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Autonomic boundary conditions for ventricular fibrillation
Author(s) -
Naggar Isaac,
Uchida Sae,
Kamran Haroon,
Lazar Jason,
Stewart Mark
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.703.8
Subject(s) - hypoxemia , medicine , cardiology , anesthesia , ventricular fibrillation , vagal tone , heart rate , vagus nerve , autonomic nervous system , stimulation , defibrillation , efferent , blood pressure , afferent
We sought to describe conditions under which changes in autonomic activity interacted with changes in oxygen availability to cause ventricular fibrillation (VF) in rats anesthetized with urethane. Parasympathetic activation was achieved by stimulation of efferent vagus nerve segments. Sympathetic activation was accomplished by varying doses of systemic isoproterenol. Hypoxemia was induced by varying the dead space attached to an endotracheal tube. BP, ECG, pulse oximetry, and echocardiograms in M‐mode were used. Ventricular fibrillation could be induced with high‐dose isoproterenol, vagotomy, and moderate hypoxemia (O 2 sat 50–60%). Lower doses of isoproterenol or non‐zero vagal tone (simulated with vagus nerve stimulation) led to bradyarrhythmia. Severe hypoxemia (O 2 sat <50%) also led to bradyarrhythmia. In addition, the dose of isoproterenol necessary to favor VF (≥16 mg/kg) was greater than the dose necessary to achieve maximal heart rate (≤12 mg/kg). We also examined defibrillation. Given that systemic hypoxemia can contribute to a specific set of autonomic conditions favorable for VF, and bradyarrhythmias result when hypoxemia is more severe or vagal tone is present, we conclude VF is an unlikely outcome of extreme autonomic overactivity.