Exam 3 - Hypo/hyperbaric Enironments Flashcards
Percentages of atmospheric oxygen, carbon dioxide and nitrogen
O2 = 20.93% CO2 = 0.03% N = 79%
How does diving disrupt homeostasis?
Disrupts internal pressure and gas concentrations within the body. Alteration in bod fluid composition and movement.
Regulation of internal pressure and gas concentration relies on…
CV an respiratory system. Injury occurs if unable to adapt.
Hyperbaric Environment
Pressure is greater than air pressure on sea level
Five physiologic stresses the body faces in hyperbaria
Elevated ambient pressure, decreased effects of gravity, altered respiration, hypothermia, sensory impairment
Hyperventilation
Prolongs time to break-point. Decreased CO2, increased O2 (arterial)
Chemoreceptors respond to
Decreased O2 (arterial), increased PCO2 (arterial) and decreased pH
Boyle’s Law
At a constant temperature, the absolute pressure and volume of a gas are inversely proportional.
Henry’s Law
Increased partial pressure = increased gas dissolved in tissue. O2 and CO2 diffusion.
Dalton’s Law
Increased ambient pressure = increased partial pressure of PO2 and PCO2
Where is the respiratory control center located?
Within medulla oblongata
Respiratory center comprised of two dense clusters of neurons
Dorsal respiratory center - primarily inspiratory neurons (control diaphragm and receive feedback on PO2, PCO2 and pH) Ventral respiratory center - both inspiratory and expiratory neurons (controls all breathing muscles)
Mechanics of breathing (immersion up to neck)
When immersed up to the neck, there is increased pressure placed on chest. Normal outward elastic recoil of chest is decreased.
Pulmonary blood flow (immersion up to neck)
Blood pooling will be decreased due to increased pressure - enhanced venous return. Colder water enhances venous return.
Mechanics of breathing (underwater breathing)
At great depths, density of gas increases, thus increasing airway resistance. Sensitivity to CO2 is decreased.
Diving Reflex
Induces bradycardia and increases vascular resistance
BHD Medical Considerations
Decreased CO2 minimizes urge to breath. O2 remains high during descent. Bottom phase CO2 rises which may cause loss of conciousness due to hypoxia.
Lung Squeeze
Excess pressure on the lungs causes fluid to move into the lungs. S/S Shortness of breath, coughing up blood, pulmonary edema.
Alveolar Rupture
Excess of movement of fluid into lungs may cause alveoli rupture. S/S: Shortness of breath.
Barotrauma
Gas expansion in the GI tract. S/S: Abdominal pain, belching, flatulence.
Pneomothorax
Ruptured lungs tissue allows a pocket of air to form between the pleura of the lungs. S/S: Shortness of breath, collapsed lungs.
Middle-ear squeeze
Closed eustachian tube does not allow for pressure between the middle and air in the lungs to equalize. S/S: Pain in the ear, blood around ear, nose or mouth.
Air Embolism
Expansion of lung gasses during ascent.
O2 Toxicity
Exposure to high oxygen for high periods of long periods of time. S/S: Primarily occur within the lungs, CNS.
Nitrogen Narcosis
Increased nitrogen diffusion into tissues. S/S: Poor judgement, slow reaction time, euphoria.
Decompression Sickness
If ascent occurs too quickly, excess N and O in the tissues will result increased pressure ultimately blocking blood and lumph vessels, inducing compartment syndrome, and rupturing cell membranes.
CO2 Toxicity
Hypoxia, hypercapnia occurs during closed-circuit suba. S/S: Breathlessness, increased VE, impaired mental function and unconciousness.
Hypoxia
Occurs when their is insufficient O2 supply to tissues.
Hypobaria
Altitude. Total pressure is less than that at sea level.
High Altitude
1500-3499m (4291-11483feet)
Very High Altitude
3500-5500m (11,500-18,000 feet)
Extreme Altitude
More then 5500m. 5985m is the population at highest altitude.
Bohr Effect
Saturation of Hb with O2 at various PO2 values. Influenced by temperature and pH. Normal conditions: 60-100mmHg, Hb will be completely saturated.
Effects of of altitude on Bohr Effect
Goes right at first then left. As pressure increases, % saturation increases (toxicity). A shift to the left is desired (increase saturation, increased partial pressure). Cool and basic preferred.
2,3-Diphosphoglycerate (DPG)
Positive effect, increases with high altitude, makes it easier for hemoglobin to release its O2.
Exposure to altitude will result in hypoxia…
Decreased rate of oxygen utilization by cells. Body relies on anaerobic means for rephosphorylation of ATP.
Respiratory Response to Altitude
Hyperventilation, Respiratory alkalosis (hypercapnia), VE increases.
Cardiovascular Response to Altitude
Q increases due to HR increase, decreased plasma volume, SV decreases slightly (venous return, contractility maintained), a-VO2 increased, increased polycythemia (stimulated by EPO in kidneys)
Central Nervous Response to Altitude
Alterations in vision, hearing, motor skills, memory, mood and hallucinations. Activities require more time and concentration.
Metabolism Changes at Altitude
Weight loss attributed to hypoxia/AMS (loss of appetite), protein metabolism inhibited, focus on physical tasks without eating or drinking, increased caloric expenditure.
Altitude on Sleep
Impaired by altitude and hypoxic stress.
Immediate Responses to Changes in Altitude
Hyperventilation, increased Q and decreased VO2, increased EPI, increased fluid loss, decreased in mental and sensory function.
Long-Term Responses to Altitude
Body fluids become more basic, decreased plasma volume, increased RBC, increased mitochondria, O2 release at tissues, decrease in lean body mass and body fat.
Altitude and Performance
Aerobic decreases due to ventilatory limitations and then improves, muscular strength and sprinting unaffected, maximal aerobic can only be maintained for short periods.
Recommendations for Training?
Live high, train low! Lower intensity until acclimatized.
Anaerobic Performance and Altitude
May decrease slightly or remain unchanged.
Benefits of training at altitude
Increased arterial O2 reduces occurrence of hypoxia, increased sensitivity of chemoreceptors, polycythemia, increased bone marrow (increased RBC production), decreased muscle CSA (less energy for more work), increased aerobic metabolism.
Deacclimatization
Occurs 2 weeks after returning to sea level.
Acute Mountain Sickness
Develops 6-12 hours following rapid ascent, peaks within 24-48 hours, acclimatization takes 3-7 days
S/S of AMS
Vascular changes (kidneys) can cause headache, fatigue, instability, GI distress (nausea, vomiting, diarrhea, loss of appetite) *EAT CARBS
Treatment of AMS
Descend, Acetazolamide, Supplemental O2
High-Altitude Cerebral Edema (HACE)
Extreme form of AMS can result in loss of conciousness, occurs between 12 hours and three days as a result of increased intracranial pressure
S/S of HACE
Loss of coordination, AMS symptoms/treatment, loss conciousness.
High-Altitude Pulmonary Edema (HAPE)
Occurs 12-96 hours post-ascent.
S/S of HAPE
Excessive, rapid breathing, increased HR, bloody cough, cyanosis (blue skin color)
PREVENTION of HAPE
Acetazolimide, ascend slowly, sleep at lower altitudes, minimize PA.
