It can be caused by drowning, inhalation of certain substances, strangulation, blockage of the airway, traumatic injury to the airway, apnea, and other means. The most immediate injury caused by asphyxia is hypoxia, which can in turn cause acute lung injury or acute respiratory distress syndrome as well as damage to the circulatory system. The most severe injury associated with asphyxiation is cerebral hypoxia and ischemia, in which the brain receives insufficient oxygen or blood, resulting in neurological damage or death. Specific injuries are associated with water inhalation, including alveolar collapse, atelectasis, intrapulmonary shunting, and ventilation perfusion mismatch. Simple asphyxia is caused by a lack of external oxygen supply. Systemic asphyxia is caused by exposure to a compound that prevents oxygen from being transported or used by the body. This can be caused by azides, carbon monoxide, cyanide, smoke inhalation, hydrogen sulfide, methemoglobinemia-inducing substances, opioids, or other systemic asphyxiants. Ventilation and oxygenation are necessary for treatment of asphyxiation, and some asphyxiants can be treated with antidotes.Injuries of overuse or overexertion can occur when the body is strained through use, affecting the bones, muscles, ligaments, or tendons. Sports injuries are often overuse injuries such as tendinopathy. Over-extension of the ligaments and tendons can result in sprains and strains, respectively. Repetitive sedentary behaviors such as extended use of a computer or a physically repetitive occupation may cause a repetitive strain injury. Extended use of brightly lit screens may also cause eye strain. Locations
Abdomen
Abdominal trauma includes injuries to the stomach, intestines, liver, pancreas, kidneys, gallbladder, and spleen.
It can also cause severe hypertension (high blood pressure) when combined with sympathomimetic drugs or MAO-A inhibitors, bradycardia (low heart rate) when combined with antiarrhythmics or mefloquine, and hypoglycemia (low blood sugar) when combined with antidiabetic drugs such as insulin. Pharmacology
Mechanism of action
Levobunolol is a non-cardioselective beta blocker, that is, it blocks beta-1 receptors as well as beta-2 receptors. The latter type dominates in the ciliary body, where it controls aqueous humour production. Blocking this type of receptor reduces aqueous humour production, lowering intraocular pressure. The substance has no relevant membrane stabilizing effect or intrinsic sympathomimetic activity. Like other beta blockers, and unlike the anti-glaucoma medication pilocarpine, levobunolol has no effect on accommodation and pupil size. Pharmacokinetics
The substance quickly penetrates the cornea and reaches the aqueous humour. It is reduced to dihydrolevobunolol, which is equally active, in the eyes tissues. The drug starts to lower intraocular pressure within an hour, reaches its maximum effect after two to six hours, and remains effective for up to 16 hours. It has an elimination half-life of six hours and is mainly excreted via the kidney. Chemistry
Levobunolol is the pure L-enantiomer of bunolol and has more than 60 times the pharmacological activity of D-bunolol. It is used as the hydrochloride, which melts at 209 to 211 °C (408 to 412 °F) and is soluble in water and methanol and slightly soluble in ethanol. References

Ishibashi T, Yokoi N, Kinoshita S (2003). "Comparison of the effects of topical levobunolol and timolol solution on the human ocular surface". Cornea. 22 (8): 709–15. doi:10.1097/00003226-200311000-00001.