This is the third installment of our 8-part series on cardiovascular complications in patients with COVID-19. The severe systemic inflammatory processes and hypercoagulability occurring with COVID-19 illness increase the risk for atherosclerotic plaque disruption and acute myocardial infarction (AMI). Patients with a previous history of coronary disease and/or other significant comorbidities are particularly predisposed to cardiovascular complications with COVID-19 infection.1 In this installment, we will discuss atrial fibrillation and other dysrhythmias in patients with COVID-19.
A 76-year-old man who was diagnosed with COVID-19 and discharged from the emergency department (ED) 2 days prior, returns to the ED with worsening shortness of breath, fatigue, and nonproductive cough. The patient has no associated fevers, chest pain, or gastrointestinal symptoms. An electrocardiogram (ECG) reveals new-onset atrial fibrillation (AF) with a ventricular rate of 115 beats per minute and elevated troponin level.
The patient’s oxygen saturation is 80% on room air. He is initially placed on a nonrebreather mask, which is quickly escalated to a high-flow oxygen therapy via nasal cannula. Oxygen saturation improves to 93% with 80% fraction of inspired oxygen on 35 L/min flow. He is admitted for COVID-19 pneumonia and initiated on dexamethasone, remdesivir, empiric IV antibiotics, and enoxaparin for venous thromboembolism prophylaxis. Cardiology and pulmonology are consulted.
Laboratory results of note include elevated white blood cell count (14,300/µL), neutrophil (1000/µL), troponin (0.52 ng/mL), creatine kinase (642 U/L), C-reactive protein (289.8 mg/dL), D-dimer (3.82 µg/mL), and N-terminal pro-BNP (brain natriuretic peptide; 700 pg/mL) levels. Mild decreases in sodium (133 mEq/L), chloride (97 mEq/L), and albumin (2.7 g/dL) are also noted. The remainder of the basic metabolic panel, liver panel, complete blood count, and coagulation studies are within normal limits.
The patient’s chest radiograph reveals bilateral interstitial pneumonitis. An echocardiogram reveals severe aortic stenosis and normal ejection fraction with moderate aortic regurgitation. Pulmonary computed tomography angiogram does not demonstrate pulmonary emboli but does show evidence of COVID-19 infection, noting bilateral ground-glass opacities with possible underlying pulmonary fibrosis.
Significant Medical History
The patient’s medical history includes hypertension, type 2 diabetes, and obesity with a BMI of 34.
The patient is a neurologically intact older man who initially presents with tachypnea and labored respirations but is breathing more comfortably on high-flow oxygen therapy via nasal cannula. Respiratory rate is 22 to 24 breaths per minute, and lungs are clear although diminished bilaterally. A systolic ejection murmur and irregular heart rhythm are noted. His abdomen is soft, nontender, and nondistended.
Recommended Diagnostic/Laboratory Tests1
|Thyrotropin and FT4 level to rule out hyperthyroidism|
|Complete blood cell count to rule out leukocytosis and anemia|
|Transthoracic ECG to evaluate atrial chamber size and ventricular function; detect valvular disease, left ventricular hypertrophy, and pericardial disease; and assess peak right ventricular pressure|
|Transesophageal ECG to identify or rule out the presence of left atrial or left atrial appendage thrombi|
Diagnosis of cardiac dysrhythmias is based on medical history, physical examination, and ECG. History should include a focus on symptoms (if any are present) and presence of any associated diseases. Identification of symptom onset, frequency and duration, qualitative characteristics, and any precipitating causes (eg, exercise or alcohol intake) should also be identified. Common associated conditions include cardiovascular or cerebrovascular disease, diabetes mellitus, hypertension, chronic obstructive pulmonary disease, obesity, obstructive sleep apnea, or potentially reversible causes such as hyperthyroidism and excessive alcohol ingestion.2
Both 12-lead ECG and continuous cardiac monitoring are important for diagnosing and monitoring dysrhythmias. A complete examination of the cardiovascular system should be performed and may reveal contributing factors such as valvular heart disease and/or problems arising secondary to the presenting dysrhythmia such as heart failure.2
With AF, as diagnosed in this case, the ECG will demonstrate irregular R-R intervals with no distinct P waves (Figure 1). Interpretation of the ventricular response rate is also important. Patients who have either a rapid ventricular response rate or a bradycardic response rate are more likely to become hemodynamically unstable and require urgent intervention.3
Other atrial dysrhythmias include atrial flutter, which is an AV nodal reentrant rhythm with atrial rates ranging from 250 to 450 beats per minute. Rather than P waves, the ECG demonstrates flutter waves that have a saw tooth or picket fence-looking pattern (Figure 2). The rhythm is typically more regular than AF, but regularity can vary. As with AF, the ventricular response rate is key to how the patient will tolerate the dysrhythmia.3
Electrocardiogram is also the primary tool for detecting ventricular ectopic beats and/or ventricular tachycardia (VT, Figure 3). With ventricular ectopic beats, the electrical impulse travels through the ventricles in an abnormal manner taking longer for both right and left ventricles to depolarize. This results in a wide QRS interval of ≥0.12 seconds. Three or more ventricular beats in a row with a rate of >100 is considered VT. Ventricular tachycardia can be monomorphic or polymorphic. With monomorphic VT the QRS complexes will have a uniform polarity. With polymorphic VT the polarity of the QRS complexes will vary, some having a positive deflection and some having a negative deflection. Ventricular tachycardias are often accompanied by hemodynamic instability and frequently require urgent intervention.3