Early aeromedical risk i was based on aeromedical standards designed to eliminate individuals ii from air operations with any identifiable medical risk, and led to frequent medical disqualification. The concept of considering aeromedical risk as part of the spectrum of risks that could lead to aircraft accidents (including mechanical risks and human factors) was first proposed in the 1980s and led to the development of the 1% rule which defines the maximum acceptable risk for an incapacitating medical event as 1% per year (or 1 in 100 person-years) to align with acceptable overall risk in aviation operations. Risk management has subsequently evolved as a formal discipline, incorporating risk assessment as an integral part of the process. Risk assessment is often visualised as a risk matrix, with the level of risk, urgency or action required defined for each cell, and colour-coded as red, amber or green depending on the overall combination of risk and consequence. This manuscript describes an approach to aeromedical risk management which incorporates risk matrices and how they can be used in aeromedical decision-making, while highlighting some of their shortcomings.

The management of cardiovascular disease (CVD) has evolved significantly in the last 20 years; however, the last major publication to address a consensus on the management of CVD in aircrew was published in 1999, following the second European Society of Cardiology conference of aviation cardiology experts. This article outlines an introduction to aviation cardiology and focuses on the broad aviation medicine considerations that are required to manage aircrew appropriately and optimally (both pilots and non-pilot aviation professionals). This and the other articles in this series are born out of a 3 year collaborative working group between international military aviation cardiologists and aviation medicine specialists, many of whom also work with and advise civil aviation authorities, as part of a North Atlantic Treaty Organization (NATO) led initiative to address the occupational ramifications of CVD in aircrew (HFM-251). This article describes the types of aircrew employed in the civil and military aviation profession in the 21st century; the types of aircraft and aviation environment that must be understood when managing aircrew with CVD; the regulatory bodies involved in aircrew licensing and the risk assessment processes that are used in aviation medicine to determine the suitability of aircrew to fly with medical (and specifically cardiovascular) disease; and the ethical, occupational and clinical tensions that exist when managing patients with CVD who are also professional aircrew.

This manuscript focuses on the broad aviation medicine considerations that are required to optimally manage aircrew with established coronary artery disease (CAD) without myocardial infarction (MI) or revascularisation (both pilots and non-pilot aviation professionals). It presents expert consensus opinion and associated recommendations and is part of a series of expert consensus documents covering all aspects of aviation cardiology.Aircrew may present with MI (both ST elevation MI (STEMI) and non-ST elevation MI (NSTEMI)) as the initial presenting symptom of obstructive CAD requiring revascularisation. Management of these individuals should be conducted according to published guidelines, ideally with consultation between the cardiologist, surgeon and aviation medical examiner. Return to restricted flight duties is possible in the majority of aircrew; however, they must have normal cardiac function, acceptable residual disease burden and no residual ischaemia. They must also be treated with aggressive cardiac risk factor modification. Aircrew should be restricted to dual pilot operations in non-high-performance aircraft, with return to flying no sooner than 6 months after the event. At minimum, annual follow-up with routine non-invasive cardiac evaluation is recommended.

Coronary events remain a major cause of sudden incapacitation, including death, in both the general population and among aviation personnel, and are an ongoing threat to flight safety and operations. The presentation is often unheralded, especially in younger adults, and is often due to rupture of a previously non-obstructive coronary atheromatous plaque. The challenge for aeromedical practitioners is to identify individuals at increased risk for such events. This paper presents the NATO Cardiology Working Group (HFM 251) consensus approach for screening and investigation of aircrew for asymptomatic coronary disease.A three-phased approach to coronary artery disease (CAD) risk assessment is recommended, beginning with initial risk-stratification using a population-appropriate risk calculator and resting ECG. For aircrew identified as being at increased risk, enhanced screening is recommended by means of Coronary Artery Calcium Score alone or combined with a CT coronary angiography investigation. Additional screening may include exercise testing, and vascular ultrasound imaging. Aircrew identified as being at high risk based on enhanced screening require secondary investigations, which may include functional ischaemia, and potentially invasive coronary angiography. Functional stress testing as a stand-alone investigation for significant CAD is not recommended in aircrew. Aircrew identified with coronary disease require further clinical and aeromedical evaluation before being reconsidered for flying status.

Cardiovascular diseases i are the most common cause of loss of flying licence globally, and cardiac arrhythmia is the main disqualifier in a substantial proportion of aircrew. Aircrew ii often operate within a demanding physiological environment, that potentially includes exposure to sustained acceleration (usually resulting in a positive gravitational force, from head to feet (+Gz)) in high performance aircraft. Aeromedical assessment is complicated further when trying to discriminate between benign and potentially significant rhythm abnormalities in aircrew, many of whom are young and fit, have a resultant high vagal tone, and among whom underlying cardiac disease has a low prevalence. In cases where a significant underlying aetiology is plausible, extensive investigation is often required and where appropriate should include review by an electrophysiologist. The decision regarding restriction of flying activity will be dependent on several factors including the underlying arrhythmia, associated pathology, risk of incapacitation and/or distraction, the type of aircraft operated, and the specific flight or mission criticality of the role performed by the individual aircrew.

It remains unknown whether hypobaria plays a role on cerebrovascular reactivity to CO2 (CVR). The present study evaluated the putative effect of hypobaria on CVR and its influence on cerebral oxygen delivery (cDO2) in five randomized conditions (i.e., normobaric normoxia, NN, altitude level of 440 m; hypobaric hypoxia, HH at altitude levels of 3,000 m and 5,500 m; normobaric hypoxia, NH, altitude simulation of 5,500 m; and hypobaric normoxia, HN). CVR was assessed in nine healthy participants (either students in aviation or pilots) during a hypercapnic test (i.e., 5% CO2). We obtained CVR by plotting middle cerebral artery velocity versus end‐tidal CO2 pressure (PETCO2) using a sigmoid model. Hypobaria induced an increased slope in HH (0.66 ± 0.33) compared to NH (0.35 ± 0.19) with a trend in HN (0.46 ± 0.12) compared to NN (0.23 ± 0.12, p = .069). PETCO2 was decreased (22.3 ± 2.4 vs. 34.5 ± 2.8 mmHg and 19.9 ± 1.3 vs. 30.8 ± 2.2 mmHg, for HN vs. NN and HH vs. NH, respectively, p < .05) in hypobaric conditions when compared to normobaric conditions with comparable inspired oxygen pressure (141 ± 1 vs. 133 ± 3 mmHg and 74 ± 1 vs. 70 ± 2 mmHg, for NN vs. HN and NH vs. HH, respectively) During hypercapnia, cDO2 was decreased in 5,500 m HH (p = .046), but maintained in NH when compared to NN. To conclude, CVR seems more sensitive (i.e., slope increase) in hypobaric than in normobaric conditions. Moreover, hypobaria potentially affected vasodilation reserve (i.e., MCAv autoregulation) and brain oxygen delivery during hypercapnia. These results are relevant for populations (i.e., aviation pilots; high‐altitude residents as miners; mountaineers) occasionally exposed to hypobaric normoxia.

Introduction: The present study evaluated the putative effect of hypobaria on resting HRV in normoxia and hypoxia. Methods: Fifteen young pilot trainees were exposed to five different conditions in a randomized order: normobaric normoxia (NN, P B = 726 ± 5 mmHg, F I O 2 = 20.9%), hypobaric normoxia (HN, P B = 380 ± 6 mmHg, F I O 2 ∼ =40%), normobaric hypoxia (NH, P B = 725 ± 4 mmHg, F I O 2 ∼ =11%); and hypobaric hypoxia (HH at 3000 and 5500 m, HH3000 and HH5500, P B = 525 ± 6 and 380 ± 8 mmHg, respectively, F I O 2 = 20.9%). HRV and pulse arterial oxygen saturation (SpO 2) were measured at rest seated during a 6 min period in each condition. HRV parameters were analyzed (Kubios HVR Standard, V 3.0) for time (RMSSD) and frequency (LF, HF, LF/HF ratio, and total power). Gas exchanges were collected at rest for 10 min following HRV recording. Results: SpO 2 decreased in HH3000 (95 ± 3) and HH5500 (81 ± 5), when compared to NN (99 ± 0). SpO 2 was higher in NH (86 ± 4) than HH5500 but similar between HN (98 ± 2) and NN. Participants showed lower RMSSD and total power values in NH and HH5500 when compared to NN. In hypoxia, LF/HF ratio was greater in HH5500 than NH, whereas in normoxia, LF/HF ratio was lower in HN than NN. Minute ventilation was higher in HH5500 than in all other conditions. Discussion: The present study reports a slight hypobaric effect either in normoxia or in hypoxia on some HRV parameters. In hypoxia, with a more prominent sympathetic activation, the hypobaric effect is likely due to the greater ventilation stimulus and larger desaturation. In normoxia, the HRV differences may come from the hyperoxic breathing and slight breathing pattern change due to hypobaria in HN.

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