Anesthesia at the Extremes of Altitude and Environment

1
Anesthesia at the Extremes of Altitude and
Environment

• Major Eric Weissend, M.D.
• Department of Anesthesiology
• Wilford Hall Medical Center
• Lackland AFB, Texas

2
Environmental Challenges in the Practice of
Anesthesiology

• Air Force anesthesiology providers are now going
  far and wide in support of combat and
  humanitarian operations. The majority of
  postings are to minimally developed areas where
  patients and providers are subject to
  environmental extremes.

3
Environmental Challenges in the Practice of
Anesthesiology

• Deployment presents numerous personal and
  professional challenges. Caring for trauma and
  surgical disease in the deployed environment can
  be physically and intellectually challenging. The
  extremes of heat, cold, and altitude further
  complicate the care of our patients.

4
Environmental Challenges in the Practice of
Anesthesiology

• Military operations in Afghanistan and Iraq serve
  to illustrate theses types of environments.

5
Heat

• Iraq Daytime temperatures in the summer
  regularly reaching well over 100 degrees F.

6
Cold

• Afghanistan, Operation Anaconda Soldiers fought
  for extended periods in temperatures well below
  freezing in the mountainous Shah-I-Khot region.

7
Altitude

• Afghanistan, Operation Anaconda (again) Combat
  Ops took place between 8,000 and 12,000 feet
  above sea level.
• Bagram Air Base located at 5,000 feet above sea
  level.

8
Environmental Challenges in the Practice of
Anesthesiology

• To provide safe and effective anesthesia services
  to our patients we must understand the effects
  that extremes of heat, cold, and altitude have on
  our patients, ourselves, and our equipment.

9
How Does Excessive Ambient Heat Effect Anesthetic
Practice?

• Effects on volatile anesthetics
• Heat injuries

10
Inhaled Anesthesia and Heat

• Temperature effects vaporizer output minimally in
  normal ranges of temperatures.
• All vaporizers in use in the EMEDS and MFST
  systems are temperature compensated.
• In a consistently climate controlled environment
  altered output should not be an issue.

11
Narkomed M
12
Inhaled Anesthesia and Heat

• Narkomed M Currently the Air Force standard
  anesthesia machine for field anesthesia
  operations. This machine is equipped with the
  Draeger Vapor 2000 anesthetic vaporizer.
• Draeger Vapor 2000 vaporizer is temperature
  compensated with an operating range of 10 to 40
  degrees C (50-104 degrees F)

13
Ohmeda Portable Anesthesia Circuit (PAC) with
Draw-over Vaporizer
14
Inhaled Anesthesia and Heat

• The Ohmeda Portable Anesthesia Circuit (PAC)
  Draw-Over Vaporizer System (primarily still in
  use with MFST).
• Operating temperature for the PAC vaporizer is 18
  to 35 degrees C (65-95 degrees F).

15
Inhaled Anesthesia and Heat

• Use above this ambient temperature range may lead
  to potentially hazardous excessive
  concentrations of anesthetic agent.

16
Inhaled Anesthesia and Heat

• Under no circumstances must the temperature of
  the anesthetic agent reach boiling point, as the
  output concentration will then become impossible
  to control.
• The boiling points for isoflurane, halothane, and
  sevoflurane are 48.5, 50.2, and 58.5 degrees C
  (119, 122.4, 137 degrees F) respectively at 760
  mm Hg.

17
Inhaled Anesthesia and Heat
18
Inhaled Anesthesia and Heat

• Is it conceivable that in Iraq, in July, the
  HV/AC system may fail intraoperatively?

19
If using volatile anesthetics at high ambient
temperatures

• Ensure you are operating in a consistent climate
  controlled environment.
• AND/OR
• Use only with end tidal anesthetic gas monitoring
  (RGM or other) to minimize the risk of volatile
  anesthetic overdose.

20
Inhaled Anesthesia and Heat

• There currently is no means of monitoring
  inspiratory or expiratory anesthetic gas in any
  Air Force deployable anesthetic system.

21
Other Anesthetic Options at High Ambient
Temperatures

• Total Intravenous Anesthesia
• Regional Anesthesia
• Neither method is known to be effected by high
  ambient temperatures.

22
Heat Injuries

• Heat illness is the inability of normal
  regulatory mechanisms to cope with a heat stress
• Minor injuries include muscle cramps, edema,
  rash, syncope, and tetany
• Major injuries are heat exhaustion and heat
  stroke
• All heat injuries are manifestations of
  dehydration

23
Heat Injuries

• Patients who are injured in and evacuated from
  areas with high ambient temperatures may suffer
  heat injuries in addition to their traumatic
  wounds.
• Medical personnel suffering heat injuries may
  have difficulty or even be unable to care for
  their patients.

24
Heat Injuries

• Any condition that increases heat gain or
  decreases heat loss may result in a major heat
  illness.
• Hot environments and physical exertion increase
  the heat load.
• Strenuous exertion can increase endogeonous heat
  production ten to twenty-fold.
• High temperatures and high humidity inhibit heat
  loss.

25
Heat Injuries
26
Heat Injuries

• Peripheral vasodilation and sweating are the
  primary mechanisms of heat loss
• Evaporation of sweat from the skin is the most
  important mechanism of heat dissipation.
• As humidity increases, the efficiency of sweating
  decreases.

27
Heat InjuriesHeat Exhaustion

• Caused by dehydration with inadequate fluid and
  electrolyte replacement.
• Usually in nonacclimatized persons who have been
  working in the heat for several days.

28
Heat InjuriesHeat Exhaustion

• Symptoms
• Weakness, fatigue, frontal headache, impaired
  judgement, vertigo, nausea and vomiting, muscle
  cramps
• Orthostatic dizziness and syncope
• Sweating persists, often profuse
• Core temperature less than 40 C
• No signs of severe CNS damage

29
Heat InjuriesHeat Exhaustion

• Volume depletion is the primary problem
• Treatment
• Rest in cool environment
• Fluid resuscitation

30
Heat InjuriesHeat Stroke

• A catastrophic life threatening medical emergency
• The failure of normal homeostatic cooling
  mechanisms
• Leads to extremely high temperatures (gt40.5C),
  multisystem tissue damage and organ dysfunction.

31
Heat InjuriesHeat Stroke

• Symptoms
• Profound CNS dysfunction is the Hallmark
• Delerium and coma are common
• Any neurologic manifestation is possible
• Dry hot skin, though sweating can persist
• Cardiovascularly hyperdynamic
• Hepatic dysfunction with massive rise in
  transaminases
• Coagulopathy
• Renal damage with acute renal failure in up to
  30 of cases.

32
Heat InjuriesHeat Stroke

• Treatment
• Core Temperature Cooling
• Evaporative cooling with fans and skin wetting
• Ice-water immersion
• Ice packs, cooling blankets, cool body
  cavity lavages
• Supportive Therapy
• Airway management (aspiration and seizures are
  common)
• Resuscitation and invasive monitoring

33
Anesthesia At Altitude

• As altitude increases atmospheric pressure
  decreases.
• Decreased atmospheric pressure has profound
  effects on inhaled anesthetics and human
  physiology.
• Safe and effective anesthesia care requires an
  understanding of all of these effects.

34
Anesthesia At Altitude

• The composition of the atmosphere is fixed and is
  independent of altitude. Oxygen is always 21
  of the ambient atmosphere pressure.
• As atmospheric pressure decreases with elevation
  however, the partial pressure of oxygen (PO2)
  declines.

35
Anesthesia At Altitude

• Recall the alveolar gas equation
• PAO2FiO2(PB-PH2O)-PaCO2/RQ
• At 5000ft elevation, PB is 632 mmHg, PaO2 is 81
  mmHg with SaO2 95.
• At 10,000ft elevation, PB is 522 mmHg, PAO2 is 59
  mmHg, SaO2 84.

36
Oxygen-Hemoglobin Dissociation Curve.
Approximate oxygen saturations are marked for
several altitudes
37
Anesthesia At Altitude

• In addition, it is important to maintain a
  higher concentration of oxygen both during and
  after administration of the anesthetic to support
  adequate oxygenation. It is suggested that 30
  oxygen be the minimum at 5000 ft and that 40
  oxygen be the minimum at 10,000 feet, for both
  intraoperative anesthetic management and
  postoperative recovery.

38
Anesthesia At Altitude

• Recommendations for anesthesia at altitude The
  major risk of anesthesia at high altitude is that
  anesthetized patients can become hypoxic despite
  the fact that adequate oxygen concentrations are
  being administered.

39
Anesthesia At Altitude

• Nitrous Oxide
• Essentially irrelevant. Unlikely to be available
  in the deployed environment. Efficacy of N2O is
  decreased by 50 at 5000 ft and essentially
  insignificant at 10,000 ft.

40
Anesthesia At Altitude

• Volatile anesthetic agents
• The saturated vapor pressure of a volatile
  anesthetic agent depends only on temperature and
  is practically independent of total environmental
  pressure

41
Anesthesia At Altitude

• Given the relative scarcity of gaseous (or
  liquid) oxygen in the deployed environment it may
  be reasonable to conduct as much anesthesia under
  regional techniques.
• At altitude, maximizing the use of regional
  anesthesia not only decreases use of scarce
  resources, but may improve patient safety
  postoperatively. Minimizing opioid use decreases
  the risk of postoperative respiratory depression.

42
Anesthesia At Altitude

• If general anesthesia is required oxygen
  requirements may be minimized using TIVA
  techniques.

43
Altitude Illness

• Military personnel deployed rapidly to high
  altitude regions are all at risk for altitude
  related illnesses.
• High altitude begins at 1500m (5000ft) above sea
  level.
• Very high altitude begins at 3500m (11,500 ft)
• Extreme altitude begins at 5500m (18,000 ft)

44
Altitude Illness

• Physiologic adjustment to altitude requires time
  and patience.
• Sudden exposure to very high and extreme altitude
  (above 11,500 ft) can be fatal.
• Unconciousness can occur within minutes and death
  may follow without supplemental oxygen.

45
Physiologic Response to Altitude

• Lower PB leads to lower PAO2, decreased SAO2 and
  PaO2 and elevated Alveolar-arterial oxygen
  gradients.
• Hypoxic Ventilatory Response to low PaO2 leads to
  hyperventilation.
• Hyperventilation leads to decreased PaCO2.

46
Physiologic Response to Altitude

• As hyperventilation is the primary means of
  adaptation to ascent, the ability to tolerate
  hypoxic environments depends largely on
  sufficient pulmonary reserve.

47
Physiologic Response to Altitude

• 2,3-DPG levels rise due to hypoxic stress,
  shifting O2-Hgb dissociation curve back toward
  the right. This facilitates O2 unloading into
  tissues.
• Erythropoiesis
• Increased cardiac output secondary to Hypoxia

48
Altitude Illness

• High Altitude Illness can take several forms that
  often overlap and share common pathophysiology.
• Acute Mountain Sickness (AMS)
• High Altitude Pulmonary Edema (HAPE)
• High Altitude Cerebral Edema (HACE)

49
Acute Mountain Sickness

• All visitors to higher altitudes are susceptible
  to AMS.
• Overexertion, poor hydration, and young age may
  contribute. Physical fitness and gender dont
  seem to effect incidence.

50
Acute Mountain Sickness

• Symptoms
• Early symptoms (12-24 hours) headache
  refractory to standard analgesics, nausea,
  anorexia, lassitude, sleep disturbances.
• Can progress to shortness of breath, intense
  snoring, vomiting, hallucinations, and impaired
  cognitive function,
• Advanced symptoms severe dyspnea, cyanosis,
  decreased SaO2, ataxia.

51
Acute Mountain Sickness

• Definitive treatment is descent.
• Often descent of 500 to 1000m leads to complete
  resolution of symptoms.
• Rest, hydration, analgesics, oxygen all can help.
• Acetazolamide 250 mg q 8-12 hours improves
  symptoms and SaO2 (especially during sleep)

52
Acute Mountain Sickness

• Prevention
• Ascend slowly, not always possible in military
  ops
• Daily altitude gain of no more than 300m above
  3000m.
• After ascending 1000m spend two consecutive
  nights.
• Rest on arrival at altitude, avoiding
  overexertion, adequate hydration
• Acetazolemide 250mg q8 hours beginning at least
  24 hours before ascent and continued for 2 to 3
  days after reaching highest altitude.

53
High Altitude Pulmonary Edema (HAPE)

• A malignant form of AMS with similar early
  symptoms. Life threatening.
• May occur in any healthy individual after rapid
  ascent above 2500 m (8200 ft)
• Dyspnea, tachypnea, chest pain, rales,
  tachycardia,dry cough, followed by the production
  of pink frothy sputum
• Respiratory failure and death can quickly ensue.

54
High Altitude Pulmonary Edema (HAPE)

• CXR shows patchy infiltrates, which spare lung
  bases and costophrenic angles.
• Elevated pulmonary artery pressure secondary to
  hypoxia.
• ECG shows right heart strain
• LV function is normal

55
High Altitude Pulmonary Edema (HAPE)

• Treatment
• Rapid descent to lower altitude
• Supplemental O2
• Morphine ?
• PEEP
• If descent is not possible, consider Gamow bag

56
High Altitude Cerebral Edema (HACE)

• Another severe form of AMS, also be life
  threatening.
• Thought to be due to increased cerebral blood
  flow and alterations in blood-brain barrier
  permeability (due to severe hypoxemia)
• Early symptoms similar to AMS.

57
High Altitude Cerebral Edema (HACE)

• Early symptoms
• Headache
• Anorexia
• Nausea
• Emesis
• Photophobia
• Fatigue
• Irritability
• Decreased socialization

• Late symptoms
• Ataxia (appendicular to truncal)
• Irrationality
• Hallucinations
• Visual disturbances
• Focal neurological deficits
• Abnormal reflexes

58
High Altitude Cerebral Edema (HACE)

• Patients may have concurrent HAPE symptoms
• Death may be imminent when symptoms of HACE
  become severe

59
High Altitude Cerebral Edema (HACE)

• Lumbar puncture may show markedly elevated CSF
  pressure.
• CT suggestive of brain edema

60
High Altitude Cerebral Edema (HACE)

• Treatment
• Immediate, rapid descent
• Dexamethasone 10 mg IV or IM, then 6 mg q 6 hrs.
• Supplemental O2, may be helpful if pulmonary
  symptoms are present
• Diuretics may reduce brain edema, but may worsen
  an already dehydrated state

61
The Gamow Bag
62
The Gamow Bag

• Portable, lightweight, fabric hyperbaric chamber.
• Can generate 103 mm Hg of pressure above ambient
  pressure.
• Simulates a descent of 4000 to 9000 ft at
  moderate altitudes.

63
Cold Injuries

• Frostbite
• Hypothermia
• Defined as core temperature below 35 degrees C

64
Cold Injuries
65
Cold InjuriesFrostbite

• Peripheral vasoconstriction limits radiant heat
  loss in cold ambient temperatures
• Occurs when tissue temperature decreases to less
  than 0 degrees C
• Ice crystal formation leads to cellular
  architectural damage
• Microvascular stasis and thrombosis
• Extent of injury is determined by duration and
  extent of cold contact with the skin

66
Cold InjuriesFrostbite

• Distal extremities, nose, ear, and penis are most
  at risk
• Numbness is most common presenting symptom

67
Cold InjuriesFrostbite

• Treatment
• Rapid rewarming by immersion bath in 37-40 degree
  C water. Reheating with static heat is much more
  injurious to tissue.
• If patient requires surgical care and anesthesia
  allow for passive rewarming to minimize risks of
  worsening injury.

68
Cold InjuriesHypothermia

• Mild Core body temperature 32-35 C
• Excitation stage, to retain and generate heat
  (shivering, increased heart rate, cardiac output,
  and blood pressure)
• Moderate 30-32 degrees C
• Slowing stage, to decrease oxygen utilization and
  CO2 production (shivering ceases, HR. CO, BP all
  decrease)
• Severe Below 30 degrees C
• ECG changes and dysrhythmias (Osborn J waves
  T-wave inversions, PR, QRS, and QT prolongation,
  sinus bradycardia to atrial fibrillation with
  slow ventricular response to ventricular
  fibrillation to asystole)

69
Cold InjuriesHypothermia
70
Cold InjuriesHypothermia

• Other Manifestations
• Pulmonary
• Tachypnea, bronchorrhea, diminished cough and gag
  reflex (increased aspiration risk)
• CNS
• Confusion, lethargy, incoordination, decreased
  consciousness, coma
• Leftward shift of Oxyhemoglobin dissociation
  curve
• Impairs release of O2 to tissues

71
Cold InjuriesHypothermia

• Other manifestations
• Renal
• Decreased renal concentrating abilities leads to
  cold diuresis and severe dehydration
• Heme
• Hemoconcentration, disseminated intravascular
  coagulation (decreased enzymatic function at
  lower core body temperatures)
• GI
• Pancreatitis, decreased hepatic function
  (impaired drug metabolism)

72
Cold InjuriesHypothermia

• Treatment
• Handle Gently
• Oxygen (warmed, humidified)
• IV fluids (warmed)
• Monitor core temperature, oxygen saturation,
  cardiac rhythm
• Dysrhythmias may be refractory to treatment until
  patient is rewarmed

73
Cold InjuriesHypothermia

• Treatment
• Rewarming
• Passive allow patients to rewarm passively and
  slowly
• Active rewarm with external (water immersion,
  radiant heat, forced warm air heating blankets)
  and core techniques (heated IV fluids, body
  cavity lavage, cardiopulmonary bypass pump
• Resuscitation with Lactated Ringers should be
  avoided as the cold liver inefficiently
  metabolizes lactate
• Neither passive nor active rewarming has been
  shown to be superior, however

74
Cold InjuriesHypothermia

• Indications for rapid rewarming
• Cardiovascular instability
• Moderate or severe hypothermia (lt32.2 C)
• Inadequate rate or failure to rewarm
• Endocrine insufficiency
• Traumatic or toxilogic peripheral vasodilation
• Secondary hypothermia impairing thermoregulation.

75
Cold InjuriesHypothermia

• As anesthesiology providers we are most likely to
  become involved with hypothermia caring for
  patients suffering from traumatic injury in
  addition to hypothermia.
• Surgical requirements will likely force active
  treatment of hypothermia while undergoing
  surgical stabilization.

76
Cold Injuries

• No known effect of cold ambient temperature to
  the delivery of any form of anesthesia.

77
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