Only 1 percent of the calcium in the human body is found in the plasma where it performs the most critical functions.

Out of this 1 percent, approximately 15% is complexed calcium bound to organic and inorganic anions, 40% is bound to albumin, and the remaining 45% circulates as free ionized calcium.

The Chvostek sign is a clinical finding associated with hypocalcaemia, or low levels of calcium in the blood. This clinical sign refers to a twitch of the facial muscles that occurs when gently tapping an individual’s cheek, in front of the ear.

Prolonged QT interval are associated with hypocalcaemia as reported in multiple studies.

Prostacyclin is a strong vasodilator. It is administered as an intravenous infusion for critical ischemia. Commercially, it is available as sodium epoprodtenol.

Atrial Natriuretic peptide (ANP) hormone secreted from the atria, kidney, and neural tissues. It primarily acts on renal vessel to maintain normal blood pressure and reduce plasma volume by: increasing the renal excretion of salt and water, glomerular filtration rate, vasodilation, and by increasing the vascular permeability. It also inhibits the release of renin and aldosterone.

Indoramin is an alpha-adrenoceptor blocking agent. which act selectively on post-synaptic-alpha adrenoreceptor, leading to decease in peripheral resistance.

Angiotensin II is a vasoconstrictor, causing high sodium retention. It also increases the secretion of antidiuretic hormone (ADH) and aldosterone level.

The umbilical vein closes once the umbilical cord is clamped following birth. This causes a rise in systemic vascular resistance, closing the ductus venosus.

Upon birth, the pulmonary vascular resistance is decreased as the lungs are aerated.

At birth, there is a rise in oxygen tension which causes the corresponding constriction of the ductus arteriosus. This prevents a left to right shunt as it stops aortic blood and blood from the pulmonary artery from mixing. The ventricles do no have an opening connecting them.

The foramen ovale closes soon after birth. It is the septum opening between the left and right atrium.

An adult’s cardiac output is expected to be 5 L/min.

The sinoatrial node receives innervation from multiple nerves arising from the complex cardiac plexus.

The cardiac plexus sends tiny branches into cardiac vessels, alongside the right and left coronary arteries.

The vagal efferent fibres originate from the vagal and accessory nerves in the brainstem, and then travel to the cardiac plexus within the heart. The resulting vagal discharge controls heart rate.

No singular nerve directly innervates the sinoatrial node.

Interleukin-4 is a cytokine which acts to regulate the responses of B and T cells.

Erythropoietin is responsible for the signal that initiated red blood cell production.

Granulocyte-colony stimulating factor stimulates the bone marrow to produce granulocytes.

Interleukin-5 is a cytokine that stimulates the proliferation and activation of eosinophils.

Thrombopoietin is the primary signal responsible for megakaryocyte and thus platelet production.
Platelets are also called thrombocytes. They, like red blood cells, are also derived from myeloid stem cells. The process involves a megakaryocyte developing from a common myeloid progenitor cell. A megakaryocyte is a large cell with a multilobulated nucleus, this grows to become massive where it will then break up to form platelets.

Immune cells are generated from haematopoietic stem cells in bone marrow. They generate two main types of progenitors, myeloid and lymphoid progenitor cells, from which all immune cells are derived.

Phase 1 is associated with assessing whether a drug is safe to use or not. The process is extensive and can take up to several months. It also involves healthy participants (less than 100) that are paid to take part in the study.

The side effects upon increasing dosage are also addressed by the study. The effects the drug has on humans including how its absorbed, metabolized and excreted are studied. Approximately 70% of the drugs pass this phase.

Selegiline is a monoamine oxidase inhibitor. Inhibition of monoamine oxidase leads to increased levels of norepinephrine and serotonin in the central nervous system.

Pethidine, also known as meperidine, is a strong agonist at the mu and kappa receptors. It inhibits pain neurotransmission and blocks muscarinic-specific actions.

Administering opioid analgesic is relatively contraindicated to individuals taking monoamine oxidase inhibitors. This is because of the high incidence of serotonin syndrome, which is characterized by fever, agitation, tremor, clonus, hyperreflexia and diaphoresis. Onset of symptoms is within hours, and the treatment is mainly through sedation, paralysis, intubation and ventilation.

The clinical findings are more consistent with Serotonin syndrome rather than exacerbation of Parkinson’s. Parkinson’s Disease (PD) exacerbations are defined as patient-reported or caregiver-reported episodes of subacute worsening of PD motor function in 1 or more domains (bradykinesia, tremor, rigidity, or PD-related postural instability/gait disturbance) that caused a decline in functional status, developed over a period of < 2 months, did not fluctuate with medication timing, and are not caused by intentional adjustments of PD medications by the treating neurologist.

Malignant hyperthermia usually occurs within minutes of administration of a volatile anaesthetic, such as halothane, or succinylcholine. There is massive release of calcium from the sarcoplasmic reticulum, leading to fever, acidosis, rhabdomyolysis, trismus, clonus, and hypertension.

In sepsis, it more common for patients to present with hypotension rather than hypertension.

The tricuspid valve allows the tip of a pulmonary artery catheter to pass through the right atrium and into the right ventricle.

The balloon will be inflated before crossing the pulmonary valve and entering the pulmonary artery, where it will eventually wedge or occlude the artery, providing an indirect measure of left atrial pressure.

0-12 mmHg in the right atrium
2-25 mmHg in the right ventricle
12-25 mmHg in the pulmonary artery
8-12 mmHg is the occlusion pressure

Flowmeters measure the rate at which a specific gas, that the flowmeter has been calibrated for, passes through. This calibration is done at room temperature and standard atmospheric pressure with an accuracy of +/- 2%.

Reading the flowmeter is done from the top of a bobbin (the midpoint of a ball). Oxygen is the last gas to be added downstream to the mixture delivered to the back bar as a safety feature. This prevents delivery of a hypoxic mixture.

Inaccurate flow measurements occur when the bobbin sticks to the inside wall of the flowmeter. Stannic oxide has been used as a successful antistatic substance thus, reducing the aforementioned risk.

Carbon dioxide being easily delivered is found on some older machines, but those attached flowmeters are limited by a maximum flow of 500 ml /min. Thus avoiding the delivery of a hypercarbic mixture.

Rifampicin is a derivative of a rifamycin (other derivatives are rifabutin and rifapentine). It is bactericidal against both dividing and non-dividing mycobacterium and acts by inhibiting DNA-dependent RNA polymerase. Thus this drug inhibits RNA synthesis.

Electrical resistivity is a measure of a material’s property to oppose the flow of electric current. This is expressed in Ohm-meters (Ω‹…m). The symbol of resistivity is usually the Greek letter Ï� (rho). A high resistivity means that a material does not conduct electric charge well.

Electrical resistivity is defined as the relation between the electric field inside a material, and the electric current through it as a consequence:

� = E/J

in which Ï� is the resistivity of the material (Ω‹…m),
E is the magnitude of the electrical field in the material (V/m),
J is the magnitude of the electric current density in the material (A/m2)

If the electric field (E) through a material is very large and the flow of current (J) is very small, it means that the material has a high resistivity.

The needle should be inserted just below the skin at the mid inguinal point which is the surface indicator for the femoral artery.

The coeliac axis refers to one of the splanchnic arteries located within the abdomen.

It arises from the aorta almost horizontally at the level of the T12 vertebrae.

The ECG changes seen in hypomagnesaemia include:

Prolonged PR interval
Prolonged QT interval
Flattening of T waves
ST segment depression
Prominent U waves

These changes are almost the same as those of hypokalaemia.

There is an increased risk of digoxin toxicity and a risk of atrial and ventricular ectopic and ventricular arrhythmias.

There is impaired synthesis and release of parathyroid hormone (PTH) in chronic hypomagnesaemia leading to impaired target organ response to PTH. This produces secondary hypocalcaemia.

The use of potassium ‘wasting’ diuretics (e.g. loop diuretics like furosemide) may lead to Hypomagnesaemia.

A tall T wave is seen in hypermagnesemia.

The response of cerebral blood flow (CBF) to hyperoxia (PaO2 >15 kPa, 113 mmHg), the cerebral oxygen vasoreactivity is less well defined. A study originally described, using a nitrous oxide washout technique, a reduction in CBF of 13% and a moderate increase in cerebrovascular resistance in subjects inhaling 85-100% oxygen. Subsequent human studies, using a variety of differing methods, have also shown CBF reductions with hyperoxia, although the reported extent of this change is variable. Another study assessed how supra-atmospheric pressures influenced CBF, as estimated by changes in middle cerebral artery flow velocity (MCAFV) in healthy individuals. Atmospheric pressure alone had no effect on MCAFV if PaO2 was kept constant. Increases in PaO2 did lead to a significant reduction in MCAFV; however, there were no further reductions in MCAFV when oxygen was increased from 100% at 1 atmosphere of pressure to 100% oxygen at 2 atmospheres of pressure. This suggests that the ability of cerebral vasculature to constrict in response to increasing partial pressure of oxygen is limited.

Increases in arterial blood CO2 tension (PaCO2) elicit marked cerebral vasodilation.

CBF increases with general anaesthesia, ketamine anaesthesia, and hypoviscosity.

Choosing an appropriate dose of local anaesthetic to reduce the chance of toxicity is the most important safety aspect in performing a caudal block.

The caudal will have to be inserted following induction of anaesthesia as performing it in an awake child is not a viable option.

The patient is placed in the lateral position and the sacral hiatus is identified. Under strict asepsis, a needle ( usually a 21-23FG needle) is advanced at an angle of approximately 55-65° to the coronal plane at the apex of the sacrococcygeal membrane. When there is loss of resistance, thats the endpoint. The needle must first be aspirated before anaesthetic agent is injected because there is a risk (1 in 2000) of perforating the dura or vascular puncture.

Alternatively, a 22-gauge plastic cannula can be used. Following perforation of the sacrococcygeal membrane, the stilette is removed and only the blunter plastic cannula is advanced. This reduces the risk of intravascular perforation.

Eliciting an appropriate end motor response at an appropriate current strength when the caudal and epidural spaces are stimulated helps in improving the efficacy and safety of neural blockade. A 22G insulated needle is advanced in the caudal canal until a pop is felt. If the needle is placed correctly, an anal sphincter contractions (S2 to S4) is seen when an electrical stimulation of 1-10 mA is applied.

The application of ultrasound guidance in identification of the caudal epidural space has been shown to prevent inadvertent dural puncture and to increase the safety and efficacy of the block in children.

During carotid endarterectomy, injury to the vagus nerve or its branches can cause hoarseness. Injury to the vagus nerve can result in adductor vocal cord paralysis. It can also cause other symptoms like dysphagia or even vocal cord immobility.

Carotid endarterectomy is the procedure to relieve an obstruction in the carotid artery by opening the artery at its origin and stripping off the atherosclerotic plaque with the intima. Because of the internal carotid artery relations, there is a risk of cranial nerve injury during the procedure involving one or more of the following nerves: CN IX, CN X (or its branch, the superior laryngeal nerve), CN XI, or CN XII.

However, only damage to the vagus would account for speech difficulties.

Monoamine oxidase (MOA) enzymes are responsible for the catalyses of monoamine oxidative deamination. It assists the degradation of serotonin, norepinephrine (NE) and dopamine.

They are found in the mitochondria of most central and peripheral nerve tissues.

There are 2 different types:

Type A: Whose main function it to inactivate dopamine, tyramine, norepinephrine and 5-hydroxytryptamine. In addition to the nervous system, it is also found in the liver, brain gastrointestinal tract, pulmonary endothelium and placenta
Type B: Whose main function is to inactivate dopamine, tyramine, tryptamine and phenylethylamine. In addition to the nervous system, it is also found in the liver, brain (especially in the basal ganglia) and blood platelets.

The study is being conducted on a smaller level with only 200 participants and is determining the effectiveness of the drug in comparison to a placebo. These characteristics are in accordance with the second phase of trial.

The arterial blood gas analysis indicates presence of acute respiratory acidosis.

Central chemoreceptors are located in the ventral medulla and respond directly to presence of hydrogen ions in the CSF. When stimulated, it causes an increase in respiratory rate.

It is believed that hydrogen ions may be the only important direct stimulus for these neurons, however, CO2 is believed to stimulate these neurons secondarily by changing the hydrogen ion concentration.

Changes in O2 concentration have virtually no direct effect on the respiratory centre itself to alter respiratory drive. Although, O2 changes do have an indirect effect by acting through the peripheral chemoreceptors.