What is the dive reflex?
The dive reflex is a physiological response to submersion (eyes, nose, mouth) in water (cold water amplifies the reflex):
- period of apnea
- vasoconstriction (cold receptors on skin) limits blood flow to the extremities and non-essential muscles, redirecting it to the brain and heart.
- bradycardia - afferent activation of chemoreceptors and baroreceptors
- Efferent activation of SNS and PSNS
Formula for pressure
Pressure = ρ x g x d
Underwater, pressure on a diver is calculated from surface atmospheric pressure plus the additional pressure exerted by water i.e., atmospheres absolute
(ATA)
Why do kids wee in a pool?
Hydrostatic pressures on lower limbs causes blood to redistribute from lower limbs to the thoracic cavity leading to an increase in arterial blood pressure and urine production. (ie increase in venous return, increases CO, increases BP)
Outline the physiological response to submersion
Redistribution of fluid from lower limbs to thoracic cavity causes ANP to be released (fast response, 1/2 life ~ 2-5 mins) and increased glomerular capillary BP -> both ANP amd GFR increase urination
Hydrostatic pressure also compresses the lungs according to Boyle’s law (P1x V1 = P2 x V2). If lung volume < residual volume:
- hemoptysis (coughing blood)
- pulmonary oedema
Calculate the depth at which a diver’s lung would compress from TLC (total lung capacity) at the surface to RV in sea water?
Female Male
4.84L 6.56L TLC
1.04L 1.39L RV
P1 x V1 = P2 x V2
P2 = P1 x V1/V2
= 1 ATA x 4.84/1.04
= 4.65 ATA
1 atm = 101.325 x 10^3 pascals
4.65 ATA = 1 atm (surface) + 3.65 atm (water)
3.65 atm = 3.65 x 101.325 x 10^3 pascals
Pressure = ρ x g x d
Depth = Pressure/(ρ x g)
1 atm = 101.325 x 10^3 pascals
4.65 ATA = 1 atm (surface) + 3.65 atm (water)
3.65 atm = 3.65 x 101.325 x 10^3 pascals
= 3.65 x 101.325 x 10^3 pascals/(1025 kg/m3 x 9.81 ms-2)
= 36.78m
But Freediver records > 36.8m ie > 100m
Why are freedivers capable of diving to depths greater than the size of their RV calculation allows?
- Redistribution of blood from periphery to the thoracic cavity provides a non-compressible material into the lungs
- Collagen and elastin fibres
(extracellular matrix) in the lung resist compression - Both above reduces the magnitude of lungh squeeze, combine with the ability of elite divers to endure lung squeeze
Why do we need pressure equalisation?
Ear barotrauma can occur:
- The external auditory canal is exposed to depth-induced hydrostatic pressure
- The liquid filled vestibulocochlear
apparatus (like blood) is under the same hydrostatic pressure
- The eustachian tube is connected to the back of the throat and allows for middle
ear pressure equalisation
- if the eustachian tube is closed or blocked (e.g., allergy induced congestion), pressure in the middle ear is not equalised
- In diving, the tympanic membrane (ear drum) is displaced inwards and ruptures => hemorrhage, hearing impairment, vertigo and nausea
- Rupture of the round window (between middle and inner ear) can cause permanent hearing loss,
Can a diver increase total lung capacity (TLC)?
Divers often use glossopharyngeal insufflation which increases vital capacity (ie does not increase residual volume). TLC = RV + VC
This increases diving depth by increasing O2 via increased TLC/RV
What is a real danger faced by deep water divers attempting to resurface?
Shallow water blackout: a loss of consciousness caused by cerebral hypoxia towards the end of a breath-hold dive in shallow water.
At depth, hydrostatic P compresses lungs so total PAO2 increases. However on returning to the surface, hydrostatic P falls hence total PAO2 falls and favours movement of O2 from the capillaries into the alveoli instead. This compromises O2 delivery to the brain (cerebral hypoxia) leading to shallow water blackout.
What is Dalton’s law?
Dalton’s law states that in a gas mixture, the sum of the partial pressure of each gas is equal to the total pressure exerted by the mixture
PTotal = PN + PO2 + Pargon + PCO2
Highlight the main differences between central and peripheral chemoreceptors
[H+] and PaCO2 are the main drivers of ventilation as detected by central and peripheral chem.
PaO2 is detected at the peripheral chemoreceptors however only drives ventilation at <60mmHg (desat point for Hb) is poses as an emergency trigger
A) Central - responds to [H+] and is most important mechanism (~80% contribution of response) governing ventilation at rest such that even small changes in PaCO2 substantially affect ventilation
B) Peripheral (carotid and aortic) detect PaCO2 and [H+] contributes 20% to response
Why are suba divers not suited to assist free divers?
Free divers experience lung compression that is comparable to the depth at which they are at. Scuba divers on the other hand, breathe compressed air matched to ambient pressure (surrounding water pressure increasing with depth) , so their lungs do not compress.
If a scuba diver were to hold his breath at functional residual capacity (FRC ~3L) at 40.3 m (5
ATA) and surface quickly to help a free diver surface, what would happen to his lungs?
P1 x V1 (at depth) = P2 x V2 (at surface)
V2 = P1 x V1/P2
= 5 ATA x 3L/1 ATA
= 15L => BAROTRAUMA
His alveoli would rupture. ie Scuba divers cannot ascend quickly
What happens during barotrauma of diving?
When scuba divers ascend quickly, tissues which are sat with gas expands and can escape out of solution (Henry’s Law) forming bubbles:
1) pneumothorax - gas leaks into the pleural space, collapsing lung
2) pneumomediastinum causing chest pain
3) subcutaneous emphysema -> the bends
4) arterial gas embolism (AGE) potentially occluding blood flow
5) cerebral gas embolism
What is prevention/treatment for decompresion sickness?
A slow ascent to allow gas to escape slowly from tissues. Treatment for decomopression sickness include the use of hyperbaric chambers where the higher pressure mitigates the formation of gas bubbles and allows the gas to be cleared through the lungs..
Why does nitrogen cause a narcotic effect?
Nitrogen is highly lipid soluble and disrupts the membranes of nerve cells. The uptake of nitrogen in tissues is greatest in perfused regions of the body. As the brain is highly perfused and rich in lipid-rich nerve cells. it is therefore susceptible to the biological effects of nitrogen
Why don’t divers use 100% O2?
O2 at high PP cause oxygen toxicity. The exact mechanism hasn’t been fully defined however a plausible mechanism is thought to be the generation of ROS which overwhelms the body’s defenses. In particular the generation of peroxynitrite (ONOO-) from NO (nitric oxide) causing neurotoxicity, seizures (above ATA 1.4-1.6), decreased capacity to carry CO2
What other gas mixers are used?
- Nitrox (60% O2, 40% N2) has O2 toxicity risk but reduced risk of decompression sickness (DS)
- Heliox (23% O2, 77% He) which reduces risk of narcosis, however He causes deep pressure neurological syndrome (DPNS)
- Trimix ( 21% O2, 35% N2, 44% He) reduces risks for narcosis and DPNS, however complex to administer
What is Deep Pressure Neurological Syndrome?
DPNS is a neurological disorder which can result from deep sea diving with the use of helium. It has symptoms of tremors, impaired motor control, nausea, dizziness
Explain dynamic airway collapse (DAC)
- Transmural pressure across the airway wall is calculated from lumen pressure minus external pressure/pleural pressure
- Transmural pressure is normally positive (distends/outward stretching of the airway wall)
- During forced expiration pleural pressure switches from negative to positive
- As pressure energy is gradually lost along the airway during forced expiration (due to resistance), positive pleural pressure eventually exceeds lumen pressure and transmural pressure becomes negative
- Negative transmural pressure compresses the airway wall, providing a ‘choke point’ (dynamic airway collapse) that accounts for effort independent flow
Why is DAC a problem during deep diving?
- deep sea divers breath a pressured gas mix. Pressured gas mixtures have higher gas density
- Dense gas promotes turbulent flow during breathing leading to greater falls in pressure along the airway
- Subsequently, dynamic airway compression occurs closer to the airway so that airflow
was restricted during much of the expiratory cycle - Dynamic airway collapse leads to effort independent flow, breathing harder is ineffective
- It however produces more CO2 which activates peripheral chemoreceptors leading to increasing hyperventilation (positive feedback loop)
- CO2 toxicity ultimately occurs
