Download Anesthesiology and the Cardiovascular Patient: Papers by Dennis T. Mangano PhD, MD (auth.), T. H. Stanley, P. L. PDF

By Dennis T. Mangano PhD, MD (auth.), T. H. Stanley, P. L. Bailey (eds.)

ISBN-10: 9401072248

ISBN-13: 9789401072243

Anesthesiology and the Cardiovascular Patient includes the edited displays of the forty first Annual Postgraduate path in Anesthesiology, February 1996. The chapters replicate new facts and ideas in the common framework of the pathophysiology and administration of surgical applicants with heart problems. The textbook will function a automobile to deliver a number of the newest thoughts in anesthesiology to people who didn't attend the convention. every one bankruptcy is a quick yet sharply centred glimpse of the present curiosity in anesthesia. This quantity, in addition to prior and destiny volumes, displays the speedy and carrying on with evolution of anesthesiology within the overdue 20th century.

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Additional resources for Anesthesiology and the Cardiovascular Patient: Papers presented at the 41st Annual Postgraduate Course in Anesthesiology, February 1996

Sample text

VENTRICULAR PRESSURE-VOLUME RELATIONS Measurement of the instantaneous change in ventricular volume and pressure forms the basis for analysis of ventricular function by the pressurevolume diagram or loop. If the recorded ventricular pressure and volumes from the Wiggers diagram are plotted simultaneously, a loop results which can be used to display various phases of the cardiac cycle (Figure 2). The changes in pressure versus volume occur in a counter-dockwise fashion over the time course of a single cardiac cycle.

If the arterioles in the perfusion territory of a totally occluded coronary artery are near maximally dilated, no further decrease in the resistance of arterioles in ischemic areas will be produced by these drugs. In fact, the effect of the small vessel dilators to lower resistance in normal zones can reduce collateral flow by decreasing the driving pressure for collateral flow at the origin of the coronary collaterals. This phenomenon is termed "coronary steal" and is independent of change in systemic hemodynamics such as heart rate and diastolic aortic pressure.

This regional difference in cardiac stiffness makes it difficult to compare studies unless data refer to the same region. As to the difference between the studies of Pagel and colleagues (20) and our own studies (21), several factors may be implicated. First, one model used the awake 34 state as control and the other used fentanyl anesthesia. Second, Pagel and colleagues studied the mid wall and not the apex or the base. As neither apical nor basal region showed any change in our study, it is unlikely that changes would have been observed if the midwall had been studied.

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