During an apnea, the oxygen in the body is used by the cells and excreted as carbon dioxide. Thus, the level of oxygen in the blood decreases, and the level of carbon dioxide increases. Increasing carbon dioxide levels lead to a stronger and stronger breathing reflex, up to the breath-hold breakpoint, at which the person can no longer voluntarily hold his or her breath. This typically occurs at an arterial partial pressure of carbon dioxide of 55 mm Hg but may differ significantly between people. The breath-hold breakpoint can be suppressed or delayed, either intentionally or unintentionally. Hyperventilation before any dive, deep or shallow, flushes out carbon dioxide in the blood resulting in a dive commencing with an abnormally low carbon dioxide level; a potentially dangerous condition known as hypocapnia. The level of carbon dioxide in the blood after hyperventilation may then be insufficient to trigger the breathing reflex later in the dive. Following this, a blackout may occur before the diver feels an urgent need to breathe. This can occur at any depth and is common in distance breath-hold divers in swimming pools. Both deep and distance free divers often use hyperventilation to flush out carbon dioxide from the lungs to suppress the breathing reflex for longer. It is important not to mistake this for an attempt to increase the bodys oxygen store. The body at rest is fully oxygenated by normal breathing and cannot take on any more.
Bladder sphincter dyssynergia (also known as detrusor sphincter dyssynergia (DSD) (the ICS standard terminology agreed 1998)  and neurogenic detrusor overactivity (NDO)) is a consequence of a neurological pathology such as spinal injury  or multiple sclerosis which disrupts central nervous system regulation of the micturition (urination) reflex resulting in dyscoordination of the detrusor muscles of the bladder and the male or female external urethral sphincter muscles. In normal lower urinary tract function, these two separate muscle structures act in synergistic coordination. But in this neurogenic disorder, the urethral sphincter muscle, instead of relaxing completely during voiding, dyssynergically contracts causing the flow to be interrupted and the bladder pressure to rise. Presentation
People with this condition generally experience daytime and night time wetting, urinary retention, and often have a history of urinary tract and bladder infections. Constipation and encopresis are often associated with this condition. Pseudodyssynergia has different causes but presents similarly. Pathology
The pathophysiology of the condition results from neuronal plasticity associated with bladder afferents and motor neurons innervating the external urethral sphincter. Treatment
Botulinum A toxin is a valuable alternative for patients who do not want surgical methods. References
Further reading


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