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Firefighters have the highest rate of line-of duty death (LODD) in the United States. More than half of these LODD are cardiovascular related occurring disproportionately around fire suppression activities. In addition, shift work, lifestyle factors, and the exposures associated with fire suppression (e.g. smoke, chemicals) may predispose the firefighter to earlier onset of heart disease or cause a pro-inflammatory state leading to endothelial dysfunction.
Fire suppression activities exacerbate cardiovascular strain and endothelial dysfunction and provide potential triggers for ischemic events (e.g. myocardial infarction, stroke). There is a rapid rise in heart rate following the activation of a fire company which may persist for as long as 20 minutes. Even in cases where heavy work is not being performed, the repetitive upper body exercise associated with tool use raises heart rate disproportionately to oxygen consumption.
Finally, there is a rapid rise in core body temperature from increased physical activity, environmental heat and impaired thermoregulation that has been shown to cause vasoconstriction and activate coagulation during heat stress (12, 13). This has recently been demonstrated in firefighters working in thermal protective clothing. The combination of triggers created during fire suppression may result in heart attack or stroke, especially in firefighters with risk factors for cardiovascular disease.
Interventions beyond basic fireground rehab may be required to minimize the effect of these triggers and enhance a firefighter's health and wellness. Fireground rehab typically focuses on cooling and rehydration of the firefighter following fire suppression or training with the assumption that these interventions will correct the underlying pathophysiology. Effective fireground rehab must deliver appropriate interventions and monitor the progress of the firefighter. While correcting hyperthermia and hypohydration are essential for continued performance, it is not clear if these therapies correct alterations in platelet or endothelial function or if other interventions are necessary to correct these physiological disturbances. Furthermore, the options for monitoring the firefighter beyond simply measuring heart and respiratory rate are limited. In our FEMA-funded Fireground Rehab Evaluation (FIRE) Trial, we demonstrated that five commercially available thermometers did not reliably measure or estimate core temperature following uncompensable heat stress (UHS) making it impossible to gauge the effectiveness of rehab interventions.
Allocation: Randomized, Control: Placebo Control, Endpoint Classification: Efficacy Study, Intervention Model: Parallel Assignment, Masking: Double Blind (Subject, Investigator), Primary Purpose: Prevention
Heat Stress Disorders
Daily aspirin (ASA), Active cooling, Acute aspirin (ASA), Passive cooling, Daily placebo, Acute placebo
University of Pittsburgh, Emergency Responder Human Performance Lab
University of Pittsburgh
Published on BioPortfolio: 2014-08-27T03:16:00-0400
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A non-steroidal anti-inflammatory agent that is less effective than equal doses of ASPIRIN in relieving pain and reducing fever. However, individuals who are hypersensitive to ASPIRIN may tolerate sodium salicylate. In general, this salicylate produces the same adverse reactions as ASPIRIN, but there is less occult gastrointestinal bleeding. (From AMA Drug Evaluations Annual, 1992, p120)
Asthmatic adverse reaction (e.g., BRONCHOCONSTRICTION) to conventional NSAIDS including aspirin use.
A drug combination of aspirin and dipyridamole that functions as a PLATELET AGGREGATION INHIBITOR, used to prevent THROMBOSIS and STROKE in TRANSIENT ISCHEMIC ATTACK patients.
ANESTHESIA achieved by lowering either BODY TEMPERATURE (core cooling) or SKIN TEMPERATURE (external cooling).
The prototypical analgesic used in the treatment of mild to moderate pain. It has anti-inflammatory and antipyretic properties and acts as an inhibitor of cyclooxygenase which results in the inhibition of the biosynthesis of prostaglandins. Aspirin also inhibits platelet aggregation and is used in the prevention of arterial and venous thrombosis. (From Martindale, The Extra Pharmacopoeia, 30th ed, p5)
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