Hypoxia PDF

The respiratory response during exposure to aerospace environment can lead to an incapacity results. The most common are: Hypoxia, Hyperventilation, and Hypercapnia. Hypoxia Hypoxia is the state of O2 deficiency in the tissues. It disrupts the intracellular oxidative process and impairs the cellul...

The respiratory response during exposure to aerospace environment can lead to an incapacity results. The most common are: Hypoxia, Hyperventilation, and Hypercapnia. Hypoxia Hypoxia is the state of O2 deficiency in the tissues. It disrupts the intracellular oxidative process and impairs the cellular functions. The brain cells/tissue, and because it’s high O2 demand, are most susceptible to low O2 tension → brain impairment, deterioration of performance, reduced visual function, and unconsciousness occur as a result of hypoxia. Causes of Hypoxia (Types) 1. Hypoxic Hypoxia Deficiency in alveolar O2, could be due to: a. b. c. d. Reduction of PO2 in inspired air (high altitude) Strangulation/Laryngospasm Severe asthma/Breath holding Breath gas mixture with insufficient PO2 *So altitude hypoxia is hypoxic hypoxia. The result is an inadequate O2 supply to the arterial blood, which in turn decreases the amount of O2 delivered to the tissues. Alveolar O2 Pressure * The Alveolar PO2 is the most critical factor in producing H.H. It determines the plasma O2 tension and the degree of O2 saturation of Hb. * Mean alveolar O2 pressure (PAO2) can be calculated from the alveolar gas equation. PAO2 = (PB-PH2O) FIO2 – PACO2 (FIO2 + ((1-FIO2))/R) PB = Ambient barometric pressure PH2O = Water vapor pressure at body temperature 37°C = 47mmHg FIO2 = The fraction of O2 in inspired air = 0.21 for air & 1.0 for O2 PACO2 = The mean alveolar CO2 pressure = 40mmHg at sea level R = Respiratory exchange ratio 760-47 = 713 713-40 = 673 673x21% = At sea level: PB=760mmHg Ambient PO2=159mmHg PAO2 = 103mmHg PACO2 = 40mmHg 2. Anemic Hypoxia – Normal ventilation and diffusion but O2 delivery to the tissue reduced because of the reduction of the O2 carrying capacity. O2 is transported principally by Hb. Hb has 4 peptide chains and 4 hemes. Each heme contains one atom of Ferrous Iron (Fe+²). One molecule of O2 bind with one atom of Ferrous Iron Hb4 + 4 O2 = Hb4 (O2)4 Some other oxidizing agents such as sulfa drugs & Carbon Monoxide which make the Hb can no longer combine with O2. * CO is significant to aircrew because it is present in the exhaust fumes of /C engines. * CO combines with Hb about 200 times more readily than does O2 and displaces O2 to form Carboxyhemoglobin * With heavy smokers, carboxyhemoglobin level may reach 7%. * Level of 15-25% produce headache and nausea, with prolonged exposure → muscle weakness, dizziness, and confusion occur. * Above 25% → ECG changes, stupor, then unconsciousness will occur. * CO can be eliminated with hyperbaric O2 treatment. * When CO toxic victim breaths fresh air → half life of carboxyHb is 5.5h. * When CO toxic victim breaths 100% O2 at S.L. → half life of carboxyHb is 1.3h. * When CO toxic victim breaths 100% O2 at 3 ATA → half life of carboxyHb is 23mins. 3. Stagnant Hypoxia Any condition that result in a reduction in total COP, pooling of the blood, or restriction of blood flow. Examples: HF, shock, continuous positive pressure breathing, and G forces sustained in flight maneuvers. Blood clots or gas bubbles (D.S.) Pathology → local cellular hypoxia 4. Histotoxic Hypoxia Inability of the cell to use molecular oxygen. Examples: Tissue poisoning by ethyl alcohol, cyanide, CO, and hydrogen sulfide, which inhibits the cytochrome complex and interfere with utilization of O2. Phase of Respiration Condition - Reduction in alveolar PO2 - Breathing air at reduced barometric pressure Strangulation/Laryngospasm Severe asthma Breath holding Malfunction of O2 equipment - Reduction in gas exchange area - Pneumonia Drowning Atelectasis/Emphysema (chronic lung disease) - Diffusion – Barriers - Hyaline membrane disease - Reduction in O2 carry capacity - Anaemia Hemorrhage Hb abnormality Drugs and chemicals - Reduction in systemic blood flow - Heart failure Shock - Reduction in regional blood flow Ventilation Diffusion Transportation Utlization Specific Course Signs and Symptoms of Hypoxia (Stages of Hypoxia) * The onset of symptoms is insidious. * The effects of H. begin immediately on ascent to altitude STAGE 1 (Indifferent Stage) Below 10,000ft.– PO2 60mmHg Saturation 99% - 88%. The deficiencies are so subtle that they go unnoticed. Only decrease in night vision usually is the only noticeable complain. STAGE 2 (Compensatory Stage) From 10,000 to 15,000ft. – PO2 (60-45)mmHg, Saturation (88% - 79%) ↑P.R., COP, and RR (Increase rate and depth of breathing) STAGE 3 (Disturbance Stage) From 15,000 to 20,000ft – PO2 (45-34)mmHg, Saturation (78% - 67%). Intellectual impairment, thinking become slow and calculations are unreliable. Fixation – tendency to repeat courses of action Memory loss, particularly for events in the immediate past. Judgment is poor and reaction time is delayed STAGE 4 (Dangerous Stage) From 20,000 to 23,000ft – PO2 (34-32)mmHg Saturation 64% - 59%. Blackout then loss of consciousness The figure shows the oxyhemoglobin saturation at different altitudes. At sea level At 10,000 feet - The healthy person has no difficulty at this altitude except for a measurable reduction – in night vision. At 18,000 feet - Oxyhemoglobin saturation is 72%. At this altitude (with this saturation), symptoms of hypoxia would be experienced within 30 minutes of exposure. Any activity or exercises would reduce this time. At 22,000 feet – Acute hypoxia and performance is lost within 5-10 minutes. Exposure to higher altitude – Further ↓ in saturation and shorter Effective Performance Time (EPT) At 25,000 feet – PAO2 may become lower than the O2 tension in the mixed venous blood. This will reverse the direction of O2 flow in the lungs. The O2 diffuses from the blood back into the alveoli. In thin altitude → the onset of hypoxia is more sudden and profound. The EPT will be very short Effects of Hypoxia * Hypoxia produces its effects at the cellular level and disrupts normal body function. The visual, myocardial, and nervous tissues are affected more as they demands the highest O2 requirement. * Increase depth of breathing → ↑ respiratory rate (chemoreceptors in aortic arch and carotid body) (compensatory effect). The ventilation will start to increase at 400ft altitude. (But significantly, when the Hb saturation decreases to 93%) or (at 8000ft). At 22,000ft, the respiratory minute volume is doubled (air hunger and ↑tidal volume). Cardio Vascular System * Symptoms of hypoxia become evident when saturation drops to 87%. * Below 65% is considered critical and symptoms of hypoxia become severe and consciousness is maintained of only a short time. * CV system is more resistant to hypoxia compared to respiratory and nervous system. ↑COP (P.R. & Stroke Volume) CNS * In addition to the reduction of O2 delivered to the cells, a ↓ in cerebral blood flow due to vasoconstriction secondary to a fall in arterial CO2 tension will may occur. * Retina and CNS are the first affected by O2 deficiency → ↓ visual and cerebral performance. Effective Performance Time (EPT) Or Time of Useful Consciousness (TUC) Defined as the amount of time an individual is able to perform useful flying duties in an environment of inadequate O2. With the loss of effective performance in flight, the individual is no longer capable of taking proper corrective or protective action. EPT for healthy, resting individual, at different altitude is as follows: At 33,000ft, reversal of O2 flow in the alveoli will occur due to a higher PO2 within the pulmonary capillaries. This will deplete the blood’s O2 reserve and reduce the EPT up to 50%. Exercise also reduce the EPT. Treatment of Hypoxia Administer 100% O2. The type of hypoxia must be determined and treated accordingly. The following steps are recommended: 1. Administer supplemental O2 under pressure. (It is the prime consideration in the treatment of hypoxia) Above 40,000ft, the hypoxia cannot be corrected without adding (Positive Pressure Breathing PPB). 2. Monitor breathing After hypoxia episode, the resulting hyperventilation must be controlled. Maintaining a breathing rate of 12-16 cycles is required. 3. Monitor equipment. 4. Descent (reduce altitude). Prevention of Hypoxia Preventing hypoxia in flying is a matter of *indoctrination which should be accomplished by instructing personnel of the proper use of O2 equipment and ensuring that they are aware of their individual symptoms of hypoxia. *Ensuring availability of sufficient O2 to maintain the normal range of PO2. This can be maintained by: a. Cabin pressurization b. Supplemental O2 c. Maintain night requirement (start O2 supply from 5,000ft) d. Maintain Pressure breathing requirement Hyperventilation It is significant in aviation because the symptoms of hyperventilation & Hypoxia are similar & often result in confusion & inappropriate corrective procedures. H.V. is a condition in which ventilation is abnormally increased → loss of CO2 from the lungs occurs (CO2 washout) → hypocapnia → Disturbed acid-base balance → Alkalosis • Hyperventilation in Aerospace operations is commonly caused by psychologic stress (fear, Anxiety, & anger) & environmental stress (pressure breathing, vibration, & heat). Effects of H.V. • The S. & S. of H.V. are easily diffused with those of H.H., The objective signs that are most frequently seen in H.V. are increased respiratory rate & depth, muscle twitching & tightness, Pallor, cold, clammy skin, muscle spasm, rigidity & unconsciousness Treatment of H.V. Requires a voluntary reduction in the rate & depth of ventilation. Breathing into a bag that collects the exhaled CO2 for rebreathing by the subject, is an additional way to treat H.V. & to differentiate it from Hypoxia.. Thank you