Firefighting: Can our arteries take the heat?

Currently, there are approximately 1.1 million volunteer and career firefighters in the United States.1 Firefighting remains one of the most hazardous and challenging lines of work with multiple occupational hazards including smoke inhalation, exposure to high-intensity heat, dehydration, potential falls and vehicular collisions. Since 1977, sudden cardiac death has accounted for the largest share of on-duty cardiac deaths among firefighters – surpassing burns, trauma, asphyxiation and smoke inhalation. Despite the steady decline in the average number of deaths among firefighters over the past decade, sudden cardiac death still accounts for 42% of the on-duty deaths in the last five years.2 Adverse cardiovascular (CV) events in firefighters, including sudden cardiac death, most commonly coincide with active strenuous duties rather than non-emergency situations. Thus, while traditional CV risk factors are prevalent in firefighters and are associated with greater CV risk in this population,3–6 the unique physical and environmental hazards faced by firefighters likely acutely magnify their CV risk in the peri-emergency setting. Research to determine the most important factors with an adverse impact remains speculative. Firefighters are subjected to high levels of dynamic and static physical exertion during performance of duties while wearing heavy, insulating protective equipment (PPE) often weighing in excess of 25 kg. Emergency situations are highly stressful and often chaotic, leading to profound sympathetic activation that manifests in part with elevated blood pressure and maximal or near maximal heart rates in firefighters during emergencies. Working under these conditions can rapidly lead to dehydration, reduced plasma volume and potentially stroke volume. Firefighting is also associated with increased number and aggregability of circulating platelets, attributable at least in part to hemoconcentration and increased sympathetic activity.7 Together with exposure to smoke containing toxic chemicals and carbon monoxide, the cardiovascular system is placed under significant strain during firefighting. Firefighters also experience significant heat stress. Firefighting produces large amounts of metabolic heat while insulating PPE limits its dissipation. In addition, fire-related heat also adds further thermal strain. The core temperature can increase as much as 0.05 degrees Celsius/min or 1°C over 20 minutes of acute firefighting activity.8,9 The increase in core temperature experienced by firefighters is significantly greater than that seen during routine aerobic exercise. Prior work by Fahs and colleagues demonstrates that three hours of firefighting activity results in impairment of microvascular endothelial function, faster wave reflection and increased vascular stiffness when assessed within 30 minutes of cessation of these activities.10 These effects were not mitigated by oral supplementation with ascorbic acid (2 grams) prior to activity.10 These data suggest firefighting activities adversely impact vascular physiology, leading to elevated blood pressure, reduced coronary perfusion and increased plaque vulnerability in a manner that is not mitigated by oral antioxidants. The specific contribution of heat stress to the acute adverse vascular effects of firefighting and whether these effects can be mitigated pharmacologically are unclear. These open questions are the subject of two articles published in the current issue of Vascular Medicine.11,12 Lefferts and colleagues explore the impact of moderate exercise induced heat stress (EIHS) compared to normothermic exercise on aortic stiffness, pressure from wave reflections and non-invasive estimates of myocardial work and coronary perfusion.11 Twelve young, healthy, and physically active men were randomized in a crossover design to two distinct alternative exercise/rest protocols: no heat stress (NHS) and heat stress (HS). Peripheral artery tonometry was performed prior to and within 15–30 minutes following each activity session. Compared to NHS, HS protocol resulted in significant increases in both rate pressure product (RPP) and systolic pressure time integral (SPTI) with concomitant decreases in both diastolic pressure time integral (DPTI) and reflected wave velocity. These data suggest heat stress results in an increase in myocardial workload with concomitant reductions in coronary perfusion. However, in contrast to prior work, no appreciable effect on aortic stiffness was noted as measured by carotid-femoral pulse wave velocity. The lack of impact of heat stress on large elastic artery stiffness reported by Lefferts and colleagues suggests that the effect on elastic arteries may require the presence of Firefighting: Can our arteries take the heat?