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The use of a new non-imaging nuclear probe (Cardioscint) capable of continuous online monitoring of left ventricular function is described in critically ill patients undergoing mechanical ventilation. Ejection fraction, measured by the Cardioscint, was compared with that measured by echocardiography. The mean difference was -1.1% (95% confidence interval -2.9 to +0.6%). Mean difference +/- 2 SD was +10.6 to -12.8% (95% confidence intervals +7.5 to 13.6% and -15.8 to -9.0%, respectively). Examples of fluid loading and inotropic support showed comparable changes in stroke counts measured by the Cardioscint and stroke index measured by thermodilution. The Cardioscint is a practical bedside method for continuous or repeated measurement of ejection fraction and for assessing the response to therapeutic interventions in critically ill patients.

To avoid factors which confound attempts to characterize the neuroendocrine response to cardiac arrest, we studied the pituitary-adrenocortical and catecholamine responses to induced ventricular fibrillation (VF) and direct current cardioversion in 10 patients undergoing testing of 'implanted cardioverter defibrillator' devices under sedation. Plasma concentrations of epinephrine were increased 5 min after VF (from a mean basal of 0.39 (S.E.M. 0.09) to a peak of 0.632 (0.212) nmol litre-1; P < 0.05) but were unchanged at other times. Plasma concentrations of norepinephrine did not change at any time. Plasma concentrations of cortisol increased significantly at 10 min (from a mean of 367 (SEM 62) to 539 (64) nmol litre-1; P < 0.001) and remained increased 30 min after VF (470 (74) nmol litre-1; P < 0.05) but had returned towards baseline at 60 min, whereas plasma prolactin concentrations were increased at 5 min (from a mean of 224 (SEM 54) to 320 (63) mu. litre-1; P < 0.01) and remained increased until the end of the sampling period at 60 min (288 (65) mu. litre-1; P < 0.05). Concentrations of adrenocorticotrophic hormone (ACTH) (n = 5) tended to increase but this was not statistically significant. We conclude that a short period of cardiac arrest in lightly sedated humans activated the pituitary-adrenocortical axis but did not appear to stimulate catecholamine secretion. These findings raise questions about the nature and mechanisms of the neuroendocrine response to cardiac arrest.

The avoidance of inappropriate shocks from the implantable cardioverter-defibrillator (ICD), together with its need to apply antitachycardia pacing to either atria or ventricles, demands considerable sophistication in the design of algorithms to interpret electrical or other cardiac signals in real-time. Methods based on rate and using single short-gap bipolar leads lack discrimination. Right ventricular electrogram morphology algorithms offer improvement but no universal algorithm exists; however, for any given patient an optimum algorithm of this type might be found. One improvement would be to provide atrial information in addition, by employing more than one electrode or a long-gap single bipolar lead. Alternatively, transducer signals could be included, once their efficacy and reliability have been improved. A different approach would be to use the much more sophisticated algorithms at present being tried with surface electrocardiograms. Integrated Circuit technology is reaching the point where this could be done but the requirement for exceptionally high reliability means that special system structures, such as a Memory Intensive Computer Architecture, may be required. When decisions on these approaches are to be made, it must also be remembered that ICDs will soon be implanted and programmed as a routine rather than a highly specialized procedure.