ECG Manifestations: The Poisoned Patient

Abstract

Emergency physicians routinely evaluate and manage poisoned patients. In 2003, more than 2 million human exposure cases were reported to poison centers throughout the United States [1]. Of those cases, 22% were treated in a health care facility with most of those cases evaluated in the emergency department. Cardiovascular drugs were listed as the fifteenth most frequently encountered human exposure (66,401) and the fifth leading cause of poisoning deaths.Drug-induced changes and abnormalities on the 12-lead electrocardiogram (ECG) are common. There are numerous drugs that can cause ECG changes and lead to cardiac dysrhythmias. The diagnoses and subsequent management of patients manifesting ECG changes following poisonings can challenge even the most experienced physician. Drugs that are advocated in Advanced Coronary Life Support protocols for cardiac dysrhythmias may not apply or may even worsen the condition of overdose patients [2].Despite that drugs have widely varying indications for therapeutic use, many unrelated drugs share a common cardiac pharmacologic effect if taken in overdose. The purpose of this article is to group together agents that cause similar electrocardiographic effects, review their pharmacologic actions, and discuss the electrocardiographic findings reported in the medical literature. The five main categories reviewed include potassium (Kþ) efflux blockers, sodium (Naþ) channel blockers, sodium-potassium adenosine-triphosphatase (Naþ/Kþ ATPase) blockers, calcium channel blockers (CCB), and beta-adrenergic blockers (BB). It is important to keep in mind, however, that many medications have actions that involve more than one of these

Toxic and Drug-Induced Changes of the Electrocardiogram

“…Toxic and Drug-Induced Changes of the Electrocardiogram 275 sign of severe poisoning, indicating that the Na + channel blockade is so profound that tachycardia does not occur, despite the clinical muscarinic antagonism or adrenergic agonism (Holstege et al, 2006). Nevertheless, bradycardia may occur because of slowed depolarization of pacemaker cells that depend on entry of Na + ions.…”

“…Direct toxin-induced blockade of cardiac Na + channels will cause QRS complex widening, and it has been described as a membrane stabilizing effect, a local anesthetic effect, or a quinidine-like effect. Some drugs in this category (Table 1) may also affect other myocardial ion transfers, such as the Ca 2+ influx and K + efflux (Holstege et al, 2006). Other abnormal QRS complex configurations are also possible.…”

“…Delay of repolarization causes the myocardial cell to have less charge difference across its membrane, and result in the activation of the inward depolarization current (early after-depolarization), which is seen on ECG as prominent U waves (Murphy et al, 2007). This may promote triggered activity, which potentially can progress to re-entry and subsequent polymorphic VT. Toxin-induced blockade of K + efflux channels during phase 3 of the action potential corresponding with repolarization and QT interval prolongation may place the patient at risk for polymorphic VT or torsades de pointes (Holstege et al, 2005;Holstege et al, 2006). The drugs and toxins reported to have this effect are listed in table 3.…”

“…Sudden shifts from bradydysrhythmias to cardiac arrest have been reported. In addition, ECG changes associated with cardiac ischemia ( fig.8) may occur as a result of the hypotension and changes in the cardiovascular status, especially in patients with preexisting cardiac disease (Patel & Benowitz, 2005;Holstege et al, 2006). …”

“…The end of the cardiac cycle is marked by the closure of the Ca 2+ channels and the activation of the K + efflux channels, which allow the action potential to return to its resting potential of -90 mV (phase 3). This K + efflux from the myocardial cell is directly responsible for the QT interval on the ECG (Holstege et al, 2006). During phase 4 of the cardiac cell action potential, some cardiac fibers allow sodium ions to enter the cell, increasing the resting membrane potential, known as spontaneous diastolic depolarization.…”