The therapeutic use of musculoskeletal paralysis with non-depolarizing paralytic agents has increased largely because of the advent of exotic mechanical ventilation modes that require subjugation of the patient's normal ventilation activity . During such ventilation modes, paralysis may benefit ventilation efficacy by decreasing chest wall muscle tension and peak airway pressure. In addition, the disparate inhalation and exhalation timing necessary for these modes is difficult for the patient to tolerate, and paralysis is necessary to avoid the patient fighting against this unequal inhalation: exhalation (I:E) ratio. Other uses for therapeutic musculoskeletal paralysis such as `chemical restraint' to protect health care personnel from violent behavior , and the decreasing of cerebral blood flow during unstable intracranial pressure following head injury , are relatively rare.
Agitation episodes that threaten hemodynaimc stability are becoming more common in the ICU as a larger range of sick patients are identified are cared for. Life threatening agitation is usually signalled by escalating musculoskeletal hyperactivity in the face of increasing sedative administration. Eventually a point is reached where the direct effects of agitation combined with suppressive side-effects of pharmacologic agents threaten respiratory and hemodynamic stability. Agitated delirium syndromes, such as ethanol withdrawal, may constitute genuine medical emergencies as they have potentially disastrous hemodynamic and metabolic consequences and may become an indication for therapeutic musculoskeletal paralysis .
Severe agitation syndromes such as delirium tremens alter physiology and can precipitate hemodynamic deterioration by increasing musculoskeletal activity and metabolic activity to the point where increasing cardiac output cannot be sustained by cardiac physiology . This can precipitate angina, heart failure, and cardiac arrhythmias by increasing myocardial work and oxygen consumption in the face of a compromised coronary artery output . In addition, musculoskeletal hyperactivity produces metabolic acidosis that can precipitate arrhythmias and compromise oxygen delivery. Hyperactivity in muscle groups not used to increased work can cause myoglobinuria and renal failure as well .
If agitation resists the titrated effects of rapid-acting, short-duration sedatives and becomes so severe that hemodynamic stability is threatened, therapeutic musculoskeletal paralysis, endotracheal intubation and mechanical ventilation, and titrated hemodynamic support may be necessary to prevent cardiorespiratory collapse. True `suspended animation' can be induced to gain complete control of the situation early, rather than chance the increased hazards of partial control in unstable circumstances. Unlike benzodiazepines that cause musculoskeletal relaxation, non-depolarizing, neuromuscular, end plate neurotransmission antagonists affect therapeutic musculoskeletal paralysis. Suspended animation using musculoskeletal paralytic agents will effectively stop the effects of muscular hyperactivity on end organs. It is also extremely important to remember that underneath therapeutic paralysis lies unprotected cerebral function. Therefore, the amount of sedation needed to ameliorate the helpless feeling of paralysis in the awake state is virtually impossible to determine from any information gained by a physical examination or an objective sedation scale such as the Ramsay Score .
For the intensivist, advantages of the computer processed EEG are that the data are more easily interpreted by physicians not specifically trained in electroencephalography . This technology uses a single bipolar lead to accentuate trends in brain wave activity (mostly frontal cortex), which may then be interpreted more quickly in the acute care setting, resulting in a faster clinical intervention where needed. Sophistication in bedside EEG hardware is increasing, with multi-channel EEG recording, various data reduction functions such as the Bispectral Index, and evoked potential analysis becoming available to the ICU.
Modern cerebral function monitors survey brain electrical activity in real time and reflect changes in brain activity caused by sedatives and other therapeutics . There is accumulating evidence that regimens utilizing continuous infusion of sedative agents can be effectively titrated, assuring patient comfort and neuronal stability under paralysis, while the search for underlying pathology and effective treatment programs follows [35,36]. Different classifications and combinations of sedatives, analgesics or antipsychotics can be tried until the combination that brings about the most appropriately calm cerebral function tracing is discovered.