More pronounced symptoms with an increase in the number of PACs can include fatigue, chest pain, SOB, and dizziness. In this patient, the observed conduction disturbance (slight widening of the QRS complex and deep terminal S pattern) is due to abnormal late depolarization. Of note, the terminal S pattern should not be confused with ST depression due to myocardial ischemia. In this example, the J point (end of the S wave and start of the T wave) is isoelectric; hence, ischemia is not present. In the context of OSA, this ECG pattern suggests a hypertrophied right outflow tract of crista supraventricularis, an important sign of worsening OSA. The presence of this ECG feature correlates with the incidence of pulmonary hypertension, which would explain the patient’s gradual development of SOB.Treatment of PACs depends largely on the symptoms and can include a reduction of known triggers and/or treatment of other conditions that may be causing the PACs. In this patient, the workup in the emergency department (physical examination, chest radiography, etc) revealed an enlarged heart and fluid in the lungs. Additionally, his blood natriuretic protein (BNP) level was high at 988 pg/mL (normal, <100 pg/mL) and his troponin I level was normal, 0.024 ng/mL (normal <0.033 ng/mL). He was subsequently diagnosed with new-onset heart failure and admitted. An echocardiogram revealed LVH with an ejection fraction of 33%, and a 12-lead ECG showed sinus rhythm at 98/min with a right bundle branch block with no ischemia present. This patient had known OSA with inconsistent treatment adherence as well as hypertension, both risk factors for the development of LVH and heart failure. On day 2, the patient was in a normal sinus rhythm with occasional PACs and his SOB had improved. Cardiac treadmill stress testing to rule out coronary artery disease was negative for ischemia and for arrhythmias. The patient was discharged with education in the following: worsening signs and symptoms of heart failure, low-sodium/low-fat diet, weight loss management, daily weight monitoring for early indication of potential fluid overload, and the importance of both medication and OSA treatment adherence.
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