Hypoxia agents causing

Various conditions and agents may change the osmolarity within the developing embryo and thereby disrupt embryogenesis. Thus, induction of hypoxia may cause hypo-osmolarity,... 

Figure 6 Redox control of PA tone, (a) The suUhydiyl oxidant diamide reverses HPV in anesthetized dogs. Preincuhation of diamide with reduced glutathione prevents this effect. (From Ref. 110.) (h) Endothehum-denuded PA rings constrict in response to the electron-shutthng agent duroquinone and this is reversed hy diamide. These data suggest that reducing agents (and, by extension, hypoxia) may cause PA constriction via a redox mechanism that involves a shift to a more reduced state. The fact that this occurs in denuded PAs suggests that this process is endothelium independent.

Asphyxiant agents cause hypoxia in the tissues following inhalation without causing damage to the lung structures. They may be divided into the following ... 

As noted in Chap. 6, toxic trauma can affect the heart and major vessels in a number of ways. A hypodynamic circulation with low blood pressure and poor central perfusion is potentially life-threatening as it is with hypovolaemic shock in physical trauma. Many chemical warfare (CW)/toxic industrial chemicals (TIC) agents give rise to potentially life-threatening cardiac dysrhythmias, for example, organophosphate (OP) agents and hydrocarbons. Profound hypoxia may cause secondary asystolic cardiac arrest which is the end stage of most toxic trauma. 

Lactic acidosis, which typically accompanies hypovolemic shock as a consequence of tissue hypoxia, is best treated by reversal of the underlying cause. Administration of alkalizing agents such as sodium bicarbonate has not been demonstrated to have any... 

The usual definition of a neuroprotectant is an agent that aims to prevent neuronal death by inhibiting one or more of the pathophysiological steps in the processes that follow injury to the central nervous system (CNS) or ischemia due to occlusion of an artery or hypoxia due to any cause. This definition has now been extended to include protection against neurodegeneration and neurotoxins. The extended definition includes interventions that slows or halts the progression of neuronal degeneration. 

Paralysis is preceded by muscular fasciculation, and this may be the cause of the muscle pain experienced commonly after its use. The pain may last 1-3 days and can be minimised by preceding the suxamethonium with a small dose of a competitive blocking agent. Suxamethonium is the neuromuscular blocker with the most rapid onset and the shortest duration of action. Tracheal intubation is possible in less than 60 seconds and total paralysis lasts up to 4 min with 50% recovery in about 10 min (t / for effect). It is particularly indicated for rapid sequence induction of anaesthesia in patients who are at risk of aspiration — the ability to secure the airway rapidly with a tracheal tube is of the utmost importance. If intubation proves impossible, recovery from suxamethonium and resumption of spontaneous respiration is relatively rapid. Unfortunately, if it is impossible to ventilate the paralysed patient s lungs, recovery may not be rapid enough to prevent the onset of hypoxia. 

Raised intracranial pressure will be made worse by high expired concentration inhalation agents, e.g. > 1% isoflurane, by hypoxia or hypercapnia, and in response to intubation if anaesthesia is inadequate. Without support from a mechanical ventilator, excessive doses of opioids will cause hypercapnia and increase intracranial pressure. 

Nerve agent exposure may cause bradycardia due to vagal stimulation or it may often cause the reverse tachycardia due to fright and hypoxia and adrenergic stimulation secondary to ganglionic stimulation. Bradyarrhythmias such as first-, second-, or third-degree heart block may also occur. Blood pressure may also be elevated because of adrenergic stimulation, but it is usually normal until the terminal decline. 

After completing decontamination, the only effective management consists of close observation for the development of respiratory distress and supportive care. There are no known antidotes for pulmonary agent exposure. Patients exposed to phosgene or diphosgene require monitoring for a minimum of 12h because of the possibility of delayed symptoms (2). Strict bed rest is essential for patients with mild and moderate exposmes, because any exertion, even minimal exertion, can shorten the clinical latent period and inaease the severity of respiratory symptoms (8). In symptomatic patients, physical activity can cause clinical deterioration and even death (8). Supportive care consists of managing secretions, bronchospasm, hypoxia, and pulmonary edema. 

---