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Initial assessment of widecomplex tachycardias (WCTs) should begin with patient history and physical examination. If there is a history of remote myocardial infarction, WCT should be considered as ventricular tachycardia until proved otherwise. In most cases, WCT is subsequently shown by electrophysiologic evaluation to be ventricular tachycardia. The presenting symptoms and degree of hemodynamic compromise should not be used to distinguish ventricular tachycardia from supraventricular tachycardia. A 12-lead electrocardiogram (ECG) should be carefully reviewed by looking for signs of ventricular tachycardia (atrioventricular dissociation, captured and fusion beats, certain QRS shapes and concordance). If the surface ECG is inconclusive, changing the position of V1 or use of a transesophageal lead may allow assessment of atrial activity. When more QRS than P waves are documented, the diagnosis is ventricular tachycardia. Cardioversion-defibrillation is required in patients with WCT who are in unstable condition. Atrioventricular node blockers are the agents of choice for arrhythmias that are atrioventricular node-dependent, but they may cause hemodynamic collapse if administered to patients with ventricular tachycardia or with atrial fibrillation and preexcitation. Lidocaine hydrochloride (Xylocaine HCl IV), preferred for ventricular tachycardia, has been reported to cause ventricular fibrillation in patients with atrial fibrillation and preexcitation. When there is doubt about the diagnosis, elective electrical cardioversion may be considered. Medical therapy should consist of intravenous magnesium sulfate and procainamide hydrochloride (Pronestyl). A beta blocker may also be considered if more aggressive blockade of the atrioventricular node becomes necessary.
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PMID:Wide-complex tachycardias. The importance of identifying the mechanism. 879 58

The purpose of this study was to determine whether lidocaine is absorbed from the trachea during the artificial circulation of cardiopulmonary resuscitation. The tissue distribution of lidocaine was investigated in eight individuals (Cases 1-8) who underwent cardiopulmonary resuscitation before being pronounced dead. In Cases 1-4, there was no restoration of heart beat during cardiopulmonary resuscitation. Heart massage had been continued for 5 min in Cases 1 and 2, and for 60 min in Cases 3 and 4. Relatively high concentrations of lidocaine (more than 0.1 mg/L) were detected in the blood left in the heart and/or in the large thoracic vessels in the four cases. In Cases 1-3, a large proportion of the lidocaine detected in these blood samples may have diffused from the trachea after cessation of cardiopulmonary resuscitation since no lidocaine was detected in the cerebrospinal fluid, cerebrum, liver, right kidney, and/or right femoral muscle. In Case 4, however, tracheal lidocaine was thought to have been absorbed during cardiopulmonary resuscitation because 0.167-0.340 mg/L or mg/kg lidocaine was detected in the cerebrospinal fluid, liver, right kidney, and right femoral muscle. This was substantiated in experiments performed in rabbit carcasses given 50 microL/kg Xylocaine jelly (a 2% lidocaine hydrochloride preparation) intratracheally, followed by rhythmical thoracic compressions (100-150 times per minute) for 60 min. A possible reason for lack of absorption of lidocaine from the trachea of Case 3 during a 60-min cardiopulmonary resuscitation procedure may have been that effective blood circulation was not obtained during cardiopulmonary resuscitation because of bleeding and pulmonary collapse. Cases 5-8 survived for 3 h to 10 days after successful cardiopulmonary resuscitation; it was obvious that lidocaine was distributed to the tissues under the influence of the natural circulation. The kidney to liver lidocaine ratio in Case 4 (0.8) was much lower than that in Cases 5-8 (1.3-4.6), although the lidocaine ratio in the blood in the left ventricle when compared to blood in the right ventricle was similar in the five cases. The kidney to liver lidocaine ratio may be helpful in judging whether the lidocaine detected was absorbed during the artificial circulation of cardiopulmonary resuscitation or naturally. Additionally, postmortem diffusion of tracheal lidocaine into the blood in the left ventricle was much greater than into the blood in the right ventricle due to their anatomical location during a supine position. The pattern of tissue distribution of lidocaine gives useful information on the state of decedents during cardiopulmonary resuscitation.
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PMID:Absorption of intubation-related lidocaine from the trachea during prolonged cardiopulmonary resuscitation. 960 14