1 / 58

HYPEROXIA AND HYPERBARIA

HYPEROXIA AND HYPERBARIA. HYPEROXIA (BREATHING OXYGEN ENRICHED AIR). BREATH-HOLDING EXERCISE.

flossie
Download Presentation

HYPEROXIA AND HYPERBARIA

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. HYPEROXIA AND HYPERBARIA

  2. HYPEROXIA (BREATHING OXYGEN ENRICHED AIR)

  3. BREATH-HOLDING EXERCISE • BENEFICIAL EFFECTS DURING BREATH-HOLDING EXERCISE DUE TO THE INCREASED CARBON DIOXIDE AND HYDROGEN IONS CONCENTRATIONS THAT ARE EXPIRED PRIOR TO EXERCISE (HALDANE EFFECT) THEREBY REDUCING RESPIRATORY STIMULATORS AND THE DESIRE FOR RESPIRATION • INCREASED PERFORMANCE TIME DURING BREATH-HOLDING EXERCISE

  4. NORMAL (BREATHING O2) EXERCISE • DURING SUBMAXIMAL EXERCISE: - LOWER HEART RATE - LOWER BLOOD LACTATE ACCUMULATION - LOWER VENTILATION RATE - INCREASED WORK TIME TO EXHAUSTION • DURING MAXIMAL EXERCISE: - GREATER ENDURANCE CAPACITY - INCREASED WORK TIME TO EXHAUSTION

  5. NORMAL (BREATHING O2) EXERCISE •BENEFITS RELATED TO THE INCREASED PARTIAL PRESSURE OF OXYGEN, WHICH INCREASES THE OXYGEN TRANSPORTED BY HEMOGLOBIN AND DISSOLVED IN THE PLASMA (PHYSICAL SOLUTION) AS WELL AS INCREASES THE DIFFUSION OF OXYGEN ACROSS THE ALVEOLAR-CAPILLARY AND MUSCLE TISSUE-CAPILLARY MEMBRANES

  6. OXYGEN-BREATHING DURING RECOVERY • MINIMAL EFFECTS ON EITHER THE RECOVERY PROCESS OR ON SUBSEQUENT WORK BOUT PERFORMANCES • NO PHYSIOLOGICAL BASIS FOR THE USE OF OXYGEN DURING RECOVERY ALTHOUGH THERE MAY BE A PSYCHOLOGICAL EFFECT

  7. HYPERBARIA

  8. HISTORY OF UNDERWATER SUBMERSION

  9. HYPERBARIA • FOR EVERY DECREASE OF 10 METERS IN SEA WATER AND 10.4 METERS IN FRESH WATER, PRESSURE INCREASE BY ONE ATMOSHPHERE (1 ATM) OR 760 mmHG

  10. OPEN-CIRCUIT SCUBA (SELF-CONTAINED UNDERWATER BREATHING APPARATUS) IS THE MOST WIDELY USED APPARATUS BY DIVERS • SCUBA USES MIXED GASES WHICH ARE SUPPLIED TO THE LUNGS AT A PRESSURE EQUIVALENT TO AMBIENT (SURROUNDING) PRESSURE • SCUBA HAS INCREASED THE DEPTH AND DURATION OF DIVING

  11. HOWEVER, THE MOST COMMON WAY TO ENTER THE WATER IS BREATH-HOLD DIVING FOR DURATIONS UP TO 3 MINUTES OR LONGER AND DEPTHS UP TO 70 METERS OR MORE

  12. IMPORTANT LAWS FOR UNDERSTANDING THE EFFECTS OF HYPERBARIA ON THE HUMAN BODY

  13. BOYLE’S LAW - PRESSURE AND VOLUME OF A GAS ARE INVERSELY RELATED • INCREASE PRESSURE, DECREASE VOLUME • DECREASE PRESSURE, INCREASE VOLUME • CHARLE’S LAW - ASSUMING PRESSURE REMAINS CONSTANT, THE VOLUME OF A GAS IS PROPORTIONAL TO ABSOLUTE TEMPERATURE OR IF VOLUME REMAINS CONSTANT, PRESSURE IS DIRECTLY PROPORTIONAL TO ABSOLUTE TEMPERATURE

  14. DALTON’S LAW - THE TOTAL PRESSURE EXERTED BY A MIXTURE OF GASES IS EQUAL TO THE SUM OF THE INDIVIDUAL PRESSURES EXERTED BY EACH OF THE GASES COMPRISING THE GAS MIXTURE • PB = PO2 + PCO2 + PN2 +Pother gases • THE AMOUNT OF GAS THAT A FLUID WILL ABSORB UNDER PRESSURE VARIES IN DIRECT PROPORTION TO THE PARTIAL PRESSURE OF THE GAS

  15. HENRY’S LAW - FOR A GAS OF LOW SOLUBILITY (DECREASED LIKELIHOOD OF BEING DISSOLVED AND THEREFORE CAN SATURATE TISSUES) , AT A GIVEN TEMPERATURE THE CONCENTRATION IN THE LIQUID WILL BE NEARLY PROPORTIONAL TO THE PRESSURE OF THAT GAS IN THE GAS PHASE • GASES WITH LOW SOLUBILITY REQUIRE LESS TIME TO SATURATE A LIQUID THAN GASES OF A HIGHER SOLUBILITY • THE LONGER AND DEEPER THE DIVE, THE GREATER THE SATURATION OF THE BODY’S TISSUES WITH GASES

  16. BREATH-HOLD (BH) DIVING • AS ONE DESCENDS THE INCREASE IN PRESSURE IS EVENLY TRANSMITTED THROUGHOUT THE BODY’S TISSUES COMPRESSING COMPLIABLE GAS CONTAINING CAVITIES (BOYLE’S LAW) • GASTROINTESTINAL TRACT IS VERY COMPLIANT OR COMPRESSIBLE • IN THE AIRWAYS, LUNGS, SINUSES, AND MIDDLE EAR, THE INTERNAL PRESSURE IS EQUALIZED WITH AMBIENT PRESSURE BY VENTING AIR BETWEEN THE COMPRESSIBLE (LUNGS) AND NONCOMPRESSIBLE CAVITIES.

  17. GENERALLY, THE VASCULATURE IS IN EQUILIBRIUM WITH EXTERNAL PRESSURE • VESSELS WHICH PASS THROUGH INTERNAL CAVIITIES WITH LOWER PRESSURE MAY RUPTURE CAUSING HEMORRHAGING • BAROTRAUMA (INJURIES RESULTING FROM PRESSURE DIFFERENCES ACROSS THE WALLS OF GAS-FILLED CAVITIES) MAY CAUSE PAIN AND TISSUE DAMAGE

  18. AS THE DEPTH OF THE DIVE INCREASES, LUNG VOLUME TENDS TO DECREASE • AT ABOUT 20 METERS LUNG VOLUME TENDS TO EQUAL RESIDUAL VOLUME

  19. BELOW 20 METERS THERE IS AN INCREASED LIKELIHOOD THAT PULMONARY VESSELS MAY RUPTURE CAUSING CONGESTION, EDEMA, AND HEMORRHAGING • DURING BH DIVING THE LOWER INTRAHORACIC PRESURE MAY RESULT IN AN INCREASE IN BLOOD FLOW TO THE THORACIC CAVITY AND THE DIAPHRAGM MAY BECOME DISPLACED TOWARD THE HEAD THEREBY FURTHER REDUCING LUNG VOLUME (AND HENCE INCREASING PRESSURE DUE TO BOYLE’S LAW) AND PREVENTING THE RUPTURE OF PULMONARY VESSELS

  20. AT SEA LEVEL, BREATH HOLDING: • DECREASED ARTERIAL AND ALVEOLAR PO2 • INCREASED ARTERIAL AND ALVEOLAR PC02 • INCREASED ARTERIAL PC02 AND DECREASED ARTERIAL P02 EVENTUALLY STIMULATES VENTILATION (BREATHING)

  21. BREATH-HOLD DIVING • DURING THE DESCENT BOTH ALVEOLAR PO2 AND PCO2 INCREASE DUE TO BOYLE’S LAW • INCREASED ALVEOLAR PC02 MAY REVERSE THE GRADIENT BETWEEN THE LUNGS AND BLOOD AND CO2 MAY MOVE BACK INTO THE BLOOD

  22. MAXIMUM ALVEOLAR P02 VALUE ACHIEVED IS DEPENDENT ON A HIGH INITIAL SURFACE VALUE, LOW METABOLIC RATE, GREATER DEPTH OF DIVE, AND DURATION/QUICKNESS OF DESCENT • QUICKER THE DESCENT, THE HIGHER THE PO2 VALUE ACHIEVED AND DEPLETION OF O2 IS MINIMIZED

  23. AT THE BOTTUM OF THE DIVE, O2 MOVES OUT OF THE LUNGS AT A RATE DICTATED BY METABOLIC DEMANDS AND ALVEOLAR PCO2 TENDS TO EQUALIZE WITH ARTERIAL PCO2

  24. DURING THE ASCENT, ALVEOLAR P02 DECREASES WHICH MAY STOP THE DIFFUSION OF O2 INTO THE BLOOD • ALVEOLAR PC02 ALSO DECREASES WHICH WILL INCREASE THE TRANSFER OF CO2 FROM THE BLOOD INTO THE LUNGS AND MAY LEAD TO A DECREASE IN VENTILATORY DRIVE

  25. MAXIMUM DURATION OF A BH DIVE (RANGE FROM 20-270 SECONDS) CAN BE INCREASED BY: • PSYCHOLOGICAL FACTORS • LARGE LUNG VOLUME AND HIGH ALVEOLAR AND ARTERIAL PO2 LEVELS • LOW ARTERIAL PC02 AS PCO2 STIMULATES RESPIRATION • REDUCED METABOLIC RATE ALTHOUGH PHYSICAL MOVEMENT MAY CAUSE CONSCIOUS DISSOCIATION AND THUS DELAY THE BREAKING POINT • INCREASED PRESSURE WHICH WILL INCREASE ALVEOLAR AND ARTERIAL O2 WHICH INCREASES TOLERANCE TO HYPERCAPNIA • INHALATION OF OXYGEN ENRICHED GAS PRIOR TO DIVE • HYPERVENTILATION PRIOR TO DIVE WHICH WILL DECREASE ALVEOLAR AND ARTERIAL PCO2 LEVELS AND HENCE VENTILATORY DRIVE; MAY BE DANGEROUS AS LIKELIHOOD OF HYPOXIA TO THE BRAIN IS INCREASED, PARTICULARLYDURING THE ASCENT PHASE OF THE DIVE WHEN THERE IS ALREADY DECREASED MOVEMENT OF OXYGEN INTO THE BLOOD

  26. METABOLIC, CARDIAC, AND CIRCULATORY FUNCTION DURING BH DIVING • NO CHANGE IN OXYGEN UPTAKE RATE, CARDIAC OUTPUT, AND OXYGEN EXTRACTION • BRADYCARDIA DUE TO INCREASED VAGUS DOMINANCE OF HR AS PNS IS STIMULATED BY COLD WATER AND APNEA • INCREASED STROKE VOLUME DUE TO ENHANCED VENOCONSTRICTION AND RETURN OF BLOOD FLOW THEREBY INCREASING END-DIASTOLIC VOLUME • INCREASED PERIPHERAL VASOCONSTRICTION (26-53%) WHICH INCREASES BLOOD PRESSURE • INCREASED VENOCONSTRICTION AND VASOCONSTRICTION DUE TO INCREASED SNS RELEASE OF NOREPINEPHRINE

  27. ADAPTATIONS TO BH DIVING • REPEATED EXPOSURE TO HIGH PRESSURE, HYPOXIA, AND HYPERCAPNIA REDUCES THE STRESS OF BH DIVING AND ENHANCES DIVING PERFORMANCE • REDUCED STRESS OF BH DIVING AND ENHANCED DIVING PERFORMANCE ARE DUE TO:

  28. INCREASED VITAL CAPACITY AND DECREASED RESIDUAL LUNG VOLUME THEREBY INCREASING THE RATIO OF TOTAL LUNG CAPACITY TO RESIDUAL LUNG VOLUME RESULTING IN GREATER LUNG COMPLIANCE • INCREASED STRENGTH IN THE RESPIRATORY MUSCLES (DIAPHRAGM AND EXTERNAL INTERCOSTALS) • DECREASED CHEMOSENSITIVITY TO HYPERCAPNIA AND POSSIBLY HYPOXIA THEREBY DECREASING VENTILATORY DRIVE (I.E., RESPIRATION) • INCREASED BRADYCARDIA WHICH DECREASES MYOCARDIAL OXYGEN REQUIREMENTS

  29. PHYSIOLOGICAL PROBLEMS ASSOCIATED WITH DEEP AND LONG DIVES

  30. OXYGEN POISONING • OCCURS WHEN PARTIAL PRESSURE OF INSPIRED OXYGEN EXCEEDS 570 mmHG (2.6 ATA OR 26 METERS) • ADVERSE PULMONARY EFFECTS (EDEMA, CONGESTION, INFLAMMATION, ATELECTASIS (COLLAPSE OF LUNGS), FIBRIN FORMATION, PNEUMONIA, BRONCHITIS, BRONCHIECTASIS, DEGENERATION OF ALVEOLAR CELLS, AND SCLEROTIC CHANGES IN PULMONARY ARTERIOLES) BEGIN AT PIO2 OF .5 ATA OR APPROXIMATELY 22-26 METERS • ADVERSE CENTRAL NERVOUS SYSTEMS EFFECTS (TWITCHING OF FACE AND HAND MUSCLES, TETANUS IN MAJOR MUSCLE GROUPS, UNCONSCIOUSNESS, AND CONVULSIONS) BEGIN AT PIO2 OF 2.0 ATA OR APPROXIMATELY 90-100 METERS

  31. NITROGEN NARCOSIS RESULTING FROM EXPOSURE TO COMPRESSED AIR • EUPHORIA, HYPEREXCITABILITY, IMPAIRED INTELLECTURAL FUNCTION (PERCEPTION AND MEMORY), IMPAIRED NEUROMUSCULAR FUNCTION • ALTHOUGH EFFECTS HAVE OCCURRED AT DEPTHS OF 30 METERS, THE EFFECTS TEND TO INCREASE AS PRESSURE INCREASES; 90 METERS HAS BEEN SET AS A PRACTICAL LIMIT FOR AVOIDANCE OF NITROGEN NARCOSIS

  32. HIGH PRESSURE NERVOUS SYNDROME (HPNS) IS FOUND IN DIVES DEEPER THAN 18 ATA OR 170 METERS AND TENDS TO INCREASE AS THE DEPTH OF THE DIVE INCREASES • DIZZINESS, NAUSEA, VOMITTING, BODY TREMORS, CHANGED EEG ACTIVITY, AND INCREASED DAYTIME SLEEP • HPNS IS DUE TO GENERAL NEURONAL HYPEREXCITABILITY IN RESPONSE TO HYDROSTATIC PRESSURE AFFECTING NERVE CELL MEMBRANES

  33. DECOMPRESSION SICKNESS RESULTS FROM NITROGEN (N2) ABSORPTION BY THE TISSUES OF THE BODY, PARTICULARLY DURING LONGER AND DEEPER (HENRY’S LAW) DIVES • TISSUES OF THE BODY CAN BE MORE EASILY SATURATED THAN DESATURATED • HIGH PN2 RESULTS IN SUPERSATURATION OF TISSUES WITH N2

  34. DURING DECOMPRESSION BUBBLES OF GAS ARE FORMED IN THE BLOOD LEADING TO DECOMPRESSION SICKNESS (THE BENDS) AS THE N2 SLOWING LEAVES THE BODY’S TISSUES DURING DESATURATION • VENOUS BUBBLES ARE NOT A MAJOR PROBLEM BUT ARTERIAL BUBBLES CAUSE NEUROLOGICAL SYMPTOMS SUCH AS SKIN RASH, MUSCLE AND JOINT DISCOMFORT, PARALYSIS, NUMBNESS, HEARING LOSS, VERTIGO, CHOCKING, CHEST PAIN, UNCONSCIOUSNESS, AND POSSIBLY DEATH

  35. DECOMPRESSION TABLES HAVE BEEN DEVELOPED BASED ON THE DEPTH AND LENGTH OF DIVE

  36. ONCE TISSUES ARE SATURATED WITH INERT GASES, CONTINUED EXPOSURE TO INCREASED PRESSURE WILL NOT INCREASE THE TIME REQUIRED FOR DESATURATION • HENCE, DIVERS CAN STAY DOWN IN WORK HABITATS OR SURFACE CHAMBERS FOR LONG PERIODS TO COMPLETE WORK OR A MISSION AND UNDERGO DECOMPRESSION ONLY ONCE AT THE END OF THE MISSION

  37. SATURATION EXCURSION DIVING INCREASES THE LIKELIHOOD OF DEVELOPING O2 POISONING IF THE PARTIAL PRESSURE OF INSPIRED OXYGEN (PIO2) EXCEEDS 0.5 ATA • THEREFORE, THE USE OF O2 COMPRESSED AIR IN SATURATION DIVING VEHICLES AND HABITATS IS LIMITED TO DEPTHS LESS THAN ABOUT 22 METERS

  38. IN SATURATION DIVING VEHICLES AND HABITATS AT DEPTHS GREATER THAN ABOUT 22 METERS, NITROX, HELIOX, AND TRIMIX BREATHING GASES ARE USED TO KEEP THE PIO2 BELOW .5 ATA THEREBY AVOIDING O2 POISONING

  39. WHICH MAMMAL IS CONSIDERED TO HAVE THE GREATEST DIVING CAPABILITIES?

  40. Sea Elephant?

  41. OR ELEPHANT SEAL?

  42. QUESTIONS??

  43. Volcanoes of the Deep Sea

More Related