Cardiac Cyanide Toxicity Induced by Nitroprusside in the Dog

Open Access
Publisher Website
Google Scholar
Abstract
Specific sodium nitroprusside(SNP)-induced myocardial cyanide (CN) toxicity was studied in 24 dogs, using a right-heart bypass preparation that enabled calculation of myocardial O2 consumption (M.ovrhdot.VO2) from direct measurements of coronary blood flow and arterial and coronary venous O2 contents. Massive doses of SNP (20 mg/kg/h) were given to obtain rapidly increasing blood CN levels. Isoelectric EEG tracings appeared at a blood CN level of 3.2 .mu.g/ml, while M.ovrhdot.VO2 did not decrease to significantly below control until blood CN had increased to 5.2 .mu.g/ml (P < .01). In 5 dogs, the addition of partial left ventricular bypass both decreased left ventricular external work and increased coronary O2 delivery, but did not appreciably delay the M.ovrhdot.VO2 decrease of ventricular fibrillation. In 7 dogs, experiments were conducted to determine the blood CN level and extent of systemic acidosis at which CN toxicity could not be reversed with standard anti-CN measures. Animals could be resuscitated when blood CN levels were less than 4 .mu.g/ml and when acidosis had not worsened beyond a base deficit of -11 mEq/l. Myocardial CN toxicity during SNP administration in dogs occurs at higher blood CN levels than those that result in isoelectric EEG tracings. Decreases in myocardial workload and increases in coronary O2 delivery are not protective. Systemic acidosis is a reasonable indicator of SNP-related whole-body CN toxicity. There is no significant decrease in M.ovrhdot.VO2 when the SNP-induced systemic CN toxicity has already become irreversible by standard anti-CN treatment. SNP-induced CN toxicity in man, even in the presence of myocardial disease, is likely to be manifested at lower blood CN levels than that which produces myocardial toxicity.