The left subclavian artery originates from the aortic arch, while the right subclavian artery originates from the brachiocephalic artery.

The subclavian artery gives off branches on both sides of the body:
1. Vertebral artery
2. Internal thoracic artery
3. Thyrocervical trunk
4. Costocervical trunk
5. Dorsal scapular artery

The superior thyroid artery is the first branch of the external carotid artery. The other branches of the external carotid artery are:
1. Superior thyroid artery
2. Ascending pharyngeal artery
3. Lingual artery
4. Facial artery
5. Occipital artery
6. Posterior auricular artery
7. Maxillary artery
8. Superficial temporal artery

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.

Adrenaline is released by the adrenal glands, acts on ? 1 and 2, ? 1 and 2 receptors, and is responsible for fight or flight response.

It acts on ? 2 receptors in skeletal muscle vessels-causing vasodilation.

It acts on ? adrenergic receptors to inhibit insulin secretion by the pancreas. It also stimulates glycogenolysis in the liver and muscle, stimulates glycolysis in muscle.

It acts on ? adrenergic receptors to stimulate glucagon secretion in the pancreas
It also stimulates Adrenocorticotrophic Hormone (ACTH) and stimulates lipolysis by adipose tissue

In first order kinetics the rate of elimination is proportional to plasma concentration.

Rate of elimination is described by the following equation:

C = C0. e^-kt

Where:
C=drug concentration,
C0= drug concentration at time zero (extrapolated),
k = rate constant and
t = time.

The initial concentration of this drug is 12 mcg/ml therefore:

The plasma concentration will have halved to 6 mcg/ml at 2 hours.
The plasma concentration will have halved to 3 mcg/ml at 4 hours and
The plasma concentration will have halved to 1.5 mcg/ml t 6 hours.

A pulse oximeter is a piece of medical equipment used as a non-invasive method of measuring the oxygen saturation of blood.

It works by measuring the ratio of absorption of red and infrared light in a section of blood flow, as red light is largely absorbed by deoxygenated blood, and infrared light is largely absorbed by oxygenated blood.

Pulse oximetry relies on photoplethysmography (PPG) waveforms. The oximeter has 2 sides, with different functions. One side houses light-emitting diodes which are responsible for transmitting 2 light wavelengths, 660nm for red light and 940nm for near infrared light. The other side is a photodetector. The light emitted travels through the body and the amount that is not absorbed is measured by the photodetector.

Smokers often have increased levels of carboxy haemoglobin (COHb). This leads to artificial increases in pulse oximeter readings as it is unable to differentiate between COHb and oxyhaemoglobin (O2HB) as they both absorb red light at 660nm. Every 1% increase of circulating carboxyhaemoglobin, results in a correlative 1% increase in oximeter readings.

Prilocaine toxicity will cause an artificial decrease in oximeter readings. This is because prilocaine metabolites cause methemoglobinemia (MetHB), which are dysfunctional haemoglobins unable to properly transport oxygen. In this case, a laboratory multiwavelength co-oximeter is recommended for a more accurate reading.

Anaemia will not affect oximeter readings as long as haemoglobins in the blood are normal.

Sickle cell disease does not affect oximeter readings despite its ability to cause hypoxia and shift the oxygen dissociation curve to the right.

Brown-red fingernail polish will cause an underestimation of pulse oximeter readings.

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)

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.

The intrinsic pathway is best assessed by the aPTT time.

D-dimer is a fibrin degradation product which is raised in the presence of blood clots.

A 50:50 mixing study is used to assess if a prolonged PT or aPTT is due to factor deficiency or a factor inhibitor.

The thrombin time is a test used to assess fibrin formation from fibrinogen in plasma. Factors that prolong the thrombin time include heparin, fibrin degradation products, and fibrinogen deficiency.

Intrinsic pathway – Best assessed by APTT. Factors 8,9,11,12 are involved. Prolonged aPTT can be seen in haemophilia and use of heparin.

Extrinsic pathway – Best assessed by Increased PT. Factor 7 involved.

Common pathway – Best assessed by APTT & PT. Factors 2,5,10 involved.

Vitamin K dependent factors are factors 2,7,9,10

The tracheobronchial tree is subdivided into the conducting and the respiratory zones.

The zones from proximal to distal are:

Trachea
Bronchi
Bronchioles
Terminal bronchioles
Respiratory bronchioles
Alveolar ducts
Alveolar sacs

from the trachea to terminal bronchioles are the conducting zone while the respiratory zone is from the respiratory bronchioles to the alveola sacs

Nausea and vomiting occur commonly due to Chemoreceptor Trigger Zone (CTZ) stimulation by dopamine (Domperidone but not metoclopramide can be used for the treatment of this vomiting)

Dopamine itself cannot cross the blood-brain barrier (BBB) but its precursor levodopa can cross BBB.

Dopamine can modulate extrapyramidal symptoms like acute dyskinesia, tardive dyskinesia, Parkinsonism, and Neuroleptic malignant syndrome.

Dopamine inhibits the secretion of prolactin from the pituitary gland.

The posterior pituitary and the hypothalamus are connected by the pituitary stalk. It contains in the pituitary sella and has the optic chiasm and hypothalamus as superior relations.

The anterior pituitary produces thyroid-stimulating hormone (TSH), luteinising hormone (LH) and follicle-stimulating hormone (FSH) . These hormones are Glycoproteins and share a common alpha subunit with unique beta subunits.

The secretion of pituitary hormones are pulsatile. Examples are LH, adrenocorticotropic hormone (ACTH) and growth hormone (GH).

An intra-operative air embolism occurs when air becomes trapped in the blood vessels during surgery.

A transoesophageal echocardiography (OE) uses invasive echocardiography to monitor the integrity and performance of the heart. It is the gold standard as it provides real-time imaging of the heart to enable early diagnosis and treatment.

Precordial doppler ultrasonography can also be used to detect into-operative air emboli. It is non-invasive and more practical, but is less sensitive.

A change in end-tidal CO2 could be indicative of and increase in physiological dead-space, but could also be indicative of any processes that reduces the excretion or increases the production of CO2, making it non-specific.

A transoesophageal stethoscope can be used to listen for the classic mill-wheel murmur produced by a large air embolus.

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.

The mechanism of action of macrolides is inhibition of bacterial protein synthesis by preventing peptidyltransferase from adding to the growing peptide which is attached to tRNA to the next amino acid.

A patient presenting with symptomatic asthma should be assessed for severity to determine appropriate management options. Indications of acute severe asthma are:

Peak expiratory flow rate (PEFR): 33-50% best/predicted
Respiratory rate: ≥25/min
Heart rate: ≥110/min
Inability to finish a complete sentence in a single breath.

Oxygen saturation should be measured. Any measurement of an oxygen saturation of 92% or less, either on air or on oxygen, indicates severe, life threatening asthma, and requires an arterial blood gas (ABG) to detect normo- or hypercarbia.

A chest x-ray would not be routine as it will not provide any relevant information. It is only required in specific cases, including:
Diagnosis of a subcutaneous emphysema
Indications of a unilateral pneumothorax
Indications of a lobar collapse of consolidation
Treatment-resistance life-threatening asthma
If mechanical ventilation is indicated

A peak expiratory flow rate (PEFR) can provide relevant information to help distinguish between acute, moderate, severe and life threatening asthma. However, it is not necessary as other parameters exist that can also help make the same distinction.

An ECG is indicated in this case as the patient has tachycardia and tachypnoea which are indicative of acute severe asthma. The ECG would indicate if arrhythmia is also present which would suggest life-threatening asthma.

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.

Recommendations from the British Thoracic Society for acute severe asthma or life-threatening asthma are:

1. Give controlled supplementary oxygen to all hypoxemic patients with acute severe asthma titrated to maintain a SpO₂ level of 94 98%.
2. Use high-dose inhaled ?₂ agonists as first-line agents in patients with acute asthma and administer them as early as possible. Reserve
intravenous ?₂ agonists for those patients in whom inhaled therapy cannot be used reliably.
3. Give steroids in adequate doses to all patients with an acute asthma attack.
4. Add nebulized ipratropium bromide (0.5 mg 4–6 hourly) to ?₂ agonist treatment for acute severe or life-threatening asthma or those with a poor initial response to ?₂ agonist therapy.
5. Consider aminophylline for children with severe or life-threatening asthma unresponsive to maximal doses of bronchodilators and steroids.

A review (including 12 case reports, three RCTs, and five other observational studies) of ketamine use in adults and children in status asthmaticus reported that ketamine is a potential bronchodilator. Still, prospective trials are needed before conclusions about effectiveness can be drawn.

Heliox has no place in the current guidelines issued by the British Thoracic Society.

The left marginal artery comes off the left circumflex artery, and runs alongside the heart.

The left circumflex artery is one of the bifurcations of the left coronary artery, and eventually forms the left marginal artery.

An occlusion in the left circumflex artery often results in a lateral MI.

The right marginal artery originates from the right coronary artery.

The left anterior descending artery (LAD) is another bifurcation of the left coronary artery. An occlusion in the LAD would often result in an anteroseptal MI as is diagnosed on ECG by noting changes in leads V1-V4.

The right coronary artery originates from the right aortic sinus of the ascending aorta, and bifurcates to give rise to many branches, including the sinoatrial artery which supplies the sinoatrial (SA) node in 50-70% of cases, the artery of the atrioventricular (AV) node in 50-60% of cases, the right acute marginal artery which supplies the right ventricle. It also supplies the right atrium, interatrial septum and the posterior inferior third of the interventricular septum.

Arrhythmias and inferior MI often occurs as a result of an occlusion in the right coronary artery, and can be diagnosed by ECG changes in leads II, III and aVF.

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

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 Purkinje system, as well as the action potentials of ventricular and atrial myocytes, have the same ionic changes. It lasts about 200 milliseconds and has a resting membrane potential, as well as fast depolarisation and plateau phases.

There are five stages to the process:

Increased Na+ and decreased K+ conductance in Phase 0 (rapid depolarisation).
1st phase (initial repolarisation) : Na+ conductance decreased, while K+ conductance increased.
Phase two (plateau phase) : Ca2+ conductance increased
Phase three (repolarisation phase) : Lower Ca2+ conductance and higher K+ conductance
4th Phase (resting membrane potential) : K+ conductance increased, Na+ conductance decreased, and Ca2+ conductance decreased.

Endothelin-1 is considered as a powerful coronary vasoconstrictor, produced by the endothelium. It acts to counter the effects of Nitric oxide (NO).
Neuropeptide-Y, angiotensin1, cocaine, vasopressin, and nicotine are some other coronary vasoconstrictors.

Chronotrophy and inotrophy occur after the activation of sympathetic nerve fibres, which in turn results in increasing the myocardial oxygen consumption, leading to increased coronary blood flow via local metabolic processes.

An alpha-receptor mediated coronary vasoconstrictor effect is also initiated that usually competes with vasodilation, resulting in decreased coronary vascular resistance. Some of the other dilators include hydrogen ions, CO2, potassium, and lactic acid. The action of endothelial NO synthase (eNOS) on L-arginine results in the formation of NO. This messenger also plays a vital role in the regulation of coronary blood flow via vasodilation, inhibition of platelet aggression, and decreasing vascular resistance.
Adenosine is considered as purine nucleoside that forms after the breakdown of adenosine triphosphate (ATP). Adenosine binds to adenosine type 2A (A2A) receptors in coronary vascular smooth muscles. These are coupled to the Gs protein. This mechanism leads to hyperpolarisation of muscle cells, resulting in relaxation and increased coronary blood flow.

GTN is an veno and arteriolar dilator, which behaves as pro-drug with NO.

The Mapleson A (Magill) and coaxial version of the Mapleson A system (Lack circuit) are more efficient for spontaneous breathing than any of the other Mapleson circuits. The fresh gas flow (FGF) required to prevent rebreathing is slightly greater than the alveolar minute ventilation (4-5 litres/minute). This is delivered to the patient through the outer coaxial tube and exhaust gases are moved to the scavenging system through the inner tube. In the Lack circuit, the expiratory valve is located close to the common gas outlet away from the patient end. This is the main advantage of the Lack circuit over the Mapleson A circuit.

The Mapleson E circuit is a modification of the Ayres T piece and the FGF required to prevent rebreathing is 1.5-2 times the patient’s minute volume.

The Bain circuit is the coaxial version of the Mapleson D circuit.

The FGF for spontaneous respiration to avoid rebreathing is 160-200 ml/kg/minute.

The FGF for controlled ventilation to avoid rebreathing is 70-100 ml/kg/min.

The external laryngeal nerve arises from the superior laryngeal nerve and provides innervation to the cricothyroid muscle.

The other muscles mentioned receive their innervations from the recurrent laryngeal nerve.

Intra-arterial blood pressure monitoring is a common place procedure in the ICU. It is used to provide accurate beat-to-beat information using a pressure wave displayed on a monitor.

It involves catheter insertion in a peripheral artery (most commonly the radial, brachial and dorsalis pedis arteries). Each subsequent contraction of cardiac muscles results in pressure wave which induces a mechanical motion of flow in the catheter. This mechanical motion is then passed on to a transducer through a rigid fluid-filled tubing. The transducer is the able to process this mechanical motion into electrical signals which are displayed as arterial waves and pressure represented numerically on the monitor.

The transducer should be placed at the same level as the heart on the phlebostatic axis, and at the level of the atria (the 4th intercostal space, in the mid-axillary line).

Air bubbles and catheter tubing with longer lengths result in wave dampening (rounding of the resulting pressure waves). This dampening causes a decrease in systolic pressure, and an increase in diastolic pressure.

The neuroleptic malignant syndrome is a rare complication in response to neuroleptic or antipsychotic medication.

The main features are:
– Elevated creatinine kinase
– Hyperthermia and tachycardia
– Altered mental state
– Increased white cell count
– Insidious onset over 1-3 days
– Extrapyramidal dysfunction (muscle rigidity, tremor, dystonia)
– Autonomic dysfunction (Labile blood pressure, sweating, salivation, urinary incontinence)

Management is supportive ICU care, anticholinergic drugs, increasing dopaminergic activity with Amantadine, L-dopa, and dantrolene, and non- depolarising neuromuscular blockade drugs

The half life of Retinol binding protein (RBP) is 10-12 hours and therefore reflects more acute changes in protein metabolism than any of these proteins. Therefore it is not commonly used as a parameter for nutritional assessment.

The half life of Transthyretin (thyroxine binding pre-albumin) is only one to two days and so levels are less sensitive and this protein is not an albumin precursor. 15 mg/dL represents early malnutrition and a need for nutritional support.

Albumin levels have been frequently as a marker of nutrition but this is not a very sensitive marker. It’s half life more than 30 days and significant change takes some time to be noticed. Also, synthesis of albumin is decreased with the onset of the stress response after burns. Unrelated to nutritional status, the synthesis of acute phase proteins increases and that of albumin decreases.

A more accurate indicator of protein stores is transferrin. It’s response to acute changes in protein status is much faster. The half life of serum transferrin is shorter (8-10 days) and there are smaller body stores than albumin. A low serum transferrin level is below 200 mg/dL and below 100 mg/dL is considered severe. Serum transferrin levels can also affect serum transferrin level.

Fibronectin is used a nutritional marker but levels decrease after seven days of starvation. It is a glycoprotein which plays a role in enhancing the phagocytosis of foreign particles.

The patient’s diagnosis is microcytic hypochromic anaemia which is often as a result of iron deficiency and thalassaemia.

Macrocytic anaemia is often caused by folate and B12 deficiencies and alcohol abuse.

Normocytic normochromic anaemia is often caused by acute blood loss, haemolytic anaemia, anaemia of chronic disease and leucoerythroblastic anaemias.

Small measurement units are denoted by the following SI mathematical prefixes:

1 deci = 0.1
1 milli = 0.001
1 micro = 0.000001
1 nano = 0.000000001
1 pico = 0.000000000001
1 femto = 0.000000000000001 (used to measure red blood cell volume)
1 atto = 0.000000000000000001

The left atrium is supplied by the left coronary artery and its major branch the left circumflex.

The heart receives blood supply from coronary arteries. The right and left coronary arteries branch off the aorta and supply oxygenated blood to all heart muscle parts.

The left main coronary artery branches into:
1. Circumflex artery – supplies the left atrium, side, and back of the left ventricle. The left marginal artery arises from the left circumflex artery. It travels along the obtuse margin of the heart.
The left marginal artery, a branch of the circumflex artery, supplies the left ventricle.
2. Left Anterior Descending (LAD) artery – supplies the front and bottom of the left ventricle and front of the interventricular septum

The right coronary artery branches into:
1. Right marginal artery
2. Posterior descending artery

The right coronary artery supplies the right atrium, right ventricle, interatrial septum, and the inferior posterior third of the interventricular septum. It also supplies the atrioventricular node + sinoatrial node in most patients. The posterior descending artery supplies the posterior third of the interventricular septum.