Tachycardia agents that cause

Agents that cause QT interval prolongation (QTc > 0.42 seconds) may produce atypical ventricular tachycardia (torsade de pointes). Torsade de pointes is characterized by polymorphous ventricular tachycardia that appears to rotate its axis continuously (Figure I-7). Torsade de pointes may also be caused by hypokalemia, hypocalcemia, or hypomagnesemia. 

Flecainide is absorbed well, has a long half-hfe of 3 to 5 days, is metabolized to -O-deaUcylated flecainide (active antiarrhythmic agent with less potency than flecainide) and to -0-deaUcylated lactam of flecainide, which is an inactive metabolite. A portion of flecainide is excreted unchanged. Flecainide, like other antiarrhythmic agents, can cause new or worsen supraventricular or ventricular arrhythmias. Ventricular proarrhythmic effects range from an increase in frequency of premature ventricular complexes (PVCs) to the development of more severe ventricular tachycardia, e.g., tachycardia that is more sustained or more resistant to conversion to sinus rhythm, with potentially fatal consequences. 

Propanidid is a nonbarbiturate ultra-short-acting anesthetic agent that may cause hypotension and tachycardia. Unlike thiopental, which is redistributed, propanidid is metabolized rapidly by pseudocholinesterases. 

Lidocaine (Xylocaine) was introduced as a local anesthetic and is still used extensively for that purpose (see Chapter 27). Lidocaine is an effective sodium channel blocker, binding to channels in the inactivated state. Lidocaine, like other IB agents, acts preferentially in diseased (ischemic) tissue, causing conduction block and interrupting reentrant tachycardias. 

Anesthesia induction with propofol causes a significant reduction in blood pressure that is proportional to the severity of cardiovascular disease or the volume status of the patient, or both. However, even in healthy patients a significant reduction in systolic and mean arterial blood pressure occurs. The reduction in pressure appears to be associated with vasodilation and myocardial depression. Although propofol decreases systemic vascular resistance, reflex tachycardia is not observed. This is in contrast to the actions of thiopental. The heart rate stabilization produced by propofol relative to other agents is likely the result of either resetting or inhibiting the baroreflex, thus reducing the tachy-cardic response to hypotension. 

Methoxyflurane (Penthmne) is the most potent inhala-tional agent available, but its high solubility in tissues limits its use as an induction anesthetic. Its pharmacological properties are similar to those of halothane with some notable exceptions. For example, since methoxyflurane does not depress cardiovascular reflexes, its direct myocardial depressant effect is partially offset by reflex tachycardia, so arterial blood pressure is better maintained. Also, the oxidative metabolism of methoxyflurane results in the production of oxalic acid and fluoride concentrations that approach the threshold of causing renal tubular dysfunction. Concern for nephrotoxicity has greatly restricted the use of methoxyflurane. 

Most adverse effects of phenoxybenzamine derive from its -receptor-blocking action the most important are orthostatic hypotension and tachycardia. Nasal stuffiness and inhibition of ejaculation also occur. Since phenoxybenzamine enters the central nervous system, it may cause less specific effects, including fatigue, sedation, and nausea. Because phenoxybenzamine is an alkylating agent, it may have other adverse effects that have not yet been characterized. 

Adverse effects of histamine release, like those following administration of histamine, are dose-related. Flushing, hypotension, tachycardia, headache, wheals, bronchoconstriction, and gastrointestinal upset are noted. These effects are also observed after the ingestion of spoiled fish (scombroid fish poisoning), and there is evidence that histamine produced by bacterial action in the flesh of the fish is the major causative agent. 

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