The area described in the question is supplied by the intercostobrachial nerve, which provides sensory innervation to the portions of the axilla, tail of the breast, lateral chest wall and medial side of the arm.

It is a common for it to be ‘missed’ during administration of local anaesthesia because of its very superficial anatomic course. It may be anesthetized by giving an analgesia from the upper border of the biceps at the anterior axillary fold, to the margin of the triceps by the axillary floor.

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.

The starling forces operate to maintain a homeostatic flow across the pulmonary capillary bed.

The outward driving force comprises of the capillary hydrostatic pressure (13 mmHg), negative interstitial fluid pressure (zero to slightly negative), and interstitial colloid osmotic pressure (17 mmHg). The inward driving force is controlled by the plasma colloid osmotic pressure (25 mmHg).

The arch of aorta gives rise to three main branches:
1. Brachiocephalic artery
2. Left common carotid artery
3. Left subclavian artery

The brachiocephalic artery then gives rise to the right subclavian artery and the right common carotid artery.

The right common carotid artery arises from the brachiocephalic trunk posterior to the sternoclavicular joint.

The coeliac trunk is a branch of the abdominal aorta.
The ascending aorta supplies the coronary arteries.

From superior to inferior, the following structures enter the orbit through the superior orbital fissure:
1. Lacrimal nerve
2. Frontal nerve
3. Superior ophthalmic vein
4. Trochlear nerve
5. Superior division of the oculomotor nerve*
6. Nasociliary nerve*
7. Inferior division of the oculomotor nerve*
8. Abducent nerve*
9. Inferior ophthalmic vein.

The superior and inferior division of the oculomotor nerve, nasociliary nerve, and abducent nerve are within the tendinous ring.

The common origin of the four rectus muscles is the tendinous ring (also known as the annulus of Zinn). The tendinous ring’s lateral portion straddles the superior orbital fissure, while the medial portion encloses the optic foramen, through which the optic nerve and ophthalmic artery pass.

Gabapentin is an amino acid-like molecules that was originally synthesized as an analogue of GABA but is now known not to act through GABA mechanisms. It is used in the treatment of focal seizures and various nonepilepsy indications, such as neuropathic pain, restless legs syndrome, and anxiety disorders.

Despite its close structural resemblance to GABA, gabapentin does not act through effects on GABA receptors or any other mechanism related to GABA-mediated neurotransmission. Rather gabapentin binds avidly to ?2?, a protein that serves as an auxiliary subunit of voltage-gated calcium channels. Moreover, it binds to NMDA receptor to modulate its transmission.

Cephalosporin belongs to a family of beta-lactam antibiotics. All ?-lactam antibiotics interfere with the synthesis of the bacterial cell walls. The ?-lactam antibiotics inhibit the transpeptidases so that cross-linking (which maintains the close-knit structure of the cell wall) does not take place i.e. they inhibit bacterial cell wall formation.

Superior vena cava is the main vein bringing blood back to the heart. It can get partially or completely blocked by various causes, the most common being due to malignant tumours of the mediastinum.

There are collateral pathways that form in long-standing cases with 60% or more stenosis and continue venous drainage in cases of superior vena obstruction. The collaterals are classified into four as follows:

1. The azygos-hemiazygos pathway
Azygos, hemiazygos, intercostal, and lumbar veins.

2. The internal and external mammary pathway
internal mammary, superior epigastric, and inferior epigastric veins and superficial veins of the thorax.

3. The lateral thoracic pathway
Lateral thoracic, thoracoepigastric, superficial circumflex, long saphenous, and femoral veins to collateralize to the IVC.

4. The vertebral pathway
Innominate, vertebral, intercostal, lumbar, and sacral veins to collateralize to the azygos and internal mammary pathways.

Adenosine is the first line for AV nodal re-entry tachycardia. An initial dose of 6 mg is given, and a consequent second dose or third dose of 12 mg is administered if the initial dose fails to terminate the arrhythmia.

Aside from Adenosine, a vagal manoeuvre (e.g. carotid massage) is done to help terminate the supraventricular arrhythmia.

Amiodarone is not a first-line drug for supraventricular tachycardias. Digoxin and Propranolol can be considered if the arrhythmia is of a narrow complex irregular type. Verapamil is an alternative to Adenosine if the latter is contraindicated.

Glyceryl trinitrate (GTN) has a significant first pass metabolism. About 90% of a dose of GTN is metabolised in the liver by the enzyme glutathione organic nitrate reductase.

An INSIGNIFICANT amount of metabolism occurs in the intestinal mucosa.

There is approximately 1% bioavailability after oral administration and 38% after sublingual administration.

GTN does NOT cause gastric irritation and it is well absorbed in the gastrointestinal tract.

The volume of distribution of GTN is 2.1 to 4.5 L/kg. This is HIGH.