Physiological changes

1. PHYSIOLOGICAL CHANGES AND
ANAESTHESIA AT HIGH ALTITUDE

2. INTRODUCTION
• Barometric pressure falls with increasing altitude, but composition of air remain
same.
• According to Dalton’s law:
Total pressure of Air= Sum of partial pressure of all gases.
• P=pO2+pN2O+pH2O
• pH2O & pCO2 determined by body so does not change with altitude
• As metabolic production of CO2, does not alter with increasing altitude, alveolar
pCO2 will not change.
• Only pO2 & pN2 change.

3. • Human body is specifically designed in such a way that it delivers
adequate O2 to the tissues only when oxygen is supplied at a pressure
close to the sea level (P=760 mmHg PO2=159 mmHg)
• So, at high altitude there is hypoxic hypoxia tissue oxygenation
suffers physiological derangements.

5. COMMON HYPOXIC EFFECTS WITH DIFFERENT ALTITUDES

6. BAROMETRIC PRESSURE AND PARTIAL PRESSURE OF GASES

7. • As the altitude increases above the sea level, the corresponding
atmospheric pressure decreases
• The partial pressure of oxygen also decreases.
• The arterial oxygen saturation levels also decreases with increase in
the altitude.

8. PHYSIOLOGICALLY CRITICAL ALTITUDES
• Up to 10,000 ft(3000m) “safe zone of rapid ascent’’ classically
defines as “high altitude”.
• At 18,000 ft(5,500m) upper limit of permanent human inhabitation.
• Above 20,000 ft(6,000m) life is endangered without supplemental
oxygen.
• At 20,000-30,000 ft O2 supplement has to be started called critical
survival altitude.
• From 40,000 ft Ozone layer starts.

9. PHYSIOLOGICAL RESPONSES TO HIGH ALTITUDE
• Divided into following two responses-
Acute response(accommodation)
Long term responses(acclimatization)
• ACCOMODATION
Refers to immediate reflex adjustments of respiratory and
cardiovascular system to hypoxia
• ACCLIMATIZATION
Refers to changes in body tissues in response to long term exposure to
hypoxia

10. ACCOMODATION AT HIGH ALTITUDE
• Immediate reflex responses of the body to acute hypoxic exposure
HYPERVENTILATION
Decrease arterial PO2 stimulation of peripheral chemoreceptors increased
rate and depth of breathing
TACHYCARDIA
Also stimulate peripheral chemo. Receptors increased cardiac output
increased oxygen delivery to the tissues
INCREASED 2,3-DPG CONC. IN RBC
Within hours, deoxy-Hb. Conc. locally pH 2,3-DPG oxygen affinity of
Hb tissue O2 tension maintained at higher than normal level.

11. NEUROLOGICAL
Considered as warning signs
Depression of CNS feels lazy, sleepy, headache
Release phenomena like effect of alcohol, lack of coordination,
slurred speech, slowed reflexes, overconfidence
At further height cognitive impairment, poor judgement,
twitching, convulsions and finally consciousness

12. ACCLIMATIZATION AT HIGH ALTITUDE
Getting used to-
People remaining at high altitude for days, weeks or years become more
and more acclimatized to low PO2.
• This causes hypoxia to cause more damaging effects.
• They can thus work harder at higher altitudes without hypoxic effects.

13. HOW DOES ACCLIMATIZATION OCCUR
• Increased:
Pulmonary ventilation
Increased diffusing capacity of lungs.
Vascularity of the peripheral tissues
Ability of tissue cells to use O2 despite low PO2.
Respiratory alkalosis
Cheyne-Stokes respiration
Increased erythropoietin
Increased no of RBC
Increased blood volume
Increased cardiac output
Increased vascularity of the peripheral tissues
Alkaline urine

14. CELLULAR ACCLIMATIZATION
Increased mitochondria
Increased Cytochrome oxidase
Increased myoglobin

15. SUSTAINED HYPERVENTILATION:
Prolonged hyperventilation CO2 wash-out respiratory alkalosis
renal compensation alkaline urine normalization of pH of blood &
CSF withdrawal of central chemo-mediated respiratory depression net
result is respiratory pulmonary ventilation due to in TV.
• SUCH POWERFUL VENTILATOR DRIVE IS ALSO POSSIBLE AS-
 sensitivity of chemo receptor to PO2 & PCO2
Somewhat work in of breathing make hyperventilation easy & less
tiring

16.  Total lung capacity: in high-landers evidence by relatively enlarged
(barrel shaped) chest ventilatory capacity in relation to body mass.
 Diffusing capacity of lungs: due to hypoxia pulmonary vasoconstriction
Pulmonary hypertension no. of pulmonary capillaries.
n

17. • VASCULARITY OF TISSUES
Growth of new circulatory capillaries in non pulmonary tissues
(angiogenesis)
This combined with systemic vasodilation leading to more oxygen
delivery to tissues
• PHYSIOLOGICAL POLYCYTHEMIA
Hypoxia induced erythropoiesis
 Hb. Conc. & RBC count(within few weeks and weeks stay)
 Expansion of blood volume
 Amount of circulating Hb
 Inspite of saturation, O2-carrying capacity is maintained at normal
limit.

18. • CVS CHANGES
Cardiac output often increases as much as 30% immediately, then gradually
return to normal in one to two weeks as the blood hematocrit increases.
Capillary density in right ventricle muscle increases because of the
combined effects of hypoxia and excess workload on the right ventricle
caused by pulmonary hypertension at high altitude.
• CHEYNE-STOKES RESPIRATIONS:
Above 10,000ft (3,000 m) most people experience a periodic breathing
during sleep. Repeated sequence of gradual onset of apnea followed by
gradual restoration of respiration.
Respiration may cease entirely for few secs & then shallow breaths begin
again. During period of breathing-arrest, person often become restless &
may wake with sudden feeling of suffocation.
Can disturb sleeping patterns exhausting the climber
Acetazolamide is helpful in relieving this.

19. BREATHING PATTERN IN CHEYNE STOKES
RESPIRATION

20. CLINICAL SYNDROME CAUSED BY HIGH ALTITUDE
• High altitude pulmonary edema
• Chronic mountain sickness
• Acute mountain sickness

21. HIGH ALTITUDE PULMONARY EDEMA(HAPO)
• Above 10,000 ft.
• Seen in
75-80% in persons doing heavy physical work in first 3-4 days
Persons who acclimatized to high altitude stay at sea levels for>2 wks
& again rapidly re-ascend.
CHARACTERISCS-
Life threatening form of non-cardiogenic pulmonary edema due to
aggravation of hypoxia.
Not develop in gradual ascent & on avoidance of physical exertion
during 3-4 days of exposure.

22. HAPO Manifestations:
Earliest symptoms are- Exercise tolerance & slow recovery from
exercise. The person feels fatigue, weakness and exertional dyspnoea.
Condition typically worsens at night & tachycardia and tachypnea
occur at rest.
Symptoms- Cough, frothy sputum, cyanosis, rales & dyspnoea
progressing to severe respiratory distress.
Other common features-low grade fever, respiratory alkalosis and
leukocytosis
In severe cases- an altered mental status, hypotension and ultimately it
may result in death.
e

23. Mechanism of development of HAPO
Sympathetic activation by physical work is over & sympathetic
stimulation by hypoxia & cold.
Vasoconstriction
Increase in pulmonary capillary hydrostatic pressure(10-15 mm hg)
Increase in capillary hydrostatic drives the fluid out of pulmonary
capillaries
Develops pulmonary edema

24. TREATMENT OF HAPO
• Standard & most imp. To descend at lower altitude as quickly as possible
( preferably by at least 1000 meters) & to take rest.
• Oxygen should also be given (if possible).
• Symptoms tend to quickly improve with descent
• The standard drug treatments for which there is strong clinical evidence are
dexamethasone & CCBs (like nefidipine)
• PDE inhibitors (eg. Tadalafil) are also effective

25. ACUTE MOUNTAIN SICKNESS
• This occurs in a small number of lowlanders who ascend rapidly to
high altitude.
• Begins from a few hours up to 2 days after their ascent.
• It’s serious and result in their death unless they are given oxygen or
taken to a low altitude.

26. ACUTE MOUNTAIN SICKNESS SYMPTOMS AND SIGNS
• Acute cerebral Edema:
Hypoxia causes cerebral vasodilatation
Increases capillary pressure
Causes fluid to out into the tissues
This leads to cerebral oedema causing:
 Severe disorientation
 Other cerebral dysfunctions like seizures or can create large areas of ischemic brain
tissue
• Acute Pulmonary Edema:
Severe Hypoxia causes Pulmonary arteriolar constriction.
In some cases it is more and causes edema.
Can be reversed within hours on oxygen therapy.

27. TREATMENT
High dose glucocorticoids
Decreasing alkalosis by giving acetazolamide- as it decreases H+ ion
excretion by kidneys by inhibiting carbonic anhydrase

28. CHRONIC MOUNTAIN SICKNESS
• Occurs in long term residents of high altitude.
• Develop-Polycythemia, cyanosis, malaise, fatigue and exercise
tolerance.
• Extreme Hb levels viscosity of blood blood flow to tissues
Widespread pulmonary vasoconstriction Pulmonary hypertension
Right ventricular hypertrophy.
Treatment- return to lower altitude(at sea level) to prevent pulmonary
oedema.

29. ANAESTHESIA AT HIGH ALTITUDE
• It can be performed by using intravenous crystalloids, colloids, blood, or
plasma.
• All intravenous fluids and blood should be warmed to body temperature
before transfusion and great care should be taken not to overload the
patients with fluid in view of risk of developing pulmonary edema
• If heavy sedation with hypnotics, narcotics, or other drugs is necessary,
oxygen should be started at the time the preoperative medication is given.
• With increased altitudes, anesthetic agents, gases, vapors, and oxygen
should be given in higher concentrations to maintain arterial partial
pressures for anesthesia

30. • With increased altitudes, anesthetic agents, gases, vapors, and oxygen
should be given in higher concentrations to maintain arterial partial
pressures for anesthesia.
• Patient should be preoxygenated for 3 to 5 minutes with 100% oxygen
before induction, in high-altitude conditions.
• Patients who have a lowered arterial PO2 may develop hypoxia more
rapidly with airway complications.
• Increasing the inspired oxygen concentration with nitrous oxide
decreases the amnesic. In this situation, nitrous oxide is unable to
achieve anesthetic partial pressures without lowering the oxygen
tension to a dangerous hypoxic level. Because of decreased barometric
pressures, low partial pressures interfere with nitrous oxide uptake.
• It is recommended that nitrous oxide be supplemented using a
balanced anesthetic technique.

31. • The increased concentrations of this less potent anesthetic agent may
decrease oxygen tensions to hypoxic levels. Therefore, the technique of
oxygen and nitrous oxide anesthesia should be avoided in higher altitudes.
• Halothane is satisfactory agent for use in higher altitudes. They permit the
use of higher concentrations of oxygen and provide rapid induction with a
rapid recovery.
• Assisted or controlled ventilation is required even with these agents to
prevent muscle fatigue and avoid hypoxia. The disadvantages of halothane
are possible bradycardia and hypotension.
• Dissociative Analgesia: Supplemental oxygen may not be available in some
of HA location so it is important to select an anesthetic technique that is
least likely to suppress ventilation.
• Ketamine anesthesia is a safe anesthesia agent used at HA if monitored
carefully.

32. • Spinal anesthesia is avoided whenever possible at the higher altitudes as
alveolar ventilation and hypoxia increases the incidence of post spinal
headache.
• With the use of muscle relaxants, deep levels of anesthesia are avoided;
therefore, the risk of hypoxia and acidosis is lessened.
• Long-acting muscle relaxants should be used with caution to avoid
prolonged muscular weakness and because specific information is not
available on the use of reversal agents at higher altitudes.
• Altitude may also affect anesthetic equipment. Flowmeters, calibrated at sea
level, deliver a higher flow than indicated due to the reduced density of
gases.
• Postoperatively, it is recommended that oxygen be given for a minimum of
1 hour.
• All patients in increased altitudes require pre- and postoperative oxygen
therapy. If inadequate ventilation is noted during the postoperative period,
controlled or assisted ventilation should be continued until the patient is
alert and muscle power is recovered.