You are in: eMedicine Specialties > Emergency Medicine > ENVIRONMENTAL Aerospace MedicineArticle Last Updated: Aug 29, 2006AUTHOR AND EDITOR INFORMATIONAuthor: John Ogle, MD, MPH, FACEP, Consulting Staff, Department of Emergency Medicine, Longmont United Hospital; Voluntary Clinical Faculty, Stanford University Medical Center John Ogle is a member of the following medical societies: Aerospace Medical Association, Alpha Omega Alpha, American College of Emergency Physicians, and Colorado Medical Society Coauthor(s): Heather Ross, MD, Faculty, Physician Assistant Program, Red Rocks Community College; Medical Educator, Flight Surgeon, United Airlines; Consulting Staff, Exempla Good Samaritan Hospital, Exempla St Joseph's Hospital, and Exempla Lutheran Hospital Editors: Joseph J Sachter, MD, FACEP, Consulting Staff, Department of Emergency Medicine, Muhlenberg Regional Medical Center; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Eddy Lang, MDCM, CCFP (EM), CSPQ, Assistant Professor, Department of Family Medicine, McGill University; Consulting Staff, Department of Emergency Medicine, The Sir Mortimer B Davis-Jewish General Hospital; John Halamka, MD, Chief Information Officer, CareGroup Healthcare System, Assistant Professor of Medicine, Department of Emergency Medicine, Beth Israel Deaconess Medical Center; Assistant Professor of Medicine, Harvard Medical School; Jonathan Adler, MD, Attending Physician, Department of Emergency Medicine, Massachusetts General Hospital; Division of Emergency Medicine, Harvard Medical School Author and Editor Disclosure Synonyms and related keywords: aerospace medicine, flight medicine, aviation medicine, aeromedical issues, dvt, thromboembolism, hypoxia, hypobarism, air transport, airline travel, in-flight emergency, in-flight medical emergency, deep vein thrombosis, DVT, pulmonary embolism, PE, airline medical kit, automated external defibrillator, AED INTRODUCTION AND BACKGROUNDSooner or later, most physicians who travel on airlines will eventually hear the overhead call from a flight attendant, "Are there any doctors on board?" This brief review of aerospace medical principles can help physicians respond with confidence. Aerospace medicine is a subdiscipline of preventive and emergency medicine that ties together physics, life support, and medicine to protect aircrew and patients in the realm of aerospace. The ambient environment quickly becomes hostile to humans with increasing altitude. From the earliest physiologic observations of balloonists in the 1700s to Paul Bert's altitude chamber experiments in 1878 to the latest findings from the Columbia Space Shuttle Accident Investigation Report, our understanding of aerospace medicine has advanced exponentially. The evolution of aerospace medicine parallels and limits our development of faster and higher flying aerospace vehicles. In daily practice, emergency physicians are often confronted with aeromedical transport issues and occasionally deal with more esoteric aerospace medicine problems.
These common problems mandate a basic familiarity of aerospace medicine among all emergency physicians. The unifying goal of this medical subdiscipline is the optimization of the health and safety of crew, passengers, and airlifted patients before, during, and after aerospace travel. This chapter provides emergency medicine practitioners with a brief overview of aerospace physiological principles and considerations. Patient Education: For excellent patient education resources, visit eMedicine's Environmental Exposures and Injuries Center. Also, see eMedicine's patient education article The Bends - Decompression Syndromes. AEROSPACE STRESSORSAtmospheric physicsThe atmosphere contains 21% oxygen, and this fraction is constant at all altitudes. As total pressure decreases with higher altitudes, however, the partial pressure of oxygen decreases proportionally (Dalton's law). In medical terms, the fraction of inspired oxygen (FIO2) of cabin air remains constant as cabin altitude increases, but the alveolar partial pressure of oxygen declines. Boyle's law states that the volume of a gas at constant temperature varies inversely with changes in pressure. As a pocket of air ascends, it expands if it is exposed to ambient (outside) air pressure. Total ambient air pressure at sea level is 760 millimeters of mercury (mm Hg). This pressure is synonymously expressed as 14.7 pounds per square inch (PSI), 760 Torr, 760 millibars, or 29.92 in Hg. Since arterial blood gas measurements are reported in mm Hg, these units are most familiar to emergency physicians; for these reasons, mm Hg is used throughout this chapter. While ascending through the first 9100-18,300 m (30,000-40,000 ft), temperature decreases linearly at an average rate of 2ºC (3.6ºF) per 305 m (1000 ft). If sea-level temperature is 16ºC (60ºF), the outside air temperature is approximately -57ºC (-70ºF) at 10,700 m (35,000 ft). HYPOBARISMIntroductionIf sea-level cabin pressure could be maintained continuously in all aircraft, the role of the clearing physician would be simplified greatly. Unfortunately, fewer than 1% of medical transport aircraft are equipped to maintain constant pressure during flights. Many factors limit an aircraft's ability to maintain continuous sea-level pressurization, including minimum safe altitude for the route of flight, different departure and arrival elevations, the aircraft's pressurization capability, and operational considerations (eg, time, distance, fuel requirements). Exposing patients to changing ambient pressures is unavoidable. This section reviews the human responses to pressure changes and countermeasures available to medical care personnel. Scuba diving and aviationFlying within 12-24 hours of scuba diving is absolutely contraindicated. Rationale for this limitation is discussed in Decompression Sickness. As air is much less dense than water, significant physiological changes usually require thousands of feet of altitude change, while 3-6 m (10-20 ft) changes in water depth are significant to divers. Scuba divers experience a constant (linear) pressure increase of 760 mm Hg per 10 m (33 ft) of depth. In contrast, atmospheric air pressure decreases nonlinearly with ascent from sea level. Unlike water, air is a compressible fluid; thus, most air is compressed into the lowest layers of the troposphere. The first 305 m (1000 ft) of ascent represent the region of greatest change per vertical 0.305 m (1 ft). The steepest pressure gradients and greatest physiological effects are experienced when climbing through the lowest levels of the atmosphere. Physiologic response to ascentHealthy aircrews initially respond with small increases in ventilation during climb. Aeromedical transport patients respond similarly, but patients with more severe illnesses or injuries are affected at lower altitudes. While ascending, the body compensates first by increasing tidal volume and second by increasing respiratory rate. In healthy flyers, increased tidal volume is first noticeable at 1500 m (5000 ft). At 3700 m (12,000 ft), the average ventilation only increases from 8.5 to 9.7 L/min, but inspired partial pressure of oxygen (PO2) decreases from a sea-level value of 103 to 54.3 mm Hg, and PCO2 decreases from 40 to 33.8 mm Hg. The resting respiratory rate is largely unchanged until climbing above 6700 m (22,000 ft). In healthy people, ventilation volume nearly doubles to 15.3 L/min at this altitude. Rapid decompressionDuring a sudden loss of cabin pressure in a commercial airliner at cruising altitude, passengers immediately are exposed to altitudes between 7600 m (25,000 ft) and 13,100 m (43,000 ft). At 7600 m (25,000 ft), steady state PO2 falls to 30.4 mm Hg, and PCO2 is 27.0 mm Hg. The pathophysiology of rapid decompression is truly unique and represents an emergency. In contrast to the physiological stress experienced by high-elevation mountaineers, passengers and crew experience instantaneous ascent (ie, no acclimatization) when their cabin loses pressurization. Initial alveolar PO2 is less than the oxygen partial pressure in the mixed venous blood; thus, oxygen diffusion in the lungs is reversed. Unless this process is halted with immediate intervention, oxygen rapidly diffuses from the body within minutes. When cabin pressurization is lost, passengers are variably exposed to bitterly cold outside temperatures of approximately -57ºC (-70ºF) at 10,667 m (35,000 ft). The flight crew should intervene immediately during rapid decompression. Once a loss of cabin pressure is detected, aircrew and able passengers should immediately don oxygen masks to reverse the diffusive loss of oxygen at the alveolar level. Simultaneously, the pilot must perform an emergency descent to less hostile altitudes. If corrective action is not taken, the effective performance time (also called time of useful consciousness) is 3-5 minutes at 7600 m (25,000 ft), 30-60 seconds at 10,700 m (35,000 ft), and 9-12 seconds at 13,100 m (43,000 ft). In people who are sick or highly active, reserves are reduced, and loss of consciousness occurs sooner. Decompression sicknessPathophysiology and risk factors Decompression sickness (DCS) is a specific hypobaric complication caused when dissolved nitrogen evolves from solution. When external pressure drops, bubbles form in various tissues. Especially vulnerable are vessels, joints, and nervous system. Often, these bubbles are asymptomatic, but DCS is defined when symptoms develop. This phenomenon is well appreciated in scuba divers, but it also has been documented in the aerospace environment since the 1930s. Risk factors for DCS include exposure to altitudes over 5500 m (18,000 ft), long duration of exposure, prior water or hyperbaric chamber dives, rapid onset of depressurization, increased physical activity after decompression, and age older than 40 years. Some authorities believe additional risk factors include obesity, prior decompression in the preceding 18 hours, timing within menstrual cycle, and traumatic injury. Women also may be at increased risk for DCS. Symptoms Onset of symptoms may be delayed, and many people with DCS do not become symptomatic until after landing. Symptoms of mild DCS include pruritus, formication (ie, crawling skin paresthesias), and pitting edema. More significant disease is marked by intense aching joint pain aggravated by active or passive movement. Free nitrogen bubbles in joint spaces cause this arthritic pain, which typically is called the bends. Large and active joints most commonly are involved. Relief of pain after inflating a blood pressure cuff over the affected joint is diagnostic of DCS. A serious presentation, called the chokes, is caused by multiple pulmonary gas emboli and manifests with pleuritic chest pain, dry cough, and dyspnea. These symptoms usually lead to shock and must be treated immediately. In severe DCS, gas emboli can affect any organ system, but the peripheral and central nervous systems frequently are affected. Treatment Treatment has 3 components as follows: (1) descend (or repressurize), (2) administer 100% oxygen (to reduce body nitrogen stores), and, if necessary, (3) refer the patient to a hyperbaric (dive) chamber. Indications for hyperbaric therapy include unrelieved or recurrent joint pain or any respiratory, cardiovascular, or neurological symptoms thought to be associated with decompression. HYPOXIAIntroductionHypoxia is insufficient tissue oxygenation and is often secondary to multiple stressors. Tissue hypoxia may be unanticipated if clinicians do not consider the additive effects of coexisting stressors prior to flight. One of the most important tasks of the consulting or transferring physician is to consider multiple sources of tissue hypoxia when clearing patients or crew for aeromedical transport. Fewer than 1% of aircraft are equipped to maintain constant pressure during flight; thus, even passengers in pressurized aircraft feel the effects of altitude. Typical cabins in pressurized aircraft are kept at pressures equivalent to 1500-2400 m (5000-8000 ft). Aviation-grade oxygen must be readily available in the event of rapid decompression. If supplemental oxygen is unavailable during a breech of hull integrity, oxygen rapidly diffuses backward through the lungs of humans exposed to cruise-altitude air pressure. At typical cruise altitudes of 10,100-11,000 m (33,000-36,000 ft), the duration of useful consciousness after rapid decompression is 30-60 seconds in healthy crewmembers and shorter in compromised patients. Cumulative hypoxic stressAltitude is particularly poorly tolerated in patients with preexisting hypoxia. Emergency physicians should consider all hypoxic conditions to be relative contraindications to aeromedical transport. One classification scheme divides hypoxia into 4 subtypes: hypoxic, hyphemic, stagnant, and histotoxic. Risk of end-organ damage is based on cumulative effects of all coexisting hypoxic insults; thus, all sources of potential tissue hypoxia must be considered when evaluating a prospective aeromedical patient. Altitude-induced tissue hypoxia is a form of hypoxic hypoxia. Hypoxic hypoxia is a deficiency of oxygen exchange at the alveolar level and exists in those exposed to high altitudes, near-drowning victims, and in patients with conditions such as asthma, atelectasis, chronic obstructive pulmonary disease (COPD), pulmonary embolism, congenital heart defects, and pneumonia. More than one hypoxic hypoxia risk factor may exist in a given patient, such as a near-drowning victim who has developed subsequent pneumonitis and requires aeromedical transport. The remaining causes of tissue hypoxia occur beyond the alveoli. Hyphemia refers to reduced oxygen-carrying capability of the blood and occurs in patients with anemia, hemoglobinopathies, and certain drug and toxic exposures. Stagnant hypoxia is secondary to reduced systemic or regional circulation and appears in patients with congestive heart failure (CHF), shock, hypothermia, poor positioning/immobility, tourniquets, hyperventilation, cerebrovascular accident (CVA), and emboli. Finally, histotoxic hypoxia refers to poisoning of the cytochrome oxidase system and interferes with cellular utilization of oxygen. Patients and aircrew exposed to carbon monoxide, ethanol, cyanide (commonly encountered in aircraft fires), and hydrogen sulfide have varying degrees of preexisting histotoxic hypoxia. Any effect of altitude-mediated tissue hypoxia is amplified in patients or aircrew with coexisting hypoxic stressors. Hypoxia countermeasuresFor many aviators, hypoxia prevention begins in the hypobaric (altitude) chamber. The experience teaches physiological self-awareness. This awareness is crucial for flight safety because hypoxia has an insidious (sometimes pleasant) onset and may present as euphoria or in other subtle ways. After this training, an aviator gains an appreciation for his or her unique hypoxic symptoms. This preventive step is an essential part of military aviation training and is highly recommended for civilian flyers. In flight, the hypoxic effects of altitude can be minimized with supplemental oxygen and maximal cabin pressurization. Supplemental oxygen increases the FIO2. Except in emergencies, hospital-grade oxygen is unacceptable for use in aerospace operations because of its moisture content. Oxygen for use in aviation must be purified to less than 0.005 mg/L of water vapor to protect against freezing and regulator interference. Pilots in high-performance/high-altitude aircraft occasionally rely on pressure breathing to counter low alveolar oxygen tension. This is analogous to continuous positive airway pressure/bilevel positive airway pressure (CPAP/BiPAP) with 100% FIO2 and is generally required at cabin altitudes above 10,400 m (34,000 ft). The usual hypobaric countermeasure involves maximizing cabin pressurization (or limiting cruise altitude). Pressurization increases the total air pressure, thereby increasing inspired and alveolar PO2 even though FIO2 is unchanged. Adding supplemental oxygen and pressurizing the cabin both independently increase alveolar partial pressure of oxygen. Remember the risk of oxygen toxicity increases in hyperbaric (ie, dive) chambers but decreases in hypobaric (ie, altitude) chambers and in actual aerospace operations. AIR TRANSPORT AND PHYSIOLOGICAL ISSUES BY ORGAN SYSTEMIntroductionCountless lives have been saved because of the rapid air transport available in modern medical systems. Specialized centers and equipment (eg, burn centers, hyperbaric chambers) are too costly to be located in every ED, so reliance on air transport continues to grow. As transferring physicians, many emergency physicians are required to prepare patients for aeromedical transport. As with any transfer, the referring physician must ensure that the patient is safe for transport. This section reviews specific conditions that the transferring or attending physician should consider when evaluating a patient for or during aeromedical transport. This chapter concludes with a brief discussion on aircrew fitness for flight. Patient clearance for flightPatient clearance falls squarely within the scope of the practicing emergency physician. Although the emergency physician retains ultimate responsibility, recall that the flight nurses and medics are formally trained in flight medicine; use them as consultants. Clearing patients or routine travelers for flight is largely based on anticipating the physiologic effects of changing cabin pressures. Most physicians are more familiar with hypoxic stress than with hypobaric stress. When ambient cabin pressures fall during ascent, free air expands and causes mass effects in unvented spaces. Pneumothorax, pneumocephalus, and intraocular air must be positively excluded in patients who are potential candidates for air transport. The following discussion is organized by organ system to facilitate quick reference by the sending physician who must make urgent decisions about suitability of air transport and prepare the patient for a safe flight. CardiovascularUnlike first-generation unipolar pacemakers, no current evidence indicates that modern pacemakers or ICDs are affected in any way with in-flight electromagnetic interference. Supplemental oxygen is strongly recommended for ill cardiac patients even when not required on the ground. Hypoxic stress may aggravate or precipitate cardiac ischemia. Ground adjuncts (eg, suction, monitors) must be provided in the cabin, and transport on a cardiopulmonary resuscitation (CPR) board is prudent though uncomfortable. Though unusual in aircraft designed for aeromedical transport, acceleration (g-forces) can be problematic, particularly during takeoff in fixed-wing aircraft. Ambulatory (seated) passengers tolerate acceleration forces well. These forces are sustained along a sagittal axis (ie, anterior to posterior) during takeoff and in the vertical axis (ie, head to toe) during turns. In patients in litters, however, acceleration and climb-out can be dangerous if blood pressure and cardiac output are tenuous and if the patient is positioned with the head toward the front of the plane. Longitudinal acceleration on the takeoff roll, combined with nose-high pitch on climb-out, creates significant reverse Trendelenburg physiology. Venous pooling and preload reduction can be significant in those with unstable hemodynamics; thus, supine patients typically are placed head rearward. Landing stresses are usually less worrisome, and nose-high landing attitude offsets deceleration forces to some degree. NeurologicalBecause of the autoregulatory mechanisms affecting cerebral blood flow, carefully consider arterial PCO2 and PO2 in brain-injured patients. At cabin altitudes of 4,600 m (15,000 ft) or below, low PCO2 effects predominate, and cerebral vessels are constricted. Above this altitude, low PO2 effects predominate, and cerebral blood flow increases. Airlifted patients with recent skull fractures or patients who are status postcraniotomy must be excluded for intracranial air as this expands at altitude, producing a mass effect. Evidence of external leakage of cerebrospinal fluid (CSF), such as otorrhea, should raise suspicion for potential pneumocephalus. Usually, patients with brain injury are best positioned with the head rearward for takeoff and forward for landing. This positioning reduces the impact of caudal acceleration forces and decreased perfusion. The benefit of greater perfusion, however, must be weighed against the risk of increasing intracranial pressure. Rapid decompression during flight can have neurological consequences for aeromedical patients and their flight crews (see Decompression Sickness). Although nitrogen bubbles can and do embolize to the CNS, in reality, hypoxic stress during depressurization is much more neurologically dangerous than nitrogen-mediated DCS. The relationship of migraines to altitude exposure remains elusive, although an association between migraines and acute mountain sickness seems apparent. Additionally, the aerospace literature suggests that exposure to altitudes over 2400 m (8000 ft) may trigger headaches in patients with a history of migraines. In these patients, the typical visual, sensory, or motor auras develop immediately after depressurization. By contrast, patients without a migraine history develop late headaches after delayed altitude exposure. OphthalmologyWhen airlifting patients with recent eye injuries or surgery, free air in the globe must be excluded, because expansion at altitude could lead to dangerous increases in intraocular pressure. OtolaryngologyEar, nose, and throat (ENT) problems encountered in aerospace medicine are similar to those in dive medicine (see Dysbarism and Barotrauma). Problems are related directly to ambient pressure changes. Barotrauma is mediated through expansion and contraction of enclosed air spaces (air cells). Problems occur when expanding gas does not communicate freely with the external environment. This may occur within the middle ear, the sinus cavities, and, occasionally, the teeth. Barotitis media is the most common problem associated with aerospace travel. Barotitis media consists of a traumatic inflammation secondary to a pressure differential between the air in the tympanic cavity and mastoid air cells and that of the ambient air (cabin pressure). Patients may report ear popping during climbs, but severe ear blocks requiring corrective maneuvers usually are limited to descent or increasing cabin pressurization. Physiologically, the eustachian tube must ventilate the middle ear and equalize pressure. The anterior two thirds of this organ is membranocartilaginous and typically rests in the closed position. Swallowing, yawning, or lower jaw movement causes contraction of the tensor and levator veli palatini muscles, which open the eustachian tube. Functionally, the anterior channel behaves as a 1-way valve. Air easily escapes the middle ear cavity when ambient pressure is reduced (ascent) but does not readily reenter this cavity when ambient pressure exceeds middle ear pressure (descent). This phenomenon is amplified in those with allergic or upper respiratory symptoms, probably because of edema and general reduced patency. Expanding air escapes from the middle ear into the back of the pharynx while climbing, thereby equalizing air pressure. This is normal physiological functioning. Problems typically arise during descent, when the eustachian tube collapses and air is prevented from reentering the middle ear. Failure to equalize pressure causes retraction of the tympanic membrane and severe pain. The flying literature is filled with anecdotes of pilots who had to abort landings because of the severe pain associated with ear blocks. The phenomenon of delayed ear blocks occurs in aviators (passengers or crew) who breathe 100% oxygen. This problem often affects those who fly late at night and then go to sleep, and it may affect patients who breathe 100% oxygen during transport, especially if heavily sedated. Oxygen-rich air remains in the middle ear cavity after landing, and slight negative pressure keeps the eustachian tube closed. Several hours after flight termination, local tissues absorb the oxygen, and the negative pressure differential is increased. The patient wakes up in the middle of the night with otalgia and a retracted tympanic membrane. ENT countermeasuresPreventing an ear block Prevention, recognition, and early reversal are the mainstays of treatment for barotitis media. Fuel and weather permitting, gradual descents permit more complete equalization of middle ear and sinus pressures. In pressurized aircraft, maintaining high cabin pressure (low-altitude equivalents) and slowly pressurizing the cabin in advance of descent are useful techniques. Sleeping during descent is risky because people swallow and yawn less when asleep, and early warning signs of mild ear discomfort may go unnoticed until a full ear block develops. For this reason, some airlines maintain a policy of waking sleeping passengers prior to descent. Infants who cry inconsolably during descent often are troubled by ear block. Nursing infants should be encouraged to suck on a pacifier during descent to help maintain eustachian tube patency. Reversing an ear block Ear block develops in a vicious cycle; the greater the middle ear/atmospheric pressure differential, the more difficult it is to restore eustachian tube patency. Pseudoephedrine, the Valsalva maneuver (ie, exhaling against a closed mouth and pinched nose), yawning, and gum chewing all have been attempted to restore pressure to the middle ear after an ear block develops. Physiologically, all of these maneuvers are designed to restore eustachian tube patency momentarily to permit equalization. Some advocate performing the Valsalva maneuver with the neck laterally flexed to one side then the other in an effort to stretch and straighten the eustachian tube. Some airline attendants and flight medics use a technique called politzerization to help those with ear blocks. Using a Politzer bag, which is essentially a reverse suction bulb, the medic attempts to force air into the nasopharyngeal opening of the eustachian tube. GastroenterologyIn contrast to ear and sinus problems, which usually are noted on descent, problems involving trapped gas that originates in the GI tract are typically present on ascent. Patients with GI problems are generally poor candidates for aeromedical transport. Infection, ischemia, ulceration, recent GI surgery, diverticulitis, or inflammation from any cause can lead to a weakened intestinal wall, which poorly withstands the increased tension present as intraluminal air expands with increased altitude. Patients with acute appendicitis, diverticulitis, strangulation, and partial or total bowel obstruction are among those who should avoid airlift if possible. Nasogastric and rectal tube decompression has been used to reduce the risk of intestinal rupture on emergency airlifts of patients with compromised GI integrity. PulmonaryUntreated pneumothorax is an absolute contraindication to flight unless sea-level cabin pressure can be strictly guaranteed. This is usually impossible; thus, placement of a chest tube with Heimlich valve is indicated. Patients with recently removed chest tubes should wait 72 hours prior to air transport because even radiologically undetectable pleural gas can expand to significant volumes in flight. All aeromedical patients must receive x-ray evaluation after subclavian or jugular vein catheterization to rule out pneumothorax. People with bullous emphysema are at risk for rupture and pneumothorax at altitude, especially during rapid loss of cabin pressure. When transporting intubated patients, some authorities recommend inflating endotracheal tube cuffs with saline instead of air to avoid gas expansion problems at altitude. If this technique is not used, pay close attention to the indicator bulb. Anticipate the need to release cuff pressure during ascent and to re-inflate during descent. Chronic obstructive pulmonary diseaseIn patients who retain carbon dioxide (eg, those with COPD), the risk of carbon dioxide narcosis is reduced at altitude for any FIO2 or flow rate. Clinicians should provide generous supplemental oxygen, even when patients are suspected or known to retain carbon dioxide. Pathophysiology in COPD patients at altitude At sea level, carbon dioxide retention in patients with COPD is a hypoventilatory response to increasing arterial PO2. People at risk for carbon dioxide retention grow tolerant of borderline high carbon dioxide and derive their ventilatory drive from blood oxygen levels. The respiratory centers rely on low-to-normal arterial PO2 to drive ventilation. Excessive exogenous oxygen can blunt ventilation at sea level and cause a dangerous buildup of carbon dioxide. On the ground, circumvention of this problem and maintenance of adequate ventilatory drive is possible by using low oxygen flow rates and minimizing FIO2. Exercise caution when applying this principle at altitude, as it can lead to inappropriate withholding of supplemental oxygen. In any given patient, carbon dioxide retention becomes less of a problem at altitude because arterial PO2 (and respiratory drive) is a function of absolute alveolar PO2, not FIO2. Example Consider a patient at sea level breathing room air (21% FIO2). Inspired PO2 is 103.0 mm Hg. When the percentage of oxygen increases to 40% FIO2, the inspired PO2 increases to 196.1 mm Hg. Even these modestly increased levels can blunt ventilatory drive in patients with COPD. This well-appreciated physiological phenomenon explains a general reluctance to blindly increase supplemental oxygen in patients who retain carbon dioxide at sea level. Now consider the respiratory physiology of this patient at altitude. At 3700 m (12,000 ft), ambient FIO2 is still 21%, but because of the total barometric pressure reduction, inspired PO2 is only 54.3 mm Hg. Increasing the oxygen concentration of inspired air at this altitude to the same 40% FIO2 results in an inspired PO Ventilatory drive depends on arterial oxygen content, which in turn depends on alveolar PO2. Clearly, the greater danger is hypoxia, not hypercarbia. Alveolar PO2 is reduced at altitude when compared to the same FIO2 at sea level, and the oxygen-dependent component of the respiratory drive is preserved or enhanced at altitude. Hypercarbia still can occur at altitude, but oxygenation is of proportionally greater concern than ventilation in the flying environment. Asthma Asthma and history of asthma are disqualifying for military candidates seeking pilot training. Asthma is also a concern to emergency physicians considering aeromedical transport because many of the stressors found in the aviation environment precipitate asthmatic exacerbation. These precipitants include temperature extremes, smoke and fumes, and, possibly, pressure breathing. Hematology and DVTsAny lengthy period of immobility is a risk factor for deep vein thrombosis (DVT). This applies to routine passengers as well as airevac patients. The New Zealand Air Traveler's Thrombosis (NZATT) study prospectively followed 878 air passengers who subsequently traveled at least 10 hours. Frequency of thromboembolism was 1.0% (9/878, 95% CI 0.5-1.9), which included 4 cases of pulmonary embolism (PE) and 5 of DVT. Among those who developed thromboembolism, 6 had preexisting risk factors, 2 traveled in business class, 5 used aspirin, and 4 wore compression stockings. A 2006 study from that country found that 65% of those admitted for DVT had undertaken air travel in the previous week, and 43% of those had undertaken travel exceeding 10 hours duration.1 Maintain a high index of suspicion for DVT and PE when evaluating passengers and crew after long flights as future studies elucidate the true incidence and effective countermeasures available for flight-related DVT. For now, it is prudent to advise ambulatory patients and passengers to stand up and move around the cabin every 2-3 hours on long flights. Aspirin or anticoagulation therapy may be warranted given the patient's risk profile and relative contraindications to antiplatelet therapy. A 2006 Cochrane Database meta-analysis found a reduction in asymptomatic DVT and leg edema when travelers wore compression stockings, but those authors cautioned against generalizing about parallel risk reduction for PE because no such events were observed in their trials.2 Occasionally, those who are extremely sensitive to marginal oxygen tensions (eg, those with sickle cell anemia) may require supplemental oxygen. Although problems are theoretically possible in individuals with sickle cell trait, restrictions are generally unnecessary. Persons with less than 41% hemoglobin S (HbS) have qualified for Air Force pilot training. When transporting patients who are anemic from other causes, supplemental oxygen is recommended for those with a hemoglobin (Hgb) level less than 8.5 g/100 mL. When Hgb falls below 8.0 g/100 mL, consider a transfusion prior to transport. Obstetrics and neonatologyTransfer of high-risk obstetric patients to tertiary facilities is commonplace. Supplemental oxygen should be available if there is any concern of fetal insufficiency. An emergency delivery pack should accompany the patient. Neonatal transport also is becoming more commonplace. In addition to oxygenation requirements, thermal stability must be ensured. Muscular and skeletalPatients with fractures can be transported by air, but recent fractures should be splinted and casts bivalved at least 48 hours prior to flight to avoid problems secondary to tissue expansion. Pneumatic splints should be avoided because of air expansion problems at elevated cabin altitudes. Airline passengers traveling with serious illnessesA 2002 Swedish study reports an estimated 50,000 passengers per year will experience a "medical event." Physicians often encounter patients who ask if it is safe to fly the next day. An understanding of the physiological stresses mentioned above along with good clinical common sense is necessary to properly address this question. First, consider the patient's general health. Is separation from the rapid response of emergency medical services (EMS) safe for the patient? Even on domestic flights, it may be unwise for a seriously ill patient to spend several hours away from definitive therapy. Beyond the obvious risk to the patient, an unscheduled flight diversion can cost an airline as much as $100,000. Given the slight decrease in PO2, any serious systemic disease could be slightly aggravated aboard a commercial airline. Some practitioners routinely discourage airline flights for those within 30 days of a myocardial infarction. Many airlines deny passage to patients in the third trimester of pregnancy. These are arbitrary restrictions that should be adjusted to the individual patient while considering the length and route of flight. Remind patients of the real but finite risks involved, and let them weigh the importance of the particular flight against those risks. Aircrew clearance for aviation dutiesOccasionally, medical practitioners are required to evaluate and treat aircrew as well as patients. State laws require physicians to report various observations to appropriate authorities. When aviators are found to have medical conditions that could impair their flying performance, supervising medical authorities must evaluate the aviator on an individual basis. Supervising agencies include the Federal Aviation Administration (FAA) and its cadre of aeromedical physicians, various branches of US and allied armed forces, and private-sector aviation organizations. Civilian and military aviators are required to self-report new medical problems to their respective aviation medical authorities, and a gentle reminder from the emergency physician is appropriate. Under 14 CFR 61.15, all pilots are required to submit a notification letter to the FAA within 60 calendar days of the effective date of an alcohol- or drug-related conviction or administrative action. When emergency physicians assist in disaster relief and evacuation missions, they may be called to confirm crewmembers' fitness for aviation duties. Physicians in this position usually are not trained in flight medicine, and differing supervising agencies define their own restrictions and standards. For these reasons, a conservative approach and referral are mandatory. Although an exhaustive discussion on aircrew physical qualifications and standards is beyond the scope of this emergency medicine text, physicians should be aware of the fundamentals of medical clearance for flight operations. Strictly speaking, only a flight physician can clear an aviator to fly. In reality, civilian aviators receive most of their urgent medical attention from nonflight physicians. During a crisis or at any time between periodic flight physical examinations (see Flight Physical), emergency physicians may be called upon to render an opinion as to a crewmember's airworthiness. Clearing an aviator for flying duties requires special training and authority. In general, aircrew are fit to fly if motor, sensory, and mental functioning are optimal and there is no increased risk of sudden incapacitation. Sudden loss of function can be caused by such conditions as vasovagal syncope, seizures, hypoglycemia, and malignant arrhythmias. There should be no impairment of hearing or vision. Confirm visual ability, including linear and distant vision, depth perception, night vision, color vision, visual field testing, and extraocular gaze performance without diplopia. Aircrew should never self-medicate, and emergency physicians must refrain from prescribing medications to those preparing to fly. If medication is required, restrict the patient from performing any flight duties until certain that all effects of the medication and underlying disease have dissipated. If any doubt exists, ground the crewmember. In all instances, refer aviators to the appropriate aeromedical authority. Air travel with minor illnessesIf major problems are considered and the risk of separation from definitive care for a few hours seems acceptably low, then it is probably safe for a patient to fly. After more serious perils are considered, address common problems that might be aggravated by high altitude. Otitis media and sinusitis are among the most common. In the US Air Force, crewmembers are restricted from flight duties if they have either sinusitis or otitis media. For the airline passenger, absolute restriction probably is not required. On examination, visualize the tympanic membrane and have the patient perform the Valsalva maneuver. If immobility is noted, advise the patient against airline travel until the condition resolves. Swollen drainage passages can create a trapped gas cavity that expands and causes problems at altitude. If the would-be flyer is adamant and ground transport alternatives are unacceptable, treat these problems aggressively with the antibiotic of choice and be sure to include oral and topical spray decongestants (eg, oxymetazoline [Afrin]) to encourage patent eustachian tubes and sinus foramina. A very different ear disorder, the perforated tympanic membrane, is not a contraindication to flight whatsoever. In fact, perforations facilitate middle ear equalization and eliminate barotitis media as a concern. German dive-bomber pilots were given prophylactic myringotomies during World War II, a truly unique occupational approach to an aeromedical hazard of the day. IN-FLIGHT MEDICAL KITSThe American Heart Association estimates that as many as 1000 lives are lost annually from cardiac arrests in commercial aircraft. Airlines are addressing this and other in-flight medical problems, but deployment of aircraft medical kits remains in a state of flux. Whether making recommendations to patients considering airline travel or responding to problems in flight, do not rely on the presence of any particular item on the airplane. The composition of such kits is only loosely regulated by the FAA and varies tremendously between airlines and even between aircraft from the same airline. In October 1996, the US Food and Drug Administration first approved the use of automated external defibrillators (AEDs) for commercial aircraft. Internationally, Qantas Airlines was the first major carrier to add AEDs to emergency medical kits. The Australian airline first brought AEDs aboard in 1991 and reported their results after 64 months of observation. They observed 27 episodes of sudden death on aircraft and 19 in terminals. AEDs were used in all cardiac arrests and on 63 other occasions for monitoring acutely ill persons. Of particular interest, most cardiac catastrophes occurred in persons who previously appeared to be in good health. Only 1 of the 27 patients who experienced cardiac arrest on the aircraft was known to be ill at check-in, and this individual was traveling with a medical escort. US airlines are carrying AEDs, but incorporation of advance resuscitation equipment has been slow and fraught with obstacles including liability, theft, and crew training problems. One major US airline reported over half its AEDs were stolen within the first few months of carrying them. A 2004 preliminary report on AED deployment on Air France describes 12 in-flight cardiac arrests over the first year. Crew defibrillated 5 patients, and 3 survived the flight and 2 survived through hospital discharge. Currently, the FAA only mandates that each aircraft carry a first-aid kit with limited emergency medications including glucose, nitroglycerin tablets, injectable diphenhydramine, and epinephrine. Medical kits usually contain additional medications, but the "airplane formulary" varies tremendously. In addition to the FAA-mandated list of medications, a 1998 report from the Aerospace Medical Association task force recommended the following:
Responding to problems while airborneThe ethical duties and liabilities of physician passengers are hotly debated. In 1998, an Aerospace Medical Association survey reported that 47 of 850 respondent physicians withheld assistance while airborne because of fear of litigation. Many other respondents reported that they feared legal ramifications, though they rendered assistance anyway. Given the litigious nature of US society, these results are unsurprising, but a 1997 review finds no punitive actions have yet been taken against passenger physicians for inappropriate actions while responding to in-flight emergencies. Airlines, however, have been sued for negligent advice from passenger physicians. If an in-flight problem arises while the physician is a passenger, the physician should ask a flight attendant to bring the medical kit so a quick inventory can be taken. The physician may be the only physician on the flight. Years may have passed since the physician delivered a baby or ran an advanced cardiac life support (ACLS)-style code; however, major airlines have flight surgeons on telephone standby 24 hours a day, and the aircrew can reach them or any needed consultant for verbal advice while airborne. Physicians should not hesitate to request this service. Though not publicized, these calls are becoming commonplace. A flight surgeon covering a single major airline typically gets 3 calls per 24-hour period requesting advice regarding onboard medical issues. DESYNCHRONY OR JET LAGCharles A. Lindbergh's observations are familiar to emergency physicians. My mind clicks on and off. . . . I try letting one eyelid close at a time while I prop the other open with my will. But the effort's too much. Sleep is winning. My whole body argues that nothing life can attain is quite so desirable as sleep. My mind is losing resolution and control.Lindbergh's observations and circadian rhythm imbalances are familiar phenomena to emergency physicians. Desynchrony is considered a contributing factor to numerous air crashes and to the Three Mile Island nuclear plant accident. US and other military flight agencies are intensely interested in medical countermeasures to offset effects of desynchrony. Troops and crewmembers often are required to transit many time zones and arrive at peak condition ready for operational missions. Air Force regulations require that flight crew be offered 12 hours of unscheduled crew rest time prior to flights, 8 hours of which should be spent sleeping. Sleep researchers and other investigators have made tremendous recent gains toward understanding these physiological cycles. Temperature, sleep-wakefulness, and hormone levels are among commonly reported markers of body cycles. Desynchrony occurs when changing environmental cues (eg, meals, daylight, work-sleep schedules) conflict with existing biological rhythms. People normally have little problem coping with short environmental shifts of 1-2 hours per day, as might be experienced by ship or car travel across time zones. Problems commonly associated with desynchrony usually manifest after transoceanic flights and, occasionally, transcontinental US flights. Symptoms of desynchrony include generalized malaise, mild nausea, reduced mental and physical energy levels, and impaired judgment and coordination. Traditionally, it was believed that recovery from jet lag (resynchronization) occurred at a fixed rate of approximately 1 hour per day. Contemporary teaching maintains that readjustment is nonlinear. The out-of-phase condition is halved every 2 days (logarithmic decay). Alcohol, increased age, and hypoxia are risk factors for symptomatic desynchrony. Generally, people have more difficulty adjusting to travel from west to east than from east to west. This is attributed to average natural circadian rhythm cycles of 24-26 hours. Eastward travel actually compresses days into shorter periods, taking a person even further from their natural cycle. In contrast, westward travel actually expands days to approximate the internal cycle more closely. Treatment and countermeasures"I hope I die peacefully in my sleep like my grandfather. . .not screaming in terror like his passengers." --Anonymous Wiley Post became the first person to circumnavigate the world in an aircraft in 1931. His desynchrony countermeasure was to gradually alter his sleep-wake pattern in advance, a method he termed preadaptation. Aeromedical circles are keenly interested in evaluating hypnotics and stimulants as pharmacologic countermeasures against desynchrony. Temazepam (Restoril), administered 30 mg PO every bedtime, was intensely evaluated by the Royal Air Force prior to the Falkland Islands War. During that conflict, temazepam proved efficacious in resynchronizing aircrews with minimal adverse effects. Melatonin is under investigation in US Air Force trials. This drug has not received FDA approval as a pharmaceutical agent, although it is widely available as an over-the-counter nutritional supplement. Recommended dosage is 3 mg PO every bedtime or 1 mg SL every bedtime. Zolpidem (Ambien), administered 5-10 mg PO every bedtime, is a recently introduced serotonergic hypnotic that shows promise in resetting circadian rhythms. As shift workers, emergency physicians experience problems related to desynchrony and usually have plenty of advice to offer. Not surprisingly, opinions about countermeasures vary widely. Counseling patients about jet lag is an opportune time to share personal remedies for this minor physiological irritant. CONCLUSIONAerospace medicine is seldom included in emergency medicine training curricula, but most ED physicians will encounter problems related to the flight environment. Excluding the immediate aftermath of the terrorist attacks of September 11, 2001, passenger miles and aeromedical transport rates have trended upward every year in the United States. As aeromedical technology advances, rescuers attempt increasingly complex air evacuations such as deep sea and remote Antarctic outposts. Whether responding to an in-flight emergency while flying as a passenger or a team member in a complex recovery, emergency physicians and their accepting EDs are usually involved. A firm grasp of aerospace physiology is imperative. The immediate airborne stressors are hypoxia and hypobarism. Without life support systems, humans respond to ascent by increasing tidal volume and respiratory rate. Emergency physicians must consider the cumulative hypoxic effects of coexisting pathology and the ambient cabin environment prior to clearing patients for flight, or while attending to them in flight. Altitude aggravates preexisting tissue hypoxia in patients with low cardiac output, anemia, and hemoglobinopathies. Delayed consequences such as DVT and PE are the feared consequences of air travel. Supplemental oxygen and cabin pressurization are first-line countermeasures. Fears of oxygen toxicity and hypercarbic narcosis are unfounded, and supplemental oxygen should be used liberally while airborne, even in patients known to retain carbon dioxide at sea level. Frequent mobility and antiplatelet therapy (if not contraindicated) are recommended by many as DVT prophylaxis. Patients with cardiac and intracranial problems must be positioned appropriately in anticipation of acceleration forces on takeoff and landing. The middle ear, sinuses, and GI tract are particularly susceptible to trapped gas expansion and compression problems. Ear blocks are among the most common problems and typically develop on descent because of the 1-way valve physiology encountered in the eustachian tube. Asthma and migraines can be induced in the flight environment, and a conservative approach is recommended for susceptible patients. Airline medical kits are often very advanced, and many carriers have AEDs and well-stocked in-flight first aid kits available. These can be used by responding physician-passengers for resuscitation and monitoring of seriously ill patients while airborne. At any time, medical professionals might be required to apply knowledge of aerospace physiology to a real patient. Physicians should be familiar with the common flight-related and flight-aggravated problems while constructing a differential diagnosis list. Many airlines have dispatch services to connect airborne passenger-physicians to ground based specialists. Most jurisdictions give "Good Samaritan" protection to voluntary responders, and the author encourages all medical professionals to volunteer their services without reservation should they find themselves airborne during an in-flight medical emergency. MULTIMEDIA
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