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Anesthesia Basics:

the Role of the nurse anesthetist

Jassin M. Jouria, MD

Dr. Jassin M. Jouria is a medical doctor, professor of academic medicine, and medical author. He graduated from Ross University School of Medicine and has completed his clinical clerkship training in various teaching hospitals throughout New York, including King’s County Hospital Center and Brookdale Medical Center, among others. Dr. Jouria has passed all USMLE medical board exams, and has served as a test prep tutor and instructor for Kaplan. He has developed several medical courses and curricula for a variety of educational institutions. Dr. Jouria has also served on multiple levels in the academic field including faculty member and Department Chair. Dr. Jouria continues to serves as a Subject Matter Expert for several continuing education organizations covering multiple basic medical sciences. He has also developed several continuing medical education courses covering various topics in clinical medicine. Recently, Dr. Jouria has been contracted by the University of Miami/Jackson Memorial Hospital’s Department of Surgery to develop an e-module training series for trauma patient management. Dr. Jouria is currently authoring an academic textbook on Human Anatomy & Physiology.

Abstract

The rapid growth of nurse anesthetists within surgical and other health settings has helped to improve available, cost-effective services for patients. Nurse anesthetists have a vital role in the management of the perioperative patient as well as in the provision of clinical support services outside the operating suite. As experienced anesthesia clinicians, they are able to assist in the education and training of new nursing and medical staff in the provision of safe and appropriate care during varied anesthesia procedures, including pre- and post-anesthesia care. With such a wide array of responsibilities, nurse anesthetists must possess a broad field of clinical knowledge.

Policy Statement

This activity has been planned and implemented in accordance with the policies of and the continuing nursing education requirements of the American Nurses Credentialing Center's Commission on Accreditation for registered nurses. It is the policy of to ensure objectivity, transparency, and best practice in clinical education for all continuing nursing education (CNE) activities.

Continuing Education Credit Designation

This educational activity is credited for 4.5 hours. Nurses may only claim credit commensurate with the credit awarded for completion of this course activity. Pharmacology content is 1 hour.

Statement of Learning Need

Nurse anesthetists need to know their role and responsibilities in the management of the patient receiving varied types of anesthesia. Importantly, as members of the anesthesia team, they are actively involved in the patient’s pre- and post-operative care relating to the preparation and planning, administration and recovery phase of anesthesia that require them to continuously update their own knowledge as practicing clinicians and as clinical leaders and educators of anesthesia practice in multiple settings, including Intensive Care Units, Palliative Care Units, and a wide array of inpatient and outpatient surgical services.

Course Purpose

To provide advanced learning for clinicians interested in the role and practice of the nurse anesthetist.

Target Audience

Advanced Practice Registered Nurses and Registered Nurses (Interdisciplinary Health Team Members, including Vocational Nurses and Medical Assistants may obtain a Certificate of Completion)

Course Author & Planning Team Conflict of Interest Disclosures

Jassin M. Jouria, MD, William S. Cook, PhD, Douglas Lawrence, MA,

Susan DePasquale, MSN, FPMHNP-BC – all have no disclosures

Acknowledgement of Commercial Support

There is no commercial support for this course.

Please take time to complete a self-assessment of knowledge, on page 4, sample questions before reading the article.

Opportunity to complete a self-assessment of knowledge learned will be provided at the end of the course.

1. _____________ is used to anesthetize an area of the body.

a. Local anesthesia

b. General anesthesia

c. Sedation

d. Regional anesthesia

2. True or False: The term “asleep” is used when anesthesia clinicians speak of a patient who is anesthetized because general anesthesia is similar to sleep in physiological terms.

a. True

b. False

3. The triad model of anesthesia means that _______________ needed to produce all three of the intended effects of anesthesia: narcosis, analgesia, and muscle relaxation.

a. sedation is

b. an anesthesia care team is

c. multiple agents are

d. only one agent is

4. Which of the following is characteristic of electrical brain activity in an anesthetized subject but not an individual who is sleeping?

a. Rapid eye movement (REM) sleep

b. Non-REM sleep

c. Burst suppression

d. Aniso-electric periods

5. Pain signals turn into perceived pain at the moment the sensory pain signals arrive at the

a. thalamus.

b. the cortex.

c. nociceptors.

d. peripheral nerves to the spinal cord.

Introduction

The anesthesia care team works in collaboration with all members of the surgical team to provide a plan that is tailored to each individual patient in terms of intraoperative life support, sedation, pain control, and postoperative management, to assure an uneventful recovery from a surgical or other emergency procedure. Outside of the operating room, medical and nursing anesthetists are involved with emergency units that provide monitoring, treatment, and support during diagnostic investigations. They often intervene in intensive care units, radiology units, acute pain units, and outside the hospital setting, such as providing care for terminal (i.e., cancer) and psychiatric (i.e., electroconvulsive therapy) patients. In the United States, the amount of autonomy that nurse anesthetists have is variable. Currently, certified registered nurse anesthetists (CRNAs) may practice without physician supervision in 17 states of the United States.3

Anesthesia Overview And General Concepts

Due to development of the state of the art surgical and exploratory tools in general surgery and the sharp rise of subspecialties in Ear, Nose and Throat (ENT), Ophthalmology, Plastic surgery and Cosmetics, among other surgical procedures, anesthesia is becoming the largest hospital medical specialty in many countries. It is estimated that 234 million surgical procedures are performed annually that necessitate the use of anesthesia.1 The proportion of non-operating room anesthesia (NORA) cases increased from 28.3% in 2010 to 35.9% in 2014. There is also a trend of increasing the volume of NORA care in the United States.2

Anesthesia involves medication given to relieve pain and sensation during a medical procedure such as during surgery. Sedation is used to make a patient calm or sleepy and sedation may also be used as part of the anesthesia process. In regional anesthesia, the anesthesiologist makes an injection near a cluster of nerves to numb the area of the body that requires surgery.

There are three types of anesthesia to consider: 1) local anesthesia performed typically at the site of the surgical incision, 2) regional anesthesia used to anesthetize an area of the body (used alone or in combination with general anesthesia), and 3) general anesthesia where the patient is made completely unresponsive to pain, in which case the patient needs assisted ventilation and close monitoring of his or her physiological status.

Sedation is another important skill area of anesthesia medical and nursing staff. Often sedation is used in combination with local anesthesia in light procedures involving the skin or subcutaneous tissues, minor biopsies, and surgeries of peripheral parts of the body that can be easily anesthetized with regional injections.

There are several levels of sedation. A mild dose allows the patient to stay awake or in a drowsy state but easily arousable, such as when the patient hears his or her name called. As sedation deepens with increasing doses, the anesthetist may need to maintain the airway open with support and assist the ventilation of the patient. In its deepest level, sedation becomes general anesthesia called total intravenous anesthesia (TIVA), and for this reason should be included in a discussion of anesthesia types.1,4

General Anesthesia and the Triad Model

Although the term asleep is used when anesthesia clinicians speak of a patient who is anesthetized, general anesthesia is very different from sleep in physiological terms. So, what is general anesthesia? First, general anesthesia is a term that refers to a state of unconsciousness deliberately produced by the action of drugs on a patient. This state is reversible in essence. At its infancy, anesthesia was introduced with the goal of eliminating pain and was usually provided by a single agent of ether or chloroform.

In 1926, John Lundy introduced the term “balanced anesthesia” to describe the use of multiple sedating agents as a premedication together with general anesthesia to improve results. Later, in the 1950s Gordon Jackson Rees and Cecil Gray proposed a triad of anesthesia consisting of narcosis (unconsciousness), analgesia, and muscle relaxation; all represented in a triangular diagram. The triad model means that one agent is no longer found sufficient to produce narcosis, analgesia, and muscle relaxation. The triad model is still taught and used with some refinement.1,4

Anesthesia Is Not ‘Asleep’

An understanding of why anesthesia is not the same as being asleep may be achieved through observing the electrical activity of the brain by means of electroencephalography (EEG). Using EEG analysis, sleep is characterized as two phases. One of these phases is rapid eye movement (REM) sleep during which vivid dreams occur and REM sleep accounts for 10% to 20% of sleep time. The other is non-REM sleep. These two types of sleep form a pattern that lasts about 90 minutes, which is a sleep cycle.4

Intense electrical activity occurs during the sleep cycle, especially during the REM phase, which resembles the EEG activity of awake subjects. In contrast to what happens in wakefulness and sleep, in anesthetized subjects, the frequency of the brain waves slows and their overall amplitude diminishes. During general anesthesia the patient may even experience short periods of silencing called burst suppression. Therefore, EEG recordings provide evidence that anesthesia is distinct from sleep.

Analgesia During Anesthesia

The aim of analgesia is to abolish pain sensation experienced by the patient during surgery and in the perioperative phase as well. The American Society of Regional Anesthesia and Pain Medicine (ASRA) define pain as “an unpleasant stimulus, which evokes an unpleasant reaction in the recipient.”4 This definition incorporates both the subjective and objective components of pain; the perception of the individual and the objective measurable effects elicited by the stimulus.

Briefly summarized, the neurophysiology of pain has been shown to comprise the following steps. First, the detection of the painful stimulus (nociception) due to the presence of nociceptors located in the skin and other organs, which upon their stimulation will produce electrical signals; second, the signals will be transmitted via the peripheral nerves to the spinal cord, and then to the thalamus which is responsible for integrating sensory signals; finally, the emerging signals from the thalamus will travel to the cortex where the pain signals turn into conscious perception, and at this moment only, pain is being perceived.

The experience of pain triggers emotional response in the patient, including fear, anger, and anxiety, which the anesthesia team strives to avoid during surgery. But the process does not end there. Pain is experienced in the subconscious part of the brain, and triggers physiological responses, activating the sympathetic system and thereby the production of adrenaline, which is responsible for pallor, sweating, rapid heart rate and breathing, and increased blood pressure. Although the patient does not respond outwardly to surgical pain while anesthetized, he or she will be under hormonal stress, which alters the healing process (by mobilizing energy stores instead of activating repair mechanisms) and leads to an uncomfortable waking of the patient.

Optimal conditions for general anesthesia require a combination of general anesthetics to produce unconsciousness and analgesics to suppress the stress response.

Muscle Relaxation

Muscle relaxation is the last component of the triad model. Sectioning a muscle of the abdominal wall for example causes a reflex spasm of the muscle, which renders the abdominal surgery more difficult to perform. Also, placing a tube in the trachea can only be performed under deep anesthesia. To circumvent these obstacles, muscle relaxants are needed both for easy access to the surgery site and intubation.

Types Of Anesthesia

The nervous system is organized hierarchically. The brain and the spinal cord constitute the central nervous system (CNS), and function to integrate various sensory inputs, process inputs, and elicit commands to the organs. Surrounding the CNS is the peripheral nervous system, made of peripheral nerves that convey information from the different parts of the body to the CNS, and convey signals from the CNS back to the body. This section highlights the types of anesthetic drugs and target sites in the body where their effect happen.1,4-8

Peripheral nerves are made of a mixture of several types of fibers and each type has a specific function. For each particular nerve, signals may be heading toward the CNS, known as afferent signals (also termed ascending), or heading away from the CNS and known as efferent signals (also termed descending).

Ascending signals are almost all sensory, which include pain, temperature, touch, vibration and proprioception (joint position sense). On one side, touch, vibration and proprioception travel through the type A-fibers, which have a coating of myelin, a lipid that increases the conduction velocity of the nerve. When they reach the spinal cord, the signals ascend in structures called the dorsal columns, on the same side of the body where the signal came from. On the other side, pain and temperature signals travel in type C-fibers; these fibers have a smaller diameter and lack myelin, so they have a slower conduction velocity. These signals travel in the spino-thalamic tracts on the opposite side of the body from the signal.

Descending signals are used to produce muscle movement; they are also called motor signals and travel via type A-fibers. Additionally, other descending signals regulating the function of internal organs such as breathing, digestion, heart rate, bladder control, are below conscious awareness and depend on the autonomic system with its two components - the sympathetic and parasympathetic pathways.

A nerve cell or neuron consists in a cell body (“soma”) from which emerge threadlike extensions or processes called dendrites and axons, which are long, slender projections of the neuron, or processes that conduct electrical impulses away from the neuron's soma. Axons can reach up to 1 meter in length. Nerve fibers are made of nerve cell axons, which can be myelinated or unmyelinated.

An individual nerve transmits its signal along the axons by a self-propagating electrical charge called an action potential. The interior of the axon is rich in potassium ions while the exterior is rich in sodium ions. This state is continually maintained by ion pumps located on the surface of the axon membrane and this imbalance is what creates the potential energy.

Opening ion channels in the membrane permits sodium and potassium to switch places leading to a depolarization lasting a few milliseconds. In response to this depolarization other channels called voltage-gated channels are activated to repolarize the cell membrane at this location. The succession of depolarization and repolarization allows the propagation of the impulse to spread along the axon, in what is called action potential. The action potential is then passed from neuron to neuron at the synaptic junction where it triggers the release of chemicals or neurotransmitters. At this level, another action potential mediated by the binding of the neurotransmitter to the dendritic site of the synapse will be initiated and so on.

Several substances found in nature are known to disrupt the propagation of action potentials. The most widely known compound that interferes with nerve conduction by blocking the voltage-gated sodium channels is cocaine, the first anesthetic drug.

Cocaine And Derived Pharmacological Products

Cocaine is an alkaloid found in the leaves of the coca plant (erythroxylum coca) native of South America. The Spanish brought the plant to Europe in the 16th century and cocaine was for the first time isolated in 1855 by Friedrich Gaedcke. Later, it was even incorporated into tonic drinks like Coca-Cola in 1866. Cocaine acts at two levels of the nervous system. Firstly, it blocks the voltage-gated sodium channels in the peripheral neurons making it an efficient local anesthetic agent. Secondly, cocaine acts on the central nervous system by blocking the reuptake of stimulatory neurotransmitters like dopamine, serotonin and noradrenaline in the synapses.

Normally, stimulatory neurotransmitters are recycled back into the transmitting neuron by a specialized protein transporter; if cocaine is present in the body, it attaches to the dopamine, serotonin or noradrenaline transporters and blocks the normal recycling process, resulting in a buildup of these stimulatory neurotransmitters in the synapses. This has the effect of enhancing their actions. It is this second action that is responsible for both cocaine’s stimulant and addictive properties.

In 1904 at the Pasteur Institute, Ernest Fourneau was able to synthesize amylocaine and completed a successful search for another drug having similar anesthetic properties without the addictive side effect. Since then, almost all local anesthetic drugs carry the suffix –caine. Amylocaine and its successors share common biochemical characteristics. They have a ring-shaped structure joined by a short linkage that is water-soluble. If the connecting link is an ester group then the drug will be hydrolyzed in the plasma by pseudocholinesterase; and, if the link is an amide bond, hydrolysis will occur in the liver. The greater the length of the connecting amino groups the greater will be potency and toxicity of the local anesthetic.

Amylocaine and procaine have an ester linkage, which can be broken down in the bloodstream and so these two drugs are known for their very short duration of action. They also have been associated with a higher incidence of allergic reactions due to one of their metabolite, para-amino benzoic acid (PABA). Eventually, an amide linkage was substituted for ester, making the molecule more stable and with a longer duration of action. This latter design led to the synthesis of lidocaine (in 1943), bupivacaine (in 1963), and ropivacaine (in 1993).

Drugs Used In Local Anesthesia

Because local anesthetic agents act by blocking both sensory and motor nerve conduction, they produce a temporary loss of sensation without loss of consciousness or depression of the central nervous system. Despite the fact that cocaine has been the first identified local anesthetic, its effects on the central nervous system, coupled with its addictive potential, have resulted in a significant decline of its clinical use. This section summarizes the characteristics of more recently developed drugs, which are currently used in local, as well as regional anesthesia. These drugs are procaine, tetracaine, lidocaine, bupivacaine and ropivacaine.1,4-7

Procaine

Procaine has a short duration of action, causes minimal systemic toxicity and creates no local irritation. The combination procaine-epinephrine decreases its rate of absorption in the bloodstream and doubles the duration of its action. A 1%-2% solution is used for nerve blocking in regional anesthesia and infiltration anesthesia, and a 5%-20% is needed for spinal anesthesia. Procaine is not efficient for topical use.

Tetracaine

Tetracaine is approximately 10 times more potent and more toxic than procaine. Its onset of action is about 5 minutes and its effect lasts between 2 and 3 hours. A 2% solution of tetracaine is used topically on mucous membranes.

Lidocaine

Lidocaine also known under the name xylocaine is rapidly absorbed, has a rapid onset of action, and causes minimal local irritation. It is more potent and has a longer duration of action than procaine. A 0.5% solution is used for infiltrative anesthesia, while a 1%-2% solution is needed for topical mucosal and nerve block anesthesia. Lidocaine is also available as an ointment, jelly and cream.

Bupivacaine

Bupivacaine is used mainly for regional anesthesia in concentrations ranging between 0.25%-0.75%. Its toxicity is similar to that of tetracaine. Its undesirable effects include hypotension, bradycardia, and prolonged duration of motor impairment, cardiotoxicity and central nervous system toxicity, which can be fatal. These severe side effects occur after an overdose or accidental intravascular injections.

Ropivacaine

Ropivacaine is nearly identical to bupivacaine in onset, quality and duration of sensory block, but it produces lesser duration of motor blockade and has a better safety profile.

Adverse Effects of Local Anesthetics

Systemic adverse effects of local anesthetics result from the passage of toxic amounts of local anesthetics into the bloodstream. As a consequence, epinephrine is prescribed in addition to the local anesthetic whenever possible to reduce the rate of systemic absorption and thus the systemic toxicity. Although rare, allergic reactions to local anesthetics have been observed. Certain local anesthetics, such as procaine and tetracaine, are associated with a higher incidence of allergic reactions due to their metabolite para-amino benzoic acid (PABA).

Local Anesthesia: Topical and Subcutaneous

Local anesthetics penetrate healthy skin poorly. Therefore, applying them as creams or gels is not the most effective way to administer local anesthetics. However, there are preparations such as tetracaine or lidocaine/prilocaine, which are used to anesthetize the skin in certain circumstances; for example, prior to blood sampling in the pediatric population.

In contrast to the skin, mucous membranes absorb topical anesthetics well. By example, the use of topical anesthetics is effective in ophthalmic procedures or surgeries. Eye drops of tetracaine can provide effective corneal anesthesia prior to the extraction of foreign objects from the eye, or even during prolonged ophthalmic surgeries involving extra-ocular muscles. Finally, infiltrative anesthesia is another technique for local anesthetics. Here the anesthesia is injected subcutaneously. This procedure is well-suited for minor surgeries such as suturing a superficial wound.

Regional Anesthesia

Regional anesthesia is obtained by blocking a nerve, so that the skin, the deeper structures, and the muscles that the nerve supplies become paralyzed. Regional anesthesia results in an inability to move muscles or to sense pain. Regional anesthesia affects temperature in the area of the affected nerve.

There are two main categories of nerve blocks. The first called neuraxial block involves the spine and can be subdivided in spinal, epidural and caudal block. The second called peripheral block may involve the eyes, breast, trunk, the upper extremity and the lower extremity. Peripheral blocks can be used alone or in combination with neuraxial anesthesia or general anesthesia.

Another alternative technique of regional anesthesia consists in the intravenous injection of anesthetic into a limb, which is isolated from the circulation by application of a tourniquet and is called Bier’s block.

Advantages of Regional Anesthesia

Besides controlling pain, regional anesthesia presents a number of advantages. It allows the patient to breathe independently without airway support, reduces postoperative nausea and vomiting, blocks the stress-induced inflammatory response to surgical trauma, and avoids airway manipulation in difficult cases. Since regional anesthesia is accompanied with vessel dilation and lower pressure within the dilated vessels, there will be less blood loss and less requirements for blood transfusions. In addition, regional anesthesia allows earlier recovery of bowel function as well as earlier rehabilitation and hospital discharge.

General Technique

The technique of regional anesthesia involves inserting the needle near enough to a nerve to deposit the anesthetic agent without injuring the nerve itself. For this, it is possible to rely on anatomical landmarks to locate the nerve, but anatomical landmarks may vary from one individual to another. Today, the nerve is located using the help of electronic nerve stimulators, which are more accurate and save time. A small electric current is passed down the needle and, as the nerve is approached, the current causes the muscles innervated by the nerve to twitch. This signals to the operator that the tip of the needle is close enough to the nerve.

Another way to avoid nerve and large vessel injuries during the injection is the use of portable ultrasound scanners, which allow a guided nerve block under direct visualization of the neighboring structures as the needle approaches its target. These two techniques complement each other since they provide important information about both nerve anatomy and function. Therefore, they are used in combination by many anesthesia teams.

Before the regional anesthesia procedure begins, the patient is positioned and connected to standard monitors for follow-up of vital signs the same as if the patient were receiving a general anesthesia. The patient is sedated in small doses to maintain the patient’s comfort but maintain the patient’s consciousness since the patient’s ability to communicate throughout the surgery is important to maintain block safety. For lengthy procedures, a plastic catheter may be inserted and left in situ, so that repeated injections, or an infusion of anesthetic may be given.

Regional blockade occurs slowly, and may take up to 30 minutes after the injection to be fully effective. Regional anesthesia is not always reliable in providing a complete analgesia during surgery. Therefore, for some types of surgeries, regional blockade is performed as an addition to general anesthesia. In this case, the regional block placed first is followed by induction of general anesthesia. This block can also provide pain relief after surgery if a nerve catheter is left in place for injection after the patient recovers from general anesthesia.

Neuraxial Block Procedure

A neuraxial block is also known as spinal block, subarachnoid block, intradural block or intrathecal block.12-15 The spinal cord is a very delicate structure. It is covered by a microscopic layer called the pia mater, and is suspended in clear watery fluid, the cerebrospinal fluid, which circulates around it. The cerebrospinal fluid is enclosed by another fragile membrane, the arachnoid, which in turn is enclosed in a tough membrane called the dura mater.

In spinal anesthesia, local anesthetic is injected into the subarachnoid space located between the pia mater and the arachnoid, using a fine needle, usually 9 cm (3.5 in) long. Spinal anesthesia provides a dense block of all spinal cord function below the level of the block. This includes loss of motor and sensitive function as well as loss of automatic reflexes that control blood pressure and heart rate depending on the level of the block. The head and the body are unaffected and the patient remains awake.

The height or level of the block depends on the injection site, which is usually done in the lumbar area, but also on the diffusion of the anesthetic solution in the cerebrospinal fluid (CSF). To prevent a higher than intended diffusion of the anesthetic drug, some solutions for spinal anesthesia are formulated with 8% dextrose, making them denser (hyperbaric solutions) than CSF. After injection, the patient will be positioned according to gravity in order to control the height of the block.

Dermatome Map

There are eight cervical nerves, twelve thoracic nerves, five lumbar nerves and five sacral nerves. Each of these nerves relays sensation from a particular region to the brain. A dermatome is an area of the skin supplied by the sensory fibers of the spinal nerve. In the head and trunk, each segment is horizontally disposed, except C1, which does not have a sensory component.8

Assessment of Neuraxial Blockade Level

Knowledge of dermatome levels is key in allowing the anesthetist to assess the level of blockade. Spinal nerves contain both sensory and motor pathways, as well as autonomic fibers. In general, small myelinated fibers are more susceptible to blockade than larger unmyelinated fibers. Moreover, with a neuraxial block there is a difference between sympathetic, sensory and motor block level. The sympathetic level being generally two to six dermatome levels higher than the sensory level. The sensory level is approximately two dermatome levels higher than the motor level.9

Contraindications

Contraindications should include patient refusal, infection, abnormal coagulation, and cardiac disease. The use of neuraxial anesthesia in patients with pre-existing neurologic disorders, such as multiple sclerosis is not recommended unless it is absolutely necessary.

Indications of Spinal Anesthesia

Spinal anesthesia is used for almost any procedure of the lower half of the body, including orthopedics, obstetrics, and prostate surgery. The use of spinal anesthesia has also been described for surgeries in the head and neck where punctures performed between the 1st and 2nd thoracic vertebrae resulted in good analgesia. Laparoscopic surgeries such as laparoscopic cholecystectomy performed under spinal anesthesia require very small incisions, produce less pain and result in shorter hospital stays. They are particularly advantageous to use in older and high-risk patients for general anesthesia.10 In the same manner, spinal anesthesia has been associated with a lower postoperative mortality risk in elective total joint replacement surgery.11

Spinal anesthesia is generally preferred over a general anesthesia in the obstetric population, as long as it is not contraindicated. The dose of local anesthetic is often reduced to one-third due to changes in the intra-abdominal pressure and effects of hormones, which increase sensitivity.

Drugs and Associated Factors Influencing Effect

The level and duration of spinal anesthesia are primarily determined by 1) baricity (the density of the drug as compared to the density of human cerebrospinal fluid), 2) contour of the spinal canal, and 3) patient position in the first few minutes after injection. To optimize lordosis, a pillow is placed under the patient’s knees; the other option is to place the patient in the lateral position. Isobaric solutions undergo less spread than hyperbaric solutions, and both of these solutions are suited for perineal or lower extremity surgery. Hypobaric solutions (sterile water or normal saline) are rarely used due the osmotic stress they might cause.

Short Duration Procedure

Lidocaine, with duration 60-90 minutes, provides good sensory and motor block. The dose of lidocaine used is between 60-75 mg. Lidocaine has been linked to transient neurologic symptoms in up to one-third of patients. Lidocaine gives less vasodilation. 

Longer Duration Procedure

Bupivacaine is the most commonly used local anesthetic. It decreases spinal and dural blood flow, and 2 to 3 ml of 0.5% in the cerebrospinal fluid provides about 2 hours of surgical anesthesia. It is administered at similar dose and duration as tetracaine (5-20 mg with duration of 90-120 minutes). However, bupivacaine gives a slightly more intense sensory anesthesia (and less motor blockade) than tetracaine.

Tetracaine provides slightly more motor blockade (although less sensory anesthesia) than bupivacaine. Its duration of action is more variable than bupivacaine. And since tetracaine is accompanied by important vasodilation, it is more profoundly affected by vasoconstrictors.

Spread of anesthesia is affected by the addition of vasoconstrictors; so the addition of epinephrine (usually 0.1 – 0.2 mg of epinephrine, i.e., 0.2 to 0.5 cc of 1:1000, or 2 – 5 mg phenylephrine) may be considered to prolong and/or improve the quality of the block.

Opioids (usually fentanyl 25 μcg) and morphine (0.1 – 0.5 mg) can be added to provide 24 hours of relief, but unlike fentanyl, morphine requires in-hospital monitoring for respiratory depression. 

Technique

Spinal anesthesia is one of the oldest techniques in anesthesia. Its use to produce surgical anesthesia dates back to 1899, and was reported in a classic paper by a German surgeon Augustus Bier.

Spinal anesthesia is considered as a routine part of any anesthetist skills. The technique of administering spinal anesthesia can be described as the “4 P’s”: preparation, position, projection, and puncture. The use of a rigorous aseptic technique during both the preparation and the procedure itself must be the rule, as reviewed further below.12-15

Preparation

Preparation refers to the preparation of the material necessary for the procedure based on the type of planned surgery and patient’s characteristics (general status, associated pathologies).12 The anesthetist will then be able to choose the appropriate anesthetic drug and formulation (hypobaric, hyperbaric, or isobaric), to match the proposed length of the surgical procedure.

Prepackaged spinal kits are normally used or can be custom made. If a prepackaged spinal kit is not available, the following equipment needs to be assembled:

• Sterile towels

• Sterile gloves

• Sterile spinal needle

• An introducer needle if using a small gauge needle (this can be a sterile 19 gauge disposable needle)

• Sterile filter needle to draw up medications

• Sterile 5 ml syringe for the spinal solution

• Sterile 2 ml syringe with a small gauge needle to localize the skin prior initiation of the spinal anesthetic

• Antiseptics for the skin (such as betadine, chlorhexidine, methyl alcohol)

• Sterile gauze for skin cleansing and to wipe off excess antiseptic at needle puncture site

• Single use preservative free local anesthetic ampoule made specifically for spinal anesthesia

Local anesthetics from multi-dose vials or those that contain preservatives should never be used for spinal anesthesia. Prior to initiating a spinal block, the clinician’s hands must be carefully washed. The patient should be attached to standard monitors including electrocardiogram, blood pressure, and pulse oximetry, and an initial set of vital signs should be recorded. Access to an intravenous route should be ensured.

Positioning of the Patient

Proper positioning of the patient is essential for a successful block.

There are three positions used for the administration of spinal anesthesia: lateral decubitus, sitting, and prone. In lateral decubitus, the patient is positioned with their back parallel with the side of the operating table. Thighs are flexed up, and the neck is flexed forward in a fetal position. The patient should be positioned to take advantage of the baricity of the spinal local anesthetic. The seated position is used for anesthesia of the lumbar and sacral levels required by urological or perineal surgeries. The patient should be sitting up straight, with feet on a stool, head flexed and arms hugging a pillow. For a lower lumbar/sacral block, the patient is left sitting for 5 minutes before assuming a supine position. The prone position is used when the patient will be in this position for the surgical procedure such as rectal, perineal, or lumbar procedures.

Approaches to Access Subarachnoid Space

There are two approaches to access the subarachnoid space: the midline and paramedian approach. The midline approach is easiest and passes through less sensitive structures. The patient is sitting up straight and with proper positioning to give access to L2-L3, L3-L4, L4-L5, and L5-S1. After identification of the top of the iliac crests, Tuffier’s line, a landmark for the placement of spinal or epidural needle, which meets the body of L4 or L4-L5 interspace, is drawn across the iliac crest. Whereas, the paramedian approach is better suited for narrow interspaces or difficulty with flexion, and typically is located 1 cm from the midline. The advantage is that by placing the needle laterally, the anatomical limitation of the spinous process is avoided. The most common error when attempting this technique is being too far from the midline, which makes encountering the vertebral lamina more likely.

Puncture

All precautions should be taken during the step that involves spinal puncture to preserve a sterile environment. The clinician should wash hands, put on sterile gloves, and use sterile technique. The tray should be prepared in a sterile fashion. The patient’s back should be prepped with an antiseptic. A skin wheal of local anesthetic is placed at the intended spinous interspace.

Smaller gauge needles will require an introducer to stabilize the needle. The introducer is placed firmly into the interspinous ligament. Grasping the introducer with one hand, the anesthetist should hold the spinal needle like a dart/pencil. Cutting needles should be inserted with the bevel parallel to the longitudinal fibers of the dura. This helps reduce cutting fibers and enhances tactile sensation as anatomical structures are crossed. Anatomical structures that will be transversed include skin, subcutaneous fat, supraspinous ligament, interspinous ligament, ligamentum flavum, epidural space, and dura.

Monitoring During Spinal Anesthesia

After successful placement, the patient should be monitored continuously for block progression and complications. The first 5-10 minutes are critical in terms of monitoring the cardiovascular response as well as the level of progression of anesthesia. The patient’s blood pressure should be taken every 3 minutes, initially. The patient should be monitored for the following:

Block Progression:

The anesthetist has to ensure that the block is adequate for the surgical procedure and does not progress too high. Numbness of the arms and hands and breathing problems may indicate that the block is too high. High spinals are often accompanied by hypotension, nausea, and agitation.

Hypotension can be severe enough to cause stroke so it should be treated aggressively if blood pressure decreases by 20% or more from baseline. Bradycardia should be treated aggressively as it may progress to cardiac arrest. A change in the level of consciousness “total spinal anesthesia” is accompanied by loss of consciousness.

Measures to prevent high spinal spread:

• Use “Heavy” Bupivacaine (0.5% + 8% dextrose)

• Inject slowly at L3/4 or L4/5

• Inject correct dose (≤ 2mls)

• Head elevated on pillow

• Monitor rising spinal level

Emergency treatment in case of high spinal spread:

• Raise the Blood pressure aggressively with vasopressors

• Bradycardia is treated with atropine and ephedrine, adrenaline in severe cases

• Intravenous fluids, colloid solutions, oxygen

• Intubate and ventilate if loss of consciousness

Postoperative Care Monitoring:

Patient’s recovering from a spinal anesthesia should receive the same vigilant monitoring as the patient recovering from general anesthesia. Patients may experience some level of hypotension in the postoperative period too. Treatment includes a Trendelenburg position, additional intravenous fluids, oxygen, and vasopressors as needed.

Urinary retention should be assessed in patients that do not have a urinary catheter. The patient should not be discharged from the recovery area until vital signs are stable and the spinal block is regressing. The patient should remain in bed until full sensory and motor function has returned. The first time a patient is ambulated, the patient should be assisted by a medical or nursing clinician to ensure full function has returned.

Epidural Anesthesia And Analgesia

This section provides a specific focus on the combination of epidural anesthesia and analgesia medication for the critical management pain control and patient cooperation during a surgical procedure. The epidural (or extradural) space is a potential space surrounding the outer envelope of the spine, which contains loose fat tissue and veins. The injection of local anesthetics in the epidural space creates a less pronounced block than a spinal injection. The anesthetics will target the spinal nerves on their path out of the vertebral canal. Myelinated nerve fibers (type C-fibers) are more resistant to local anesthetics. This means that unmyelinated sensory nerve fibers, which carry pain signals, are blocked earlier and more completely than myelinated fibers. This explains why a moderate dose of anesthetic will produce analgesia without impairing the motor and touch function. However, to obtain a dense block much like a spinal, one would need a dose about ten times greater than the dose required for a spinal.1,4-8,12-19

Neural Blockade

As with spinal anesthesia, a number of parameters determine how far neural blockade will spread after epidural injection. Some variables are intrinsic to the patient’s anatomy; others depend on variations in the techniques and the drugs given. The combination of all of these variables can make the spread of the solution in the epidural space unpredictable.

Epidural analgesia is commonly indicated during labor and childbirth because it provides pain relief while still allowing the mother to push with her pelvic muscles when needed (at this stage the anesthetist has to simply discontinue the anesthetic infusion). Also, when labor does not proceed as expected and a cesarean section is planned in an emergency, the anesthetist needs only to inject a more concentrated local anesthetic to achieve a denser anesthesia to the lower abdomen for the surgical incision.

In addition to obstetrics indications, any lower limb procedure such as hip replacement, knee replacement or fracture repair can benefit from epidural anesthesia. Furthermore, epidural analgesia has proved useful during the recovery from surgeries performed under general anesthesia such as, upper abdominal or thoracic procedures which can be quite painful. In this scenario, epidural anesthesia has been shown to provide a better postoperative pain management than opioids or morphine, in the same time it decreases postoperative ileus and improves patient recovery. The latter advantages are particularly important in elderly patients as well as in patients with pre-existing pathologies.

Types of Epidural Anesthesia

Single-shot technique is easiest and provides the most uniform spread of anesthetic. Always begin with a negative aspiration and a test dose (3 ml of 1.5% lidocaine with 1:200,000 epinephrine) followed by a 3 minute waiting period. If the test dose is adequate, the total amount is injected in fractionated aliquots of 5 ml each.

Continuous epidural techniques involve placement of a catheter 3-5 cm beyond the needle (any longer than has the risk of penetrating into a vein, exiting the foramen, or wrapping around a nerve root). In a standard technique the catheter can be left in place for up to 72 hours and the retrieval of the catheter should never be done through the needle due to the risk of nerve transection.

Caudal blocks are epidural injections placed through the sacrococcygeal ligament and sacral hiatus, absent in 10% of patients. The technique consists in passing the needle through the ligament until it hits the sacrum, and then retracting slightly before aiming cephalad (towards the head), and then readvancing 2 cm and injecting air; if no crepitus is felt, it is likely placement is in the caudal canal and the anesthetist can inject. As with all neuraxial procedures, caudal block should be executed with a rigorous aseptic technique.

Duration and Influencing Factors

Dose and volume are important for epidural anesthetics, while concentration is not. By decreasing concentration and increasing volume, one can obtain greater anesthetic spread.

In contrast to spinal anesthesia, baricity does not matter in epidurals, but negative intrathoracic pressure does in terms of levels. Lumbar epidurals tend to flow cephalad due to negative intrathoracic pressure, whereas thoracic epidurals tend to stay in place. L5/S1 anesthesia is more difficult, likely due to the large fiber size. Chlorprocaine is used for rapid onset and short procedures. Lidocaine is intermediate, and bupivacaine/L-bupivacaine/ropivacaine has slower onset and prolonged duration. Tetracaine and procaine are not used because of their long latency times.

On a practical level, for a one-shot epidural, a 20 cc dose via lumbar injection is assumed to provide a mid-thoracic level block and then the volume is adjusted according to the desired level, for example, a decrease in the volume if only lower dermatomes are the aim. Bupivacaine produces a significant sensory block with minimal motor block, as opposed to etidocaine, which has a more pronounced motor block. Epinephrine at 1:200,000 can prolong a lidocaine block, but not a bupivacaine block. The mechanism for the latter is unknown; a decreased blood flow, an intrinsic analgesia provided by epinephrine, or an increased volume of distribution has been hypothesized.

Adjuvant Medications

Epinephrine (1:200,000 or 5μcg/mL) can prolong an epidural, especially if chlorprocaine or lidocaine is used. One has to be aware however that the mild B-stimulation may accentuate the fall in blood pressure that generally occurs with neuraxial anesthesia. On the other side, other studies report that the use of epinephrine seem to be preferable to phenylephrine at an equivalent dose as it has been shown to preserve cardiac output in contrast to the latter.

The use of opioids can enhance analgesia, with the degree of side effects largely related to lipid solubility. Morphine (hydrophilic or lipophobic) injected epidurally stays in place or spreads rostrally (distribution of medication within the cerebrospinal fluid), whereas fentanyl (hydrophobic/liphophilic) will be rapidly absorbed.

Sodium bicarbonate is known to promote a more rapid onset of epidural anesthesia.

Neuraxial Anesthesia Complications

Neuraxial techniques are generally considered safer than general anesthesia, particularly in patients with difficult airway management, elderly debilitated patients and even the premature newborn. However, several studies demonstrate that the setting in which a neuraxial block is performed, as well as the technique used, make a difference in the risk of complications. Adverse effects of neuraxial anesthesia may be as minimal as discomfort but may have more serious consequences such as disability or even death.

Hypotension

Hypotension is the most frequent immediate adverse effect. It occurs in one third of patients, initially due to decreased vascular resistance but in severe cases it may be due to decreased venous return and cardiac output. Risk factors for hypotension include arterial hypertension, obesity, increased fetal weight, chronic alcohol use, and a high level of blockade. Hypotension may cause intraoperative nausea and vomiting. Bradycardia may also be present if the block involves the heart-accelerating fibers (T1-T4 level), or from a decreased venous return.

A slight head-down position (5-10 degrees) to increase venous return without altering the spread of anesthetic and the maintenance of an adequate hydration are able to correct the situation.

High Blockade or High Spinal

Due to excessive spread of the anesthetic to higher levels of the dermatome, hemodynamic and respiratory effects are expected to occur. It can happen both in spinal and epidural anesthesia. A total spinal blockade is characterized by sympathetic blockade and respiratory arrest needs immediate and aggressive treatment as described in the section above on monitoring.

Cardiac Arrest

Cardiac arrest is most frequently seen in spinal anesthesia with an incidence estimated at 2.73 per 10,000 patients. A high block, dehydration, deep sedation, and inadvertent intravascular injection of the anesthetic, are considered risk factors for this complication.

Urinary Retention

Studies have shown that the sensation of urgency to void disappears 30-60 seconds after spinal injection of anesthetic solution; as for the detrusor muscle, contraction is completely abolished 2-5 minutes after. Opioid administration also affects bladder function and contributes to urinary retention.

Urinary retention is a complication which is more common in men older than 50 years with a history of urologic dysfunction as well as in anorectal surgery, inguinal hernia repair, hip surgery and gynecological surgery. Other risk factors include perfusion of large amount of fluids, the use of long acting anesthetics, and the site of the injection for epidurals. A lumbar site is more often associated with urinary retention than a thoracic site. Postoperative urinary retention causes unnecessary pain, vomiting, bradycardia, hypotension, and can be complicated by urinary infection. Bladder catheterization is recommended in high-risk patients.

Adverse Effects: CNS and Technique

Central nervous system toxicity can occur whereby the initial excitatory phase is characterized by the onset of facial numbness, metallic taste and tinnitus followed by agitation or confusion and seizures. A depressive phase occurs that involves respiratory depression and coma following the above symptoms. Cardiovascular toxicity can also occur and is initially manifested by tachycardia and hypertension followed by hypotension and myocardial depression, and then by vasodilation and arrhythmias.

Adverse effects due to technique are highlighted below:

Paresthesia

Paresthesia may be experienced as sharp discomfort by the patient, during the insertion of the needle or the catheter, radiating to the buttocks, pelvis or legs. In such case, it is recommended to stop advancing the needle or injecting the anesthetic at the site as it may result in nerve injury; in fact, this is the main reason that anesthetists conduct spinal procedures while the patient is still alert to be able to report such sensations.

Postdural Puncture or Spinal Headaches

Postdural puncture or spinal headaches are postural; they are due to a leak of cerebrospinal fluid through the hole left by the needle. They are experienced by the patient while sitting and resolve in a supine position. They are less common now due to the availability of smaller needles for spinal anesthetics injection.

Spinal headaches are treated most successfully with bed rest and an increase in fluid for 24 hours. If they persist, the next therapeutic option will be to perform an epidural blood patch, which consists in drawing blood from the patient and injecting it in the epidural space to help seal the hole.

Spinal or Epidural Hematoma

Spinal or epidural hematoma is a rare and potentially catastrophic complication of neuraxial anesthesia because of the nature of the bleeding into a fixed and noncompressible space. The incidence of hematoma in epidural anesthesia is about 1 in 50,000 and above 1 in 200,000 in spinal procedures.

The higher incidence of epidural hematoma can be explained by the increased vascularity of the epidural space. The clinical manifestations are due to the compression and ischemia of the spinal cord or spinal nerves; they may include legs or backache, motor weakness and dysfunction of the rectal and bladder sphincters. In the event of spinal hematoma, a prompt diagnosis and intervention are critical to ensure a recovery of the patient. Spinal cord ischemia tends to be reversible in patients who underwent laminectomy within the 8 hours of onset of the neurologic symptoms.

Often patients who are candidates for procedures where a regional technique would be advantageous are receiving anticoagulant or antiplatelet therapy, for example, pregnant patients with preeclampsia, and orthopedic patient under thromboprophylaxis. In such cases, regional anesthesia can still be safely performed provided there is appropriate timing of needle placement and catheter removal relative to the timing of anticoagulant drug administration.

The patient’s coagulation status should be optimized at the time of spinal or epidural needle or catheter placement and the level of anticoagulation must be carefully monitored during the period of epidural catheterization. Indwelling catheters should not be removed in the presence of therapeutic anticoagulation, as this appears to significantly increase the risk of spinal hematoma. Vigilance is therefore again emphasized in monitoring to allow early evaluation of neurologic dysfunction and prompt intervention.

Although spinal anesthesia seems to be safe to perform in patients with bleeding disorders (provided there is a platelet count between 50,000 and 80,000) the decision should be based on careful weighing of the risk of spinal hematoma with the benefits of regional anesthesia for a specific patient.

Infections

Bacterial contamination can lead to meningitis or to an epidural abscess, which can cause spinal cord compression. Bacterial meningitis after a neuraxial anesthesia is rare with an incidence of 0-2 cases per 10,000, and a high mortality rate of 30% even when antibiotherapy has been applied. Meningitis may be differentiated from postdural spinal headache based on the presence of fever accompanying the neurological signs. Streptococcus salivarus, which is regularly present in the skin, oral cavity, gastrointestinal and genitourinary tracts has been found responsible of more than 90% of post spinal meningitis.

Viral contamination may also occur after neuraxial techniques though they are less frequent and benign.

Inadvertent germ inoculation during neuraxial anesthesia can be prevented by a rigorous preparation of the injection site with sterile equipment, and by maintaining a sterile environment.

Failure

The incidence of failure with neuraxial anesthesia is variable and highly dependent on institutions and patient population, among other factors. Experienced clinicians might consider it to be around 1%, while hospital series reported incidences reaching 47%. Block failure in general can be attributed to one or the combination of the following parameters: 1) the experience of the operator, 2) the technique, 3) the spreading of the anesthetic agent, 4) the dosing of the anesthetic solution, 5) the solution itself, which can be ineffective, and 6) possibly related to the patient’s preoperative and intraoperative management.

Failed Lumbar Puncture

Failed lumber puncture is the only cause that is immediately obvious. It can be caused by a blocked lumen of the needle, thus the requirement to check the material before use, by an incorrect positioning of the patient, or a spine anomaly. Obesity, anxiety and pain due to the pathology presented by the patient can hamper the positioning of the patient. Gentle, reassuring handling of the patient, light anxiolytic premedication and systemic analgesia can prevent movement during the procedure. Good knowledge of spinal anatomy will be necessary to understand the different structures and potential resistance encountered when orienting and advancing the spinal needle.

Dosing and Spread

Spinal needle insertion followed with appearance of cerebrospinal fluid is a prerequisite but not a guarantee of success during lumbar puncture. The injection of the appropriate dose should be done after verification that the connection between the needle and the syringe is firm to prevent a leak. Similarly, unwanted anterior or posterior displacements of the needle tip during CSF fluid aspiration (a necessary step before injection) can result in misplaced injection (spinal versus epidural).

Inadequate spread of the anesthetic solution can stem again from inadequate positioning after injection, or from anatomical abnormality such as kyphosis, scoliosis, which could have been anticipated, within certain limits, by the preoperative examination. Another rare and not apparent possibility, lies in the presence of septae within the anatomical supportive structures of the spine, which act as barriers to the spread of the anesthetic solution. This can result in unilateral blocks or insufficient cephalad spread despite the appropriate baricity of the anesthetic solution and the positioning of the patient. Furthermore, in rare instances, a larger than usual volume of CSF associated with dural ectasia (widening of dural sac surrounding the spinal cord) seen in patients with connective tissue disorders, may limit anesthesia spread.

In addition to solution density (baricity), which influences the spread through gravity, a correct location of the site of the injection must be carefully selected to avoid a too low block or, to the contrary, a dangerous and unnecessary higher level spread.

Ineffective Drug versus Medical Error

A well-prepared spinal anesthesia procedure including the preparation of the required material and the verification that it is adequate and properly functioning should leave no room for confusion in the solution preparation. Nonetheless, reports of failure have been attributed to the loss of solution effectiveness due to prolonged storage or induced by the sterilization process.

Management of Failure

If all the preventive and corrective measures described above do not lead to a positive outcome, then the anesthetist has to accept the idea of failure and move to a back-up plan. A back-up plan should have been already discussed with the well-informed patient during the preoperative evaluation. The consequences of a failed block that is discovered in the course of the surgery have more severe implications for the patient’s safety, not to mention the medico-legal aspects.

Minor Adverse Effects of Regional Anesthesia

Shivering is partly related to vascular dilation and heat loss from the skin, and possibly due also to the direct effect of anesthesia on the thermoregulation center. Temperature regulation is a challenge in both regional and general anesthesia.

Itching is observed when opioids are injected into the spinal fluid to control for postoperative pain. Itching may also occur after intravenous administration of the same drugs.

Intravenous Regional Anesthesia

Intravenous regional anesthesia (IVRA) or Bier’s block is named after the German surgeon A.G. Bier who described it first in 1908. The IVRA is a highly popular procedure, versatile and useful in other settings than the surgical suite, such as in emergency departments during reduction of limb fractures and dislocations. It is considered safer than general anesthesia, especially for those patients who are elderly or carry diagnoses such as cardiac or respiratory disease. This section briefly highlights the IVRA procedure.1,4,18,19

With this technique, anesthesia is obtained by the intravenous injection of a local anesthetic, typically, 12-15 mL of 2% lidocaine for upper extremities, or 30-40 mL of 0.5% lidocaine, in a previously exsanguinated vascular space, isolated from the rest of the circulation by two Esmarch bandages used as tourniquets. The exact mechanism of IVRA is not completely understood. The likely mechanism is that the local anesthetic, via the vascular bed, reaches both peripheral nerves and nerve trunks (vasae nervorum), and nerve endings. Diffusion of local anesthetic into the surrounding tissues, ischemia and compression of the peripheral nerves at the level of the inflated cuff may also contribute to the mechanism of IVRA.

Contraindications

Contraindications to this technique are crush injuries, skin infection, compound fractures, allergy to local anesthetics and severe peripheral vascular disease. Disadvantages include incomplete muscle relaxation (where important) and lack of postoperative pain relief.

Indications

Bier’s block is a widely accepted technique for short duration surgeries such as wrist or hand surgery, carpal tunnel syndrome, Dupuytren contractures, and reduction of fractures. Since the duration of anesthesia depends on the length of time the tourniquet is inflated, there is no need to use long-acting or more toxic agents. Its application for longer surgical procedures is however impeded by the discomfort caused by the tourniquet, which occurs typically within 30 to 45 minutes.

General Anesthesia

General anesthetics act on the central nervous system or autonomic nervous system to produce analgesia, amnesia or hypnosis. They are used alone, or most frequently, as we will see, in combination with other agents to provide an optimal depth of anesthesia. General anesthesia can be achieved by inhalation of anesthetic gases or intravenously. Introduced around 1846, ether and nitrous oxide were the first inhalation anesthetics to be accepted by the medical community. Beginning with halothane in the 1950s, halogenated anesthetics replaced the routine use of ether and chloroform.20

Intravenous agents are used mostly for induction of anesthesia but they can be used also for some other longer procedures, which are 1) Neuroleptanesthesia, where a narcotic analgesic is combined with a neuroleptic in association with inhalation of nitrous oxide and oxygen, 2) Dissociative anesthesia with ketamine which produces rapid analgesia and amnesia while maintaining the laryngeal reflexes, and 3) Preanesthetic medication (also called premedication) which includes sedatives opioids, tranquilizers, and anticholinergic agents.4,6

Mechanism of Action of Anesthesia Drugs

There are two levels of understanding how the anesthetic agents work. Firstly, the molecular basis, which addresses what effect anesthetics have at a molecular level; and, secondly, the anatomical basis, which focuses on what part of the body they act on.

The molecular basis of anesthesia is complex and still incomplete. Although, it seems the predominant molecular mechanism lies in a transmembrane protein called GABAA receptor with five subunits, found widely in the central nervous system. The five subunits are the potential binding sites for general anesthetic agents.

The neurotransmitter GABA (gamma amino butyric acid) is inhibitory, for example, it makes the postsynaptic cell fire less. Specific binding sites have been identified for volatile agents as well as for intravenous drugs such as propofol (potent GABA agonist) and etomidate. More recently, the intervention of the two pore-domain potassium channels, which are also widely distributed in the mammalian central nervous system, have been described. Experimental studies with halothane, isoflurane sevoflurane, and desflurane have shown an enhancement of potassium channels leading to hyperpolarization of the neuronal plasma membrane.1,4,20

As for the mechanism of action of other anesthetics, such as Nitrous oxide, xenon and ketamine, they are likely mediated by N-methyl-D-aspartate (NMDA) receptors. Moreover, apart from its well accepted NMDA blockade, ketamine has been reported to interact with a wide range of other intracellular neuronal processes. It seems likely that its hypnotic effects are caused by a combination of immediate channel blockade of NMDA and HCN1 channels.21

With regard to the anatomic basis of anesthesia action, the macroscopic level of the neuroanatomy must be considered. Immobility induced by inhalational anesthetics is produced in the spinal cord, precisely it is due to a decreased transmission of afferent noxious information to the cerebral cortex via the thalamus; in addition, there is an inhibition of the spinal motor response which explains the reduction of the withdrawal movement. On the other hand, amnesia and hypnosis (the two other end points of anesthesia) are mediated by the brain. Inhalational agents have been shown to depress cerebral blood flow and glucose metabolism.

Amnesia probably involves among other structures, the hippocampus, amygdala, and the mediotemporal lobe. Hypnosis or unconsciousness concerns the cerebral cortex, thalamus and reticular formation.1,4,20

Inhalation Agents

Current volatile anesthetic agents are colorless liquids that evaporate into a vapor, which produces general anesthesia when inhaled. They are chemically stable and not likely to breakdown into poisonous products. They can be distinguished from each other by their specific properties; such as, potency, speed of onset, smell and partition coefficient, as further highlighted here.1,4,6,18,20

The potency of anesthetic gases is expressed as minimum alveolar concentration (MAC) at 1 atmosphere (atm) required to keep 50% of adults unmoving in response to a standard skin incision. MAC concept is a useful concept introduced for the first time by Ted Eger, Giles Merkel and collaborators in 1963. It helps comparing potencies of different agents. Isoflurane has a MAC value of 1.2%; it means that at equilibrium, with the concentration of 1.2% of isoflurane in the lungs, 50% of adults will not move in response to a skin incision. Sevoflurane, on the other hand, is less potent with a MAC of 2% and desflurane even less with a MAC of 6%. At equilibrium, it is considered that the lung’s concentration is equivalent to the concentration in the blood stream, and this in turn is equivalent to the concentration in the brain. Therefore, the measurement of the volatile agent in the expired breath of the patient gives a close approximation to the brain concentration of the anesthetic gas.

The MAC values are additive, so a patient with 0.5% MAC of isoflurane and 0.5% MAC of sevoflurane is said to have a 1.0 MAC of anesthetic in total. Since giving more than 1 MAC will result in less than 50% of adults moving in response to a painful stimulus, it is understood that MAC correlates with the depth of anesthesia. Interestingly, whereas immobility is produced around 1.0 MAC, amnesia is produced at a much smaller dose of typically 0.25% MAC, and unconsciousness at 0.5 MAC. This implies that a patient might move in response to the surgical stimulus without being conscious or remembering it afterwards.

Potency has also been shown to correlate with lipid solubility. This property is known as Meyer-Overton correlation.

Speed of onset is inversely proportional to water solubility. Desflurane is the least water-soluble of all agents and has the most rapid onset and offset. It is followed by nitrous oxide, sevoflurane and isoflurane.

Pungency is not a desirable property for an anesthetic agent during the induction of general anesthesia. In contrast to isoflurane and desflurane, sevoflurane has a fruity smell, which makes it more suitable for inhalational induction.

Partition coefficient is the concentration of an inhalation anesthetic in blood or tissue is the product of its solubility and partial pressure. This solubility is commonly expressed as blood-gas (alveolar) or tissue- blood partition coefficient. An agent with a blood:gas partition of 2 will reach twice the concentration in the blood phase as in the gas phase when the partial pressure is the same in both phases (at equilibrium). Ether, a very soluble gas, has a very high blood-gas partition coefficient equal to 12, while a relatively insoluble agent like nitrous oxide has a coefficient less than 1. Because high solubility constantly decreases the alveolar gas pressure, the lower the blood-gas partition coefficient of anesthetic agent then the more rapid the induction with that agent.

Influencing Factors

Blood-gas partition coefficients are affected by the concentration of serum constituents such as albumin, globulin, triglycerides and cholesterol. These molecules bind to anesthetics increasing their blood solubility.20

Drug uptake from the lung and delivery to the tissues, particularly the brain, is increased by a higher cardiac output although this does not lead to faster induction since the alveolar concentration is lowered by the high uptake. In contrast, a decreased cardiac output will be accompanied with a slow uptake, higher alveolar pressure and thus faster induction. A larger fat compartment in obese individuals leads to a longer equilibration time after induction and a slower emergence due the high absorption of anesthetic agents in the fat tissue and their slow release. Infants and children have a faster rate of induction than adults; this has been attributed to a larger ratio of alveolar ventilation to functional residual capacity, a greater delivery to a richer healthier vasculature, as well as to lower albumin and cholesterol levels.

Halogenated Anesthetics and Other Gases

Halogenated inhalational anesthetics are currently the most common drugs used for the induction and maintenance of general anesthesia.

Halothane (Fluothane)

The first chlorofluorocarbon to be developed from chloroform in 1951 is halothane. It was once considered an ideal anesthetic agent in that it was volatile and non-inflammable and had a high anesthetic potency with a MAC of 0.75%.20,22,23

Pharmacologic Effects of Halothane

Respirations become rapid and shallow with a reduction in the minute volume causing a reduction in the ventilatory responses to carbon dioxide; fluothane produces bronchiolar dilation.

Arterial blood pressure is decreased in a dose-dependent manner; there is an increase in cutaneous blood flow, and depression of myocardial contractility. Halothane antagonizes the sympathetic response to arterial hypotension and decreases cardiac sympathetic activity, which results in a slow heart rate. Although uncommon, arrhythmias have been associated with the use of halothane.

As anesthesia deepens, fast, slow voltage electroencephalogram waves are replaced by slow, high voltage waves. At 1 MAC, the glomerular filtration drops by 50%.

Halothane causes muscular relaxation by both central and peripheral mechanisms, increases the sensitivity to neuromuscular blocking agents, and like all inhalation compounds can trigger malignant hyperthermia, a very severe complication. It can also depress liver function and may lead to hepatic necrosis.

Excretion of Halothane

About 70% of Halothane is eliminated through the lungs in the first 24 hours after administration. The remaining is metabolized by the cytochrome p-450 system in the endoplasmic reticulum of the liver, which causes hepatic injury.22

Enflurane

Enflurane is a potent anesthetic obtained from the fluorination of ether; it has a MAC of 1.68%. Enflurane causes mild stimulation of salivation, produces tracheobronchial secretions and suppresses laryngeal reflexes. All of these parameters need to be taken in account during the ventilation of the patient.20

Like halothane, enflurane produces a dose-dependent respiratory depression and has similar effects on blood pressure and myocardium as well as on the renal glomerular filtration. However, bradycardia and cardiac output are not as much decreased as with halothane. Enflurane also acts directly on the neuromuscular junction providing adequate relaxation to the muscles, including uterine smooth muscle. On the other side, enflurane increases intracranial pressure and produces an electroencephalic pattern similar to seizure activity or frank seizures. Therefore, it is contraindicated in epileptic patients. It is eliminated in 80% as expired gas; free fluoride is released and as little as 5% are metabolized in the liver. Nevertheless, hepatic necrosis cases have also been reported after repeated administration of enflurane.

Isoflurane

Isoflurane a methyl-ethyl diether-like desflurane, while sevoflurane is a methyl-isopropyl ether; all of these gases derive from the fluorination of ether. Isoflurane is actually an isomer of enflurane. It also produces respiratory depression and a fall in arterial blood pressure, with the advantage of being a better myorelaxant than halothane and enflurane. Moreover, unlike enflurane, isoflurane does not cause seizures; and, unlike halothane, isoflurane does not induce arrhythmias. For these reasons, isoflurane is the anesthetic of choice among the halogenated volatiles compounds.20

Adverse Effects of Halogenated Anesthetics

About 25% of halothane is metabolized by oxidative phosphorylation via hepatic cytochrome P450 systems. The major metabolite is trifluoroacetic acid (TFA), which is protein-bound and this TFA–protein complex (neoantigens) has been shown to induce a T-cell-mediated immune response resulting in hepatitis ranging from mild to fulminant hepatic necrosis, and possibly death. According to the National Halothane Study, the risk of fatal hepatic necrosis is one in 10,000 anesthetic procedures.

Current volatile gases such as enflurane, isoflurane and desflurane are also metabolized in the liver through the metabolic pathway involving cytochrome P-450 2E1 (CYP2E1) which produces trifluoroacetylated components; however, in comparison with halothane, only 2–5% of isoflurane, sevoflurane, and desflurane are metabolized; the remaining is excreted unchanged in exhaled air.20

The severity of hepatotoxicity of these compounds is associated with the degree by which they undergo hepatic metabolism by cytochrome P-450.20,22 Enflurane, isoflurane, desflurane, and sevoflurane have different molecular structures to that of halothane and they seem to be associated with less hepatotoxicity; however, rare cases of acute liver injury have also been reported with all of these agents. The pattern of liver injury described with enflurane, isoflurane and desflurane has common features with that of halothane, and evidence of autoimmune response to trifluoroacetylated liver proteins has been reported.20,22

Unlike other halogenated anesthetics, sevoflurane is not metabolized to hepatotoxic trifluoroacetylated proteins; nevertheless, very few reports have described liver injury after sevoflurane exposure. Consequently, a history of anesthesia-induced hepatitis is a contraindication to halothane or other halogenated anesthetics re-exposure. The susceptibility to malignant hyperthermia is another contraindication.4,18

Nitrous Oxide

Nitrous oxide (N2O) is an inorganic inert, odorless, gas which can be compressed into a liquid. Although, chemically different (with respect to their properties) from halogenated gases mentioned above, it has similar behavior. The MAC of nitrous oxide is 105.2%, which means that it needs hyperbaric conditions to reach a level of I MAC. For maintaining anesthesia a concentration of 75%-80% is required. Although nitrous Oxide is a powerful analgesic that is well tolerated and has rapid onset of action and recovery, it is a weak anesthetic. Therefore, to achieve a more complete anesthesia, the use of nitrous oxide needs to be supplemented by a narcotic agent as well as a neuromuscular blocking agent. More often, nitrous oxide is used in combination with other potent anesthetic agents, and because of that it is probably the most widely used general anesthetic agent.1,6,19

An inhalation of 50:50 mixture of nitrous oxide with oxygen known as “gas and air” is offered sometimes to women in labor because it is effective enough to relieve pain without causing general anesthesia.

Moreover, at 50% concentration, its effects on breathing are minimal.

N2O is excreted primarily through the lungs as expired air.1,6

Adverse Effects and Contraindications of N2O

Because of its high partial pressure in blood and its low blood:gas partition coefficient, N2O diffuses into air–containing cavities and thus expands the volume of gas in air pockets. This effect can result in bowel distension, rupture of a pulmonary cyst, rupture of the tympanic membrane in the middle ear, and pneumocephalus. In the blood it can enlarge the volume of air embolus. Therefore, the use of N2O is contraindicated in bowel obstruction, air embolism and chronic obstructive pulmonary disease. It can lead to diffusion hypoxia at the end of anesthesia if a patient starts breathing room air all of a sudden.

An outward movement of N2O causes hypoxia from the tissues to the blood and then to the alveoli where it decreases alveolar tension and, by the same token, lowers arterial oxygen levels. To circumvent this drawback, one has to administer 100% oxygen for a short period of time at the end of the N2O anesthesia. N2O is also associated with a higher incidence of postoperative nausea and vomiting and should be avoided whenever possible in patients with a positive history of PONV.6,23

Xenon

Xenon (Xe) is odorless and nonirritant to the airway, which favors a smooth induction; and with a MAC of 71% it is considered as potent enough to be given alone with oxygen. Its blood:gas partition coefficient is 0.12, which means that it provides a rapid onset and recovery from anesthesia. It is a more potent intraoperative analgesic than sevoflurane.1,20

Xenon produces depression of postsynaptic excitatory transmission via NMDA receptor block. It has minimal cardiovascular side effects, even in cases of severely limited myocardial reserve. Although a mild respiratory depressant, xenon decreases respiratory rate and increases tidal volume, in contrast to volatile agents. Experimental models suggest that it has a significant neuroprotective action, but this benefit seems to be offset by an increase in cerebral blood flow, which elevates intracranial pressure.

Xenon causes an increase in pulmonary resistance due to its high relative density. Because of this, it should be used with caution in patients with severe chronic obstructive pulmonary disease and premature infants. It is not metabolized in the liver or kidneys, has no negative environmental effect and it does not trigger malignant hyperpyrexia. Despite all these advantages its use is still very marginal due to higher cost of production and its rapid diffusion through ordinary anesthetic hoses thus requiring specialized equipment.1,20

Oxygen

Oxygen (O2) is produced by distillation of liquid atmospheric air. At ordinary temperatures, oxygen cannot be liquefied so it is stored as compressed gas in cylinders. Medical air is atmospheric air filtered to remove particles (such as pollen, oil droplets), and dehydrated to remove moisture then compressed into cylinders. In addition to being used throughout anesthesia procedure, compressed medical air may be used in the operating room to power surgical tools. In anesthesia oxygen is used in combination with air or nitrous oxide but rarely alone as it can be harmful to the lungs if the administration is prolonged.1,19

Delivery Methods of Inhalation Anesthesia

The three most common methods used to control the airway during general anesthesia are: the mask (facemask), the laryngeal mask airway and the endotracheal tube.1,19

Mask Ventilation

Mask ventilation is performed with proper airway maintenance maneuvers during induction of general anesthesia. The mask has an airtight seal around the mouth and nose allowing the patient to breathe the anesthetic gas mixture efficiently. Ideal mask position is obtained by lifting the patient’s chin upward positioning the head in the so-called “sniffing” position and bringing the mandible forward to move the tongue from the oropharynx.

Mask ventilation can be challenging in neck and head surgeries, including ophthalmic procedures, as the anesthesiologist and the surgeon share a focus on the airway. Mask ventilation is frequently employed in short procedures, when the anesthetist has access to the patient’s airway or when tracheal intubation is difficult or impossible. Some studies report an incidence of impossible mask ventilation ranging between 1.4 to 5 percent.

Sleep disordered-breathing (SDB) in particular has been identified as a non-negligible risk factor for difficult mask ventilation, given the fact that the prevalence of SDB is as high as 69% of the general surgical population. Reports show that patients with SDB who undergo general anesthesia have pharyngeal airways that are narrower and more collapsible when compared to non-SDB patients.25,26 Mask ventilation has changed little in contrast to significant improvement of tracheal intubation techniques and devices in the past decade.

Laryngeal Mask Airway

The laryngeal mask airway (LMA) is made of soft rubber and is inserted via the mouth into the back of the throat resting just above the vocal cords. Its distal extremity is connected to the anesthesia machine breathing circuit. Because the laryngeal mask does not penetrate into the trachea, it is less irritating to the vocal cords and the throat than the endotracheal tube. However, the LMA tube does not protect against aspiration pneumonia and ventilation cannot be controlled as reliably as it can be done with the endotracheal tube.

Endotracheal Tube

Intubation with endotracheal tube was a major progress in the field of anesthesia as it has allowed for controlled mechanical ventilation and more invasive surgeries. Typically, the endotracheal tube is placed in the patient after the induction phase of anesthesia and will be removed before awakening. The process by which the endotracheal tube is inserted in the trachea is called intubation. Optimal intubating conditions are achieved when the tragus of the ear is aligned with the sternum allowing a direct visualization of the vocal cords while performing direct laryngoscopy.

The endotracheal tube is made of soft plastic, and is inserted through the mouth or the nose and guided with a laryngoscope through the vocal cords into the trachea. The distal end coming out of the mouth is connected to the anesthesia breathing circuit. A balloon (low pressure cuff) on the outer portion of the endotracheal tube is positioned inside the trachea and inflated to produce an airtight seal between the tube and the trachea in order to prevent any gastric fluid or secretions from entering the lungs. The incidence of aspiration pneumonia has been considerably reduced by the use of cuffed endotracheal tubes. In preparation for the intubation, the anesthetist’s preoperative evaluation of the patient should be focused on airway conditions, including mouth opening, dentition, receding jaw, and limitations in neck anatomy and range of motion.

Difficult laryngoscopy/intubation has been reported to occur in 5.8% of general anesthesia;26 various scoring systems based on orofacial measurements have been used to predict difficulties during intubation. The most widely known is the Mallampati score, which identify patients in whom the pharynx is not well visualized through the open mouth. It may be obtained on a seated patient with the mouth open and the tongue protruding without phonating. If a predisposing factor has been detected during this assessment, a more appropriate strategy for intubation should therefore be planned.

Intravenous Induction Agents

As opposed to anesthesia, analgesia is the relief of pain without loss of consciousness. This section covers combination anesthesia and pain medications used during the anesthesia induction phase.1,6,19-21,27-29

Morphine is the most abundant analgesic opiate found in opium; it is extracted from the poppy seed and is a potent pain reliever. Opioid on the other side is a term used in reference to both naturally occurring opiates and synthetic drugs having similar actions. Opioid substances impair pain sensation through opiate receptors of several types that have been identified in the central nervous system. These receptors are found in:

• The limbic system, including the hypothalamus

• The medial and lateral thalamus and the area postrema, site of the trigger zone for nausea and vomiting (emesis)

• The nucleus of the solitary tract, location of the cough center

• The spinal cord

Neuroleptanesthesia

A combination of a neuroleptic (also called antipsychotic or major tranquilizer) with a powerful narcotic is used to provide neuroleptanalgesia; and, the addition of nitrous oxide and oxygen to the combination of neuroleptic/narcotic agents produces neuroleptanesthesia.

The most frequently used agents to achieve neuroleptanalgesia are droperidol, a butyrophenone derivative, and fentanyl, an opioid with a short duration of action. However, both of them exert a marked respiratory depressant effect, which outlasts the analgesic effect and they both induce hypotension. Fentanyl should be administered slowly over 5 to 10 minutes and adequate ventilation and oxygenation are required. After neuroleptanalgesia, nitrous oxide administration starts. This latter method is useful in obstetrics and in minor procedures such as diagnostic explorations if the patient is cooperative. The most common adverse effects after neuroleptanesthesia are confusion and mental depression.

Dissociative Anesthesia

Dissociative anesthesia is a state similar to neuroleptanalgesia in which patients feel totally dissociated from their surroundings. Ketamine is the only drug used at the present time to produce this state. Ketamine was introduced as a derivative of the hallucinogenic drug phencyclidine in 1965. It is a very atypical induction agent as it does not suppress consciousness as most general anesthetics do, but disrupts it. With ketamine the patient has a rather normal muscular tone, the eyes may remain open, and by observing the electroencephalogram tracings it may wrongly be concluded that the patient is awake.

Ketamine produces profound analgesia and amnesia. Unlike other agents, skeletal muscle tone, heart rate, arterial blood pressure and cerebrospinal fluid pressure can be increased by ketamine. Moreover, ketamine does not affect the laryngeal reflexes and maintains a normal respiratory cycle with a strong bronchodilator effect. To counteract ketamine’s known excessive salivation effect, which poses a potential risk of aspiration in the deeply sedated patient, atropine is added in the premedication to reduce mucous and salivary secretions.

Several routes including oral, rectal and intramuscular can be used to administer Ketamine. Its duration of action is between 10 to 20 minutes; therefore, it is commonly used in children and adults for short diagnostic procedures. Because of its hallucinogen effect, recovery from ketamine anesthesia is accompanied by emergence delirium and agitation. Ketamine is contraindicated in patients with psychiatric disorders, with a cerebrovascular disease, intracranial hypertension, arterial hypertension and glaucoma.

Barbiturates

Thiopental:

Thiopental is a short acting barbiturate, brought into practice for the first time in 1934. Although it provides a rapid and stable induction of general anesthesia, it is cleared very slowly from the body. So it is not suitable for maintenance of anesthesia and an alternative volatile agent must be used for that matter. It also causes a dose-dependent depression of heart rate and blood pressure.

Etomidate:

Etomidate, which has been introduced in 1973, is an ultra-short acting hypnotic, which can induce amnesia within 5 to 15 seconds after a single bolus dose and unlike thiopental, has virtually no cardiovascular effects. However, it has other drawbacks such as pain on injection, myoclonic movements at induction, and post-operative nausea and vomiting especially in combination with opioid use. Its use as a sedative in the intensive care unit has also been reported to be associated with suppression of synthesis of endogenous steroids by adrenal glands. Therefore, etomidate should not be used in the maintenance of anesthesia.

Propofol

Propofol was introduced in 1985; it is a short-acting intravenous anesthetic that can induce unconsciousness within 1 minute, but it has a short-lived effect of 3-5 minutes due to its rapid redistribution. These properties make propofol suitable for induction and maintenance of general anesthesia. Moreover, it produces a rapid clear-headed recovery, which is useful in ambulatory surgery.

Pre-anesthetic Medications

A well-thought and planned premedication not only will foster an uncomplicated anesthesia and post-operative course by reducing the anxiety of the patient, and by improving the rapidity and the smoothness of induction, but it will also compensate for the side effects of the anesthetics including salivation, bradycardia, and post-operative nausea and vomiting. Pre-anesthetic medications include sedatives, opioids, tranquillizers and anticholinergic agents.

Sedatives or barbiturates, such as secobarbital and pentobarbital are the most commonly used sedatives as they produce less nausea and vomiting than opioids. Opioids such as fentanyl and morphine are given to patients in combination with nitrous oxide and thiopental. They can also be administered with a barbiturate for regional anesthesia.

Phenothiazine derivatives like promethazine are often administered with opioids due to their potentiation effects on analgesia without increasing the side effects. Tranquilizers are useful as preoperative sedation, and they help to prevent central nervous system stimulation caused by the local anesthetics and provide amnesia. Anticholinergic agents such as atropine and scopolamine are commonly used to reduce salivation.

Muscle Relaxants/Neuromuscular Blockers

They are valuable adjuncts to general anesthesia and should be administered only to anesthetized patients. They should not be used to stop patient’s movement because they have no analgesic or amnestic effect.

Neuromuscular blockers act at the neuromuscular junction via their effects on acetylcholine, which is the major neurotransmitter at the motor endplate. There are two levels of action; the post junctional effects such as those produced by depolarizing neuromuscular blockers like succinylcholine (which consist in a prolonged depolarization by desensitization of acetycholine receptors), inactivation of voltage-gated sodium channels at the neuromuscular junction, and increases in potassium permeability of the cell membrane, resulting in a failure of action potential generation and muscular block. As for the prejunctional effects, they are produced by nondepolarizing neuromuscular blockers, which affect the receptors on motor nerve endings involved in the modulation of acetycholine release and preventing it from being made available.

The main advantages of neuromuscular blocking agents are improvement of face mask ventilation and facilitation of tracheal intubation. They also provide surgical relaxation. The required intensity of neuromuscular blockade that is desired depends on the type of surgical procedure. There are, however, important safety issues with their use due to their cardiovascular and respiratory side effects.

Succinylcholine, a rapid onset, short-acting depolarizing muscle relaxant has been traditionally used when rapid tracheal intubation is needed in emergency or during an elective surgery. It can provide muscle relaxation in 60 to 90 seconds and its effect lasts only 6 to 10 minutes. However, it has numerous side effects, which include severe effects such as cardiac arrest, severe arrhythmias, prolonged respiratory depression, and malignant hyperthermia. Further, it is contraindicated in patients with known hyperkalemia, major crush injuries, and muscular dystrophy. Succinylcholine has also been associated with increase in intracranial and intraocular pressures.

Intermediate-acting neuromuscular blockers include steroid-based compounds, pancuronium, vecuronium, atracurium and cisatracurium; however, none is as rapid as succinylcholine. Rocuronium, which is also a steroid based non-depolarizing muscle relaxant, has been proposed as a replacement for succinylcholine. However, due to its longer duration of action (37 to 72 minutes), rocuronium has to be used with caution in patients with myasthenia gravis, hepatic disease, neuromuscular disease, severe cachexia and carcinomatosis. Allergy is the only contraindication to the use of rocuronium.

Except for the relatively new drugs atracurium and cisatracurium, the kidney generally excretes muscle relaxants that are metabolized in the plasma (Hofmann elimination), and thus can be used in case of renal or hepatic impairment.

Reversal of Neuromuscular Blockade

The neuromuscular blockade induced at the beginning of the general anesthesia needs to be reversed at the end of surgery with the use of anticholinesterases drugs which act primarily by inhibiting acetylcholine esterase, thus prolonging the existence of acetylcholine at the motor endplate. Neostigmine, a commonly used reversal agent, is administered at 60-80 μg/kg and usually combined with atropine to antagonize the muscarinic side effects of neostigmine.

Sugammadex (modified gamma-cyclodextrin) is a selective relaxant binding agent which complexes with steroid-based neuromuscular blocking agents, helping in rapid removal from plasma and excretion through the kidney. The recommended dose for sugammadex is between 2-16 mg/kg of body weight.

To avoid relying only on neuromuscular blocking agents, it is important to keep in mind that there are other alternatives that will provide adequate relaxation in the operating room. These options are the adjustment of the depth of anesthesia, regional anesthesia, and proper positioning of the patient on the operating table. The anesthetist has a choice to make depending on the estimated time remaining before the end of the surgery, the anesthetic technique and the type of surgery.

Intravenous Administration of Fluids

Anesthetists commonly administer intravenous fluids for a wide variety reasons.4,18, Bleeding is the most obvious one. Patients may also be dehydrated preoperatively due to the disease, particularly a bowel disease, or fasting. In such cases the anesthetist must estimate the patient’s fluid status and correct it if necessary, using urine output if the patient is catheterized, central venous pressure and blood tests.

Five categories of intravenous fluids need to be mentioned: 1) 5% Dextrose in water (D5W) is useful because this solution has the same concentration of the blood plasma. When D5W is administered the cells rapidly absorb dextrose, which leaves only water in the circulation. This is therefore an effective way to deliver water to the body as pure water is harmful causing the cells to rupture. 2) 0.9% normal saline solution (sodium chloride) is commonly used during surgery for immediate venous/arterial access for intravenous medication. 3) Compound sodium lactate (Hartmann solution) is another salty solution that contains sodium, potassium, calcium chloride and lactate in levels similar to those of human blood. When a patient loses blood the most important measure is to maintain the circulating volume. If blood is not immediately available, salt-containing solutions are used. However, in this scenario each volume of blood lost needs to be replaced by twice or three times the volume of salty solutions due to the fact that they leak out to the tissues over time. 4) Solutions, known as colloids, containing large molecules like certain proteins (gelatin) or carbohydrates (dextran) are retained much longer in the bloodstream and can fulfill the purpose. Unfortunately, they can be responsible for severe allergic reactions and also interfere with blood coagulation. 5) Blood products include red cells fraction, platelets, coagulation factors, and they are replaced according to the need of the patient.

General Anesthesia Procedure

Before proceeding it is important for the anesthetist to verify that all the necessary equipment and material needed are available and ready for use. The mnemonic DAMMIS is a reminder of what should be checked: Drugs, Airway equipment, Machine, Monitors, IV, Suction

The stages of general anesthesia include:4,18,29

• Stage I:

Stage of induction or analgesia

• Stage II:

Stage of excitement or delirium (dilated reactive pupil due to the preponderance of the sympathetic system)

• Stage III:

Stage of surgical anesthesia (normal pupil); it is divided into four planes (Guedel’s classification). Stage III is the state into which the patient should be maintained for general anesthesia.

• Stage VI:

Stage of medullary paralysis (dilated non-reactive pupil)

General anesthesia has three phases, which are important to consider: these are the induction, maintenance and recovery phase.

Induction

Induction is the period between the administration of inductions agents and loss of consciousness where the patient status evolves from analgesia without amnesia to analgesia with amnesia. It is considered as the most dangerous time since the medications can result in hemodynamic instability, apnea and loss of airway tone. Coughing, breath-holding and laryngospam may occur at this phase.

Overdose or an inadequate choice of medication for induction is one of the most common causes of death during general anesthesia. A review of anesthesia-related cardiac arrest based on a database of 217,365 procedures showed that 64% of anesthesia-attributable cardiac arrest were caused by airway complications that occurred during induction, emergence or in the postoperative period, with a 29% rate of mortality. On the other hand, anesthesia-contributory cardiac arrest occurred during all phases of anesthesia and led to a 70% mortality rate.

As seen previously, induction can be performed using either intravenous route, or via inhalation of an anesthetic gas. The latter method is used especially in the pediatric population before the anesthetist can have access to an intravenous route. Intravenous induction involves also the administration of an analgesic (fentanyl) in anticipation of the pain the patient may feel during endotracheal intubation and which may raise the blood pressure and the heart rate. Since the next step will be to secure the airway, muscle relaxants will be added to facilitate endotracheal intubation if needed, and thus mechanical ventilation. However, if during the patient’s preoperative assessment, the anesthetist has identified predictors of difficult airway access, then intubation of the patient should be performed before induction using an advanced tool like a fiberoptic bronchoscope.

After induction, eyelids should be taped gently in a closed position to avoid corneal exposure or accidental erosion and to prevent nerve injuries, the patient should be positioned with the arms at less than 90 degrees in relation to the body, padding of the regions in contact with hard surfaces and a neutral neck position are recommended.

In general, intubation is indicated in an emergent case with a potential for airway contamination including full stomach, altered state of consciousness, and polytrauma. In elective surgery, the indication may be, among other reasons, gastroesophageal reflux, pharyngeal bleeding, surgical need of deep muscle relaxation with long-acting muscle relaxants (abdominal or thoracic surgery), and predictable difficulty to use mask ventilation (i.e., due to facial anomaly, orofacial surgery, or surgery requiring a lateral or prone positioning of the patient).

The induction phase is characterized by an intense and frequent monitoring of the patient’s parameters. In addition to clinical observation of the patient, a routine practice is to measure blood pressure every minute along with a continuous electrocardiogram, pulse, temperature, oxygen saturation, and end-tidal carbon monoxide concentrations.

Rapid Sequence Induction

A specific type of induction called rapid sequence induction (RSI), consists of rapid sequential intravenous administration of an induction anesthetic, a sedative and a muscle relaxant with or without a narcotic; this is followed by endotracheal intubation within one minute of injection of the muscle relaxant (usually succinylcholine due to its fast onset and duration). RSI is indicated in emergency situations where the patient is unstable or considered to be at high risk for aspiration or in elective surgery and if there is increased intracranial pressure.

Maintenance of Anesthesia

Maintenance of anesthesia is the continuation of general anesthesia with the use of intravenous or inhalational agents, independently from the mode of induction. Most frequently, the patient will be kept anesthetized with the administration of inhalational agents via the breathing system of the anesthesia machine. The patient may be breathing spontaneously the oxygen/anesthetic mixture, or artificially under pressure by a ventilator, particularly if the surgery required the use of deep muscular blocking agents which indiscriminately impede the function of respiratory muscles.4,18

The maintenance phase is usually the most stable part of the anesthesia process. Nevertheless, the anesthetist should still keep the same level of vigilance and ensure a regular monitoring of the patient. The measurement of the blood pressure, respiratory rate, heart rate, oxygen saturation, temperature, oxygen administration and gases, end-tidal carbon dioxide, will be recorded. Depending on the type of surgery and/or preexisting medical conditions of the patient, additional parameters such as central venous pressure, urinary output will have to be included.

It is also critical for the anesthetist to stay updated about the progress of the surgical procedure, as clear communication with the surgical team supports planning of the next phases of anesthesia. As the surgical procedure progresses, adjustments in anesthetic doses might be needed to maintain the required level of anesthesia, while keeping the patient safe with the minimum amount of medications. The depth of anesthesia can be estimated via the electroencephalographic (EEG) recording on the monitor screen, as well as by the bispectral index monitoring, if available. However, experienced anesthetists should be able to recognize inadequate anesthesia when the patient moves or coughs.

If the patient has been administered myorelaxants, the anesthetist should be alerted by an onset of hypertension, tachycardia, sweating and capillary dilation and determine whether adjustment of the level of anesthesia depth is required. Conversely, a decreased heart rate and hypotension may mean excessive depth and must be corrected immediately to prevent severe complications.

It is worth mentioning that the drugs administered during the induction phase may still continue their effects during the maintenance phase. Similarly, effects of the drugs used during the induction and maintenance phase may still be exerting their effect during the recovery phase. This should be taken into account to estimate the doses for maintenance and to evaluate possible adverse effects due to drug interactions.

Recovery from Anesthesia

Recovery from anesthesia, also called the emergence phase, is planned in collaboration with the surgeon as the surgery is drawing to a close. Again, vigilance and close monitoring by the anesthetist of all the parameters are of paramount importance during this critical phase, which is marked by exacerbated autonomic responses and instability.4,19,30-33

First, the anesthetic gas administration level is lowered or even interrupted. Assisted ventilation is stopped and the patient is restored to breathing independently and progressively emerging to consciousness. In a second step, if muscular blocking agents were part of the anesthesia regimen their action is reversed. Traditionally, anticholinesterases drugs (neostigmine) have been used to reverse this action. However, their efficacy has not been consistent in resolving deep levels of neuromuscular block. A more selective agent sugammadex is now available. Concurrently, the regression of muscle paralysis should be monitored and its reversal objectively assessed.

Clinical evaluation of the muscle blockade relies on the return of muscle strength (head lift, jaw clench and grip strength) or respiratory parameters (vital capacity and tidal volume). However, clinical signs are not considered sensitive enough to serve as criteria upon which the anesthetist should base his/her decision to extubate the patient. Therefore, the prevalent opinion within the medical community is more in favor of using a peripheral nerve stimulator to evaluate the blockade. Most commonly, the anesthetist will observe the contraction of the adductor pollicis muscle elicited by the stimulation of the ulnar nerve either at the wrist or at the elbow. If patient positioning limits access to the arms to stimulate the ulnar nerve, then the peroneal nerve or the facial nerve may be used for monitoring.

Objective evaluation of the depth of neuromuscular blockade is important for the determination of the appropriate dose of sugammadex to be administered, as well as the timing of tracheal extubation to ensure no residual weakness is present at the end of the anesthetic procedure.

Postperative residual neuromuscular block has been associated with impaired pharyngeal function, increased aspiration risk, upper airway weakness and partial upper airway obstruction. It can considerably jeopardize the recovery of the patient as it has been shown to lead to postoperative pulmonary complications in 28% of the cases and even to tracheal reintubation. Therefore, regardless of the clinical experience of the anesthetist, objective assessment of neuromuscular function has become mandatory.

Once the patient has regained his/her airway reflexes, the anesthetist will proceed with extubation and observe/monitor the patient until complete stabilization and communication by the patient is made. If the procedure was performed in an ambulatory setting, under no circumstances should the patient be allowed to leave the health facility unaccompanied or drive on the same day of having a surgical procedure.

Total Intravenous Anesthesia

Total intravenous anesthesia (TIVA) is defined as a procedure that achieves general anesthesia without inhaled hypnotics. This method has several advantages. It is generally quicker and easier to perform in a patient who does not need to be intubated.1,4,18

Main Indications of TIVA

• Risk of malignant hyperthermia

• Long QT syndrome

• History of severe postoperative nausea and vomiting

• Tubeless Eye nose and throat, and thoracic surgery

• Patients with difficult intubation/extubation

• Neurosurgery patients

• Neuromuscular disorders/myasthenia gravis

• Ambulatory exploration or surgery

Criteria for Pharmacologic Agents and System Requirements for TIVA

Drugs with fast onset and offset times are preferred because they balance hypnosis and analgesia with rapid recovery. For example, the co-administration of propofol and remifentanyl are synergistic and considered a good drug combination. The use of target-controlled infusions is key for the maintenance of adequate concentrations both in the brain and the plasma, and the best way to achieve this level is with pharmacokinetic infusion pump systems.1 Target controlled infusion systems have the following components: 1) a user interface, 2) a microprocessor with pharmacokinetic software, 3) an infusion pump which delivers up to 1200 ml/hr, and 4) a visual and audible alarm system.

Preparing And Planning For Anesthesia

When the need for and type of anesthesia is being considered, the patient interview with the anesthetist is a very important step. This is particularly true in elective surgery. It will bring to light the patient’s temperament, mental status, level of cooperation, personal habits, history of addictions (with their potential to interact with the anesthesia drugs), and allergic antecedents. The patient’s family history is also very important; for example, family history may include malignant hyperthermia in a parent or sibling, which is crucial to help guide the patient make an informed decision about the choice of anesthesia and agents that should be avoided.18,23,25,53,58,59,60-63

A pertinent assessment related to pathological conditions in the patient’s personal history with potential to lead to difficult airway management during anesthesia gives certain cues as to what would be required for airway management. For example, a positive history for gastroesophageal reflux disease, dysphagia, and gastrointestinal disorder may represent an increased risk of regurgitation and pulmonary aspiration and will indicate a need for tracheal intubation.

The awareness about pre-existing diseases such as diabetes, hypertension, coronary insufficiency, and hepatic or kidney impairments, will help determine necessary preoperative investigations, monitoring parameters, and the choice of premedication, adjuvant and anesthetic drugs. Furthermore, it will increase awareness of known potential intraoperative and postoperative complications.

Past History and Prior Anesthesia

Routinely asking about prior anesthetic experiences should be an integral part of proper preparation for anesthesia. While doing so, patients in need of psychological help can be detected, and those at risk for adverse effects from anesthesia, such as post-op nausea and vomiting (PONV), allergies, or susceptibility to malignant hyperthermia can be identified.

A prior experience of inadvertent intraoperative awareness (the unexpected and explicit recall by patients of events that occurred during anesthesia) should be carefully researched as this has been recognized as a strong predictor of another similar event. The issue of inadvertent awareness is not only relevant to the patient’s safety but also to the standards for monitoring, as well as research in the field of neural correlates of consciousness. The approximate incidence of awareness in the general population is estimated to be 1-2 per 1000, while patients with a history of intraoperative awareness with recall have an incidence of 1 in 50.

The hypothesis of a genetic contribution is controversial. Since there is established evidence that incidence of awareness without recall is higher than with recall, it is safe to assume that this risk is somewhat underestimated. Intraoperative awareness with recall can lead to post-traumatic stress disorder (PTSD). The distress experienced by the aware patient is particularly more intense when neuromuscular agents have been administered.

Current Medications

A history of medication should be obtained and documented in all patients, during the process of evaluation of general anesthesia. Especially, in the geriatric population which consumes more systemic medications than any other group.

Generally, administration of most drugs, with some exceptions, should be continued up to the morning of surgery. The dosage of antihypertensive drugs and insulin will have to be adjusted, while oral hypoglycemic drugs should be discontinued. Diuretics, including angiotensin converting enzyme (ACE) inhibitors, should be discontinued the day before surgery due to their effects on water and electrolyte balance; ACE inhibitors, which are routinely used in hypertensive patients contribute to hemodynamic instability by interfering with the renin-angiotensin-aldosterone system, a key player in the blood pressure regulation. The group of monoamine oxidase inhibitors should be interrupted 2 to 3 weeks before surgical procedure due to the risks of interaction with anesthesia drugs. Oral contraceptives should be discontinued at least 6 weeks before elective surgery because of the risk of venous thrombosis.

The use of medications that potentiate bleeding needs to be carefully evaluated taking in account the risk benefit ratio and the recommended time frame for a discontinuation will be based on drug clearance and half-life properties. Aspirin should be discontinued 7-10 days before surgery and oral anticoagulants must be stopped 4-5 days prior to surgery. The American Society of Anesthesiologists also recommends discontinuing herbal supplements at least 2 weeks before surgery.

Allergies

The clinical spectrum of allergic manifestations ranges from mild reactions such as skin rash to the most severe forms with difficulty breathing and anaphylaxis. As a first approach, preanesthetic interview with the patient may reveal a history of allergic reaction to known products or drugs including foods, latex, disinfectants, antibiotics and local anesthetics. This information will be recorded in the medical file and used to exclude exposure to the sensitizing agent, and select an appropriate alternative.

Asthma and Chronic Rhinitis

These two pathological conditions with underlying allergic mechanisms are the most common chronic airway diseases and as such, merit a close evaluation when planning anesthesia in patients with these conditions.

Two types of asthma can be distinguished. The allergic and the nonallergic types, and although they may overlap, the allergic type is the most frequent in children and adults. The development of asthma is thought to be due to both genetics and environmental factors such as tobacco smoke, air pollutants, and exposure to allergens, which may trigger its onset.

Allergic rhinitis is characterized by symptoms such as sneezing, nasal blockage and itching of the nose, which can be intermittent or permanent. More than 80% of asthmatic patients have rhinitis, and 10% to 40% of rhinitis patients have asthma. Because of this association, patients with severe or uncontrolled rhinitis should be evaluated for asthma before anesthesia.

Another meaningful association is sleep-disordered breathing which has been found to be more prevalent in asthmatic individuals than in the normal population.

Preoperative assessment and physical examination in asthmatic patients should focus on preoperative pulmonary risk assessment. The anesthetist should ask about exercise tolerance and clearly document any drug sensitivities, especially aspirin given the high prevalence of aspirin-induced asthma. The presence of decreased breath sounds, sibilants, rhonchi, and prolonged expiratory phase, a recent exacerbation with wheezing, cough, and dyspnea increases the risk of perioperative pulmonary complications, in addition to an increased risk of bronchospasm induced by tracheal intubation.

If the physical examination reveals the presence of an active bronchospasm, elective surgery should be postponed until the patient becomes free of wheezing, cough and dyspnea. Furthermore, asthmatics who are smokers are strongly advised to abstain from smoking at least 2 months before surgery.

Preparatory Phase

The key parameters in the prevention of perioperative bronchospasm in asthmatic patients are the control of airway inflammation and reduction of the associated symptoms. Spirometry evaluation of the lung function is useful. The drugs used to control asthma should be continued perioperatively.

General Anesthesia and Associated Drugs

Drugs associated with histamine release (morphine, atracurium) should be avoided and intubation should be performed under adequate analgesia (fentanyl). Short-acting anesthetic agents include propofol, and ketamine, which is a bronchodilator. Extubation will be carried out in a sitting position and breathing oxygen.

Intraoperative bronchospasm has been reported to occur in asthmatic patients. Based on published literature, bronchospasm induced by irritation of the airway, occurred more frequently in patients who had predisposing factors such as asthma, heavy smoking or bronchitis, during induction and maintenance phase of anesthesia. Other studies showed that an allergic mechanism was present in a significant number of the cases experiencing bronchospasm during induction.

The treatment of bronchospasm aims at relieving as quickly as possible the airway obstruction to reestablish normal oxygenation. For this purpose, oxygen concentration should be increased to 100% and manual bag ventilation started to assess the pulmonary compliance. The concentration of the volatile anesthetic (sevoflurane or isoflurane, but not desflurane, which is an irritant) will be increased. Propofol or ketamine will be added to rule out an inadequate depth of anesthesia as a cause for the bronchospasm.

Quick acting beta 2-selective adrenergic agonists should be administered with a nebulizer or a metered-dose inhaler to relieve the bronchoconstriction. As an example, 8-10 puffs of salbutamol whose onset of action is 5 minutes with a peak at 60 minutes and duration of action extending to 4-6 hours, will be repeated at 15 to 30 min intervals. Finally, steroids will be administered intravenously to speed up the resolution of the airway inflammation.

Regional anesthesia is best suited for peripheral surgery in poorly controlled asthmatic patients. In these cases, spinal technique is considered safe.

Summary

There has been rapid growth and development of varied clinical roles within anesthesia and surgical health teams to deliver inpatient and outpatient treatment with the goal to improve available, cost-effective patient care. Nurse anesthetists have a vital role in the management of the perioperative patient as well as in the provision of clinical support services outside the operating suite. As experienced anesthesia clinicians, nurse anesthetists are able to assist in the education and training of new nursing and medical staff in the provision of varied anesthesia procedures, including pre- and post-anesthesia care.

Nurse anesthetists specifically have a vital role in the care of surgical patients. This article provided an overview of local, regional and general anesthesia, as well as the nurse’s responsibilities in the management of the patient while under anesthesia. The responsibilities of the anesthetist to deliver pre- and post-operative care relating to the administration of anesthesia were discussed. This includes knowledge of the side effects and contraindications of the different anesthesia techniques, as well as an understanding of the three phases of anesthesia: induction, maintenance and recovery.

Anesthesia care teams work in collaboration with all members of the surgical team, as well as in other health settings to provide a plan of care tailored to each individual patient. This plan may include intravenous sedation, pain control, or varied types of anesthesia during emergency, surgical or other procedures, such as palliative types, which nurse anesthetists might be called upon to manage and to responsibly work in concert with their health teams in the delivery of safe and appropriate anesthesia care for patients.

Please take time to help course planners evaluate the nursing knowledge needs met by completing the self-assessment of Knowledge Questions after reading the article, and providing feedback in the online course evaluation.

Completing the study questions is optional and is NOT a course requirement.

1. _____________ is used to anesthetize an area of the body.

a. Local anesthesia

b. General anesthesia

c. Sedation

d. Regional anesthesia

2. True or False: The term “asleep” is used when anesthesia clinicians speak of a patient who is anesthetized because general anesthesia is similar to sleep in physiological terms.

a. True

b. False

3. The triad model of anesthesia means that _______________ needed to produce all three of the intended effects of anesthesia: narcosis, analgesia, and muscle relaxation.

a. sedation is

b. an anesthesia care team is

c. multiple agents are

d. only one agent is

4. Which of the following is characteristic of electrical brain activity in an anesthetized subject but not an individual who is sleeping?

a. Rapid eye movement (REM) sleep

b. Non-REM sleep

c. Burst suppression

d. Aniso-electric periods

5. Pain signals turn into perceived pain at the moment the sensory pain signals arrive at the

a. thalamus.

b. the cortex.

c. nociceptors.

d. peripheral nerves to the spinal cord.

6. Peripheral nerve signals that head towards the central nervous system (CNS) are known as

a. efferent signals.

b. descending signals.

c. isoelectric signals.

d. afferent signals.

7. True or False: General anesthesia require the use of analgesics to produce unconsciousness.

a. True

b. False

8. _____________ in the central nervous system produce muscle movement.

a. Efferent signals

b. The dorsal columns

c. Afferent signals

d. Nociceptors

9. An individual nerve transmits its signal along the axons by a self-propagating electrical charge called

a. propagation.

b. an action potential.

c. infusion.

d. a resting potential.

10. The succession of depolarization and repolarization allows the propagation of the impulse to spread along _________, in what is called action potential.

a. the synapse

b. the receptor

c. the vesicle

d. the axon

11. The most widely known compound that interferes with nerve conduction by blocking the voltage-gated sodium channels is

a. sodium

b. potassium

c. opium

d. cocaine

12. True or False: Muscles relaxants are needed both for easy access to the surgery site, and intubation.

a. True

b. False

13. The action potential is passed from neuron to neuron at the _____________ where it triggers the release of chemicals or neurotransmitters.

a. synaptic junction

b. dorsal columns

c. axon

d. nociceptors

14. As the action potential is passed from neuron to neuron, another action potential mediated by the binding of the neurotransmitter to the __________ site of the synapse will be initiated and so on.

a. axon

b. dendritic

c. junction

d. nociceptors

15. If cocaine is present in the body, it attaches to the dopamine, serotonin or noradrenaline transporters and blocks the normal recycling process, resulting in a

a. buildup of stimulatory neurotransmitters in the synapses.

b. reduction of stimulatory neurotransmitters in the synapses.

c. reduction of the effects of stimulatory neurotransmitters.

d. block of the stimulant effects of cocaine.

16. True or False: Cocaine acts as an efficient local anesthetic agent because it blocks the voltage-gated sodium channels in the peripheral neurons.

a. True

b. False

17. The drug procaine has a short duration of action

a. is efficient for topical use.

b. and causes minimal systemic toxicity

c. but creates no local irritation.

d. is approximately 10 times more potent than tetracaine.

18. The combination of procaine and __________ decreases its rate of absorption in the bloodstream and doubles the duration of its action.

a. sodium

b. potassium

c. ropivacaine

d. epinephrine

19. A 2% solution of _____________ is used topically on mucous membranes.

a. ropivacaine

b. procaine

c. tetracaine

d. epinephrine

20. True or False: A 1%-2% solution of procaine is used for nerve blocking in regional anesthesia and infiltration anesthesia, and a 5%-20% is needed for spinal anesthesia.

a. True

b. False

21. Regional anesthesia is obtained by blocking the nerve, so that the skin, the deeper structures, and the muscles it supplies become

a. slowed.

b. numbed.

c. paralyzed.

d. infused.

22. The regional anesthesia known as a neuraxial block involves

a. upper extremities.

b. lower extremities.

c. the trunk of the body.

d. the spine.

23. A regional anesthesia known as ______________involves the use of a tourniquet to isolate an intravenous injection of anesthetic into a limb.

a. neuraxial block

b. Bier’s block

c. epidural block

d. epidural block

24. The technique of regional anesthesia involves inserting a needle

a. into the nerve to deposit the anesthetic agent.

b. near enough to a nerve to deposit the anesthetic agent.

c. into the nerve, which invariably injures the nerve.

d. far from the nerves to protect it from injury.

25. _____________ is used to help gain accuracy and avoid nerve and large vessels injuries during the injection of a regional anesthesia.

a. A plastic catheter

b. A tourniquet

c. An ultrasound scanner

d. A dermatome map

26. True or False: Pain is experienced in the subconscious part of the brain, and triggers physiological responses, activating the sympathetic system.

a. True

b. False

27. Regional anesthesia offers a number of advantages in addition to pain control; for example, during surgery regional anesthesia

a. vessel contraction within the anesthetized vessels.

b. stress-induced inflammatory response to function.

c. higher pressure within the dilated vessels.

d. allows a patient to breathe without airway support.

28. True or False: When an anesthesiologist is inserting a needle to deposit an anesthetic agent, the anesthesiologist may rely on a patient’s anatomical landmarks because these do not vary from one individual to another.

a. True

b. False

29. In order to improve accuracy and speed when administering an anesthetic agent in a patient, the anesthesiologist finds the location for insertion of the needle, using the help of

a. a plastic catheter.

b. an electronic nerve stimulator.

c. a dermatome map.

d. anatomical landmarks.

30. For lengthy regional anesthesia procedures,

a. the patient is sedated in larger doses to maintain comfort.

b. a Bier’s block must be used.

c. the patient must be unconscious.

d. a plastic catheter may be inserted and left in situ.

31. To prevent a higher than intended diffusion of the anesthetic drug in the cerebrospinal fluid (CSF), some solutions for spinal anesthesia are formulated with

a. 8% dextrose.

b. 10% sodium.

c. epinephrine.

d. 4% fentanyl.

32. True or False: The use of portable ultrasound scanners and electronic nerve stimulators are used in combination by many anesthesiologists to avoid nerve and large vessels injuries during anesthetic drug injections.

a. True

b. False

33. Knowledge of dermatome levels is key in allowing the anesthetist to assess

a. the location of the blockade.

b. whether to use a portable ultrasound scanner.

c. the level of blockade.

d. whether anatomical landmarks are accurate.

34. With a neuraxial block, which of the following has the highest dermatome level?

a. Unmyelinated fiber level

b. Sensory level

c. Sympathetic level

d. Motor level

35. Spinal nerves contain

a. sensory pathways.

b. motor pathways.

c. autonomic fibers.

d. All of the above

36. The use of neuraxial anesthesia in patients with pre-existing neurologic disorders, such as multiple sclerosis

a. is recommended as the preferred technique.

b. is never recommended.

c. is not recommended unless it is absolutely necessary.

d. is recommended unless the patient refuses the procedure.

37. True or False: In general, larger unmyelinated fibers are more susceptible to blockade than small myelinated fibers.

a. True

b. False

38. Spinal anesthesia is used for the following procedures except for

a. surgeries in the head and neck.

b. prostate surgery.

c. surgeries involving the lower half of the body.

d. None of the above

39. _______________________ performed under spinal anesthesia require very small incisions, produce less pain and result in shorter hospital stays.

a. Laparoscopic cholecystectomy

b. Total joint surgery

c. Head and neck surgery

d. None of the above

40. The level and duration of spinal anesthesia are primarily determined by three factors, including ___________, which is the density of the drug when compared to the density of human cerebrospinal fluid.

a. lordosis

b. hypobaricity

c. baricity

d. osmosis

41. To optimize ____________, a pillow may be placed under the patient’s knees or the patient may be set in the lateral position.

a. postoperative pain

b. baricity

c. lordosis

d. osmosis

42. Sterile water or 1/2 normal saline solutions, known as _________________, are rarely used due the osmotic stress they might cause.

a. isobaric solutions

b. hypobaric solutions

c. dextrose solutions

d. glucose solutions

43. True or False: Opioids (usually 25 μcg fentanyl) and morphine (0.1 – 0.5 mg) can be added to provide 24 hours of relief, but unlike fentanyl, morphine requires in-hospital monitoring for respiratory depression.

a. True

b. False

44. One of the three phases of general anesthesia is the ___________ phase, which is the period between the administration of the agents and loss of consciousness.

a. induction

b. maintenance

c. recovery

d. emergence

45. __________________ tend to flow cephalad due to negative intrathoracic pressure.

a. Thoracic epidurals

b. Neuraxial blocks

c. Bier’s blocks

d. Lumbar epidurals

46. Neuraxial techniques are generally considered safer than general anesthesia, particularly in patients with

a. with difficult airway management.

b. thrombocytopenia.

c. anticoagulation therapy.

d. All of the above

47. ________________ is the most frequent, immediate adverse effect of neuraxial anesthesia, which occurs in one third of patients.

a. Bradycardia

b. Airway obstruction

c. Hypotension

d. Hydrocephaly

48. The _______________ is usually the most stable part of the anesthesia process.

a. emergence phase

b. induction phase

c. recovery phase

d. maintenance phase

49. True or False: If muscular blocking agents were part of the anesthesia regimen their action should be reversed using anticholinesterases drugs such as neostigmine.

a. True

b. False

50. _______________ induced by irritation of the airway, occurred more frequently in patients who had predisposing factors, such as asthma, during induction and maintenance phase of anesthesia.

a. Systemic toxicity

b. Bronchospasm

c. Bradycardia

d. Hypertension

CORRECT ANSWERS:

1. _____________ is used to anesthetize an area of the body.

d. Regional anesthesia

“There are three types of anesthesia to consider: 1) local anesthesia performed typically at the site of the surgical incision, 2) regional anesthesia is used to anesthetize an area of the body, and it may be used alone or in combination with general anesthesia, and 3) general anesthesia where the patient is made completely unresponsive to pain, in which case the patient needs assisted ventilation and close monitoring of his or her physiological status.”

2. True or False: The term “asleep” is used when anesthesia clinicians speak of a patient who is anesthetized because general anesthesia is similar to sleep in physiological terms.

b. False

“Although the term asleep is used when anesthesia clinicians speak of a patient who is anesthetized, general anesthesia is very different from sleep in physiological terms.”

3. The triad model of anesthesia means that _______________ needed to produce all three of the intended effects of anesthesia: narcosis, analgesia, and muscle relaxation.

c. multiple agents are

“In 1926, John Lundy introduced the term “balanced anesthesia” to describe the use of multiple agents “sedatives” as a premedication together with general anesthesia, to improve the results. Later, in the 1950s Gordon Jackson Rees and Cecil Gray proposed a triad of anesthesia consisting of narcosis (meaning unconsciousness), analgesia, and muscle relaxation; all represented in a triangular diagram. The triad model means that one agent is no longer found sufficient to produce of narcosis, analgesia, and muscle relaxation. The triad model is still taught and used with some refinement.”

4. Which of the following is characteristic of electrical brain activity in an anesthetized subject but not an individual who is sleeping?

c. Burst suppression

“Intense electrical activity occurs during the sleep cycle, especially during the REM phase, resembling that of awake subjects. In contrast to what happens in wakefulness and sleep, in anesthetized subjects, the frequency of the brain waves slows and their overall amplitude diminishes. During general anesthesia the patient may even experience short periods of silencing called burst suppression. Therefore, as shown by EEG recordings, anesthesia is distinct from sleep. Burst suppression (BS) is an electroencephalogram (EEG) pattern that is characterized by brief bursts of spikes, sharp waves, or slow waves of relatively high amplitude alternating with periods of relatively flat EEG or isoelectric periods. The pattern is usually associated with coma, severe encephalopathy of various etiologies, or general anesthesia.”

5. Pain signals turn into perceived pain at the moment the sensory pain signals arrive at the

b. the cortex.

“…first the detection of the painful stimulus (nociception) due to the presence of nociceptors located in the skin and other organs, which upon their stimulation will produce electrical signals; in a second step the signals will be transmitted via the peripheral nerves to the spinal cord, then to the thalamus which is responsible for integrating sensory signals; finally the emerging signals from the thalamus will travel to the cortex where the pain signals turn into conscious perception, and at this moment only, pain is being perceived.”

6. Peripheral nerve signals that head towards the central nervous system (CNS) are known as

d. afferent signals.

“Peripheral nerves are made of a mixture of several types of fibers and each type has a specific function. For each particular nerve, signals may be heading towards the CNS, known as afferent signals (also termed ascending), or heading away from the CNS and known as efferent signals (termed as descending).”

7. True or False: General anesthesia require the use of analgesics to produce unconsciousness.

b. False

“Therefore, optimal conditions for general anesthesia require a combination of general anesthetics to produce unconsciousness and analgesics to suppress the stress response.”

8. _____________ in the central nervous system produce muscle movement.

a. Efferent signals

“For each particular nerve, signals may be heading towards the CNS, known as afferent signals (also termed ascending), or heading away from the CNS and known as efferent signals (termed as descending)…. As for the descending signals, they are used to produce muscle movement; they are also called motor signals and travel via type A-fibers.”

9. An individual nerve transmits its signal along the axons by a self-propagating electrical charge called

b. an action potential.

“An individual nerve transmits its signal along the axons by a self-propagating electrical charge called an action potential.”

10. The succession of depolarization and repolarization allows the propagation of the impulse to spread along _________, in what is called action potential.

d. the axon

“The succession of depolarization and repolarization allows the propagation of the impulse to spread along the axon, in what is called action potential.”

11. The most widely known compound that interferes with nerve conduction by blocking the voltage-gated sodium channels is

d. cocaine

“The most widely known compound that interferes with nerve conduction by blocking the voltage-gated sodium channels is cocaine,….”

12. True or False: Muscles relaxants are needed both for easy access to the surgery site, and intubation.

a. True

“… muscles relaxants are needed both for easy access to the surgery site, and intubation.”

13. The action potential is passed from neuron to neuron at the _____________ where it triggers the release of chemicals or neurotransmitters.

a. synaptic junction

“The action potential is passed from neuron to neuron at the synaptic junction where it triggers the release of chemicals or neurotransmitters.”

14. As the action potential is passed from neuron to neuron, another action potential mediated by the binding of the neurotransmitter to the ________ site of the synapse will be initiated and so on.

b. dendritic

“At this level, another action potential mediated by the binding of the neurotransmitter to the dendritic site of the synapse will be initiated and so on.”

15. If cocaine is present in the body, it attaches to the dopamine, serotonin or noradrenaline transporters and blocks the normal recycling process, resulting in a

a. buildup of stimulatory neurotransmitters in the synapses.

“Cocaine acts on the central nervous system by blocking the reuptake of stimulatory neurotransmitters like dopamine, serotonin and noradrenaline in the synapses. Normally, stimulatory neurotransmitters are recycled back into the transmitting neuron by a specialized protein transporter, i.e., a dopamine transporter. If cocaine is present in the body, it attaches to the dopamine, serotonin or noradrenaline transporters and blocks the normal recycling process, resulting in a buildup of these stimulatory neurotransmitters in the synapses. This has the effect of enhancing their actions. It is this second action that is responsible for both cocaine’s stimulant and addictive properties.”

16. True or False: Cocaine acts as an efficient local anesthetic agent because it blocks the voltage-gated sodium channels in the peripheral neurons.

a. True

“Cocaine acts at two levels of the nervous system. Firstly, it blocks the voltage-gated sodium channels in the peripheral neurons making it an efficient local anesthetic agent.”

17. The drug procaine has a short duration of action

b. and causes minimal systemic toxicity

“Procaine has a short duration of action, causes minimal systemic toxicity and creates no local irritation. The combination procaine-epinephrine decreases its rate of absorption in the bloodstream and doubles the duration of its action. A 1%-2% solution is used for nerve blocking in regional anesthesia and infiltration anesthesia, and a 5%-20% is needed for spinal anesthesia. Procaine is not efficient for topical use. Tetracaine is approximately 10 times more potent and more toxic than procaine.”

18. The combination of procaine and __________ decreases its rate of absorption in the bloodstream and doubles the duration of its action.

d. epinephrine

“The combination procaine-epinephrine decreases its rate of absorption in the bloodstream and doubles the duration of its action.”

19. A 2% solution of _____________ is used topically on mucous membranes.

c. tetracaine

“A 2% solution of tetracaine is used topically on mucous membranes.”

20. True or False: A 1%-2% solution of procaine is used for nerve blocking in regional anesthesia and infiltration anesthesia, and a 5%-20% is needed for spinal anesthesia.

a. True

“Procaine has a short duration of action, causes minimal systemic toxicity and creates no local irritation. The combination procaine-epinephrine decreases its rate of absorption in the bloodstream and doubles the duration of its action. A 1%-2% solution is used for nerve blocking in regional anesthesia and infiltration anesthesia, and a 5%-20% is needed for spinal anesthesia. Procaine is not efficient for topical use.”

21. Regional anesthesia is obtained by blocking the nerve, so that the skin, the deeper structures, and the muscles it supplies become

c. paralyzed.

“Regional anesthesia is obtained by blocking the nerve, so that the skin, the deeper structures, and the muscles it supplies become paralyzed.”

22. The regional anesthesia known as a neuraxial block involves

d. the spine.

“There are two main categories of nerve blocks. The first called neuraxial block involves the spine and can be subdivided in spinal, epidural and caudal block. The second called peripheral block may involve the eyes, breast, trunk, the upper extremity and the lower extremity. Peripheral blocks can be used alone or in combination with neuraxial anesthesia or general anesthesia.”

23. A regional anesthesia known as ______________involves the use of a tourniquet to isolate an intravenous injection of anesthetic into a limb.

b. Bier’s block

“Another alternative technique of regional anesthesia consists in the intravenous injection of anesthetic into a limb, which is isolated from the circulation by a system of tourniquet and called Bier’s block.”

24. The technique of regional anesthesia involves inserting a needle

b. near enough to a nerve to deposit the anesthetic agent.

“The technique of regional anesthesia involves inserting the needle near enough to a nerve to deposit the anesthetic agent without injuring the nerve itself. For this, it is possible to rely on anatomical landmarks to locate the nerve, but they may vary from one individual to another. Nowadays, the technique is performed with the help of electronic nerve stimulators, which are more accurate and time saving. A small electric current is passed down the needle and, as the nerve is approached, the current causes the muscles innervated by the nerve to twitch, signaling to the operator that the tip of the needle is close enough to the nerve.”

25. _____________ is used to help gain accuracy and avoid nerve and large vessels injuries during the injection of a regional anesthesia.

c. An ultrasound scanner

“Another way to gain in accuracy and avoid nerve and large vessels injuries during the injection is permitted by the use of portable ultrasound scanners, which allow a guided nerve block under direct visualization of the neighboring structures as the needle approaches. These two techniques complement each other in fact, since they provide important information about both nerve anatomy and function. Therefore, they are used in combination by many anesthesiologists.”

26. True or False: Pain is experienced in the subconscious part of the brain, and triggers physiological responses, activating the sympathetic system.

a. True

“Pain is experienced in the subconscious part of the brain, and triggers physiological responses, activating the sympathetic system….”

27. Regional anesthesia offers a number of advantages in addition to pain control; for example, during surgery regional anesthesia

d. allows a patient to breathe without airway support.

“Besides controlling pain, regional anesthesia presents a number of advantages. It allows the patient to breathe on his own without airway support; it reduces postoperative nausea and vomiting; it blocks the stress-induced inflammatory response to surgical trauma; and it avoids airway manipulation in difficult cases. Since regional anesthesia is accompanied with vessel dilation and lower pressure within the dilated vessels, there will be less blood loss and less requirements for blood transfusions. In addition, regional anesthesia allows earlier recovery of bowel function as well as earlier rehabilitation and hospital discharge.”

28. When an anesthesiologist is inserting a needle to deposit an anesthetic agent, the clinician uses and may rely on a patient’s anatomical landmarks because these do not vary from one individual to another.

b. False

“The technique of regional anesthesia involves inserting the needle near enough to a nerve to deposit the anesthetic agent without injuring the nerve itself. For this, it is possible to rely on anatomical landmarks to locate the nerve, but anatomical landmarks may vary from one individual to another.”

29. In order to improve accuracy and speed when administering an anesthetic agent in a patient, the anesthesiologist finds the location for insertion of the needle, using the help of

b. an electronic nerve stimulator.

“The technique of regional anesthesia involves inserting the needle near enough to a nerve to deposit the anesthetic agent without injuring the nerve itself. For this, it is possible to rely on anatomical landmarks to locate the nerve, but they may vary from one individual to another. Nowadays, the technique is performed with the help of electronic nerve stimulators, which are more accurate and time saving. A small electric current is passed down the needle and, as the nerve is approached, the current causes the muscles innervated by the nerve to twitch, signaling to the operator that the tip of the needle is close enough to the nerve.”

30. For lengthy regional anesthesia procedures,

d. a plastic catheter may be inserted and left in situ.

“Before the regional anesthesia procedure begins, the patient is positioned and connected to standard monitors for follow-up of vital signs the same as if the patient were receiving a general anesthesia. The patient is sedated in small doses to maintain the patient’s comfort but maintain the patient’s consciousness since the patient’s ability to communicate throughout the surgery is important to maintain block safety. For lengthy procedures, a plastic catheter may be inserted and left in situ, so that repeated injections, or an infusion of anesthetic may be given.”

31. To prevent a higher than intended diffusion of the anesthetic drug in the cerebrospinal fluid (CSF), some solutions for spinal anesthesia are formulated with

a. 8% dextrose.

“The height or level of the block depends on the injection site, which is usually done in the lumbar area, but also on the diffusion of the anesthetic solution in the cerebrospinal fluid (CSF). To prevent a higher than intended diffusion of the anesthetic drug, some solutions for spinal anesthesia are formulated with 8% dextrose, making them denser than CSF (hyperbaric solutions); after the injection, the patient will be positioned according to gravity in order to control for the height of the block.”

32. True or False: The use of portable ultrasound scanners and electronic nerve stimulators are used in combination by many anesthesiologists to avoid nerve and large vessels injuries during anesthetic drug injections.

a. True

“Today the nerve is located using the help of electronic nerve stimulators, which are more accurate and save time. A small electric current is passed down the needle and, as the nerve is approached, the current causes the muscles innervated by the nerve to twitch, signaling to the operator that the tip of the needle is close enough to the nerve…. Another way to avoid nerve and large vessels injuries during the injection is the use of portable ultrasound scanners, which allow a guided nerve block under direct visualization of the neighboring structures as the needle approaches its target. These two techniques complement each other in fact, since they provide important information about both nerve anatomy and function. Therefore, they are used in combination by many anesthesiologists.”

33. Knowledge of dermatome levels is key in allowing the anesthetist to assess

c. the level of blockade.

“Knowledge of dermatome levels is key in allowing the anesthetist to assess the level of blockade.”

34. With a neuraxial block, which of the following has the highest dermatome level?

c. Sympathetic level

“Moreover, with a neuraxial block there is a difference between sympathetic, sensory and motor block level. The sympathetic level being generally two to six dermatome levels higher than the sensory level. The sensory level is approximately two dermatome levels higher than the motor level.”

35. Spinal nerves contain

a. sensory pathways.

b. motor pathways.

c. autonomic fibers.

d. All of the above [correct answer]

“Spinal nerves contain both sensory and motor pathways, as well as autonomic fibers.”

36. The use of neuraxial anesthesia in patients with pre-existing neurologic disorders, such as multiple sclerosis

c. is not recommended unless it is absolutely necessary.

“The use of neuraxial anesthesia in patients with pre-existing neurologic disorders, such as multiple sclerosis is not recommended unless it is absolutely necessary.”

37. True or False: In general, larger unmyelinated fibers are more susceptible to blockade than small myelinated fibers.

b. False

“In general, small myelinated fibers are more susceptible to blockade than larger unmyelinated fibers.”

38. Spinal anesthesia is used for the following procedures except for

a. surgeries in the head and neck.

b. prostate surgery.

c. surgeries involving the lower half of the body.

d. None of the above [correct answer]

“Spinal anesthesia is used for almost any procedure of the lower half of the body, including orthopedics, obstetrics, and prostate surgery. The use of spinal anesthesia has also been described for surgeries in the head and neck where punctures performed between the 1st and 2nd thoracic vertebrae resulted in good analgesia.”

39. _______________________ performed under spinal anesthesia require very small incisions, produce less pain and result in shorter hospital stays.

a. Laparoscopic cholecystectomy

“Laparoscopic surgeries such as laparoscopic cholecystectomy performed under spinal anesthesia require very small incisions, produce less pain and result in shorter hospital stays. They are particularly advantageous to use in older and high risk patients for general anesthesia. In the same manner, spinal anesthesia has been associated to a lower postoperative mortality risk in elective total joint replacement surgery.”

40. The level and duration of spinal anesthesia are primarily determined by three factors, including ___________, which is the density of the drug when compared to the density of human cerebrospinal fluid.

c. baricity

“The level and duration of spinal anesthesia are primarily determined by 1) baricity (the density of the drug as compared to the density of human cerebrospinal fluid), 2) contour of spinal canal, and 3) patient position in the first few minutes after injection.”

41. To optimize ____________, a pillow may be placed under the patient’s knees or the patient may be set in the lateral position.

c. lordosis

“To optimize lordosis, a pillow is placed under the patient’s knees; the other option is to place the patient in the lateral position.”

42. Sterile water or 1/2 normal saline solutions, known as _________________, are rarely used due the osmotic stress they might cause.

b. hypobaric solutions

“Isobaric solutions undergo less spread than hyperbaric solutions; both of these solutions are suited for perineal or lower extremity surgery. Hypobaric solutions (sterile water or 1/2 normal saline), are rarely used due the osmotic stress they might cause.”

43. True or False: Opioids (usually 25 μcg fentanyl) and morphine (0.1 – 0.5 mg) can be added to provide 24 hours of relief, but unlike fentanyl, morphine requires in-hospital monitoring for respiratory depression.

a. True

“Opioids (usually 25 μcg fentanyl) and morphine (0.1 – 0.5 mg) can be added to provide 24 hours of relief, but unlike fentanyl, morphine requires in-hospital monitoring for respiratory depression.”

44. One of the three phases of general anesthesia is the ___________ phase, which is the period between the administration of the agents and loss of consciousness.

a. induction

“Induction is the period between the administration of inductions agents and loss of consciousness where the patient status evolves from analgesia without amnesia to analgesia with amnesia.”

45. __________________ tend to flow cephalad due to negative intrathoracic pressure.

d. Lumbar epidurals

“Lumbar epidurals tend to flow cephalad due to negative intrathoracic pressure, whereas thoracic epidurals tend to stay in place. L5/S1 anesthesia is more difficult, likely due to the large fiber size.”

46. Neuraxial techniques are generally considered safer than general anesthesia, particularly in patients with

a. with difficult airway management.

“Neuraxial techniques are generally considered safer than general anesthesia, particularly in patients with difficult airway management, elderly debilitated patients and even the premature newborn.”

47. ________________ is the most frequent immediate adverse effect of neuraxial anesthesia, which occurs in one third of patients.

c. Hypotension

“Neuraxial Anesthesia Complications: Hypotension is the most frequent immediate adverse effect. It occurs in one third of patients, initially due to decreased vascular resistance but in severe cases it may be due to decreased venous return and cardiac output. Risk factors for hypotension include arterial hypertension, obesity, increased fetal weight, chronic alcohol use, and a high level of blockade. Hypotension may cause intraoperative nausea and vomiting. Bradycardia may also be present if the block involves the heart- accelerating fibers (T1-T4 level), or from a decreased venous return.”

48. The _______________ is usually the most stable part of the anesthesia process.

d. maintenance phase

“The maintenance phase is usually the most stable part of the anesthesia process.”

49. True or False: If muscular blocking agents were part of the anesthesia regimen their action should be reversed using anticholinesterases drugs such as neostigmine.

b. False

“… if muscular blocking agents were part of the anesthesia regimen their action should be reversed. Traditionally, anticholinesterases drugs (neostigmine) have been used to reverse this action. However, their efficacy has not been consistent in resolving deep levels of neuromuscular block. A more selective agent sugammadex is now available.”

50. _______________ induced by irritation of the airway, occurred more frequently in patients who had predisposing factors, such as asthma, during induction and maintenance phase of anesthesia.

b. Bronchospasm

“Based on published literature, bronchospasm induced by irritation of the airway, occurred more frequently in patients who had predisposing factors, such as asthma, heavy smoking or bronchitis, during induction and maintenance phase of anesthesia.”

References Section

The References below include published works and in-text citations of published works that are intended as helpful material for your further reading.

1. O’Donnell A. (2012). Anesthesia, a very short introduction. 1st ed. UK: Oxford University Press.

2. Nagrebetsky A, Gabriel RA, Dutton RP, Urman RD. (2016). Growth of Nonoperating Room Anesthesia Care in the United States: A

Contemporary Trends Analysis [abstract]. Anesthesia & Analgesia.

3. Quintana J. (2016). Answering Today’s Need for High‐Quality Anesthesia Care at a Lower Cost; American Association of Nurse Anesthetists.

4. Orebaud SL. (2012). Understanding Anesthesia: what you need to know about sedation and pain control. Baltimore: The John Hopkins University Press.

5. Lexicomp (2016). UpToDate. Retrieved online at .

6. Physicians Desk Reference (2017). Retrieved online at .

7. Bhat, S.N, Himaldev, Upadya M. (2013). Comparison of efficacy and safety of ropivacaine with bupivacaine for intrathecal anesthesia for lower abdominal and lower limb surgeries. Anesth Essays Res. 2013; 7(3): 381–385.

8. Hadzic A and Franco C. (2013). Essentials of Regional Anesthesia Anatomy. New York School of regional anesthesia.

9. Gelb, Douglas (2016). The detailed neurologic examination in adults. Up To Date. Retrieved online at .

10. Ellakany M. (2013). Comparative study between general and thoracic spinal anesthesia for laparoscopic cholecystectomy. Egyptian Journal of Anesthesia; 29: 375–381

11. Perlas A, Chan VWS, Beattie S. (2016). Anesthesia Technique and Mortality after Total Hip or Knee Arthroplasty A Retrospective, Propensity Score–matched Cohort Study. Anesthesiology; 125:724-31.

12. DeLeon, A.M. and Wong, C.A. (2016) Spinal anesthesia: Technique. UpToDate. Retrieved online at .

13. Spinal Anesthesia (2013). New York School of regional anesthesia. Retrieved online at

14. Kooij F.O, Schlack W.S, Preckel B, Markus W. Hollmann M.W. (2014). Does Regional Analgesia for Major Surgery Improve Outcome? Focus on Epidural Analgesia. Anesthesia& Analgesia; 119 (3): 740-744.

15. Gallego Molina MB, Loras Borraz P, Guerrero-Orriach JL. (2015). Neuraxial Anesthesia Complications. Medical & Clinical Reviews; 1(14): 1-7.

16. Youssef MMI and Abdelnaim HE. (2014). Failed spinal anesthesia in addicts: Is it an incidence or coincidence? Egyptian Journal of Anesthesia; 30:247–253.

17. Grant, G.J., et al. (2017). Adverse effects of neuraxial analgesia and anesthesia for obstetrics. UpToDate. Retrieved online at .

18. Falk, S.A. and Fleisher, L.A. (2017). Overview of anesthesia and anesthetic choices. UpToDate. Retrieved online at .

19. Hsu, D.C. (2017). Subcutaneous infiltration of local anesthetics. UpToDate. Retrieved online at 's%20block&selectedTitle=5~36.

20. Khan S.K, Hayes I, and Buggy D.J. (2013). Pharmacology of anaesthetics II: inhalation anaesthetic agents. Continuing Education in Anesthesia, Critical Care & Pain.

21. Sleigh J, Harvey M, Voss L, Denny B. (2014). Ketamine More mechanisms of action than just NMDA blockade. Trends in Anesthesia and Critical Care; 10: 76-81.

22. Kurth M.J, Yokoi T and Gershwin M.E. (2014). halothane-induced hepatitis: paradigm or paradox for drug-induced liver injury. Hepatology; 60(5): 1473–1475.

23. Myles PS, Chan MTV, Kasza J and al. (2016). Severe Nausea and Vomiting in the Evaluation of Nitrous Oxide in the Gas Mixture for Anesthesia II Trial. Anesthesiology; 124:1032-40.

24. Sato S., et al. (2017). Mask Ventilation during Induction of General Anesthesia Influences of Obstructive Sleep Apnea. Anesthesiology; 126 (1):28-38.

25. Walls, R.M. and Brown, C.A. (2017). Approach to the difficult airway in adults outside the operating room. UpToDate. Retrieved online .

26. Kheterpal S, Healy D, Aziz M.F., et al. (2013). Multicenter Perioperative Outcomes Group (MPOG) Perioperative Clinical Research Committee: Incidence, predictors, and outcome of difficult mask ventilation combined with difficult laryngoscopy: A report from the multicenter perioperative outcomes group. Anesthesiology; 119:1360–9.

27. Thompson Bastin M.L., Baker S.N., Weant K.A. (2014). Effects of Etomidate on Adrenal Suppression: A Review of Intubated Septic Patients. Hosp Pharm; 49(2): 177–183.

28. Tran D.T.T., et al. (2015). Rocuronium versus succinylcholine for rapid sequence induction intubation (review). Cochrane database syst rev., issue 10, Art. No: [CD 002788] DOI: [DOI 10.1002/14651858.CD002788.pub3.]

29. Pani N., et al. (2015). Reversal agents in anaesthesia and critical care. Indian J Anaesth.; 59(10): 664–669.

30. Ellis S.J., et al. (2014). Anesthesia-related Cardiac Arrest. Anesthesiology.; 120:829-38.

31. Brull S.J. and Prielipp R.C. (2015). Reversal of Neuromuscular Blockade “Identification Friend or Foe” Anesthesiology; 122:1183-5

32. Bulka C.M., et al. (2016). Nondepolarizing Neuromuscular Blocking Agents, Reversal, and Risk of Postoperative Pneumonia. Anesthesiology; 125:647-55

33. Moi D. (2013). Residual neuromuscular blockade anaesthesia tutorial.

34. McCann M.E and Soriano S.G. (2014). Progress in anesthesia and management of the newborn surgical patient. Seminars in Pediatric Surgery; 23:244–248.

35. Pani N and Panda C.K. (2012). Anaesthetic consideration for neonatal surgical emergencies Indian J Anaesth.; 56(5): 463–469.

36. McPherson C. and Grunau R.E. (2014). Neonatal pain control and neurologic effects of anesthetics and sedatives in preterm infants. Clin Perinatol.; 41(1): 209–227.

37. Bang S.R. (2015). Neonatal anesthesia: how we manage our most vulnerable patients. Korean J Anesthesiol; 68(5): 434-441

38. Taneja B, Srivastava V, Saxena K.N. (2012). Physiological and anaesthetic considerations for the preterm neonate undergoing surgery. Journal of Neonatal Surgery; 1(1):14

39. Hatfield L.A, Meyers MA, Messing TM. (2013). A systematic review of the effects of repeated painful procedures in infants: Is there a potential to mitigate future pain responsivity? Journal of Nursing Education and Practice; 3( 8):99-112.

40. McCann M.E and Soriano S.G. (2012). General anesthetics in pediatric anesthesia: Influences on the developing brain. Curr Drug Targets; 13(7): 944–951.

41. Nasr V.G and Jonathan M. Davis J.M. (2015). Anesthetic use in newborn infants: the urgent need for rigorous evaluation. Pediatric Research; 78(1): 1-6.

42. Baidee Z, Vakiliamini M and Mohammadizadeh M. (2013). Remifentanil for endotracheal intubation in premature infants: A randomized controlled trial. J Res Pharm Pract.; 2(2): 75–82.

43. Ceelie I, de Wildt SN, van Dijk M, et al. (2013). Effect of intravenous paracetamol on postoperative morphine requirements in neonates and infants undergoing major noncardiac surgery: a randomized controlled trial. JAMA.; 309:149–154

44. Wong I, St John-Green C, Walker SM. (2013). Opioid-sparing effects of perioperative paracetamol and nonsteroidal anti-inflammatory drugs (NSAIDs) in children. Pediatric Anesthesia; 23: 475–495.

45. Pang, L.M. (2017). Anesthesia for ex-premature infants and children. UpToDate. Retrieved online at .

46. Davidson A.J, Morton N.S, Arnup S.J et al. (2015). Apnea after awake-regional and general anesthesia in infants: The General Anesthesia compared to Spinal anesthesia (GAS) study: comparing apnea and neurodevelopmental outcomes, a randomized controlled trial. Anesthesiology; 123(1): 38–54

47. Kurth C.D, Coté C.J. (2015). Postoperative Apnea in Former Preterm Infants General Anesthesia or Spinal Anesthesia—Do We Have an Answer? Anesthesiology; 123:15-7

48. Strømn C, Rasmussen L.S . (2014). Challenges in anaesthesia for elderly. Singapore Dental Journal; 35: 23–29.

49. Chu CC, Weng SF, Chen KT et al. (2015). Propensity Score–matched Comparison of Postoperative Adverse Outcomes between Geriatric Patients Given a General or a Neuraxial Anesthetic for Hip Surgery A Population-based Study. Anesthesiology; 123:136-47

50. Ogden CL, Carroll MD, Fryar CD, Flegal KM. (2015). Prevalence of Obesity among Adults and Youth: United States, 2011–2014. NCHS Data Brief, No. 219, November 2015.

51. Nightingale CE, Margarson MP, Shearer E et al. (2015). Association of Anaesthetists of Great Britain and Ireland Society for Obesity and Bariatric Anesthesia. Peri-operative management of the obese surgical patient. Anesthesia; 70: 859–876

52. Chung F, Abdullah HR and Pu Liao P. (2016). STOP-Bang Questionnaire A Practical Approach to Screen for Obstructive Sleep Apnea. Chest; 149(3):631-638

53. Rosenblatt, W.H. and Artime, C. (2017). Management of the difficult airway for general anesthesia. UpToDate. Retrieved online at .

54. Ankichetty S., et al. (2013). Case report: Rhabdomyolysis in morbidly obese patients: anesthetic considerations. Can J Anesth. 2013; 60:290–293

55. Tolone S, Pilone V, Musella M et al. (2016). Rhabdomyolysis after bariatric surgery: a multicenter, prospective study on incidence, risk factors, and therapeutic strategy in a cohort from South Italy [abstract]. Surg Obes Relat Dis.;12(2):384-90.

56. Chung H.S. (2014). Awareness and recall during general anesthesia. Korean J Anesthesiol; 66(5): 339-345.

57. Mashour GA and Avidan MS. (2015). Intraoperative awareness: controversies and non-controversies. Br J Anaesth.; 120-126

58. Complex Information for Anesthesiologists Presented Quickly and Clearly. Anesthesiology. 2017; 126 (1) .

59. Muluk V., et al. (2017). Perioperative medication management. UpToDate. Retrieved online at .

60. Gaëlle Abittan G. (2014). Preoperative medication management for noncardiac elective surgeries. Date of revision – 3rd version November 2014

61. Serra M.F., Anjos-Valotta E.A., Olsen P.C., et al. (2012). Nebulized Lidocaine Prevents Airway Inflammation, Peribronchial Fibrosis, and Mucus Production in a Murine Model of Asthma. Anesthesiology; 117:580 –91

62. Dobyns, J.B. (2017). Anesthesia for adult patients with asthma. UpToDate. Retrieved online at .

63. Dewachter P, Mouton-Faivre C, Emala CW, Beloucif S. (2011). Case Scenario: Bronchospasm during Anesthetic Induction. Anesthesiology; 114:1200 –10

64. Alcohol Facts and Statistics (2014). National Institutes of Health.

65. Gordon, A. (2017). Identification and management of unhealthy alcohol use in the perioperative period.

66. Adams C. (2010). Anaesthetic implications of acute and chronic alcohol abuse. Southern African Journal of Anesthesia and Analgesia;16 (3): 42-49

67. Warner D.O., et al. (2015). Decision Aid for Cigarette Smokers Scheduled for Elective Surgery. Anesthesiology; 123:18-28

68. Bryson EO, Frost EAM. (2011). The Perioperative Implications of Tobacco, Marijuana, and Other Inhaled Toxins. International anesthesiology clinics; 49 (1): 103–118.

69. Jackson KL, Devine JG. Global Spine J. (2016). The Effects of Smoking and Smoking Cessation on Spine Surgery: A Systematic Review of the Literature; 6:695–701

70. Dr Narmatha Thiagarajan (2011). SMOKING AND ANAESTHESIA ANAESTHESIA TUTORIAL OF THE WEEK 221 2ND MAY 2011. totw.

71. Bala, N., Kaur, G., Attri, L.P., et al. (2015). Psychiatric and anesthetic implications of substance abuse: Present scenario. Anesth Essays Res.; 9(3): 304–309.

72. Karam K, Abbasi S and Khan FA. (2015). Anaesthetic Consideration in a Cannabis Addict. Journal of the College of Physicians and Surgeons Pakistan.; 25 (Suppl 1): S2-S3

73. An Updated Report by the American Society of Anesthesiologists Committee on Standards and Practice Parameters. Practice Guidelines for Preoperative Fasting and the Use of Pharmacologic Agents to Reduce the Risk of Pulmonary Aspiration: Application to Healthy Patients Undergoing Elective Procedures. Anesthesiology. 2011; 114(3)495-511

74. ASA physical status classification system. Last approved by the ASA House of Delegates on October 15, 2014 

75. Checketts M.R., Alladi R., Ferguson K., et al. (2016). Recommendations for standards of monitoring during anaesthesia and recovery: Association of Anaesthetists of Great Britain and Ireland. Anesthesia; 71: 85-93.

76. The American Society of Anesthesiologists (2015). Standards for basic anesthetic monitoring. Approved by the ASA House of Delegates on October 21, 1986, last affirmed on October 28th, 2015

77. Jain RK  and Swaminathan S. (2013). Anesthesia ventilators. Indian J Anaesth.; 57(5): 525–532.

78. Deschamps A, Hall R, Grocott H. (2016). Cerebral Oximetry Monitoring to Maintain Normal Cerebral Oxygen Saturation during High-risk Cardiac Surgery A Randomized Controlled Feasibility Trial. Anesthesiology; 124:826-36

79. Walsh M, Devereaux P.J, Garg A.X., et al. (2013). Relationship between Intraoperative Mean Arterial Pressure and Clinical Outcomes after Noncardiac Surgery: Toward an Empirical Definition of Hypotension. Anesthesiology; 119 (9): 507-515.

80. Salmasi V, Maheshwari K, Yang D. et al. (2017). Relationship between Intraoperative Hypotension, Defined by Either Reduction from Baseline or Absolute Thresholds, and Acute Kidney and Myocardial Injury after Noncardiac Surgery: A Retrospective Cohort Analysis. Anesthesiology; 126(1): 47-65.

81. Broussard, D. and Ural, K., (2016). Cardiovascular problems in the post-anesthesia care unit (PACU). UpToDate. Retrieved online at .

82. Krauss, Baruch, et al (2017). Carbon dioxide monitoring (capnography). UpToDate. Retrieved online at .

83. Sessler D.I. (2014). Temperature monitoring: the consequences and prevention of mild perioperative hypothermia. South Afr Anaesth Analg.; 20(1):25-31

84. Saad and Aladawy. (2013). Temperature management in cardiac surgery. Global Cardiology Science & Practice.; 7: 44-62

85. Manjuladevi M and  Upadhyaya KSV. (2014). Perioperative blood management. Indian J Anaesth.; 58(5): 573–580.

86. Fayeda N, Mourad W, Yassena K, Görlinger K. (2015). Preoperative Thromboelastometry as a Predictor of Transfusion Requirements during Adult Living Donor Liver Transplantation. Transfus Med Hemother.; 42:99–108

87. Fayad, A. (2017). Anesthesia for open abdominal aortic surgery. UpToDate. Retrieved online at .

88. Sher-Lu, Pai (2017). Delayed emergence and emergence delirium in adults. UpToDate. .

89. Retrieved online at Goren O. and Matot I. (2015). Perioperative acute kidney injury. Br J Anaesth.; 115 (suppl 2): 3–14

90. Grams M.E. and Rabb H. (2012). The distant organ effects of acute kidney injury. Kidney International.; 81: 942–948.

91. Yazdi M.G, Shoghli A, Faghihi S, Baratloo A. (2016). Central Venous Pressure Monitoring; Introduction of a New Device. Emerg (Tehran).; 4(2): 52-54

92. Vincent J.L , De Backer D, M.D. (2013). Circulatory Shock. N Engl J Med.; 369: 1726-34

93. Saugel B, Cecconi M, Wagner J.Y, Reuter A. (2015). Noninvasive continuous cardiac output monitoring in perioperative and intensive care medicine. Br J Anaesth.[ Advance Access published January 16, 2015 1-14]

94. Schneider G, Jordan D, Schwarz G., et al. (2014). Perioperative Medicine | April 2014.Monitoring Depth of Anesthesia Utilizing a Combination of Electroencephalographic and Standard Measures. Anesthesiology.; 120(4): 819-828.

95. Mali S. (2012). Anaphylaxis during the perioperative period. Anesth Essays Res.; 6(2): 124–133.

96. Reddy J.I., et al. (2015). Anaphylaxis Is More Common with Rocuronium and Succinylcholine than with Atracurium. Anesthesiology. 2015; 122:39-45

97. Mills ATD, Sice PJA, Ford SM. (2013). Anesthesia-related anaphylaxis: investigation and follow-up. Continuing Education in Anesthesia, Critical Care & Pain J.: 1-6

98. Apfel, C. C., et al. (2012). "Evidence-based analysis of risk factors for postoperative nausea and vomiting." Br J Anaesth 109(5): 742-753.

99. Gan T.J, Diemunsch P, Habib A.S et al. Consensus Guidelines for the Management of Postoperative Nausea and Vomiting. Anesth Analg. 2014; 118 (1):85–113

100. Feinleib, J., et al. (2017). Postoperative nausea and vomiting. UpToDate. Retrieved online at .

101. Neufeld K.J., Leoutsakos JMS, Frederick E. Sieber F.E., et al. (2013). Outcomes of Early Delirium Diagnosis After General Anesthesia in the Elderly. Anesth Analg.; 117:471–8

102. Mashour GA, Avidan MS. (2014). Postoperative Delirium Disconnecting the Network? Anesthesiology.; 121:214-6

103. Barnett, S. (2016). Anesthesia for the older adult. UpToDate. Retrieved online at .

104. Li Y.W , Li H.J , Li H.J , Feng Y. , Yu Y , Xiang-Yang Guo X.Y., et al. (2015). Effects of two different anesthesia-analgesia methods on incidence of postoperative delirium in elderly patients undergoing major thoracic and abdominal surgery: study rationale and protocol for a multicenter randomized controlled trial. BMC Anesthesiology.; 15:144

105. Viswanath O., Kerner B, Jean Y.K. Soto R., Rosen G. (2015). Emergence delirium: a narrative review. Journal of Anesthesiology & Clinical Science.; 4 (2): 1-8

106. Riazi S., et al. (2014). Malignant Hyperthermia in Canada: Characteristics of index Anesthetics in 129 malignant Hyperthermia Susceptible Probands. Anesth Analg.; 118: 381-7

107. Rosenberg H, Sambuughin N, Riazi S, Dirksen R. (2013). Malignant Hyperthermia Susceptibility. NCBI Bookshelf. National Institutes of Health.

108. Larach M.G, Gerald A, Gronert G.A, Allen G.C, Brandom,B.W, Lehman E.B. (2010). Clinical Presentation, Treatment, and Complications of Malignant Hyperthermia in North America from 1987 to 2006. Anesth Analg.;110:498 –507

109. McGlothlin JD, and Moenning JE. (2013). Waste Anesthetic Gases (WAGs) among Employees in the Healthcare Industry.

110. Stahl, S. (2013). Essential Psychopharmacology, 4th Edition. Cambridge University Press.

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