Document Sample
					        OXYGEN THERAPY
        AND DURING
     DR ROHAN K.

                     DR ROHAN
• Oxygen delivery to the tissues depends on an adequate
  supply of oxygen at each step of the oxygen transport
  chain from the inspired air to the mitochondria.
• The inspired partial pressure of oxygen is
  approximately 21% of the atmospheric pressure, which
  decreases predictably at altitudes above sea level.
• There is a fall in the total atmospheric pressure and the
  partial pressure of oxygen as the altitude increases.
• Humans at high altitude, therefore, must overcome the
  disadvantage of ambient hypoxia by making a number
  of adaptations to optimize the availability of oxygen to
  the tissues.
   ALTITUDE (feet)     BAROMETRIC        PO2 in Air(mm Hg)
                     PRESSUSRE(mm Hg)
            0              760                  159
       10,000              523                  110
       20,000              349                   73
       30,000              226                   47
       40,000              141                   29
       50,000               87                   18

•This decrease in barometric pressure is the basic cause
of all the hypoxia problems at high altitudes.
• As the barometric pressure decreases the atmospheric
oxygen partial pressure decreases proportionately.
Alveolar Po2 At Different Elevations:
• CO2 is continually excreted from the pulmonary blood into
  alveoli even at high altitudes.
• Also water vaporizes into the inspired air from the
  respiratory surfaces.
• These two gases dilute the oxygen in the alveoli, thus
  reducing the O2 conc.
• Alveolar water vapor pressure remains 47 mm Hg at normal
  body temperature regardless of the altitude.
• At very high altitudes, the alveolar Pco2 falls from the sea
  level values of 40mm Hg to lower values .
• The pressure changes of this two gases affects the alveolar
                                             BREATHING PURE
                   BREATHING AIR
                 Alveolar     Alveolar      Alveolar     Alveolar
               Pco2(mm Hg)   Po2(mm hg)   Pco2(mm Hg)   Po2(mm hg)
        0        40(40)       104(104)        40           673
  10,000         36(23)        67(77)         40           436
  20,000         24(10)        40(53)         40           262
  30,000          24(7)        18(30)         40           139
  40,000                                      36            58

 *Numbers in parentheses are acclimatized values.
                                                        Breathing pure
                                        Breathing air
                    0                       97(97)           100
           10,000                           90(92)           100
           20,000                           73(85)           100
           30,000                           24(38)            99
           40,000                                             84

*Numbers in parentheses are acclimatized values.
Effect of high altitude on arterial oxygen
       saturation when breathing
 air and when breathing pure oxygen
• Up to an altitude of about 10,000 feet, even when
  air is breathed, the arterial saturation remains at
  least as high as 90%
• Above 10,000 feet, SaO2 falls rapidly, until it is
  slightly less than 70 per cent at 20,000 feet and
  much less at still higher altitudes.
• The red curve in the above graph shows arterial
  blood hemoglobin oxygen saturation at different
  altitudes when one is breathing pure oxygen.
• Note that the saturation remains above 90 per cent
  until the aviator ascends to about 39,000 feet; then
  it falls rapidly to about 50 per cent at about 47,000
      Acute Effects of Hypoxia
• Important acute effects of hypoxia in the
  unacclimatized person breathing air, beginning
  at an altitude of about 12,000 feet, are
  drowsiness, lassitude,mental and muscle
  fatigue, sometimes headache, occasionally
  nausea, and sometimes euphoria.
• These effects progress to a stage of twitchings
  or seizures above 18,000 feet and end, above
  23,000 feet in the unacclimatized person, in
  coma, followed shortly thereafter by death.
      Acute Effects of Hypoxia
• One of the most important effects of hypoxia is
  decreased mental proficiency, which decreases
  judgment, memory, and performance of
  discrete motor movements.
• If an unacclimatized aviator stays at 15,000
  feet for 1 hour, mental proficiency ordinarily
  falls to about 50 per cent of normal, and after
  18 hours at this level it falls to about 20 per
  cent of normal.
       Acclimatization to Low PO2
• A person remaining at high altitudes for days, weeks, or years
  becomes more and more acclimatized to the low Po2, so that it
  causes fewer deleterious effects on the body.
• It becomes possible for the person to work harder without
  hypoxic effects or to ascend to still higher altitudes.
• The principal means by which acclimatization comes about are
 a great increase in pulmonary ventilation,
 increased numbers of red blood cells,
 increased diffusing capacity of the lungs,
 Increased vascularity of the peripheral tissues, and
 Increased ability of the tissue cells to use oxygen despite low
   Natural Acclimatization of Native Human
       Beings Living at High Altitudes
• Many native human beings live at altitudes above
  13,000 feet.
• Acclimatization of the natives begins in infancy.
• The chest size, especially, is greatly increased, whereas
  the body size is somewhat decreased, giving a high
  ratio of ventilatory capacity to body mass.
• In addition, their hearts, which from birth onward pump
  extra amounts of cardiac output, are considerably larger
  than the hearts of lowlanders.
• Delivery of oxygen by the blood to the tissues is also
  highly facilitated in these natives.
Oxygen-hemoglobin dissociation curves for blood of high-altitude
residents (red curve) and sea-level residents (blue curve), showing the
respective arterial and venous PO2 levels and oxygen
contents as recorded in their native surroundings.
• A small percentage of people who ascend rapidly to
  high altitudes become acutely sick and can die.
• The sickness begins from a few hours up to about 2
  days after ascent.
• Rapid ascent to much lower altitudes (2500 to 4000 m)
  can also lead to problems.
• A trip to and from high altitude on the same day is
  much less stressful than an overnight stay because
  hypoxia is accentuated during sleep and because of
  more prolonged exposure.
       Disorders Associated with High

                                 In High-Altitude     Problems Potentially
 In the Unacclimatized
                                    Residents        Aggravated (Partial List)

Acute mountain sickness Chronic mountain sickness          Hypertension

                                                       Arteriosclerotic heart
    Cerebral edema         Reentry pulmonary edema
   Pulmonary edema          Problems of pregnancy     Congestive heart failure
   Peripheral edema                                    Chronic lung disease

                                                     cerebrovascular disease

Thromboembolic problems                              Pulmonary hypertension

                                                      Disorders of pregnancy
Sleep periodic breathing
                                                          and childbirth
• Clinical Presentation.
• Headache is the most common and prominent
  symptom of AMS
• Associated symptoms and signs in
  approximate order of frequency are lassitude,
  insomnia, anorexia, nausea, dizziness,
  breathlessness, reduced urination, and
  vomiting, which are accompanied by evidence
  of fluid retention.
• The key to successful treatment is early diagnosis.
• Persons with mild illness may resolve their symptoms
  by resting or a descent of as little as 300 m, whereas
  more severe illness requires further descent.
• At times, field conditions may be such that descent is
  impractical or impossible.
• Pressurization to 2 psi (110 mm Hg) is equivalent to a
  descent of approximately 1500 m.
• By means of a foot pump, sufficient gas flow is
  maintained to keep the carbon dioxide concentration
  low and the oxygen concentration close to 21%
• Supplemental oxygen can also be added to the bag.
• Studies have documented the chamber to be as effective as
  administering 26% to 30% oxygen; the critical factor for
  resolution of illness is the PO2.
• These devices are particularly useful when oxygen is not
  readily available.
• In areas with medical facilities, persons suffering from AMS
  or HAPE prefer oxygen breathing to being treated in a
• With oxygen therapy, relief of symptoms is generally
  immediate, but treatment is necessary for a number of hours
  for continued clinical improvement .
• The duration of therapy depends on the severity of illness
High-Altitude Pulmonary Edema
• High-Altitude Pulmonary Edema (HAPE) is the most
  common cause of death from high-altitude illness.
• The severe hypoxia causes the pulmonary arterioles
  to constrict potently.
• The constriction is much greater in some parts of the
  lungs than in other parts, so that more and more of the
  pulmonary blood flow is forced through fewer and
  fewer still unconstricted pulmonary vessels.
High-Altitude Pulmonary Edema
• The postulated result is that the capillary
  pressure in these areas of the lungs becomes
  especially high and local edema occurs.
• Extension of the process to progressively more
  areas of the lungs leads to spreading
  pulmonary edema and severe pulmonary
  dysfunction that can be lethal
• It is grouped with the pulmonary edemas of
  noncardiogenic origin.
A, Typical roentgenograph of high-altitude pulmonary edema in a 29-year-old female skier. Note
that the edema is unilateral, right sided, and predominantly in the right middle lobe. B,
Roentgenograph of the same patient 1 day later, after descent and oxygen. Note the rapid
clearing. C, Severe unilateral pulmonary edema in a 21-year-old male with no history of any
previous illness. D, Severe pulmonary edema of altitude. Note normal heart size
High-Altitude Pulmonary Edema
• High altitude pulmonary oedema is immediately life
  threatening and requires urgent treatment.
• If HAPE is diagnosed early, recovery is rapid with a descent
  of only 500 to 1000 m.
• Oxygen administration is immediately required pending the
  descent to a lower altitude.
• A portable hyperbaric chamber, or supplemental oxygen
  will immediately increase arterial SO2 and reduce
  pulmonary artery pressure, heart rate, respiratory rate, and
• Oxygen is administered at a high FiO2 of upto 1 to achieve
  immediate relief.
High-Altitude Pulmonary Edema
• The use of an expiratory positive airway pressure mask was
  shown to improve oxygenation in HAPE.
• Complete resolution of the edema may require 24 to 72 hours
  of oxygen therapy if treated near the altitude of onset.
• Higher concentrations of oxygen do not seem to be more
  useful as long as arterial SO2 is maintained above 90%.
• Occasionally, life-threatening HAPE being treated at a medical
  facility will require descent to a lower altitude as well as a
  high inspired oxygen concentration if arterial saturation cannot
  be maintained or if severe encephalopathy develops.
High-Altitude Pulmonary Edema
• Intubation may then be required, as well as
  therapy directed to the cerebral edema.
• However oxygen therapy may not always succeed
  and some of the patients may fail to respond.
• Pulmonary embolism, pneumothorax, myocardial
  infarction, and congestive heart failure should
  also be suspected in patients not responding
  rapidly to oxygen therapy.
             High-Altitude Cerebral
• HACE is defined as the presence of a change in mental status or
  ataxia, or both, in a person with AMS, or the presence of both central
  nervous system abnormalities in a person without AMS who has
  recently ascended to altitude.
• The initial symptoms of HACE are usually those of severe AMS
  plus neurologic abnormalities
• Headache may be incapacitating, nausea and vomiting persistent,
  and lassitude debilitating.
• Ataxic gait, usually present and associated with altered mental
  status, is a reliable diagnostic sign.
• Among the protean neurologic signs accompanying the illness are
  papilledema, visual changes, cranial nerve palsies, bladder
  dysfunction, abnormal reflexes, paresthesias, pareses, aphasia,
  clonus, hallucinations, seizures, and behavioral changes, terminating
  in coma and death.
 High-Altitude Cerebral Edema
• The definitive treatment of HACE is descent.
• However, recovery is not as rapid as in AMS
  and HAPE, and a descent in altitude of more
  than 1000 m may be necessary.
• Oxygen or hyperbaric therapy may be a
  lifesaving temporizing measure
    Chronic Mountain Sickness
• Chronic mountain sickness (CMS) occurs in persons born
  and living at high altitude(Primary Monge’s disease) as well
  as in lowlanders who move to high altitudes but are unable
  to acclimatize.
• People with chronic hypoxaemic and other diseases known
  to chronic hypoxemia at even sea level can have more
  serious consequences when superimposed on the hypoxia of
  high altitude.These include patients with gross
• Symptoms of CMS include: headache, dizziness, lethargy,
  impaired memory and mentation, and poor sleep.
• Consistent findings are cyanosis, plethoric appearance, and
  elevated hematocrit and hemoglobin.
    Chronic Mountain Sickness
• The following effects occur:
1) the red cell mass and hematocrit become exceptionally
2) the pulmonary arterial pressure becomes elevated even
   more than the normal elevation that occurs during
3) the right side of the heart becomes greatly enlarged,
4) the peripheral arterial pressure begins to fall,
5) congestive heart failure ensues, and
6) Death often follows unless the person is removed to a
   lower altitude.
    Chronic Mountain Sickness
• The causes of this sequence of events are
  probably threefold:
 First, the red cell mass becomes so great that the
  blood viscosity increases several fold.
 Second, the pulmonary arterioles become
  vasoconstricted because of the lung hypoxia.
 Third, the alveolar arteriolar spasm diverts much
  of the blood flow through non-alveolar pulmonary
  vessels, thus causing an excess of pulmonary
  shunt blood flow where the blood is poorly
    Chronic Mountain Sickness
• Oxygen therapy has no role in the treatment of primary
  Monge’s disease.
• It may lower the pulmonary hypertension temporarily
  but not revert the condition.
• Oxygen is however required for respiratory
  insufficiency which may occur in patients with chronic
  hypoxaemic disorders.
• Oxygen therapy in these conditions is administered on
  standard principles as anywhere else
• But early and more vigorous therapy may be required.
         Atmospheric physics
• The atmosphere contains 21% oxygen, and this fraction is
  constant at all altitudes.
• As total pressure decreases with higher altitudes, however, the
  partial pressure of oxygen decreases proportionally (Dalton's
• In medical terms, the fraction of inspired oxygen (FIO2) of
  cabin air remains constant as cabin altitude increases, but the
  alveolar partial pressure of oxygen declines.
• Boyle's law states that the volume of a gas at constant
  temperature varies inversely with changes in pressure.
• As a pocket of air ascends, it expands if it is exposed to
  ambient (outside) air pressure.
 Air Travel And Cabin Pressures
• The inside cabin pressure in the aircraft is maintained at about
  445mm Hg above the outside barometric pressure or equivalent to
  that of 5000-8000 feet.
• If sea-level cabin pressure could be maintained continuously in all
  aircraft, air travel could have been considred safe for all individuals.
• Unfortunately, fewer than 1% of aircrafts are equipped to maintain
  constant pressure during flights.
• Many factors limit an aircraft's ability to maintain continuous sea-
  level pressurization, including minimum safe altitude for the route
  of flight, different departure and arrival elevations, the aircraft's
  pressurization capability, and operational considerations (eg, time,
  distance, fuel requirements).
• Exposing patients to changing ambient pressures is therefore
  Physiologic Response To Ascent
• While ascending, the body compensates first by increasing
  tidal volume and second by increasing respiratory rate.
• In healthy flyers, increased tidal volume is first noticeable
  at 1500 m (5000 ft).
• At 3700 m (12,000 ft), the average ventilation only
  increases from 8.5 to 9.7 L/min, but inspired partial
  pressure of oxygen (PO2) decreases from a sea-level value
  of 103 to 54.3 mm Hg, and PCO2 decreases from 40 to 33.8
  mm Hg.
• The resting respiratory rate is largely unchanged until
  climbing above 6700 m (22,000 ft).
• In healthy people, ventilation volume nearly doubles to 15.3
  L/min at this altitude.
         Hypoxia and Air Travel
• Hypoxia is insufficient tissue oxygenation and is often
  secondary to multiple stressors.
• If the additive effects of coexisting stressors is not
  considered prior to flight unanticipated tissue hypoxia may
• Typical cabins in pressurized aircraft are kept at pressures
  equivalent to 1500-2400 m (5000-8000 ft).
• At an altitude of 6000 feet, the alveolar oxygen pressure is
  about 75mm Hg.
• Due to sigmoid shape of the oxygen dissociation curve, the
  SaO2 is above 90%.
• Therefore the healthy passengers do not encounter problem.
         Hypoxia and Air Travel
• But patients with compromised cardio-pulmonary function and
  a degree of hypoxia are near the steep part of the O2
  dissociation curve.
• Their PaO2 may fall further necessitating oxygen
• Aviation-grade oxygen must be readily available in the event
  of rapid decompression.
• If supplemental oxygen is unavailable ,oxygen rapidly diffuses
  backward through the lungs of humans exposed to cruise-
  altitude air pressure.
• At typical cruise altitudes of 10,100-11,000 m (33,000-36,000
  ft), the duration of useful consciousness after rapid
  decompression is 30-60 seconds in healthy crewmembers and
  shorter in compromised patients.
          Hypoxia and Air Travel
    Cumulative hypoxic stress
•   Altitude is particularly poorly tolerated in patients
    with preexisting hypoxia.
•   All hypoxic conditions should be considered to be
    relative contraindications to air travel.
•   Risk of end-organ damage is based on cumulative
    effects of all coexisting hypoxic insults; thus, all
    sources of potential tissue hypoxia must be
    considered when evaluatin
•    Altitude-induced tissue hypoxia is a form of
    hypoxic hypoxia.
        Hypoxia and Air Travel
 Hypoxia countermeasures
• For aviators, hypoxia prevention begins in the
  hypobaric (altitude) chamber.
• The experience teaches physiological self-awareness.
• This awareness is crucial for flight safety because
  hypoxia has an insidious (sometimes pleasant) onset
  and may present as euphoria or in other subtle ways.
• This preventive step is an essential part of military
  aviation training and is highly recommended for
  civilian flyers.
       Hypoxia and Air Travel
 Hypoxia countermeasures.
• The hypoxic effects of altitude can be minimized
  with supplemental oxygen and maximal cabin
• Supplemental oxygen increases the FIO 2 .
• Except in emergencies, hospital-grade oxygen is
  unacceptable for use in aerospace operations
  because of its moisture content.
• Oxygen for use in aviation must be purified to
  less than 0.005 mg/L of water vapor to protect
  against freezing and regulator interference.
         Hypoxia and Air Travel
 Hypoxia countermeasures.
• Pilots in high-performance/high-altitude aircraft
  occasionally rely on pressure breathing to counter low
  alveolar oxygen tension.
• This is analogous to continuous positive airway
  pressure/bilevel positive airway pressure (CPAP/BiPAP)
  with 100% FIO 2 and is generally required at cabin altitudes
  above 10,400 m (34,000 ft).
• The usual hypobaric countermeasure involves maximizing
  cabin pressurization.
• Pressurization increases the total air pressure, thereby
  increasing inspired and alveolar PO 2 even though FIO 2 is
     Patient Clearance For Flight
• A careful preflight evaluation is required regarding the
  safety of flight as well as the requirement of oxygen during
  the flight.
• Clearing patients or routine travelers for flight is largely
  based on anticipating the physiologic effects of changing
  cabin pressures.
• Preflight evaluation for a patient with respiratory disease
  consists of a good clinical examination, chest X-ray, ECG,
  blood counts and serum electrolytes, spirometry and blood
  gas analysis
• Pneumothorax, pneumocephalus, and intraocular air must be
  positively excluded in patients who are potential candidates
  for air transport as free air expands and causes mass effects
  in unvented space
     Patient Clearance For Flight
• Some of the indicators of altitude intolerance are:
1. Dyspnoea at rest,
2. Those who cannot walk >50 meter/climb one flight of stairs
3. Chronic cor pulmonale or cyanosis.
1. Vital capacity< 50% predicted,
2. Maximum voluntary ventilation < 40 L/min.
1. Respiratory acidosis and,
2. PaO2 <50 mm Hg
•   Presence of one or more of the above criteria is a contraindication
    for air travel.
    Patient Clearance For Flight
• Sea level arterial PO2 can be used as an
  excellent predictor of arterial PO2 at altitudes
  upto 2400 m, in normocapnic patients.
• Hypobaric chamber simulating air travel
  condition can be used to assess the overall
  response to altitude stress.
• A more practical method is to use the hypoxic
  gas mixtures that simulate the inspired PO2 at
  desired altitudes.
     Patient Clearance For Flight
• It comprises of administration of hypoxic gas mixture with oxygen
    tension equivalent to those at an altitude between 5000-10,000 feet.
• A regression equation and normogram derived with the help of
    HAST, can be used to estimate PaO2 at those altitudes in patients
    with normocapnic chronic airway obstruction.
• The expected PaO2 at altitude can be calculated with the help of the
    following formula:
Predicted PaO2 at altitude =22.8-2.74x+0.68 y
(x is the anticipated cabin altitude in thousands of feet; y is resting
    PaO2 in mmHg at ground level ,on room air).
• Although the formula provides a reliable prediction of the
    anticipated PaO2, it is important to actually perform the HAST to
    assess the cardiovascular and symptomatic response,as well as
    efficacy of supplemental oxygen.
   Patient Clearance For Flight
• Even HAST will not necessarily predict that a
  patient will or will not run into trouble.
• Empirically oxygen is often prescribed if the
  in-flight PaO2 at 8000 ft, estimated from the
  above equation or by experimentation, is less
  than 7 kPa or 86% SaO2.
• This is not evidence-based, so a simple
  recommendation based on sea level oximetry
  measurements is likely to be as valid.
   Patient Clearance For Flight
• Simple recommendations for oxygen when
      SaO2            OXYGEN
      >92%              No oxygen required

      90-92%           Perform challenge test

      <90%              Recommend oxygen
     Patient Clearance For Flight
Pulmonary diseases and air travel
• Untreated pneumothorax is an absolute contraindication to
  flight unless sea-level cabin pressure can be strictly
• This is usually impossible; thus, placement of a chest tube
  with Heimlich valve is indicated.
• Patients with recently removed chest tubes should wait 72
  hours prior to air transport because even radiologically
  undetectable pleural gas can expand to significant volumes
  in flight.
• People with bullous emphysema are at risk for rupture and
  pneumothorax at altitude, especially during rapid loss of
  cabin pressure
    Patient Clearance For Flight
Pulmonary diseases and air travel
• In patients who retain carbon dioxide (eg, those with
  COPD), the risk of carbon dioxide narcosis is reduced
  at altitude for any FIO2 or flow rate.
• Clinicians should provide generous supplemental
  oxygen, even when patients are suspected or known to
  retain carbon dioxide.
• Many of the stressors found in the aviation environment
  precipitate asthmatic exacerbation. These precipitants
  include temperature extremes, smoke and fumes, and,
  possibly, pressure breathing.
          Rapid decompression
• During a sudden loss of cabin pressure in a commercial
  airliner at cruising altitude, passengers immediately are
  exposed to altitudes between 7600 m (25,000 ft) and 13,100
  m (43,000 ft).
• At 7600 m (25,000 ft), steady state PO2 falls to 30.4 mm
  Hg, and PCO2 is 27.0 mm Hg.
• The pathophysiology of rapid decompression is truly unique
  and represents an emergency.
• In contrast to the physiological stress experienced by high-
  elevation mountaineers, passengers and crew experience
  instantaneous ascent (ie, no acclimatization) when their
  cabin loses pressurization.
• Initial alveolar PO2 is less than the oxygen partial pressure
  in the mixed venous blood; thus, oxygen diffusion in the
  lungs is reversed
          Rapid decompression
• Unless this process is halted with immediate intervention,
  oxygen rapidly diffuses from the body within minutes.
• Once a loss of cabin pressure is detected, aircrew and able
  passengers should immediately don oxygen masks to
  reverse the diffusive loss of oxygen at the alveolar level.
• If corrective action is not taken, the effective performance
  time (also called time of useful consciousness) is 3-5
  minutes at 7600 m (25,000 ft), 30-60 seconds at 10,700 m
  (35,000 ft), and 9-12 seconds at 13,100 m (43,000 ft).
• In people who are sick or highly active, reserves are
  reduced, and loss of consciousness occurs sooner.
       Decompression sickness
• Decompression sickness (DCS) is a specific hypobaric
  complication caused when dissolved nitrogen evolves from
• When external pressure drops, bubbles form in various
  tissues. Especially vulnerable are vessels, joints, and nervous
• Risk factors for DCS include exposure to altitudes over 5500
  m (18,000 ft), long duration of exposure, prior water or
  hyperbaric chamber dives, rapid onset of depressurization,
  increased physical activity after decompression, and age
  older than 40 years.
• Many people with DCS do not become symptomatic until
  after landing.
• Symptoms of mild DCS include pruritus, formication (ie,
  crawling skin paresthesias), and pitting edema.
       Decompression sickness
• More significant disease is marked by intense aching
  joint pain which typically is called the bends.
• A serious presentation, called the chokes, is caused by
  multiple pulmonary gas emboli and manifests with
  pleuritic chest pain, dry cough, and dyspnea.
• Treatment has 3 components as follows:
1) descend (or repressurize),
2) administer 100% oxygen (to reduce body nitrogen
   stores), and, if necessary,
3) refer the patient to a hyperbaric (dive) chamber.
Thank You