Basic Science

Atmospheric pressure has a non-linear decrease as altitude increases. Half of the atmosphere is below 18 000 ft and the remaining half extends up to >100 000 ft. Increased altitudes are often categorized to denote their increasing effect of physiology:

• 
  

  “High altitude” begins at 1500 m (~5000 ft) above sea level.

  
  
• 
  

  “Very high altitude” begins at 3500 m (~11 500 ft)

  
  
• 
  

  “Extreme altitude” begins at 5500 m (~18 000 ft)

Anesthetics delivered between 5000 and 11 500 ft require only modest changes from standard sea-level practices. Anesthetic care above 11 500 ft becomes increasingly problematic. The distinction and risks of “extreme altitude” are self-explanatory.

Fractional atmospheric oxygen concentration remains approximately 21% at all altitudes. As atmospheric pressure decreases with elevation, the absolute partial pressure of oxygen in air declines according to Dalton’s Law – “The sum of all the partial equals the total pressure.” (Pbar × 0.21) calculates the atmospheric oxygen pressure at any altitude. The alveolar gas equation defines a partial pressure for alveolar oxygen based on barometric pressure. A simplified form of the equation is:

PAlveolarO2=FiO2PBar-47mmHg-PaCO2RQ

where P_Alveolar is the partial pressure of oxygen in the alveolus (mmHg) – “PAO_2,” FiO₂ is the fractional concentration of oxygen in inhaled gas (21% unless enhanced), P_Bar is the barometric (atmospheric) pressure (mmHg), 47 mmHg is the vapor pressure of water at body temperature (altitude does not change), PaCO₂ is the partial pressure of CO₂ in the alveolus (mmHg), and RQ is the respiratory quotient (moles CO₂ produced per moles O₂ consumed – typically about 0.82 for normal diet).

Using the alveolar gas equation, the effects of altitude and carbon dioxide on alveolar and arterial oxygen become very evident (calculations assume PaCO₂ = 40 – no compensation with hyperventilation):²

At sea level – P_Bar is 760 mmHg, PAO₂ is 101 mmHg, and hemoglobin saturation (SaO₂) is 98%.

At 5000 ft – P_Bar is 632 mmHg, PAO₂ is 73 mmHg, and SaO₂ is 95%

At 10 000 ft – P_Bar is 522 mmHg, PAO₂ is 51 mmHg, and SaO₂ is 86%.

At 15 000 ft – P_Bar is 438 mmHg, PAO₂ is 32 mmHg, and SaO₂ is 62%.

At 20 000 ft – P_Bar is 364 mmHg, PAO₂ is 17 mmHg, and SaO₂ is 24%.

(This last altitude is only sustainable with hyperventilation/hypocarbia or supplemental oxygen.)

With PaCO₂ = 20 mmHg – note the effect of hyperventilation on saturation

At 20 000 ft – P_Bar is 364 mmHg, PAO₂ is 42 mmHg, and SaO₂ is 78%.

Demographics

All people are subject to the normal physiological effects of altitude. Rapid ascent to high altitude without adequate acclimatization additionally risks altitude-related illnesses. Physiologic adjustment to altitude requires both time and patience.

Adaptation

Acute adaptation to high altitude involves hyperventilation and increased cardiac output. Lower P_Bar leads to lower PAO₂, decreased SaO₂, and PaO_2. Increased hypoxic ventilatory drive from low PaO₂ leads to hyperventilation. Hyperventilation leads to decreased PaCO₂ and PACO₂, enhancing alveolar oxygen tension (per above illustration). As hyperventilation is the primary means of acute adaptation to ascent, the ability to rapidly tolerate hypobaric environments depends largely on sufficient pulmonary reserve. The degree of hypocapnia can be striking. End-tidal CO₂ on Mt Everest has been measured at 7.5 mmHg, clearly low enough to modify cerebral and other organ blood flow. Decreased gas density offsets some of the adverse work of breathing from hyperventilation. Cardiac output is increased by sympathetic signaling due to hypoxemia, particularly through increased heart rate. This acute response may be detrimental to individuals with ischemic or valvular cardiac disease or with pre-existing pulmonary hypertension.

Longer-term adaptation occurs over days to weeks. Mechanisms include:

• 
  

  Increased 2,3-DPG levels due to hypoxic stress, shifting O₂–Hgb dissociation curve toward the right and facilitating O₂ unloading in tissues

  
  
• 
  

  Increased erythropoiesis – polycythemia toward >50% Hct

  
  
• 
  

  Increased cardiac output secondary to hypoxemia

  
  
• 
  

  Renal compensation for the alkalosis of hypocarbia – largely bicarbonate wasting to improve left-shifted O₂–Hgb dissociation curve

  
  
• 
  

  Genetic differences modify adaptive responses

  
  
• 
  

  The complete mechanism of adaptation is not fully elucidated.

Pathophysiology at Altitude

Both anesthesia providers and their patients arriving acutely at high altitudes are susceptible to hypobaric illnesses. Over-exertion, poor hydration, and young age may contribute to risk. Physical fitness and gender do not seem to affect incidence. Sudden exposure to very high or extreme altitudes (>11 500 ft) can be fatal. Unconsciousness can occur within minutes and death may follow without supplemental oxygen. Although discussion of these illnesses may seem tangential to “high-altitude anesthesia,” these conditions may affect either the provider or the patient. Prolonged emergence, refractory hypoxemia, and other adverse anesthetic patient outcomes may be explained by these mechanisms. Providers impaired by these conditions constitute a substantial hazard to their patients. Cerebral hypoxia impairs judgment – perhaps your judgment!

Acute high-altitude exposure can cause several forms of illness, overlapping in both pathophysiology and clinical presentation:

• 
  

  acute mountain sickness (AMS)

  
  
• 
  

  high-altitude pulmonary edema (HAPE)

  
  
• 
  

  high-altitude cerebral edema (HACE).

Acute Mountain Sickness

AMS is the mildest mild form of hypobaric illness.

Symptoms

• 
  

  Early symptoms (12–24 hours): headache refractory to standard analgesics, nausea, anorexia, lassitude, sleep disturbances, peripheral edema. Judgment may be impaired.

  
  
• 
  

  Late symptoms: can progress to shortness of breath, intense snoring, vomiting, hallucinations, and severely impaired cognitive function.

  
  
• 
  

  Advanced symptoms: severe dyspnea, cyanosis, decreased SaO₂, ataxia.

Treatment

• 
  

  If severe, definitive treatment is descent! Often descent of only 500–1000 m leads to complete resolution of symptoms. Most symptoms resolve in several days, even at altitude.

  
  
• 
  

  Rest, hydration, analgesics, oxygen all can help.

  
  
• 
  

  Acetazolamide 250 mg q 8–12 hours improves symptoms and SaO₂ (especially during sleep).

  
  
• 
  

  Dexamethasone 4 mg q 6 hours.

Prevention

• 
  

  Ascend slowly (not always possible in military or disaster operations)

  
  
• 
  

  Oxygen, particularly at night while sleeping

  
  
• 
  

  Daily altitude gain of no more than 300 m above 3000 m

  
  
• 
  

  After ascending 1000 m spend two consecutive nights

  
  
• 
  

  Rest on arrival at altitude, avoiding over-exertion, adequate hydration

  
  
• 
  

  Acetazolamide 250 mg q8 hours beginning at least 24 hours before ascent and continued for two to three days after reaching highest altitude.

Two additional forms of altitude-induced illness are, though less common, more severe and life threatening.

Only gold members can continue reading. Log In or Register to continue

Share this:

• Click to share on Twitter (Opens in new window)
• Click to share on Facebook (Opens in new window)

Related

Related posts:

Chapter 5 – Inhaled Anesthetics and Draw-Over Devices in Disaster Response Chapter 4 – Total Intravenous Anesthesia in Disaster Medicine Chapter 14 – Considerations When Working with Children and Families Chapter 15 – Chemical and Radiologic Exposures in Trauma and Disasters Chapter 23 – Pharmacy in Disaster Anesthesia Chapter 21 – Operation Tomodachi: Anesthetic Implications

Stay updated, free articles. Join our Telegram channel

Join