The upper five cervical segments of the spinal cord give rise to the XI cranial nerve. They connect with a few smaller branches before exiting the skull through the jugular foramen. The sternomastoid and trapezius muscles get their motor supply from the accessory root. Except for the palatoglossus, the hypoglossal nerve supplies motor supply to all tongue muscles.

The inability to shrug the shoulder on the affected side and rotate the head to the side against resistance is caused by damage to the spinal accessory nerve. This is due to the trapezius and sternomastoid muscles’ weakness.

The hypoglossal nerve is damaged, resulting in tongue wasting and inability to move from side to side.

The stylopharyngeus receives motor supply from the glossopharyngeal nerve. It also carries taste sensory fibres from the back third of the tongue, as well as the carotid sinus, carotid body, pharynx, and middle ear.

Motor supply to the larynx, pharynx, and palate; parasympathetic innervation to the heart, lung, and gut; and sensory fibres from the epiglottis and valleculae are all provided by the vagus nerve.

The National Institute for Health and Care Excellence (NICE) has published guidelines on infective endocarditis prophylaxis (IE). The goal was to create clear guidelines for antibiotic prophylaxis in patients undergoing dental procedures as well as certain non-dental interventional procedures. A number of studies have found an inconsistent link between recent interventional procedures and the development of infective endocarditis in both dental and non-dental procedures.

Antibiotic prophylaxis against infective endocarditis is not advised or required in the following situations:

Dental patients undergoing procedures
Patients undergoing procedures involving the upper and lower gastrointestinal tracts, the genitourinary tract (including urological, gynaecological, and obstetric procedures, as well as childbirth), and the upper and lower respiratory tract (including ear, nose and throat procedures and bronchoscopy).

Antibiotic resistance can be exacerbated by the indiscriminate use of prophylactic antibiotics, but this is not the primary reason for avoiding their use in these situations.

To reduce the risk of endocarditis, any patient who is at risk of developing IE should be investigated and treated as soon as possible. Patients with the following conditions are at risk of developing IE:
acquired valvular heart disease with regurgitation or stenosis
previous valve replacement
structural congenital heart disease
past history of IE, or
hypertrophic cardiomyopathy (HOCM)

It would also be appropriate for high-risk dental procedures and those with severe gingival disease.

Although this patient may not have structural heart disease, ABs should be administered on a case-by-case basis.

Observers may subconsciously measure or report data in a way that favours the expected study outcome. Therefore, by blinding the study we can eliminate expectation bias.

Recall bias is a systematic error that occurs when the study participants omit details or do not remember previous events or experiences accurately.

Verification can occur during investigations when there is a difference in testing strategy between groups of individuals, which might lead to biasness due to differing ways of verifying the disease of interest.

Nonresponse bias is the bias that occurs when the people who respond to a survey differ significantly from the people who do not respond to the survey.

A distortion that modifies an association between an exposure and an outcome because a factor is independently associated with the exposure and the outcome. Randomization is the best way to reduce the risk of confounding.

The vertebral artery originates from the subclavian artery and ascends through the neck in the transverse foramen of the C1-C6 vertebrae. C2 vertebra is called the axis vertebra. A part of the vertebral artery lies in a groove on the upper surface of the atlas’s (C1) posterior arch. It enters the vertebral canal below the inferior border of the posterior atlantooccipital membrane. The vertebral arteries then enter the skull via the foramen magnum.

Ciprofloxacin belongs to the quinolone group of antibiotics, and doxycycline and minocycline are tetracyclines. So, they are not affected by beta-lactamase.
However, amoxicillin is a beta-lactam antibiotic and beta-lactamase cleaves the beta-lactam ring present in amoxicillin. This results in the breakdown of the antibiotic and thus the area of erythema dramatically increased.
Co-amoxiclav contains amoxicillin and clavulanic acid which protects amoxicillin from beta-lactamase.

Phase 0 trials assist the scientists in studying the behaviour of drugs in humans by micro dosing patients. They are used to speed up the developmental process. They have no measurable therapeutic effect and efficiency.

Phase 1 is associated with assessing whether a drug is safe to use or not. The process is extensive and can take up to several months. It also involves healthy participants (less than 100) that are paid to take part in the study. The side effects upon increasing dosage are also addressed by the study. The effects the drug has on humans including how its absorbed, metabolized and excreted are studied. Approximately 70% of the drugs pass this phase.

Phase 2 trials involve patients that are suffering from the disease under study and are associated with determining the efficiency and the optimum dosage of the drug.

Phase 3 also assesses the efficacy but at a higher scale with larger population sample.

Phase 4 trials are involved with the long term effects and side effects of the drug.

The structures in the porta hepatis from anterior to posterior are:

The ducts: Most anterior are the left and right hepatic ducts.

The arteries: Next are the left and right hepatic arteries

The veins: Next is the portal vein

The epiploic foramen of Winslow lies most posterior at the porta hepatis.

Microshock refers to ventricular fibrillation caused by miniscule amounts of currents or voltages (100-150 microamperes) passing through the myocardial tissue from external cables arising from electrical components within the cardiac muscle, for example, pacemaker electrodes or saline filled venous catheters.
The risk of shock changes with the construction of electrical equipment in question. The main classes of electrical equipment include: I: Appliances have a protective earth connected to an outer casing which prevents live elements from coming in contact with conductive elements. A fault in this equipment class will result in live elements coming in contact with the outer casing and allowing electrical flow into the protective earth. This triggers the protective fuse to disconnect the electric supply to the appliance.
II: These appliances have reinforced insulation. In the event of a fault which causes the first layer of insulation to fail, the second layer is able to prevent contact of live elements with outer casing.
III: These appliances have no insulation to provide safety, and rely solely on the use of separated extra low voltage source (SELV) which limits voltage to 25V AC or 60V DC allowing for a person to come in contact with it without risk of a shock under normal dry conditions. Under wet conditions, voltage supply should be lowered to reduce risk of shock. These devices have no risk of macroshocks, but some risk of microshocks.
Class I and II electrical appliances are further divided into subtypes developed to limit current leakage in the event of a singular fault:
B (body): Upper limit of current leakage is 500 µA. This current can cause skin tingling and microshocks, but is not sufficient to cause injury.
BF (body floating): These appliances have an isolating capacitor or transformer which separate the secondary circuit from the protective earth. The upper limit of current leakage is the same as type B.
CF (cardiac floating): Upper limit of leakage current during a singular fault is 50 microamps. It is least likely to result in a microshock.

Noradrenaline also called norepinephrine belongs to the catecholamine family that functions in the brain and body as both a hormone and neurotransmitter.

They have sympathomimetic effects acting via adrenoceptors (α1, α2, β1, β2, β3) or dopamine receptors (D1, D2).

May cause reflex bradycardia, reduce cardiac output and increase myocardial oxygen consumption

The incidence of Pulmonary aspiration in children is about 0.07%€�0.1%.

The Association of Paediatric Anaesthetists of Great Britain and Ireland, The European Society of Paediatric Anaesthetists and L’Association Des Anesthésistes€�Réanimateurs Pédiatriques d’Expression Française produced a consensus statement in April 2018 with revised starvation times in children prior to elective surgery.

The preoperative fasting for elective procedures for children aged 0-16 years of age are:

Solid food/formula milk – 6 hours
Breast milk – 4 hours
Clear fluid – 1 hour

A liberal clear fluid fasting regime does not affect the incidence of pulmonary aspiration in children as long as there are no specific contraindications (e.g. gastro-oesophageal reflux, cerebral palsy). Prolonged periods of fasting in children are associated with increase thirst and irritability and can lead to other adverse physiological and metabolic effects.

Clear fluids are defined as water, clear (nonopaque) fruit juice or squash/cordial, ready diluted drinks, and non-fizzy sports drinks.

Electrical resistivity is a measure of a material’s property to oppose the flow of electric current. This is expressed in Ohm-meters (Ω‹…m). The symbol of resistivity is usually the Greek letter Ï� (rho). A high resistivity means that a material does not conduct electric charge well.

Electrical resistivity is defined as the relation between the electric field inside a material, and the electric current through it as a consequence:

� = E/J

in which Ï� is the resistivity of the material (Ω‹…m),
E is the magnitude of the electrical field in the material (V/m),
J is the magnitude of the electric current density in the material (A/m2)

If the electric field (E) through a material is very large and the flow of current (J) is very small, it means that the material has a high resistivity.

The following terms are used in medical testing:

True negative – The test is negative and the patient does not have the disease.
True positive – The test is positive and the patient has the disease.
False positive – The test is positive but the patient does not have the disease.
False negative – The test is negative but the patient has the disease.

The sensitivity of a predictive test = true positives / (true positives + false negatives).

The specificity of a test = true negatives / (false positives + true negatives).

The negative predictive value of a test = true negatives / (false negatives + true negatives).

Pulse oximeters combine the principles of oximetry and plethysmography to noninvasively measure oxygen saturation in arterial blood. A sensor containing two or three light emitting diodes and a photodiode is placed across a perfused body part, commonly a finger, to be transilluminated. Oximetry depends on oxyhaemoglobin and deoxyhaemoglobin, and their ability to absorb the beams of light produced by the light emitting diodes: red light at 660 nm and infrared light at 960 nm.

The isosbestic point is the point wherein two different substances absorb light to the same extent. For oxyhaemoglobin and deoxyhaemoglobin, the points are at 590 nm and 805 nm. These are considered reference points where light absorption is independent of the degree of saturation.

Non-constant absorption of light is often due to the presence of an arterial pulsation, whilst constant absorption of light is seen in non-pulsatile tissues.

Most pulse oximeters are inaccurate at low SpO2, but is accurate at +/- 2% within the range of 70% to 100% SpO2. All pulse oximeters demonstrate a delay in between changes in SaO2 and SpO2, and display average readings every 10 to 20 seconds, hence they are unable to detect acute desaturation episodes.

Phase IIa studies are usually pilot studies designed to demonstrate clinical efficacy or biological activity (‘proof of concept’ studies) whereas phase IIb studies determine the optimal dose at which the drug shows biological activity with minimal side-effects (€˜definite dose-finding’ studies).

Phase III and Phase IV studies are performed on larger set of participants (usually hundreds to thousands) when safety and efficacy have been established.

According to European Group protocol for the investigation of MH susceptibility, muscle biopsy should be performed on quadriceps muscle (either vastus medialis or vastus lateralis), using regional anaesthesia (avoiding local anaesthetic infiltration) or general anaesthetic techniques. Local anaesthetic solution within muscle fibres may affect in vitro contraction testing.

Desflurane is a weak triggering anaesthetic of malignant hyperthermia so is avoided in MH susceptible patients. This includes all volatile inhalational agents and suxamethonium.

General anaesthetic with the volatile free anaesthetic machine may be considered but spinal anaesthesia is a better choice due to the possibility of airway problems.

Dose response curves are plotted as % response to drug against Logarithm of drug concentration. The graph is usually sigmoid shaped.

Any drug that has high affinity and high intrinsic activity is likely an agonist. A drug with high affinity but no intrinsic activity will act as an antagonist. Displacement of an agonist also depends on the relative concentrations of the two drugs at the receptor sites.

Maximal response may be achieved by activation of a small proportion of receptor sites.

Arrhythmias and/or hypotension are the most common causes of death from tricyclic antidepressant (TCA) overdose.

The quinidine-like actions of tricyclic antidepressants on cardiac tissues are primarily responsible for their toxicity. Conduction through the His-Purkinje system and the myocardium slows as phase 0 depolarisation of the action potential slows. QRS prolongation and atrioventricular block are caused by slowed impulse conduction, which also contributes to ventricular arrhythmias and hypotension.

Arrhythmias can also be caused by abnormal repolarization, impaired automaticity, cholinergic blockade, and inhibition of neuronal catecholamine uptake, among other things.

Acidaemia, hypotension, and hyperthermia can all exacerbate toxicity.

The anticholinergic effects of tricyclic antidepressants, as well as the blockade of neuronal catecholamine reuptake, cause sinus tachycardia. Sinus tachycardia is usually well tolerated and does not require treatment. It can be difficult to tell the difference between sinus tachycardia and ventricular tachycardia with QRS prolongation.

A QRS duration of more than 100 milliseconds indicates a higher risk of arrhythmia and should be treated with systemic sodium bicarbonate.

The tricyclic is dissociated from myocardial sodium channels by serum alkalinization, and the extracellular sodium load improves sodium channel function.

Maintenance therapy aims to replace water and electrolytes lost under ordinary conditions. In the perioperative period, maintenance fluid administration may not sufficiently account for the increased fluid requirements caused by third-space losses into the interstitium and gut. Specific recommendations vary with the patient, the procedure, and the type and amount of fluid administered during the operation. The fluid for maintenance therapy replaces deficits arising primarily from insensible losses and urinary or gastrointestinal (GI) losses.

The maintenance fluid volume can be computed using the Holliday-Segar method.

Body weight Fluid volume
first 10 kg 4 ml/kg/hr
next 10-20 kg 2 ml/kg/hr
>20 kg 1 ml/kg/hr

In the past few years, there has been growing recognition of the increased risk of hyponatremia in hospitalized children in intensive care and postoperative settings who receive hypotonic maintenance fluids. Several studies, including a randomized controlled trial and a Cochrane analysis, found that the use of isotonic fluids is associated with fewer electrolyte derangements and concluded that isotonic maintenance fluids are preferable to hypotonic solutions in hospitalized children.

A European consensus statement suggests that an intraoperative fluid should have an osmolarity close to the physiologic range in children in order to avoid hyponatremia, an addition of 1-2.5% in order to avoid hypoglycaemia, lipolysis or hyperglycaemia and should also include metabolic anions as bicarbonate precursors to prevent hyperchloremic acidosis.

A rate of 40 ml/hr is suboptimal.

If 0.9% NaCl with 0% glucose is given at a rate of 65 ml/hr, despite of the correct infusion rate, large volumes can lead to hyperchloremic acidosis.

If 0.18% NaCl with 4% glucose is given at a rate of 65 ml/hr, infusion of this fluid regimen can lead to hyponatremia because of its hypotonicity.

End-tidal carbon dioxide (ETCO2) monitoring has been an important factor in reducing anaesthesia-related mortality and morbidity. Hypercarbia, or hypercapnia, occurs when levels of CO2 in the blood become abnormally high (Paco2 >45 mm Hg). Hypercarbia is confirmed by arterial blood gas analysis. When using capnography to approximate Paco2, remember that the normal arterial€“end-tidal carbon dioxide gradient is roughly 5 mm Hg. Hypercarbia, therefore, occurs when PETco2 is greater than 40 mm Hg.

The most likely explanation for the changes in capnograph is either exhaustion of the soda lime and a progressive rise in circuit dead space.

Inspect the soda lime canister for a change in colour of the granules. To overcome soda lime exhaustion, the first step is to increase the fresh gas flow (FGF) (Option A). Then, if need arises, replace the soda lime granules. Other strategies that can work are changing to another circuit or bypassing the soda lime canister, but remember that both these strategies are employed only after increasing FGF first. Exclude other causes of equipment deadspace too.

There are also other causes for hypercarbia to develop intraoperatively:
1. Hypoventilation is the most common cause of hypercapnia. A. Inadequate ventilation can occur with spontaneous breathing due to drugs like anaesthetic agents, opioids, residual NMDs, chronic respiratory or neuromuscular disease, cerebrovascular accident.
B. In controlled ventilation, hypercapnia due to circuit leaks, disconnection or miscalculation of patient’s minute volume.
2. Rebreathing – Soda lime exhaustion with circle, inadequate fresh gas flow into Mapleson circuits and increased breathing system deadspace.
3. Endogenous source – Tourniquet release, hypermetabolic states (MH or thyroid storm) and release of vascular clamps.
4. Exogenous source – Absorption of CO2 from pneumoperitoneum.

Among the breathing circuits, the Lack circuit is the most efficient for spontaneous breathing.

An outer coaxial tube is present to deliver fresh air; exhaust air is routed to an inner tube, which is then delivered to a scavenging system. An expiratory valve is seen at the patient end, which is an advantage over other circuits. Moreover, the Lack circuit prevents rebreathing slightly greater than the alveolar minute ventilation at 4-5 litres per minute.

The Bain circuit prevents rebreathing at 160-200ml/kg per minute, and is a co-axial version of the Mapleson D circuit.

The Mapleson E circuit prevent rebreathing at a fresh gas flow (FGF) of approximately twice the patient’s normal minute volume. A modification of this, the Mapleson F, has a reservoir bag at the opposite end for the FGF. This circuit is appropriate for paediatric patients with a body weight less than 20 kg.

To denote large measured units, the following SI mathematical prefixes are used:

1 deca = 10 bytes (101)
1 hecto (h) = 100 bytes
1 kilo (k)= 1,000 bytes
1 mega (M) = 1,000,000 bytes
1 giga (G) = 1,000,000,000 bytes
1 Tera (T) = 1,000,000,000,000 bytes
1 Peta (P) = 1,000,000,000,000,000 bytes.

A nominal volume of 2 litres is contained in a CD cylinder. It has a pressure of 230 bar when full and contains litres 460 L of useable oxygen at STP.

For every 1000 mL 100% oxygen there will be an entrainment of 1000 mL or air (20% oxygen) in an air/oxygen mix.

The average concentration is, therefore, 120/2=60% or 0.6.

Cardiac conduction

Phase 0 – Rapid depolarization. Opening of fast sodium channels with large influx of sodium

Phase 1 – Rapid partial depolarization. Opening of potassium channels and efflux of potassium ions. Sodium channels close and influx of sodium ions stop

Phase 2 – Plateau phase with large influx of calcium ions. Offsets action of potassium channels. The absolute refractory period

Phase 3 – Repolarization due to potassium efflux after calcium channels close. Relative refractory period

Phase 4 – Repolarization continues as sodium/potassium pump restores the ionic gradient by pumping out 3 sodium ions in exchange for 2 potassium ions coming into the cell. Relative refractory period

Selection of a chest drain will depend on the external circumference.

A cannula, whether intravenous or intra-arterial, are classified according to standard wire gauge, which refers to the number of wires that can fit into the same hole. If a cannula is labelled 22G, then 22 wires will fit into the standard size hole.

A more popular measurement than SWG nowadays is cross sectional area.

When the concern for selecting equipment is the rate of flow, then it is important to consider the diameter and the radius of a parallel sided tube. These, however, are not routinely considered when comparing sizes of a cannula.

The response of cerebral blood flow (CBF) to hyperoxia (PaO2 >15 kPa, 113 mmHg), the cerebral oxygen vasoreactivity is less well defined. A study originally described, using a nitrous oxide washout technique, a reduction in CBF of 13% and a moderate increase in cerebrovascular resistance in subjects inhaling 85-100% oxygen. Subsequent human studies, using a variety of differing methods, have also shown CBF reductions with hyperoxia, although the reported extent of this change is variable. Another study assessed how supra-atmospheric pressures influenced CBF, as estimated by changes in middle cerebral artery flow velocity (MCAFV) in healthy individuals. Atmospheric pressure alone had no effect on MCAFV if PaO2 was kept constant. Increases in PaO2 did lead to a significant reduction in MCAFV; however, there were no further reductions in MCAFV when oxygen was increased from 100% at 1 atmosphere of pressure to 100% oxygen at 2 atmospheres of pressure. This suggests that the ability of cerebral vasculature to constrict in response to increasing partial pressure of oxygen is limited.

Increases in arterial blood CO2 tension (PaCO2) elicit marked cerebral vasodilation.

CBF increases with general anaesthesia, ketamine anaesthesia, and hypoviscosity.

Atrial natriuretic peptide (ANP) is secreted mainly from myocytes of right atrium and ventricle in response to increased blood volume.
It is secreted by both the right and left atria (right >> left).

It is a 28 amino acid peptide hormone, which acts via cGMP
degraded by endopeptidases.

It serves to promote the excretion of sodium, lowers blood pressure, and antagonise the actions of angiotensin II and aldosterone.

Resistance pulmonary arteries constrict in response to alveolar and airway hypoxia, diverting blood to better-oxygenated alveoli.

In atelectasis, pneumonia, asthma, and adult respiratory distress syndrome, hypoxic pulmonary vasoconstriction optimises O2 uptake. Hypoxic pulmonary vasoconstriction helps maintain systemic oxygenation during single-lung anaesthesia.

A redox-based O2 sensor within pulmonary artery smooth muscle cells is involved in hypoxic pulmonary vasoconstriction. The production of reactive oxygen species by smooth muscle cells in the pulmonary artery varies in proportion to PaO2. Hypoxic removal of these redox second messengers inhibits voltage-gated potassium channels, depolarizing smooth muscle cells in the pulmonary artery.

L-type calcium channels are activated by depolarization, which raises cytosolic calcium and causes hypoxic pulmonary vasoconstriction. Some anaesthetics suppress this response, increasing the risk of further deterioration in ventilation perfusion mismatch.

Agents that inhibit HPV are ether, halothane, and desflurane (>1.6 MAC).
Agents with no effect on HPV include thiopentone, fentanyl, desflurane (1MAC), isoflurane (<1.5MAC), sevoflurane(1MAC), and propofol.

Hydrochloric acid is lost when you vomit for a long time (HCl). As a result, the following can be expected, in varying degrees of severity:

Hypokalaemia
Hypochloraemia
Increased bicarbonate to compensate for chloride loss and metabolic alkalosis

The alkalosis causes potassium to move from the intracellular to the extracellular compartment at first. Long-term vomiting and dehydration cause potassium to be excreted by the kidneys in order to conserve sodium. Dehydration can cause urea and creatinine levels to rise.

The actual base excess is always greater than the standard base excess.

The actual base excess (BE) is a measurement of a base’s contribution to a blood gas picture’s metabolic component. It’s the amount of base that needs to be added to a blood sample to bring the pH back to 7.4 after the respiratory component of a blood gas picture has been corrected (PaCO2 of 40 mmHg or 5.3 kPa). The BE has a normal range of +2 to 2. A large positive BE indicates a severe metabolic alkalosis, while a large negative BE indicates a severe metabolic acidosis. As a result, the actual BE in vitro is unaffected by CO2.

In vivo, however, standard BE is not independent of pCO2 because blood with haemoglobin acts as a better buffer than total ECF.

As a result, it is impossible to tell the difference between compensating for a respiratory disorder and compensating for the presence of a primary metabolic disorder.

The differences between in vitro and in vivo behaviour can be mostly eliminated if the BE is calculated for a haemoglobin concentration of 50 g/L (the ‘effective’ or virtual value of Hb if it was distributed throughout the extracellular space) rather than the actual haemoglobin. Because haemoglobin has a lower buffering capacity, the standard BE is higher than the actual BE. It reflects the BE better in the extracellular space rather than just the intravascular compartment.

The AAGBI and the British Hypertension Society has published guidelines for the measurement of adult blood pressure and management of hypertension before elective surgery.

The objective is to ensure that patients admitted for elective surgery have a known systolic blood pressure below 160 mmHg and diastolic blood pressures below 100 mmHg. The primary health care teams, if possible, should ensure that this is the case and provide evidence to the pre-assessment clinic staff or on admission.

Avoiding cancellation on the day of surgery because of white coat hypertension is a secondary objective.

Patients with blood pressures below 180 mmHg systolic and 110 mmHg diastolic (measured in the preop assessment clinic), who present to pre-operative assessment clinics without documented evidence of primary care blood pressures should proceed to elective surgery.

In this question, the history/assessment does not appear to point to obvious end-organ damage so there is no indication for further investigation for secondary causes of hypertension or an echocardiogram at this point. Further review and treatment at this point is not required.

However, you should write to the patient’s GP and encourage serial blood pressure measurements in the primary health care setting.

Carbon dioxide absorbs the most infrared (IR) light between the wavelengths of 4.2-4.4m (4.26m is ideal).

Nitrous oxide absorbs infrared light at wavelengths of 4.4-4.6m (very similar to CO2) and less so at 3.9m.

At a frequency of 4.7m, carbon monoxide absorbs the most IR light.

At 3.3 m and throughout the ranges 8-12 m, the volatile agents have strong absorption bands.

Although oxygen does not absorb infrared light, it collides with CO2 molecules, interfering with absorption. The absorption band is widened as a result of this (so called collision or pressure broadening). A drop of 0.5 percent in measured CO2 can be caused by 95% oxygen.

Nitrous oxide causes a greater inaccuracy of 0.1 percent per ten percent of nitrous oxide.

Water vapour absorbs infrared light as well, resulting in absorption band overlap, collision broadening, and partial pressure dilution. Water traps and water permeable tubing are used to reduce inaccuracies.

Collision broadening is compensated for in modern gas multi-gas analysers.