Diving mechanics and gas laws for pulmonology and medical students

1. Physiology of Diving
Dr. Athul Francis
2nd
Year Junior Resident
Department Of Pulmonary Medicine

2. DIVING &
LUNG

4. Introduction
SCUBA – Self Contained Underwater Breathing Apparatus.
1942-1943 :Cousteau and Gagnan-First Scuba Device : aqua
lung
DAN(Divers Alert Network ):Most accurate statistics of diving
injuries

5.  Leading COD:Drowning (70 % )
 Disabling Injuries:
 A)Asphyxia (29 %)
 B)Cardiac Events (26 %)
 C)Trauma (5 %)
 D)Decompression sickness (3%)

6. Fundamental Concepts
 Pressure = Force/Area
 1 ATM=760 mm Hg=101.3 kPa
 For every 33 ft of sea Water-Pressure increases by 1 ATM
 By 99 ft- 4 ATM
 As subject ascends- pressure reduces

7. Behavior of gases and
pressure changes during
descent and ascent.
Clinical manifestations seen
during diving or up to 24
h after it.

8. Gas Laws

9. Boyle’s Law
o For any gas at a constant
temperature, the volume of the gas
will vary inversely with the
pressure, and the density of the
gas will vary directly with the
pressure.
o P1V1=P2V2=N

10. HENRY’S LAW
The amount of any given gas that will dissolve in a liquid at
a given temperature is proportional to the partial pressure
of that gas in equilibrium with that liquid.
 An increase in pressure will increase absorption

11. • At sea level, the dissolved gases in the blood and tissues are
in proportion to the partial pressures of the gases in the
person's lungs at the surface.
• As the diver descends ,the ambient pressure increases, and
therefore the pressure of the gas inside the lungs
increases.

12. Dalton’s law of partial pressures
Daltons law states that the total pressure exerted by gas
mixture is equal to sum of partial pressure of each
individual gas.
P absolute=pN2+pO2+pco2 +…
As absolute pressure increases,the amount of gas also
increases- leading to adverse effects

14. Main Pathologies
1.Barotrauma – Ear, Sinus,
Pulmonary barotrauma.
2. Decompression illness:
Dysbaric AGE
DCS
3. Pulmonary edema
4.Pharmacological and toxic
effects of increased partial
pressures of gases

15. Ear Barotrauma
 Most common disorder among divers (Middle ear
involvement).
 Unable to equilibrate the pressure between the
nasopharynx and the middle ear through the eustachian
tube can result in middle ear pain.
 Tinnitus, dizziness, hearing loss.
 In severe cases, rupture of the ear drum can occur.

16. Sinus Barotrauma
 Second most common
disorder among divers.
 During descent, increase
in ambient
environmental pressure
can lead to mucosal
engorgement, edema and
inflammation producing
blockage of the sinus
Ostia.
 Frontal sinus – most
commonly affected.
 Headache, epistaxis.
 Pneumocephalus.

17. Pulmonary barotrauma
Diver Descends
Increase in atmospheric pressure
Lung decreases in volume and may go into collapse
Inorder to prevent collapse ,and to prevent tear to vessels and
parenchyma,diver has to breathe in a mixture containing O2

18. Nitrogen narcosis
 • Caused by raised partial pressure
of
 nitrogen in nervous system tissue.
 Usually occurs at depths greater
than 100 feet.
 Direct toxic effect of high nitrogen
pressure on nerve conduction.
 Variable sensation but always
depth related.

19. Nitrogen Narcosis
Some divers experience no
narcotic effect at depths up to
40 m. whereas others feel
some effect at around 25 m.
 The diver may feel and act
totally drunk.
 Takes the regulator out of
their mouth and hands it to a
fish !
MARTINI EFFECT

20. Arterial gas Embolism
 Any person using
SCUBA equipment
presenting with
neurologic deficits
during or
immediately after
ascent, should be
suspected of air
embolism
Form of
barotrauma of
ascent.

21. Very serious condition in which air bubbles enter
the circulatory system through rupture of small
pulmonary vessels.
 Air can also be trapped in blebs, air pockets,
within the pulmonary tissue

22. Air Embolism- Pathophysiology
 Arterial gas embolism is the most serious potential sequel
of pulmonary barotrauma.
 Arterial gas emboli can result from any of three process:
1. 1.Passage of gas bubbles into the pulmonary veins and
from there into the systemic circulation
2. Development of venous gas emboli (either from
barotrauma or decompression sickness), which overwhelm
the filtering capacity of the pulmonary capillaries to
appear in the systemic arterial circulation.

24. 3. Development of venous gas emboli that reach the arterial circulation
"paradoxically" via a functional right-to-left shunt, such as a patent
foramen ovale.
 Reach the systemic arterial circulation.
 Gas emboli typically break up as they reach vascular branch points.
.
 Lodge in vessels with diameters ranging from 30 to 60 μm
.
 They produce distal ischemia and local activation of inflammatory
cascades

25. Air Embolism-Clinical features
 Cardiac-: Dysrhythmias, myocardial infarction, and/or cardiac arrest (0.5ml air
can cause)
 CNS-: focal motor, sensory, or visual deficits to seizures, loss of consciousness,
apnea, and death.
 Skin-: cyanotic marbling of the skin, focal pallor of the tongue.
 Renal-: hematuria, proteinuria, and renal failure.
 Uterine & GI bleeds

26.  About 5 %-critically injured and die even when recompression given within
minutes
 Neurological symptoms are the most common

27. Treatment
 Immediate administration of 100 percent oxygen.
 Shift to hyperbaric oxygen facility as soon as possible

28. Air Embolism-Treatment
1. Assess ABCs.
2. Administer oxygen.
3. Place patient in left lateral
Trendelenburg
position/Supine
position
4. Monitor vital signs
frequently.
5. Administer IV fluids.
6. Corticosteroid.
7. Lidocaine.
8. combination of
prostacyclin,
indomethacin, and heparin

29. Pneumomediastinum
 Alveolar rupture- gas can dissect along the perivascular sheath into the
mediastinum.
 Clinical Features:
 Substernal chest pain.
 Irregular pulse.
 Abnormal heart sounds.
 Reduced blood pressure/narrowing pulse pressure.
 Change in voice.
 May or may not be evidence of cyanosis.
 Crepitation in the neck
 Haman’s sign

30. Pneumomediastinum - Treatment
 Administration of high-concentration oxygen via non-rebreathing face mask
 Treatment generally ranges from observation to
recompression

31. Decompression Sickness (Bends)
 Condition that develops in divers
subjected to rapid reduction of
air pressure after ascending to
the surface following exposure to
compressed air.

32. Decompression Sickness (Bends)
 “Caisson disease“
 First recognized in 1843 among tunnel workers following
return from the compressed environment of the caisson to
atmospheric pressure.
 Term "the bends" is frequently applied to this illness.
 Laborers with decompression sickness sometimes walked
with a slight stoop.

33. Pathophysiology
Diver descends
breathes air under increased pressure.
.
Tissues become loaded with increased quantities of oxygen and
nitrogen as predicted by Henry's law.
.

34. Diver ascends-Decreased solubility of gas
the sum of the gas tensions in the tissue may exceed
the ambient pressure.
Leads to the liberation of free gas from the tissues
in the form of bubbles

35.  The liberated gas bubbles can alter organ function:
1) By blocking vessels, rupturing or compressing tissue,
2) activating clotting and inflammatory cascades.
 The volume and location of these bubbles
determine if symptoms occur or not.
 Effects on the body can be direct or indirect.

36. Direct Effects
 Intravascular: blood flow will be decreased, leading to ischemia or infarct.
 Extravascular: tissues will be displaced, which further results in pressure on
neural tissue
 vestibular: air can diffuse into the audiovestibular system, causing vertigo.

37. Indirect Effects
 Surface of air emboli may initiate platelet aggregation and
intravascular coagulation
 Extravascular plasma loss may lead to edema
 Electrolyte imbalances may occur
 Lipid emboli are released.

38.  Decompression sickness divided into
two types based on the presenting
signs and symptoms.

39. Type I
 Usually referred to as the bends.
 Musculoskeletal-: Joint Pain
Caused by expansion of gases present in the joint
space. (Elbow & shoulder)
 Skin manifestations -:
pruritus (itch), localized erythema.
cutis marmorata-rash with reticulated marbled
appearance is path gnomic of DCS.
 Lymphatic-: lymphadenopathy and localized edema

42. TYPE 2
Neurologic
 60% of divers
 Damage to spinal cord.
 Paresthesias and weakness
 Paraplegia
 Loss of bladder control
 Memory loss
 Ataxia
 Visual and speech
disturbances.
Pulmonary
 Venous gas embolism (5%)
 Gas bubbles – occlude
portions of Pulmonary
circulation.
 Chest pain, dyspnea
 Right ventricular outflow
obstruction
 Circulatory collapse

43. DECOMPRESSION SICKNESS SEQUENCE

44. Treatment
 Hydration
 Administration of 100 percent oxygen
 Positioning the patient in the left lateral decubitus
(Durant's maneuver).
 Mild Trendelenburg (bed angled downward toward
head) position in an effort to restore forward blood
flow by placing the right ventricular outflow tract
inferior to the right ventricular cavity, permitting air
to migrate superiorly to a non obstructing position

45. Treatment
 Hyperbaric oxygen therapy – definitive treatment
 In a recompression chamber initiated as quickly as possible.
 Time to initiation of treatment is one of the main determinants of
outcome .
 Hyperbaric oxygen therapy decreases the volume of air bubbles according
to Boyle's law.
 Provides oxygenation to hypoxic tissue by increasing the dissolved oxygen
content of arterial blood.

46. NSAID-TENOXICAM .
LIDOCAINE- class1b antiarrythmic agent and local anesthetic has been shown to
have cerebroprotective effects.

47. HYPERBARIC OXYGEN CHAMBER

48. HYPERBARIC OXYGEN THERAPY FOR DECOMPRESSION
ILLNESS
HBOT involves inhalation of 100% oxygen at a pressure greater than 1 ATA.
Typical treatment pressure range is 2-3ATA.
HBOT allows for dramatic increase in both arterial and tissue oxygen tensions.

50. Hyperbaric chambers are generally classified as either multiplace or monoplace
chambers.
AGE and DCS the primary aims of therapy are:
reduction in bubble volume.
accelaration of bubble resolution.
maintanence of tissue oxygenation.

51. Resolution of bubbles in DCS and AGE is hastened by breathing oxygen at
increased pressure because the associated elimination of nitrogen from all
body tissues and concurrent bubble compression combine to maximize the
outward diffusion gradient for bubble nitrogen.