A major source of caloric expenditure and oxygen consumption in the body is work of breathing (WOB) and 70% of this is to overcome elastic forces. The remaining 30% is for flow-resistive work

In a normal patient breathing normally, the total area of hysteresis pressure volume curve represents the flow-resistive WOB.

The area of the expiratory resistive work increases during an asthma attack making the compliance curve larger in area. The larger the area the greater the work required to breathe.

With regards to the autonomic nervous system (ANS)

1. It is not under voluntary control
2. It uses reflex pathways and different to the somatic nervous system.
3. The hypothalamus is the central point of integration of the ANS. However, the gut can coordinate some secretions and information from the baroreceptors which are processed in the medulla.

With regards to the central nervous system (CNS)
1. There are myelinated preganglionic fibres which lead to the
ganglion where the nerve cell bodies of the non-myelinated post ganglionic nerves are organised.
2. From the ganglion, the post ganglionic nerves then lead on to the innervated organ.

Most organs are under control of both systems although one system normally predominates.

The nerves of the sympathetic nervous system (SNS) originate from the lateral horns of the spinal cord, pass into the anterior primary rami and then pass via the white rami communicates into the ganglia from T1-L2.

There are short pre-ganglionic and long post ganglionic fibres.
Pre-ganglionic synapses use acetylcholine (ACh) as a neurotransmitter on nicotinic receptors.
Post ganglionic synapses uses adrenoceptors with norepinephrine / epinephrine as the neurotransmitter.
However, in sweat glands, piloerector muscles and few blood vessels, ACh is still used as a neurotransmitter with nicotinic receptors.

The ganglia form the sympathetic trunk – this is a collection of nerves that begin at the base of the skull and travel 2-3 cm lateral to the vertebrae, extending to the coccyx.

There are cervical, thoracic, lumbar and sacral ganglia and visceral sympathetic innervation is by cardiac, coeliac and hypogastric plexi.

Juxta glomerular apparatus, piloerector muscles and adipose tissue are all organs under sole sympathetic control.

The PNS has a craniosacral outflow. It causes reduced arousal and cardiovascular stimulation and increases visceral activity.

The cranial outflow consists of
1. The oculomotor nerve (CN III) to the eye via the ciliary ganglion,
2. Facial nerve (CN VII) to the submandibular, sublingual and lacrimal glands via the pterygopalatine and submandibular ganglions
3. Glossopharyngeal (CN IX) to lungs, larynx and tracheobronchial tree via otic ganglion
4. The vagus nerve (CN X), the largest contributor and carries ¾ of fibres covering innervation of the heart, lungs, larynx, tracheobronchial tree parotid gland and proximal gut to the splenic flexure, liver and pancreas

The sacral outflow (S2 to S4) innervates the bladder, distal gut and genitalia.

The PNS has long preganglionic and short post ganglionic fibres.
Preganglionic synapses, like in the SNS, use ACh as the neuro transmitter with nicotinic receptors.
Post ganglionic synapses also use ACh as the neurotransmitter but have muscarinic receptors.

Different types of these muscarinic receptors are present in different organs:
There are:
M1 = pupillary constriction, gastric acid secretion stimulation
M2 = inhibition of cardiac stimulation
M3 = visceral vasodilation, coronary artery constriction, increased secretions in salivary, lacrimal glands and pancreas
M4 = brain and adrenal medulla
M5 = brain

The lacrimal glands are solely under parasympathetic control.

The follicle is the functional unit of the thyroid gland. The follicular cells surround the follicle which is filled with colloid. Suspended within the colloid is the is a pro-hormone complex thyroglobulin.

The synthesis and storage of thyroid hormones is done by follicular cells and the thyroglobulin within the colloid.

Iodide ions (I−) are actively transported against a concentration gradient into the follicular cell under the influence of thyroid stimulating hormone (TSH). It then undergoes oxidation to active iodine catalysed by thyroid peroxidase (TPO). The synthesis of thyroglobulin is in the follicular cells and it contains up to 140 tyrosine residues. The tyrosine residues of thyroglobulin and active iodine are merged to form mono- and di-iodotyrosines (MIT and DIT). The iodinated thyroglobulin is then taken up into the colloid where it is stored and dimerised. Two DIT molecules are joined to produce thyroxine (T4) while one MIT and one DIT molecule are joined to produce tri-iodotyrosine (T3) by a process catalysed by TPO.

Thyroglobulin droplets are taken up as vesicles into follicular cells by pinocytosis. This process is stimulated by TSH. When these vesicles fuse with lysosomes, hydrolysis of the thyroglobulin molecules and subsequent release of T4 and T3 into the circulation occurs.

ICP is significant because it influences cerebral perfusion pressure and cerebral blood flow. The normal ICP ranges from 5 to 13 mmHg.

The components within the skull include the brain (80%/1400 ml), blood (10%/150 ml), and cerebrospinal fluid (CSF) (10%/150 ml).

Because the skull is a rigid box, if one of the three components increases in volume, one or more of the remaining components must decrease in volume to compensate, or the ICP will rise (Monroe-Kellie hypothesis).

Primary brain injury occurs as a result of a head injury and is unavoidable unless precautions are taken to reduce the risk of head injury. A reduction in oxygen delivery due to hypoxemia (low arterial PaO2) or anaemia, a reduction in cerebral blood flow due to hypotension or reduced cardiac output, and factors that cause a raised ICP and reduced CPP are all causes of secondary brain injury. Secondary brain injury can be avoided with proper management.

The most important initial management task is to make certain that:

There is protection of the airway and the cervical spine
There is proper ventilation and oxygenation
Blood pressure and cerebral perfusion pressure are both adequate (CPP).

Following the implementation of these management principles, additional strategies to reduce ICP and preserve cerebral perfusion are required. The volume of one or more of the contents of the skull can be reduced using techniques that can be used to reduce ICP.

Reduce the volume of brain tissue
Blood volume should be reduced.
CSF volume should be reduced.

The following are some methods for reducing the volume of brain tissue:
Abscess removal or tumour resection
Steroids (especially dexamethasone) are used to treat oedema in the brain.
To reduce intracellular volume, use mannitol/furosemide or hypertonic saline.
To increase intracranial volume, a decompressive craniectomy is performed.

The following are some methods for reducing blood volume:

Haematomas must be evacuated.
Barbiturate coma reduces cerebral metabolic rate and oxygen consumption, lowering cerebral blood volume as a result.
Hypoxemia, hypercarbia, hyperthermia, vasodilator drugs, and hypotension should all be avoided in the arterial system.
PEEP/airway obstruction/CVP lines in neck: patient positioning with 30° head up, avoid neck compression with ties/excessive rotation, avoid PEEP/airway obstruction/CVP lines in neck

The following are some methods for reducing CSF volume:

To reduce CSF volume, an external ventricular drain or a ventriculoperitoneal shunt is inserted (although more a long term measure).

Selective ?1 -Blockers like prazosin, terazosin, doxazosin, and alfuzosin cause a decrease in blood pressure with lesser tachycardia than nonselective blockers (due to lack of ?2 blocking action.

The major adverse effect of these drugs is postural hypotension. It is seen with the first few doses or on-dose escalation (First dose effect).

Its half-life is approximately three hours.

It is excreted primarily through bile and faeces (not through kidneys)

The fall in plasma concentration of a drug with time decreases exponentially in a single compartment pharmacokinetic model (wash-out curve).

A straight line is produced when the logarithm (ln) of a drug’s plasma concentration is plotted against time because a constant proportion of the drug is removed from the plasma per unit time. The line’s gradient or slope can be expressed mathematically as k. (the rate constant). The gradient is related to the half life (T1/2) because it can be used to predict a drug’s plasma concentration at any time.

According to the following formula, clearance (CL), volume of distribution (Vd), and elimination rate constant (k) are mathematically related.

CL = Vd x k

For drug A, CL = 1 x 0.1 = 0.1units per minute

For drug B, Cl = 2 x 0.2 = 0.4 units per minute

Hence, it is proved that Drug A has a lower clearance than drug B.

The internal carotid artery passes through the carotid canal in the petrous part of the temporal bone into the cranial cavity. It does NOT groove the sphenoid bone.

The internal carotid artery gives off no branches in the neck and is a terminal branch of the common carotid artery.

These structures pass between the external and internal carotid arteries: the styloglossus and stylopharyngeus muscles, the glossopharyngeal nerve (CN IX), and the pharyngeal branch of the vagus.

Accompanied by its sympathetic plexus, the internal carotid artery, passes through the cavernous sinus and is crossed by the abducent nerve.

Number needed to treat can be defined as the number of patients who need to be treated to prevent one additional bad outcome.

It can be found as:

NNT=1/Absolute Risk Reduction (rounded to the next integer since number of patients can be integer only).

where ARR= (Risk factor associated with the new drug group) — (Risk factor associated with the currently available drug)

So,

ARR= (0.04-0.03)

ARR= 0.01

NNT= 1/0.01

NNT=100

Barbiturates are derived from barbituric acid, which itself is nondepressant, but appropriate side-chain substitutions result in CNS depressant activity that varies in potency and duration with carbon chain length, branching, and saturation.

Oxybarbiturates retain an oxygen atom on number 2-carbon atom of the barbituric acid ring.

Thiobarbiturates replace this oxygen atom with a sulphur atom, which confers greater lipid solubility. Generally speaking, a substitution such as sulphuration that increases lipid solubility is associated with greater hypnotic potency and more rapid onset, but shorter duration of action.

Addition of a methyl group to the nitrogen atom of the barbituric acid ring, as with oxybarbiturate methohexital, also results in a compound with a short duration of action.

An ipsilateral phrenic nerve block will result from a successful interscalene block (ISB).

The phrenic nerve is the diaphragm’s sole motor supply, and ipsilateral hemidiaphragmatic paresis affects up to 100% of patients who receive ISBs. Phrenic nerve palsy is usually well tolerated and goes unnoticed by healthy people. However, forced vital capacity decreases by approximately 25%, which can produce ventilatory compromise in patients with limited pulmonary reserve, requiring assisted ventilation.

Vocal cord palsy occurs when the recurrent laryngeal nerve is inadvertently blocked, causing hoarseness and possibly acute respiratory insufficiency. Unless bilateral laryngeal nerve palsy occurs, which can cause severe laryngeal obstruction, this complication is usually of little consequence.

ISB can also cause cranial nerve X and XII palsy (Tapia’s syndrome). One-sided cord paralysis, aphonia, and the patient’s tongue deviating toward the block’s side are all symptoms.

When a local anaesthetic spreads to the stellate ganglion and its cervical sympathetic nerves, Horner’s syndrome can develop. Ptosis of the eyelid, miosis, and anhidrosis of the face are all symptoms. Horner’s syndrome, on the other hand, may not indicate that the brachial plexus is sufficiently blocked.

Calcium channel blocker (CCB) blocks L-type of voltage-gated calcium channels present in blood vessels and the heart. By inhibiting the calcium channels, these agents decrease the frequency of opening of calcium channels activity of the heart, decrease heart rate, AV conduction, and contractility.

Three groups of CCBs include
1) Phenylalkylamines: Verapamil, Norverapamil
2) Benzothiazepines : Diltiazem
3) Dihydropyridine : Nifedipine, Nicardipine, Nimodipine, Nislodipine, Nitrendipine, Isradipine, Lacidipine, Felodipine and Amlodipine.

Even though verapamil as good absorption from GIT, its oral bioavailability is low due to high first-pass metabolism.

Nimodipine is a Cerebro-selective CCB, used to reverse the compensatory vasoconstriction after sub-arachnoid haemorrhage and is more lipid soluble analogue of nifedipine

Calcium channel antagonist can potentiate the effect of non-depolarising muscle relaxants.

Chi-square test is used to determine the statistically significant different between categorical variables. It also determines the difference between expected frequencies and the observed frequencies.

Mann Whitney U test is used to determine the statistically significant different between two independent groups.

Wilcoxon’s test is the test of dependency. it determines the statistically significant difference between two dependent groups.

Student t-test is one of the most commonly used method to test the hypothesis. It determines the significant difference between the means of two different groups.

ANOVA (analysis of variance) is similar to student’s t-test.

ANOVA is a statistical method used to determines the statistically significant difference between the mean of more than two group. In this experiment as we are dealing with three different group, ANOVA is most suitable test to determine the difference between each groups.

The answer is anterior to the spermatic cord.

The inguinal canal in men contains the ilioinguinal nerve, the genitofemoral nerve and the spermatic cord.

The ilioinguinal nerve arises of the L1 nerve root with the Iliohypogastric nerve, before entering the inguinal canal from the side, through the muscles of the abdomen, travelling superficial to the spermatic cord.

The sternocleidomastoid muscle divides the neck into anterior and posterior triangles on both sides of the neck.

The posterior triangle has the following boundaries:
anteriorly – sternocleidomastoid muscle
posteriorly – trapezius
roof – investing layer of deep cervical fascia
floor – prevertebral fascia overlying splenius capitis, levator scapulae, and the scalene muscles

The contents of the posterior triangle are:
1. fat
2. lymph nodes (level V)
3. accessory nerve
4. cutaneous branches of the cervical plexus (A major branch of this plexus is the phrenic nerve, which arises from the anterior divisions of spinal nerves C3-C5)
5. inferior belly of omohyoid
6. branches of the thyrocervical trunk (transverse cervical and suprascapular arteries)
7. third part of the subclavian artery
8. external jugular vein

Pituitary tumours that compress the optic chiasma primarily affect the neurones that decussate at this location. Bitemporal hemianopia is caused by neurones that emerge from the nasal half of the retina and transmit the temporal half of the visual field.

The axons of ganglion cells in the retina form the optic nerve.

It exits the orbit through the optic foramen and projects to the thalamic lateral geniculate body. The optic chiasma forms above the sella turcica as the nasal fibres decussate along the way. The optic radiation travels from the lateral geniculate body to the occipital cortex.

Lesions at various points along this pathway cause the following visual field defects:

Scotoma implies partial retinal or optic nerve damage.
Monocular vision loss occurs when the optic nerve is completely damaged.
Pathology at the optic chiasma causes bitemporal hemianopia.
Cortical blindness with occipital cortex pathology and homonymous hemianopia with lesions compromising the optic radiation.

An intercostal nerve block is used for therapeutic and diagnostic purposes. Intercostal nerve blocks manage acute and chronic pain in the chest area. Common indications are chest wall surgery and shingles or postherpetic neuralgia.

An intercostal nerve block is also an effective option for the management of pain associated with chest trauma and rib fractures. These blocks have been shown to improve oxygenation and respiratory mechanics, and offer pain relief that is comparable to that of epidural analgesia.

This technique, however, is limited by the relatively large doses of local anaesthetic required, and relatively high intravascular uptake from the intercostal space, increasing risk of local anaesthetic toxicity.

Attributable proportion is the proportion of disease that is caused due to exposure. It refers to the proportion of disease that would be eradicated from a particular population if the disease rate was diminished to match that of the unexposed group.

Risk ratio (relative risk) compares the probability of an event in an exposed (experimental) group to that of an event in the unexposed (control) group. Thus two are not the same.

The attributable risk is the rate of a disease in an exposed group to that of a group that has not been exposed to it i.e. how many deaths did the exposure cause.

Closing capacity refers to volume of gas within the lungs at which the conducting small airways begin to close, that is, the point during expiration when small airways close.

It is calculated mathematically as:

Closing capacity = Closing volume (CV) + Residual volume (RV)

Functional residual capacity (FRC) is the volume of gas still present within the lungs post expiration.

Closing capacity is lower than the functional residual capacity in younger adults, but begins to rise to eventually equal, and then exceed it with increasing age (at about middle age), increasing intrabdominal pressure, decreasing blood flow in the pulmonary system and parenchymal disease within the pulmonary system.

The formula for calculating air: oxygen entrainment ratio is given as :
100% − FiO2 = air/oxygen entrainment ratio
Since FiO2 − 21% and the entrainment ratio is already known. Substituting the values in the equation: x = FiO2.

100 − x = 9
x − 21
100 − x = 9(x − 21)
100 − x = 9x − 189
10x = 289
x = 289/10
x = 28.9%

There are different models of flowmeters determined by the applied pressure and its orifice. For instance, the watersight flowmeter functions through applying variable pressure, and it has a variable orifice. In contrast, the bubble flowmeter is operated using a constant pressure and orifice. Flowmeters such as rotameters, Heidbrink and Peak have a constant pressure but variable orifice. On the other hand, flowmeters including a simple pressure gauge, water depression, and pneumotachograph have a constant orifice but variable pressure.

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 inferior phrenic nerves are at the highest risk of damage as they are the first branches of the abdominal aorta. The potential space at the level of the diaphragmatic hiatus is a potentially useful site for aortic occlusion. However, leaving the clamp applied for more than 10 -15 minutes usually leads to poor outcomes.

The superior phrenic artery branches from the thoracic aorta.

The abdominal aorta begins at the level of the body of T12 near the midline, as a continuation of the thoracic aorta. It descends and bifurcates at the level of L4 into the common iliac arteries.

The branches of the abdominal aorta (with their vertebra level) are:
1. Inferior phrenic arteries: T12 (upper border)
2. Coeliac artery: T12
3. Superior mesenteric artery: L1
4. Middle suprarenal arteries: L1
5. Renal arteries: Between L1 and L2
6. Gonadal arteries: L2 (in males, it is the testicular artery, and in females, the ovarian artery)
7. Inferior mesenteric artery: L3
8. Median sacral artery: L4
9. Lumbar arteries: Between L1 and L4

With regards to the autonomic nervous system (ANS)

1. It is not under voluntary control
2. It uses reflex pathways and different to the somatic nervous system.
3. The hypothalamus is the central point of integration of the ANS. However, the gut can coordinate some secretions and information from the baroreceptors which are processed in the medulla.

With regards to the central nervous system (CNS)
1. There are myelinated preganglionic fibres which lead to the
ganglion where the nerve cell bodies of the non-myelinated post ganglionic nerves are organised.
2. From the ganglion, the post ganglionic nerves then lead on to the innervated organ.

Most organs are under control of both systems although one system normally predominates.

The nerves of the sympathetic nervous system (SNS) originate from the lateral horns of the spinal cord, pass into the anterior primary rami and then pass via the white rami communicates into the ganglia from T1-L2.

There are short pre-ganglionic and long post ganglionic fibres.
Pre-ganglionic synapses use acetylcholine (ACh) as a neurotransmitter on nicotinic receptors.
Post ganglionic synapses uses adrenoceptors with norepinephrine / epinephrine as the neurotransmitter.
However, in sweat glands, piloerector muscles and few blood vessels, ACh is still used as a neurotransmitter with nicotinic receptors.

The ganglia form the sympathetic trunk – this is a collection of nerves that begin at the base of the skull and travel 2-3 cm lateral to the vertebrae, extending to the coccyx.

There are cervical, thoracic, lumbar and sacral ganglia and visceral sympathetic innervation is by cardiac, coeliac and hypogastric plexi.

Juxta glomerular apparatus, piloerector muscles and adipose tissue are all organs under sole sympathetic control.

The PNS has a craniosacral outflow. It causes reduced arousal and cardiovascular stimulation and increases visceral activity.

The cranial outflow consists of
1. The oculomotor nerve (CN III) to the eye via the ciliary ganglion,
2. Facial nerve (CN VII) to the submandibular, sublingual and lacrimal glands via the pterygopalatine and submandibular ganglions
3. Glossopharyngeal (CN IX) to lungs, larynx and tracheobronchial tree via otic ganglion
4. The vagus nerve (CN X), the largest contributor and carries ¾ of fibres covering innervation of the heart, lungs, larynx, tracheobronchial tree parotid gland and proximal gut to the splenic flexure, liver and pancreas

The sacral outflow (S2 to S4) innervates the bladder, distal gut and genitalia.

The PNS has long preganglionic and short post ganglionic fibres.
Preganglionic synapses, like in the SNS, use ACh as the neuro transmitter with nicotinic receptors.
Post ganglionic synapses also use ACh as the neurotransmitter but have muscarinic receptors.

Different types of these muscarinic receptors are present in different organs:
There are:
M1 = pupillary constriction, gastric acid secretion stimulation
M2 = inhibition of cardiac stimulation
M3 = visceral vasodilation, coronary artery constriction, increased secretions in salivary, lacrimal glands and pancreas
M4 = brain and adrenal medulla
M5 = brain

The lacrimal glands are solely under parasympathetic control.

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.

Campylobacter is the commonest bacterial cause of infectious intestinal disease in the UK. The majority of cases are caused by the Gram-negative bacillus Campylobacter jejuni which is spread by the faecal-oral route. The incubation period is 1-6 days.

Features include a prodrome phase with headaches and malaise, then diarrhoea occurs which is often bloody.
There is often abdominal pain which may mimic appendicitis.

It is usually self-limiting but treatment is warranted if the infection is severe or the infection occurs in an immunocompromised patient.
Severe infection comprises of high fever, bloody diarrhoea, or more than eight stools per day or symptoms last for more than one week.
This management would include antibiotics and the first-line antibiotic is clarithromycin.
Ciprofloxacin is an alternative but there are strains with decreased sensitivity to ciprofloxacin which can be frequently isolated.

Complications include:
1.Guillain-Barre syndrome may follow Campylobacter
2. Jejuniinfections
3. Reactive arthritis
4. Septicaemia, endocarditis, arthritis

The ventilation/perfusion ratio varies in different areas of the lung. In an upright individual, although both ventilation and perfusion increase from the apex to the base of the lung, the increase in ventilation is less than the increase in blood flow. As a result, the normal V̇ /Q̇ ratio at the apex of the lung is much greater than 1 (ventilation exceeds perfusion), whereas the V̇ /Q̇ ratio at the base of the lung is much less than 1 (perfusion exceeds ventilation).

There is more volume in the alveoli found in the apices than in the bases of the lungs. This is due to the weight of the lung stretching the apical alveoli to the maximum size. Also, the weight of the lungs pull themselves away from the chest wall, creating a negative intrapleural pressure. These factors, however, do not directly affect the PAO2.

The pituitary gland plays a crucial role in the neuro-endocrine axis. It is located at the base of the skull in the sella turcica of the sphenoid bone. It is connected superiorly to the hypothalamus, third ventricle, and visual pathways, and laterally to the cavernous sinuses, internal carotid arteries, and cranial nerves III, IV, V, and VI.

Pituitary tumours make up about 10-15% of all intracranial tumours. The majority of adenomas are benign. Over-secretion of pituitary hormones (most commonly prolactin, growth hormone, or ACTH), under-secretion of hormones, or localised or generalised pressure effects can all cause symptoms.

Compression of the optic chiasm can result in visual field defects, the most common of which is bitemporal hemianopia. This is caused by compression of the nasal retinal fibres, which carry visual impulses from temporal vision across the optic chiasm to the contralateral sides before continuing to the optic tracts.

The interruption of the visual pathways distal to the optic chiasm causes a homonymous visual field defect. The loss of the right or left halves of each eye’s visual field is referred to as homonymous hemianopia. It’s usually caused by a middle or posterior cerebral artery territory stroke that affects the occipital lobe’s optic radiation or visual cortex.

Binasal hemianopia is a condition in which vision is lost in the inner half of both eyes (nasal or medial). It’s caused by compression of the temporal visual pathways, which don’t cross at the optic chiasm and instead continue to the ipsilateral optic tracts. Binasal hemianopia is a rare complication caused by the internal carotid artery impinging on the temporal (lateral) visual fibres.

A monocular visual loss (that is, loss of vision in only one eye) can be caused by a variety of factors, but if caused by nerve damage, the damage would be proximal to the optic chiasm on the ipsilateral side.

A central scotoma is another name for central visual field loss. Every normal mammalian eye has a scotoma, also known as a blind spot, in its field of vision. The optic disc is a region of the retina that lacks photoreceptor cells and is where the retinal ganglion cell axons that make up the optic nerve exit the retina. When both eyes are open, visual signals that are absent in one eye’s blind spot are provided for the other eye by the opposite visual cortex, even if the other eye is closed.

Scotomata can be caused by a variety of factors, including demyelinating disease such as multiple sclerosis, damage to nerve fibre layer in the retina, methyl alcohol, ethambutol, quinine, nutritional deficiencies, and vascular blockages either in the retina or in the optic nerve.

Bilateral scotoma can occur when a pituitary tumour compresses the optic chiasm, causing a bitemporal paracentral scotoma, which then spreads out to the periphery, causing bitemporal hemianopsia. A central scotoma in a pregnant woman could be a sign of severe pre-eclampsia.

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.