ACUTE%20EFFECTS%20OF%20HIGH%20ALTITUDE%20(HYPOBARIA)

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ACUTE EFFECTS OF HIGH ALTITUDE (HYPOBARIA)
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• 1. REVIEW BASIC PHYSIOLOGY OF GAS TRANSPORT AND
  EXCHANGE MECHANISMS
• 2. VENTILATORY RESPONSES, PULMONARY DIFFUSION,
  AND OXYGEN TRANSPORT
• 3. MAXIMAL EXERCISE RESPONSES
• 4. SUBMAXIMAL EXERCISE RESPONSES
• 5. MUSCULAR STRENGTH AND ENDURANCE
• 6. NEUROENDOCRINE AND METABOLIC RESPONSES
• 7. BODY FLUID LEVELS
• 8. NEUROPSYCHOLOGICAL FUNCTIONING
• 9. HYPOBARIC ILLNESSES

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PLASMA TRANSPORT OF OXYGEN (02)

• 1. DISSOLVED 02 IN PLASMA
• - 0.3 ML 02/100 ML BLOOD (1)
• 2. O2 BOUND TO HEMOGLOBIN (Hb-02)
• - 20.0 ML O2/100 ML BLOOD (99)
• - IT TAKES lt .01 SEC FOR 02 TO BIND TO Hb
  ONCE IT HAS DIFFUSED INTO THE BLOOD
• - REVIEW EX PHYS FIGURES 2-6

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CO2 TRANSPORT

• 1. 7-10 DISSOLVED IN PLASMA
• 2. 60-70 TRANSPORTED AS BICARBONATE ION, MOST
  OF WHICH
• IS CONVERTED TO BICARBONATE ION BY CARBONIC
  ANHYDRASE IN RBC
• 3. 23-30 TRANSPORTED AS CARBAMINOHEMOGLOBIN
• - REVIEW EX PHYS FIGURE 2-12

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GAS EXCHANGE

• O2 AND CO2 DIFFUSE FROM AN AREA OF HIGH PARTIAL
  PRESSURE TO AN AREA OF LOW PARTIAL PRESSURE
• P02 PB X 02
• PC02 PB X C02
• C02 DIFFUSES 20 TIMES AS FAST AS O2 THEREFORE,
  LOWER PRESSURE GRADIENT IS NEEDED FOR EXCHANGE

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GAS EXCHANGE

• HALDANE EFFECT HIGH P02 IN THE LUNGS STIMULATES
  THE RELEASE OF C02 AND H FROM HEMOGLOBIN IN
  ALVEOLAR CAPILLARIES
• BOHR EFFECT HIGH PC02 AND H IN MUSCLE
  CAPILLARIES FROM METABOLISM STIMULATES THE
  RELEASE OF 02 FROM HEMOGLOBIN
• REVIEW EX PHYS FIGURE 2-3

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ALTITUDE AND P02

• AS ALTITUDE INCREASES, P02 DECREASES
• REVIEW ALTITUDE AND PRESSURE FIGURE, TABLE 12-1,
  AND FIGURE 12-1

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• AT SEA LEVEL (PB 760 mmHg), THE FOLLOWING
  ALTITUDES CORRESPOND TO THESE 02
• SEA LEVEL 20.93
• 5,000 FT 17.27
• 10,000 FT 14.38
• 14,100 FT 12.34
• 18,000 FT 10.44
• NOTE PO2 O2 X ATM PRESSURE

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VENTILATORY RESPONSES
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• THRESHOLD FOR STIMULUS TO INCREASE VENTILATION
  (VE)
• PIO2 110 TORR OR PaO2 60 TORR ABOUT 3,100 M
  OR 10,000 FT
• 1 TORR 1/760 OF NORMAL ATMOSPHERIC PRESSURE IT
  IS THE PRESSURE NEEDED TO SUPPORT MERCURY 1 MM AT
  0o C AND STANDARD GRAVITY 1 TORR 1 mmHg
• BEYOND THRESHOLD, VE INCREASES AS P02 DROPS
  FURTHER

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• INITIAL INCREASE IN VE IS DUE TO AN INCREASE IN
  TIDAL VOLUME FOLLOWED BY AN INCREASE BREATHING
  FREQUENCY DURING EXTENDED EXPOSURE OR INCREASED
  SEVERITY OF HYPOXIC CONDITIONS
• THE INCREASE IN VE AS PIO2 OR Pa02 DROP BELOW
  THRESHOLD INCREASES PA02 AND DECREASES PACO2
• INCREASE IN PA02 INCREASES SIZE OF GRADIENT
  BETWEEN PAO2 AND PaO2, WHICH INCREASES ARTERIAL
  02 SATURATION

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• PERIPHERAL CHEMORECEPTORS, LOCATED IN THE CAROTID
  BODY AND AORTIC ARCH, AND CENTRAL CHEMORECEPTORS
  IN THE MEDULLA OBLONGATA STIMULATE VE DURING
  HYPOXIA
• BECAUSE OF THE HALDANE EFFECT (HIGH P02 IN LUNGS
  STIMULATES RELEASE OF CO2 AND H FROM
  HEMOGLOBIN), PRIOR TO ACCLIMATION THE INCREASED
  VENTILATORY DRIVE MAY BE PARTIALLY OFFSET BY A
  DECREASE IN PaCO2 AND H CONCENTRATION, DUE TO
  BOTH CENTRAL AND PERIPHERAL FEEDBACK MECHANISMS

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• ALSO, THE DECREASE IN PaCO2 AND INCREASE IN pH
  (BECAUSE OF DECREASE IN H) DUE TO INCREASED
  VENTILATION WILL SHIFT THE Hb-O2 CURVE TO THE
  LEFT, WHICH WILL INCREASE THE AMOUNT OF O2 BOUND
  TO Hb IN THE MUSCLE CAPILLARIES (I.E., PERCENT
  SATURATION OF Hb WITH O2) FOR ANY GIVEN PO2
  (I.E., DECREASED RELEASE OF O2 FROM Hb TO MUSCLE
  TISSUE)

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PULMONARY DIFFUSION

• REVIEW FIGURE 12-2 AND EX PHYS OH 2-3 REGARDING
  PULMONARY DIFFUSION TRANSIT TIME AT REST
• (.75 SEC) AND DURING EXERCISE
• (.25-.4 SEC)

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• ALTITUDE INCREASES PULMONARY DIFFUSION TRANSIT
  TIME NEEDED FOR COMPLETE MOVEMENT OF OXYGEN INTO
  THE BLOOD DUE TO THE LOWER DIFFUSION GRADIENT AND
  HENCE, MAY LIMIT THE OXYGEN CARRYING CAPACITY OF
  THE BLOOD

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• INCREASED DILATION OF PULMONARY CAPILLARIES
  DURING EXERCISE INCREASES PDC
• TRAINING INCREASES PULMONARY DIFFUSION CAPACITY
  DUE TO
• INCREASED ALVEOLAR CAPILLARIZATION, INCREASED
  LUNG VOLUME OR ALVEOLI SIZE, AND INCREASED Hb
  CONCENTRATION AND PLASMA VOLUME

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TEN FACTORS AFFECTINGPULMONARY DIFFUSION

• TRAINING STATUS
• Hb CONCENTRATION AND PLASMA VOLUME
• PAO2, WHICH IS DECREASED BY ALTITUDE DUE TO A
  DECREASE IN THE PIO2 DECREASED PAO2 WILL
  DECREASE THE DIFFUSION GRADIENT BETWEEN THE
  ALVEOLI AND ALVEOLAR CAPILLARIES
• TRANSIT TIME AVAILABLE FOR EXCHANGE ALTITUDE
  INCREASES THE TRANSIT TIME REQUIRED FOR GAS
  EXCHANGE DUE TO THE DECREASE IN THE DIFFUSION
  GRADIENT

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• PULMONARY EDEMA INCREASES BELOW 447 TORR (I.E.,
  ABOVE 12,500 FT)
• VA-Q MATCHING AT REST, VA gt IN UPPER LOBES, Q gt
  IN LOWER LOBES DURING EXERCISE VA-Q MATCHING
  IMPROVES ALTITUDE TENDS TO DECREASE OR HINDER
  VA-Q MATCHING DURING EXERCISE
• ALVEOLAR MEMBRANES
• INTERSTITIAL FLUID LEVELS
• CAPILLARY MEMBRANES
• PLASMA, RBC, AND HB CONCENTRATIONS

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ARTERIAL OXYGEN SATURATION (SaO2) DURING EXERCISE

• DURING HEAVY EXERCISE AT SEA LEVEL, NO EFFECTS ON
  SaO2

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• SaO2 IS INVERSELY RELATED TO ALTITUDE (INCREASE
  IN ALTITUDE, DECREASE IN SaO2)

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• ARTERIAL DESATURATION AT ALTITUDE IS DUE TO
• 1. DIFFUSION LIMITATION AS TIME REQUIRED
  FOR DIFFUSION OF 02 INCREASES AT
  ALTITUDE (FIGURE 12-2)
• 2. DECREASE OR WORSENING OF THE VA-Q
  MATCHING
• 3. INCREASED SHUNTING OF BLOOD AWAY FROM THE
  LUNGS (??) IF THIS OCCURS, IT MAY BE RELATED TO
  INCREASED SYMPATHETIC NERVOUS SYSTEM ACTIVITY
  AND HENCE, INCREASED CIRCULATING
  NOREPINEPHRINE LEVELS THAT CAUSES
  VASOCONSTRICTION OF THE ALVEOLAR CAPILLARIES
  HOWEVER, THIS IS NOT LIKELY AS CATECHOLAMLINES
  GENERALLY CAUSE VASODILATION OF ALVEOLAR
  CAPILLARIES

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OXYGEN TRANSPORT Hb-O2 DISSOCIATION CURVE
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• 99 OF O2 IS TRANSPORTED BY Hb FROM THE LUNGS TO
  THE MUSCLE TISSUE
• Hb SATURATION WITH O2 IS DIRECTLY RELATED TO PO2
  IN THE BLOOD A DECREASE IN PaO2 AT ALTITUDE
  WOULD DECREASE THE SATURATION OF HEMOGLOBIN WITH
  OXYGEN

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• AN INCREASE IN PC02, TEMP, 2,3-DPG OR A DECREASE
  IN pH WILL SHIFT CURVE TO THE RIGHT BECAUSE OF
  THE SIGMOIDAL SHAPE OF THE CURVE, THE SHIFT TO
  THE RIGHT DOES NOT AFFECT O2 LOADING TO Hb IN THE
  LUNGS BUT O2UNLOADING FROM Hb IN THE MUSCLE
  TISSUE IS INCREASED THEREBY INCREASING O2
  AVAILABILITY TO THE MUSCLE TISSUE

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• ALTITUDE WILL FURTHER ACCENTUATE THE INCREASE IN
  PCO2, TEMP,
• AND 2,3-DPG AND THE DECREASE IN pH DURING
  EXERCISE
• HOWEVER, BECAUSE ALTITUDE WILL DECREASE PIO2 AND
  PA02, SaO2 IS REDUCED AS PREVIOUSLY DISCUSSED AND
  OVERALL THERE IS A SUBSTANTIAL DECREASE IN OXYGEN
  EXTRACTION

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• Hb-O2 DISSOCIATION CURVE IS SIGMOIDAL SHAPED
  BECAUSE Hb IS AN ALLOSTERIC PROTEIN WHICH
• 1. WORKS IN CONJUNCTION WITH DIFFUSION
  GRADIENT TO INCREASE 02 AVAILABILITY BY
• 2-FOLD
• 2. IMPLIES COOPERATIVITY (I.E., BINDING OF
  02 TO 1 HEME ENHANCES THE BINDING OF 02 TO
  OTHER HEMES AND THE UNLOADING OF 02 FROM 1
  HEME ENHANCES THE UNLOADING OF 02 FROM OTHER
  HEMES

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BLOOD-TISSUE O2 TRANSPORT

• AT SEA LEVEL, P02 IN MUSCLE TISSUE IS 10 TORR
• AT 5,500 M, PO2 IN MUSCLE TISSUE IS 5 TORR
• ONLY A 1-3 TORR GRADIENT IS NECESSARY BETWEEN
  CYTOPLASM AND MITOCHONDRIA TO SUPPORT OXIDATIVE
  REACTIONS (I.E., MYOGLOBIN WHICH TRANSPORTS O2
  INTRACELLULARLY IS FULLY SATURATED WITH O2 AT
  VERY LOW PO2 OR TORR VALUES) HENCE, ONLY IN
  EXTREME HYPOBARIC CONDITIONS (E.G., TOP OF MT.
  EVEREST) DURING HEAVY EXERCISE IS THIS APPROACHED

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AFFECTS OF ALTITUDE ON MAXIMAL EXERCISE
PERFORMANCE

• VO2 CARDIAC OUTPUT X OXYGEN EXTRACTION
• VO2 SV X HR X (A - V O2 DIFFERENCE)
• ALTITUDE DECREASES VO2MAX

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• AT PIO2 OF 120 TORR OR 1,500 M, Hb IS MORE THAN
  90 SATURATED WITH 02 AND VO2MAX IS NOT
  SIGNIFICANTLY AFFECTED
• ABOVE 1,500 M, THERE IS A 10 DECREASE IN VO2MAX
  FOR EACH 1,000 M INCREASE IN ALTITUDE AS SaO2 IS
  SUBSTANTIALLY REDUCED THEREFORE, THE A - V O2
  DIFFERENCE (I.E., OXYGEN EXTRACTION) IS REDUCED
• REVIEW FIGURE 12-4

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• NO AFFECT ON SVMAX OR HRMAX, AND HENCE QMAX
• NO AFFECT ON VEMAX
• IMPROVED MAXIMAL VENTILATORY EFFICIENCY (VE/VO2)
  WHICH IN PART WILL HELP MAINTAIN PAO2
• DECREASED MAXIMAL EXERCISE INTENSITY, WHICH MAY
  PRESENT PROBLEMS IN TRAINING AND EVENTUALLY
  PERFORMANCE DUE TO CHANGES IN MOTOR UNIT
  RECRUITMENT PATTERNS
• NO AFFECT ON MAXIMAL BLOOD LACTATE LEVELS

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AFFECTS OF ALTITUDE ON SUBMAXIMAL EXERCISE
PERFORMANCE

• NO CHANGE IN V02 REQUIRED TO PERFORM A GIVEN
  ABSOLUTE WORKLOAD AS Q INCREASES TO OFFSET THE
  DECREASE IN
• A - V O2 DIFFERENCE (I.E., OXYGEN EXTRACTION)
  DUE TO THE DECREASE IN ARTERAL SATURATION WITH
  OXYGEN
• INCREASE IN Q IS DUE TO AN INCREASE IN HR
  RESULTING FROM INCREASED SYMPATHETIC NEURAL
  STIMULATION

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• SINCE VO2MAX IS DECREASED, RELATIVE VO2 (VO2MAX)
  TO DO THE SAME ABSOLUTE WORKLOAD IS INCREASED
  THEREFORE, HYPOXIA INCREASES THE RELATIVE STRESS
  ON THE BODY
• WHILE PERFORMING THE SAME ABSOLUTE WORKLOAD,
  VENTILATION RATE (FIGURE 12-5), OXYGEN DEFICIT
  AND DEBT, BLOOD LACTATE ACCUMULATION, AND CORE
  TEMPERATURE ARE INCREASED DUE TO AN INCREASE IN
  RELATIVE EXERCISE INTENSITY
• DECREASED ENDURANCE TIME OR TIME TO FATIGUE WHILE
  PERFORMING THE SAME ABSOLUTE WORKLOAD

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• WHEN WORKING AT THE SAME ABSOLUTE WORKLOAD, THE
  SMALL AND GENERALLY INSIGNIFICANT INCREASE IN
  OXYGEN UPTAKE RATE THAT MAY BE OBSERVED IS
  PROBABLY DUE TO THE INCREASED OXYGEN NEEDS OF THE
  RESPIRATORY AND CARDIAC MUSCLES AS VENTILATION
  RATE AND HEART RATE ARE INCREASED

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• WHEN WORKING AT THE SAME RELATIVE WORKLOAD
  (VO2MAX), HIGH ALTITUDE HAS MINIMAL EFFECTS (IF
  ANY) ON HR, VENTILATION RATE, O2 DEFICIT AND
  DEBT, RESPIRATORY EXCHANGE RATIO, LACTATE
  ACCUMULATION, AND ENDURANCE TIME TO EXHAUSTION
  IN ORDER TO WORK AT THE SAME RELATIVE WORKLOAD,
  ABSOLUTE WORKLOAD IS REDUCED TO ADJUST FOR THE
  ALTITUDE INDUCED DECREASE IN MAXIMAL OXYGEN
  UPTAKE RATE

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MUSCLE STRENGTH AND ENDURANCE

• ALTHOUGH CONFLICTING RESULTS EXIST IN THE
  LITERATURE, IT IS GENERALLY BELIEVED THAT
  ALTITUDE HAS NO SUBSTANTIAL EFFECTS ON MUSCLE
  STRENGTH AND ENDURANCE AS THEY ARE NOT DEPENDENT
  ON THE AEROBIC, OXIDATIVE MECHANISMS

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NEUROENDOCRINE AND METABOLISM RESPONSES TO HIGH
ALTITUDE

• AT REST, SYMPATHETIC NERVOUS SYSTEM ACTIVITY IS
  INCREASED RESULTING IN INCREASED CIRCULATING
  LEVELS OF NOREPINEPHRINE WHICH GENERALLY HAS A
  WIDESPREAD VASOCONSTRICTION EFFECT THROUGHOUT THE
  BODY AND INCREASES HEART RATE, VENTILATION RATE,
  AND VASODIALATION OF SKELETAL, HEART, AND
  ALVEOLAR CAPILLARIES.
• REVIEW EX PHYS FIGURE 2-10

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• AT REST, OTHER HORMONES AND METABOLISM (E.G.,
  BLOOD GLUCOSE, FREE FATTY ACIDS, LACTATE (LA),
  CORTISOL, GLUCAGON, ANDROSTENEDIONE,
  TESTOSTERONE, LUTEINIZING HORMONE (LH), INSULIN,
  GROWTH HORMONE, PROLACTIN, ANTIDIURETIC HORMONE,
  THYROXIN, ALDOSTERONE, RENIN, AND ANGIOTENSIN II)
  ARE MINIMALLY AFFECTED

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• GENERALLY, HYPOXIA DOES NOT ALTER HORMONAL AND
  METABOLIC RESPONSES WHEN WORKING AT THE SAME
  RELATIVE WORKLOAD (E.G., THE RELEASE OF
  NOREPINEPHRINE, EPINEPHRINE, AMMONIA, LACTIC
  ACID, TESTOSTERONE, CORTISOL, GROWTH HORMONE, AND
  LUTEINIZING HORMONE INCREASE WHILE THE RELEASE OF
  INSULIN DECREASES) HOWEVER, IF WORKING AT THE
  SAME ABSOLUTE WORKLOAD RELATIVE EXERCISE
  INTENSITY IS INCREASED, WHICH RESULTS IN GREATER
  RELEASE OF HORMONES SUCH AS EPINEPHRINE,
  NOREPINEPHRINE, GLUCAGON, GROWTH HORMONE,
  THYROXIN, AND CORTISOL

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BODY FLUID LEVELS

• HYPOXIA DECREASES ANGIOTENSIN CONVERTING ENZYME
  (ACE) ACTIVITY IN THE LUNGS, WHICH LEADS TO A
  DECREASE ANGIOTENSIN II AND ALDOSTERONE SECRETION
  BY THE ADRENAL CORTEX, WHICH LEAD TO SODIUM AND
  WATER RETENTION BY THE KIDNEYS
• THIS RESULTS IN A DECREASE IN EXTRACELLULAR
  FLUID, WHICH MAY RESULT IN DEHYDRATION DURING
  EXERCISE AS WELL AS LEAD TO MOUNTAIN SICKNESS

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• NORMALLY, DECREASED BLOOD FLOW TO THE KIDNEYS
  STIMULATES RENIN SECRETION WHICH CONVERTS THE
  PLASMA PROTEIN ANGIOTENSINOGEN INTO ANGIOTENSIN
  I, WHICH IS CONVERTED BY ANGIOTENSIN CONVERTING
  ENZYME (ACE) INTO ANGIOTENSIN II ANGIOTENSIN II
  STIMULATES ALDOSTERONE SECRETION FROM THE ADRENAL
  CORTEX, WHICH PROMOTE SODIUM AND WATER RETENTION
  BY THE KIDNEYS.

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NEUROPSYCHOLOGICAL IMPAIRMENT

• HIGHER CORTICAL AREAS ARE VERY SENSITIVE TO SMALL
  DECREASES IN CaO2 (CEREBRAL CORTEX IS THE MOST
  SENSITIVE FOLLOWED BY THE CEREBELLUM, MEDULLA,
  SPINAL CORD, AND SYMPATHETIC GANGLIA)
• WHEN PIO2 FALLS BELOW 100 TORR (I.E., ABOVE 3,000
  M OR 10,000 FT, "TIMBERLINE"), THE SMALL
  DECREASES IN CaO2 CAN SIGNIFICANTLY AFFECT MENTAL
  AND MOTOR FUNCTIONING

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• FACTORS AFFECTING DEGREE OF IMPAIRMENT
• SEVERITY OF HYPOXIA
• TYPE OF TASK OR FUNCTION
• FAMILIARITY WITH TASK
• COMPLEXITY OF TASK
• MASTERY OF TASK
• REVIEW FIGURE 12-6

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HIGH ALTITUDE (HYPOXIC) ILLENESSES
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QUESTIONS??