Abstract
For some time it has been known that alterations in blood pressure, heart rate, cardiac output, and other body functions occur after the introduction of contrast media into the vascular system. The full nature and extent of the hemodynamic changes, however, are often not well appreciated, nor has there been general realization of their significance. It is the purpose of this paper to describe these changes, relate their mechanisms so far as they are known, gauge their importance, and indicate avenues available to the radiologist for minimizing them. The morbidity and mortality which still accompany several types of angiography are not a small concern, and we should endeavor to improve our present practices. Basic to this approach are the assumptions that any deviation from the patient's pre-examination hemodynamic status is undesirable and that the propensity of a contrast material to cause deviations from the prior hemodynamic status is a measure of its toxicity. The consequences of the surgical events by which a vessel is entered or the mechanical and electrical events due to the catheter and the injector apparatus will not be considered at this time. The Hemodynamic Responses The hemodynamic reactions to contrast media can be conveniently considered first on the basis of the type and site of injection. In general, introduction methods are of two main types: the slow injection of a compound into a peripheral vein for its excretion by the kidney or liver to visualize the collecting systems of those organs and the rapid injection of a more concentrated solution to visualize the vasculature of an organ or a region of the body. Intravenous Injection The relatively slow intravenous injection of urographic and Cholangiographie agents results in a degree of systemic hypotension due to a lowering of peripheral vascular resistance (38). Hypertonic solutions of many kinds have long been known to cause similar responses, and it is likely that the hemodynamic responses secondary to the urographic and Cholangiographic agents are in part due to their hypertonicity. Tachycardia is probably compensatory, as is the increase in venous pressure and pulmonary artery pressure which occurs concomitantly. Although there may be accompanying subjective responses, these hemodynamic reactions are not often serious. We are excluding from the present discussion patients who respond with abnormal intensity to the chemical nature of the material, the so-called drug idiosyncrasy reactions. Rapid peripheral intravenous injection of concentrated contrast media for angiocardiography produces a brief rise in arterial blood pressure followed by a prolonged fall. The diastolic pressure decreases more than the systolic, causing a rise in pulse pressure. The pulse rate also falls, and there are marked changes in the contour of the pulse. Venous pressure rises characteristic electrocardiogram changes consist of flattening, splitting, or inversion of T waves.