Nerve agents cardiovascular effects

Fusek, J., Bajgar, J., Herink, J., Skopec, F. (1996b). New group of nerve agents cardiovascular and respiratory effects and blood cholinesterase activity during acute intoxication with 2-dimethylaminoethyl-(dimethylamido)-fluorophosphate in rats. Int. Rev. Arm. Forces Med. Serv. 69 291-4. 

The cardiovascular effects of local anesthetics result partly from direct effects upon the cardiac and smooth muscle membranes and partly from indirect effects upon the autonomic nerves. As described in Chapter 14 Agents Used in Cardiac Arrhythmias, local anesthetics block cardiac sodium channels and thus depress abnormal cardiac pacemaker activity, excitability, and conduction. At very high concentrations, they may also block calcium channels. With the notable exception of cocaine, local anesthetics also depress the strength of cardiac contraction and cause arteriolar dilation, both effects leading to severe hypotension. Cardiovascular collapse and death are rare and usually occur only after large doses of 0.75% bupivacaine. 

Notes X = A known adverse effect by an agent CNS = Central nervous system ANS = Autonomic nervous system CV = Cardiovascular system PB = Pyridostigmine bromide OP = Organophosphates CB = Carbamates Pyreth = Pyrethroids Lind = Lindane NA = Nerve agents Mus = Mustard agents Du = Depleted uranium. 

Toxic effects occur within seconds to 5 min of nerve agent vapor or aerosol inhalation. The muscarinic effects include ocular (miosis, conjunctival congestion, ciliary spasm), nasal discharge, respiratory (bronchoconstriction and increased bronchial secretion), gastrointestinal (anorexia, vomiting, abdominal cramps, and diarrhea), sweating, salivation, and cardiovascular (bradycardia and hypotension) effects. The nicotinic effects include muscular fa-sciculation and paralysis. CNS effects can include ataxia, confusion, loss of reflexes, slurred speech, coma, and paralysis. 

Few data on the cardiovascular effects of nerve agents in humans exist. In mild-to-moderate intoxi-... 

As noted in Chap. 4, toxic trauma to the RS and cardiovascular system (CVS) may occur as a direct effect on the lungs and the respiratory tree and also indirectly due to the effects on the brainstem-controlled breathing. Airways may be blocked by direct action (e.g. sulphur mustard) and by pharmacological actions (e.g. nerve agents). Box 7.4 summarises the presenting signs of toxic agents effects on the airways. 

Anesthetic techniques that have minimized adverse effects include the use of muscle relaxants and, more recently, nerve stimulators to assess adequacy of relaxation, the introduction of very rapid acting, short-duration barbiturates, and the use of atropinic agents to minimize the cardiovascular response to a combination of a seizure and anesthesia (93). In addition, 100% oxygenation (adequacy monitored by a pulse oximeter) with positive-pressure ventilation can minimize related cardiac events and memory disruption. 

Cardiovascular adverse effects are minimal with pancuronium. Ganglion blockade does not occur. Shght dose-dependent rises in heart rate, blood pressure, and cardiac output are common (5), but are often masked by the actions of other co-administered agents, such as fentanyl or halothane, which cause bradycardia or hypotension. These adverse effects of pancuronium are thus often beneficial and can be deliberately harnessed. Several mechanisms contribute vagal blockade via selective blockade of cardiac muscarinic receptors (6), release of noradrenaline from adrenergic nerve endings (7), increased blood catecholamine concentrations (8), inhibition of neuronal catecholamine reuptake (9-11), and direct effects on myocardial contractility (12). These have been reviewed (13-15). 

---