Asystole Associated with Lidocaine Use in a Hyperkalemic Patient during Advanced Cardiac Life Support

A case report of fatal asystole associated with use of lidocaine in a hyperkalemic patient is presented. The patient was a 61–year-old man with a rapidly increasing serum potassium level related to acute renal failure. Ventricular tachycardia with a pulse developed twice, for which lidocaine was administered according to the American Heart Association's ACLS protocol. Both episodes were immediately followed by asystole, the second of which was terminal. Available information suggests that this phenomenon can be explained by a synergistic effect on membrane responsiveness and conduction velocity. Thus, extreme caution should be exercised in the use of lidocaine when ventricular tachycardia complicates severe hyperkalemia.

Electrophysiological effects of encainide and its metabolites in normal canine Purkinje fibers and Purkinje fibers surviving infarction

In this study, we assessed the effects of O-demethyl encainide (0.5 μM), the most active metabolite of encainide, and the combination with 3-methoxy-O-demethyl encainide (0.5 μM) and encainide (0.1 μM) on cardiac action potential characteristics in normal canine Purkinje fibers and Purkinje fibers surviving 24 h of myocardial ischemia. O-demethyl encainide decreased [Formula: see text] and conduction in normal Purkinje fibers and Purkinje fibers surviving infarction. Further decreases were observed with the combination. Action potential duration at both 50 and 95% repolarization was decreased by O-demethyl encainide. The combination of O-demethyl encainide, 3-methoxy-O-demethyl encainide, and encainide had no further effect. The combination of O-demethyl encainide, 3-methoxy-O-demethyl encainide, and encainide produced a smaller change in effective refractory period than O-demethyl encainide in normal Purkinje fibers and in Purkinje fibers surviving infarction. O-demethyl encainide and the combination shifted the membrane responsiveness curve to more negative potentials in both normal Purkinje fibers and Purkinje fibers surviving infarction. It is apparent from this study that there are differences in the effects of O-demethyl encainide and the combination of O-demethyl encainide, 3-methoxy-O-demethyl encainide, and encainide in normal Purkinje fibers compared with Purkinje fibers surviving infarction. Also, the combination used in this study had different electrophysiological effects than those of O-demethyl encainide alone.Key words: encainide, metabolites, electrophysiological effects, Purkinje fibers, infarction.

Developmental changes in the response of cardiac Purkinje fibers to SC-72-14

We used standard microelectrode techniques to study the effects of SC-72-14, a monoclonal antibody to eel electroplax, and tetrodotoxin (TTX) on the electrophysiological properties of neonatal and adult canine Purkinje fibers. SC-72-14, 7 ng/ml, depressed maximum upstroke potential (Vmax) and membrane responsiveness of adult but not neonatal fibers. In contrast, we previously had shown TTX to have a greater effect on neonatal than adult fibers (29). Even in the presence of SC-72-14, TTX continued to have a greater effect on the neonatal fibers. The effects of TTX and SC-72-14 were cumulative over the concentration range studied, and our results are consistent with their acting at different sites.

Control of the erythrocyte membrane shape: recovery from the effect of crenating agents.

Intact erythrocytes become immediately crenated upon addition of 2,4-dinitrophenol (DNP) or pyrenebutyric acid (PBA). However, when cells are incubated at 37 degrees C in the presence of the crenating agents with glucose, they gradually (4--8 h) recover the normal biconcave disc form. The recovery process does not reflect a gradual inactivation of DNP or PBA since fresh cells are equally crenated by the supernatant from the recovered cells. Further, after recovery and removal of the crenating agents, cells are found to be desensitized to the readdition of DNP as well as to the addition of PBA, but they are more sensitive to cupping by chlorpromazine. This alteration in the cell membrane responsiveness was reversible upon further incubation in the absence of DNP. Recovery is dependent upon cellular metabolic state since an energy source is needed and incubation with guanosine but not adenosine will accelerate conversion to the disc shape. It is suggested that the conversion of cells from crenated to disc shape in the presence of the crenators, represents an alteration or rearrangement of membrane components rather than a redistribution of the crenators within the membrane. This shape recovery process may be important for erythrocyte shape preservation as well as shape control in other cells.

Action potential correlates of pressure-induced changes in cardiac conduction

Microelectrode studies were undertaken to determine the cellular bases for hydrostatic pressure effects on impulse propagation and refractoriness in cardiac muscle. Canine Purkinje fibers, at 37 degrees C, were exposed to increases in hydrostatic pressure to 150 ATA. At 150 ATA membrane excitability was depressed and the maximum upstroke velocity (Vmax) of the action potential was reduced by 10%. Furthermore, the curve relating Vmax to takeoff potential (membrane responsiveness relation) shifted downward and to the right with the half inactivation voltage shifting in the hyperpolarizing direction by about 4 mV. Decreases in excitability and responsiveness occurred concomitantly with pressure-induced decreases in impulse conduction. Action potential duration (APD) increased significantly at 150 ATA. APD measured at -20 mV, -60 mV, and at maximum repolarization averaged 20.7, 15.5, and 13.5% longer than their respective 1-ATA values. The combined effects of increased APD and depressed responsiveness account for increased tissue refractoriness. The implications of the findings with regard to the arrhythmogenic nature of high hydrostatic pressure are discussed.

Effects of lidocaine in rabbit atria

Standard microelectrode recordings were obtained from rabbit right and left atria. Lidocaine (1 × 10−5 M) had no effect on these, but 5 × 10−5 M lidocaine significantly slowed rate and Vmax. This concentration had no effect on the duration of the action potential, a result clearly different from the effect of this drug in Purkinje tissue. Lidocaine had much less effect on the 'steady-state' relation of membrane potential to Vmax of phase 0 of the action potential than on the 'membrane responsiveness curve obtained by the extra stimulus technique. We have demonstrated time-related recovery from sodium inactivation in rabbit left atria and have shown that lidocaine slows recovery in this tissue as it does in Purkinje fibres.