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

The inferior thyroid artery is derived from the thyrocervical trunk.

For estimating a child’s weight, the Resuscitation Council (UK) and European Resuscitation Council teach the following formula:

Weight = (age + 4) × 2

The weight of the child will be around 20 kg.

This formula is used in the Primary FRCA exam by the Royal College of Anaesthetists.

In ‘developed’ countries, the traditional ‘APLS formula’ for estimating weight in children based on age (wt in kg = [age+4] x 2) is acknowledged as underestimating weight by 33.4 percent on average, with the degree of underestimation increasing with increasing age.

However, more recently, the APLS formula ‘Weight=3(age)+7’ has been found to provide a mean underestimate of only 6.9%. This formula is applicable to children aged 1 to 13 years.

The estimated weight based on age using this formula is 25 kg.

The minimal alveolar concentration (MAC) is the concentration of an inhalation anaesthetic agent in the lung alveoli required to stop a response to the surgical stimulus in 50% of the patient.

Following factors don’t affect the MAC of the inhaled anaesthetic agents:

Gender, acidosis, alkalosis, hypothyroidism, hyperthyroidism, body weight, serum potassium level, and the duration of the anaesthesia.

MAC increase in children, elevated temperature, high metabolic rate, sympathetic increase and chronic alcoholism.

MAC decrease in low temperature, low oxygen level, old age, hypotension ( 120mmHg is being used in anesthetic-Hinkman as an additive effect to decrease MAC, however, increase concentration of CO2 activates the sympathetic system resulting the MAC increases.

Adenosine receptors are expressed on the surface of most cells.
Four subtypes are known to exist which are A1, A2A, A2B and A3.

Of these, the A1 and A2 receptors are present peripherally and centrally. There are agonists at the A1 receptors which are antinociceptive, which reduce the sensitivity to a painful stimuli for the individual. There are also agonists at the A2 receptors which are algogenic and activation of these results in pain.

The role of adenosine and other A1 receptor agonists is currently under investigation for use in acute and chronic pain states.

Severity of a reduction in restrictive defect (%FVC) or obstructive defect (V1/FVC) predicted are classified as follows:

Mild 70-80%
Moderate 60-69%
Moderately severe 50-59%
Severe 35-49%
Very severe <35%

This patient has a %FVC predicted of 60.4% and this corresponds to a moderate restrictive deficit. V1/FVC ratio is 93.5%.

FEV1/FVC ratio 80% < predicted and VC < 80% = mixed picture.

FEV1/FVC ratio 80% < predicted and VC > 80% = obstructive picture.

FEV1/FVC ratio 80% > predicted and VC > 80% = normal picture.

FEV1/FVC ratio 80% > predicted and VC < 80% predicted= restrictive picture.

The integrity of the alveolar-capillary barrier is measured by carbon monoxide transfer factor (TLCO) and carbon monoxide transfer coefficient (KCO). These values are seen to be reduced in emphysema, interstitial lung diseases and in pulmonary vascular pathology. However, the KCO (as % predicted) is high in extrapulmonary restriction (pleural, chest wall and respiratory neuromuscular disease), and in loss of lung units provided the structure of the lung remaining is normal. The KCO distinguishes extrapulmonary (high KCO) causes of 'restriction' from intrapulmonary causes (low KCO).

Approximately 20% of halothane and 0.02% desflurane undergo hepatic biotransformation. Desflurane, halothane, and isoflurane are metabolised in the liver by cytochrome p450 to trifluoroacetate. Through an immunological mechanism involving trifluoroacetyl hapten formation, trifluoroacetate is thought to be responsible for hepatotoxicity.

Potency of inhaled anaesthetic agents is measured using the minimal alveolar concentration (MAC). The MAC of halothane is 0.74% while that of desflurane is 6.3%. The potency can also be compared using the oil: gas partition coefficient (224 and 18.7 for halothane and desflurane respectively).

Onset of action of volatile agents depends on the blood:gas partition coefficient. A lower blood:gas partition coefficient and insolubility in blood means faster onset and offset of action. The blood gas coefficient for halothane is 2.4 while that of desflurane is 0.42. Desflurane is less soluble than halothane in blood. Halothane has a pungent smell that can irritate the airway which limits its use for a gaseous induction especially in paediatric anaesthesia. desflurane is not pungent.

Desfluranes boiling point is only slightly above normal room temperature (22.8°C) making it extremely volatile while the boiling point of halothane is approximately 50.2°C.

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.

The ‘ideal’ alveolar PO2 minus arterial PO2 is the alveolar-arterial (A-a) oxygen difference.

The ‘ideal’ alveolar PO2 is derived from the alveolar air equation and is the PO2 that the lung would have if there was no ventilation-perfusion (V/Q) inequality and it was exchanging gas at the same respiratory exchange ratio as real lung.

The amount of oxygen in the blood is measured directly in the arteries.

The A-a oxygen difference (or gradient) is a useful measure of shunt and V/Q mismatch, and it is less than 2 kPa in normal adults breathing air (15 mmHg). Because the shunt component is not corrected, the A-a difference increases when breathing 100 percent oxygen, and it can be up to 15 kPa (115 mmHg).

An abnormally low or abnormally high V/Q ratio within the lung can cause an increased A-a difference, though the former is more common. Atelectasis, which results in a low V/Q ratio, is the most likely cause of an A-a difference in a healthy adult breathing 100 percent oxygen.

Hypoventilation may cause an increase in alveolar (and thus arterial) CO2, lowering alveolar PO2 according to the alveolar air equation.

The alveolar PO2 is also reduced at high altitude.

Healthy people are unlikely to have a right-to-left shunt or an oxygen transport diffusion defect.

Selective α1 -Blockers like prazosin, terazosin, doxazosin, and alfuzosin cause a decrease in blood pressure with lesser tachycardia than nonselective blockers (due to lack of α2 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)

Dinamap continuously measures the systolic, diastolic and mean arterial pressure along with pulse rate, thereby providing a continuous monitoring of the blood pressure using the osscillitonometric principle of measurement.

The device loses accuracy towards the extremes of BP and is more accurate with systolic compared with diastolic pressure. In arrhythmias such as AF, the devices are also inaccurate due to the major fluctuations associated with the individual pulse pressure variations.

The manual BP device is still the gold standard for BP measurement and monitoring.

With a history of drug abuse, the patient is likely dependent on and tolerant to opioids. He is also likely to experience significant pain from his injuries. Providing adequate pain relief with regular paracetamol and NSAIDs in combination with a pure opioid agonist while at the same time avoiding occurrence of acute withdrawal syndrome is the goal.

Administering a baseline dose of opioid corresponding to the patient’s usual opioid use plus an opioid dose required to address the level of pain the patient experience can help prevent opioid withdrawal. The best approach is by empowering the patient to use patient controlled analgesia (PCA). The infusion rate, bolus dose and lock-out time are adjusted accordingly. Using PCA helps in avoiding staff/patient confrontations about dose and dosing interval.

2.5 mg heroin is equivalent to 3.3 mg morphine. This patient is usually on 200 mg of heroin per 24 hours. The equivalent dose of morphine is 80 × 3.3 =254 mg per 24 hours (11 mg/hour).

Epidural or spinal opioids might be the best choice for providing a systemic dose of opioids when patients are in remission to avoid withdrawal. Lumbar vertebral fractures is a contraindication to this route of analgesia.

The long half life of Oral methadone make titration to response difficult. Also, absorption of methadone by the gastrointestinal tract is variable. It is therefore NOT the best choice for acute pain management.

Each kidney is composed of about 1.2 million uriniferous tubules. Each tubule consists of two parts that are embryologically distinct from each other. They are as follows:
a) Excretory part, called the nephron, which elaborates urine
b) Collecting part which begins as a junctional tubule from the distal convoluted tubule.

There are two types of nephrons in the kidney:
The cortical nephron comprises 80% of the total nephron and its major function is the excretion of waste products in urine whereas the juxtamedullary nephron comprises 20% of the total nephron and its major function is the concentration of urine by counter current mechanism.
In the superficial (cortical) nephrons, peritubular capillaries branch off the efferent arterioles and deliver nutrients to epithelial cells as well as serve as a blood supply for reabsorption and secretion. In juxtamedullary nephrons, the peritubular capillaries have a specialization called the vasa recta, which are long, hairpin-shaped blood vessels that follow the same course as a loop of Henle. The vasa recta serve as osmotic exchangers for the production of concentrated urine.

The kidney receives about 25% of cardiac output and about 20% of this is filtered at the glomeruli of the kidney. Thus, renal blood flow is 1200 ml/minute and renal plasma flow is 650 ml/minute.

Mean, also known as the average, is the most common measure of central tendency. It is the sum of all observed values divided by the number of observation. It is not useful for skewed data, which has an abnormal distribution. It is useful, instead, for numerical data that have symmetric distribution. It reflects the contributions of each data in the group, and are sensitive to outliers.

The median is the value that falls in the middle position when the observations are ranked in order from the smallest to the largest. If the number of observations is odd, the median is the middle number. If it is even, the median is the average of the two middle numbers. Unlike the mean, the median is useful on skewed data, and can be used for ordinal or numerical data if skewed.

The mode is the value that occurs with the greatest frequency in a set of observations, and is utilized for bimodal distribution.

The variance and the standard deviation are not measures of central tendency, but of dispersion.

The drug of choice for the treatment of anaphylaxis is adrenaline. It has an intravenous route of administration. Since the patient already has intravenous access, the intramuscular route is not appropriate.

Second-line pharmacological intervention includes the use of chlorpheniramine 10mg intravenous, Hydrocortisone 200mg.

Pipeline gases (in the UK this includes: Oxygen, Nitrous oxide, Medical air, and Entonox) are supplied at 4 bar (or 400 kPa), and compressed air is supplied at 7 bar for power tools.

Carbon dioxide and nitric oxide are usually only supplied in cylinders.

The toxicity of organophosphorus (OP) nerve agents is manifested through irreversible inhibition of acetylcholinesterase (AChE) at the cholinergic synapses, which stops nerve signal transmission, resulting in a cholinergic crisis and eventually death of the poisoned person. Oxime compounds used in nerve agent antidote regimen reactivate nerve agent-inhibited AChE and halt the development of this cholinergic crisis.

30mL 0.5% bupivacaine, 1mL 1 in 1,000 adrenaline and 89mL 0.9% N. Saline is the correct answer.
Initial concentration of bupivacaine is 0.5% with a volume of 30mL

The volume is doubled (60mL) by the addition of 0.9% N. saline (30mls) and the concentration of bupivacaine is halved to (0.25%).

If the volume is doubled again (120mL) by the addition of further 0.9% N. saline (59mls) the final concentration of bupivacaine is halved again to 0.125%. Total N. saline = 89mls

The 1 mL of 1 in 1000 adrenaline has also been diluted into the final volume of 120 mL making it a 1 in 120000 concentration.

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.

When drugs are bound to proteins, drugs cannot cross membranes and exert their effect. Only the free (unbound) drug can be absorbed, distributed, metabolized, excreted and exert pharmacologic effect. Thus, when amide local anaesthetics are bound to α1-glycoproteins, their duration of action are reduced.

The potency of local anaesthetics are affected by lipid solubility. Solubility influences the concentration of the drug in the extracellular fluid surrounding blood vessels. The brain, which is high in lipid content, will dissolve high concentration of lipid soluble drugs. When drugs are non-ionized and non-polarized, they are more lipid-soluble and undergo more extensive distribution. Hence allowing these drugs to penetrate the membrane of the target cells and exert their effect.

Tissue pKa and pH will determine the degree of ionization.

The tenth cranial nerve (vagus nerve) has both sensory and motor divisions.

It emerges from the anterolateral surface of the medulla in a groove between the olive and the inferior cerebellar peduncle as a series of 8-10 rootlets . It leaves the skull through the middle compartment of the jugular foramen and descends within the carotid sheath between the internal carotid artery and internal jugular vein. The right vagus crosses in front of the first part of the subclavian artery. It gives off the right recurrent laryngeal nerve at this point.

The left recurrent laryngeal nerve passes around the ligamentum arteriosum.

The external laryngeal nerve supplies the cricothyroid muscle while the recurrent laryngeal nerve supplies the other laryngeal muscles.

The cranial part of the accessory nerve supplies all the muscles of the palate, via the pharyngeal plexus and the pharyngeal branch of the vagus nerve, except the tensor veli palatini which is supplied by the mandibular branch of the trigeminal nerve.

The Sternothyroid, Sternohyoid, and Omohyoid muscles are supplied by the ansa cervicalis while the thyrohyoid muscle is supplied by the hypoglossal nerve.

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.

This patient’s limited haematological profile includes mild normocytic anaemia and a normal platelet count.

Iron deficiency is the most common cause of anaemia during pregnancy. It affects 75 to 95 percent of patients. A haemoglobin level of less than 110 g/L in the first trimester and less than 105 g/L in the second and third trimesters is considered anaemia. There will usually be a low mean cell volume (MCV), mean cell haemoglobin (MCH), and mean cell haemoglobin concentration in addition to a low haemoglobin (MCHC). The MCV may be normal in mild cases of iron deficiency or coexisting vitamin B12 and folate deficiency.

To determine whether you have an iron deficiency, you’ll need to take more tests. Low serum ferritin (15 g/L) and less reliable indices like serum iron and total iron binding capacity are among them.

A number of factors contribute to iron deficiency in pregnancy, including:

Insufficient dietary iron to meet the mother’s and foetus’ nutritional needs
Multiple pregnancies
Blood loss, as well as
Absorption of iron from the gut is reduced.

The volume of plasma increases by about 50% during pregnancy, but the mass of red blood cells (RBCs) increases by only 30%. Dilutional anaemia is the result of this situation. From the first trimester to delivery, the RBC mass increases linearly, while the plasma volume plateaus, stabilises, or falls slightly near term. As a result, between 28 and 34 weeks of pregnancy, haemoglobin concentrations are at their lowest. The effects of haemodilution will be negated in this patient because she is 37 weeks pregnant.

Vitamin B12 and folate deficiency are less common causes of anaemia in pregnancy. The diagnosis could be ruled out if the MVC is normal.

During pregnancy, the platelet count drops, especially in the third trimester. Gestational thrombocytopenia is the medical term for this condition. It’s due to a combination of factors, including haemodilution and increased platelet activation and clearance. Pre-eclampsia and HELLP syndrome are common causes of thrombocytopenia. Pre-eclampsia isn’t the only cause of anaemia during pregnancy.

A typical blood picture of a haemoglobinopathy like sickle cell disease shows quantitative and qualitative defects, with the former leading to a severe anaemia exacerbated by haemodilution and other factors that contribute to iron deficiency. Microcytic cells are the most common type.

Meta analysis performed upon the results, presented by the diamond, is clear from the no effect line. It presents a substantial increase in the probability of another heart attack.

During glycolysis, 2,3-diphosphoglycerate (2,3-DPG) is
created in erythrocytes by the Rapoport-Luebering shunt.

The production of 2,3-DPG increases for several conditions
in the presence of decreased peripheral tissue O2 availability.
Some of these conditions include hypoxaemia, chronic lung
disease anaemia, and congestive heart failure. Thus,
2,3-DPG production is likely an important adaptive mechanism.

High levels of 2,3-DPG cause a shift of the curve to the right.
Low levels of 2,3-DPG cause a shift of the curve to the left,
as seen in states such as septic shock and hypophosphatemia.

Ventricular fibrillation (VT) is an arrhythmia caused by a distortion in the organized contraction of the ventricles leading to an inability to pump blood out into the body.

Amiodarone is an anti arrhythmic drug used for the treatment of ventricular and atrial fibrillations. It is the gold standard of treatment for refractory pulseless ventricular tachycardia (VT) and ventricular fibrillation (VF).

Guidelines for emergency treatment state that only the rescuer carrying out chest compressions on the patient may stand near the defibrillator as it charges.

Cardio-pulmonary resuscitation (CPR) during cardiac arrest is required for 2 minute cycles.

Hypovolaemia is as a cause of pulseless electrical activity (PEA) can be reversed using fluid resuscitation, whereas hypotension during cardiac arrest is either persistent or undetectable and is therefore irreversible.

Hyperkalaemia and hypocalcaemia are treated using calcium salts, but calcium chloride is often preferred over calcium gluconate.

During a pulseless VT or VF, a single precordial thump will be effective if administered within the first seconds of the occurrence of a shockable rhythm.

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.

Porphyria is a group of disorders in which there is excess production and excess excretion of porphyrins and their precursors. They are usually genetic and are caused due to defects in the haem metabolic pathway. However, other factors like infection, pregnancy, mensuration, starvation may precipitate the attack.

Sulphonamides, barbiturates (methohexitone and thiopental), and phenytoin are considered to be precipitants so are not safe to use
Chloral hydrate is thought to be safe to use.
Etomidate lacks proper studies and may be used with caution but it is generally advised not to use this drug especially if other alternatives are available.

Using a lean body weight metric encompasses a more scientific approach to weight-based dosing. Lean body weight reflects the weight of all €˜non-fat’ body components, including muscle and vascular organs such as the liver and kidneys. As lean body weight contributes to approximately 99% of a drug’s clearance, it is useful for guiding dosing in obesity.

This metric has undergone a number of transformations. The most commonly cited formula derived by Cheymol is not optimal for dosing across body compositions and can even produce a negative result. A new formula has been developed that appears stable across different body sizes, in particular the obese to morbidly obese.

A practical downfall of the calculation of lean body weight (and other body size descriptors) is the numerical complexity, which may not be palatable to a busy clinician. Often limited time is available for prescribing and an immediate calculation is required. Lean body weight calculators are available online, for example in the Therapeutic Guidelines.

Using total body weight assumes that the pharmacokinetics of the drug are linearly scalable from normal-weight patients to those who are obese. This is inaccurate. For example, we cannot assume that a 150 kg patient eliminates a drug twice as fast as a 75 kg patient and therefore double the dose. Clinicians are alert to toxicities with higher doses, for example nephro- and neurotoxicity with some antibiotics and chemotherapeutics, and bleeding with anticoagulants. Arbitrary dose reductions or €˜caps’ are used to avoid these toxicities, but if too low can result in sub-therapeutic exposure and treatment failure.

Body surface area is traditionally used to dose chemotherapeutics. It is a function of weight and height and has been shown to correlate with cardiac output, blood volume and renal function. However, it is controversial in patients at extremes of size because it does not account for varying body compositions. As a consequence, some older drugs such as cyclophosphamide, paclitaxel and doxorubicin were €˜capped’ (commonly at 2 m^2) potentially resulting in sub-therapeutic treatment. Recent guidelines suggest that unless there is a justifiable reason to reduce the dose (e.g. renal disease), total body weight should be used in the calculation of body surface area, until further research is done. Little research into dosing based on body surface area has been conducted for other medicines.

Ideal body weight was developed for insurance purposes not for drug dosing. It is a function of height and gender only and, like body surface area, does not take into account body composition. Using ideal body weight, all patients of the same height and sex would receive the same dose, which is inadequate and generally results in under-dosing. For example a male who has a total body weight of 150 kg and a height of 170 cm will have the same ideal body weight as a male who is 80 kg and 170 cm tall. Both could potentially receive a mg/kg dose based on 65 kg (ideal body weight).

There are two types of defibrillators
AC defibrillator
DC defibrillator

AC defibrillator,
consists of a step-up transformer with primary and secondary winding and two switches. Since secondary coil consists of more turns of wire than the primary coil, it induces larger voltage. A voltage value ranging between 250V to 750V is applied for AC external defibrillator. And used to enable the charging of a capacitor.

DC defibrillator,
consists of auto transformer T1 that acts as primary of the high voltage transformer T2. Is an iron core that transfers energy between 2 circuits by electromagnetic induction. Transformers are used to isolate circuits, change impedance and alter voltage output. transformers do not convert AC to DC.

Diode rectifier composed of 4 diodes made of semiconductor material allows current to flow only in one direction. Alternating current (AC) passing through these diodes produces direct current (DC). Capacitor stores the charge in the form of an electrostatic field.

Capacitor is used to convert the rectified AC voltage to produce DC voltage but capacitors do not directly convert AC to DC.

Inductor induces a counter electromotive force(emf) that reduces the capacitor discharge value.

In step-down transformer primary coils has more turns of wire than secondary coil, so induced voltage is smaller in the secondary coil.

Crystalloids recommended for fluid resuscitation include 0.9% N saline and Hartmann’s solution(a physiological solution). 0.9% N. saline is not a physiological solution for the following reasons:

Compared with the normal range of 98-102 mmol/L, its chloride concentration is high (154 mmol/L)
It lacks calcium, magnesium, glucose and potassium
It does not have bicarbonate or bicarbonate precursor buffer necessary to maintain plasma pH within normal limits

There is a difference in the activity (concentration) of strong ions at a physiological pH. This imbalance can explain abnormalities of acid base balance. A normal strong ion difference (SID) is in the order of 40.

SID = ([Na+] + [K+] + [Ca2+] + [Mg2+]) – ([Cl-] + [lactate] + [SO42-])

This imbalance is made up with the weaker anions to maintain electrical neutrality.
Administration of a large volume of 0.9% normal saline during resuscitation results in excessive chloride administration and this impairs renal bicarbonate reabsorption. The SID of 0.9% normal saline is 0 (Na+ = 154mmol/L and Cl- = 154mmol/L = 154 – 154 = 0). A large volume of NS will decrease the plasma SID causing an acidosis.

Other causes of a hyperchloremic acidosis are:

Diabetic ketoacidosis
Total Parenteral Nutrition
Overdose of ammonium chloride and hydrochloric acid
Gastrointestinal losses of bicarbonate like in diarrhoea and pancreatic fistula
Proximal renal tubular acidosis with failure of bicarbonate reabsorption

The central venous pressure (CVP) waveform depicts changes of pressure within the right atrium. Different parts of the waveform are:

A wave: which represents atrial contraction. It is synonymous with the P wave seen during an ECG. It is often eliminated in the presence of atrial fibrillation, and increased tricuspid stenosis, pulmonary stenosis and pulmonary hypertension.

C wave: which represents right ventricle contraction at the point where the tricuspid valve bulges into the right atrium. It is synonymous with the QRS complex seen on ECG.

X descent: which represents relaxation of the atrial diastole and a decrease in atrial pressure, due to the downward movement of the right ventricle as it contracts. It is synonymous with the point before the T wave on ECG.

V wave: which represents an increase in atrial pressure just before the opening of the tricuspid valve. It is synonymous with the point after the T wave on ECG. It is increased in the background of a tricuspid regurgitation.

Y descent: which represents the emptying of the atrium as the tricuspid valve opens to allow for blood flow into the ventricle in early diastole.

According to the Ohm’s law, the potential difference is defined as

V(potential difference) = I(current) x (R) resistance

So, for one resistor of 5 ohms, a 10 ampere current will generate:

V = I x R
V = 10 x 5
V = 50 volts

The formula for resistors in series can be defined as:

R(total) = R1+R2

Hence, when a current of 10 amperes passes through two 5 ohms resistors that are connected in series, the potential difference is:

V = I x (R1+R2)
V = 10 x (5+5)
V = 10 x 10
V = 100 volts

The formula for resistors that are connected in a parallel circuit is:

1/ Rtotal = 1/R1 + 1/R2

Hence, when a current of 10 amperes passes through two 5 Ω resistors that are connected in a parallel circuit, the potential difference is:

Rtotal = R1 × R2/ R1 + R2
Rtotal = 25/10
Rtotal = 2.5
V = I x R
V = 10 x (R1xR2 / R1 + R2)
V = 10 x (25/10)
V = 10 x 2.5
V = 25 volts

Capacitors are electronic components that have the ability to store energy and charge (Q). The derived SI unit of capacitance (C) is the farad (F), which is equivalent to one coulomb per volt (V). The typical capacitors usually have a very small capacitance range, that ranges from pico to microfarads. On the contrary, supercapacitors can have a capacitance of up to 1-5000 F.

There are a number of factors that eventually determine the capacitance (C). They are as follows:

– Larger plate area (A)
– Closer plate spacing (d)
– Permittivity (ε) of the material (dielectric) between the plates (vacuum<<<glass), – C = ε × A/d

The units of stored charge are coulombs (Q), which is equal to the pathway of one ampere of current per second.
Stored charge, capacitance and voltage can be defined by the following equation:

V (potential difference across capacitor) = Q(charge) / C (capacitance)

In a parallel circuit, the formula of capacitors is:

Ctotal = C1 + C2

Hence, two 5 farad capacitors in a parallel circuit arrangement with a charge of 100 coulomb and capacitance 10 F will give a potential difference of::

V = 100/10
V = 10 volts

In a series circuit, the formula for capacitors is:

1/Ctotal = 1/C1 + 1/C2

Hence, two 5 farad capacitors with a charge of 100 coulomb will give:

Ctotal = C1 × C2/C1 + C2

In the example total capacitance = 25/10 = 2.5 F

V = 100/2.5
V = 40 volts.

Professor Mapleson classified non-rebreathing circuits based on the position of the APL valve, which controls fresh gas flow.

The Mapleson A (Magill) circuit is most effective in spontaneous breathing, requiring only 70-100 ml/kg (the patient’s minute volume) of fresh gas flow. The patient inhales fresh gas from the reservoir bag and tubing during inspiration. During expiration, the patient adds dead space gas (gas that hasn’t been exchanged) to the tubing and reservoir bag in addition to the fresh gas flow. At the patient’s end, alveolar gas is vented through the APL valve. During the expiratory pause, the fresh gas flow causes more gas to be released.

The Mapleson A is inefficient during controlled ventilation. Venting occurs during inspiration rather than during the expiratory phase, as it does during spontaneous ventilation. As a result, unless a high fresh gas flow of >20 L/minute is used, alveolar gas is rebreathed.

During spontaneous ventilation, the Mapleson D circuit is inefficient.

The oxygen concentration in a Hudson mask is insufficient to allow for adequate pre-oxygenation.

The emulsification and absorption of fats requires Bile salts.

Absorption of fats is associated with the activation of lipases in the intestine.

Bile salts are involved in fat soluble vitamin absorption and are reabsorbed in the terminal ileum (B12 is NOT fat soluble).

Although Vitamin B12 is also absorbed in the terminal ileum, it is a water soluble vitamin (as are B1, nicotinic acid, folic acid and vitamin C) .

The gastric parietal cells secretes Intrinsic factor that is essential for the absorption of B12.

The Wolff-Parkinson-White syndrome (WPWS) is linked to an additional electrical conduction pathway between the atria and ventricles. This accessory pathway (bundle of Kent), unlike the atrioventricular (AV) node, is incapable of slowing down a rapid rate of atrial depolarization. In other words, a short circuit bypasses the AV node. Patients with a rapid ventricular response or narrow complex AV re-entry tachycardia are more likely to develop atrial fibrillation or flutter.

Digoxin can promote impulse transmission through this accessory pathway if a patient with WPWS develops atrial fibrillation because it works by blocking the AV node. This can cause ventricular fibrillation and an extremely rapid ventricular rate. As a result, it’s not advised.

Adenosine, beta-blockers, and calcium channel blockers, among other drugs that interfere with AV nodal conduction, are also generally contraindicated.

The class III antiarrhythmic drugs amiodarone and ibutilide (K+ channel block) and procainamide (Na+ channel block) are the drugs of choice.

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.

Multiple regression analysis revealed that velocity of lactate accumulation (VOBLA) accounted for 92 percent of the variation in marathon running velocity (VM), and VOBLA plus training volume prior to the marathon accounted for 96 percent of the variation. Percent ST muscle fibre distribution (r = 0.55-0.69) and capillary density (r = 052-0.63) were found to be positively correlated with all performance variables. As a result, marathon running performance was linked to VOBLA and the ability to run at a pace close to it during the race. The percent ST, capillary density, and training volume were all related to these properties.

Another metabolic adaptation compared to normal people is the early selection of fat for oxidation by muscle, especially when glucose availability is limited during high-intensity exercise. This helps to delay the onset of muscle fatigue, but it does not prevent VOBLA.

For a given level of exercise, training can also result in cardiovascular adaptation, such as increased heart size, increased contractility, and a slower heart rate. All of these factors contribute to an increase in maximal oxygen consumption (VO2 max), but genetic factors, despite intensive training, play a large role in an athlete’s performance.

A damped sine wave is a smooth, periodic oscillation with an amplitude that approaches zero as time goes to infinity. In other words, the wave gets flatter as the x-values become larger.

Critical damping is defined as the threshold between overdamping and underdamping. In the case of critical damping, the oscillator returns to the equilibrium position as quickly as possible, without oscillating, and passes it once at most.

In overdamping, the system moves slowly towards the equilibrium. An underdamped system moves quickly to equilibrium, but will oscillate about the equilibrium point as it does so.

Optimal damping has a damping coefficient of around 0.64-0.7. It maximizes frequency response, minimizes overshoot of oscillations, and minimizes phase and amplitude distortion.

In an undamped system, the amplitude of the waves that are being generated remain unchanged and constant over time.

When there is a fall in ionised plasma calcium levels, the chief cells of the parathyroid glands are stimulated to secrete parathyroid hormone (PTH).

50% of extracellular calcium occurs as non-ionised, protein- (albumin-)bound calcium.

The degree of ionisation increases with low ph and decreases with high pH.

There is increased renal calcium excretion with secretion of calcitonin.

The level of statistical significance required influences the sample size used. This is because sample size is used in the calculation of SD/SE.

Sample size does not affect

The level of acceptance
The alternative hypothesis with a general level set at p<0.05
The test to be used.

Experience of the investigator and the type of patient recruited should have no bearing on the required sample size.

Bucks fascia refers to the layer of loose connective tissue, nerves and blood vessels that encapsulates the penile erectile bodies, the corpa cavernosa and the anterior part of the urethra, including the entirety of the spongiose part of the urethra.

It runs with the external spermatic fascia and the penile suspensory ligament.

The respiratory quotient is the ratio of CO2 produced to O2 consumed while food is being metabolized:

RQ = CO2 eliminated/O2 consumed

Most energy sources are food containing carbon, hydrogen and oxygen. Examples include fat, carbohydrates, protein, and ethanol. The normal range of respiratory coefficients for organisms in metabolic balance usually ranges from 1.0-0.7.

Granulated sugar is a refined carbohydrate with no significant fat, protein or ethanol content.

The RQ for carbohydrates is = 1.0

The RQ for the rest of the compounds are:

Fats RQ = 0.7
The chemical composition of fats differs from that of carbohydrates in that fats contain considerably fewer oxygen atoms in proportion to atoms of carbon and hydrogen.

Protein RQ = 0.8
Due to the complexity of various ways in which different amino acids can be metabolized, no single RQ can be assigned to the oxidation of protein in the diet; however, 0.8 is a frequently utilized estimate.

Haemorrhage, including intracranial bleeding, is a common and potentially fatal side effect of warfarin therapy, and reversing anticoagulation quickly and completely can save lives. When complete and immediate correction of the coagulation defect is required in orally anticoagulated patients with life-threatening haemorrhage, clotting factor concentrates are the only viable option.

For rapid reversal of vitamin K anticoagulants, prothrombin complex concentrates (PCC) are recommended. They contain the vitamin K-dependent clotting factors II, VII, IX, and X and are derived from human plasma. They can be used as an adjunctive therapy in patients with major bleeding because they normalise vitamin K dependent clotting factors and restore haemostasis.

The most common treatments are fresh frozen plasma (FFP) and vitamin K. The efficacy of this approach is questioned due to the variable content of vitamin K-dependent clotting factors in FFP and the effects of dilution. Significant intravascular volume challenge, as well as the possibility of rare complications like transfusion-associated lung injury or blood-borne infection, are all potential issues.

To avoid anaphylactic reactions, vitamin K should be given as a slow intravenous infusion over 30 minutes. Regardless of the route of administration, the reversal of INRs with vitamin K can take up to 24 hours to reach its maximum effect.

Reversal of anticoagulation in patients with warfarin-associated intracranial haemorrhage may be considered with factor VIIa (recombinant), but its use is controversial. There are concerns about thromboembolic events following treatment, as well as questions about assessing efficacy in changes in the INR. If the drug is to be administered, patients should be screened for an increased risk of thrombosis before the drug is given.

The clinical potency of the anaesthetic agent is measured using minimal alveolar concentration(MAC).

MAC and oil: gas partition coefficient is inversely related. Anaesthetic agent Oil/gas partition coefficient and Minimal alveolar concentration (MAC) is given respectively as

Desflurane 18 6
Isoflurane 90 1.2
Nitrous oxide 1.4 104
Sevoflurane 53.4 2
Xenon 1.9 71

With these data, we can conclude Isoflurane is the most potent with the highest oil/gas partition coefficient of 90 and the lowest MAC of 1.2

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 (Iˆ’) 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.

An elevated arterial blood lactate level and an increase anion gap ([Na + K] – [Cl + HCO3]) of >20mmol gives rise to lactic acidosis. It can also be a result of overproduction and/or reduced metabolism of lactic acid.

The liver and kidney are the main sites of lactate metabolism, not skeletal muscle.

The two types of lactic acidosis that are known are:

Type A – due to tissue hypoxia, inadequate tissue perfusion and anaerobic glycolysis. These may be seen in cardiac arrest, shock, hypoxaemia and anaemia. The management of type A lactic acidosis involves reversing the underlying cause of the tissue hypoxia.

Type B – occurs in the absence of tissue hypoxia. Some of the causes of this include hepatic failure, renal failure, diabetes mellitus, pancreatitis and infection. Some drugs can also cause this lie aspirin, ethanol, methanol, biguanides and intravenous fructose.

The mainstay of treatment involves:
1. Optimising tissue oxygen delivery
2. Correcting the cause
3. Intravenous sodium bicarbonate

In resistant cases, peritoneal dialysis can be performed.

Sugammadex is a modified cyclodextrin that works as an aminosteroid neuromuscular blocking (nmb) reversal agent. By encapsulating each molecule in the plasma, it rapidly reverses rocuronium and, to a lesser extent, vecuronium-induced neuromuscular blockade. Consequently, a  concentration gradient favours the movement of these nmb agents away from the neuromuscular junction.  Pancuronium-induced neuromuscular blockade at low levels has also been reversed.

By inhibiting voltage-dependent calcium channels at the neuromuscular junction, antibiotics in the aminoglycoside group potentiate neuromuscular blocking agents. This can be reversed by giving calcium but not neostigmine or sugammadex.

Sugammadex will not reverse the effects of mivacurium, which belongs to the benzylisoquinolinium class of drugs.

A phase II or desensitisation block occurs when the motor end-plate becomes less sensitive to acetylcholine as a result of an overdose or repeated administration of suxamethonium. The use of neostigmine has been shown to be effective in reversing this weakness.

Foramen ovale, ductus arteriosus (DA) and ductus venosus (DV) are the three important cardiac shunts in-utero.

At birth the umbilical vessels constrict in response to stretch as they are clamped. Blood flow through the ductus venosus (DV) decreases but the DV closes passively in 3-10 days.

As the pulmonary circulation is established, there is a drastic fall in pulmonary vascular resistance and an increased pulmonary blood flow. This increases flow and pressure in the Left Atrium that exceeds that of the right atrium. The difference in pressure usually leads to the IMMEDIATE closure of the foramen ovale.

The DA is functionally closed within the first 36-hours of birth in a healthy full-term newborn. Subsequent endothelial and fibroblast proliferation leads to permanent anatomical closure within 2 – 3 weeks.

Oxygenated blood from the placenta passes via the umbilical vein to the liver. Blood also bypasses the liver via the ductus venosus into the inferior vena cava (IVC). The Crista dividens is a tissue flap situated at the junction of the IVC and the right atrium (RA). This flap directs the oxygen-rich blood, along the posterior aspect of the IVC, through the foramen ovale into the left atrium (LA).

The Eustachian valve also known as the valve of The IVC is a remnant of the crista dividens.

pH is the negative log to the base 10 of hydrogen ion concentration:

So, what power produces the answer?

pH = – log10 [H+]

Making [H+] the subject:

[H+] = 10-pH

Substituting, [H+] = 10-7

One nanomole = 1 x 10-9 or 0.000000001

10-7 = 1x 0.0000001 or 10 x 0.00000001 or 100 x 0.000000001

100 nanomole.

Smoking is a major risk factor associated with perioperative respiratory and cardiovascular complications. Evidence also suggests that cigarette smoking causes imbalance in the prostaglandins and promotes vasoconstriction and excessive platelet aggregation. Two of the constituents of cigarette smoke, nicotine and carbon monoxide, have adverse cardiovascular effects. Carbon monoxide increases the incidence of arrhythmias and has a negative ionotropic effect both in animals and humans.

Smoking causes an increase in carboxyhaemoglobin levels, resulting in a leftward shift in which appears to represent a risk factor for some of these cardiovascular complications.

There are two mechanisms responsible for the leftward shift of oxyhaemoglobin dissociation curve when carbon monoxide is present in the blood. Carbon monoxide has a direct effect on oxyhaemoglobin, causing a leftward shift of the oxygen dissociation curve, and carbon monoxide also reduces the formation of 2,3-DPG by inhibiting glycolysis in the erythrocyte. Nicotine, on the other hand, has a stimulatory effect on the autonomic nervous system. The effects of nicotine on the cardiovascular system last less than 30 min.