PHYSIOLOGICAL%20CHANGES%20AND%20ANAESTHESIA%20AT%20HIGH%20ALTITUDE.pptx

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.

4. COMMON HYPOXIC EFFECTS WITH DIFFERENT ALTITUDES

5. BAROMETRIC PRESSURE AND PARTIAL PRESSURE OF GASES

6. 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 .

7. 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 .

8. 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

9. 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.

10. 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

11. 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 .

12. 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

13. CELLULAR ACCLIMATIZATION Increased mitochondria Increased Cytochrome oxidase Increased myoglobin

14. 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

15. 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

16. 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.

17. 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.

18. BREATHING PATTERN IN CHEYNE STOKES RESPIRATION

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

20. 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.

21. 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

22. 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

23. 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

24. 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 .

25. 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.

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

27. 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.

28. 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

29. 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.

30. 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 .

31. 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.