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Trekking to Everest: Part II

This is a three part series about Linda Sanders’ trek to the Everest base camp, and is accompanied by an interview about the journey. See Part II of the interview here:


High Altitude Illness Prevention We often say the air is thin at altitude. Actually, the FiO2 is still 21%, but because the barometric pressure drops by half, the partial pressure of inspired oxygen (PiO2) drops dramatically. The alveolar gas equation helps demonstrate this:

PiO2 = FiO2 x (PB – 47mmHg) – 1.2 (PaCO2)

PB = barometric pressure.

Of course sea level barometric pressures (PB) are 760mmHg, while at EBC the PB drops to just under 400mmHg. So if we do the math, the PiO2 is about half: 75mmHg at EBC vs 150 at sea level, if we keep the PaCO2 at normal physiologic levels (40).

This converts to a PaO2 of just 27mmHg compared to 100mmHg at sea level. If you look at the Oxygen hemoglobin dissociation curve, you’ve fallen off the steep part of the curve. So if you were breathing at a normal respiratory rate and tidal volume, your O2 Sat would be 44%. That’s a problem.

Fortunately we can breath faster, and the PaCo2 is the other half of this equation. At a respiratory rate of 20 you can clear out that CO2 and bump up your O2 Sat to 77%. Thus extreme hyperventilation is key to avoiding altitude illness. This ability to hyperventilate at these altitudes is called the hypoxic ventilator response (HVR) and if this is response is blunted by genetics, alcohol, or other sedating medications the individual is at increased risk of hypoxia and thus altitude illness.

This is why it is advised to take acetazolamide prophylactically before going to altitude. Acetazolamide is a carbonic anhydrase inhibitor and it causes a diuresis of bicarbonate which leads to a metabolic acidosis. This causes us to increase our respiratory rate to compensate. And we need a faster respiratory rate to maintain our O2 Saturation at altitude. Unfortunately it takes some time to work, so it is advised to take acetazolamide a couple of days before reaching altitude and its less effectivea once you’re already feeling sick.

Acetazolamide is an amazing drug that helped 16/17 of our group achieve their goal of reaching Everest Base Camp. Our group started taking it a day or two prior to arriving at Lukla (9000 feet). The major side effects included nocturia and pretty significant paresthesias. The recommended dosage is 125mg BID to start but can be increased to TID or 250mg BID at higher altitudes. We did have one group member with a sulfa allergy. He did not take acetazolamide and had a terrible headache at 10,000 feet where the rest of us felt very well. In these cases, dexamethasone is recommended for prophylaxis.

The impact of increased Hematocrit and Mitochondria at high altitude on acclimatization is often overemphasized. In reality this takes several weeks to occur. In the meantime it’s all about increasing one’s sympathetic drive and Diamox helps achieve this goal.

High Altitude Illnesses: AMS, HACE, & HAPE

Acute Mountain Sickness (AMS) is basically a headache plus GI symptoms (nausea, vomiting, anorexia) or insomnia, fatigue or dizziness. You can use the Lake Louise Criteria to determine the extent. But generally if one is experiencing AMS, it is recommended that one stop ascending to allow further acclimatization and wait 24 hours before further ascent. I found that AMS usually responds well to simply ibuprofen and odansetron. Clinical investigations are ongoing regarding the use of other antiemetic options. Several of our group members developed varying levels of AMS and first experienced mild AMS at 15,000 feet where my first symptoms were a headache, nausea and dizziness. One of our fellow trekkers was evacuated by helicopter for severe AMS at 17,000 feet.

Thankfully none of our group members developed High Altitude Cerebral Edema (HACE). HACE is basically worsening AMS resulting in life-threatening cerebral edema. HACE is characterized by a severe headache with altered mental status, which may manifest as ataxia, neurologic deficits, or simply confusion. Individuals with HACE must descend or risk death from cerebral herniation. There are some temporizing measures – supplemental oxygen, which is often in limited supply (our porters carried a single tank), and medications like acetazolamide and dexamethasone. In case of severe HACE or HAPE, our group carried a Gamow bag, a portable hyperbaric chamber. A Gamow bag is a large inflatable duffel bag that fits a person inside and is attached to a foot pump, which is used to pressurize the bag. A Gamow bag can simulate descent of 3000 to 9000 feet, the amount depends on the altitude at which it is used. Typically the ill individual will enter the Gamow bag for up to at least 2 to 4 hours and then be reassessed. Unfortunately when they exit the bag, they’re still at very high altitudes, so descent is often times still indicated.

At around 16,500 feet I myself started to develop High Altitude Pulmonary Edema (HAPE). HAPE is a form of non-cardiogenic pulmonary edema caused by the patchy vasoconstrictor response of the pulmonary vasculature to hypoxia. This leads to high pulmonary artery pressures and subsequent capillary leakage. The illness is most commonly characterized by decreased exercise tolerance, dyspnea, and cough. My story is a good example of HAPE and so I will share it here.

The first thing I noticed at 16,500 feet was my poor tolerance for uphill trekking. Every incline was becoming a problem for me. I felt myself slowing down. And I was developing what felt like exertional GERD, except that GERD shouldn’t be exertional so I was worried. My lungs were burning, perhaps filling with fluid. I finished ascending another 1,000 feet to our summit (EBC) and had my pulse oximetry taken at the Everest Base Camp ER tent. I knew it would be low, but the number was a shocking 60%. Somehow I was still mentating. At that point I had trekked six hours that day, and had another two to get back to our teahouse in Gorak Shep.

I made it back to the teahouse, slow and steady. But exertion is known to worsen HAPE. That night I slept sitting up in bed. I figured I had HAPE, so I took 20mg of extended release nifedipine in an attempt to abate the vasoconstriction of my pulmonary arteries that was causing all of this edema. I barely slept at all. At one point I had to get up to use the bathroom thanks to acetazolamide but I couldn’t do it. I was too short of breath to walk to the bathroom. Later I tried to take off a sock and felt my heart rate reach 160.

As it reached morning I was just thankful that I had made it through the night and I took another dose of nifedipine plus my dexamethasone and acetazolamide. Both of which were given to me by my roommate grabbed because I couldn’t move from bed. I had a severe headache which was also concerning. HAPE is known to be concomitant with HACE. I was still mentating, so our tour guides decided against the Gamow bag and I waited for them to contact a Helicopter. But as fate would have it was six hours before they were able to get a phone signal and by then I was feeling much better. Still, nifedipine and dexamethasone are temporizing measures for this condition. The definitive management for HAPE is descent.

Our group had planned to descend that morning and thanks to the help of pharmaceuticals and my fellow travellers looking out for me, I was able to join them for the rest of the trek. I had a horrendous cough but I was on my own two feet. I gave my daypack to a porter for the first day of descent and lowered the weight in my daypack on the following days in an attempt to decrease the exertion on the way down.

According to the Wilderness Medical Society guidelines, the next time I attempt an ascent or visit high altitude it will be advised that I take nifedipine prophylactically (Bartsch et al. 1991; Luks et al. 2014). Of course the best prevention is a slow ascent (less than 300-500 meters per day) with low sleeping altitudes and rest days built in after every 3 to 4 days of ascent.

PART THREE

Auerbach, PS (2012). Wilderness Medicine, Sixth Edition. Philadelphia, PA: Elsevier.

Bartsch P, Maggiorini M., Ritter M, Noti C, Vock P, & Oelz O (1991). Prevention of High-Altitude Pulmonary Edema by Nifedipine. The New England Journal of Medicine 325 (8): 1284-1289.

Luks AM, McIntosh SE, Grissom CK, Auerbach PS, Rodway GW, Schoene RB, Zafren K, & Hackett PH (2014). Wilderness Medical Society Practice Guideliens for the Prevention and Treatment of Acute Altitude Illness: 2014 Update. Wilderness & Environmental Medicine 25: S4-S14.

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