What is the empirical evidence that hospitals with higher-risk adjusted mortality rates provide poorer quality care? A systematic review of the literature

<p>Abstract</p> <p>Background</p> <p>Despite increasing interest and publication of risk-adjusted hospital mortality rates, the relationship with underlying quality of care remains unclear. We undertook a systematic review to ascertain the extent to which variations in risk-adjusted mortality rates were associated with differences in quality of care.</p> <p>Methods</p> <p>We identified studies in which risk-adjusted mortality and quality of care had been reported in more than one hospital. We adopted an iterative search strategy using three databases – Medline, HealthSTAR and CINAHL from 1966, 1975 and 1982 respectively. We identified potentially relevant studies on the basis of the title or abstract. We obtained these papers and included those which met our inclusion criteria.</p> <p>Results</p> <p>From an initial yield of 6,456 papers, 36 studies met the inclusion criteria. Several of these studies considered more than one process-versus-risk-adjusted mortality relationship. In total we found 51 such relationships in a widen range of clinical conditions using a variety of methods. A positive correlation between better quality of care and risk-adjusted mortality was found in under half the relationships (26/51 51%) but the remainder showed no correlation (16/51 31%) or a paradoxical correlation (9/51 18%).</p> <p>Conclusion</p> <p>The general notion that hospitals with higher risk-adjusted mortality have poorer quality of care is neither consistent nor reliable.</p

Hämodynamik von Koronarstenosen

Under physiological conditions the resistance component of large epicardial coronary branches is very small in relation to total coronary resistance and can be neglected. The pressure losses across minor stenoses can be compensated by a decrease of resistance in the more peripheral coronary bed (autoregulation). This compensatory mechanism is limited to luminal obstructions less than 85%. Above this limit, when collateral vessels are not available, perfusion of the periphery becomes a function of the flow across the stenosis. As a consequence coronary reserve becomes abolished with an increasing obstruction. Coronary reserve describes an increase of coronary flow up to a factor of five, which, under normal conditions, is induced by dilation of resistors (arterioles) in the coronary bed. After exhaustion of coronary reserve the hemodynamic impact of a vascular narrowing can be expressed as the pressure loss across a coronary lesion (delta p). delta p is composed of viscous losses (AV) that are in linear relation to flow and inertial components that are related to the square of flow (B). Accordingly pressure loss across a stenosis can be expressed in a general form as delta p = AV X Q + B X Q2. In vitro data show that an approximation of delta p can be calculated on the basis of stenosis geometry including normal and minimal diameter, length, angle of entrance and exit, velocity of flow, viscosity and density of blood. Pressure losses across a stenosis can be divided in three components: the entrance, the narrow part, and the exit. Turbulence arises at the exit. This fact leads to a variable interaction of consecutive vascular lesions.(ABSTRACT TRUNCATED AT 250 WORDS