Spontaneous respiration

Ethanol is classified for medical purposes as a central nervous system (CNS) depressant. Its effects—that is, being drunk—resemble the human response to anesthetics. There is an initial excitability and increase in sociable behavior, but this results from depression of inhibition rather than from stimulation. At a blood alcohol concentration of 0.1% to 0.3%, motor coordination is affected, accompanied by loss of balance, slurred speech, and amnesia. When blood alcohol concentration rises to 0.3% to 0.4%, nausea and loss of consciousness occur. Above 0.6%, spontaneous respiration and cardiovascular regulation are affected, ultimately leading to death. The LD50 of ethanol is 10.6 g/kg (Chapter 1 Focus On). 

Ingestion of ethanol acts on the central nervous system. In moderate amounts, it affects Judgment and lowers inhibitions. Higher concentrations cause nausea and loss of consciousness. Even at higher concentrations, it interferes with spontaneous respiration and can be fatal. 

A rare genetic variant is found in some patients who possess a form of butyrylcholinesterase, the metabolizing enzyme, for which succinylcholine has a very low affinity. The consequences are greatly prolonged duration of achon of the relaxant. Patients fail to resume spontaneous respiration, and often have to be artihcially ventilated, sometimes for days, before the relaxant effect disappears. 

Rarely, prolonged apnea may occur in those susceptible because of an inability to adequately metabolize succinylcholine (i.e., increased pseudocholinesterase levels). This condition requires continued positive-pressure ventilation until the patient begins spontaneous respiration. 

Dosages and routes of administration Alfentanil is only used parenterally. Because of strong respiratory depression administration under spontaneous respiration has to be confined to a dose range up to 200 pg/h. Higher doses as used in anesthesia need assisted ventilation. 

Stage IV. Medullary Paralysis. This stage is marked by the cessation of spontaneous respiration because respiratory control centers located in the medulla oblongata are inhibited by excessive anesthesia. The ability of the medullary vasomotor center to regulate blood pressure is also affected, and cardiovascular collapse ensues. If this stage is inadvertently reached during anesthesia, respiratory and circulatory support must be provided or the patient will die.39... 

All enteral feeds were stopped. The baby was given intravenous glucose, L-arginine, sodium benzoate, and sodium phenylacetate. Hemodialysis was initiated. At this time, there were no spontaneous respirations, there was no response to painful stimuli, and brainstem reflexes were absent. The plasma amino acid results revealed a glutamine level of 1500 pmol/L (normal 254-823), and citrulline was undetectable (normal 10-34 pmol/L). Quantitative carnitine, plasma acylcarnitine, and urine organic acid profiles were normal. The urine orotic acid concen-... 

A Statham pressure transducer is placed into the right femoral artery for continuous measurement of blood pressure. Spontaneous respiration is maintained through a tracheal tube. 

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. 

Apnea of variable duration results from muscle paralysis. The return of spontaneous respiration is normally rapid, but it may be delayed if phase II block develops. This will only be of consequence if it is not detected and spontaneous respiration is permitted before it is adequate. Exacerbation of muscle weakness in Duchenne muscular dystrophy after injection of suxamethonium can lead to delayed respiratory failure postoperatively (29). 

It is common to find a pharmacist as a member of the hospital cardiopulmonary resuscitation (CPR) team, which responds to emergent situations that may require immediate patient care. These scenarios usually involve a patient who suddenly becomes nonresponsive, ceases spontaneous respirations, and/or experiences a life-threatening cardiac arrhythmia. The CPR team responds to such patients by implementing advanced cardiac life support (ACLS), which involves quick provision of an airway and electrical (defibrillation) and/or pharmacologic interventions to sustain cardiac function. The pharmacist s role on such a team involves the preparation of intravenous infusions needed in an emergent situation, dose calculations, and consultation regarding appropriate medication use. 

The nature of the dose-response curves for succinylcholine in subjects with atypical esterase has one important consequence for the understanding of abnormal clinical events. A usual dose of succinylcholine (50 to 100 mg) injected intravenously into a subject lacking cholinesterase activity causes complete paralysis of the respiratory muscles for 1 hour or so in clinical practice, this means that as much as 2 hours may elapse before adequate spontaneous respiration is restored—perhaps in exceptional cases, even 3 hours. However, an effect which lasts still longer than this period cannot be explained solely as a consequence of cholinesterase dysfunction, and the fault is likely to be in muscle. The elimination of the drug in subjects lacking esterase function is probably due to renal excretion and nonenzymatic hydrolysis. 

A. Supportive Measures. Measures should be taken to lower temperature relieve pain maintain spontaneous respiration and secure an intravenous access for the administration of drugs and fluids. Symptomatic treatment and treatment of coexisting injuries should follow established principles. 

Stage IV Spontaneous respiration ceases. Inhibition of medullary vasomotor centers leads to circulatory collapse. Circulatory and respiratory support must be maintained, or death rapidly ensues. (See Figure.)... 

Respiratory System Spontaneous respiration is rapid and shallow during halothane anesthesia. The decreased alveolar ventilation results in an elevation in arterial CO tension from 40 mm Hg to >50 mm Hg at 1 MAC. The elevated CO does not provoke a compensatory increase in ventilation, because halothane causes a concentration-dependent inhibition of the ventilatory response to COj. Halothane also inhibits peripheral chemoceptor responses to arterial hypoxemia. Thus, neither hemodynamic (tachycardia and hypertension) nor ventilatory responses to hypoxemia are observed during halothane anesthesia, making it prudent to monitor arterial oxygenation directly. 

In summary, spontaneous respiration will stop within several minutes after onset of effects caused by exposure to a lethal amount of nerve agent. Antidotes alone are relatively ineffective in restoring spontaneous respiration. Attempts at ventilation are hindered by the high resistance of constricted bron-chiolar muscles and by copious secretions, which may be thick and plug the bronchi. Ventilatory assistance may be required briefly (20-30 min) or for a much longer period. In several instances, assistance was required for 3 hours18,63 this seems to be the longest reported use of ventilation. 

The triad of consciousness, lack of convulsive activity, and spontaneous respiration is an indicator of a good outcome, provided adequate therapy is given early. 

Supporting this view is a report from the Tokyo subway terrorist incident of 1995. One hospital received two casualties who were apneic with no heartbeat. With vigorous resuscitation, cardiac activity was established in both. One resumed spontaneous respiration and walked out of the hospital several days later, and the other did not start breathing spontaneously and died days later. These anecdotes suggest that when circumstances permit, resuscitation should be attempted. In a contaminated area where resources, including personnel, are limited, the use of ventilatory support and closed chest cardiac compression must be balanced against other factors (see above), but the immediate administration of diazepam and additional atropine requires little effort and can be very rewarding in the casualty who still has apparent cardiopulmonary function. Cyanide... 

Determine whether patient is conscious and has spontaneous respirations and palpable carotid pulse. 

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