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Objective: To reduce the time between arrival at hospital of a patient with acute myocardial infarction and administration of thrombolytic therapy (door to needle time) by the introduction of nurse initiated thrombolysis in the accident and emergency department. Methods: Two acute chest pain nurse specialists (ACPNS) based in A&E for 62.5 hours of the week were responsible for initiating thrombolysis in the A&E department. The service reverts to a "fast track" system outside of these hours, with the on call medical team prescribing thrombolysis on the coronary care unit. Prospectively gathered data were analysed for a nine month period and a head to head comparison made between the mean and median door to needle times for both systems of thrombolysis delivery. Results: Data from 91 patients were analysed; 43 (47%) were thrombolysed in A&E by the ACPNS and 48 (53%) were thrombolysed in the coronary care unit by the on call medical team. The ACPNS achieved a median door to needle time of 23 minutes (IQR=17 to 32) compared with 56 minutes (IQR=34 to 79.5) for the fast track. The proportion of patients thrombolysed in 30 minutes by the ACPNS and fast track system was 72% (31 of 43) and 21% (10 of 48) respectively (difference=51%, 95% confidence intervals 34% to 69%, p<0.05). Conclusion: Diagnosis of acute myocardial infarction and administration of thrombolysis by experienced cardiology nurses in A&E is a safe and effective strategy for reducing door to needle times, even when compared with a conventional fast track system.

Cardiac haemodynamics are deranged in chronic heart failure but fail to predict the exercise capacity of the patient. Cardiac power output is a descriptor of cardiac function derived from preload, blood pressure and cardiac output. Forty-one patients with moderately severe and severe chronic heart failure were exercised on a cycle ergometer to determine the relationship between traditional haemodynamics and cardiac power output and exercise capacity. Resting cardiac power output was no more predictive of exercise capacity than resting stroke-work index or resting cardiac index (r = 0.53, 0.61 and 0.51 respectively). Maximum cardiac power output and the ability to increase cardiac power output, however, were correlated with exercise capacity (r = 0.79 and 0.80). It is concluded that resting cardiac power output does not predict subsequent exercise capacity but that maximum cardiac power output and the ability to increase cardiac power output on stimulation are good descriptors of functional cardiac reserve.

Fifteen patients with moderately severe and severe chronic congestive heart failure were studied to determine the central haemodynamic results of short term increases in lower body positive pressure. Central haemodynamic variables were determined by Swan-Ganz thermodilution catheterisation and arterial cannulation. Graded increases in lower body positive pressure were applied to supine patients using Medical Anti-Shock Trousers (MAST). Increasing lower body positive pressure by 25 mm Hg and 55 mm Hg caused increases in mean right atrial pressure (6.0 to 13.2 to 17.9 mm Hg; p less than 0.001 and p less than 0.0001 respectively) and mean pulmonary artery pressure (26.8 to 35.5 to 41.3 mm Hg; p less than 0.05 and p less than 0.01 respectively). No significant changes were seen in left heart filling pressures or in pulmonary vascular resistance. Furthermore, there were no significant increases in indices of cardiac work (cardiac index, left ventricular stroke work index, right ventricular stroke work index or cardiac power output) despite the increased right heart filling pressures. These results show that in patients with longstanding severe congestive heart failure, short term increases in cardiac return may increase right heart pressures but do not appear to cause either beneficial or detrimental changes in left heart haemodynamic indices.