Cardiopulmonary toxicity

Tong, H. et al. (2009) Influence of acid functionalization on the cardiopulmonary toxicity of carbon nanotubes and carbon black particles in mice. Toxicology and Applied Pharmacology, 239 (3), 224—232. 

Belej MA, Aviado DM Cardiopulmonary toxicity of propellants for aerosols. J Clin Pharmacol 15 105-115, 1975... 

White RL Jr, Schwartzentruber DJ, Guleria A, MacFarlane MP, White DE, Tucker E, Rosenberg SA. Cardiopulmonary toxicity of treatment with high dose interleukin-2 in 199 consecutive patients with metastatic melanoma or renal cell carcinoma. Cancer 1994 74(12) 3212-22. 

After administration of vinorelbine, chest pain occurs in up to 5% of patients. However, subsequent analysis showed that most patients had underlying cardiovascular disease or a tumor in the chest, making interpretation difficult (2,20). Three patients developed acute cardiopulmonary toxicity after vinorelbine therapy (25). The symptoms mimicked acute cardiac ischemia, but with no electrocardiographic changes or raised cardiac enzymes. In two patients, tachypnea, rales, wheezing, and severe dyspnea responded to inhaled salbutamol. One patient developed pulmonary edema and bilateral pleural effusions, which contained no malignant cells when drained. 

Karminsky N, Merimsky O, Kovner F, Inbar M. Vmorelbme-related acute cardiopulmonary toxicity. Cancer Chemother Pharmacol 1999 43(2) 180-2. 

In dogs, high doses of BCNU resulted in severe bone marrow hypoplasia with delayed, reversible thrombocytopenia. The other major toxicides observed were cardiopulmonary (pulmonary edema, myocardial infarction, and pericardial hemorrhage), intestinal mucosal damage with hemorrhage, renal toxicity, and delayed hepatotoxicity. Similar toxicity was seen in monkeys except that cardiopulmonary toxicity did not occur. In rats, initially well-tolerated doses may cause death later. There is sufficient evidence for the carcinogenicity of BCNU in rats. BCNU is embryo-and fetolethal in rats and rabbits at doses nontoxic to the mother and can induce a variety of teratogenic effects in rats. 

Allen DR, Ferens JM, Cheney FW, Nelp WB (1978) Critical evaluation of acute cardiopulmonary toxicity of microspheres. J Nucl Med 19 1204-1208 Aim A (1975) Radioactively labelled microspheres in regional cerebral blood flow determinations. 

Kobayashi S, Hutcheon DE, Regan J. 1982. Cardiopulmonary toxicity of tetrachloroethylene. J Toxicol Environ Health 10 23-30. 

Choi S, Hoffmann S, Cooling L. Another case of acute cardiopulmonary toxicity with cord blood infusion is dexlran the culprit Transfusion January 2012 52(l) 207-8. http //dx.doi.Org/10.llll/j.1537-2995.2011.03424.x. 

Oral poisoning after accidental phenol ingestion has caused fulminant central nervous system depression, hepatorenal and cardiopulmonary failure [20]. No hepatorenal or central nervous system toxicities with properly performed chemical peels have been reported in the literature [21]. 

Death. 1,2-Dibromoethane can be fatal to humans after oral or dermal exposure. Acute deaths following toxic doses are related to cardiopulmonary arrest or, if affected individuals survive for a period of time, to hepatic and renal failure. These results are supported by animal studies in which acute death occurred after oral, dermal, and inhalation exposure. 

Resuscitation from bupivacaine cardiovascular toxicity is extremely difficult. However, prompt resuscitation has been successful with standard cardiopulmonary support, including the prompt correction of acidosis by hyperventilation and administration of bicarbonate as well as epinephrine, atropine, and bretylium. Local anesthetics, especially bupivacaine, also inhibit basal and epinephrine-stimulated cAMP production. This finding places greater emphasis on aggressive epinephrine therapy during bupivacaine-induced cardiotoxicity. The (SJ-isomer, levobupivacaine, appears to have a lower propensity for cardiovascular toxicity than the racemic mixture or the (R)-isomer and has recently been approved for clinical use. Ropivacaine, another newer local anesthetic, has clinical effects similar to those of bupivacaine but may be associated with a lower potential for cardiovascular toxicity. Ropivacaine is available only as the (S)-stereoisomer, which has inherently less affinity for the cardiac sodium channel. 

Dysrhythmias seem to be the most likely cause of sudden death from cocaine, but cardiac conduction disorders are more common in patients with acute cocaine toxicity. Severe cocaine toxicity also causes acidemia and cardiac dysfunction (96). Four patients developed seizures, psychomotor agitation, and cardiopulmonary arrest two of these are briefly summarized here. 

Lee DL, Ayoub C, Shaw RK, Fontes ML. Grand mal seizure during cardiopulmonary bypass probable lidocaine toxicity. J Cardiothorac Vase Anesth 1999 13(2) 200-2. 

A patient due to have a bronchoscopy was given an overdose of lidocaine to anesthetize the airway by an inexperienced health worker. He was then left unobserved and subsequently developed convulsions and cardiopulmonary arrest (354). He survived with severe cerebral damage. His lidocaine concentration was 24 micrograms/ml about 1 hour after initial administration (a blood concentration over 6 micrograms/ml is considered to be toxic). 

High doses of penicillins, in the order of several million units/day of penicillin G, can produce myoclonic jerks, hyper-reflexia, seizures, or coma. Drowsiness and hallucinations can occur occasionally (18-20). Such reactions are due to a direct toxic effect and are more likely with high concentrations, as seen with intravenous administration (21,22) and with cardiopulmonary bypass in open-heart surgery (23,24). 

Toxic reactions can occur in patients with pre-existing cerebral damage or during cardiopulmonary bypass. Embolic reactions can have severe consequences in patients with pre-existing cardiac or pulmonary disease. 

A 15-year-old woman survived a total of 65 minutes cardiac arrest after taking 7200 mg of verapamil and 240 mg of paroxetine, which potentiates verapamil toxicity (19). Despite the length of cardiopulmonary resuscitation, with evidence of subsequent myocardial damage and renal impairment, she was discharged 17 days after admission, having made a full recovery, without evidence of neurological impairment. 

A In this patient with well-documented CAD who is sip CABG, either terbutaline or nifedipine would be contraindicated. It is not entirely clear which would be the safest, but based on studies, the use of nifedipine in patients with documented CAD can lead to an increase in mortality. Of the other three, the next most dangerous medication is likely to be MgS04, which can lead to cardiopulmonary arrest at toxic levels. The safest choice between indo-methacin and the oxytocin antagonist is difficult to sort out. Indomethacin has a higher risk characterization at baseline than the oxytocin antagonist, and in a patient with CAD, there should be concerns about renal function which is an issue with NSAIDs. 

Nitrous oxide (laughing gas) has been used as an inhalant anesthetic since 1844 and is still widely used in human anesthesia because of its potent analgesic actions. Although it has many desirable properties, including rapid onset and recovery, limited cardiopulmonary depression and minimal toxicity, it is a weak anesthetic. Its lack of potency, its relatively high cost and its possible contribution to hypoxia and accumulation in gas-filled spaces limits its use in the horse. 

Currently, there are no antidotes of choice for selenium toxicity. Ethylenediaminetetraacetic acid and BAL (British antilewisite 2,3-dimercaptopropanol) should not be used because they may enhance selenium toxicity. Treatment is symptomatic (e.g., cardiopulmonary). Often, supplemental oxygen is needed. Corrosive selenious acid (in gun-bluing solution) should be treated similar to other agents that cause esophageal burns. 

These acid metabolites are responsible for much of the toxicity of ethylene glycol, the clinical manifestations of which include neurological abnormalities (CNS depression in severe cases, coma and convulsions), severe metabolic acidosis, acute renal failure, and cardiopulmonary failure. The serum concentration of glycolic acid correlates more closely with clinical symptoms and mortality than does the concentration of ethylene glycol. Secause of the rapid elimination of ethylene glycol (ti/2 3 hours), its serum concentration may be low or undetectable at a time when that for glycolic acid remains elevated. Thus the determi-... 

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