Drug Effects, Electrolyte Abnormalities, and Metabolic Factors

Chapter 10 Drug Effects, Electrolyte Abnormalities, and Metabolic Factors


The ECG is importantly affected by a number of factors, including drug effects, electrolyte abnormalities, and a variety of other metabolic conditions. Indeed, the ECG may be the major, initial indicator of a life-threatening abnormality, such as hyperkalemia or tricyclic antidepressant toxicity. These topics are introduced in this chapter, along with a brief review of nonspecific versus more specific ST-T changes.



Drug Effects



Drugs Used to Treat Arrhythmias


Numerous drugs, both “cardiac” and “noncardiac,” can affect the ECG. These changes may be mediated by direct effects on the electrical properties of a pacemaker, specialized conduction system, and atrial or ventricular cells. Drugs that alter autonomic nervous system activity (vagal and sympathetic) may also have important effects on pacemaker activity and conduction properties.


Cardiologists often use a shorthand classification system when referring to drugs primarily used to treat arrhythmias (Box 10-1). This system has a number of flaws, but is widely employed—so students and clinicians need to be aware of it.



Class 1 drugs have a sodium channel blocking action, so they may prolong the QRS duration. The class I drugs are subdivided into A, B, and C groups. Class 1A drugs also prolong repolarization via potassium channel blocking effects. Therefore, they may prolong the QT(U) interval, leading to increased risk of torsades de pointes and sudden cardiac arrest (Chapters 16 and 19; Figs. 2-13 and 19-7). Class 1B drugs include lidocaine and mexiletine. Class IC drugs, such as flecainide and propafenone, used to treat atrial fibrillation and other supraventricular tachycardias, are the most likely to produce clinically important widening of the QRS complex (intraventricular conduction delays) due to their prominent sodium channel blocking effects.


All “antiarrhythmic” class 1 (sodium channel blocking) drugs, along with many other pharmaceutical agents, may, paradoxically, induce or promote the occurrence of life-threatening ventricular arrhythmias by altering basic electrical properties of myocardial cells. These so-called proarrhythmic drug effects, which are of major clinical importance, are discussed further in Chapters 16 and 19.


Prolongation of the QT(U) interval with a life-threatening risk of torsades de pointes, another type of ventricular proarrhythmia, can also occur with class 3 drugs, notably ibutilide, dofetilide, sotalol (also has beta-blocking effects), amiodarone (also beta-blocking, among other, effects), and dronedarone (Fig. 10-1). This effect is also related to blocking of potassium channel function with prolongation of myocardial cellular repolarization.



Beta blockers (class 2) and certain calcium channel blockers (class 4) primarily depress the sinus node and atrioventricular (AV) node, so that bradycardias related to these actions may occur, ranging from mild to severe. Combinations of drugs (e.g., metoprolol and diltiazem) may produce marked sinus node slowing or AV (nodal) block, especially in the elderly. Carvedilol has both β-adrenergic and α1-adrenergic (vasodilatory) effects.


Weaknesses of this classification scheme include its failure to account for drugs with “mixed” effects (like amiodarone and sotalol) and the fact that important drugs, such as adenosine and digoxin, do not fit in. Instead, they are placed under the class 5 or “other” category. The therapeutic and toxic effects of digitalis-related drugs, like digoxin, are discussed separately in Chapter 18.


Jun 11, 2016 | Posted by in CARDIOLOGY | Comments Off on Drug Effects, Electrolyte Abnormalities, and Metabolic Factors
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