Should i sleep before anesthesia

You'll get specific instructions based on your age, medical condition, and the time of day of the procedure. Why is eating before surgery an issue? Because the body normally has reflexes that prevent food from being aspirated or inhaled into the lungs when it's swallowed or regurgitated thrown up.

But anesthetic medications can suspend these reflexes, which could cause food to become inhaled into the lungs if there is vomiting or regurgitation under anesthesia. Sometimes, though, the anesthesiologist will say it's OK to drink clear liquids or take specific medications a few hours before surgery. To ensure your safety during the surgery, you'll need to answer all of the anesthesiologist's questions as honestly and thoroughly as possible. Things that may seem harmless could interact with or affect the anesthesia and how you react to it.

You also can ask plenty of your own questions. If you don't meet the anesthesiologist before the day of the operation, you may want to ask your doctor or surgeon the following questions beforehand so you can have all the answers you need:.

You might be given a sedative before going into the operating room, but for minor procedures, this might not be needed. In fact, some people may prefer not to be sedated. The decision of whether or not to sedate you beforehand is made by the anesthesiologist, using your input. If general anesthesia is used, the anesthesiologist will start transitioning you from the normal awake state to the sleepy state of anesthesia. This is called induction , which is usually done by either injecting medicine through an IV or by inhaling gases through a mask.

If, like lots of people, you're afraid of needles, the good news is that you may not have to get one while awake. In this respect, the disk-over-water paradigm used in this study has been validated as able to produce near-total sleep deprivation while allowing nearly normal amounts of sleep when applied randomly.

This duration of rotation translated into 1. It is thus unlikely that fatigue or environmental stress was responsible for our observations. We did not measure end-tidal isoflurane levels or blood levels of propofol in this study. It is thus possible that our observations may have been partly the result of effects of sleep deprivation on pharmacokinetic properties of isoflurane and propofol.

Dehydration during the deprivation period, for example, may have altered drug disposition similarly with both anesthetic agents. We believed, however, that such effects were unlikely to fully explain our findings. First, the magnitude and direction of the sleep deprivation effect was similar for isoflurane and propofol.

To ascribe these effects solely to pharmacokinetic changes induced by sleep deprivation would require that deprivation affect the uptake and distribution of propofol and isoflurane equally. Because sleep deprivation with the disk-over-water paradigm typically induces polyphagia, 24 significant hypovolemia probably did not occur.

Second, no known mechanism links sleep deprivation to a pharmacokinetic change large enough to produce the results we observed.

In normal rats, a continuous infusion of propofol produces increasing blood levels for at least 30 min, indicating a reasonable correlation between blood levels and infusion duration.

With the disk-over-water paradigm, sleep deprivation results ultimately in death, but it requires approximately 2 weeks of continuous application to do so and is preceded by marked physical changes. Our results imply that adequacy of preoperative sleep may affect perioperative management. In addition to altering anesthetic potency, sleep deprivation in humans affects respiratory muscle strength, 27 adrenergic state, and cortisol secretion.

Finally, enhanced respiratory depressant effects of benzodiazepines and narcotics have been noted in patients with sleep apnea. In conclusion, we report a significant enhancing effect of sleep deprivation on the ability of isoflurane and propofol to reduce responsiveness to external stimuli in a rat model. When compared with rested rats, administration of either anesthetic in sleep-deprived rats resulted in more rapid loss of righting reflex and a delayed recovery.

Our results suggest that mechanisms involved in the regulation of naturally occurring sleep can affect anesthetic potency and increase the possibility that naturally occurring sleep and the anesthetized state may act via common neurophysiologic pathways. Further work is needed to clarify the mechanisms linking sleep deprivation and anesthetic action. Sign In or Create an Account. Advanced Search. Sign In. Skip Nav Destination Article Navigation. Close mobile search navigation Article navigation.

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View large Download slide. Table 1. Weights and Ages of Rats in Each Arm of the Study Four separate experiments are represented: sleep deprivation versus ad-lib activity for both propofol and isoflurane and timed wheel rotation versus ad-lib activity for both propofol and isoflurane. View large. View Large. Br J Anaesth ; —8. A nesthesiology ; —9. Anesth Analg ; — J Clin Monit Comp ; 37— Life Sci ; — Children may prefer to go to sleep with a mask.

Once you're asleep, the anesthesiologist may insert a tube into your mouth and down your windpipe. The tube ensures that you get enough oxygen and protects your lungs from blood or other fluids, such as stomach fluids.

You'll be given muscle relaxants before doctors insert the tube to relax the muscles in your windpipe. Your doctor may use other options, such as a laryngeal airway mask, to help manage your breathing during surgery. Someone from the anesthesia care team monitors you continuously while you sleep.

He or she will adjust your medications, breathing, temperature, fluids and blood pressure as needed. Any issues that occur during the surgery are corrected with additional medications, fluids and, sometimes, blood transfusions.

When the surgery is complete, the anesthesiologist reverses the medications to wake you up. You'll slowly wake either in the operating room or the recovery room. You'll probably feel groggy and a little confused when you first wake. You may experience common side effects such as:. You may also experience other side effects after you awaken from anesthesia, such as pain. Your anesthesia care team will ask you about your pain and other side effects. Side effects depend on your individual condition and the type of surgery.

Your doctor may give you medications after your procedure to reduce pain and nausea. Explore Mayo Clinic studies of tests and procedures to help prevent, detect, treat or manage conditions.

Mayo Clinic does not endorse companies or products. Advertising revenue supports our not-for-profit mission. This content does not have an English version. This content does not have an Arabic version. Overview General anesthesia is a combination of medications that put you in a sleep-like state before a surgery or other medical procedure. Share on: Facebook Twitter. Benzodiazepines also significantly affect respiratory status of patients.

Midazolam lowers the muscle activity during deep anesthesia, thereby increases the possibility of airway stenosis than it does in natural sleep. Genta et al. On the other hand, diazepam possibly reduces sleep apnea and increases the percentage of NREM sleep in rats [ 20 ]. Also, Wedzicha et al. However, the usage potentially leads to adverse effects including hypothermia, tachycardia, hypertension, and partial memory impairment [ 22 — 24 ].

Intravenous Anesthetic Agent: Propofol and Ketamine Propofol is one of intravenous anesthetic agents that has characteristically short half life, thereby does not have prolonged effect [ 25 ]. To back up further, it exacerbated poor sleep quality of critically ill patients and reduced percentage of REM sleep [ 27 ].

Besides, there were conflicting findings that propofol improved sleep quality in patients in Intensive Care Unit [ 28 ]. In consistent with such findings, propofol therapy improved polysomnographic and Leeds Sleep Evaluation Questionnaire result of patients with refractory chronic primary insomnia [ 29 ]. Thus, in depth research is recommended to examine the effect of propofol infusion on sleep since it varies by circumstances.

However, propofol shows consistent postoperative outcome in patients with OSAS. According to the fact that propofol deters genioglossus activity [ 30 ], abundant studies have revealed that propofol infusion instigates significantly higher rate of airway collapse in dose dependent manner [ 30 , 31 ]. Along with the aforementioned results, the symptoms of OSAS measured by apnea-hypopnea index and oxygen desaturation level remained constant during the propofol sedation [ 32 — 36 ].

Ketamine is another intravenous anesthetic agent that affects sleep significantly. Indeed, it increased slow wave for the first night of usage, while it subsequently increased total sleep and reduced number of awakenings for the second night [ 39 ]. However, it also demonstrated deleterious impact on sleep electrophysiology by inducing psychotropic side effects and unpleasant dreams during drug-induced sleep [ 40 , 41 ]. In case of cats, it triggered hallucination due to malfunction in central nervous system [ 42 ].

Mounting evidence has suggested that ketamine favorably acts on respiratory tract during anesthesia. Studies on pharmacology of ketamine indicate that it alters airway muscle movement and tranquilizes respiratory activity by reducing the release of acetylcholine in medial pontine reticular formation [ 38 , 43 , 44 ].

In rat model, ketamine has found to be doing so by increasing viscoelasticity of lung and influencing alveoli [ 45 ]. Aforementioned results demonstrate ketamine as a promising sedative for the patients with OSAS because it highly avoids respiratory events during anesthesia [ 46 , 47 ]. Analgesic Agent: Opioids Opioid is an analgesic agent frequently used as pain reliever. There have been contentions about the effect of opioids on sleep, whether it is beneficial or not [ 48 ].

Meanwhile, many studies have implied that opioid has detrimental effect on sleep. Polysomnographical results and sleep diaries of opioid dependent patients have suggested that opioid is linearly correlated to poor sleep quality and reduction of SWS [ 49 , 50 ].

A significant decrease in SWS is highly liable to opioid, because opioid antagonist naloxone application successfully revitalizes SWS [ 51 ]. Disadvantageous consequence of opioid on sleep also has been recognized in other sleep stages. For instance, it significantly reduces REM sleep and increases Stage 1 sleep by impeding acetylcholine release in medial pontine reticular formation [ 51 — 54 ].

As respiratory depressant, opioid also detrimentally affects sleep disordered breathing and thereby increases number of awakenings. Numerous studies have exposed high correlation between opioid and respiratory deficiency, such as central sleep apnea and hypoxemia [ 52 , 55 — 64 ].

The severity of respiratory obstruction increases in dose dependent manner [ 56 , 65 ]. However, we need to consider that the patients who receive opioid prescription already have low quality of sleep as a result of pain.

Mostly pain causes higher number of arousal, thus patients may accommodate daytime sleepiness and napping regardless of opioid [ 66 , 67 ]. Indeed, Cronin et al. He also articulates that there has been no incident of airway obstruction when patients without OSAS used opioid [ 68 ].

Additionally, one review article even states that opioid analgesia significantly improves the sleep quality of patients [ 70 ]. For instance, opioid has been found to be a useful treatment of restless leg syndrome or periodic limb movement [ 71 ]. In several studies, opioid significantly reduced periodic limb movement index and increased percentage of SWS [ 72 , 73 ].

Benzodiazepine Antagonist: Flumazenil Benzodiazepine antagonist such as flumazenil deters sleep and increases alertness through GABAergic pathway [ 74 ]. Thus, it is commonly applied in order to reverse sedation during the recovery after anesthesia. Extent research has disclosed that flumazenil treated hypersomnolence or excessive daytime sleepiness by improving nocturnal sleep quality. Specifically, polysomnographic outcome reveals that flumazenil increases sleep efficiency and SWS, and reduces sleep onset latency [ 75 , 76 ].

However, for the sleep deprived patients, it rather lengthens sleep onset latency and disturbs SWS [ 77 ]. Other Adjuvant: Dexmedetomidine Dexmedetomidine is common adjuvant used in the process of anesthesia. Alike most of analgesic drugs, it follows GABAergic pathway and shares a common biological pathway with natural sleep [ 79 ].

Since it maintains high level of thalamic connectivity, patient anesthetized with dexmedetomidine tends to be more aroused after the surgery [ 81 ]. As well as ketamine, it is known to provide sedation without the risk of respiratory depression.

The need for artificial airway support during anesthesia has been significantly less in dexmedetomidine than that in other analgesic drugs [ 82 ]. Therefore, it is beneficial to patients with sleep apnea, especially children and adolescents who have unsettled airway [ 80 ]. Anesthesia alleviates fatigue and fatigue itself may further promote anesthesia vice versa [ 83 ].

In rat model, 12 hours of sleep deprivation led to more rapid loss of consciousness in sevoflurane-induced anesthesia [ 84 ]. Other studies that induced anesthesia with propofol or intralipid control in rats with sleep deprivation also have revealed similar outcome.

After 6 hours of anesthesthetic process, sleep deprived rats did not demonstrate any distinguishable deprived characteristic in REM sleep and NREM sleep [ 83 ]. Isoflurane, desflurane and halothane also successfully supplemented sleep deprivation, while isoflurane and desflurane compensated NREM sleep debt twice faster than that of propofol [ 84 — 86 ]. However, in the case of inhaled anesthetic agent halogenated ethers , the anesthetic state was subsequent to NREM sleep, and REM sleep debt was not compensated [ 87 ].

Clinical trials with healthy persons were not significantly different with aforementioned outcomes. Induction of isoflurane reduced sleepiness and increased Stage 2 sleep in sleep deprived patients [ 88 ]. As it can be seen in multiple animal and human models, sleep deprivation complementation varies depending on the analgesic drugs.

Narcolepsy Narcolepsy is a sleep disorder mostly characterized by intolerable excessive daytime sleepiness, cataplexy, and orexin deficiency. Orexinergic neurons are most divergent at wake state and generally remain low during sleep. Since it is highly correlated with gamma waves and muscle activity, an abnormality in orexinergic signaling pathway causes narcolepsy [ 89 ]. Several studies have concordantly delineated that orexin and analgesic drugs are highly correlated.

Kushikata et al. Moreover, when orexin was injected to the cortex, the anesthetic effect of propofol was reduced [ 92 ]. Hypothetical mechanism is that orexinergic system promotes arousal under propofol-induced anesthesia, which is mediated by noradrenergic and dopaminergic neurotransmission of the cerebral cortex [ 93 ]. Likewise, when orexin was injected into the basal forebrain of anesthetized rats, they were alert and the time to fully anesthesize them was reduced [ 94 , 95 ].

Conversely, the activity of orexinergic neurons reduced in rats injected with sevoflurane and isoflurane [ 96 ]. Interestingly, this phenomenon did not appear when halothane was injected, suggesting that halothane-induced anesthesia did not participate in orexinergic signaling pathway [ 97 ].

Following issue is anesthesia in narcolepsy patients would look different from that in normal patients. Indeed, patients with narcolepsy have demonstrated similar intraoperative course and recovery period that are similar to healthy controls [ 98 ].

Also, their risk of postoperative complications have not been significantly higher than that of other groups [ 99 ]. To back up further, propofol and remifentanil have been found to be safe during heart surgery in narcoleptics [ ].

Besides, Hu et al. In general, when anesthesia is conducted to patients with narcolepsy, sedation should be prevented and the treatment of narcolepsy should be continued until the day of operation. Use of short-acting anesthetics, such as propofol and remifentanil, is recommended [ ]. Meanwhile, bispectral index monitoring is advantageous to preserve sevoflurane concentration at a reasonable level and to observe changes in status which are due to oversedation and preoperative drug use [ ].

Furthermore, studies on mice with orexin deficiency have indicated that the control of temperature is important in patients with narcolepsy during anesthesia [ ].

For neurosurgical anesthetic operations involving the hypothalamus or the third and fourth ventricles, postoperative symptoms of narcoleptics should be checked after the surgery [ ]. Circadian Rhythm Disorder Patients conceivably experience sleep disturbances after anesthesia because anesthesia distresses circadian rhythm after surgery. Both animal and human models have shown that anesthesia impedes the rhythm of the daily cycle and changes the molecular clock.

Recent study has displayed that sevoflurane-induced anesthesia suppresses the expression of clock genes [ ]. Also, benzodiazepines influence the major neurotransmitter systems, which is associated with circadian rhythm control [ ]. Plenty of studies have revealed that diurnal rhythm would be interfered when an animal is anesthetized during its active time [ ].

However, much more evidence is needed to validate how anesthesia-induced change in the molecular clock renders change in behavior. Disruption of circadian rhythm after anesthesia is heavily correlated to melatonin, an important agent that maintains circadian cycle.

In fact, the level of melatonin metabolites has been increased while that of cortisol has been decreased after anesthesia [ ]. Hence, melatonin is commonly used as a stabilizer when performing surgery with anesthesia. Oral administration of melatonin to patients undergoing local anesthesia has provided satisfactory surgical conditions due to anxiolytic effects, pain relief, and reduction of ocular motility disorders [ — ].

Indeed, a study illustrates that oral melatonin reduces the incidence of excitement after sevoflurane anesthesia [ ]. Furthermore, several study approaches have presented that melatonin acts to mitigate apoptotic neurodegeneration caused by anesthesia. A study conducted on rats that were exposed to pro-apoptotic anesthesia cocktail such as midazolam, isoflurane, and nitrous oxide for seven days has reported that their anesthesia-induced brain damage significantly decreased after the application of melatonin [ , ].

In conclusion, melatonin is an effective treatment to reduce patient anxiety, to reduce the pain associated with hemostasis, and to improve preoperative damage before and after anesthesia [ ].