Principles Of Anaesthesiology Muscle Relaxants Reversal Of Neuromuscular Blockade Notes

Principles Of Anaesthesiology

Principles Of Anaesthesiology Introduction:

Surgery has been practised for ages. However, the advent of modern techniques of anaesthesia has allowed surgery to develop by leaps and bounds. If there is a well-informed, vigilant and safe anaesthesiologist taking care of the patient, the surgeon is able to concentrate on the surgical procedure unhindereAn anaesthesiologist is also a perioperative physician.

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An anaesthesiologist’s understanding of anatomy, physiology and pharmacology, and his expertise of management of critical illness and pain give him a wider scope of practice including intensive care, pain and palliative care.

A good understanding of the physiology and pharmacology, complemented by continuous and vigilant monitoring, has made the practice of anaesthesia safer. Safe practice of anaesthesia comprises the following steps: A good rapport with the patient, a thorough preoperative preparation and premedication, monitoring and perioperative care.

Types Of Anaesthesia

The choice of anaesthesia depends on several factors: The site and duration of surgery, general condition of the patient, expertise of the anaesthesiologist and preference of the patient.

Anaesthesia can be classified into two main categories: General anaesthesia and regional anaesthesia

General Anaesthesia (GA):

In this type of anaesthesia, the patient is rendered unconscious by the administration of anaesthetic agents. These agents produce a generalised and reversible depression of the central nervous system.

The components of general anaesthesia include anaesthesia (unconscious with no sensation), analgesia (no pain), amnesia (no recall) and muscle relaxation.

Indications for General Anaesthesia:

• When the surgical procedure involves areas that cannot be easily performed under regional anaesthesia such as head and neck procedures
• Prolonged surgical procedures that make it uncomfortable for patients to lie in the same position for a long period of time
• Extensive surgical procedures involving body cavities (thorax, abdomen)
• Surgeries involving multiple parts of the body
• Haemodynamically unstable patients
• Patients with coagulation disorders
• Patient request

Contraindications:

The only absolute contraindication to general anaesthesia is patient refusal. However, if the patient’s general condition is poor and is at risk of deterioration with the administration of general anaesthesia, one may attempt to avoid general anaesthesia by adopting regional anaesthesia, if possible or defer surgery till the patient is optimized to tolerate it.

Techniques of General Anaesthesia:

General anaesthesia (GA) has three important phases:

Induction, maintenance and emergence. GA may be provided using administration of either inhalational anaesthetic agents, intravenous anaesthetics or a combination.

Preoperative assessment, preparation and premedication: Induction of general anaesthesia alters the physiology of the patient in many ways and it is important to do a preoperative assessment (described in detail later) to know the baseline condition.

The patient is then prepared for surgery if he has any condition that needs to be optimized before surgery.

For example, the patient is given preoperative instructions regarding fasting before surgery. Certain medications may be prescribed as premedication (to reduce anxiety, pain. etc.).

Induction and airway management: In the operation theatre, intravenous access is secured (called the ‘lifeline’ of the patient) and monitoring commences once the anaesthetist is satisfied that the patient’s vitals are within acceptable limits, he/she proceeds to induce general anaesthesia by either intravenous or inhalation anaesthesia patient becomes unconscious and as a consequence, the tongue and the epiglottis fall back into the pharynx and the airway gets obstructed overcome this, the anaesthetist maintains a patent airway using an endotracheal tube or a supraglottic airway such as laryngeal mask airway or I-gel after the induction of general anaesthesia (described in detail later).

Anaesthesia Maintenance: The induction agents are short-acting and hence, maintenance of anaesthesia must be done with continued administration of inhalation anaesthetic agents or infusion of intravenous anaesthetic agents. Muscle relaxants may be given to facilitate surgery, especially for intracavitary surgeries. The patient is monitored throughout surgery and interventions are made as required

Emergence: Once surgery is complete, the patient is allowed to wake up, after adequate reversal of neuromuscular blockade and the circulation anaesthetics. The artificial airway is removed after a full return of consciousness and airway reflexes. The patient is shifted to the postoperative care unit where the patient will be cared for till discharge.

Preoperative Assessment And Premedication

Every patient is anxious when he comes into the operating room. The causes of anxiety can be varied: Fear of the disease condition, surgery, anaesthetic and the anticipated pain. A good rapport developed between the patient and the anaesthesiologist can build up his confidence and help allay many of these fears.

Anaesthesia is associated with changes in the internal homeostasis. Normally, these are well tolerated by the different systems. However, if the patient has a preexisting derangement, his capacity to withstand changes in his internal milieu may be limiteIt is thus very important to assess preoperatively the baseline condition of the patient, irrespective of the scheduled surgery and anaesthesiThis will be detailed in an elective case and a more directed assessment in an emergency.

Preoperative Assessment And Premedication History:

A detailed history of the patient with symptoms pertaining to the presenting complaint must be The patient should be questioned about symptoms pertaining to the presence of any comorbidities such as hypertension, diabetes, ischaemic heart disease, respiratory illness, neurological illness, renal and hepatic dysfunction. History of previous surgery, exposure to anaesthetics, medication history, allergies, smoking, alcohol, recent respiratory infections and his current effort tolerance should also be elicited.

Physical Examination:

A detailed physical examination is done and the relevant history specially borne in general physical examination includes:

Vital signs: Blood pressure, heart rate, respiratory rate, temperature and oxygen saturation.

PICCLE: Pallor, icterus, cyanosis, clubbing, lymphadenopathy, oedema and raised jugular venous pulse.

Spine: To rule out infection over the skin covering the spine, tenderness, stiffness or fractures of spine, to check spaces.

Veins: Ease of obtaining venous access is also assesse

Assessment of Airway:

Whenever a person becomes unconscious, the tongue and epiglottis fall back onto the pharynx and obstruct the airway. Since the patient may need sedation or may be made unconscious during a general anaesthetic, the anaesthetist must ensure ability to secure the patient’s airway. Hence, preoperative assessment of the airway becomes important.

The assessment is done as follows:

The 1–2–3 Test:

• When a person opens his mouth, one should be able to insinuate one finger in the temporomandibular joint.
• There should be at least two finger breadths’ distance between his incisors.
• There should be at least three finger breadths’ distance between the chin and the thyroid cartilage (thyromental distance) of the patient.

Mallampati Test:

The patient is made to sit upright, open his mouth wide and protrude his tongue. The structures visualised are classifieThese classes roughly correlate with the following grades of laryngoscopic views. Difficult airway may be anticipated in Mallampati Class 3 and 4 and the anaesthesiologist must be prepared to secure airway in such patients.

Neck Movements:

Restriction of neck movements, especially extension makes endotracheal intubation more difficult.

Systemic Examination:

A detailed examination of the various systems is then carried out and relevant findings noted.

Preoperative Assessment And Premedication Investigations:

There is no place for routine investigations to be ordered before any surgery. Investigations that are required to assess the baseline status of the patient and have a bearing on the perioperative course must be done. Thus, they should be tailored to the individual patient.

The common investigations ordered are as follows:

Haemoglobin estimation: All patients.

Electrocardiogram, blood sugar estimation, blood urea, serum creatinine and electrolytes: Male patients >40 years, smokers and female patients above 50 years.

Total and differential white cell count: If infection is suspected.

Platelet count and coagulation profile:

• If any abnormality is suspected or bleeding is anticipated.
• Chest X-ray is ordered if a major abdominal or thoracic surgery is planned, postoperative ventilation is expected or cardiorespiratory disease is suspecte Stress test, echocardiogram, pulmonary function test or a blood gas analysis are obtained as necessary.
• Blood grouping and cross-matching are requested if the surgery may be associated with major blood loss.

ASA Physical Status Classification:

The patient’s preoperative physical status can be classified into five different categories.

The American Society of Anaesthesiologist’s classification of Physical Status is as follows:

• ASA 1: Healthy patient, no medical problems
• ASA 2: Mild systemic disease
• ASA 3: Severe systemic disease, but not incapacitating
• ASA 4: Severe systemic disease that is constant threat to life
• ASA 5: Moribund, not expected to survive without the operation

A suffix E is added if the surgery is of emergent nature. A sixth category called ASA VI is given to the patient who is declared brain dead, whose organs are being removed for donor purposes.

The risks associated with anaesthesia in a patient with concurrent diseases must be assesseAlgorithms by different organisations are available to help decisionmaking in individual patients: For example, American Heart Association recommendations for evaluation of ischaemic heart disease in a patient posted for noncardiac surgery. The goal of preoperative assessment and preparation is thus to ensure that the patient is optimised and is in the best possible condition prior to surgery and anaesthesi

Informed Consent:

The patient is explained about the planned anaesthetic, the problems anticipated and the risks involved in his own language and a written and informed consent is obtained.

Preoperative Instructions:

The patient is permitted to take solids and milk up to 6–8 hours and clear fluids up to 3 hours prior to surgery. This may be relaxed for neonates and infants where a four-hour fast for breast milk is sufficient. Formula feeds and milk from any other source are treated as solids. If the last food intake contained a considerable amount of fat, gastric emptying time may be delayed.

Premedication:

This term refers to the administration of certain medications prior to anaesthesia drugs used and their objectives are as follows:

1. To allay anxiety: A certain degree of anxiety is felt by most patients before surgery. A good rapport developed between the patient and the anaesthesiologist helps relieve this anxiety. Any of the following medications may be used to reduce anxiety.

• Adults (night before and morning of surgery)
• Tab Alprazolam 0.25–0.5 mg
• Tab Lorazepam 2–4 mg orally
• Children: To enable easy separation from parents.
• Midazolam 0.5 mg/kg (maximum 10 mg) mixed with 5 ml of paracetamol syrup is given orally 15–20 minutes prior to the procedure.
• Triclofos syrup, 75–100 mg/kg, one hour prior to surgery.

2. To relieve pain: If the patient has any painful condition that could get aggravated on movement, a narcotic in appropriate doses can be added to reduce the pain during shifting from the ward, e.g. fractures.

Care must be taken to avoid excessive sedation and respiratory depression.

3. To dry secretions: An anticholinergic such as glycopyrrolate (0.2 mg) is added if fibreoptic intubation is planned so that oral secretions do not hinder vision. Local anaesthetic agents produce better local anaesthesia of the upper airway when the mucosa is dry. It may be given intravenously just prior to surgery in ENT surgeries and oral surgeries.

4. To help anaesthesia induction: Premedication with a narcotic provides analgesia and helps induce anaesthesia more smoothly.

5. To blunt baroreceptor reflexes: A small dose of β-blockers or clonidine may be given in certain patients to blunt baroreceptor reflexes during intubation.

6. To reduce gastric volume and acidity: Some patients are at risk of regurgitation of gastric contents and aspiration. They may be premedicated with a prokinetic such as metoclopramide (10 mg) and a H₂ blocker such as ranitidine (150 mg orally). Pantoprazole 40 mg may be given instead of ranitidine. The consequences of aspiration of gastric contents depend on its quantity and acidity. Particulate matter, if aspirated, can cause mechanical blockage of the airways. Metoclopramide reduces residual gastric content by hastening gastric emptying and ranitidine reduces the acidity.

Sometimes, a nonparticulate antacid such as sodium citrate may be given to neutralise existing gastric aci Multiple factors during anaesthesia and surgery increase the chances of nausea and vomiting. Since anaesthesia involves blunting of airway reflexes, patients are at risk of aspiration. This is why patients are kept fasting before elective surgery. This may not be possible for patients who are posted for emergency surgery. It is assumed that these patients are ‘fullstomach’ and appropriate precautions are taken.

Airway Management

General anaesthesia involves induction of unconsciousness during which the patient’s ability to maintain his airway and breathing are impaireIt thus becomes necessary that the anaesthesiologist maintains and protects the patient’s airway. In addition, not only anaesthesia but also oxygenation and ventilation are maintained well only if the airway is patent and secured.

Management of airway is one of the basic skills acquired by an anesthesiologist. This is relatively easy in most individuals. Difficult airway is the term given when there is difficulty with mask ventilation, endotracheal intubation, or both.

BAG-Mask Ventilation

When a person becomes unconscious, the tongue and the epiglottis fall back and obstruct the airway. Since they are attached to the mandible, lifting up of the mandible also lifts these two structures and opens the airway. This is usually done by head-tilt and chin-lift method as during cardiopulmonary resuscitation. Jaw thrust is more popular with anesthesiologists. The patient may be ventilated using a ‘bag’ (either a selfinflating bag or anaesthetic circuit) and a facemask. The mask is triangular in shape, the narrow portion of which is placed at the bridge of the nose and the base placed in the depression between the lower lip and chin. The mask is held in place by an E-C technique.

Endotracheal Intubation

Endotracheal intubation is the most definitive way of maintaining airway in patients who require muscle paralysis and require intermittent positive pressure ventilation. It involves the introduction of a tube into the trachea for maintaining the patency and protecting the airway as well as to ensure adequate oxygenation and ventilation. Whenever general anaesthesia is induced and needs to be maintained for long periods, endotracheal intubation is done.

Airway Management Indications:

• To administer general anaesthesia for long (>1–2 h) periods.
• To maintain patency of the airway in unconscious patients.
• To protect lungs from aspiration of regurgitated gastric contents.
• To ensure delivery of adequate tidal volumes to the lungs.
• To clear excessive and retained secretions from the lungs.

Contraindications:

Endotracheal intubation may be extremely difficult or even impossible and a tracheostomy may be better in certain situations:

• When the upper airway integrity is lost as in extensive maxillofacial injury with bilateral fractures of the mandible and maxillae.
• Injuries to the neck with laryngeal rupture
• Large tumours of the upper airway.

Equipment:

Laryngoscopes:

These consist of a handle and a blade:

• The handle contains batteries. The blade has a flange to push the tongue towards the left side. This ensures more room for visualisation of the glottis. A bulb nearer the tip of the blade lights up when the handle and blade are at right angles to each other and electrical contact is made.
• There are several types of laryngoscopes to aid in different situations.
  • Macintosh-type blade is curved and is popular for use in adults
  • The Miller blade is straight and is used in children and in adults with difficult airway
  • The McCoy laryngoscope has a tiltable tip.
  • Fibreoptic laryngoscopes are flexible.

• • Videolaryngoscopes have a small camera on the blade a little proximal to the tip and provide a better view of the ‘difficult to see’ larynx.
  • Short-handled laryngoscopes are available for use in difficult airways, e.g. pregnant women, and obese patients.

Endotracheal Tubes:

It is a C-shaped tube and is commonly made of polyvinyl chloride (PVC). The machine end has a standard 15 mm diameter connector. The patient end is bevelled and has an opening on the side just proximal to the tip called the Murphy’s eye. This ensures patency of the tube even if the bevelled tip is against the tracheal wall.

Endotracheal tube size:

Endotracheal tubes are available in different sizes. Their size is indicated as the internal diameter in millimetres. However, the correct size will depend on the growth of the child.

Depth of insertion:

• The distance of several points on the tube from the patient end is marked in centimetre along the tube. The tube is fixed at 22 or 23 cm in adult men and at 20 or 21 cm in adult women.
• In children, the following formula is used: Age/2 + 12 cm.

The tube should be positioned such that its tip must lie above the carina but well below the glottis. Air entry should be heard bilaterally on auscultation of the chest.

Airway Management Position:

A pillow (7–10 cm) under the patient’s head enables mild flexion at the cervical spine. The head is then extended at the atlanto-occipital joint. This is called the intubating position or “sniffing position”.

Airway Management Route:

Endotracheal intubation can be done either orally or nasally. It can be done either under direct vision or indirectly using a fibreoptic scope. It may need to be done blindly when visualisation of the glottis by direct means is not possible and a fibreoptic scope is not available.

In such cases, if the regular antegrade technique (mouth or nose to larynx) is not possible, retrograde intubation (larynx to mouth) may be trieIn the retrograde technique, a guidewire is passed from the cricothyroid membrane upward into the mouth or nose and the endotracheal tube is guided over it towards the larynx.

Airway Management Procedure:

The patient’s head is placed in the sniffing position. The mouth is opened and the laryngoscope blade is introduced through the right angle of mouth along the tongue into the pharynx. Once the epiglottis is seen, the tip of the laryngoscope blade is pressed into the valleculThis lifts up the epiglottis to reveal the glottis.

The glottis is identified by the two pearly white vocal cords. Once the cords are seen, the endotracheal tube is inserted between them into the trache It may also be done with the patient awake after administering local anaesthesia to the upper airway when a difficult intubation is anticipated.

Many airway adjuncts are available for use when a difficult airway is encountered, especially when it is unanticipateThese include oropharyngeal airway, nasopharyngeal airway, laryngeal mask airway and Combitube.

Confirmation of Correct Placement of Endotracheal Tube:

The correct position of the endotracheal tube may be confirmed by the following:

• Endotracheal intubation under vision
• Bilateral visible chest rise
• Bilateral equal air entry in the lungs
• Absent breath sounds in the epigastrium
• A square wave normal capnogram—gold standard
• Prompt inflation of the deflated bulb of oesophageal detector device.

Airway Management Complications:

The complications of endotracheal intubation may be classified as follows:

Airway Management Immediate:

• Trauma to teeth, lips, tongue, pharynx or larynx
• Haemodynamic changes—tachycardia, hypertension, myocardial ischaemia
• Misplaced tube—accidental extubation, oesophageal intubation.

Delayed:

Laryngeal granuloma, laryngeal or subglottic stenosis.

Oropharyngeal Airway:

• It is available in various sizes. The correct size is chosen such that when it is placed along the side of the patient’s face, it should extend from the angle of mouth up to the tragus. This is inserted along the tongue and reaches up to the posterior pharyngeal wall.

• Care should be taken not to push the tongue backwards with the airway itself.
• To avoid that, the airway is inserted with its concavity towards the palate and then turned once 50% of it is inserted and passed further.
• Please note that an oropharyngeal airway is excellent in patients who are completely unconscious. Patients who are conscious do not tolerate it. In patients who are semiconscious, it may initiate a gag reflex and induce vomiting. In such patients, a nasopharyngeal airway is a better choice.

Nasopharyngeal Airway:

• It is a soft tube made of latex or silicon. It is available in various sizes. The correct size is the same size as an endotracheal tube for that patient.

The correct length is chosen such that when it is placed along the side of the patient’s face, it should extend from the nostril up to the tragus. This is inserted along the nose and reaches up to the posterior pharyngeal wall.

Laryngeal Mask Airway:

This is a supraglottic airway that has revolutionised airway management during anaesthesiIt has a tube or a shaft with a standard 15 mm connector at the proximal end to connect to the anaesthetic circuit. The patient end has an oval-shaped inflatable cuff which when inserted rests just above the larynx and creates an airtight seal.

Airway Management Uses:

• To administer anaesthesia
• To maintain airway in patients with difficult airway where endotracheal intubation is not possible and are at risk of hypoxia
• It may also be used as a conduit for passage of the endotracheal tube, either blindly or with the use of a fibreoptic bronchoscope.

Endotracheal Extubation:

Endotracheal extubation is as important as intubation. A patient’s trachea may be extubated when the following criteria are met

• Oxygenation and ventilation are satisfactory
• The patient is haemodynamically stable
• The patient is fully conscious
• Able to maintain his airway patency
• Airway reflexes are intact
• Able to cough and clear airway.

Equipment for reintubation and personnel skilled in intubation should be readily available. After a good oropharyngeal suction to clear the secretions, the cuff is deflated and the tube is removed should be administered by face mask and the patient monitored till he is stable and ready to go to the ward.

Monitoring In Anaesthesia

The administration of anaesthesia is associated with changes in the internal homeostasis of the patient, especially the cardiac and respiratory systems. Constant monitoring of the various body systems is necessary to ensure the well-being of the patient and prompt recovery from anaesthesia at the end of surgery. Identification and prompt treatment of any untoward changes should alleviate complications due to anaesthesia.

• Monitoring used in anaesthesia may be classified into: Noninvasive and invasive monitoring. The extent of monitoring depends on the patient’s preoperative condition, the extent of surgery, the type of anaesthesia and the facilities available.
• Most patients are noninvasively monitoreBasic noninvasive monitoring includes clinical observation of the patient and monitoring of the patient’s haemodynamic parameters. Adequate cardiac output is associated with good urine output, warm and well-perfused peripheries and good capillary refill. Heart rate may be monitored with a finger on the pulse. Blood pressure may be measured using a standard sphygmomanometer. More conveniently and accurately, heart rate and rhythm are continuously monitored using the electrocardiogram and blood pressure using automated noninvasive blood pressure monitoring systems.
• Invasive monitoring becomes necessary when considerable haemodynamic instability exists or is expected to occur perioperatively. This may include invasive arterial pressure, central venous pressure and several others as required.
• Minimum monitoring standards (according to guidelines from Indian Society of Anaesthesiologists) for a patient undergoing any type of anaesthesia are:
  • Noninvasive blood pressure (NIBP)
  • Electrocardiogram (ECG)
  • Pulse oximetry

Monitoring capnography, although not mandatory in India, is an important monitor in patients undergoing anaesthesiIn addition, monitoring of body temperature, anaesthetic gases and neuromuscular blockade is desirable.

Regional Anaesthesia

This involves injection of local anaesthetic agents in close proximity to the nerves, nerve plexuses or spinal cord segments supplying the site of surgery. There are three types of regional anaesthesia: Central neuraxial block, peripheral nerve block and local anaesthesia.

Central Neuraxial Block:

Regional anaesthesia induced by injecting the local anaesthetic agents around the spinal cord is called a central neuraxial block. It includes spinal, epidural and caudal anaesthesia/analgesia the drug is injected into the cerebrospinal fluid (subarachnoid space), it is called subarachnoid block or spinal anaesthesiIf the drug is injected into the epidural space, it is called epidural anaesthesiThe drug can also be injected into the sacral epidural space accessed through the sacral hiatus. This is called caudal epidural block.

Peripheral Nerve Block:

When regional anaesthesia is induced by injecting the local anaesthetic agents around nerve plexuses (plexus block) or individual nerves, it is called a peripheral nerve block.

Monitoring In Anaesthesia Indications:

Surgeries that can be done by blocking nerve supply to the surgical areFor example: Surgeries on the lower limbs or below umbilicus can be done under spinal or epidural anaesthesia surgeries on the upper limb can be done under brachial plexus block.

Contraindications:

• Patient refusal
• Infection at the site of injection
• Coagulation abnormalities

Advantages of Regional Anaesthesia:

• Only the part that needs to be operated upon is anaesthetize
• The patient will be able to resume oral fluid intake early after surgery.
• There is minimum cardiorespiratory depression, especially after peripheral nerve blocks.
• Systemic effects of anaesthetics can be avoided.

Monitoring In Anaesthesia Disadvantages:

It is difficult for a patient to lie immobile for long periods of time.

• The patient can get restless and irritable.
• Occasionally, neurological injury and other complications (as described below) can occur.
• Regional anaesthesia has a small failure rate and certain surgeries may outlast the duration of block provided by the regional block, in which case general anaesthesia may need to be given. Thus, even though the primary anaesthetic contemplated is regional anaesthesia, it must be ensured that the patients are also fit for general anaesthesia before taking up for surgery.

Local Anaesthetics

Local anaesthetics are drugs when injected around the nerves block impulse conduction distal to the site of injection and produce analgesia and anaesthesia in that area.

Local Anaesthetics Classification:

Local anaesthetics consist of a hydrophilic tertiary amine group linked to a lipophilic aromatic group. They are classified into two main categories based on this linking group: The aminoamides and the aminoesters.

• Aminoesters: Procaine, chloroprocaine, tetracaine.
• Aminoamides: Lignocaine, bupivacaine, ropivacaine.

Mechanism of Action:

A nerve impulse is transmitted by progressive opening of sodium channels across the membrane and sudden influx of sodium into the intracellular fluiLocal anaesthetics produce sodium channel blockade. They block the fast sodium channels and the sodium influx, thus blocking all impulse transmission across the membrane.

Local anaesthetic exists in two forms: Ionised and nonioniseThe nonionised form is lipophilic and crosses the phospholipid membrane more easily. The ionised form is hydrophilic, blocks the channel in the open state and blocks nerve transmission (usedependent blockade). The drug blocks the channel from the intracellular direction.

Factors Influencing Activity:

Lipid solubility:

Higher the lipid solubility, higher is its ability to penetrate the lipoprotein membrane and hence greater is its potency.

pKa:

The pKa of a drug is the pH at which the ionised and nonionised portions of the drug are equal. The lower the pKa, lower is the degree of ionisation for any given pH. The nonionised portion is lipophilic and crosses the cell membrane more easily hastening the onset of nerve blockade. For example, lignocaine has a pKa of 7.9 and acts faster than bupivacaine with a pKa of 8.1.

pH

Acidosis decreases the proportion of the nonionised drug and reduces the amount of drug able to cross the membrane. That is why local anaesthetics do not work optimally when injected into an infected tissue (pH is acidic in these tissues).

Protein binding:

The greater the degree of protein (membrane proteins) binding, longer is the duration of action.

Choice of Local Anaesthetic Agents:

• Lignocaine: Skin infiltration—0.5–1% Minor nerve block—1% Epidural—1.5–2%
• Spinal anaesthesia—5% hyperbaric (heavy)
• Two topical preparations—2% lignocaine jelly and 4% lignocaine spray for the mucosal surfaces of the body. Note: 1% means each ml contains 10 mg of the drug, 2% to 20 mg/ml, and so on.
• Bupivacaine: Skin infiltration, epidural—0.25%, 0.5%
• Spinal anaesthesia—0.5%, hyperbaric (heavy).
• Levobupivacaine: Bupivacaine is a racemic mixture containing levo and dextrorotatory forms. The dextrorotatory form is cardiotoxiThe levorotatory form of bupivacaine is now available as levobupivacaine (0.25 and 0.5%) and is much safer.
• Ropivacaine: Available as 0.2% for providing post-operative analgesia, labour analgesia and as 0.75% for spinal and epidural anaesthesia and nerve blocks.
• Chloroprocaine: This is a short-acting ester local anaesthetic now reintroduced for clinical use. There were a few cases of cauda equina syndrome in the 1980s when it was used for subarachnoid block and its use was abandoneThe cause of the neurological injury was then traced to the metabisulfite added to the solution as a preservative. It has now been reintroduced in a concentration of 1% for intrathecal use in a preservative-free form. It is approved for use in the US and Europe. Its advantages are its short duration of action (40 min approximately) and is suitable for procedures of short duration.

Maximum Recommended Doses of Local Anaesthetics for Infiltration and Blocks:

• Lignocaine—3 mg/kg
• Lignocaine with adrenaline—7 mg/kg
• Bupivacaine—2 mg/kg
• Ropivacaine—2.5 mg/kg, not to exceed 200 mg for minor nerve blocks.

Local Anaesthetics Clinical Effects:

Local Anaesthetics Local effects:

Local anaesthetics block the sodium channels in the neuronal membrane and thus the propagation of impulses across it.

Local Anaesthetics Systemic effects:

These drugs can produce systemic effects when high plasma levels of the drug are achieved may also be deliberate as and when lignocaine is used as an antiarrhythmic agent. It is classified as a Class Ia drug (sodium channel blockers) in the Vaughan Williams classification of antiarrhythmic agents.

When high plasma concentrations of local anaesthetics are achieved, either due to accidental intravenous injection of the drug or due to intravascular absorption of a large amount of drug infiltrated in a region, systemic toxicity can occur.

Adrenaline-containing preparations should not be used for nerve blocks of fingers, toes and penis as it can cause ischaemia.

Toxicity of Local Anaesthetics:

Systemic toxicity:

If a significant amount of local anaesthetics reaches the tissues of the heart and brain, they exert the same membrane stabilising effect as on the peripheral nerve, resulting in progressive depression of function. The toxicity of local anaesthetics is dose-dependent. These drugs always produce central nervous system (CNS) toxicity first. As the plasma level rises, cardiovascular toxicity and collapse occur.

The plasma levels of lignocaine required to produce cardiovascular collapse (CVS toxicity) is seven times that required to produce convulsions (CNS toxicity).

Bupivacaine requires only three times the plasma level to produce cardiac toxicity as for CNS toxicity. Thus, bupivacaine has a greater potential for cardiotoxicity. With all local anaesthetics, central nervous system toxicity always comes first. This is followed by cardiac toxicity.

Clinical features of local anaesthetic toxicity are related to the plasma level of the local anaesthetic clinical effects and their relation to plasma level.

The likelihood of toxicity of local anaesthetics depends on several factors:

1. Amount of drug injected
2. Site of injection—vascularity
3. Addition of vasoconstrictors
4. Rapidity of injection
5. Nature of drug given
6. Presence of associated conditions such as low cardiac output or renal failure.

Amount and nature of drug injected:

Lignocaine is mostly used to produce peripheral neural conduction blockade. It can be used in doses not exceeding 5 mg/kg body weight for plexus blocks or infiltration. When combined with vasopressors such as adrenaline (1:200,000 = 5 µm/ml), the dose can be increased up to 7 mg/kg. The intravenous dose of lignocaine is 1–1.5 mg/kg when used as an antiarrhythmiHowever, even a small dose such as 20 mg in an adult when injected accidentally into the carotid artery may be sufficient to produce convulsions.

The clinical effects and their relation to plasma level of lignocaine:

Bupivacaine is used only for nerve blocks or infiltration. It is not an antiarrhythmic drug. Bupivacaine is cardiotoxic and care should be taken not to exceed the prescribed doses. Circulatory collapse and cardiac arrest due to large doses of bupivacaine can be very resistant to resuscitation. It can be used in a dose of up to 2.5 mg/ kg body weight.

Ropivacaine is a newer amide local anaesthetic agent which is similar to bupivacaine but with less cardiotoxicity. A levo isomer of bupivacaine, called levobupivacaine is also less cardiotoxic and has been put into clinical use recently.

Site of injection:

Certain sites are very vascular as compared to others. A higher plasma level of local anaesthetic is reached when the same amount of local anaesthetic is used for multiple intercostal nerve blocks as compared to the brachial plexus block.

Prevention of toxicity:

• Do not exceed recommended doses.
• Aspirate to rule out presence of the needle tip in a vessel before injecting the drug.
• Avoid injecting large boluses at once. Small boluses, given slowly to achieve the desired effect, are safer.

Treatment of local anaesthetic toxicity:

The toxicity of local anaesthetics manifests as CNS depression and convulsions. Maintenance of airway, breathing and circulation must be a priority. These convulsions generally last for a short period of time.

• Patency of the airway must be maintained.
• Oxygen by face mask.
• Ventilation, if apnoea occurs.
• Convulsions are treated with intravenous diazepam or thiopentone in incremental doses.
• Cardiovascular collapse with ephedrine, inotropes and vasoconstrictors, and CPR as needed
• Arrhythmias must be treated appropriately.
• Intralipid 20%: This is now recommended for use in local anaesthetic toxicity with cardiovascular collapse. Intralipid molecules act like a sink to mop up local anaesthetic molecules. When LA toxicity with cardiovascular collapse occurs, it is advised to give intralipid in a dose of 1.5 ml/kg over 2–3 min followed by 0.25 ml/kg/min for 15–20 min. If the patient is still unstable, can repeat the bolus once or twice at the same dose and the infusion rate can be The maximum dose of intralipid is 12 ml/kg.

Spinal And Epidural Anaesthesia

• Injection of local anaesthetics around the spinal cord to produce a reversible blockade of impulses that pass through it, is called central neuraxial blockade.
• When the local anaesthetic is injected into the cerebrospinal fluid bathing the spinal cord, it is called spinal anaesthesia (subarachnoid block).
• When local anaesthetics are injected into the epidural space to block the nerves that emerge from the spinal cord, it is called epidural anaesthesia.

Spinal Anaesthesia

Physiological Effects:

Nervous system:

The local anaesthetics spread from the site of injection by mixing with the cerebrospinal fluid (CSF). They reach the nerve fibres in the spinal cord and block transmission of impulses below the highest level of sprea The concentration of the drug is higher in the caudal regions and reduces with increasing distance cranially. A lower concentration of the drug is sufficient to block smaller fibres (C and Aδ), whereas the thick motor fibres (Aα) require a larger concentration to get blockeThus, a differential blockade is seen after a spinal anaesthetic and is as follows:

• Motor block up to a certain level (depends on the dose of drug injected).
• The sensory level of block 2 segments higher than motor block.
• Sympathetic block about two to four segments above the level of sensory block.

Cardiovascular system:

• Hypotension: Due to the blockade of sympathetic nerves below the level of spinal block, there is profound vasodilatation in the affected areas. A relative hypovolaemia occurs and hypotension is usually seen. The extent of hypovolaemia depends on the preoperative volume status, level of block and ability to compensate for the vasodilatation. The vessels in the upper limbs constrict to compensate for vasodilatation in the lower limbs. This is described as pink trousers, blue jacket phenomenon.
• Bradycardia: Heart rate is maintained in low blocks, but in higher blocks (high thoracic), sympathetic nerve block of the cardioaccelerator nerves can occur causing unopposed action of the parasympathetic system and bradycardia.
• Cardiac output also reduces in high spinal anaesthetics.

Respiratory system:

• No changes in respiratory function are seen in spinal anaesthetics below T10 level.
• When the level of spinal anaesthesia ascends, the intercostal nerves are gradually blocked.
• The diaphragm is not easily paralysed as the phrenic nerve is a thick and strong nerve and arises from cervical nerve roots (C3, C4, C5).
• In high spinals, the alveolar ventilation reduces and may lead to hypoxia and hypercarbia.

Gastrointestinal system:

• Unopposed parasympathetic activity leads to constriction of gut with increased peristaltic activity.
• Nausea, retching or vomiting may occur and may be the symptom of impending hypotension. These symptoms disappear when the hypotension is correcteOccasionally, it may need administration of an anticholinergic or an antiemetic agent.
• However, since the bowel is contracted and small and the skeletal muscle relaxation produced is greater, the surgeons find it easier to operate on such a gut.

Spinal And Epidural Anaesthesia Indications:

• Lower abdominal surgery
• Lower limb surgery
• Caesarean section
• Prostate surgery

Spinal And Epidural Anaesthesia Contraindications:

Absolute:

• Patient refusal
• Infection at the site of injection
• Bleeding tendencies

Relative:

• Hypovolaemia
• Severe stenotic valvular heart disease

Limitation:

Limited duration of block.

Pre-procedure Check:

A preprocedure check of the anaesthesia equipment, resuscitation equipment and drugs is made. An intravenous line is placed and monitoring commenceThe patient is then positioned for spinal anaesthesia.

Spinal And Epidural Anaesthesia Position:

The spinal anaesthetic may be administered with the patient in lateral or sitting position.

Lateral: The patient lies either in the left or right lateral position. The back should be parallel to the edge of the operating table and perpendicular to the grounThe legs should be flexed at the hips as much as possible.

Sitting position: The patient sits on the table, with the back bent forwarHe is allowed to rest his arms on pillows. The back is cleaned with spirit and betadine and drapeUnder aseptic precautions, the vertebral spines are identified in the lumbar region.

The highest point of the iliac crest corresponds to L3–4 space. The L2–3, L3–4, L4–5 intervertebral spaces can also be useA space higher than this is not used as the spinal cord ends at L1 in adults. This point is lower in children and should be borne in mind in paediatric spinals.

Approach:

The subarachnoid space may be approached either from the midline or by a paramedian technique. A subcutaneous wheal of local anaesthetic is raised in the chosen intervertebral space.

Midline approach: The lumbar puncture needle is inserted in the midline, midway between the spines and perpendicular to the skin. The spinal needle passes through the following structures to reach the subarachnoid space:

• Skin
• Subcutaneous tissue
• Supraspinous ligaments
• Interspinous ligaments
• Ligamentum flavum
• Dura and arachnoid

Paramedian approach: The needle is inserted a fingerbreadth lateral to the spine and advanced in a slightly cephalad direction towards the midline. If the needle touches the lamina, it should be redirected medially.

The correct position of the needle is identified by obtaining a free flow of CSF. This approach helps access the subarachnoid space in those patients whose interspinous and supraspinous ligaments are calcified or in patients unable to bend enough to open the interspaces well. The local anaesthetic is now injected into the CSF, taking care not to displace the needle

Spinal And Epidural Anaesthesia Complications:

These may be classified into Minor and Major based on the reversibility and seriousness of the complication.

Minor:

Hypotension:

This is treated with intravenous fluids to compensate for the vasodilatation. If necessary, incremental doses of a vasoconstrictor may also be used.

Bradycardia:

If the cardioaccelerator nerves (T1–T4) are blockeThis is usually easily treated with an anticholinergic such as atropine or glycopyrrolate. If profound, a small dose of adrenaline may be required (very rare).

Postdural puncture headache (PDPH):

The incidence of PDPH depends on the size of the needle used, number of punctures made, fluid status and ambulation. With finer needles (25 or 26 G) and good hydration of the patient, PDPH is uncommon. This may be treated with rest, increased fluid intake, plenty of coffee and NSAIDs. Rarely, an epidural blood patch (vide infra) may be required.

Respiratory depression:

If the level of spinal anaesthesia is high and all intercostal muscles are paralysed, respiratory depression may occur. However, diaphragm, the principal muscle of respiration is supplied by the thick phrenic nerve which does not get blocked easily. Any respiratory depression seen during spinal anaesthesia is more due to hypoperfusion of the respiratory centre (due to hypotension). This can be treated with respiratory support as required and stabilisation of blood pressure.

Retention of urine:

Backache: This is not a problem of spinal anaesthesia per se but may be due to faulty positioning during surgery.

Major:

• Infection: Arachnoiditis, meningitis.
• Nerve injury: Cauda equina syndrome.

Epidural Anaesthesia

In this type of central neuraxial blockade, local anaesthetic is injected in the space around the dura (epidural space). The local anaesthetic blocks the nerves as they emerge through the intervertebral foramen. Some of it diffuses through the meninges into the spinal cord and acts on the spinal cord.

Pre-procedure Check:

A pre-procedure check of the anaesthesia equipment, resuscitation equipment and drugs is made. An intravenous line is placed and monitoring of heart rate, electrocardiogram, blood pressure and oxygen saturation is established and the baseline note

Comparison of spinal and epidural anaesthesia:

Spinal And Epidural Anaesthesia Position:

The epidural puncture can be done with the patient in sitting position or in the lateral decubitus position.

Spinal And Epidural Anaesthesia Technique:

The patient’s back is cleaned with an antiseptic and then drapeUnder aseptic precautions, epidural puncture is done using a 16 or 18# Tuohy needle. This needle has a blunt tip to reduce the risk of dural puncture. The needle is inserted either in the midline or by a paramedian approach. It passes through the same tissues as in lumbar puncture except the subarachnoid space.

The needle is inserted along with its stylet and always advanced slowly from skin onwards. Once the subcutaneous tissue is entered, the stylet is removeA 2 ml or 5 ml syringe with a freely moving plunger and containing either air, saline or both is then connected to the needle huA gentle attempt at injection of this air or saline is made as the needle advances through the tissues. The entry of the needle into the epidural space is heralded when it penetrates the ligamentum flavum and there is a loss of resistance to injection of air or saline. This is taken as the end-point. An epidural catheter is passed through this needle and advanced to about 3–4 cm into the space. The needle is removed and the catheter taped and fixed to the back. A bacterial filter is attached to the injection port of the catheter.

The epidural needle or catheter may accidentally enter an epidural vein or the subarachnoid space. To avoid injecting a large dose of local anaesthetic into either of these spaces, a test-dose containing a small amount of local anaesthetic (3 ml of 2% = 60 mg lignocaine) and 15 µg of adrenaline is injecteAny sensory or motor block following this dose would suggest an accidental dural puncture resulting in spinal anaesthesiAn accidental intravascular injection is identified by an increase in the heart rate and blood pressure within a minute of the injection. In either situation, the epidural catheter may need to be withdrawn or replaceIf neither response is seen, an epidural placement is assumed and the full dose of local anaesthetic is injected in divided doses. The patient should be continuously monitored till the block wears off.

Spinal And Epidural Anaesthesia Complications:

1. Postdural puncture headache (PDPH):

The epidural needles are large and dural puncture results in a larger leak of cerebrospinal fluid (CSF). This results in low CSF pressures. Whenever the patient sits up or becomes ambulatory, a drag occurs on the brain and the meninges due to gravity and loss of CSF. This results in a typical postural headache referred to the occipital region. The pain disappears when he lies down supine. This is more common in obstetric patients. It may occur up to 2 to 7 days after lumbar puncture and may persist for up to 6 weeks.

Spinal And Epidural Anaesthesia Treatment: Plenty of oral fluids may increase CSF production. Rest, plenty of coffee and NSAIDs may also help. Rarely, an epidural blood patch may be require

Epidural blood patch: If the headache is very severe, an epidural blood patch may be given. 15–20 ml of the patient’s own blood is drawn under aseptic precautions.

Simultaneously, epidural puncture is made in the same space as the previous epidural puncture. The freshly drawn blood is injected into the epidural space which clots and seals the puncture hole. This is nearly 100% effective in relieving the headache.

2. Total spinal block:

When a large dose of local anaesthetic is injected intrathecally inadvertently, all spinal nerves are blocked, causing profound hypotension, bradycardia and collapse. If the patient is continuously monitored and treated promptly, this is completely reversible.

Spinal And Epidural Anaesthesia Treatment:

1. Volume infusion and vasopressors
2. Endotracheal intubation and ventilation as necessary
3. Urinary retention
4. Meningitis, if aseptic precautions are not followed.
5. Cauda equina syndrome, adhesive arachnoiditis: Extremely rare.

Other Regional Techniques

Caudal Analgesia

This is a very popular technique in providing postoperative analgesia in children. It involves injection of local anaesthetics with or without opioids in the caudal epidural space.

Other Regional Techniques Procedure:

Other Regional Techniques Position:

The patient is positioned in lateral position with the knees flexed and the back perpendicular to the groun It can also be given with the patient in prone position.

The area over the sacrum and the gluteal region is cleaned and draped.

Needles:

A 22 or 23 G hypodermic needle or a scalp vein set is used to administer the block.

Technique:

The needle is inserted at the apex of the sacral hiatus at a 60° angle to the skin. A distinct ‘pop’ or a ‘give way’ is felt as the needle punctures the sacrococcygeal membrane. The angle of the needle is then changed to about 15° to 20° to the skin and advanced a little further into the sacral epidural space. The latter step is optional and has to be done with caution as the dural sac may end relatively low in infants. After careful aspiration to rule out blood or CSF, a small dose of local anaesthetic is injecteThere should be no resistance to injection. A subcutaneous injection should also be ruled out.

Other Regional Techniques Drugs:

0.25% bupivacaine in a dose of 0.5 ml/kg is sufficient for perineal and low sacral procedures, 1 ml/kg for lumbosacral procedures and 1.5 ml/kg for lower abdominal procedures. However, a total volume of 20 ml and a total dose of 2.5 mg/kg of bupivacaine may not be exceeded.

Other Regional Techniques Indications:

• Postoperative pain relief in children for perineal and lumbosacral procedures.
• It is also used to supplement general anaesthesia for perianal procedures in adults.

Other Regional Techniques Contraindications:

• Absence of consent from parents/patients
• Local infection
• Bleeding tendencies.

Other Regional Techniques Complications:

• The intrathecal injection is possible, especially in smaller infants who have an extension of dural sac down to S3.
• Intravascular injection of large dose of local anaesthetics.

Brachial Plexus Block

Injection of local anaesthetics injected around the brachial plexus produces analgesia and even surgical anaesthesia in the upper limThe brachial plexus can be blocked by four different approaches: Interscalene, supraclavicular, infraclavicular and the axillary. Peripheral nerve blocks are most often given under direct visualization using ultrasounOther methods include use of a peripheral nerve stimulator or landmark-guided techniques.

Ankle Block

This is a popular technique in providing intra- and postoperative analgesia in adults undergoing procedures on the foot.

Other Regional Techniques Position:

The patient is positioned supine. The foot is raised by an assistant and the area around the ankle is cleaned and draped.

Needles:

A 22 G hypodermic needle is used to administer the block.

Technique:

Ankle block involves the blocking of 5 nerves.

1. The posterior tibial nerve is blocked with 3–5 ml of local anaesthetic at a point midway between the medial malleolus and the heel, just behind the posterior tibial arterial pulsations.
2. The sural nerve may be blocked at a point midway between the lateral malleolus and the heel, just lateral to the Achilles tendon.
3. The deep peroneal nerve is blocked at a point midway between the lateral and the medial malleoli lateral to the tendon of extensor hallucis longus and anterior tibial artery.
4. The saphenous nerve and the superficial peroneal nerves are easily blocked by raising a subcutaneous wheal of local anaesthetic between the malleoli anteriorly.

Other Regional Techniques Drugs:

Lignocaine plain not exceeding 5 mg/kg or bupivacaine not exceeding 2.5 mg/kg may be used.

Other Regional Techniques Indications:

Postoperative pain relief in adults for procedures on the foot.

Other Regional Techniques Contraindications:

Absence of consent from patients, local infection, bleeding tendencies.

Complications Of Anaesthesia

The practice of anaesthesia has become very safe due to better preoperative evaluation and preparation, careful choice of patients, better monitoring, availability of safer drugs and safer anaesthetic techniques. The incidence of complications has come down drastically.

However, complications can still occur. The perioperative (pre-, intra-, and postoperative periods) complications can be classified as follows.

Complications Of Anaesthesia Respiratory:

• Airway obstruction
• Bronchospasm
• Respiratory failure

Cardiovascular:

• Hypertension
• Hypotension
• Arrhythmias
• Shock

Central Nervous System:

• Postoperative drowsiness
• Postoperative nausea and vomiting
• Neurologic complications of regional blockade.

Renal and Hepatic Failure:

Impairment of urea, creatinine and liver enzymes can occur.

Respiratory Complications

Airway Obstruction:

Airway obstruction may occur during the induction of general anaesthesiWhen a person becomes unconscious, the tongue and the epiglottis fall back and can obstruct the airway. The patency of the airway is usually maintained fairly easily by the anaesthesiologist by using chin lift or jaw thrust manoeuvres. A definitive airway such as an endotracheal tube may then be inserted into the trachea.

Occasionally, the chin lift or jaw thrust manoeuvres are inadequate to maintain a patent airway as in patients with abnormal airways. Insertion of an endotracheal tube may also prove to be difficult in certain individuals.

An oral or nasopharyngeal airway may be inserted to overcome this obstruction and maintenance of the airway for a short duration. If there is difficulty in inserting the endotracheal tube due to supraglottic causes and oral or nasopharyngeal airways are not sufficient to relieve the obstruction, insertion of a laryngeal mask airway or a Combitube® may be attempte If the problem is at the glottis or subglottis and the airway is obstructed, an emergency cricothyrotomy or a tracheostomy may be required.

Perioperative airway obstruction may also be due to any of the following causes:

• Trauma—maxillofacial, head injury
• Foreign body aspiration
• Laryngospasm
• Infection—Ludwig’s angina, retropharyngeal abscess
• Oedema—laryngeal/pharyngeal oedema
• Neurological—recurrent laryngeal nerve injury
• Endocrine—thyroid enlargement
• Tumour—malignancy of the airway (tongue, cheek, larynx or the pharynx)

A thorough assessment of the airway must be done preoperatively and a management plan A formulate Plan B and Plan C also should be considered in the eventuality of failure of Plan Generally loss of life occurs not because of inability to intubate but due to an inability to oxygenate and ventilate the patient. This situation, also called, ‘cannot intubate—cannot ventilate’ (CVCI) is one of the most dreaded situations faced by an anaesthesiologist.

Bronchospasm:

Bronchospasm may occur in a patient under anaesthesiThe possible causes are as follows:

• Irritable airways as in a known asthmatic, chronic obstructive airways disease, i.e. exacerbation of preexisting bronchospastic disease.
• Endobronchial intubation and carinal stimulation
• As part of allergic reaction to anaesthetic drugs, antibiotics
• Aspiration of regurgitated gastric contents
• Pneumothorax
• Upper airway obstruction and laryngospasm can reflexly stimulate bronchospasm.

Treatment involves treatment of the precipitating cause and bronchodilators.

Respiratory Failure:

A patient is said to be in respiratory failure if he is unable to maintain adequate oxygenation and ventilation, i.e. arterial blood gas tension of O2 less than 60 mmHg (when patient is breathing 60% O2) and CO2 more than 50 mmHg. This could be acute or acute exacerbation of chronic respiratory failure.

Complications Of Anaesthesia Causes:

Central:

• Head injury
• Depressant drugs—anaesthetics, opioids
• Hypoxic encephalopathy
• Metabolic causes such as hyponatraemia, hypoglycaemia, hypokalaemia, and hyperglycaemia.

Peripheral:

• Lung parenchymal disorders such as pneumonia, atelectasis, aspiration, pneumothorax, and pulmonary embolism.
• Inadequate respiratory excursion due to pain or thoracic cage abnormalities such as kyphoscoliosis.
• Weakness of muscles, e.g. prolonged effect of muscle relaxants, myasthenia gravis.

Complications Of Anaesthesia Treatment:

• Treat the cause
• Intermittent positive pressure ventilation and ventilatory support till the patient improves.

Cardiovascular Complications

Hypertension, hypotension and arrhythmias occur perioperatively due to various reasons such as inadequate preoperative treatment, surgical stress, inadequate anaesthesia, metabolic or endocrine causes or even drug interactions. Brief periods of haemodynamic instability, although common are welltolerated by healthy individuals. Continuous and appropriate monitoring and prompt treatment should avoid long-term complications.

Hypotension may be due to decreased preload, reduced contractility or decreased afterload to the left ventricle. If not identified or treated in time, it may progress to shock and cardiac arrest. Hypovolaemic shock is the commonest type of shock encountered during surgery. However, cardiogenic shock due to perioperative myocardial infarction, anaphylactic shock due to allergic reaction to anaesthetics or neurogenic shock due to vasovagal attack, high spinals may also occur in susceptible individuals.

Perioperative myocardial infarction (MI) is a complication that occurs in susceptible individuals. It may be caused due to extreme and sustained variations in haemodynamics such as hypotension, hypertension or tachycardiIt may also be caused due to thrombosis as the patient is in a hypercoagulable state due to stress of surgery. The highest incidence of perioperative MI is seen not on the day of surgery (when the patient is under the vigilant care of the anaesthesiologist) but on the second or the third day when the attention given to him is less in terms of pain relief or haemodynamic changes.

Central Nervous System Complications

Awareness:

Rarely, a patient under general anaesthesia (GA) might recall events that occurred during the procedure. This is termed awareness during anaesthesia and is one of the most dreaded complications by both anaesthesiologist and the patient. This is more likely to occur if the patient’s haemodynamics are very unstable (as in postpartum haemorrhage, trauma) and the anaesthesiologist fears further cardiac depression may occur with the use of inhalation agents. The use of opioids and nitrous oxide may provide analgesia but not the amnesia and anaesthesia requireWith increased awareness of this complication among anaesthesiologists coupled with the use of benzodiazepines and modern anaesthetic agents which are more cardiostable, the incidence of this is reduceA ‘depth of anaesthesia’ monitor is called BIS index monitor provides some information of the conscious state of the patient but is not widely available yet.

Postoperative Drowsiness:

A patient may be slow to awaken after anaesthesia due to persistent effect of the anaesthetic agents or opioids administered during the anaesthesiHowever, it may be due to metabolic causes such as hypoxia, hypothermia, hypo- or hypernatraemia, hypo- or hyperglycaemiIf all these causes are ruled out, a neurological consultation is obtained to rule out any space-occupying lesions in the central nervous system, stroke or hypoxic encephalopathy.

Postoperative Nausea and Vomiting (PONV):

PONV is a frequent complication of anaesthesiIt is common in women, after laparoscopic surgeries, squint surgeries and is associated with the use of nitrous oxide and opioids or even early oral intake postoperatively. It may be treated with IV metoclopramide (10 mg), ondansetron (4–8 mg) or dexamethasone (4–8 mg) in an average adult.

Nerve Injuries:

Nerve injuries may arise as a complication of regional blockade. Complications such as adhesive arachnoiditis, cauda equina syndrome or paraplegia have been reported after spinal and epidural anaesthesia but are extremely rare. The use of tourniquet, if prolonged or if very high pressures are used, can also cause nerve injuries.

Peripheral nerve injuries may occur perioperatively due to improper positioning under regional or general anaesthesia common peroneal nerve and the sciatic nerve can be injured during lithotomy position. The ulnar and the radial nerves may be affected in the arm or at the elbow due to inadequate attention to positioning. Brachial plexus stretch injury can occur if the arms are allowed to be abducted more than ninety degrees. Injury to optic nerves or the retina may occur in prone position due to compression of the eyeball. Corneal injury may occur due to exposure in an unconscious patient.

Renal Failure

Renal failure, usually prerenal is associated with large fluid shifts or major haemodynamic instability. Direct injury to the kidneys (acute tubular necrosis) may occur if adequate attention is not given to prerenal failure.

Methoxyflurane, an inhalation anaesthetic agent can cause renal failure but is no longer in clinical use. Renal failure can also occur as part of hepatorenal syndrome or after a mismatched blood transfusion.

Hepatic Failure

A patient with compromised hepatic function may proceed to hepatic failure perioperatively, e.g. cirrhosis of liver, obstructive jaundice. Hepatic failure may also occur due to infective complications such as hepatitis or sepsis. Massive hepatic necrosis has been reported after repeated use of halothane. The incidence of this is very rare and must be a diagnosis of exclusion.

General Anaesthetic Agents

General anaesthetic agents are of two main types: Inhalational anaesthetic agents or Intravenous anaesthetic agents.

Inhalational Anaesthetic Agents

• Volatile anaesthetics: The volatile anaesthetic agents need a vaporiser to calibrate and deliver the vapour accurately in measured doses, e.g. isoflurane.
• Nonvolatile anaesthetics: For example, nitrous oxide.

General Anaesthetic Agents Classification:

1. Agents of mainly historical interest:

1. Ethyl chloride
2. Chloroform
3. Trichloroethylene
4. Cyclopropane
5. Methoxyflurane
6. Enflurane
7. Diethyl ether
8. Halothane

2. Agents in clinical use:

1. Isoflurane
2. Sevoflurane
3. Desflurane
4. Nitrous oxide

3. Agent undergoing clinical trials—Xenon:

A comparison of clinical effects of common inhalational anaesthetic agents in use is given in Table 64.3. Only important effects have been mentioned for the benefit of students.

Halothane

This was a very popular anaesthetic agent till recently but is largely replaced by isoflurane.

The reasons for dwindling popularity are:

• Myocardial depression
• Arrhythmogenicity
• Remote possibility of halothane hepatitis
• Easier availability of isoflurane (a safer agent).

Halothane Hepatotoxicity:

Two types of halothane-induced hepatic dysfunction are recognised:

• Type 1: It is mild, self-limiting and more common. It is associated with mild increases in liver enzymes but not jaundice. It is caused by reductive metabolism of halothane.
• Type 2: On extremely rare occasions (widely quoted incidence 1:35,000), the administration of halothane may be associated with the production of hepatitis.

This entity, known as halothane hepatitis, is largely a diagnosis of exclusion. It is fulminant with a high mortality rate (up to 50%). It is associated with fever, jaundice and grossly elevated liver enzymes. The toxic metabolite, trifluoroacetic acid reacts with liver proteins and triggers immune-mediated reaction in genetically susceptible individuals. Risk factors for development of halothane hepatitis are female gender, obesity, prior history of postanaesthetic jaundice, genetic susceptibility, repeated administration and enzyme-inducing drugs such as phenobarbitone.

Halothane is metabolised up to 20%, and sevoflurane (2%) and isoflurane (0.2%). Thus, hepatic dysfunction, although reported with sevoflurane and isoflurane, is extremely rare.

Comparison of different inhalation anaesthetics:

Isoflurane

• It is a halogenated ether.
• It is not expensive.
• It causes less cerebral vasodilatation than halothane.
• It is associated with only a remote risk of hepatitis
• Isoflurane is now routinely used for all cases because it produces less arrhythmias and myocardial depression.
• It has a pungent smell and hence cannot be used for inhalation induction.

Sevoflurane

It is a newer general anaesthetic agent and has a sweet smell.

• Useful for inhalation induction, especially in children.
• Induction and recovery are faster than with halothane.
• It produces minimal myocardial depression.
• It is also a useful agent for induction of anaesthesia in patients with difficult airways.
• It is expensive but more affordable than previously. Thus, it is being increasingly used for neurosurgery, cardiac surgery and in patients who can afford it, because of better haemodynamic stability and faster recovery.

Desflurane

• It is another new volatile anaesthetic agent.
• It causes vasodilatation and increase in heart rate.
• Induction and recovery are very fast.
• However, it is irritant to the respiratory tract and hence is not suitable for inhalational induction.
• It also requires a specially constructed heated vaporiser because of its high volatility.
• Desflurane has a very low blood-gas solubility coefficient. Hence, emergence from desflurane anaesthesia is very fast and thus it is an ideal agent to use in obese patients. It is very expensive.
• Desflurane is a greenhouse gas and can contribute to air pollution. Hence its use has reduced and many hospitals across the world have stopped its use.

Nitrous Oxide

• It is an anaesthetic gas which is compressed and supplied as a liquid in blue cylinders.
• It is sweet smelling and nonirritant.
• It provides analgesia but is insufficient to produce an adequate depth of anaesthesia when used alone.
• It enhances induction of anaesthesia with the volatile anaesthetics and reduces their requirement.
• It does not produce significant depression of the cardiovascular system.

General Anaesthetic Agents Uses:

• It is used along with volatile anaesthetic agents as part of balanced anaesthesia.
• A combination of 50% nitrous oxide and 50% oxygen is available as Entonox. It can be used to provide labour analgesi
• It may also be used to provide analgesia for small procedures in dentistry.

General Anaesthetic Agents Side Effects:

• It can diffuse into closed gas spaces such as pneumothorax, obstructed intestines, sinuses and middle ear, and can cause barotraumThe volume of a cavity can increase 3 to 4 times within 1–2 hours. Hence, nitrous oxide is best avoided in patients in whom such expansion may be anticipated.
• Its use is associated with an increased incidence of postoperative nausea and vomiting.
• In prolonged administrations, it can affect vitamin B12 synthesis causing megaloblastic anaemia.
• Teratogenicity: This has been observed in pregnant rats exposed to nitrous oxide for prolonged periods but not been proven in human beings. Nitrous oxide is best avoided in early pregnancy.
• Like desflurane, nitrous oxide is also a greenhouse gas and its clinical use has reduced considerably.

Intravenous Anaesthetic Agents

Intravenously administered anaesthetic agents are more popular for induction of anaesthesia because it is more rapid and smooth than that associated with inhalational agents. They can also be used for the maintenance of anaesthesia, sedation during regional anaesthesia, sedation in the ICU and treatment of status epilepticus.

They can be classified into rapidly-acting (acting within one arm-brain circulation time) and slower-acting (those that take longer than one arm-brain circulation time).

Intravenous Anaesthetics:

Rapidly-acting: Thiopentone, propofol, etomidate.

Slower-acting: Ketamine, high dose opioids, benzodiazepines.

Thiopentone Sodium

It is an ultra-short-acting barbiturate, available as a yellowish powder. It is used as a 2.5% solution (25 mg/ ml). It is used in a dose of 4–5 mg/kg intravenously.

Thiopentone Sodium Clinical Effects:

CNS:

• Generalised depression of the CNS is observed within 15 to 20 seconds of IV injection of thiopentone. Loss of eyelash reflex is used as an end-point.
• It is a potent anticonvulsant.
• It is not an analgesiTo the contrary, it increases pain sensation (antanalgesic). Consciousness is regained within 5 to 10 minutes.

CVS:

It produces myocardial depression, peripheral vasodilatation and hypotension especially when large doses are administered rapidly.

Profound hypotension may occur, especially in a patient with hypovolaemia or cardiac disease. It may induce tachycardia.

RS:

• It reduces respiratory drive. A short period of apnoea is common.
• It can precipitate asthma following airway obstruction in susceptible individuals.

Skeletal muscle:

There is poor muscle relaxation with thiopentone.

Uterus and placenta:

• There is little effect on resting uterine tone.
• It crosses the placenta rapidly, although foetal blood concentration is far less than that observed in the mother.

Eye:

• It reduces intraocular pressure.
• The corneal, eyelash and eyelid reflexes are abolished.

Intravenous Anaesthetic Agents Side Effects:

• Hypotension, tachycardia
• Respiratory depression
• Irritant to veins and can cause thrombophlebitis. If it extravasates, can cause tissue necrosis.
• Intra-arterial injection: Accidental intra-arterial injection of thiopentone results in severe arterial spasm and pain. This may be treated with vasodilators and heparin.
• Allergic reactions: Very rare.

Contraindications:

Absolute :

1. Airway obstruction 1. Hypovolaemia
2. Acute intermittent porphyria
3. Previous hypersensitivity reaction

Relative:

1. Hypovolaemia
2. Asthma

Propofol

This drug became commercially available in 1986. It is comparable to thiopentone but is five times more expensive. It is highly lipid soluble and is formulated in a white, aqueous emulsion containing soya bean oil and egg phosphatide. It is used in a dose of 2–2.5 mg/kg intravenously. The dose should be reduced in the elderly and in haemodynamically unstable patients.

Propofol Clinical Effects:

CNS:

Propofol depresses the central nervous system within 20 to 40 seconds of injection. Loss of verbal contact is used as an end-point.

Recovery is rapid and there is a minimal “hang-over” effect even in the immediate post-anaesthetic period.

CVS:

The arterial pressure decreases more than with thiopentone. This is due to peripheral vasodilatation. The degree of hypotension can be reduced by slowing the rate of administration. Heart rate increases slightly.

RS:

• After induction, apnoea occurs commonly and for a longer duration than with thiopentone.
• It causes ventilatory depression, particularly with opioids.
• It may prevent development of bronchospasm because it blunts airway reflexes.

GIT, uterus and placenta: Propofol has no significant effect on GI motility but causes a mild transient decrease in or hepatorenal function.

Intravenous Anaesthetic Agents Uses:

• As an induction agent
• As an infusion, can be used to provide total intravenous anaesthesia
• To provide conscious sedation
• As continuous infusion to sedate patients in the ICU, since its half-life is very short.

Intravenous Anaesthetic Agents Adverse Effects:

• Cardiovascular depression
• Respiratory depression
• Pain on injection
• Allergic reactions.

Comparison of different intravenous anaesthetics:

Etomidate

• Etomidate is a rapidly acting intravenous anaesthetic agent with a short duration of action of 3–5 minutes.
• It is a very cardiostable agent and is used to induce anaesthesia in cardiac patients and in haemodynamically unstable patients.
• However, continuous infusions are not advisable as it is known to depress synthesis of cortisol by the adrenal gland and impair response to ACTH.
• It is used in a dose of 0.2–0.3 mg/kg IV.

Intravenous Anaesthetic Agents Adverse Effects:

1. Adrenocortical suppression when used as infusion
2. Excitatory phenomena: Involuntary movements, cough
3. Pain on injection and venous thrombosis
4. Nausea and vomiting

Ketamine Hydrochloride

Ketamine differs from other intravenous anaesthetic agents in many respects and produces dissociative anaesthesia, rather than generalised depression of the central nervous system. It is used in a dose of 1–2 mg/ kg IV or 4–5 mg/kg IM.

Intravenous Anaesthetic Agents Clinical Effects:

CNS:

• It induces anaesthesia within 30–60 seconds of intravenous injection and lasts for 10–20 minutes. It is effective within 3–4 minutes of intramuscular injection and lasts for 15–25 minutes.
• It produces anaesthesia by dissociating the cerebral cortex from the limbic system.
• It is a potent analgesi
• It increases cerebral blood flow and intracranial pressure.

CVS:

The heart rate, blood pressure and cardiac output increase.

RS:

• Respiration is usually well-maintained with ketamine although transient apnoea may occur occasionally.
• Ketamine is a good bronchodilator.

Skeletal muscle:

There is increased muscle tone. Some spontaneous and involuntary movements may occur.

GIT:

Increased salivation can occur and can be prevented by using anticholinergic agents.

Eye:

Intraocular pressure increases.

Uterus and placenta:

It readily crosses the placental barrier and hence should be given in lower doses in pregnant patients.

Intravenous Anaesthetic Agents Adverse Effects:

• Emergence delirium
• Hypertension and tachycardia
• Increased intracranial pressure
• Vivid and unpleasant hallucinations are known with ketamine and can be prevented by prior injections of benzodiazepines.

Intravenous Anaesthetic Agents Uses:

• Patients in severe hypotension, shock
• Paediatric anaesthesia
• Analgesia and sedation
• Bronchial asthma
• Difficult locations: Accident sites, war casualties.

Physiology Of Neuromuscular Junction

When a nerve impulse arrives at the neuromuscular junction through the motor neuron, acetylcholine (ACh) molecules are liberated from the nerve endings into the junctional cleft. Acetylcholine molecules act as neurotransmitters by interacting with the nicotinic ACh receptors on the postjunctional muscle membrane at the motor end plates. This induces the opening of ionic channel of the receptor to allow ionic (sodium, calcium) flux into the muscle. The sudden influx of sodium results in depolarisation and muscle contraction.

Acetylcholine Receptor:

The acetylcholine receptor is flower-shaped with five petal-like structures. These five subunits are named α(2), β(1), ε(1) and δ(1). Each alpha subunit must be occupied by an acetylcholine molecule to open the channel. This acetylcholine receptor at the neuromuscular junction is nicotinic in nature and thus different from those in the rest of the body.

Muscle Relaxants

These are drugs that interfere with the combination of acetylcholine molecules with their receptors. These block neuromuscular transmission and cause relaxation of the muscle resulting in muscle paralysis.

Neuromuscular blockers are of two types: Depolarising and nondepolarising muscle relaxants.

Depolarising Muscle Relaxants (Succinylcholine)

It is the only depolarising muscle relaxant in clinical use. It has a molecular structure similar to acetylcholine. It combines with the alpha subunit of the ACh receptor and produces muscle contraction. However, unlike acetylcholine, it has a prolonged action. Continued depolarisation of a muscle results in accommodation blockade and the muscle relaxes.

• Dose: 1–1.5 mg/kg intravenously.
• Onset of action: Within 60 seconds.
• Duration of action: 3–5 minutes.
• Metabolism: By plasma cholinesterase.

Physiology Of Neuromuscular Junction Uses:

Succinylcholine is the only muscle relaxant which has the shortest time to onset of action (60 seconds) and shortest duration of action (3–5 minutes). It is used:

• To facilitate endotracheal intubation in ‘full-stomach’ patients.
• It is useful in patients with difficult airway because it gives very good relaxation to facilitate intubation but if intubation fails, the patient is likely to resume spontaneous breathing early and hypoxic brain injury may be avoided.
• To maintain paralysis for short procedures.

Physiology Of Neuromuscular Junction Adverse Effects:

• Muscle pains: The initial depolarisation that occurs due to succinylcholine causes uncoordinated contraction (fasciculations) of different groups of muscle fibres. This can cause severe muscle pain postoperatively.
• Bradycardia, especially if a second dose of succinylcholine is given. It is easily avoided by pretreatment with atropine.
• Hyperkalaemia in patients with renal failure, burns, massive crush injury, etc.
• Increase in intracranial pressure
• Increase in intraocular pressure
• Prolonged action in patients deficient in pseudocholinesterase (plasma cholinesterase). This occurs as a genetic problem in a small number of patients but may be an acquired problem as in severe liver disease.
• Malignant hyperthermia is a disorder that is unique and life-threatening precipitated by exposure to inhalation anaesthetics and succinylcholine in susceptible patients. In malignant hyperthermia, the metabolic rate of muscle cells is increased tremendously due to a defective ryanodine receptor which is necessary for reuptake of calcium after a depolarisation.

Those with a family history of anaesthetic mishaps, neuromuscular diseases such as muscular dystrophy may be susceptible to this disorder and succinylcholine is best avoided in these patients. It is not always possible to identify latent muscular dystrophies in infants and children. Administration of succinylcholine in these patients can be disastrous. Hence, the use of succinylcholine should be avoided in children less than 2 years unless an indication such as a full stomach exists. Even then, rocuronium may be considered as an alternative.

Nondepolarising Muscle Relaxants

Pancuronium, vecuronium, rocuronium, atracurium and cisatracurium are drugs belonging to this group in clinical use. The nondepolarising muscle relaxants combine with the ACh receptors but do not have any intrinsic effect on the muscle. They cause muscle paralysis by preventing the ACh molecules that are released from the nerve terminal from combining with the ACh receptors on the postsynaptic membrane and producing their action (competitive inhibition). Even if one alpha subunit is combined with a molecule of nondepolarising muscle relaxant, the muscle cannot contract in response to a nerve impulse and gets paralyseThe muscle regains its power when the muscle relaxant gets metabolised.

The nondepolarising muscle relaxants can be classified according to their duration of action as follows:

• Short-acting (10–20 min): Mivacurium
• Intermediate-acting (20–30 min): Atracurium, vecuronium and rocuronium
• Long-acting (>45 min): d-Tubocurarine and pancuronium.

Physiology Of Neuromuscular Junction Uses:

1. To facilitate endotracheal intubation
2. To maintain paralysis during anaesthesia and in the ICU.

Reversal Of Neuromuscular Blockade

At the end of anaesthesia, the muscle relaxation produced by the nondepolarising muscle relaxant is usually reverseThis is to ensure good recovery of muscle power to maintain airway and respiration. ACh molecules are broken down by cholinesterases. Anticholinesterases such as neostigmine block the action of cholinesterase, thus allowing ACh molecules to accumulate in the neuromuscular junction. The block produced by the nondepolarising muscle relaxants is competitive. When ACh molecules increase in number due to the action of the anticholinesterase, and nondepolarising muscle relaxant molecules decrease in number due to metabolism, muscle power returns.

Neostigmine is the only anticholinesterase in clinical use. Its dose is 0.05 mg/kg body weight. Neostigmine increases the amount of ACh not only at the neuromuscular junction but also in the entire body. It can cause the muscarinic effects of ACh such as bradycardia, bronchoconstriction, etHence, neostigmine is always combined with atropine (0.025 mg/kg) or glycopyrrolate (0.01 mg/kg) to counter the muscarinic effects.

Recovery from Neuromuscular Blockade:

Physiology Of Neuromuscular Junction Clinical indicators:

• Opening of eyes without furrowing of forehead
• Good handgrip
• Raising arms against gravity
• Good cough
• Ability to lift head against gravity (sustained head lift) for at least five seconds.
• Good cough and sustained head-lift are reliable indicators of adequate recovery, whereas simple opening of eyes and handgrip may still be associated with incomplete recovery.

Objective criteria:

The amount of neuromuscular blockade can be checked using a peripheral nerve stimulator. The ulnar nerve is stimulated and the response of the adductor pollicis muscle is checked If good muscle contractions are seen in response to the nerve stimulation, the muscle power is said to have Similarly, posterior tibial nerve and facial nerve may also be used to monitor neuromuscular junction.

The patient is allowed to breathe spontaneously and his trachea extubated only when there is clinical evidence of complete recovery from neuromuscular blockade. If there is inadequate recovery of muscle power, the patient may need to be ventilated artificially till muscle power is normal.

Principles of Anaesthesiology  Multiple Choice Questions

Question 1. With the mouth wide open and tongue protruding in a patient in a sitting position, if only soft and hard palate are seen, his airway is classified as Mallampati class:

1. 1
2. 2
3. 3
4. 4

Answer: 3. 3

Question 2. The following period is adequate fasting before the administration of anaesthesia after taking a glass of cow’s milk:

1. 2 hours
2. 4 hours
3. 6 hours
4. 8 hours

Answer: 3. 6 hours

Question 3. American Society of Anaesthesiologists physical status (ASA–PS) 6 would be appropriate to describe the following patient:

1. Patient with moderately controlled diabetes mellitus on insulin
2. Patient posted for surgery for 6 times before
3. Patient in severe hypovolaemic shock undergoing fluid resuscitation
4. Brain dead patient for organ donation

Answer: 4. Brain-dead patient for organ donation

Question 4. The following is an ideal anaesthetic agent for inhalation induction:

1. Isoflurane
2. Sevoflurane
3. Desflurane
4. Diethyl ether

Answer: 1. Isoflurane

Question 5. Succinylcholine is contraindicated in all of the following except:

1. Full stomach
2. Raised intracranial pressure
3. Open eye injury
4. Crush injury

Answer: 1. Full Stomach

Question 6. The following inhalation anaesthetic requires a heated vaporiser:

1. Isoflurane
2. Sevoflurane
3. Desflurane
4. Diethyl ether

Answer: 3. Desflurane

Question 7. The following anaesthetic can be given by nasal, intramuscular and intravenous routes for induction of anaesthesia:

1. Thiopentone
2. Ketamine
3. Etomidate
4. Propofol

Answer: 2. Ketamine

Question 8. The following intravenous anaesthetic is useful in status asthmaticus for its bronchodilatory effect:

1. Thiopentone
2. Ketamine
3. Etomidate
4. Propofol

Answer: 2. Ketamine

Question 9. The following intravenous anaesthetic produces dissociative anaesthesia:

1. Thiopentone
2. Ketamine
3. Etomidate
4. Propofol

Answer: 2. Ketamine

Question 10. The following local anaesthetic is also Class 1b antiarrhythmic agent:

1. Lignocaine
2. Bupivacaine
3. Prilocaine
4. Cocaine

Answer: 1. Lignocaine

Question 11. The following local anaesthetic is very cardiotoxic:

1. Lignocaine
2. Bupivacaine
3. Prilocaine
4. Ropivacaine

Answer: 2. Bupivacaine

Question 12. The following anaesthetic is described as an antanalgesic:

1. Thiopentone
2. Ketamine
3. Etomidate
4. Propofol

Answer: 1. Thiopentone

Question 13. The following drug is absolutely contraindicated in acute intermittent porphyria:

1. Thiopentone
2. Ketamine
3. Etomidate
4. Propofol

Answer: 1. Thiopentone

Question 14. The following muscle relaxant produces ‘accommodation blockade’:

1. Succinylcholine
2. Atracurium
3. Vecuronium
4. Tubocurarine

Answer: 1. Succinylcholine

Question 15. The gold standard for confirmation of endotracheal tube position is:

1. Presence of bilateral air entry
2. Absent breath sounds in the epigastrium
3. A square wave capnogram
4. Bilateral visible chest rise

Answer: 3. A square wave capnogram