WILDERNESS MEDICINE
Navigating Toxic Flora: A Guide to Common Cardiac Glycoside Plants in North America
SAEM PULSE | NOVEMBER-DECEMBER 2023
By Kailee Pollock and Kevin Watkins on behalf of the SAEM Wilderness Medicine Interest Group
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The toxic plant classification systems have been debated for years. A recent effective system, outlined by James H. Diaz in his study "Poisoning by Herbs and Plants: Rapid Toxidromic Classification and Diagnosis," offers valuable insights. Diaz's classification, beneficial for frontline providers, includes four primary toxic plant categories: cardiotoxic, neurotoxic, cytotoxic, and GI/hepatotoxic plants. Among these, cardiotoxic plants, like foxglove, are widely known. They can be divided into three main groups: cardiac glycosides, sodium channel activators, and sodium/calcium channel blockers. This article will focus on cardiac glycosides. Nature boasts over 200 cardiac glycosides, present in both plants and animals. Structurally, they consist of a steroid backbone, lactone ring, and sugar moiety. These toxins
predominantly bind to Na/K ATPase enzymes in cardiac myocytes, skeletal muscle, and baroreceptors, leading to a digoxin toxidrome. Inhibiting this enzyme elevates intracellular sodium and calcium, increasing automaticity. While cardiac effects are their hallmark, these plants can also impact the GI system, with symptom onset and duration varying among different plant species but are not well-known for some plant species. In cases of acute toxic ingestion of cardiac glycosides, the initial gastrointestinal distress is followed by cardiac toxicity, characterized by heightened vagal tone on the sinoatrial (SA) or atrioventricular (AV) node, leading to bradycardias or AV blocks, notably in younger patients with naturally higher baseline vagal tone levels. Additionally, these toxins increase atrial and ventricular automaticity, potentially causing abnormal heart rhythms like
atrial or ventricular tachycardias. While bidirectional ventricular tachycardia is often considered indicative of cardiac glycoside toxicity, similar patterns can also result from other plant toxins. These conduction affects are the most common cause of death. The ECG may display nonspecific ST and T wave changes, and patients might experience visual disturbances, altered mental status, and weakness during acute toxicity, although these symptoms are more commonly associated with chronic digoxin exposure rather than acute ingestion. Due to their impact on the Na/K ATPase enzyme, cardiac glycosides can cause hyperkalemia that produce typical changes on ECG. The degree of hyperkalemia aids in prognosis prediction. Comprehensive electrolyte panels, including renal function studies, should be obtained. Elevated digoxin serum assays confirm exposure, but levels don't correspond with illness severity.