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TITLE: Anesthesia
SOURCE: Grand Rounds Presentation, UTMB, Dept. of Otolaryngology
DATE: February 2, 2000
RESIDENT PHYSICIAN:Russell D. Briggs, M.D.
FACULTY PHYSICIAN: Francis B. Quinn, M.D.
SERIES EDITOR: Francis B. Quinn, Jr., M.D.
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Despite the synthesis of ether in 1540 by Valerius Cordus, the use of anesthetic agents in a medical setting represents a totally American contribution to medicine. Dr. Crawford W. Long, a rural doctor in Georgia, first used inhalational ether to anesthetize a patient for neck surgery in 1842. Unfortunately, his work was not publicized. In 1846, Boston dentist William Morton demonstrated the anesthetic effects of ether in front of a live audience at Massachusetts General Hospital. He anesthetized a patient undergoing resection of a submandibular mass by a prominent surgeon of the time, Dr. John C. Warren. With its publication in the Boston Daily Journal the next day, the civilized world came to know of the discovery of surgical anesthesia. That same year, nitrous oxide was also used as an anesthetic agent, although its use was well known in England at social events to induce frolicking. The next year, Dr. James Simpson used chloroform to relieve the pain of labor. The use of chloroform gained public acceptance after Queen Victoria in 1853 was administered this drug by Dr. John Snow, the first physician to devote his life to anesthesia.
Numerous other developments paved the way for modern anesthesia to flourish. The endotracheal tube was discovered in 1878 which protected against the drug-induced respiratory failure. Nerve block anesthesia with cocaine was popularized by Halsted in 1885 with epidural and spinal anesthesia emerging shortly thereafter. Intravenous agents became increasingly popularized after sodium thiopentone was first used in 1934. The current concept of "balanced anesthesia" was first introduced after curare was used in anesthetic practice in 1942. Over the next fifty years, many additional anesthetic agents have been developed and refined with anesthesia emerging as an important specialized field in medicine.
Basic Principles of General Anesthesia
Anesthesia is defined as the absence or abolition of sensation. This term should be differentiated from analgesia which is defined as the absence or abolition of pain. General anesthesia involves rendering a patient unconscious whereas local anesthesia (or more correctly local analgesia) is aimed at blocking conduction of nerves to the operative site. In order to provide safe,as well as adequate general anesthesia, the anesthesiologist must combine the need for unconsciousness, the need for analgesia, and the need for muscle relaxation to provide the best operative conditions for the surgeon. This so-called triad of anesthesia can be achieved with the use of only one drug, however side effects have limited the successful application of single line agents in modern anesthesia. Therefore, utilizing various drugs for their particular muscle relaxing, sleep producing, and analgesic properties, anesthesia can be safely and properly maintained.
Four main stages of general anesthesia are recognized regardless of the method in which the anesthesia is delivered. These stages are based upon the patients body movements, respiratory rhythm, oculomotor reflexes, and muscle tone. In general, a patient in stage one is conscious and rational, however the perception of pain is diminished. Stage one is commonly termed the analgesia stage. Stage two, the delirium stage, is marked by the patient becoming unconscious, however the body responds reflexively and irrationally to stimuli. Breath holding may be present and can result in hypoxia, however tone is maintained in pharyngeal muscles and a patient can maintain and protect their own airway. Pupils generally become dilated. Stage three, the surgical anesthesia stage, is characterized by increasing degrees of muscular relaxation. Protective pharyngotracheal reflexes are absent and the patient is unable to protect the airway. Stage four is medullary depression. This stage is characterized by cardiovascular and respiratory collapse due to depression of the cardiovascular and respiratory centers in the brain stem.
Each anesthetic agent has a varying effect on the pattern of surgical anesthesia. For example, certain agents are highly analgesic (nitrous oxide) whereas others do not show stage I (thiopental). For a particular agent, the stage or depth of anesthesia must be judged with reference to the known sequence of signs for that agent. Various anesthetic agents are used to achieve the aforementioned stages for general anesthesia. These include inhalational agents, intravenous agents, analgesic agents, and muscle relaxants. Local anesthetics represent a category of anesthesia outside the realm of general anesthesia and will be discussed separately.
Inhalational Anesthetic Agents
Inhalational anesthesia refers to the delivery of gases or vapors into the body via the respiratory tract to produce anesthesia. Through uptake and distribution, some portion of the anesthetic agent is presented to the nervous system, resulting in the absence of sensation. Understanding the induction, maintenance, and recovery from an inhalational anesthetic requires applications of the pharmacokinetics of the particular drug. In general, the aim in giving an inhalational anesthetic is to readily achieve a partial pressure of that anesthetic in the brain sufficient to keep the patient asleep and maintain that partial pressure until the operation is complete. Certain factors such as the solubility of the anesthetic agent, cardiac output of the patient, and alveolar ventilation of the patient will influence the ability of the anesthetic to achieve its result.
An important concept in comparing inhalational anesthetics is knowing their measure of potency called the minimum alveolar concentration (MAC). It is defined as the concentration of a particular inhalational anesthetic at one atmosphere pressure in which 50 percent of patients do not move in response to a skin incision. Minimum alveolar concentration is analogous to the ED50 value computed from a pharmacological dose-response curve. Therefore, the potencies (as well as side effects at similar potencies) of different inhalational agents can be compared; so can combinations of agents. In general, a half MAC of each of two inhalational anesthetics is equivalent to one MAC of either. This concept not only has clinical applications but also suggests that the fundamental mechanisms by which these inhalational agents induce anesthesia are similar. The use of MAC in comparing the potency of different anesthetic gases has been criticized because it measures only a single point, the abolition of muscular response to pain. The concept fails to recognize the importance of the slope of the response curve. Other comparisons have been advocated (e.g. MAC/AWAKE ratios) however the MAC is the most widely used.
All the inhalational agents impair respiratory and circulatory function as well as influencing every organ system in one way or another. Some of these actions do not accompany the anesthetic effect but are side effects that must be appreciated when these agents are utilized. The potency, systemic effects, and specific side effects of the most commonly used inhalational agents will be discussed.
Nitrous Oxide
Nitrous oxide (N2O) was first prepared by Priestly in 1776 (prior to the isolation of oxygen) and its anesthetic properties described by Humphry Davy in 1799. Dr. Davys thought was that this inorganic gas might "be used with advantage during surgical operations" went unheeded until the mid 1800s. Nitrous oxide is characterized by its inert nature--it undergoes only minimal metabolism. It is colorless, tasteless, and odorless. It does not burn but will support combustion, so it cannot be taken for granted in a high-risk environment (laser surgery). It is stored as a liquid at 50 atmospheres in a cylinder.
The major difference between nitrous oxide and the rest of the inhalational agents is its low potency. The MAC of this agent is 105%, unreachable at normal atmospheric pressure in oxygen concentrations compatible with survival. The value of this agent is its ability to produce different effects over a wide range of inspired concentrations. It is a weak anesthetic but powerful analgesic. Patients will have some degree of analgesia at 50% nitrous oxide and may become amnestic at 66 2/3 %. Its drawback is the need for some additional agent to achieve full surgical anesthesia. It is poorly soluble in blood, and thus the onset and recovery times for nitrous anesthesia are brief (three to ten minutes).
Systemic Effects
Despite its relatively low potency, nitrous oxide affects most of the major body systems. It does cause direct mild myocardial depression, and although its general effects on heart rate and blood pressure are innocuous, it can cause major cardiovascular depression in patients with underlying hemodyamic compromise (hypovolemia, myocardial dysfunction, or septic shock). Nitrous has little effect on respiration and does not affect the neuromuscular junction to alter the requirement for a nondepolarizing neuromuscular blocking agent.
Side Effects
There are a number of special concerns with nitrous oxide that are not present with the other agents. Nitric oxide and nitrogen dioxide are both highly toxic to the lung and fortunately have largely been eliminated as impurities from the manufacturing process. There is a very real danger of administering a hypoxic mixture of nitrous oxide-oxygen mixture to a patient. The large volume of gas administered poses another problem. Although nitrous oxide is the least soluble anesthetic agent, it is still much more soluble than nitrogen. This means that the two agents take time to equilibrate across the alveolo-capillary membrane. At the beginning of anesthesia, nitrous oxide leaves the alveoli faster than nitrogen enters the lung, thereby raising the concentrations of oxygen, carbon dioxide, and any other inhalational agent used. Increasing the concentration of other inhalational anesthetics can speed induction at the beginning of a case, a phenomenon known as the second gas effect. At the end of anesthesia, the opposite is true. The alveolus fills rapidly with nitrous oxide and the nitrogen in the alveolus is unable to equilibrate as rapidly with the blood. This dilutes the oxygen present within the alvelous potentially creating hypoxemia especially if low levels of supplemental oxygen are used and the patient has a depressed state of consciousness at the end of a case. This phenomenon is termed diffusion hypoxia. The same principle applies when some portion of the body has trapped air, such as in a pneumothorax, bowel obstruction, air embolism, or with middle ear surgery. The displacement of tympanic membrane grafts is well described with the use of nitrous oxide anesthesia. Nitrous oxide also interferes with cell division. High concentrations will stop white cell formation after 36 hours of administration. It may also inhibit methionine synthetase thereby resulting in a megaloblastic or aplastic anemia. Under a similar mechanism, it can also inhibit vitamin B-12 metabolism producing its associated neurologic deficits.
Halothane for many years has been the most commonly used supplement to nitrous oxide anesthesia. It was synthesized by Suckling in 1956 with the hopes of being an ideal anesthetic agent. It exists as a volatile liquid with a distinctive aroma and is added to the gas mixture delivered to the patient by means of a vaporizer added to the anesthesia machine. It is a comparably stable compound, nonflammable, and easy to vaporize.
Halothane has a MAC of 0.75%, indicating that it is highly potent. It has poor direct analgesic properties which makes it a perfect complement to nitrous oxide. Halothane is very soluble in blood and fatty tissues and awaking from halothane anesthesia may be prolonged if attention is not given at the time of emergence.
Systemic Effects
Halothane has profound effects on various body systems. In addition to depressing consciousness, halothane reduces or eliminates the sympathetic response to painful stimuli. This depressant effect on the sympathetic nervous system also reduces the protective baroreflex response to conditions such as hypovolemia. Depression of the respiratory drive is also produced by halothane. Both the central response to carbon dioxide and the peripheral response to tissue hypoxia are depressed. The pattern of respiration produced by halothane is rapid, shallow, and monotonous with no sighs. Such a pattern predisposes to atelectasis. Halothane also depresses protective airway reflexes thereby placing the patient at higher risk of aspiration at induction. Halothane directly decreases myocardial contractility and heart rate and slows conduction through the AV and ventricular Purkinje system. Although some vasodilation occurs with halothane, the hypotension produced by this agent is primarily the result of myocardial depression and decreased cardiac output. Exogenous doses of catecholamines (e.g. during facial plastic surgery) may produce severe ventricular dysarrhythmias due to the myocardial sensitization.
Side Effects
One of the well-known complications of halothane is "halothane hepatitis". This syndrome appears following exposure to halothane and may produce fever, jaundice, and possibly massive hepatic necrosis and death. The mechanism is not clear but allergic reactions to halothane byproducts are implicated. It is an extremely rare occurrence but is seen in increased frequency in those patients who have suffered hepatic anoxia thereby increasing the concentrations of hepatotoxic metabolites. Halothane is also a well-known trigger for malignant hyperthermia. This anesthetic reaction is usually detected in young fit individuals who have inherited a susceptibility to this problem. It is characterized by masseter spasm, sustained muscle rigidity, myoglobinuria, and a rapidly rising core body temperature. These symptoms and signs are manifestations of a hypermetabolic state initiated by an inhibition of calcium reuptake into the sarcoplasmic reticulum of skeletal muscle. It is universally fatal unless total body cooling, vigorous hydration, and administration of dantrolene is delivered expeditiously.
Because of the disadvantages of the available anesthetics at the time, enflurane was developed in 1963 by Terrell and released for use in 1972. It is a stable, nonflammable liquid that is somewhat less volatile than halothane. It has a distinctive pungent odor that creates an unpleasant induction in a nonpremedicated patient.
Enflurane is slightly less potent than halothane with a MAC of 1.68%. Onset and elimination is similar to that of halothane.
Systemic Effects
The respiratory drive is depressed to a greater extent with enflurane than halothane, and the ventilatory response to hypoxemia is also decreased. Enflurane depresses cardiac contractility and heart rate more than halothane and produces a similar baroreflex response depression as halothane although sensitization to exogenous catecholamines is much less with enflurane than halothane. The metabolism of enflurane is one-tenth that of halothane thereby reducing its potential as a hepatotoxic agent. Its metabolism does release one fluoride ion which is potentially nephrotoxic but is rarely sufficient to produce clinical concern except in hyperthyroid patients and in patients taking rifampin. Fluoride toxicity presents as nephrogenic diabetes insipidus and, in extreme cases, high-output renal failure can occur.
Side Effects
There is one unusual side effect that is not seen with the other agents. At deep levels of anesthesia and with a lowered PaCO2, some patients show an epileptiform pattern on EEG. Even though no post-anesthetic neurologic sequalae have been attributed to this pattern, this drug should be avoided in patients with seizure disorders.
Isoflurane was synthesized in 1965 by Terrell but its development lagged behind that of its isomer enflurane because of difficulties in its synthesis, purification, and now refuted claims of carcinogenesis. It is nonflammable, and has properties similar to that of halothane and enflurane with a few striking exceptions.
Isoflurane is less soluble in blood than halothane or enflurane which affords a more rapid induction and recovery from anesthesia. Its disadvantage is its pungent odor which is difficult to administer to a conscious patient. With a MAC of 1.3%, isoflurane is less potent than halothane but more potent than enflurane in producing general anesthesia.
Systemic Effects
Isoflurane depresses the respiratory drive and the ventilatory response to hypoxemia in a similar degree to that of halothane, much less than its isomer enflurane. Although isoflurane is a direct cardiac depressant, cardiac output decreases less than with either halothane or enflurane. The baroreflex is inhibited but again less than either halothane or enflurane. Isoflurane is much less likely than halothane to produce arrythmias in the presence of circulating catacholamines. Isoflurane does however cause a significant reduction in the systemic vascular resistance, with a marked increase in blood flow to the muscle and skin. It is the most potent vasodilator of the previous three inhalational agents and the hypotension that results with its use is a result of it peripheral effects rather than its direct effects on cardiac depression.
Side Effects
Isoflurane does not create the elipetiform activity as seen with enflurane and may be used in seizure prone individuals. A major difference in this agent compared with the other is its extremely low level of metabolism in the body, thereby nearly eliminating the possibility of nephrogenic or hepatic toxicity.
Sevoflurane is a new fluorinated ether compound that has similar properties to the other fluorinated inhalational agents. It can produce mild respiratory and cardiac depression. It is not bronchoirritative and is characterized by a rapid degree of induction and recovery due to its low lipid solubility. It has a similar biotransformation profile as enflurane and may induce nephrogenic and hepatic side effects.
Desflurane is another new halogenated inhalational agent. It is also characterized by a low blood and lipid solubility which allows for rapid induction and emergence from anesthesia. It does produce bronchoirrative effects with a high incidence of breath holding, coughing, and laryngeal spasm. This agent is not as widely used for induction as the other inhalational agents. It is not metabolized to any appreciable degree and its side effect profile is advantageous.
Intravenous Anesthetic Agents
There are many ways to design an anesthetic plan to meet the requirements for general anesthesia: muscle relaxation appropriate for the procedure, unconsciousness, and analgesia. Intravenous anesthetics can meet these requirements and may be classified as nonopoids, opoids, and muscle relaxants. The nonopoid intravenous anesthetic drugs principally provide hypnosis and blunting of reflexes whereas the opoids (narcotics) and neuromuscular blockers provide analgesia and muscle relaxation respectively. In most surgical procedures, the induction of anesthesia is carried out by the use of an intravenous agent and is not an unpleasant experience. It has become customary to induce general anesthesia with an intravenous agent regardless of the subsequent agents to be used for maintenance.
Barbiturates and other Nonopoid Compounds
Barbiturates are commonly separated into classes based on duration of action and onset. In general, anesthesiologists prefer to use drugs that have a rapid onset of action but a short duration of action. Such drugs allow rapid titration to the required effect and are usually used to induce anesthesia. Thiopental sodium is the prototype drug in this class.
Thiopental is water soluble and stable in aqueous solution for weeks. It is generally prepared as the sodium salt and is quite alkaline in solution with a pH of 10.5. This alkalinity makes thiopental incompatible with many other acidic agents such as opiates, catacholamines, and some neuromuscular blockers. Because of this alkalinity, thiopental must be injected into a freely flowing intravenous line as extravasation can produce skin necrosis. Inadvertent intraarterial injection is a serious complication. A chemical endarteritis occurs and thrombosis of the artery may follow. Tissue ischemia and gangrene are potential complications. The use of less concentrated suspensions of thiopental (2.5%) can decrease this risk and is now the standard concentration used in practice today.
Thiopental is generally delivered as a bolus dose of 3-5 mg/kg. The drug is rapidly diffused into vessel-rich areas such as the brain and unconsciousness ensues within 10-15 seconds. Unconsciousness from thiopental results from dose-dependent suppression of neuronal activity within the central nervous system. This suppression is associated with a general decrease in cerebral metabolic rate. Despite this depression in metabolic rate, thiopental and other barbiturates are poor analgesics and, in low doses, may even increase the perception of pain. The CNS effects of thiopental go beyond producing unconsciousness. Adequate levels of thiopental depress cortical brain activity measured on an EEG to the point of electrical silence. The metabolism when the EEG is flat presumably represents the basal metabolic requirements of cell function. Thus, in patients with severe brain injury and increased intracranial pressure, an induction dose can reduce pressure in most cases.
The effect of thiopental on the cardiovascular system is varied. It may have a profound effect in some patients, whereas virtually no effect in others. Healthy patients may experience a transient decrease in arterial blood pressure with a mild compensatory tachycardia and return of blood pressure to normal. In this situation, cardiac depression is limited. In large doses, or in patients with limited ability to activate a baroreceptor response (patients taking antihypertensives or hypovolemic patients), myocardial depression is more pronounced. Adequate volume repletion and sympathomimetic drugs all play a role in treating the hypotension in these patients.
Thiopental also produces a dose-dependent depression of medullary and pontine respiratory centers. Carbon dioxide responsiveness is blunted as are ventilatory responses to hypoxia.
The short duration of thiopental was originally thought to be a result of rapid metabolism. It is now clear that this is due to the rapid redistribution of the drug into tissues. Metabolism eventually occurs via the liver.
Several newer drugs have been introduced to avoid the drowsiness associated with prolonged metabolism of the barbiturates. Etomidate is one of these newer agents and has a structural appearance similar to ketoconazole. In terms of onset, elimination, and reliability in producing unconsciousness, etomidate is similar to thiopental. It produces unconsciousness in less than 60 seconds at the usual induction dose of 0.2-0.4 mg/kg. As with thiopental, drug redistribution from the brain to other tissue accounts for its short duration of activity. Bolus doses cause less change in blood pressure and heart rate than thiopental and this drug has less depressant effect on cardiovascular function in patients with depressed myocardial function. It also produces less respiratory depression than thiopental. It does have several disadvantages that limit its use. There is a high frequency of myoclonic movements and pain with injection (due to propylene glycol). It has also been shown to produce cortisol suppression and Addisonian crises when used in debilitated patients.
Ketamine is an alkylamine structurally similar to phencyclidine (PCP) and produces a state of "dissociative anesthesia". An IV dose of 1-2 mg/kg may produce a cataleptic state characterized by intense analgesia, amnesia, and commonly a slow nystagmus with the eyes open. Systemic effects are characteristic of sympathetic nervous system stimulation. The more commonly observed include increases in heart rate, blood pressure, and cardiac output. Respiratory function is not depressed in normal patients and laryngeal reflexes are maintained. The onset of action is rapid (within a few minutes) and consciousness returns within 10-15 minutes although retrograde amnesia may be prolonged. A major disadvantage associated with its use occurs during emergence and consists of unpleasant dreams or even hallucinations. Benzodiazapines greatly reduce these side effects.
Propofol is a substituted phenol whose action is characterized by a rapid onset and short duration of action. Therefore, propofol is suitable for induction and can be used as a maintenance agent. The usual induction dose of 1.5-3 mg/kg produces unconsciousness within a matter of minutes and is metabolized quickly by the body. The major hemodynamic and respiratory effects of propofol are similar to those of thiopental. Like, thiopental, propofol decreases systemic blood pressure by dilating peripheral blood vessels. In patients with a blunted sympathetic response, profound hypotension may occur. Propofol mimics the action of thiopental by inducing a short period of apnea after bolus. Side effects are rare; the most common being the venous irritation upon administration (due to the soybean solvent in its emulsion). This can be diminished by the use of a large vein or injecting lidocaine IV prior to its administration.
Many benzodiazepines are available in the United States and are used primarily for the treatment of anxiety disorders. These agents are excellent in producing amnestic and sedative responses. Three benzodiazepines are available for IV injection and are commonly used in anesthesia practice: diazepam, lorazepam, and midazolam. Benzodiazepines induce amnesia and sedation secondary to potentiation of the inhibitory neurotransmitter gamma amino-butyric acid (GABA). Although sleep inducing doses of diazepam (0.3-0.6 mg/kg) or midazolam (0.2-0.4 mg/kg) may produce unconsciousness in two to three minutes, these drugs have a slower onset of action and a longer post anesthetic recovery period than thiopental. Because of this, benzodiazepines are less commonly used as induction agents, but are commonly used for sedation and to ensure amnesia. Diazepam is commonly used for premedication with a 5-10 mg IV dose. Induction with diazepam varies from 0.2-1.8 mg/kg dose and is marked by variability in onset and prolonged reactions. The effects of diazepam on the cardiovascular system are minimal. Mild decreases in blood pressure and heart rate are indicative of its sedative effect. There have been reports of respiratory depression with diazepam, however this response is dose dependent and can be marked if concomitant doses of narcotics are used. It is known to produce venous irritation when injected. Lorazepam (0.04 mg/kg) is slow in onset of action (10-20 minutes) and is not typically used as an induction agent. It is commonly utilized as an adjunct to regional anesthesia because of its profound anxiolytic and sedative effects. Pharmacological actions are similar to diazepam but longer in duration. Similar to diazepam, the parenteral form produces venous irritation and pain when injected. Midazolam is water-soluble and has a lower incidence of injection pain. As with the other benzodiazepines, induction with midazolam is slow and recovery is prolonged. Midazolam is twice as potent as diazepam and doses of 0.1 mg/kg are generally adequate. Because of its potential for depressing respiration, especially if given with narcotics, the respiratory response of these patients needs to be monitored. Intravenous benzodiazepines should be titrated to effect and the benzodiazepine antagonist flumazenil should be immediately available.
Narcotic Agonists (Opiods) and Antagonists
Narcotics have been used for centuries to control perioperative pain and anxiety. In the past twenty years, very large doses of narcotics have been used not only for analgesia but also to produce unconsciousness and suppress the usual hyperdynamic responses to surgery. The predominant effects of narcotics include analgesia, a depressed sensorium, and respiratory depression. These effects are dose related. Narcotics have minimal effects on the cardiovascular systems of healthy patients. Narcotics do not produce direct cardiac suppression and are widely used for induction and maintenance of anesthesia in patients with myocardial disease. In hypovolemic patients, morphine may precipitate hypotension from its vasodilatory effects. Bradycardia with large doses of narcotics can occur due to direct stimulation of the vagal nucleus, however in normal patients cardiac output is not compromised due to an increase in stroke volume. Side effects include nausea and vomiting, chest wall rigidity, seizure activity, and decreased gastrointestinal motility.
The mechanism of action of these agents is receptor mediated. The sites of this receptor activity are opiod-specific and are most commonly found in the amygdala and spinal cord. Many opiod receptors have been identified and three appear related to the analgesic and anesthetic effects of the narcotics. Stimulation of the mu receptor results in analgesia, respiratory depression, euphoria, and physical dependence. Kappa receptors mediate spinal analgesia, sedation, and meiosis. The omega receptors mediate hallucinations, dysphoria, and tachycardia. Meperidine, morphine, fentanyl, sufentanil, and remifentnil are commonly used increasingly potent narcotic agonists. Nalorphine is a concomitant narcotic agonist and antagonist which has less analgesic effects as well as less respiratory depression. Naloxone produces pure antagonistic effects with no known agonistic properties. It reverses analgesia and respiratory depression nonselectively. The duration of action is approximately 30 minutes with a typical dose of 1-2 ug/kg and additional doses may need to be delivered should the respiratory depression recur as the naloxone is metabolized. Hypertensive crises can occur in narcotic dependent patients in whom naloxone is delivered producing acute withdrawal symptoms.
Muscle Relaxants
There is more to anesthesia than simply rendering a patient unconscious and free of pain. In order to provide an optimal surgical field, an anesthetist must also control muscle tone as the current use of inhalational and intravenous agents do not fully achieve this goal. Since their first use in the 1940s, neuromuscular blocking agents have been developed to decrease the incidence of side effects, decrease their duration, and increase their onset of action. Muscle relaxants produce their desired effect at the neuromuscular junction, but also have nonspecific effects at other sites. In order to understand the mechanism of action of neuromuscular relaxing agents, it is necessary to understand the depolarization of nerves and subsequent muscle contraction. An action potential travels down an efferent nerve to the terminal neuromuscular junction or motor end plate. Upon arrival, the action potential stimulates the release of acetylcholine from the synaptic vesicles into the postsynaptic cleft. The acetylcholine subsequently attaches to nicotinic receptors located on the postjunctional membrane. Should two acetylcholine molecules attach to the acetylcholine nicotinic receptor, the receptor will open allowing an influx of sodium ions into the muscle cell and depolarizing the motor end plate. The acetylcholine rapidly diffuses away from the motor end plate and is hydrolyzed by the enzyme acetylcholinesterase. The end-plate potential returns to resting potentials due to an active Na-K pump and prepares for the next stimulus. Neuromuscular blockade occurs when the normal events are disrupted at one or more sites. The two classes of commonly used neuromuscular relaxing agents include nondepolarizing and depolarizing agents.
Nondepolarizing Muscle Relaxants
All nondepolarizing muscle relaxants bind to and competitively inhibit the end plate nicotinic cholinergic receptor. With the competitive blockade, an increase in the concentration of a nondepolarizing relaxant at the multiple neuromuscular junctions of each myofibril will increase the density of muscle paralysis. Conversely, drugs that inhibit acetylcholinesterase increase the amount of acetylcholine near the end-plate and competitively "reverse" the neuromuscular blockade.
Nondepolarizing neuromuscular blocking agents can be classified into intermediate acting (15-60 minutes) and long-acting agents (over 60 minutes). This characteristic is arbitrary as the duration of action is dose dependent. Intermediate acting nondepolarizing agents include atracurium, vecuronium, and mivacurium, whereas the long acting drugs include pancuronium, metocurine, d-tubocurarine, and gallamine. The intermediate acting drugs in comparison to the long acting muscle relaxants have a similar rate of onset of neuromuscular blockade (3-5 minutes) but are relatively independent of renal function for clearance and evoke less circulatory effects. Most of these drugs have hemodynamic effects. Tubocurarine is known to block autonomic ganglia which can suppress sympathetic discharge and can decrease systemic vascular resistance. In addition, tubocurarine is known for its potential in mast cell degranulation with subsequent histamine release and severe hypotension. Pancuronium is well known for its inhibition of vagal and muscarinic receptors and commonly produces tachycardia with its use.
When muscle relaxation is no longer needed, any residual effects of the neuromuscular blocking agent are "reversed" to ensure appropriate muscle function and to sustain ventilation. Anticholinesterases inhibit actylcholinesterase, thereby increasing the concentration of acetylcholine. The three commonly used drugs for this purpose are neostigmine, edrophonium, and pyridostigmine. The increased concentration of acetylcholine may cause bradycardia and hypotension due to stimulation of the muscarinic cholinergic receptors on the heart. These unwanted side effects can be reduced by the preadministration of a muscarinic blocker such as atropine or glycopyrrolate prior to its administration.
Depolarizing Muscle Relaxants
Depolarizing muscle relaxants bind and depolarize the end-plate acetylcholine nicotinic receptors. This depolarization continues as long as the receptor is occupied. Succinylcholine is the only depolarizing muscle relaxant used clinically. Its duration of action with the typical induction dose of 1 mg/kg is very short (five minutes) because of rapid hydrolysis by plasma cholinesterases. Patients with abnormal production of plasma cholinesterase due to genetic abnormalities cannot hydrolyze the succinylcholine resulting in prolonged paralysis.
There are several characteristics unique to succinylcholine that may cause undesired effects. The sustained depolarization by the administration of succinylcholine typically produces transient fasiculations. Fasiculation of damaged or weakened myocytes may cause myocyte rupture and intracellular extravasation of potassium in patients at risk (burn patients, trauma patients, and patients with neuromuscular disease). Postoperative myalgias of the muscles of the neck, back, and abdomen are occasionally seen with its use. It is speculated that unsynchronized contractions of skeletal muscle fibers may lead to this side effect. Prior administration of a nondepolarizing muscle relaxant (tubocurarine) can attenutate its incidence. Sinus bradycardia, junctional rhythms, and even sinus arrest may follow its administration. These responses likely reflect the action of succinylcholine at cardiac postganglionic muscarinic receptors where this drug mimics the normal response of acetylcholine. These effects are more likely to occur with doses given close together. Atropine, the muscarinic receptor blocker, can attenuate these effects if given prior to its administration. Increases in intraocular pressure, intragastric pressure, and trismus have been associated with the use of succinylcholine. Patients who develop severe trismus with the use of this drug should be considered susceptible to the triggering effect of succinylcholine on malignant hyperthermia.
Techniques in General Anesthesia
Prior to the initiation of general anesthesia, a thorough history and physical examiniation is warranted. Previous reactions to any of the general anesthetics or a family history of reactions should be noted. Any potential cardiac or pulmonary risk factors should be elicited as these two organ systems are the most commonly affected by general anesthesia. An extensive cardiac and pulmonary evaluation should be made in those patients at risk so that potential risk-reducing interventions can be performed preoperatively.
With an adequate understanding of the drugs used in achieving general anesthesia, it is useful to understand the techniques used to induce and to maintain general anesthesia throughout a surgical case. As discussed earlier, induction of general anesthesia is most often accomplished by the intravenous administration of thiopental. Shortly thereafter, succinylcholine is also administered to produce skeletal muscle relaxation so as to facilitate direct laryngoscopy for intubation of the trachea. This injection of drugs (barbiturates, benzodiazepines, opoids, etomidate, ketamine, or propofol) to produce unconsciousness followed immediately by succinylcholine is referred to as a "rapid sequence induction". Preoxygenation prior to the administration of the drugs minimizes the likelihood of arterial hypoxemia developing during the period of apnea. A dose of tubocurarine prior to the succinylcholine can reduce the fasciculations induced by the depolarizing muscle relaxant. An alternative to this rapid sequence induction is the inhalation of nitrous oxide plus a volatile anesthetic. An inhalational induction is commonly utilized for pediatrics patients, particularly when insertion of an IV catheter is not practical.
After successful induction and intubation of the patient, maintenance of anesthesia aims at the aforementioned goals of analgesia, unconsciousness, skeletal muscle relaxation, and control of sympathetic responses to the noxious stimuli. These objectives are most commonly met by the use of a combination of drugs discussed earlier. Typically, nitrous oxide is the most frequently used inhalational anesthetic. It is commonly used in conjunction with an opoid or volatile anesthetic. For muscle relaxation, a nondepolarizing muscle relaxant is also commonly utilized to maintain a motionless surgical field.
Local Anesthetics
The introduction of local anesthesia followed that of general anesthesia by about 40 years. In 1884, Koller introduced cocaine as an effective topical anesthetic for the eye. Later that year, American surgeon Halsted employed cocaine to produce the first nerve block by local injection. Because of cocaines ability to produce psychologic dependence and its irritant properties when used topically, a search was made for improved local anesthetics. In 1905, Einhorn synthesized the first synthetic local anesthetic, procaine, and by 1943, lidocaine was successfully synthesized and employed for use.
Local anesthetic drugs are used clinically to reversibly inhibit the generation and conduction of impulses from an area of the body. Local anesthetics produce conduction blockade of nerve impulses by preventing increases in permeability of nerve membranes to sodium ions. Failure of this permeability to sodium ions slows the rate of depolarization such that threshold potentials are not reached and action potentials are not propagated. It is likely that the local anesthetic enters the sodium channel from the axioplasmic (inner) side of the nerve membrane and attaches to a receptor about halfway down the channel. While the local anesthetic is within the sodium ion channel, it prevents the sodium ion movements necessary for depolarization. Although a local anesthetic drug is injected to produce blockade of nerve impulses, the drug is subsequently absorbed away from the nerve site and appears in the circulation. The concentration of the drug in the blood is directly related to the systemic effects of the local anesthetic. Local injection into highly vascularized areas such as the hypopharynx, nose, and trachea produces maximal levels that approach that of intravenous injection. Topical application, however, results in blood levels that are one-third that of IV injection. Most of the local anesthetics (with the notable exception of cocaine) are vasodilators, thus necessitating the addition of epinephrine or phenylephrine to aid in vasoconstriction. This addition minimizes the risk of systemic toxicity and allows for a bloodless field. Of interest, the addition of 1:100,000 or 1:200,000 provides the same vasoconstricting effects at the doses typically used for injection. The site of metabolism of a local anesthetic drug is determined by the chemical structure of the drug. Local anesthetics can be divided into two groups, depending on whether they have an ester linkage (cocaine, procaine, benzocaine, and tetracaine) or an amide linkage (lidocaine, bupivacaine, prilocaine, mepivacaine). The metabolism of local anesthetics with an ester linkage are metabolized in plasma by plasma cholinesterase (the same agent that metabolizes succinylcholine), whereas the local anesthetics with an amide bond are broken down in the liver by hydrolysis and deakylation by the cytochrome p-450 enzyme system.
Local anesthetics tend to be linear molecules consisting of a lipophilic end and a hydrophilic end. The lipophilic end typically contains a benzoic acid moiety while the hydrophilic end contains a hydrocarbon chain that is ionizable. This is of use clinically because the non-ionized form readily penetrates membrane barriers (when the pH is high more is in the non-ionized state) whereas the cationic form binds more readily to the sodium receptor (typically when the pH is lower). Thus, tissue acidosis render local anesthetics ineffective because the local anesthetic is relatively cationic in this state and cannot cross the nerve membrane to bind to the receptor. The addition of sodium bicarbonate into the local anesthetic provides more anesthetic in the non-ionized form which allows it to readily cross the nerve membrane and produces local analgesia for extended periods of time (in addition to decreasing the pain involved with injection of the parent weak acid compound).
The major systemic toxicity of local anesthetic agents involves the central nervous system and the cardiovascular system. Because local anesthetics cross the blood brain barrier, toxic levels can produce both CNS excitability and depression. Initially, toxicity is manifested by light-headedness, circumoral numbness, and dizziness, followed by auditory (tinnitus) and visual disturbances. Drowsiness, disorientation, and a temporary loss of conciousness may follow. Slurred speech, shivering, muscle twitching, and tremors precede a generalized convulsive state (CNS excitability). Further increases in the local anesthetic dose results in cessation of convulsive activity, flattening of brain wave patterns, and respiratory depression, consistent with generalized CNS depression. Local anesthetics can produce profound cardiovascular changes by direct cardiac and peripheral vascular effects. It is manifested by myocardial depression and peripheral vasodilation. Inadvertent, rapid intravenous injection of an excessive dose can cause significant myocardial contractility and peripheral vasodilation resulting in profound hypotension and circulatory collapse. Other systemic effects of local anesthetics include methemoglobinemia and allergic reactions. Prilocaine when administered in large doses may result in accumulation of the metabolite, ortho-toludine, an oxidizing compound capable of converting hemoglobin into methemoglobin. With sufficient methemoglobin, the patient can appear cyanotic and the blood chocolate colored. This is easily revered by IV administration of methyline blue. Allergic reactions to local anesthetics are rare, despite their widespread use. Indeed, it is estimated that less than one percent of all reaction to local anesthetics are related to allergic etiology. Preservatives in the local anesthetic (methylparabenor) or breakdown products particularly of the ester groups (para-aminobenzoic acid) can produce typical allergic systems such as rash, laryngeal edema, bronchospasm. It is more likely that a systemic toxicity has occurred should any neurological or cardiovascular symptoms present. Treatment for a true allergic reaction is supportive. As there is no cross reactivity between classes of local anesthetics, the use of an amide local anesthetic may be used when an allergic reaction is documented for an ester group drug.
Preventing Toxicity
Local anesthetic toxicity primarily results from accidental intravascular injection or injection of an excessive dose. This must always be anticipated. Resuscitative equipment (oxygen, airways, bag and mask, suction), CNS-depressant drugs (diazepam, midazolam, and thiopental), and cardiovascular drugs (ephedrine, phenylephrine, epinephrine) should be on hand at all times. An IV should be started prior before any major regional anesthetic is started. Toxic reactions are best avoided by frequent aspirations during injection and slow, intermittent injection of the local anesthesia. When large doses are injected slowly and intermittently, the patient should be asked about symptoms related to CNS toxicity such as ringing in the ears, circumoral numbness, feeling of light-headedness, etc. Further, the slow injection rate allows dilution of the local anesthetic in the blood, so that high concentrations are not reached quickly. If signs or symptoms of systemic toxicity occur, the injection should be stopped immediately. In cases where large doses of anesthetic are used, monitoring should be employed including the maintenance of verbal contact, continuous ECG monitoring, noninvasive BP checks, and monitoring oxygen saturations. If convulsions or cardiac arrest occur due to local anesthetic usage, establishment of an airway, adequate ventilation, and support of circulation is mandatory. If the patient cannot be adequately ventilated, insertion of an oral airway after administration of succinylcholine (20 mg) can be useful. Should mask ventilation not be possible, tracheal intubation should be performed. CNS excitability (seizures) should be treated with small amounts of benzodiazepines (diazepam 5-10 mg). Hypotension is treated with alpha and beta agonists (ephedrine 5-10 mg or pheylephrine 40-80 micrograms). ACLS protocol should be instituted when life threatening cardiac dysrhythmias occur.
The use of cocaine dates back to the sixth century with South American Indians using the drug to induce euphoria, to reduce hunger, and increase work tolerance. With the placement of cocaine on the list of controlled narcotics in 1914, its legal use has been limited to topical application of anesthesia, particularly in the head and neck region. It is excellent for this purpose, having a rapid onset of action and a prolonged duration of activity. In addition, its strong vasoconstricting effects are unique among local anesthetics, providing decongestion and decreased risk of hemorrhage, obviating the need for epinephrine. The mechanism of action of cocaine is similar to other local anesthetics by blocking the sodium channel of the nerve membrane. It also is the only local anesthetic known to interfere with the reuptake of norepinephrine by the adrenergic nerve terminal and, in addition, prevents the uptake of exogenously administered epinephrine. This action leads to increased levels of circulating catecholamines and sensitizes target organs to the effects of sympathetic stimulation-- tachycardia leading to ventricular and atrial ectopy, vasoconstriction leading to severe hypertension, mydriasis, and an increase in body temperature. While theorectically being a contraindication, the subcutaneous injection of lidocaine with various doses of epinephrine in combination with topically applied cocaine is safe. The use of such dilute solutions of epinephrine and its slow release from subcutaneous tissues result in such low concentrations of circulating epinephrine as to be inconsequential if used with cocaine. Many references state that the safe maximal limit for cocaine is 200 mg (a 4% vial). Other authors mention 300-400 mg. Interestingly, the "safe" level for topically applied cocaine has not been based on scientific evidence, rather on early clinical experience when cocaine was injected for tonsillectomy anesthesia.
Special Anesthetic Techniques in Otolaryngology
Ear Surgery
Ear surgery provides numerous areas of concern for the surgeon as well as the anesthesiologist. A bloodless field for microsurgery is important and various techniques are employed to maintain this state. Preoperatively, local injection with a solution containing epinephrine can produce sufficient vasoconstriction. Maintaining low-normal blood pressure without excessive elevations and keeping the neck veins free of compression can do much to limit the bleeding associated with middle ear surgery. The middle ear is an anatomic air cavity that is prone to diffusion of nitrous oxide. If nitrous oxide is used during middle ear surgery and is not allowed to diffuse out of the middle ear space, an increase in intracavitary pressure can exist which can dislodge a tympanic membrane graft. Simply stopping nitrous oxide 15 minutes prior to placement of the TM graft can prevent this occurrence. Facial nerve monitoring is also an important concern in ear as well as parotid surgery. Eliciting a facial grimace or the use of facial nerve monitors are easily used methods of identifying and avoiding the facial nerve. The judicious use or elimination of muscle relaxants allows the facial nerve to be identified by these methods. The use of potent inhalational anesthetics during ear surgery cases can maintain a relaxed patient with preservation of facial nerve conductance.
The tonsillectomy is a common procedure performed in children and adults, however, numerous challenges are provided in anesthetic management. Patients commonly present with upper airway obstruction from enlarged tonsils, peritonsillar abcess, or sleep apnea syndrome. Careful attention to these possibilities is needed in order to anticipate the possibility of a difficult airway. Teeth should be inspected so that these do not become dislodged during induction or placement of the mouth gag. A patient that bleeds after a tonsillectomy represents a high risk induction. There is high rate of morbidity if not handled appropriately. The patient is at high risk for aspiration of digested blood and for the development of severe hypotension during induction due to hypovolemia. Adequate intravenous infusion should be started immediately. Blood should be immediately available for transfusion particularly if evidence of hypovolemic shock occurs.
The patient who is bleeding should be transported to the operating room in the semiprone position to facilitate the gravity drainage of blood from the oral cavity. Once in the operating room, the patient should be placed in the same position with the right side down (for a right-handed anesthesiologist). Assistants should hold the patient in this position during induction of anesthesia. A full size smaller tube should be available to deal with potential edema from the previous intubation. A high volume suction must be available. The patient is preoxygenated and an inhalation induction is employed. When adequate depth is reached for laryngoscopy, the patient is turned to the full lateral position with no support under the head. This allows the head and bleeding points to be below the level of the larynx. The laryngoscope is introduced and is lifted 45 degrees upward to give adequate view for intubation. An older child or adult may be intubated awake however effective use of topical anesthesia is unlikely in the face of severe hemorrhage in addition to the higher risk of inducing vomiting with laryngoscopy.
Facial Fractures
In severe facial fractures, the anesthetic management is complicated by the presence of blood, teeth, and bone fragments in the oral cavity and possibly the airway. Severe facial injury can be accompanied by fractures of the larynx or cervical spine. In addition, mandibular or maxillary fractures can present with significant trismus or airway obstruction. If one is called to evaluate a newly injured patient in acute respiratory distress prior to cervical spine X-rays, the airway should be established by cricothyrotomy or tracheotomy without manipulation of the neck. If the patient is known to be free of spinal fracture and is to be intubated for surgery, a decision must be made for oral or nasal intubation versus a tracheotomy. In the patient with severe midface fractures in the cribiform or nasoethmoid complex area, nasal intubation should be avoided whenever possible, both to avoid contributing to infection of the CSF and to avoid inadvertent insertion of the tube into the cranium. In the patient with a midface or mandible fracture, the tube may interfere with surgical manipulation. A major hazard with an endotracheal tube is the risk of carrying foreign bodies into the airway with the tube. In these cases, awake intubation with preparations for immediate tracheotomy should be performed.
Laryngeal Surgery
Surgery of the larynx provides numerous anesthetic considerations for both the surgeon and anesthesiologist. The anesthetic objectives are to maintain oxygenation and ventilation while the surgeon must have access to an unobstructed operating field. Communication is critical so that both goals can be met safely for the patient. For some cases with cooperative patients, topical laryngeal anesthesia can be achieved. Cocaine or aerosolized lidocaine is effective in achieving appropriate anesthesia of this area. Alternatively, a superior laryngeal nerve block can be performed. In most procedures, however, general anesthesia is usually required. The use of a small diameter cuffed endotracheal tube can allow for most laryngeal work to be performed safely and adequately. Should an endotracheal tube be a hindrance to the surgery planned, the intermittent apneic technique, jet-Venturi technique, or spontaneous respiration anesthesia technique can be considered. The use of neuromuscular relaxants and intravenous agents allow for appropriate oxygenation and ventilation in those circumstances where these methods are used. At other times, a small catheter placed just superior to the carina allows for adequate oxygenation and ventilation as well. With any of these methods, pulse oximetry and capnography is essential.
A carbon dioxide laser is also commonly used during laryngeal surgery. The risk of fire is always of concern when the laser is used. Certain measures should be undertaken to help reduce the risk of a fire. It has been determined that polyvinyl endotracheal tubes, even if wrapped in protective metallic tape, should not be used. Instead, laser resistant endotracheal tubes such as the Xomed Laser-Shield or Rusch red rubber tubes should be used and wrapped with metallic tape as an added protective mechanism. The safest anesthetic gas mixture has been found to be 30% oxygen in helium and up to 2% halothane has not been found to add any further fire risk. Additionally, the tube cuff should be protected by inflation with saline colored with methylene blue, neurosurgical cottonoids should be covered with saline, and the patients face should be fully covered with saline impregnated gauze. Finally, the use of pulse mode for laser use provides a significantly decreased risk of laser induced fire than that used in the continuous mode.
DiFazio, Cosmo A. Local Anesthetics: Action, Metabolism, and Toxicity. Otolaryngologic Clinics of North America 1981; 14: 515-519.
Dripps, Robert D., Eckenhoff, James E., and Leroy D. Vandam. Introduction to Anesthesiology: The Principles of Safe Practice. 1988; Saunders: Philadelphia.
Ellis, F.R. and I.T. Cambell. Essential Anesthesia. 1986; Blackwell Scientific Publishing: London.
Kem, William. General Anesthetics. Phase B Pharmacology 1996; University of Florida College of Medicine; 101-106.
Kem, William. Neuromuscular Blocking Agents. Phase B Pharmacology 1996; University of Florida College of Medicine; 115-118.
Kem, William. Pharmacological Basis of Local Anesthetics. Phase B Pharmacology 1996; University of Florida College of Medicine; 107-112.
Liu, Phillip L. Principles and Procedures in Anesthesiology. 1992; Lippincott: Philadelphia.
Longnecker, David E. and Frank L. Murphy. Introduction to Anesthesiology. 1992; Saunders: Philadelphia.
Ossoff, Robert H. Laser Safety in Otolaryngology-Head and Neck Surgery: Anesthetic and Educational Considerations for Laryngeal Surgery. Laryngoscope 1989; 99: 1-26.
Reynolds, Robert C. General Anesthetic Agents (What Every Surgeon Should Know About Anesthesia, But Has Been Afraid to Ask). Otolaryngologic Clinics of North America 1981; 14: 489-500.
Stern, Yoram, McCall, John E., et al. Spontaneous Respiration Anesthesia for Respiratory Papillomatosis. Annals of Otology, Rhinology, and Laryngology 2000; 109: 72-76.
Stoelting, Robert K. and Ronald D. Miller. Basics of Anesthesiology. 1989; Churchill Livingstone Inc.: New York.
Verlander, J. Michael and Michael E. Johns. The Clinical Use of Cocaine. Otolaryngologic Clinics of North America 1981; 14: 521-531.
Walts, Leonard F. Neuromuscular Blocking Agents. Otolaryngologic Clinics of North America 1981; 14: 501-513.
Younker, Dirk. Anesthesiology. In Bailey, B.J., ed. Head and Neck Surgery-Otolaryngology. Second ed. Lippincott-Raven: Philadelphia, 1998.
Posted 2/22/2000


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You're watching...
The Benefits of Moving Your Business to the Sunshine State
Former LPL Managing Director Steven Black on why he moved his business to Florida.
Feb 14, 2013
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Former LPL Managing Director Steven Black on why he moved his business to Florida.
Feb 14, 2013
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To the sunshine state Cheryl Casone is live in Miami Beach with more on that hi -- Well good morning Diane and taxes we'll pay -- but it's not just the taxes you pay on an annual basis every here.
Come April 15 -- tax you pay every single day every thing that you buy your gasoline your -- I don't -- things like that your rent but obviously there are expensive that businesses have to cover it -- something the difference between.
New York and Florida -- it comes to state and local taxes paid on a daily basis in New York.
At about eight and a half percent -- what if you look at Florida that combined state and local tax burden.
It is six and a half percent of the numbers right then and there.
They are astounding so -- -- business owners leaving new York and -- down to sunny and warm.
Florida outlook Stephen black is a former managing director LPL financial he did just that he joins me now here at the news cafe and Stephen you know latest figures -- years -- New York.
Europe Merrill Lynch your Bank of America -- -- you teamed up -- up want.
-- I love the warm weather and climate.
But it also has -- tax benefits not not for a person but also for the businesses.
From a business perspective.
You can save significant dollars.
Also took -- this is that a relocating now there acts to state is actually -- -- Tax benefits and tax savings to relocate.
There's also.
Tax credits to build capital infrastructures of new buildings.
So Florida is really looking just like these businesses.
To the states.
Talk about the stated and one of the things that governor Rick Scott has been doing it's a big initiative here Florida little bit controversial.
Is to -- get international businesses of course businesses from the United States that come and to Florida.
Set -- -- manufacturing facilities but it really -- the brokerage.
Houses the hedge funds that have been coming down the Florida the last couple for years but is it is -- technology is just easier to do business in Florida.
It is I think they try to make it with less regulations.
It's not as up -- and from our regulations standpoint no they edit plus two to monitor.
And -- report.
These regulations is very closely right.
But also there is also a lot of -- benefits for the employee standpoint.
You have but he did -- we'll cross delivered.
Compared to New York -- able -- -- -- quite a larger house maybe 3040%.
So what does that mean your family that a has it that a quality of life.
There's also the ability to Sharia and who who employees -- a lot of companies in New York having difficulties.
Recruiting people because they just don't wanna have that lifestyle and -- those according tax.
So I'm twentysomething.
Broker freshman -- college not got maybe a white and a couple of kids.
The -- -- have a New York City conventional less -- haven't Florida I mean there's just no comparison there is no -- Paris and I know that from an example I worked in Merrill -- new York and and I relocated.
Merrill Lynch in Florida years ago.
And it and it is it's night and day.
And I I just truly believed.
When you have a better quality of life -- have that if staff that are more productive.
Do you think that you know what everything he's he told me earlier that really that that -- New York is no longer the financial.
-- the world that we -- just become anti business what do you mean by that.
Well -- chest.
Everyday you turn around there's a new regulation there is more taxes.
And there is.
And then the cost of real estate there's no incentive for these businesses to stay in new York and with the modern age of technology.
You really could run your business elsewhere.
If you look around a lot of the New York trading systems.
There at a New Jersey they're not even in New York.
So it just shows that you don't have to be in the -- Manhattan I believe Charlotte's another example that they they became one of the largest pubs so unreal.
I don't mean I think it's highly -- tell you -- at this summit of the group of Brooklyn and that as you note.
Is that you know you're doing pretty well cared Florida's great to have you thank you very much server about a Donovan is that they -- -- say.
-- I mean really when you look at the overall structure the corporate tax structure of the art vs Florida and that's we're gonna be covering all day today it's very very different.
Capital in the 11 o'clock hour of markets now the -- -- how -- grants -- some -- it actually lives in new York and Florida he has a residence in both places.
I advisory chief analyst Erik Howard believes that is exactly what Steve was saying that that it's easier and to get.
Better talent better employees down her Florida off several -- tomorrow.
Fox Business called a -- -- -- -- -- -- Miami international -- -- big economic.
Boat coming to Florida Diane from the boat show that's all -- tomorrow right here on Fox Business back -- -- -- -- -- Casone live from Florida thanks Sheryl.
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Dating & Single Living
So you are finally going to meet that dream gal or guy for the very first time. What is your ideal setting for such an occasion?
Or if she's a dog person, maybe bring our dogs for a walk and play in the dog park. Dogs are perfect chaperones
Mass and Adoration. Then go for a stroll and perhaps end up having a pic nic by the beach or in some park where we can talk and have a laugh. Id leave the dinners and films perhaps for a second date.
Anna, absolutely right on, in my opinion.
depends on the person and what she is comfortable with... here are some examples of "first dates" I've had via CM:
- Lunch and the Mall of America
- Dinner and then a service at Church
- the State Fair
- met at a Cathedral, visited a future saint's tomb, and then to lunch and a walk by the lake
- met at a baseball game
- picked up at the airport, taken to dinner, and then to a thrift store, and a walk by the river (this being a long distance f2f, after six months of correspondence to get comfortable with each other)
Nothing overtly romantic, but rather meetings in safe places, with lots of other people around, with casual, pressure free converation, and at some point the opportunity to share our Spritual sides, even if only to stop to say grace before eating.


text:
STRATFORD, TEXAS -- Stratford resident Josh Willey is determined to make Congress and other lawmakers aware of the plight of Bowe Bergdahl.
Army Sergeant Bergdahl has been a Taliban prisoner since 2009.
Willey says he came across Bergdahl's story on Facebook and one thing led to another.
Soon he was actively lobbying for Bergdahl's release, enlisting the help of family, friends and authorities.
He says he's probably made at least 200 calls to legislators.
He says, "In one of his last videos he says, "I want to come home," over and over. For him to be over there, lonely, around people who don't like him…God only knows what's going on over there."
Sherman County Sheriff Joe Powell says, "It doesn't surprise me we have a citizen so willing to reach out…We're wearing the bracelets. What Josh did, he had bracelets made with Bowe's name, U.S. Army, the day he disappeared."
Stratford Police Chief Aaron Sheehan says, "If one guy can do that on his own, think what hundreds of us can do."
Willey says that's what he intends to do, to get more people involved, one person at a time, one phone call at a time.


text:
Tonight's the night Carrie Underwood plays her dream role of Maria von Trapp in the live television broadcast of The Sound of Music. Carrie has been learning the lines, the music and even a few dance steps for the three-hour show. Before you tune in, however, Carrie wants to make one thing perfectly clear -- this is NOT an adaptation of the movie version of the beloved classic. Watch The Sound of Music Live! tonight on NBC beginning at 8 p.m. The soundtrack is currently in stores. The DVD will be released on December 17th.
Photo: Pearl Records Inc.
Move over Duck Dynasty Christmas album…there's a new #1 on the country albums chart! Garth Brooks claims the top spot with his new boxed set called Blame It All On My Roots. The eight-CD compilation sold more than 163,000 copies in just three days. You can pick it up exclusively at Walmart.
Photo: Getty Images
Danielle Bradbery has been named the new face of SKECHERS and will appear in the company's global marketing and social media campaigns through 2015. The 17 year-old winner of The Voice will make her first appearance in the Spring of 2014 television and print ads.
Just 20 days til Christmas…Only NINE days until The Bull's Country Christmas Show at Wild Bill's with Cole Swindell! It's just five bucks to get in…get your tickets before the show sells out by clicking Cole's pic above! See ya there!


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We went thru this on another thread a year ago.
I was the dude that worked up the cockpit displays and weapon control algorithms for the Northrop-Grumman entry. Navy chose GD-McD entry.
Requirements were for a plane to replace the A-6 for interdiction and SEAD. Hornets would still be around as all-purpose jets.
Two-seater, plenty of range, and bays for the ordnance. There was also a requirement for AMRAAM and 'winders, so I had to allow for the internal carraige on those guys. No cannon. So look up the Intruder data and there you are, except the bad guys wouldn't be able to see the A-12 on radar until it was too late.
I never got to see the prototype and was really pissed.
One biggie is that stealth and carrier ops are hard to match up. This is especially true if you want the range that was required. The big delta of the finalist seemed to have good range capabilities, but we'll never know.


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text: There are some Bellefonte residents who eat here every day or every week. As a local I can say it may be an acquired taste but as a traveler I like to eat where the locals do so you don't end up in a dive. Jim's has been around for many years. Most love the house dressing and when it... More


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6 months ago
Apollo 79 Piece Multi-purpose Tool Kit for $32.99
@ kmart.com | 0 comments | tools, home-repair, diy
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7 months ago
Bicycle Puncture Tire Repair Kit w/ Patches, Tube, Rasp, Glue for $1.89 + free shipping
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7 months ago
2 Pack - Magnum Steel Incredible Epoxy Putty for $4.99 + free shipping
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8 months ago
12pc Computer Repair Tool Kit for $6.99 + free shipping
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12' Foot 10 Gauge Automotive Jumper Cable for $6.99
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Hakko FM204-CP Conversion Port for $640.36 + free shipping
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Techspray 1804-100F Size #4 Pro Wick Desoldering Braid for $24.95 + free shipping
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Jack Stands, 3 Ton Heavy Duty - Save $21 for $13.99
@ harborfreight.com | 13 comments | automotive, mechanic, repair, jack-stands
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Hakko FR802-11 Hot Air Rework System for $752.65 + free shipping
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Aquaseal UV - Ultra-Fast Sunlight Curing Adhesive for $7.99 + free shipping
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Mighty Mendit - As Seen on TV - See Video for $8.49 + free shipping
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16pc Deluxe T-Handle Ratchet Screwdriver Set w/ Assorted Bits for $7.99
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Sponsored Deals
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OK, yes, companies pay a little something to be Sponsored Deals. But we don't allow just any old crap in this section. Sponsored Deals are proposed to us by other retailers, manufacturers, and even other daily deal sites. If we find the deal compelling enough that our members will appreciate us bringing it to their attention, we'll feature it here. Believe it or not, we have a reputation to uphold. If your store would like to be considered for this space, please contact us for details. But if your deal is lame, or sketchy, no amount of money will let you buy your way in.
Community Deals
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Pretty much, anyway. This is where you find the deals that wooters like you have ferreted out and brought to light. We're thinking it'll turn into a massive database of discounted products from around the Web, constantly expanding to absorb the newest deals from the very moment their prices are slashed, with each deal immediately rated by hordes of savvy voters to spotlight the very greatest deals in the world today. Hey, we can dream, right?
We use a fancy algorithm to determine which deals are catching the most buzz – they're under the Popular tab, which is the default view of this section. You can look for the most popular deals today, this week, or this month. The Fresh tab features the most recently submitted deals, so that's where to look for deals that everybody else doesn't know about yet. And the Search bar does what a Search bar does, only, uh, much wootier! Yeah! Right on!
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Organic bullets? Vegetarian haggis? Cheap tickets to Antarctica? The best high-performance sweatsocks for under $100? If you're looking for a deal that doesn't appear to show up in our Community Deals section, throw the question to your fellow cheapskates. Or answer a question for one of your fellow cheapskates. Or vote for your favorite questions, or your favorite answers, or… maybe we should call this section "Ask, Answer, Comment On, And Vote In The Community", but that won't fit on the page.


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Posts Tagged 'Yogyakarta'
Student's Financial Management
Yogyakarta or Jogja is well-referred to as town of education student because it has numerous trustworthy colleges and schools along with other facilities that support learning atmosphere. Thus, many people all over Indonesia have an interest to carry on their study within this city. For college students who originate from another city, they generally rent an area inside a boarding house or employ a house using their buddies in the same city, or stick with their relatives.
Surely for 'migrant student', understanding how to be independent is essential since they're now from their parents' supervision. This means they need to manage themselves for instance controlling their time, keeping their companionship around the 'track', as well as controlling their financial.
For many wealthy students, it's not easy to handle financial factor given that they you can spend their cash with no 'buy this…' or 'don't buy that certain…' using their parents. Consequently, ultimately of month their cash frequently expires. The living cost in Jogja is low also it helps make the cost in Jogja cheap rival other metropolitan areas. So, a number of them enjoy spending their cash to visit shopping to purchase either books or clothes, to visit some areas in Jogja, or perhaps to possess some entertainment here.
However, students who've inadequate money are often more careful to invest their cash to ensure they are survive before the finish from the month. A number of them prepare their very own food and visit the college by feet and bicycle to become economical. They often search for a component-time job to assist their financial.
Finally, controlling cash is essential for 'migrant students' to be able to make sure they are learn to be independent as well as how you can be careful in handling and investing money. It's helpful then should they have listing of 'urgent needs' and 'wants' to allow them to have priority by bearing in mind the primary factor they need to buy. -Student


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Do they haul food to the bike kitchen with it? One track mind.
Fun until your 10th friend needs to move to a new apartment (all in one month) : )
Nice.... they could haul a lot of beer!
spiderLegGreen/ beer=foodadrienne/ that's a good point. mmmh.nick/ yes we'll take 3. make that kegs. wink
I read every comment. Sincere thanks for your readership.---xxo♥meligrosa /san pancho, califas.


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Vintage Trailer of the Day: The Odd Couple (1968)
Features By Scott Beggs on July 19, 2011 | Be the First To CommentThe movie that sparked an incredibly successful television show, this adaptation of the Neil Simon play (adapted by Neil Simon) was only the second film from Gene Saks – a director with a remarkably low output in his career. He worked almost exclusively with plays, and even though he didn't direct many movies, he churned out this classic alongside Mame, Cactus Flower and Brighton Beach Memoirs.
Walter Matthau and Jack Lemmon are in top form here in a surprisingly touching comedy that has sitcom sensibilities. This is the second movie they made together (out of ten), the first being The Fortune Cookie. As it happens, Robert Evans wanted their director there, the brilliant Billy Wilder, to write and direct here as well. As usual, money got in the way, but the movie turned out more than fine.
It makes a great double feature with Grumpy Old Men, and who could forget that theme music?
Let the film marketers of the past sell you on their movie by checking out more VTOTDs
Scott Beggs | Email
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Creamy Hot Apple Cider
apple cider
cinnamon candies (red hots)
dollop of vanilla or cinnamon ice cream
cinnamon sticks
Heat any amount of apple cider in a crockpot or in a mug in the microwave. Add red hots to taste. When hot, add a dollop of vanilla or cinnamon ice cream to each mug. Serve with a cinnamon stick to stir.
Sharry Waldriff
Lazy Man's Pierogi
1 - 16 oz. pkg. rotelle pasta
1/2 lb. bacon, chopped
2 onions, chopped
1/2 lb. mushrooms, quartered or 8 oz. canned, sliced mushrooms, drained
1 T. butter
1 - 16 oz. can sauerkraut, rinsed (but not too much) and drained
2 - 10.75 oz. cans condensed cream of mushroom soup
salt and pepper to taste
Preheat the oven to 350 degrees. Bring a large pot of lightly salted water to a boil. Add pasta and cook for 8 to 10 minutes or until al dente: drain. Place the bacon in a large deep skillet. Cook over medium high heat until evenly browned. Stir in onions and cook until translucent. In a separate pan, saute the mushrooms in butter. In a large bowl, combine the pasta, bacon, onion, mushrooms, sauerkraut and soup. Season with salt and pepper to taste. If it seems too thick, add a bit of milk to thin. Pour into a 9 x 13 inch baking dish. Bake in the preheated for 45 minutes.
Cynthia Amitrano
Wild Rice Hotdish
1 lb. ground beef, browned
1 c. celery, chopped
¾ c. onion, chopped
1 c. mushrooms, drained
1 can cream of mushroom soup
1 can beefy mushroom soup
½ lb. wild rice, cooked
1 - 8 oz. pkg. shredded cheddar cheese
1 T. butter
Brown the hamburger, onion and celery in the butter. Put it in a casserole. Add the rice, soups, and mushrooms. Top with cheese. Bake for 45 minutes at 350 degrees. For a quick version use 2 cans of cooked wild rice.
Kathy Oberg
Two Harbors
Tags: scrapbook, life, recipes, food


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We are probably all used to taking care of our own teeth, brushing twice a day and flossing once a day, but do you know when to start brushing your baby's first teeth? Do you know how to coax your opinionated toddler to brush their teeth twice a day? When to take your child for their first dental visit?
I always tell my patients that good oral health habits are formed before their children can walk or talk. If you start good habits early, it will likely make it easier to continue reinforcing good oral health habits that they can carry into their independent adult life.
When should I start brushing my child's teeth?
It is important for parents to know that tooth decay can start as soon as their
child's first tooth breaks through the gums, and this is when they should start
brushing their children's teeth. This could happen as early as 4 months or as late as 14 months. For children under the age of 2 we advise brushing with a soft child's size toothbrush and water. When your child turns 2, you can start using a pea sized amount of toothpaste on the toothbrush. If you are considering using fluoride toothpaste, you should speak with your child's dentist so they can monitor how much fluoride they are getting via supplements and other sources.
My child won't let me brush his/her teeth-what can I do?
It is important for parents to know that brushing your child's teeth is extremely
important in preventing cavities. It will be much easier to get them to brush than it will be to get them to sit through a cavity being filled! We can offer a few strategies that you can try:
- Try making brushing time fun, let them sit somewhere special, and sing them a favorite song as you brush.
- Try brushing your own teeth with your own toothbrush so your child can see that it's fun! Let your child brush your teeth with your toothbrush. Then tell your child it's her/his turn and use their toothbrush to brush their teeth.
- Try the 'I brush then you brush' technique. Here, you as the parent will brush your child's teeth, then your child will get a turn to brush their own teeth. Kids at this age tend to like being in control and this gives them that chance.
- Teach your child about brushing their teeth and then take them to a store where they can pick out their own special toothbrush. This will make it exciting for them to brush when they get to use the toothbrush that they picked out.
- Routine is extremely important, brush their teeth, read a book, and then sing a special song (or your own variation). It helps kids feel secure when they have structure and a routine that they can expect every morning and evening.
- There are many books you can purchase or find in the library that can help teach your child about taking care of their teeth. This can get your kids excited about brushing-first read a book about their favorite character getting their teeth brushed and visiting the dentist, and then it's their turn to brush!
When should I take my child for his first dental visit?
Dr. Magid recommends that you take your child for their first dental visit within 6
months of their first tooth appearing, and most definitely by their first
What should I expect at my child's first dental visit?
- At his or her first dental exam you can expect your child's dentist to check for cavities, oral injuries, or other problems.
- The dentist will clean your child's teeth and explain to you how you should be teaching them to take care of their teeth on a daily basis.
- Talk with you about any oral risk factors or thumb or pacifier sucking habits your child may have.
Dr. David Magid is a Family General and Cosmetic Dentist in Livingston, NJ. He graduated in 2002 from the University of Pennsylvania School of Dental Medicine and completed a residency at Columbia University in 2003. His office is located at 315 E Northfield Road, Livingston, NJ 07039. You can reach the office at (973) 992-8800 or find us on the web at LivingstonSmileDesign.com


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Recycle those doodads you've been saving for a good purpose by putting them on top of garden stakes. You'll have decorative stakes that can serve as garden art or be used to support veggies and vines.
What you'll need: • Material for stakes, such as bamboo, wood dowels, plastic pipe or broom handles • Nails, screws or epoxy glue • Everyday objects to top your stakes, such as drawer knobs, fishing bobs, large wooden beads, plastic Christmas ornaments, doorknobs, or twists of copper wire strung with beads and stuck in a cork
How to do it: Use a nail, screw or glue to attach the topper to the stakes. Make several at a time, then enjoy them in your garden.
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quick_silver (quick_silver) wrote in athinblackline, @ 2009-05-27 13:16:00 |
Entry tags: | quicksilver |
Who: Pietro Maximoff, OTA
When: Wednesday, May 27
Where: Blue Block--Amusement Park
What: Pietro ventures out on his own.
Of all people he should know better by now, but Pietro was dying for a smoke. He'd been cautious about getting friendly with any of the faces that didn't belong to his sister. This wasn't home, he didn't want to make attachments, he didn't want to make friends he'd be forced to leave behind, or fight, if things didn't work out as quickly as he hoped.
But he could no longer stand being coped up, and Wanda needed her space...he still felt guilty for their training experience. Hands in his pockets, he strolled in the direction of the amusement park, eyes darting about, hoping to come across someone he might be able to buy a smoke off of.


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Tommy Hanson's new delivery: where's the velocity?
by Kyle BoddyJuly 17, 2012
In February of this year, reporters noted that Atlanta Braves phenom Tommy Hanson would be altering his mechanics to reduce strain on his shoulder. In June of 2011, Hanson had been shelved on the 15-day disabled list due to shoulder tendinitis—more specifically, inflammation in the posterior (rear) aspect of the rotator cuff.
On the mechanical changes:
"I'm really just cutting out that pause," Hanson said. "I felt like I was throwing with all arm. Also, by changing, I could kill two birds with one stone as far as cutting down the running game. Somebody gets on and they have just run all day. I think it's going to help both."
However, it's no secret that, Hanson has started to struggle. He was beaten badly by the Mets on July 14, giving up six earned runs in 5.1 innings pitched, his strikeout rate has dropped significantly in the last year, and his fastball velocity has declined for a second straight year. It went from 92.7 mph on average in 2010 to 91.1 mph in 2011 (his injury probably played a big role here) and just 89.8 mph so far in 2012.
Some have wondered if Hanson's mechanical changes have caused the reduction in fastball velocity and have also questioned whether changing his mechanics will actually help protect his shoulder.
Hanson's mechanics: a comparison
Here's a look at Hanson's mechanics when comparing his 2010 version (93 MPH) to a 2012 version (90 MPH):
I used to be a big fan of Hanson's mechanics, but upon a closer look, I notice some deceleration issues. When comparing the videos, you can clearly see that in the 2010 version (dark jersey) he has significant arm recoil at the end of the throwing phase. Recoil tends to indicate poor deceleration/follow through and overly stresses the posterior aspect of the shoulder. In the 2012 version, you can see Hanson has significantly less arm recoil (almost none).
Hanson's arm recoil in 2010 is very clear in this slow-motion clip from the side:
While Hanson said his arm slot hadn't changed, PITCHf/x seems to disagree. Look at how his release point has morphed between last year and this year (controlling for time period):
(if it doesn't loop, right-click and open in new window to see the animation)
Hanson seems to use less violent rotation in the lower half in his revamped delivery, which he alluded to when interviewed about the subject. While he's cut down the "pause," it's still noticeable. I think it's misguided to say that the "pause" in his delivery is responsible for posterior shoulder stress; Hanson's upper body is simply too linear into follow through, which cuts off the deceleration path his arm can follow. Better shoulder rotation and sticking the pitching arm shoulder into the target will help with this; a great example is Trevor Bauer:
Mechanical conclusion
I think it's pretty clear that Hanson has cut down on some of the things that will stress his posterior shoulder: The recoil has been significantly diminished. However, so is his fastball velocity, and I highly doubt that will return. A better solution to cutting down on unnecessary posterior shoulder stress and retaining the fastball velocity may be learning to use the shoulders in a more complete manner to provide a longer, more efficient deceleration path. The "dart-throwing" aspect of his arm action is far down the list of things to worry about, if it's even something to focus on at all.
However, this is a perfect example that shows that rotation = velocity. Cutting down on rotation in hopes of solving another problem will come at a price. Can Hanson use these mechanics and diminished fastball velocity to return to form as a 3.20 - 3.80 xFIP kind of pitcher, a clear No. 2 in the rotation? Only time will tell. But while going from 93 to 90 might not be too bad, going from 90 to 88 could be a drastic difference to hitters, as fastball effectiveness does not diminish in a 1:1 ratio with lost velocity.
Kyle Boddy is the owner of Driveline Baseball and Driveline Biomechanics Research, both in Seattle, Washington. At his facility, he's melded statistical analysis, strength & conditioning, prehab/rehab, and advanced biomechanical analysis concepts to develop improved efficiency, durability, and fastball velocity of baseball pitchers. He is the author of The Dynamic Pitcher, a comprehensive book and video set dedicated to developing elite youth baseball pitchers.
He can be reached via email at email@example.com and found on Twitter: @drivelinebases.
<< Return to Article


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Five area golf teams and four local individuals advance to Division 2 District Golf tournaments after Tuesday's sectionals at Jaycees and Shawnee courses.
At Jaycees, Washington CH wins the team title, followed by Unioto, Fairfield Union, Adena and Logan Elm. Individuals to advance include Southeastern's Eli McKee and Westfall's Andrew Pettenski.
At Shawnee, Chesapeake takes the team title, followed by Wheelersburg, Portsmouth, Gallia Academy and Piketon. Daniel Heffner of Waverly and Lynchburg Clay's Tristen Willbanks also advance.
For complete details of the Jaycees match, click here...View Document


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Gucci Suede-Trimmed Alpaca, Angora And...
Men's Fashion Shopping Information for Australia
Buy Men's Fashion in Australia and compare prices on Men's Fashion before you buy in store on Lasoo, Australia's Shopping search engine. Find a cheap Men's Fashion sale at major Australian retailers. Our retailers have offers on Men's Fashion in shops in Sydney, Melbourne, Brisbane, Adelaide, Perth, Canberra, Hobart, Darwin and other cities around Australia, with new Men's Fashion offers added daily.
To read Men's Fashion reviews check out the Lasoo blogs for daily professional and consumer Australian product reviews.


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G.SKILL – world renowned for producing memory modules at extreme speeds, has once again proven as "a brand to be reckoned with" in the DDR3 memory sector by announcing the world's fastest DDR3 32GB Memory kit, adding 32GB kit to the world's dominating DDR3 Series – G.SKILL "Trident X." The new Trident X 32GB kit - F3-2800C11Q-32GTXD features 4 sticks of 8 GB memory modules, which will fit perfectly on Z77 chipset & IVY Bridge CPU, and it's also the one and only 32 GB Memory kit running @ 2800 MHz CL11 in the market today. Being the first to introduce such large capacity memory kit running at an incredible speed of 2800MHz, G.SKILL continues to impress power users/professional overclockers by offering the best memory solution with highest quality.
The last screenshot is not small and compressed enough. Please do the needful. Also, cannot wait for a review of those, or even some comparison tests to see if is really worth buying those over email@example.com for example..
I'll see what I can do. I'll have a G.skill review up very soon, but not these sticks. Perhaps after. Unfortunately, not many chips can run 4 sticks with 2800 MHz really. 2666 MHz seems to be the true max for IVB. Maybe G.skill poured some secret sauce on these here sticks though. Would be interesting to see.
Other than for entertainment, there isn't much value in DDR3 RAM above 1600 MHz. for typical desktop PCs as it's not a system bottleneck as extensive testing has proven. I know the RAM makers don't want consumers to know this but it's been documented by numerous reliable sources and you can test it yourself or read the tests at Tom's or Anandtech - to name just a few sources. DDR4 is a technology that may be useful for mobile devices and servers, but it doesn't offer anything tangible in performance for typical desktop PCs. LV DDR3 provides 98% of the power reduction and cost a whole lot less then DDR4 will. PCIe 3.0 is also a "paper advantage" that no one can derive a performance benefit from at this point in time. Those who don't know any better get all excited about stuff they don't understand and spend like drunks - which is exactly why Press Releases are sent out.
Maybe you mean GDDR? Best not to confuse DDR and GDDR. DDR4 spec is here, there is no reason why they would wait this long again just to develop another revision. There are a lot of changes to DDR4 that should prove to be rather interesting. As for skipping GDDR4, I have a Radeon HD 2600 XT with GDDR4 in it. I use it at work on my workstation.


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Assault on HAWORTH HALL, LAWRENCE, KS |
Assault - HAWORTH HALL, LAWRENCE, KS
Email to a friend Submit a Crime Tip |
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Google Streetview Disclaimer: This is a Google Maps Street View of the approximate area where the crime occurred. It is not necessarily the exact address view of the crime.
Local news for Lawrence provided by
Lawrence man charged with attempted second-degree murder (by The Capital-Journal)
John P. Barton, 23, was scheduled for a first appearance Thursday in the pro tem division of Douglas County District Court.
Jayhawks And Tigers: A Sports Rivalry Born Of Blood (by GPB.org)
Would you go to a bar to celebrate a massacre? That's a choice people in Kansas City are facing.
Lawrence police see uptick in home invasions (by Salina Journal)
Police are seeing a troubling rise in the number of drug-related home invasions committed in Lawrence, especially against young people who are considered easy targets.
Re: 150 years later, Quantrill's raid on Lawrence still stirs... (by The Wichita Eagle)
Pat Kehde is the great-granddaughter of Ralph and Jetta Dix. Ralph was shot and killed by one of William Quantrill's Raiders on Aug. 21, 1863.