Key Point: While finding out confidence intervals, standard errors are used. Standard error and Standard deviation are two distinct entities and should not be confused.

For 99.7% confidence interval, you can find the range as follows:

Multiply the standard error by 3.

Subtract the answer from mean value to get the lower limit.

Add the answer obtained in step 1 from the mean value to get the upper limit.

The range turns out to be 1-13 mmol/L.

For a confidence interval of 68%, multiply the standard error with 1 and repeat the process. The range found for this interval is 3-11 mmol/L.

For a 95% confidence interval. Standard Error is multiplied by 1.96 which gives us the limit ranging from 3.08 to 10.92 mmol/L which could be approximated to 3-11 mmol/L.

A prospective randomised double blind controlled trial against cyclizine in multiple centres is the most likely to change your practice.

Case controlled studies are efficient in identifying an association between a drug treatment and outcome and are usually conducted retrospectively. They are generally less valued than prospective randomised trials. They cannot generate incidence data, are subject to bias, have difficult selection of controls and can be made more difficult if note keeping is not reliable.

The gold standard in intervention-based studies is randomised controlled double blind trials. Its features are:

Treating all intervention groups identically
Reduction of bias by random allocation to intervention groups
Patients and researchers unaware of which treatment was given until at completion of study
Patients analysed within the group to which they were allocated, and
Analysis focused on estimating the size of the difference in predefined outcomes between intervention groups.

New healthcare interventions should be evaluated through properly designed randomised controlled trials (though there are some potential ethical disadvantages)

Conducting trials in multiple centres is an accepted way of evaluating a new drug as it may be the only way of recruiting sufficient number of patients within a reasonable time frame to satisfy the objectives of the trial. Type II statistical errors will occur if a small numbers of patients is used in study group.

The bispectral index (BIS) is one of several systems used in anaesthesiology as of 2003 to measure the effects of specific anaesthetic drugs on the brain and to track changes in the patient’s level of sedation or hypnosis. It is a complex mathematical algorithm that allows a computer inside an anaesthesia monitor to analyse data from a patient’s electroencephalogram (EEG) during surgery. It is a dimensionless number (0-100) that is a summative measurement of time domain, frequency domain and high order spectral parameters derived from electroencephalogram (EEG) signals.

Sleep and anaesthesia have similar behavioural characteristics but are physiologically different but BIS monitors can be used to measure sleep depth. With increasing sleep depth during slow-wave sleep, BIS levels decrease. This correlates with changes in regional cerebral blood flow when measured using positron emission tomography (PET).

BIS shows a dose-response relationship with the intravenous and volatile anaesthetic agents. Opioids produce a clinical change in the depth of sedation or analgesia but fail to produce significant changes in the BIS. Ketamine increases CMRO2 and EEG activity.

BIS is unable to predict movement in response to a surgical stimulus. Some of these are spinal reflexes and not perceived by the cerebral cortex.

BIS is used during cardiopulmonary bypass to measure depth of anaesthesia and an index of cerebral perfusion. However, it cannot predict subtle or significant cerebral damage.

This patient is morbidly obese and has a high risk of developing hypoxia. This will be exacerbated by the patient’s supine position, as a result of:

Functional residual capacity has been reduced (FRC)
Increased closing capacity (CC)
Reduced tidal volume due to increased airway resistance, decreased thoracic cage compliance, and decreased respiratory muscle strength and endurance
Following induction of general anaesthesia, there is a tendency for atelectasis and increased O2 consumption due to the increased workload of respiratory muscles and the overall increase in metabolism.

Pre-oxygenation with 100 percent oxygen via a tight-fitting mask can be done using either tidal volume breaths for three to five minutes or four vital capacity breaths in normal circumstances. In the head-up position, this patient is much more likely to be adequately pre-oxygenated, maximising the FRC and minimising the CC. In spontaneously breathing patients, the Mapleson A and circle systems are both effective, but the Mapleson D requires 160-200 ml/kg/minute to prevent rebreathing.

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

The heart has two venous drainage systems:
1. Greater venous system – it parallels the coronary arterial circulation and provides 70% venous drainage to the heart
2. Lesser venous system – includes the thebasian veins and provides up to 30% of the venous drainage to the heart

Thebasian veins (also called venae cordis minimae) are the smallest coronary veins and run in the myocardial layer of the heart. They serve to drain the myocardium and are present in all four heart chambers. They are more abundant on the right side of the heart and, more specifically, are most abundant in the right atrium. Thebesian veins drain the subendocardial myocardium either directly, via connecting intramural arteries and veins, or indirectly, via subendocardial sinusoidal spaces.

The pectinate muscles (musculi pectinati) are parallel muscular ridges that extend anterolaterally on the right atrial walls. The most prominent pectinate muscle, which forms the bridge of the sulcus terminalis internally, is the taenia sagittalis (second crest or septum spurium).

In the left atrium, the pectinate muscles are confined to the inner surface of its atrial appendage. They tend to be fewer and smaller than in the right atrium. This is due to the embryological origin of the auricles, which are the true atria.

Pectinate muscles of the atria are different from the trabeculae carneae, which are found on the inner walls of both ventricles.

The interior of the right atrium has five distinct features:
1. Sinus venarum – smooth, thin-walled posterior part of the right atrium where the SVC, IVC, and coronary sinus open
2. Musculi pectinati – a rough anterior wall of pectinate muscles
3. Tricuspid valve orifice – the opening through which the right atrium empties blood into the right ventricle
4. Crista terminalis – separates the rough (musculi pectinati) from the smooth (sinus venarum) internally
5. Fossa ovalis – a thumbprint size depression in the interatrial septum, which is a remnant of the oval foramen and its valve in the foetus

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.

Systemic vascular resistance (SVR), also known as total peripheral resistance (TPR), is the amount of force exerted on circulating blood by the vasculature of the body. Three factors determine the force: the length of the blood vessels in the body, the diameter of the vessels, and the viscosity of the blood within them. The most important factor that determines the systemic vascular resistance (SVR) is the tone of the small arterioles.

These are otherwise known as resistance arterioles. Their diameter ranges between 100 and 450 µm. Smaller resistance vessels, less than 100 µm in diameter (pre-capillary arterioles), play a less significant role in determining SVR. They are subject to autoregulation.

Any change in the viscosity of blood and therefore flow (such as due to a change in haematocrit) might also have a small effect on the measured vascular resistance.

Changes of blood temperature can also affect blood rheology and therefore flow through resistance vessels.

Systemic vascular resistance (SVR) is measured in dynes·s·cm-5

It can be calculated from the following equation:

SVR = (mean arterial pressure − mean right atrial pressure) × 80 cardiac output

PaCO2 is one of the most important factors that regulate cerebral vascular tone. CO2 induces cerebral vasodilatation and as a result, it increases CBF. Between 20 mmHg (2.7 kPa) and 80 mmHg (10.7 kPa), there is a linear increase of PaCO2.

Sometimes, there are areas where auto regulation has failed locally but not globally. Similarly, local vs. systemic acidosis will have similar effects. When the PaO2 falls below 50 mmHg (6.5 kPa), the CBF progressively increases.

An increase in the cerebral metabolic rate for oxygen (CMRO2) and therefore CBF can be caused by hyperthermia.
A late feature of cerebral injury is hyperthermia secondary to hypothalamic injury. Therefore this is not the most likely cause of an increased CBF in this scenario.