131 Scuba Diving and Dysbarism Flashcards
Leading cause of death amonst divers
drowning
2 major mechanism of injury in diving dysbarisms
1) barotrauma (pressure)
2. decompression illness
Baotrauma - related to ? of descent and ascent vs time and depth
speed of
not rel to time or depth
Bubble formation from nitrogen and nitrogen narcosis - dep on depth for extended period of time?
yes
Boyle’s law
diver related barotrauma: at constant temp, absolute pressure and vol of gas are inversely proportional
ie as pressure incr with descent, gas vol is reduced
changes in vol of gas caised bu change of pressure due to depth defining this relationship in gas supplies
Pascal’s law
pressure applied to any part of a liquid will transmit throughout
pressure in contaned space transmitted throughout (ie relevant inner ear and middle ear barotrauma)
Charles’ law
at constant pressure, vol of directly = to change in absolute temp
incr pressure (filling scuba tank) - causes heat and cooling tank decr pressure
General gas law
P1 x V1/T1 = P2 x V2/T2
Daltons’ law
total pressure exerted by mix of gases is equal to sum total of of each of different gases making up mixture
N2 under pressure acts as if gases are not present
Henry’s law
amount of gas dissolving into liquid at a given temp is directly proprtional to partial pressure at that gas
more N2 taken into solution (serum) at high pressures than comes out of a solution at lower pressures
Fractional changes in vol are greater where proprtional pressure changes are highest - generally more in ___ water
shallow
Henry’s law explains what type of illness?
decompression
Decompression sickness - how does this ocur?
rapid ascent - reduce pressure at higher rate than body can accommodate and bubbles (ie n2) accumulate, disrupting body tissue and systems
Disorders relevant to descent/barotrauma
- middle ear barotrauma
- inner ear “
- ext ear “
- barosinusitis
- reverse middle ear squeeze
- alternobaric vertigo
- facial barotrauma/mask squeeze
Key q for diving hx
When was the first onset of symptoms?
What type of equipment was used? Compressed air, mixed gas, enriched air,
rebreather? What was the source of the gas?
Did the dive approach or exceed decompression limits? Was a dive computer
used?
What were the number, depth, bottom time, total time, and surface intervals
for all dives in the 72 hours preceding symptoms (the dive “profiles”)? Were decompression stops used? Was in-water decompression attempted? What was the time delay from the last dive to air travel?
Did the diver experience difficulty with ear or sinus equilibration? Did the pain
occur on descent or ascent?
Was the diver intoxicated? Dehydrated? Working strenuously?
How long after the dive did symptoms present? Were they present at surfac-
ing? Delayed? Progressive?
Is a medical history of ear or sinus infections or abnormalities present? Emphy-
sema or asthma? Coronary artery disease? Patent foramen ovale (PFO)? Neurologic illness?
Why does middle ear barotrauma occur in diving
Typically, a diver performs various equaliza- tion maneuvers to force air into the middle ear through the ET. The ET may become blocked or collapse related to the pressure differential or inflammation, making subsequent attempts at equalization virtu- ally impossible. This is typically painful
How does inner ear trauma occur in diving?
Inner ear barotrauma (IEBT) results in damage to the cochleovestibular apparatus. It is less common than MEBT (reported as 0.5% lifetime incidence in divers) but is associated with greater morbidity. If the diver is unable to equalize the middle ear during descent, pressure is transmitted across the labyrinthine windows (oval and round) leading to inner ear hemorrhage. Intralaby- rinthine membrane tears which effect the Reissner, tectorial or basilar membranes can also occur or cause a tear of the labyrinthine windows, leading to perilymphatic fistula formation (PLF)
Rev middle ear squeeze: what is this?
opposite of middle squeeze and occurs during ascent. As the pressure lessens, a pressure gradient can cause the TM to bulge outward and even rupture causing pain. This is much less common than middle ear squeeze during descent.
Why does barosinusitis occur?
The air-filled maxillary, frontal, and eth- moidal sinuses are susceptible to volume-pressure changes on ascent or descent; the most commonly affected is the maxillary sinus, fol- lowed by the frontal. The most common symptoms are facial pain and epistaxis.
Alternobaric vertigo - what is this?
common but usually transient, self-limited vertigo secondary to asymmetric ear pressure transmitting from the middle ear to the inner ear.
Facial barotrauma: what is this?
Mask squeeze” is a type of facial barotrauma injury that occurs more commonly in novice divers or in masks that cannot be exhaled into (e.g., free diving masks) The difference in pressure inside and outside the mask can lead to baro- trauma to the contents inside the mask leading to injury of blood vessels and tissue of the eyes and face. This can lead to facial and conjunctival edema, diffuse petechial hemorrhages on the face, and subconjunctival hemorrhages which are generally self-limited. Rarely, optic nerve damage
Disorders at descent
nitrogenic narcosis
o2 toxicity
contaminated air
N2 narcosis: what is this?
occurs when exposed to the intoxicating increases of partial pres- sures of nitrogen and is considered a significant contributing factor in diving-related accidents. Narcosis is characterized by an impairment of psychomotor coordination and alterations in mood (such as eupho- ria or increased anxiety) and behavior (lowering of inhibitions and impairment in reasoning).
N2 narcosis: what depth?
require time at depth and may become apparent at a depth of 100 ft (30 m) and increase with fur- ther increases in depth.
N2 narcosis: recommended for deeper depths to prevent this and how to resolve?
Use of mixed gases with lower concentration of nitrogen is recommended for technical, military, commercial or sport diving to deeper depths. The effects of nitrogen narcosis resolve with gradual and controlled ascent to shallower depths.
When is O2 considered toxic? (pp)
partial pressure exceeds 1.6 atmosphere absolute (ata). Oxygen partial pressures below 1.4 ata are unlikely to produce CNS toxicity. A diver breathing compressed air would attain a partial pressure of 1.6 ata of oxygen at a depth of 218 fsw. This far exceeds the depth to which most recreational divers would dive. Most profes- sional divers prevent oxygen toxicity by breathing mixed gases with decreased oxygen and nitrogen content to decrease the possibility of oxygen toxicity (and nitrogen narcosis)
Low pressure oxygen toxicity/low pressure o2 poisoning can occur after 24h with pp of o2 in excess of ? ata
0.6
Pulmonary oxygen toxicity sx
burn sensation
pain on inspiration and cough
cns: h/a, dizzy, irritable, anx, visual change, extremity twitching, tinitus and hearing
nausea
seizure
death
Concern for contaminated air: what kind of sx seen?
hypercarbia or CO poison
Rebreathers use absorbent material to remove carbon dioxide from the circuit. A hose rupture allowing seawater contamination of the circuit may create a caustic alkaline-based liquid containing calcium or sodium hydroxide, which can cause burns to the mouth, throat, and airways.
Disorders arising on ascent
alternobaric vertigo
barodontalgia
GI barotrauma
pulm barotrauma
decompression sickness
Barodontalgia
air that is trapped beneath a poorly filled dental cavity or within a dental abscess and expands on ascent, leading to dental pain. This condition affects up to 10% of divers but is relatively benign and self-limited.
GI barotrauma: how does this occur?
expansion of bowel gas in the small intestine and colon on ascent after diving. Predisposing factors include consumption of carbonated beverages, large meals, or gas-producing foods before diving, as well as performance of the Valsalva maneuver in the head- down position.
