Aerospace medicine involves investigating and optimizing human physiology in esoteric environments such as undersea, flight, mountain, and space. As opposed to the majority of medical disciplines in which pathophysiology gets addressed in a normal environment, here effects on normal physiology get addressed in an abnormal environment, which presents a myriad of challenges regarding environmental exposures and physiologic function.
Humans in the aerospace environment are exposed to an increased ionizing radiation index, leading to genetic and cytogenetic changes. One concern is that an unpredicted solar particle event (e.g., solar flares) may expose space crew to unacceptably high radiation levels and cause acute radiation syndrome, which typically manifests following whole-body or partial-body exposure greater than 0.5 Gy. Symptoms occur as a spectrum, dependent on the type, route, and dose of exposure, and typically lead to hematopoietic, gastrointestinal, neurovascular, and cutaneous manifestations. Of additional concern is chronic exposure to low-dose cosmic radiation. This exposure may be a factor for space crew, as well as long-haul commercial pilots or transport aircrew who experience exposure to increased cosmic and ultraviolet radiation at the typical cruising altitudes of modern aircraft (i.e., 10000 to 13000 m). Chronic exposure has been shown to increase the risk of nuclear cataracts in pilots compared with non-pilots. Although anecdotal evidence suggests that aircrews are at an increased risk for malignancy, studies have reported conflicting results. Further research is warranted to ascertain the extent to which exposure to cosmic radiation affects subsequent long-term pathology. Aircrew and space crew may also sustain increased radiation exposure from vehicle systems (e.g., radar systems), which are specific to the aircraft, although there is only limited research regarding this factor. Humans in space are unavoidably exposed to further increased amounts of cosmic radiation, and spacecraft employ radiation protection material to mitigate this risk. Additionally, limits to cumulative radiation exposure are enforced.
Microgravity refers to an environment in which gravitational force is less than that experienced at the surface of Earth, including weightlessness. Primary musculoskeletal effects include loss of bone mineral density and deconditioning of skeletal muscle. Negative sequelae include reduced strength, increased fracture risk, and potential renal calculi formation due to aberration in calcium metabolism. Reduced gravity also affects the cardiovascular system due to a decrease in hydrostatic pressure, which leads to a fluid shift from extravascular to intravascular spaces, as well as the cephalad movement of intravascular fluid. Carotid baroreceptors perceive a hypervolemic state and enact a compensatory diuresis and reduce peripheral vascular resistance, resulting in orthostatic dysfunction sustained upon reentry and return to the normal gravity environment; baroreceptor reflex must again reset to normal gravitation force.
Acceleration is typically a factor during flights involving aggressive maneuvering. Importantly, the mechanics of rotational acceleration about various flight axes produce an effective increase in the force of gravity sustained by aircrew in the physiologic vertical axis (cephalad to foot). This effect becomes quantified in multiples of the normal acceleration due to gravitational force, expressed as G. For example, a 70-kg pilot executing a 9-G turn would experience the effects equivalent to a weight of 630 kg, resulting in pooling of blood volume in capacitance vasculature of the lower extremities, which reduces the ability of the cardiovascular system to ensure cerebral perfusion. Manifestations of reduced cerebral perfusion range from peripheral vision loss, to total gray-out (temporary loss of full visual field), to G-induced loss of consciousness (G-LOC), in which aircrew are rendered completely unconscious and incapacitated. The threshold of susceptibility to G force is individualized. Conversely, negative G force leads to abnormally increased cerebral vascular pressures that may result in “redout” (total reddening of the visual field). Negative G force is not as frequently encountered as it tends to be less comfortable. Acceleration effects are also present in the lateral and longitudinal axes but are generally not as substantial.
Musculoskeletal challenges are frequently incurred in high-performance aircraft as they undergo close air combat maneuvering against another maneuvering aircraft. These aircraft routinely attain and even sustain 9-G rotational acceleration, subjecting the pilot to an axial force of 9 times the force of gravity. This force frequently coincides with the pilot attempting to maneuver physically within the cockpit to maintain sight of the adversary aircraft, requiring the pilot to aggressively rotate, flex, and extend the neck and upper trunk against this force. As a result, fighter pilots often experience acute strain injuries of the cervical and paraspinal musculature of the upper back. High G force subjects the spinal column to significant stress. Pilots exposed to high G forces have an increased incidence of chronic neck and back pain compared with pilots exposed to low G forces. Additionally, maneuvering under high G forces has been associated with a 4.9-mm decrease in body height. Aircrew exposed to increased whole-body vibration, such as those associated with helicopters, report a high incidence of low back pain. Lastly, life support equipment, cockpit ergonomics, and cockpit posture may not be optimal and may subject the aircrew to increased musculoskeletal stress.
Ventilation must occur in various environments, from undersea divers breathing compressed air to mountain climbers ascending through hypoxic environments. A range of variables presents to the respiratory system for compensation, including changes in partial pressures of breathing gas as well as their relative concentrations. Hypoxia, which refers to inadequate delivery of oxygen to the tissues, can occur in the aerospace medicine environment in the form of hypoxic hypoxia, in which there is the inadequate environmental partial pressure of oxygen (PO2). Symptom onset presents with interpersonal variability but generally begins to occur above 3048 m (10000 ft) and may include dyspnea, fatigue, and reduced cognitive capacity. High-altitude cerebral edema (HACE) and high-altitude pulmonary edema (HAPE) are more severe, potentially lethal sequelae that may occur with altitude sickness. The body compensates for increased altitude and reduced PO2 with increased respiratory rate, increased depth of respiration, and increased cardiac output in an attempt to maintain oxygenation. Individuals who spend increased amounts of time at high altitudes also develop an increased concentration of hemoglobin to augment the oxygen-carrying capacity of the blood, as well as increased hemoglobin–oxygen affinity. Above 7620 to 10363 m (25000 to 34000 ft), death occurs without supplemental oxygen in individuals who have not undergone acclimatization to high altitude. At approximately 18300 m (60000 ft), the atmospheric pressure becomes so reduced that physiologic fluids will reach their boiling point in a phenomenon known as ebullism. Spacecraft and large aircraft maintain cabin pressurization to permit flight at high altitudes and enable adequate oxygenation for the occupants. High-performance tactical aircraft typically maintain cockpit pressurization and pressurized mask breathing through an independent ventilation circuit for the duration of the flight.
Both hyperbaric and hypobaric conditions present unique challenges to the cardiovascular system. The hypobaric environment below 2500 m (8200 ft) is usually well tolerated by healthy individuals, but the rate of ascent, genetic factors, age, and underlying pathophysiology will influence changes in the body during ascents. The greatest influencing factor to physiologic changes at altitude is the height of elevation and the resultant reduction in the partial pressure of inspired oxygen (PiO2), the partial pressure of alveolar oxygen (PAO2), and the partial pressure of arterial oxygen (PaO2). Since the fraction of inspired oxygen (FiO2) remains relatively constant at all altitudes (21%), reductions in barometric pressure will cause a decrease in PiO2, PAO2, and PaO2 leading to relative hypoxia without compensation. In addition to respiratory compensation by increasing minute ventilation, the hypobaric hypoxia will increase pulmonary artery pressures (hypoxic vasoconstriction), which can contribute to pulmonary edema in some individuals. To maximize oxygen delivery to tissues, cardiac output increases with the augmentation of heart rate and stroke volume, further increasing myocardial oxygen demand. With repeated or long-term exposures to high-altitude environments, the body undergoes several long-term adaptive mechanisms, including increased red blood cell counts, a rightward shift on the oxygen dissociation curve, and a reduction in parasympathetic activity to maintain a chronically elevated heart rate.
The hyperbaric environment is less frequently encountered and is most commonly associated with scuba diving or artificial depth in a hyperbaric chamber. Although an oversimplification, it is easy to conceptualize the physiologic changes at altitude as an inverse to that which occurs at depth; however, it is important to understand that the significant difference in density between water and air leads to more abrupt changes in partial pressures of gases at depth. Whereas the atmospheric pressure drops to one-half of its value at nearly 20000 ft, it requires a depth of only 33 ft of seawater to double atmospheric pressure. Thus, the short-term physiologic changes are mostly related to the behaviors of gas under pressure (Henry’s law and Boyle’s law) and give rise to many unique disease states when ascent, descent, and time at depth are not under strict control. Although there are notable and expected cardiovascular changes at normally encountered depths (reduction in heart rate, cardiac output, and preservation of stroke volume),  more pronounced changes and concerns relate to barotrauma, arterial gas embolism, and decompression sickness. Since the volume of gas is inversely related to the pressure at which it is subjected, failure to equalize pressure in the sinuses, lungs, ears, and other gas-filled pockets can result in barotrauma. As a diver ascends, especially against a closed glottis, increases in trans-alveolar pressure can cause overexpansion injury, alveolar rupture, pneumomediastinum, and even pneumothorax. Both pulmonary barotrauma and the precipitation of gas from blood during ascent can act as a conduit for gaseous infiltration of the cardiovascular system. Venous gas emboli are common after diving and usually well tolerated at low levels in the absence of a right to left shunt. In circumstances of overwhelming venous gas emboli or shunts (i.e., patent foramen ovale, or entry of gas into the pulmonary veins), and arterial gas embolism can occur with catastrophic ischemic sequelae occurring in the coronary and cerebral vasculature. As a diver ascends, the partial pressures of gases dissolved in bodily fluids can exceed that of ambient pressure. Depending on the location of gas precipitation, multiple symptoms of decompression sickness can ensue. Mild forms of decompression sickness (type I) occur with small gas embolism in the joints and skin, resulting in musculoskeletal pain and pruritis. More severe forms of decompression sickness (type II) usually result in neurological deficits and pulmonary involvement.
Traditional medicine involves the diagnosis and treatment of pathology in a normal environment. The aerospace medicine clinician must remain cognizant of the fact that, in general, addressing the physical effects of the aerospace environment on professional aviators, divers, astronauts, etc., does not primarily comprise considerations of pathology but instead focuses on strategies to mitigate the deleterious effects of an extreme environment on normal human physiology. For example, high-performance tactical fighter pilots are exhaustively screened to ensure optimal health. They are also the population most frequently involved in G-LOC occurrences. Interventions to mitigate this have included aircrew training and conditioning to maximize G resistance and the development of novel garments (G suit) to compress the lower extremities under G and reduce pooling of blood in the extremities and optimize cerebral perfusion. Consequently, the frequency of G-LOC has been reduced, augmenting the safety and efficacy of flying operations. Aerospace medicine continues to evolve, integrating the knowledge of environmental factors with a precise understanding of physiology to remain on the frontier of human exploration.
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