Cardiac blocking potency

Table 6. Anti-anginal and Anti-hypertensive Dose Compared to Experimental Cardiac 3-blocking Potency...

Explt.Cardiac 3-blocking potency Anti-anginal dose mg/day Anti-hypertensive dose mg/day... 

The anti-hypertensive dose is clearly related to the dose used to treat angina although the former is a good deal higher than the latter. Both doses however clearly correlate with the experimental cardiac 3-blocking potency. 

Bupivacaine is more cardiotoxic than equi-effective doses of Udocaine. Clinically, this is manifested by severe ventricular arrhythmias and myocardial depression after inadvertent intravascular administration of large doses of bupivacaine. Bupivacaine dissociates slowly during diastole, so a significant fraction of No channels at physiological heart rates remains blocked with bupivacaine at the end of diastole. Thus, the block by bupivacaine is cumulative and substantially more than would be predicted by its local anesthetic potency. Bupivacaine-induced cardiac toxicity can be very difficult to treat, and its severity is enhanced by coexisting acidosis, hypercarbia, and hypoxemia. The S-enantiomer and the racemate are equally efficacious and potent, but levobupivacaine may be less cardiotoxic. 

They antagonize the positive inotropic and chronotropic effects of catecholamines. Cardiac arrhythmias associated with excessive adrenergic stimulus, released endogenous catecholamines or sensitization of the heart by anes-thetics or cardiac glycosides may effectively be treated by 6-blockade. Some B-blockers also possess membrane or local anesthetic action and are effective against arrhythmias due to ischemia or cardiac glycoside toxicity as well. This membrane action was shown to be independent of 6-blockade since resolved isomers of B-blockers possessed equal antiarrhythmic potency but unequal B-blocking action. 

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