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“If I could only fly … if I could only fly … I’d bid this place goodbye … to come and be with you.”
‘If there is a physician on board, can you identify yourself to the cabin crew?’
You are nearly 4 hours into a trans-Atlantic flight from New York City to Amsterdam – well into your ‘It’s Always Sunny in Philadelphia’ viewing marathon – when a 21 year old man complains of feeling faint. He is flushed, nauseous and complains of bilateral hand tingling. He stands up to visit the lavatory when he wobbles and collapses into his seat. You see this transpire and identify yourself to the crew and make your way to the ailing passenger. The young man is fully conscious and states that prior to the flight that he and his girlfriend shared a large shellfish platter and bottle of red-wine. He has no known medical history, is on no mediations and has no allergies. There is nothing focal on a cursory neurological survey and absolutely no signs of upper airway compromise. You open the emergency medical kit, check his fingerstick glucose – which is normal – and attempt to measure his blood pressure with stethoscope and sphygmomanometer, but ambient engine noise prevents you from hearing the Korotkoff sounds. By palpation, he has a systolic blood pressure of 90-100 mmHg and a heart rate of 98 beats per minute. A crew member states, “Doctor, the pilot is ready to land in Reykjavik if needed.”
Commercial Flight Physiology
The cabin of a commercial aircraft is hypobaric, that is, pressurized to an altitude of 5000 to 8000 feet above sea level. More specifically, however, in a study from the late 1980s cabin pressure was determined to be up to 9000 feet [2715 metres] in some instances with a median cabin pressure just above 6000 feet. Newer aircraft, such as my favourite the Boeing 787, keep the ambient cabin pressure on the lower end of this range for improved passenger well-being. The rationale for keeping ambient pressure below 6000 feet is based on a study presented in the New England Journal of Medicine which showed that passenger discomfort increased the most during simulated altitudes of 7000 to 8000 feet with differences becoming most pronounced after 3 to 9 hours of exposure. It was postulated that these symptoms may have been secondary to mild acute mountain sickness and hypobaric hypoxemia. For instance, at an altitude of 8000 feet, ambient pressure falls from 760 mmHg to 565 mmHg. Thus, alveolar oxygen tension falls by about 25-30% based on the alveolar gas equation. Note that while the fraction of inspired oxygen remains 21% at altitude, it’s the total pressure that falls and reduces alveolar oxygen. In those with healthy lungs and a normal A-a gradient, a fall in alveolar oxygen occasions an arterial oxygen tension above 60 mmHg – on the flat portion of the hemoglobin dissociation curve. In those with pulmonary pathology – i.e. with an elevated A-a gradient – diminished alveolar oxygen can easily push arterial oxygen below 60 mmHg onto the descending portion of the hemoglobin dissociation curve. The aforementioned changes in arterial oxygen tension may be the cause of in-flight, mild respiratory distress endorsed by patients with chronic obstructive pulmonary disease.
While diminished cabin pressure alters gas-exchange physiology, it can also cause gas-expansion – described by Boyle’s law – in various body cavities leading to discomfort or even perforation. Accordingly, patients with recent abdominal, ENT or neurosurgical interventions or pneumothorax should refrain from flying for roughly 2-to-3 weeks [see this reference for specifics].
A clinician ready to assist is never alone. Typically, before an on-board announcement is made, ground-based medical consultative services are contacted by the flight crew. The assisting clinician can speak with these consultants and this is often helpful as the ground-based services are familiar with the medically-austere in-flight environment. One evaluation found that consultation with ground-based medical professionals reduced the need for diversion by upwards of 70%.
Pre-Syncope & Syncope
This is the most common in-flight medical event – accounting for 38% of incidents, but only 5% of all diversions and 6.5% of all hospital admissions. As a contributing factor, dehydration may accompany the dry conditions of most commercial airline cabins and subtle hyperventilation from hypobaric hypoxemia may accelerate insensible fluid loss. Capillary glucose and vital signs should be obtained as well as a brief medical history. Rather than determining an exact etiology, it is recommended that the clinician risk stratify the patient based on age and underlying cardiac conditions. Elderly patients at high risk for more sinister causes of syncope should prompt consideration for diversion. Nevertheless, in a previous commentary, the phenomenon of ‘benign in-flight syncope’ was described and, in general, vasovagal syncope can usually be managed simply by raising the legs and encouraging rehydration. The topic of pulmonary embolus as a cause of syncope has been previously discussed, and may not be as prevalent as formerly thought.
Cardiac symptoms make up about 8% of all in-flight events and roughly 18% of all flight diversions. Just as in any emergency department, the differential diagnosis of chest pain is quite broad. In the air, however, an approach similar to syncope may be adopted – that is, a method based upon risk stratification. While the clinical diagnosis of acute coronary syndrome is far-from-perfect, a middle-aged or elderly patient with concerning symptoms and a known history is reasonably treated with aspirin. While nitroglycerine may be found in the emergency medical kits, extreme care should be used with this drug as ACS with RV infarction cannot be diagnosed without an electrocardiogram; similarly, acute pulmonary embolus remains in the differential making RV preload reduction tenuous. It has previously been suggested that the flying altitude be reduced to increase cabin pressure, but this carries aviation risk and driving oxygen saturation above 90% in acute coronary syndrome has recently proved ineffective. The broad differential diagnosis of chest pain, clearly also includes other catastrophic events such as pulmonary embolus, dissection, pneumothorax, etc. While these etiologies would be difficult to discern in a commercial airline cabin, persistent, severe chest pain – especially with dyspnea – should trigger diversion. In a previous review, the use of an antacid was suggested to help differentiate cardiac chest pain from gastrointestinal sources and this was appropriately challenged in an accompanying commentary.
To Be Continued …
Dr. Kenny is the cofounder and Chief Medical Officer of Flosonics Medical; he is also the creator and author of a free hemodynamic curriculum at heart-lung.org