The fibrotendinous ring formed by the congregation of the rectus muscles at the apex of the orbit does not include superior oblique. This muscle is completely outside the ring and so it is the most difficult muscle to anaesthetise completely. A good grasp of the anatomy of the area being anaesthetised is important with all regional anaesthetic techniques so that potential problems and complications with a block can be anticipated.

The borders of this pyramid whose apex points upwards and outwards of the bony orbit are as follows:
Floor – Zygoma and Maxilla
Roof – frontal bone
Medial wall – maxilla, ethmoid, sphenoid and lacrimal bones.
Lateral wall – greater wing of the sphenoid and the zygoma.

The four recti muscles (superior, medial, lateral and inferior) originate from a tendinous ring (the annulus of Zinn) and extend anteriorly to insert beyond the equator of the globe. Bands of connective tissue are present between the rectus muscles forming a conical structure and hinder the passage of local anaesthetic.

The superior oblique muscle is situated outside this ring and is the most difficult muscle to anaesthetise completely, particularly with a single inferotemporal peribulbar injection. An additional medial injection may help to prevent this.

The cranial nerve supply to the extraocular muscles are:
3rd (inferior oblique, inferior recti, medial and superior)
4th (superior oblique), and
6th (lateral rectus).

The long and short ciliary nerves provide the sensory supply to the globe and these are branches of the nasociliary nerve, (which is itself a branch of the ophthalmic division of the trigeminal nerve).

To achieve anaesthesia for the eye, these nerves which enter the fibrotendinous ring need to be fully blocked to anaesthetise the eye for surgery.

The diaphragm divides the thoracic cavity from the abdominal cavity. Structures penetrate the diaphragm at different vertebral levels through openings in the diaphragm to communicate between the two cavities. The diaphragm has openings at three vertebral levels:

T8: vena cava, terminal branches of the right phrenic nerve
T10: oesophagus, vagal trunks, left anterior phrenic vessels, oesophageal branches of the left gastric vessels
T12: descending aorta, thoracic duct, azygous and hemi-azygous vein

The posterior tibial artery originates from the popliteal artery in the popliteal fossa. It passes posterior to the popliteus muscle to pierce the soleus muscle. It descends between the tibialis posterior and flexor digitorum longus muscles.

The posterior tibial artery supplies blood to the posterior compartment of the lower limb. The artery can be palpated posterior to the medial malleolus.

There are 4 main pulse points for the lower limb:

1. Femoral pulse 2-3 cm below the mid-inguinal point
2. Popliteal partially flexed knee to loosen the popliteal fascia
3. Posterior tibial behind and below the medial ankle
4. Dorsal pedis dorsum of the foot over the navicular bone

In any alveolar unit, the V/Q ratio affects alveolar oxygen (PAO2) and carbon dioxide tension (PACO2).

The partial pressure of alveolar carbon dioxide (PACO2) is plotted against the partial pressure of alveolar oxygen in a Ventilation-Perfusion (V/Q) ratio graph (PAO2). Given a set of model assumptions, the curve represents all of the possible values for PACO2 and PAO2 that an individual alveolus could have.

In the case of an infinity V/Q ratio (ventilation but no perfusion or dead space), the PACO2 of the alveolus will equal zero, while the PAO2 will approach that of external air (150mmmHg). At the apex of the lung, the V/Q ratio is 3.3, compared to 0.67 at the base.

PACO2 and PAO2 approach the partial pressures for these gases in the venous blood when the V/Q ratio is zero (no ventilation but perfusion). At the base of the lung, the V/Q ratio is 0.67, whereas at the apex, it is 3.3.

PAO2 at the apex is typically 132mmHg, and PACO2 is typically 28mmHg.

The average PAO2 at the base is 89 mmHg, while the average PACO2 is 42 mmHg.

Accumulation of morphine-6-glucuronide is a risk factor for opioid toxicity during morphine treatment. Morphine is metabolized in the liver to morphine-6-glucuronide and morphine-3-glucuronide, both of which are excreted by the kidneys. In the setting of renal failure, these metabolites can accumulate, resulting in a lowering of the seizure threshold. However, it does not occur in all patients with renal insufficiency, which is the most common reason for accumulation of morphine-6-glucuronide; this suggests that other risk factors can contribute to morphine-6-glucuronide toxicity.

The active metabolites of codeine are morphine and the morphine metabolite morphine-6-glucuronide. The enzyme systems responsible for this metabolism are: CYP2D for codeine and UGT2B7 for morphine, codeine-6-gluronide, and morphine-6-glucuronide. Both of these systems are subject to genetic variation. Some patients are ultrarapid metabolizers of codeine and produce higher levels of morphine and active metabolites in a very short period of time after administration. These increased levels will produce increased side effects, especially drowsiness and central nervous system depression.

The deep inguinal ring is the entrance of the inguinal canal. It is an opening in the transversalis fascia around 1 cm above the inguinal ligament. Therefore, the superolateral wall is made by the transervalis fascia.

The inferior epigastric vessels run medially to the deep inguinal ring forming its inferomedial border.

The inguinal canal extends obliquely from the deep inguinal ring to the superficial inguinal ring.
An indirect inguinal hernia arises through the deep inguinal ring lateral to the inferior epigastric vessels.

Boyle’s law is correctly stated as it states that the volume of a gas of known mass is inversely proportional with absolute pressure, at a constant temperature.

Beer’s law states that radiation absorption by a solution of known thickness and concentration is identical to that of a solution of double thickness and half concentration.

Bougner’s (or Lambert’s) law states that every layer with the same thickness will absorb the same amount of radiation as it passes through.

Graham’s law states that the diffusion rate of a gas is inversely related to the square root of its molecular weight.

Raoult’s law states that the reduction of a solvent’s vapour pressure is directly proportional to the solute’s molar concentration.

The external carotid artery has eight important branches:
1. Superior thyroid artery
2. Ascending pharyngeal artery
3. Lingual artery
4. Facial artery
5. Occipital artery
6. Posterior auricular artery
7. Maxillary artery (terminal branch)
8. Superficial temporal artery (terminal branch)

There is no mandibular artery but the first part of the maxillary artery is called the mandibular part as it is posterior to the lateral pterygoid muscle.
The maxillary artery is divided into three portions by its relation to the lateral pterygoid muscle:
first (mandibular) part: posterior to the lateral pterygoid muscle
second (pterygoid or muscular) part: within the lateral pterygoid muscle
third (pterygopalatine) part: anterior to the lateral pterygoid muscle

Dopamine (DA) is a dopaminergic (D1 and D2) as well as adrenergic ? and?1 (but not ?2 ) agonist.

The D1 receptors in renal and mesenteric blood vessels are the most sensitive: i.v. infusion of a low dose of Dopamine dilates these vessels (by raising intracellular cAMP). This increases g.f.r. In addition, DA exerts a natriuretic effect by D1 receptors on proximal tubular cells.

Moderately high doses produce a positive inotropic (direct?1 and D1 action + that due to NA release), but the little chronotropic effect on the heart.

Vasoconstriction (?1 action) occurs only when large doses are infused.

At doses normally employed, it raises cardiac output and systolic BP with little effect on diastolic BP. It has practically no effect on nonvascular ? and ? receptors; does not penetrate the blood-brain barrier—no CNS effects.

Dopamine is less arrhythmogenic than adrenaline

Regarding dopamine part of the dose is converted to Noradrenaline in sympathetic nerve terminals.

The surface marking for locating the femoral artery is the mid-inguinal point, which is the halfway point between the anterior superior iliac spine (ASIS) and the pubic symphysis.

The other mentioned options are not specific for any landmark.

However, it is important to note the difference between the mid inguinal point and the midpoint of the inguinal ligament, which is travels from the ASIS to the pubic tubercle.

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.

A ‘double blind crossover study’ happens when every patient receive both treatments.

It is incorrect to say that only half of the patients do not know which treatment they receive because in a double blind placebo control clinical trial ALL of the patients are blind to their treatment choice .

If some of the patients are not treated, they would be aware that they were not being treated and it could not be considered a blind trial.

In a double blind placebo control clinical trial both the clinician and the patient are blind to the treatment choice. The clinician assessing the effects of the treatment, therefore, does not know which treatment the patient has been given.

Epinephrine is used for the treatment of cardiac arrest because it causes vasoconstriction via the alpha-adrenergic (?1) receptor. This vasoconstriction increases cerebral and coronary blood flow by increasing mean arterial, aortic diastolic, and cerebral pressures. Furthermore, epinephrine is also a?1 and ?2 adrenoreceptor agonist which shows inotrope, chronotrope, and bronchodilator effects.
– Adrenaline is also used to prolong the duration of action and decrease the systemic toxicity of local anaesthetics.
– Preferred route of adrenaline in patients with cardiac arrest is i.v. followed by intra-osseous and endotracheal

Propofol is considered a safe drug to use in porphyria because even if causes mild elevation of porphyrins inpatient, it does not cause any symptoms.

Since barbiturates are inducers of ALA synthetase, they are contraindicated in porphyria patients. So, thiopentone most not be used.

Etomidate is a potent inhibitor of adrenal 11 beta-hydroxylase and 17 alpha-hydroxylase reducing cortisol and aldosterone synthesis in the adrenal cortex and has been associated with exacerbations of porphyria in animal studies and it is advisable not to use it in this condition.

Ketamine should be reserved for the hemodynamically unstable patient, however, it is a safe drug.

Diazepam is safe in porphyria but is not usually used for a rapid sequence induction.

Malignant hyperthermia (MH) is a autosomal dominant inherited medical condition which predisposes affected individuals to a clinical syndrome of hypermetabolism which involves abnormal ryanodine receptors in skeletal muscle causing a deregulation of calcium in muscle.

It is a life threatening condition requiring immediate medical intervention. It often lies dormant until triggered in susceptible individuals mostly by volatile inhaled anaesthetic agents and succinylcholine which is a muscle relaxant.

The signs and symptoms of MH are related to this hypermetabolism, which includes an increase in carbon dioxide production, metabolic and respiratory acidosis, accelerated oxygen consumption, heat production, activation of the sympathetic nervous system, hyperkalaemia, disseminated intravascular coagulation (DIC), and multiple organ dysfunction and failure.

Early signs of MH to look out for in patients includes an uptick in end-tidal carbon dioxide (even with increasing minute ventilation), tachycardia, muscle rigidity, tachypnoea, and hyperkalaemia. Later signs include fever, myoglobinuria, and multiple organ failure.

In vitro muscle contracture test (IVCT) is the standard for determining individual susceptibility to MH. It is conducted by measuring the force of muscle contraction after exposing the patient’s muscle sample to halothane and caffeine., the sample is normally taken from the vastus medialis or lateralis under regional anaesthesia.

If there is no change in preload and myocardial contractility, there will be decrease in end-diastolic volume and stroke volume. So there must be increase in end-systolic volume.

Codeine is easily absorbed from the gastrointestinal tract and converted to morphine and norcodeine in the liver via O- and N-demethylation. Morphine and norcodeine are excreted almost entirely by the kidney, primarily as conjugates with glucuronic acid.

By glucuronidation, phase II metabolism enzyme UDP-glucuronosyl transferase-2B7 converts morphine to morphine-3-glucuronide (M3G) and morphine-6-glucuronide (M6G) (UGT2B7).

Approximately 60% of morphine is converted to M3G, with the remaining 6-10% converted to M6G. M3G is inactive, but M6G is said to be 4 to 650 times more potent on the MOP receptor than morphine.

When codeine is consumed, cytochrome P450 2D6 in the liver converts it to morphine (CYP2D6).

Some people have DNA variations that increase the activity of this enzyme, causing codeine to be converted to morphine more quickly and completely than in others. After taking codeine, these ultra-rapid metabolisers are more likely to have higher than normal levels of morphine in their blood.

Respiratory depression/obstruction can be caused by high levels of morphine and M6G, especially in people who have a history of obstructive sleep apnoea. The estimated number of ultra-rapid metabolisers ranges from 1 to 7 per 100 people, but some ethnic groups may have as many as 28 per 100 people.

The pectinate muscles (musculi pectinati) are parallel muscular ridges that extend anterolaterally on the right atrial walls. The most prominent pectinate muscle, which forms the bridge of the sulcus terminalis internally, is the taenia sagittalis (second crest or septum spurium).

In the left atrium, the pectinate muscles are confined to the inner surface of its atrial appendage. They tend to be fewer and smaller than in the right atrium. This is due to the embryological origin of the auricles, which are the true atria.

Pectinate muscles of the atria are different from the trabeculae carneae, which are found on the inner walls of both ventricles.

The interior of the right atrium has five distinct features:
1. Sinus venarum – smooth, thin-walled posterior part of the right atrium where the SVC, IVC, and coronary sinus open
2. Musculi pectinati – a rough anterior wall of pectinate muscles
3. Tricuspid valve orifice – the opening through which the right atrium empties blood into the right ventricle
4. Crista terminalis – separates the rough (musculi pectinati) from the smooth (sinus venarum) internally
5. Fossa ovalis – a thumbprint size depression in the interatrial septum, which is a remnant of the oval foramen and its valve in the foetus

The autonomic nervous system is divided into the sympathetic and parasympathetic nervous system. They are anatomically and physiologically different.

The sympathetic nervous system arises from the thoracolumbar outflow (T1-L5 ) at the lateral horns of grey matter of the spinal cord. Their preganglionic neurones are usually short myelinated and synapse in ganglia lateral to the vertebral column and have acetyl choline (Ach) as the neurotransmitter. Their postganglionic neurones are longer and unmyelinated and synapse with effector organ where the neurotransmitter is either adrenaline or noradrenaline.

The outflow of the parasympathetic nervous system is craniosacral. The cranial part originates from the midbrain and medulla (cranial nerves III, VII, IX and X) and the sacral outflow is from S2, S3 and S4. Their preganglionic neurones are usually long myelinated and synapse in ganglia close to the target organ and has Ach as its neurotransmitter. The unmyelinated postganglionic neurones is shorter and they synapse with effector organ. The neurotransmitter here is also Ach.

Both sympathetic and parasympathetic preganglionic neurons are cholinergic. Only the postganglionic parasympathetic neurons are cholinergic.

Nonsteroidal anti-inflammatory drugs (NSAIDs) cause bronchospasm, rhinorrhoea, and nasal obstruction in some asthma patients.

The inhibition of cyclooxygenase-1 (Cox-1) appears to be the cause of NSAID-induced reactions. This activates the lipoxygenase pathway, which increases the release of cysteinyl leukotrienes (Cys-LTs), which causes bronchospasm and nasal obstruction.

The following changes in arachidonic acid (AA) metabolism have been observed in NSAID-intolerant asthmatic patients:

Prostaglandin E2 production is low, possibly due to a lack of Cox-2 regulation.
An increase in leukotriene-C4 synthase expression and
A decrease in the production of metabolites (lipoxins) released by AA’s transcellular metabolism.

Phospholipase A produces membrane phospholipids, which are converted to arachidonic acid.

TXA2 causes vasoconstriction as well as platelet aggregation and adhesion.

PGI2 causes vasodilation and a reduction in platelet adhesion.

PGE2 is involved in parturition initiation and maintenance, as well as thermoregulation.

The pulse oximeter provides a continuous non-invasive measurement of the arterial oxygen saturation. The light emitting diodes (LEDs) produce beams of red and infrared light at 660 nm and 940 nm respectively (not 640 and 960 nm), which travel through a finger (toe, ear lobe or nose) and are then detected by a sensitive photodetector.

The light absorbed by non-pulsatile tissues is constant (DC), and the non-constant absorption (AC) is the result of arterial blood pulsation. The DC and AC components at 660 and 940 nm are then analysed by the microprocessor and the result is related to the arterial saturation.

An isosbestic point is a point at which two substances absorb a wavelength of light to the same degree. In pulse oximetry the different absorption profiles of oxyhaemoglobin and deoxyhaemoglobin are used to quantify the haemoglobin saturation (in %). Isosbestic points occur at 590 and 805 nm (not 490 and 805 nm), where the light absorbed is independent of the degree of saturation, and are used as reference points.

The pulse oximeter is accurate to within +/- 2% in the range of 70% to 100% saturation, and below 70% the readings are extrapolated. Pulse oximeters average their readings every 10 to 20 seconds and thus they cannot detect acute desaturation events. Consequently, they are often referred to as ‘lag’ monitors, due to the time delay in identifying the desaturation episode.

Funnel plot is essentially a scatterplot of the effect of treatment against a particular measure of study precision. Its primal purpose is to serve as a visual aid and help in detection of bias or systematic heterogenity.

Loop diuretics act by causing inhibition of Na+ K+ 2Cl– symporter present at the luminal membrane of the ascending limb of the loop of Henle.

Furosemide, torsemide, bumetanide, ethacrynic acid, furosemide, piretanide, tripamide, and mersalyl are the important members of this group

The main use of loop diuretics is to remove the oedema fluid in renal, hepatic, or cardiac diseases. Thus they are useful in the treatment of acute heart failure. These can be administered i.v. for prompt relief of acute pulmonary oedema (due to vasodilatory action).

Hypokalaemia, hypomagnesemia, hyponatremia, alkalosis, hyperglycaemia, hyperuricemia, and dyslipidaemia are seen with both thiazides as well as loop diuretics

The basilic vein is one of the primary veins that drain the upper limb, like the cephalic vein. It begins as the dorsal venous arch. The basilic vein originates from the ulnar side of the dorsal arch of the upper limb passes along the posteromedial aspect of the forearm, moving towards the anterior surface of the elbow.

The basilic vein pierces the deep fascia at the elbow and joins the venae commitantes of the brachial vein to form the axillary vein.

The basilic vein passes deep under the muscles as it moves midway up the humerus. At the lower border of the teres major muscle, the anterior and posterior circumflex humeral veins feed into it.

After a paediatric case, you’ll frequently have to calculate and prescribe maintenance fluids. The ‘4-2-1 rule’ should be used as a guideline:

1st 10 kg – 4 ml/kg/hr
2nd 10 kg – 2 ml/kg/hr
Subsequent kg – 1 ml/kg/hr

Hence

1st 10 kg = 4 × 10 = 40 ml
2nd 10 kg = 2 × 10 = 20 ml
Subsequent kg = 1 × 1 = 1 ml
Total = 61 ml/hr

61 × 12 = 732 ml over 12 hrs.

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.

The mandibular branch of the trigeminal nerve passes through the foramen ovale. Other structures that pass through this foramen are the accessory meningeal artery, and occasionally, the lesser petrosal nerve.

These are the structures that pass through the other openings in the cranial fossa:

Foramen rotundum – Maxillary branch of the trigeminal nerve

Foramen lacerum – Greater petrosal nerve, traversed by the internal carotid artery

Superior orbital fissure – Oculomotor nerve; trochlear nerve; lacrimal, frontal and nasociliary branches of the ophthalmic branch of the trigeminal nerve; abducens nerve, superior ophthalmic vein

Stylomastoid foramen – facial nerve

The sacral hiatus is shaped by incomplete midline fusion of the posterior elements of the distal portion of S4 and S5. This inverted U shaped space is covered by the posterior aspect of the sacrococcygeal membrane and is an important landmark in caudal anaesthetic block. Distal most portion of the dural sac and the sacral hiatus usually terminate between levels S1 and S3. The dural sac ends at the level of S2 in adults and S3 in children.

An equilateral triangle is formed between the apex of the sacral hiatus and the posterior superior iliac spines. This triangle is used to determine the location of the sacral hiatus during caudal anaesthetic block.

A compound that contains an asymmetric centre (chiral atom or chiral centre) and thus can occur in two non-superimposable mirror-image forms (enantiomers) are called chiral compounds.

Desflurane, Halothane, and isoflurane are chiral compounds but Sevoflurane is not a chiral compound.

The data is ideal for chi square test evaluation as it will help determine if observed outcomes are in line with expected outcomes, and also if results are significant or due to chance.

The student’s t test is not ideal as it requires comparison of means from different populations, rather than proportions.

Pearson’s coefficient of linear regression is not ideal as it requires the plotting of a linear regression.

The numbers should be analysed before determining if there are any statistical conclusions that can be drawn from the population.

Statistical analysis is always required to determine the performance of any treatment during a clinical drug trial. Conclusions cannot be drawn simply by looking at the data.