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Excerpt
The effects of inhaled volatile anesthetics on the patient with coronary artery disease have been a topic of debate for many years. Early studies on the effects of volatile anesthetics involving the coronary circulation suggested that halothane, enflurane, and isoflurane had minimal direct effects [1-3]. But, as time passed, research showed that all inhaled anesthetics had certain potential drawbacks that could affect this patient population. Halothane has been shown to exacerbate catecholamine-induced cardiac arrhythmias, while enflurane has been shown to be a potent cardiac depressant, and isoflurane may potentially cause a phenomenon known as "coronary steal" under certain hemodynamic conditions. All of this has prompted anesthetists to question which inhalation agent to use for the patient with coronary artery disease.
The debate continues with the recent findings of Park et al. [4]. In the November 1994 issue of Anesthesiology, they presented material relating to isoflurane's effect on the diameter of isolated segments of coronary arteries in rabbits during varying conditions. Their results showed differing effects depending on the initial diameter of the vessels. This prompted an editorial by Merin and Johns in that same issue. These findings are contrary to previous work by Sill et al. [5], which showed isoflurane dilated small coronary arterioles and had little effect on large epicardial coronary arteries. The resultant redistribution of blood flow was felt to be responsible for the so-called "coronary steal" phenomenon, and in 1987 Lewis stated that "isoflurane is dangerous for the patient with coronary artery disease" because of its dilating effects on small vessels, which may result in regional myocardial ischemia in these patients [6,7].
While coronary steal has been demonstrated in animals by Buffington et al. [8], the evidence from human studies is less conclusive [8]. A study by Reiz et al. [9] on the effects of isoflurane and coronary steal involved the administration of enough isoflurane to decrease the mean arterial pressure by 50%. Therefore, any recorded myocardial ischemia may have been attributed to the hemodynamic changes caused by isoflurane rather than true coronary steal [9]. Indeed, the separation of hemodynamically related ischemia from coronary steal has been a major stumbling block with isoflurane studies in humans.
Proponents of isoflurane have shown its beneficial effects in managing the hypertensive responses to surgery in patients anesthetized primarily with opioids [10]. Also, recovery of the "stunned" myocardium may be enhanced by the use of isoflurane [11]. Recently, two large studies involving more than 2000 patients addressed the issue of anesthetic technique and outcome directly [12,13]. Neither study was able to demonstrate any influence of primary anesthetic agent or technique on postoperative outcome. In fact, the most important determinants of outcome are severity of disease process [related to the incidence of hemodynamically silent ischemia, shown by Knight et al. [14]] and surgical technique.
The literature is full of conflicting data on the issue of inhalation agents and their effects on coronary artery disease. There is no consensus on whether one inhaled anesthetic is better than another for this patient population. Throughout my anesthetic training in Boston, I was taught that one inhalation agent is superior for use in patients with coronary artery disease. But, in my travels throughout the world, it has been opined that other inhalation agents are superior. What I have found is that no one inhalation agent is superior and that overall outcome depends on the strength of the individual anesthetist.
The true goal lies in the anesthetist's ability to avoid additional detrimental changes in the myocardial dynamics (i.e., increased oxygen demand and/or decreased oxygen supply) and to actively improve oxygen balance, thus preventing ischemia.
