Intravenous beta-blocking drugs are being increasingly used in early myocardial infarction but little is known of the comparative haemodynamic effects of drugs with different ancillary pharmacological properties. In patients with stable coronary heart disease all intravenous beta-blocking drugs reduce left ventricular pumping function in a dose-response fashion. The reduction in cardiac mechanical activity is directly related to the dose and inversely related to the degree of intrinsic sympathomimetic activity possessed by each drug; it is independent of the property of 'cardioselectivity'. The lesser depression of left ventricular pumping performance after beta-blocking drugs with intrinsic sympathomimetic activity is probably due to two primary pharmacodynamic effects: a) increased myocardial contractile activity due to stimulation of post-synaptic beta 1- and presynaptic beta 2-adrenoceptors in the sinus node and ventricular myocardium; b) reduction in left ventricular afterload consequent upon the fall in systemic vascular resistance resulting from stimulation of vasodilator beta 2-adrenoceptors in peripheral resistance vessels. A similar but less marked haemodynamic separation of beta-blocking drugs with and without intrinsic sympathomimetic activity is observed in patients with acute myocardial infarction. The quantitative difference in the haemodynamic effects of intravenous beta-blocking drugs in angina pectoris compared to their effects in acute myocardial infarction is probably due to the higher level of sympathetic stimulation and sensitivity to beta-blockade in the latter. It has yet to be shown by formal clinical trial that the haemodynamic advantages attributable to the possession of intrinsic sympathomimetic activity by a beta-blocking drug are translated into clinical benefit.