Atrial fibrillation (AF) has been associated with lung diseases like pneumonia and chronic obstructive pulmonary disease but has only infrequently been associated with inhalational lung injury. We report two cases of resistant AF, which developed in young healthy manual laborers shortly after inhalational lung injury due to massive quantity of pesticides and anhydrous ammonia, respectively. They had no evidence of valvular or structural heart disease and did not have any previous medical problems. The AF was resistant to antiarrhythmic drugs and required pulmonary vein isolation in first patient and possibly the second patient who is currently being evaluated for this procedure. These arrhythmias may reflect direct myocardial injury during and after exposure. Alternatively, multiple mechanisms can cause atrial fibrillation in lung diseases, including hypoxemia, acidemia, inflammatory mediators, and structural changes in the atria and ventricle, and these could lead to AF in inhalational lung injury cases. AF needs to be excluded when patients present with palpitations after inhalational lung injury, especially since, if unrecognized, AF may lead to complications, like thromboembolic phenomenon and tachycardiomyopathy.
Age adjusted multivariate analyses have shown that the major risk factors for atrial fibrillation (AF) are hypertension, heart failure, diabetes, and valvular heart diseases [
The first patient is a 35-year-old man who worked as an insecticide sprayer on a potato farm. He was accidentally sprayed with over 900 gallons of a mixture of four agricultural chemicals when the valve holding the chemicals ruptured. The pesticides included a mixture of Venom insecticide (neonicotinoid), EPI-MEK meticide/insecticide (avernectin), Super-10 (permethrin), and Manzate Pro-Stick (fungicide). He presented with shortness of breath and hemoptysis to the emergency department immediately after the event. He subsequently developed diffuse interstitial lung disease, identified as desquamative interstitial pneumonia on lung biopsy (Figure
CT Chest of the first patient showing diffuse interstitial thickening, patchy infiltrates and areas of consolidation of the left lower lobe.
The second patient is a 36-year-old man who was accidentally exposed to anhydrous ammonia when the tube transferring ammonia broke. He sustained lung injury and was brought to the emergency department. He developed persistent atrial fibrillation within hours after hospitalization. He was electrically cardioverted twice to sinus rhythm, but atrial fibrillation recurred in spite of treatment with propafenone and dronedarone. He recently underwent chemical cardioversion with dofetilide but had recurrence within one week of cardioversion. His echocardiogram revealed a left ventricular ejection fraction of 65–69%, normal diastolic function and chamber dimensions, and left atrial dimension of 2.7 cm. His thyroid stimulating hormone was within normal range. He is currently being evaluated for pulmonary vein isolation. Although this patient initially had respiratory failure after the exposure and required intubation, his lung function recovered. His PFTs later revealed a FVC of 6.2 L (110% predicted), FEV1 of 3.6 L (80% predicted), and a FEV1/FVC 72% of predicted. His initial X-ray revealed bilateral basilar infiltrates and atelectasis. His X-ray seven months later was within normal limits.
These patients were young healthy men without cardiac or respiratory disease prior to their inhalational lung injury. They did not have congenital or valvular heart disease, did not have hyperthyroidism, and did not use or abuse sympathomimetic drugs. The time course suggests that their AF developed as a consequence of inhalational lung injury, possibly secondary entry of high concentrations of chemicals and inflammatory mediators into the pulmonary veins with direct delivery into the left atrium. The atrial fibrillation in these patients was persistent and refractory to antiarrhythmic drugs.
Histological studies of atrial tissue in patients with AF demonstrate that these patients have myocarditis (64%), localized noninflammatory cardiomyopathy (17%), and patchy fibrosis (17%) [
High blood pressure, bradycardia, and cardiac arrest have been reported in humans as a result of acute exposure to highly concentrated aerosols of ammonium compounds [
AF could also develop during acute lung disease as a consequence of acute sympathetic stress, hypoxemia, and inflammatory mediators. For example, seven patients (4.1% of 170) had new onset atrial fibrillation during an episode of pneumococcal pneumonia [
AF has also been associated chronic lung disease. Shibata and coworkers studied 2917 subjects 40 years or older who participated in a community-based annual health survey. AF was associated with decreased FEV1 and FVC independent of age, gender, left ventricular hypertrophy, and levels of brain natriuretic peptide [
Reduced pulmonary function could directly lead to the development of AF. Hypoxia, hypercarbia, respiratory and metabolic alkalosis, the release of inflammatory mediators, and the effects of drugs used to treat respiratory diseases could cause AF. Lung dysfunction causes hypoxia, and this increases sympathetic drive which could induce ectopy. In turn, ectopic foci in the pulmonary veins potentially trigger AF. The synergistic interactions among hypoxia, respiratory acidosis, and cor pulmonale have a proarrhythmic effect [
In summary, multiple mechanisms, especially if significant pulmonary impairment develops, could potentially contribute to the development of AF in patients with acute inhalational injury; these would include hypoxemia, acidemia, inflammatory mediators, and structural changes in the atria. The possibility of cardiac arrhythmias should be considered when these patients present to physicians. These arrhythmias potentially contribute to the physical limitations of these patients and have important complications, such as tachycardia mediated cardiomyopathy and thromboembolic phenomena.
The authors declare that they have no conflict of interests.