ABSTRACT
As part of a public health response to severe heat waves in the midwestern and northeastern United States in the summer of 1999, the authors actively solicited the number of heat-related deaths from 38 medical examiner and coroner jurisdictions comprising 35 metropolitan areas to enumerate heat-related deaths in areas affected by heat waves. They also determined the usefulness of these data for surveillance and rapid investigation of heat-related deaths. A total of 334 heat-related deaths were reported during the study period of July 1 - August 31. Minor changes in data collection and diagnostic criteria in some medical examiner and coroner jurisdictions would allow for greater comparability among jurisdictions. The National Association of Medical Examiners' position paper on heat-related mortality diagnosis provides important guidance to medical examiners and coroners regarding the certification of heat-related deaths and may require some refinement to address certain issues. Among these are certifying manner of death and classifying potential causes of heat-related death not involving hyperthermia or heat stroke, but where heat is a potential contributing factor to death. Medical examiners and coroners are an important resource for heat-related mortality research, and improvements in data collection and reporting could yield tremendous benefits to our understanding of and interventions for heat-related deaths.
Subject(s)
Cause of Death , Heat Stress Disorders/mortality , Cities/epidemiology , Coroners and Medical Examiners/statistics & numerical data , Death Certificates , Heat Stress Disorders/diagnosis , Humans , Population Surveillance/methods , Seasons , United States/epidemiologyABSTRACT
We compared the effects of elevated left atrial pressure of central nervous system origin (bicuculline-induced seizures) with an identical pulmonary vascular pressure elevation induced in six sheep by inflation of a balloon in the left atrium. The degree and duration of the consequent elevation in pulmonary lymph flow and the alteration in protein movement in the two groups was identical. Alterations in pulmonary fluid and protein flux resulting from generalized seizures can be explained by the pressor response alone; specific brain-lung neural interactions need not be postulated.
