Asthma is a lung condition that causes reversible narrowing and swelling of airway passages. It is classified by the frequency and severity of symptoms.

The following are symptoms of moderate asthma:

Symptoms include cough, wheezing, chest tightness, or difficulty breathing which occurs daily
Decreased activity levels due to flare-ups
Night-time symptoms 5 or more times a month
Lung function test FEV1 is 60-80% of predicted normal values
Peak flow has more than 30% variability

With moderate asthma attacks, the arterial pCO2 levels may decrease, but as severity increases, so does the pCO2, reaching normal levels, and then exceeding them in severe asthma attacks.

Airway obstruction increases the functional residual capacity.

Concentration of serum bicarbonate would not increase in moderate asthma, but it could possibly increase in life-threatening asthma via the same mechanism as what increases arterial PCO2.

FEV1 is a good measure of airway obstruction. and is reduced in acute asthma attacks.

In the case of a pneumothorax, a decrease in arterial PO2 is higher.

Once the decision to deliver a baby by caesarean section has been made, it should be carried out with a level of urgency commensurate with the risk to the baby and the mother’s safety.

There are four types of caesarean section urgency:

Category 1 – Endangering the life of the mother or the foetus
Category 2 – Maternal or foetal compromise that is not immediately life threatening
Category 3 – Early delivery is required, but there is no risk to the mother or the foetus.
Category 4: Elective delivery at a time that is convenient for both the mother and the maternity staff.

Caesarean sections for categories 1 and 2 should be performed as soon as possible after the decision is made, especially for category 1. For category 1 caesarean sections, a decision to deliver time of 30 minutes is currently used.

In most cases, Category 2 caesarean sections should be performed within 75 minutes of making the decision.

The condition of the woman and the unborn baby should be considered when making a decision for a quick delivery, as it may be harmful in some cases.

There is no evidence of foetal compromise in the example above (early foetal pulse decelerations and a pH of less than 7.25). Early foetal pulse decelerations are most likely caused by the uterus compressing the foetal head. The foetus is not harmed by these. A spinal anaesthetic is preferred over a general anaesthetic whenever possible.

If the foetal scalp blood pH is greater than 7.25, it’s a good idea to repeat the test later and look for any changes. When a foetus decelerates, the mother should be given oxygen, kept in a left lateral position, and kept hydrated to avoid the need for a caesarean section.

Prerenal failure has a serum urea: creatinine ratio of >100, while acute kidney injury has a ratio of 40.
In prerenal failure, ADH levels are typically high, resulting in water, urea, and sodium resorption. The fractional sodium excretion is less than 1%, but it is greater than 2% in acute tubular necrosis.
Prerenal azotaemia has higher serum urea nitrogen/serum creatinine ratios (>20), whereas acute tubular necrosis has lower ratios (10-15). The normal range is between 12 and 20.
Urinary sodium is less than 20 in prerenal failure and greater than 40 in acute tubular necrosis.
Prerenal failure has a urine osmolality of >500, while acute tubular necrosis has an osmolality of 350.
Prerenal failure has a urine/serum creatinine ratio of >40, while acute tubular necrosis has a urine/serum creatinine ratio of 20.

The concentrations of serum urea or creatinine change in inverse proportion to glomerular filtration. Changes in serum creatinine concentrations are more reliable than changes in serum urea concentrations in predicting GFR. Creatinine is produced at a constant rate from creatine, and blood concentrations are almost entirely determined by GFR.

A number of factors influence urea formation, including liver function, protein intake, and protein catabolism rate. Urea excretion is also influenced by hydration status, the amount of water reabsorption, and GFR.

A high serum creatinine level, as well as a urine output of less than 10 mL/hour and the production of concentrated looking urine, do not necessarily indicate a specific cause of oliguria.

This may be the classical case of blood transfusion reaction due to ABO incompatibility.

Here red cells are destroyed in the bloodstream with the release of haemoglobin in circulation (causing haemoglobinuria). Here, IgM or IgG anti-A or anti-B antibody can cause rapid activation of complement cascade usually the classical pathway. This is called intravascular haemolysis.

There may be extravascular haemolysis by cells of the mononuclear phagocyte system situated in the liver and spleen. Extravascular red cell destruction can increase breakdown products of haemoglobin, such as bilirubin and urobilinogen.

Her symptoms are suggestive of trigeminal neuralgia which is a short, sudden, severe sharp unilateral pain in the facial region. The pain often follows the sensory distribution of the trigeminal nerve (CN V).

The trigeminal nerve gives rise to 3 sensory and 1 motor nuclei. Neuralgia can arise from any of the 3 sensory divisions.

The ophthalmic division gives rise to 3 further sensory branches, which are the frontal, lacrimal and nasociliary.

The frontal branch of the ophthalmic division of the trigeminal nerve is responsible for the innervation of the area in question.

The superior alveolar dental, zygomatic and sphenopalatine nerves are all branches arising from the maxillary division of the trigeminal nerve.

The mandibular division of the trigeminal nerve provides sensory and motor innervation. The sensory innervation is carried out by the auriculotemporal nerve which supplies the lower third of the face, while the motor fibres are responsible for controlling the muscles of mastication.

The somatic sensory branches of the vagus nerve are responsible for sensory innervation of the external acoustic meatus and tympanic membrane.

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 (I−) 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.

The posterior pituitary is made up mostly of neural tissue. It is responsible for the storage and release of 2 hormones:
– antidiuretic hormone (ADH)
– oxytocin.

These two hormones are synthesised in the supraoptic and paraventricular nuclei of the hypothalamus.

Every surgical procedure is associated with a stress response which comprises a number of endocrine, metabolic, and immunological changes triggered by neuronal activation of the hypothalamic-pituitary-adrenal axis. The overall metabolic effect of the stress response to surgery includes an increase in secretion of catabolic hormones, such as cortisol and catecholamine, and a decrease in secretion of anabolic hormones, such as insulin and testosterone. The increase in levels of catabolic hormones in plasma stimulates glucose production, and there is a relative lack of insulin together with impaired tissue insulin sensitivity and glucose utilization, which is called insulin resistance. Consequently, blood glucose concentrations will increase, even in the absence of pre-existing diabetes.

A study compared the effects of spinal and general anaesthesia on changes in blood glucose concentrations during surgery in nondiabetic patients. Although mean blood glucose concentrations showed a significant proportional increase during surgery in both groups, this effect was much more significant with general anaesthesia than with spinal anaesthesia. These results indicate that spinal anaesthesia is more effective than general anaesthesia in attenuating the hyperglycaemic response to surgery.

The hormone parathyroid hormone (PTH) and the receptor parathyroid hormone type 1 (PTH1-Rc) are important regulators of blood calcium homeostasis.

PTH can cause a rapid release of calcium from the matrix in bone, but it also affects long-term calcium metabolism by acting directly on bone-forming osteoblasts (by binding to PTH1-Rc) and indirectly on bone-resorbing osteoclasts.

PTH causes changes in the synthesis and/or activity of several proteins, including osteoclast-differentiating factor, also known as TRANCE or RANKL, when it acts on osteoblasts.

RANK receptors are found on the cell surfaces of osteoclast precursors. The osteoclasts are activated when RANKL binds to the RANK receptors. Osteoclasts lack PTH receptors, whereas osteoblasts do. Osteoclasts are activated indirectly when the RANK receptor binds to the RANKL secreted by osteoblasts, resulting in bone resorption. PTH1 receptors are found in osteoclasts, but they are few.

PTH activates G-protein coupled receptors in all target cells via adenylate cyclase.

The PTH2 receptor is most abundant in the nervous system and pancreas, but it is not a calcium metabolism regulator. It is abundant in the septum, midline thalamic nuclei, several hypothalamic nuclei, and the dorsal horn of the spinal cord, as well as the cerebral cortex and basal ganglia. Expression in pancreatic islet somatostatin cells is the most prominent on the periphery.

The distribution of the receptor is being used to test functional hypotheses. It may play a role in pain modulation and hypothalamic releasing-factor secretion control.

The patellar (knee jerk) reflex is a monosynaptic stretch reflex arising from L2-L4 nerve roots. It occurs after a tap on the patellar tendon which causes the spindles of the quadriceps muscles to stretch.

The afferent nerve pathway occurred through A gamma fibres.

Wesphal’s sign refers to a reduction, or absence of the patellar reflex. It is often indicated of a neurological disease affecting the PNS.

A transection of the spinal cord results in a degree of shock which causes all reflexes to be reduced or completely absent, and required a period of approximately 6 weeks to recover.

Glutamic acid decarboxylase is responsible for the catalyses of glutamate to gamma-aminobutyric acid (GABA)

Catechol-o-methyl transferase catalyses the degradation and inactivation of dopamine into 3-methoxytyramine, epinephrine into metanephrine, and norepinephrine into normetanephrine and vanylmethylmandelic acid (VMA).

Monoamine oxidase catalyses the oxidation of norepinephrine to vanylmethylmandelic acid (VMA) and serotonin to 5-hydeoxyindole acetic acid (5-HIAA).

Cholinesterase functions to catalyse the split of acetylcholine into choline and acetic acid.

Two mechanisms are responsible for autoregulation of RBF and GFR: one mechanism that responds to changes in arterial pressure and another that responds to changes in [NaCl] in tubular fluid. Both regulate the tone of the afferent arteriole. The pressure-sensitive mechanism, the so-called myogenic mechanism, is related to an intrinsic property of vascular smooth muscle: the tendency to contract when stretched. Accordingly, when arterial pressure rises and the renal afferent arteriole is stretched, the smooth muscle contracts in response. Because the increase in resistance of the arteriole offsets the increase in pressure, RBF, and therefore GFR, remains constant.

The second mechanism responsible for autoregulation of GFR and RBF is the [NaCl]-dependent mechanism known as tubuloglomerular feedback. This mechanism involves a feedback loop in which a change in GFR leads to alteration in the concentration of NaCl in tubular fluid, which is sensed by the macula densa of the juxtaglomerular apparatus and converted into signals that affect afferent arteriolar resistance and thus the GFR (Fig. 33.19). For example, when the GFR increases and causes [NaCl] in tubular fluid in the loop of Henle to rise, more NaCl enters the macula densa cells in this segment (Fig. 33.20). This leads to an increase in formation and release of adenosine triphosphate (ATP) and adenosine (a metabolite of ATP) by macula densa cells, which causes vasoconstriction of the afferent arteriole and normalization of GFR. In contrast, when GFR and [NaCl] in tubule fluid decrease, less NaCl enters the macula densa cells, and both ATP and adenosine production and release decline. The fall in [ATP] and [adenosine] results in afferent arteriolar vasodilation, which returns GFR to normal. NO, a vasodilator produced by the macula densa, attenuates tubuloglomerular feedback, whereas angiotensin II enhances tubuloglomerular feedback. Thus the macula densa may release both vasoconstrictors (e.g., ATP and adenosine) and a vasodilator (e.g., NO) that oppose each other’s action at the level of the afferent arteriole. Production plus release of either vasoconstrictors or vasodilators ensures exquisite control over tubuloglomerular feedback.

Renal autoregulation, thus, reduces the effect of changes in arterial blood pressure on renal sodium excretion.

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 European Group protocol for the investigation of MH susceptibility, muscle biopsy should be performed on quadriceps muscle (either vastus medialis or vastus lateralis), using regional anaesthesia (avoiding local anaesthetic infiltration) or general anaesthetic techniques. Local anaesthetic solution within muscle fibres may affect in vitro contraction testing.

Desflurane is a weak triggering anaesthetic of malignant hyperthermia so is avoided in MH susceptible patients. This includes all volatile inhalational agents and suxamethonium.

General anaesthetic with the volatile free anaesthetic machine may be considered but spinal anaesthesia is a better choice due to the possibility of airway problems.

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

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

Breathing 100% oxygen for three minutes will provide the best reservoir of oxygen during apnoea by oxygenating the functional residual capacity (FRC).

Sitting at 45 degrees might increase the FRC and improve oxygen reserve but not compared with 100% oxygenation.

The following table compares the oxygen reserves in the body following pre-oxygenation with room air and 100% oxygen:

Compartment Factors Room air (mL) 100% O2 (mL)
Lung FAO2, FRC 630 2850
Plasma PaO2, DF, PV 7 45
Red blood cells Hb, TGV, SaO2 788 805
Myoglobin – 200 200
Interstitial space – 25 160

FAO2 = alveolar fraction of oxygen.
FRC = Functional residual capacity.
PaO2 = partial pressure of oxygen dissolved in arterial blood
DF = dissolved form.
PV = plasma volume.
TG = total globular volume .
Hb = haemoglobin concentration.
SaO2 = arterial oxygen saturation

Stopping smoking one month prior to surgery will not be more effective than pre-oxygenation with 100% oxygen though it may reduce postoperative pulmonary complications. Note that both long term and short term abstinence reduces pulse rate and blood pressure thus reducing oxygen consumption and also reduce carboxyhaemoglobin levels.

Blood transfusion will not make a big difference in oxygen reserve, particularly if a blood transfusion is administered within 12-24-hours before surgery.

Heliox (79% helium and 21% oxygen) despite its lower viscosity is unlikely to be more effective than 100% oxygen .

Chest compressions are an essential part of cardiopulmonary resuscitation (CPR) which helps restore spontaneous circulation (ROSC).

Sodium bicarbonate is only prescribed in patients with cardiac arrests as a result of an overdose of tricyclic antidepressants or hyperkalaemia. Its use causes the body to produce more CO2 which causes:

Exacerbation of intracellular acidosis
Negative inotropy to ischaemic myocardium
Increased osmotic load of sodium into failing brain and body
Shift of oxygen dissociation curve to the left.

THAM is often used to treat metabolic acidosis as a result of cardiac bypass surgery and also cardiac arrest, when other standard methods have failed.

Carbicarb (Na2CO3 0.33 molar NaHCO3 0.33 molar) has only mild effects on acidosis. It also causes an increase in arterial CO2 pressure and lactate concentration.

The thyroid gland is a gland shaped like a butterfly which lies at the base of the anterior neck. It controls metabolism using hormone secretion.

Iodine is extremely important for the synthesis of hormones within the thyroid. It is internalised into the thyroid follicular cells via the sodium/iodide symporter (NIS).

The parathyroid glands are found posterior to the thyroid gland, with the recurrent laryngeal nerves running posteromedially.

The expected weight of a normal thyroid gland is about 30 grams.

According to the Safe Anaesthesia Liaison Group, the most important factor to consider the cannula access, and if the patient is properly receiving the total intravenous anaesthesia. The cannula access must be regularly checked for kinks, leaks and disconnections.

Below are the safety precautions and policies to be followed for total intravenous anaesthesia among children and adults:

When administering TIVA, a non-return valve must be used on any intravenous fluid line;
When using equipment, it is essential that clinical staff know its limitations and uses;
Sites of intravenous infusions should be visible so they may be monitored for disconnection, leaks or perivenous infusion into the subcutaneous tissues; and,
Organisations must give preference to clearly labelled intravenous connectors and valves.

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.

Classification of hemorrhagic shock according to Advanced Trauma Life Support is as follows:

– Class I haemorrhage (blood loss up to 15%) in which there is no change in blood pressure, RR, or pulse pressure.

– Class II haemorrhage (15-30% blood volume loss) where there is tachycardia, tachypnoea, and a decrease in pulse pressure.

– Class III haemorrhage (30-40% blood volume loss) where clinical signs of inadequate perfusion, marked tachycardia, tachypnoea, significant changes in mental state, and measurable fall in systolic pressure is seen. It almost always requires a blood transfusion.

– Class IV haemorrhage (> 40% blood volume loss) in which marked tachycardia, significant depression in systolic pressure and very narrow pulse pressure, and markedly depressed mental state with cold and pale skin are seen.

Loss of >50% results in loss of consciousness, pulse, and blood pressure.

The option that is most responsible is the progressive decrease in venous return of blood to the right atrium. The heart rate does not usually change with PEEP so the fall in cardiac output is due to a reduction in left ventricular (LV) stroke volume (SV).

Note that the interventricular septum does shift toward the left and there is an increased pulmonary vascular resistance (PVR) from overdistention of alveolar air sacs that contribute to the reduction in cardiac output. Any increase in PVR will be associated with reduced pulmonary vascular capacitance.

Iron is a necessary micronutrient for proper erythropoietic function, oxidative metabolism, and cellular immune responses. Although dietary iron absorption (1-2 mg/d) is tightly controlled, it is only just balanced by losses.

The adult body contains 35-45 mg/kg iron (about 4-5 g)

Iron can be found in a variety of forms, including haemoglobin, ferritin, haemosiderin, myoglobin, haem enzymes, and transferrin bound proteins.

During normal tissue metabolism, there is production of CO2 (acid) which is then expired by the lungs. If metabolism switches from aerobic to anaerobic due to a lack of oxygen, the tissues are unable to completely oxidise sugars to CO2. As a consequence, the sugars can only be partially oxidised to lactic acid. Since lactic acid cannot be expired by the lungs, it remains in the circulation leading to metabolic acidosis.

Also, normal tissue metabolism leads to the production of some amount of acid from the breakdown of proteins. These acids are excreted from the body by kidney filtration. Renal failure will therefore results in acidosis after several days.

An increased acidosis stimulates the brain’s respiratory centres to increase the respiratory rate. This lowers the CO2 in the blood, leading to a decrease in its acidity. Renal excretion removes the excess acid, resulting in a normal pH, and a reduced PaCO2 and HCO3.

pH PaCO2 (kPa) HCO3
Compensated respiratory acidosis 7.34 7.2 29
Acute respiratory acidosis 7.25 7.3 22
Compensated metabolic acidosis 7.34 3.6 14
Metabolic acidosis 7.21 5.3 15
Metabolic alkalosis 7.51 5.1 30

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

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

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

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.

When using dry soda lime for VOCs, very high amounts of carbon monoxide may be produced, regardless of the inhalational anaesthetic agent used. The carbon monoxide produced is sufficient enough to cause cytotoxic and anaemic hypoxia. To prevent this, soda lime canisters are shaken well to even out the packing of granules. This can help to evenly distribute gas flow for proper CO2 absorption and ventilation.

Compound A is formed when dry soda lime, or soda lime in high temperature, reacts with the inhalational anaesthetic Sevoflurane. Animal studies have shown renal toxicity in rats, but renal adverse effects in humans are yet to be observed.

When monitors are not employed with VOCs, deleterious effects are not for certain. However, monitors not employed with vaporiser inside the circuit (VIC) can lead to significant adverse events.

Standard wire gauge cannulas for intravenous and intraarterial use are available (SWG or G). The SWG is a former imperial unit (which requires metric conversion). The cross sectional area of wires is becoming more popular as a size measurement.

The number of wires that will fit into a standard hole template is referred to as SWG.

This standard sized hole can accommodate 22 thin wires side by side (each wire the diameter of a 22 gauge cannula)
In the same hole, 14 thicker wires would fit (each wire the diameter of a 14 gauge cannula)

While the diameter and thus radius of a parallel sided tube are the most important determinants of fluid flow rate, they are not commonly used to compare cannula sizes.

The circumference of French gauge (FG) catheters (urinary or chest drains) is measured. Sizes of double lumen tracheal tubes are FG. Internal diameter is used to measure single lumen tubes.

The AAGBI and the British Hypertension Society has published guidelines for the measurement of adult blood pressure and management of hypertension before elective surgery.

The objective is to ensure that patients admitted for elective surgery have a known systolic blood pressure below 160 mmHg and diastolic blood pressures below 100 mmHg. The primary health care teams, if possible, should ensure that this is the case and provide evidence to the pre-assessment clinic staff or on admission.

Avoiding cancellation on the day of surgery because of white coat hypertension is a secondary objective.

Patients with blood pressures below 180 mmHg systolic and 110 mmHg diastolic (measured in the preop assessment clinic), who present to pre-operative assessment clinics without documented evidence of primary care blood pressures should proceed to elective surgery.

In this question, the history/assessment does not appear to point to obvious end-organ damage so there is no indication for further investigation for secondary causes of hypertension or an echocardiogram at this point. Further review and treatment at this point is not required.

However, you should write to the patient’s GP and encourage serial blood pressure measurements in the primary health care setting.

The vertebral (spinal) column is the skeletal central axis made up of approximately 33 bones called the vertebrae.

Cervical disc herniations occur when some or all of the nucleus pulposus extends through the annulus fibrosus. The most commonly affected discs are the C5-C6 and C6-C7 discs. Each vertebrae has a corresponding nerve root which arises at a level above it. This means that a hernation of the C5-C6 disc will cause a compression of the C6 nerve root.

The foramen transversarium is a part of the transverse process of each cervical vertebrae, however, the vertebral artery only runs through the C1-C6 foramen transversarium.

The costal facets are the point of joint formation between a rib and a vertebrae. As such, they are only present on the transverse processes of T1-T10.

The lumbar vertebrae do not form a joint with the ribs, nor do they possess a foramina in their transverse process.

Intervertebral discs are thickest in the cervical and lumbar regions of the spinal column. However, there are no discs between C1 and C2.

Pituitary macroadenoma is a benign tumour with growth larger than 10mm (those under 10mm are called microadenoma)

Compression of optic chiasm by pituitary adenoma is responsible for causing visual field defects like bitemporal hemianopia, optic neuropathy.

At rest, the heart has the greatest a-vO2 difference, a high capillary to myocyte ratio, short diffusion distances, and a high mitochondrial density. The flow of blood through the coronary arteries is also tightly controlled. At rest, 70-80 percent of the oxygen available to the cardiac muscle is extracted, increasing to 90 percent during exercise.

The a-vO2 difference indicates the body’s or an individual organ’s ability to extract oxygen from the blood.

CaO2 is influenced by a number of factors, including Hb concentration, PaO2 and pulmonary diffusion capacity.

CvO2 is influenced by a number of factors, including capillary density, regional blood flow, heart, resting skeletal muscle, kidney, intestine and skin.

Oxygen delivery is related to blood flow as most of the oxygen binds to haemoglobin in red blood cells, although a small amount is dissolved in the plasma. Blood flow per 100 g of tissue is greatest in the kidneys.

The following is the oxygen consumption rate of different organs in ml/minute/100g

Hepatoportal = 2.2
Kidney = 6.8
Brain = 3.7
Skin = 0.38
Skeletal muscle = 0.18
Heart = 11

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.

The ventilatory anaerobic threshold (VAT), formerly referred to as the anaerobic threshold, is an index used to estimate exercise capacity. During the initial (aerobic) phase of CPET, which lasts until 50–60% of Vo2max is reached, expired ventilation (VE) increases linearly with Vo2 and reflects aerobically produced CO2 in the muscles. Blood lactate levels do not change substantially during this phase, since muscle lactic acid production is minimal.

During the latter half of exercise, anaerobic metabolism occurs because oxygen supply cannot keep up with the increasing metabolic requirements of exercising muscles. At this time, there is a significant increase in lactic acid production in the muscles and in the blood lactate concentration. The Vo2 at the onset of blood lactate accumulation is called the lactate threshold or the VAT. The VAT is also defined as the point at which minute ventilation increases disproportionately relative to Vo2, a response that is generally seen at 60–70% of Vo2max.

The VAT is a useful measure as work below this level encompasses most daily living activities. The ability to achieve the VAT can help distinguish cardiac and non‐cardiac (pulmonary or musculoskeletal) causes of exercise limitation, since patients who fatigue before reaching VAT are likely to have a non‐cardiac problem.

When VAT is detected, patients with PVo2 of ⩽10 ml/kg/min have a high event rate.

Hydrochloric acid is lost when you vomit for a long time (HCl). As a result, the following can be expected, in varying degrees of severity:

Hypokalaemia
Hypochloraemia
Increased bicarbonate to compensate for chloride loss and metabolic alkalosis

The alkalosis causes potassium to move from the intracellular to the extracellular compartment at first. Long-term vomiting and dehydration cause potassium to be excreted by the kidneys in order to conserve sodium. Dehydration can cause urea and creatinine levels to rise.

The actual base excess is always greater than the standard base excess.

The actual base excess (BE) is a measurement of a base’s contribution to a blood gas picture’s metabolic component. It’s the amount of base that needs to be added to a blood sample to bring the pH back to 7.4 after the respiratory component of a blood gas picture has been corrected (PaCO2 of 40 mmHg or 5.3 kPa). The BE has a normal range of +2 to 2. A large positive BE indicates a severe metabolic alkalosis, while a large negative BE indicates a severe metabolic acidosis. As a result, the actual BE in vitro is unaffected by CO2.

In vivo, however, standard BE is not independent of pCO2 because blood with haemoglobin acts as a better buffer than total ECF.

As a result, it is impossible to tell the difference between compensating for a respiratory disorder and compensating for the presence of a primary metabolic disorder.

The differences between in vitro and in vivo behaviour can be mostly eliminated if the BE is calculated for a haemoglobin concentration of 50 g/L (the ‘effective’ or virtual value of Hb if it was distributed throughout the extracellular space) rather than the actual haemoglobin. Because haemoglobin has a lower buffering capacity, the standard BE is higher than the actual BE. It reflects the BE better in the extracellular space rather than just the intravascular compartment.

Whatever the age, the dead space ratio is 0.3. It’s the dead space (Vd) to tidal volume ratio (Vt).

The glottis is the narrowest point of the upper airway in an adult, while the cricoid ring is the narrowest point in a child.

A child’s airway resistance is much higher than an adult’s. The resistance to airflow increases as the diameter of a paediatric airway shrinks. The radius (r) to the power of 4 is inversely proportional to airway resistance (r4). As a result, paediatric patients are more susceptible to changes in airflow caused by a small reduction in airway diameter, such as caused by oedema.

The compliance of a newborn’s lungs is very low (5 mL/cmH2O), but it gradually improves as lung size and elasticity grow. Lung compliance in an adult is 200 mL/cmH2O.

In children, minute ventilation (mL/kg/minute) is much higher.

Paediatric life support differs from adult life support in that hypoxia is the primary cause of deterioration.

After checking for danger, the child should be given a gentle stimulus (such as holding the head and shaking the arm) and asked, Are you alright? according to current advanced paediatric life support (APLS) guidelines. Safety, Stimulate, Shout is a phrase that is frequently remembered. Any airway assessment should be preceded by these actions.

Although the algorithm includes five rescue breaths, they are performed after the airway assessment.

It is not recommended to ask parents to leave unless they are obstructing the resuscitation. A team member should be with them at all times to explain what is going on and answer any questions they may have.

CPR should not begin until the child has been properly assessed and rescue breaths have been administered.

Nitric oxide is generated from L-arginine by nitric oxide synthase. It is produced in response to haemodynamic stress by the vascular endothelium, and it produces both smooth muscle relaxation and reduced vascular resistance.

Nitric oxide may be inactivated through interaction with other oxygen free radicals, (e.g. oxidised low-density lipoprotein (LDL)).

Nitric oxide causes the production of the second messenger, cyclic guanosine monophosphate (cGMP).

Endotoxins are the lipopolysaccharides found in the outer cell wall of Gram-negative bacteria. They are responsible for providing the structure and stability of the cell wall.

They cannot be destroyed by normal sterilisation as they are heat stable molecules. They require the use of certain sterilant such as superoxide, peroxide and hypochlorite to be neutralised.

They stimulate strong immune responses, but can only be destroyed partially by specific antibodies. Repeat infections occur as memory T cells cannot be formed.

It can cause septicaemia and associated symptoms such as fever, shock, hypotension and nausea.

It activates the alternative complement pathway and the coagulation pathway using secreted cytokines.

It is not involved in botulism as clostridium botulinum, the responsible organism, secretes a neurotoxic exotoxin.

Among the types of muscles, cardiac muscles have the greatest number if mitochondria due to the heart energy requirements.

Approximately 35% of the cardiac muscle volume is due to the mitochondria. While in skeletal and smooth muscles, it comprises 3-8% of the muscle volume.

Type I muscle fibre has a slow contraction velocity, with a red fibre colour, and predominantly uses oxidative phosphorylation to produce a sustained contraction. It contains more mitochondria and myoglobin than type II, and is often used for endurance training.

Type II muscle fibre has a fast contraction velocity, a white fibre colour, and predominantly uses anaerobic glycolysis. It has fewer mitochondria and myoglobin, and is often used for weight or resistance training and sprinting.

Organophosphate poisoning occurs most often due to accidental exposure to toxic amounts of pesticides. Signs and symptoms include diarrhoea, urination, miosis, bradycardia, emesis, lacrimation, lethargy and salivation.

Organophosphates are classified as indirect acting cholinomimetics, and their mode of action involves: (1) the inhibition of acetylcholinesterase (AChE) by forming a stable covalent bond on the active site serine; and, (2) amplification of endogenously release acetylcholine (ACh), hence the clinical manifestation.

There are 4 types of bonds or interactions: ionic, covalent, hydrogen bonds, and van der Waals interactions. Ionic and covalent bonds are strong interactions that require a larger energy input to break apart. When an element donates an electron from its outer shell, a positive ion is formed. The element accepting the electron is now negatively charged. Because positive and negative charges attract, these ions stay together and form an ionic bond. Covalent bonds form when an electron is shared between two elements and are the strongest and most common form of chemical bond in living organisms. Covalent bonds form between the elements that make up the biological molecules in our cells. Unlike ionic bonds, covalent bonds do not dissociate in water.

When polar covalent bonds containing a hydrogen atom form, the hydrogen atom in that bond has a slightly positive charge. This is because the shared electron is pulled more strongly toward the other element and away from the hydrogen nucleus. Because the hydrogen atom is slightly positive, it will be attracted to neighbouring negative partial charges. When this happens, a weak interaction occurs between the slightly positive charge of the hydrogen atom of one molecule and the slightly negative charge of the other molecule. This interaction is called a hydrogen bond.

Magnesium is a very important cation due to its various physiological roles in the body. This includes:
– playing the role of a cofactor in many enzymatic reactions
– influencing hormone receptor binding
– affecting calcium channels
– impact on cardiac, vascular and neural cells

Magnesium sulphate is used as first line in the treatment of eclampsia. Moreover, it has some preventive role in patients with severe pre-eclampsia. All the clinical effects of magnesium are in line with its plasma concentration.

The first sign of magnesium toxicity in obstetric patients is the loss of patellar reflex, which is regularly monitored during treatment. The other options are all late signs of magnesium toxicity.

Whenever there is a doubt, serum magnesium levels should always be monitored.

The table below correlates the effects of increased levels of magnesium on the body:

Plasma Concentration
(mmol/L) Effect
0.7-1.2 Normal
4-8 Decreased deep tendon reflexes, nausea, headache, weakness, malaise, lethargy and facial flushing
5-10 ECG changes (prolonged PR, prolonged QT, and widened QRS)
10 Muscle weakness, loss of deep tendon reflexes, hypotension
15 SA/AV nodal block, respiratory paralysis and depression
20 Cardiac arrest

Tonic-clonic (Grand mal) epilepsy is characterised by a general loss of consciousness with violent involuntary muscle contractions.

The NICE guidelines for treatment indicates the use of sodium valproate and lamotrigine, but sodium valproate unsuitable in this case and she is a woman of reproductive age and it is known to have teratogenic effects. Lamotrigine is a more suitable choice, prescribed as 800mg daily.

NICE guidelines also advice an additional prescription of 5mg of folic acid daily for women on anticonvulsant therapy looking to get pregnant. It also warns of the need for extra contraceptive precaution as there is a possibly that the anticonvulsant agent can reduce levels of contraceptive agents.

Stimulation of the vagal nerve stimulation is only necessary in patients who are refractory to medical treatment and not candidates for surgical resection.

The trochlear nerve (CN IV) is the fourth and smallest cranial nerve. It’s role is to provide somatic motor innervation of the superior oblique muscle which is responsible for oculomotion.

Injury to the trochlear nerve will result in vertical diplopia, which worsens when looking downwards or inwards. This diplopia presents as an upward deviation of the eye with a head tilt away from the site of the lesion.

The abducens nerve (CN VI) provides somatic motor innervation for the lateral rectus muscle which functions to abduct the eye. Injury to this nerve will cause diplopia and an inability to abduct the eye, causing the patient to have to rotate their head to look sideways.

The facial nerve (CN VII) provides sensory, motor and parasympathetic innervations. It’s motor aspect controls the muscles of facial expression. Damage will cause paralysis of facial expression.

The oculomotor nerve (CN III) provides motor and parasympathetic innervations. Its motor component controls most of the other extraocular muscles. Damage to it will result in ptosis, dilatation of the pupil and a down and out eye position.

The ophthalmic division of the trigeminal nerve (CN VI) is responsible for sensory innervation of skin, mucous membranes and sinuses of the upper face and scalp.

Automated blood gas analysers are commonly used to analyse blood gas samples, and they measure specific components of the arterial blood gas sample, whether directly or indirectly.

The following are the components of arterial blood gas:

pH = measured (directly determined) acid-base balance of the blood

PaO2 = measured partial pressure of oxygen in arterial blood

PaCO2 = measured partial pressure of carbon dioxide in arterial blood

HCO3 = calculated (indirectly determined) concentration of bicarbonate in arterial blood

Base excess/deficit = calculated relative excess or deficit of base in arterial blood

SaO2 = calculated arterial oxygen saturation unless a co-oximetry is obtained, in which case it is measured

Type I – immediate hypersensitivity reaction

Examples are: Atopy, urticaria, Anaphylaxis, Asthma( IgE mediated).

Type II – Antibody mediated cytotoxic reaction

Examples are: Autoimmune haemolytic anaemia, Thrombocytopenia( IgM or IgG mediated).

Type III – Immune complex mediated reaction

Examples are: Serum sickness,SLE – IgG., Farmers lungs, rheumatoid arthritis

Type IV – Delayed hypersensitivity reaction

Examples are: Contact dermatitis, drug allergies.

Type V – Autoimmune

Graves’
Myasthenia – IgM or IgG.

The incidence of vertebral canal haematoma following neuraxial blockade was reported (third National Audit Project (NAP3)) as 0.85 per 100 000 (95% CI 0-1.8 per 100 000). The incidence following neuraxial blockade in coagulopathic patients is likely to be higher hence coagulopathy remains a relative contraindication for conducting a spinal or epidural. When indicate, risk and benefits are weighed, and it is only performed by experienced personnel in this case.

Acceptable time to perform a block after the last dose of rivaroxaban in a patient with a creatinine clearance of greater than 30mL/minute is 18 hours.

Acceptable time to perform a block after the last dose of subcutaneous LMWH as prophylaxis is 12 hours.

Acceptable time to perform a block after the last dose of subcutaneous UFH as prophylaxis is 4 hours.

Acceptable time to perform a block after the last dose of thrombolytic therapy (streptokinase or alteplase) is 10 days.

Clopidogrel should be stopped 7 days prior to surgery, particularly if a central neuraxial procedure is considered.

The volume expired in the first second of maximal expiration after a maximal inspiration is known as forced expiratory volume in one second (FEV1), and it indicates how quickly full lungs can be emptied. It is the most commonly measured parameter for bronchoconstriction assessment.

The maximum volume of air exhaled after a maximal inspiration is known as the ‘slow’ vital capacity (VC). VC is normally equal to FVC after a forced vital capacity (FVC) or slow vital capacity (VC) manoeuvre, unless there is an airflow obstruction, in which case VC is usually higher than FVC.

The FEV1/FVC (Tiffeneau index) is a clinically useful index of airflow restriction that can be used to distinguish between restrictive and obstructive respiratory disorders.

The average expired flow over the middle half (25-75 percent) of the FVC manoeuvre is the forced expiratory volume (FEF25-75). The airflow from the resistance bronchioles corresponds to this. It’s a more sensitive indicator of mild small airway narrowing than FEV1, but it’s difficult to tell if the VC (or FVC) is decreasing or increasing.

The maximum expiratory flow rate achieved is called the peak expiratory flow (PEF), which is usually 8-14 L/second.

The renal effects of atrial natriuretic peptide (ANP) secretion are as follows:

Increased glomerular filtration rate by dilating the afferent glomerular arteriole. Moreover, it constricts the efferent glomerular arteriole, and relaxes the mesangial cells.
Reduces sodium reabsorption in the collecting ducts and distal convoluted tubule.
The renin-angiotensin system (RAS) is inhibited.
Blood flow in the vasa recta is increased.

Because plasma osmolality is unlikely to change, hypothalamic osmoreceptors are unaffected.

The plasma protein has a molecular weight of 66 kDa, is not normally filtered into the proximal convoluted tubule, and has no osmotic diuretic effect.

The following are some basic assumptions:

Extracellular fluid (ECF) makes up one-third of total body water (TBW), while intracellular fluid makes up the other two-thirds (ICF)
One-quarter plasma and three-quarters interstitial fluid make up ECF (ISF)
The volume receptors in the atria have a 7-10% blood volume change threshold.
The osmoreceptors are sensitive to changes in osmolality of 1-2 percent.
The normal plasma osmolality before the transfusion is 287-290 mOsm/kg.
The plasma protein solution is a colloid that is only delivered to the intravascular compartment. The tonicity remains unchanged.
The blood volume increases by 20%, from 5,000 mls to 6,000 mls. This is higher than the volume receptor threshold of 7 to 10%.

Amyl nitrate is part of the treatment of cyanide poisoning. The short acting nitrate causes oxidation of Fe2+ in haemoglobin to Fe3+ in methaemoglobin. Methaemoglobin combines with cyanide (cyanmethemoglobin), which reacts with sodium thiosulfate to convert nontoxic thiocyanate and methaemoglobin.

Methaemoglobin is formed when the iron in haemoglobin is converted from the reduced state (Fe2+) to the oxidized state (Fe3+). The oxidized form of haemoglobin (Fe3+) does not bind oxygen as readily as Fe2+, but has high affinity for cyanide. It also results to high affinity of bound oxygen to haemoglobin, thus leading to tissue hypoxia. Arterial oxygen tension is normal despite observations of cyanosis and dyspnoea. Methemoglobinemia can be treated with methylene blue and vitamin C.

Carboxyhaemoglobin can be due to carbon monoxide poisoning. In such cases, patients experience headache and dizziness, but do not develop cyanosis.

2,3-diphosphoglycerate causes a shift in the oxygen dissociation curve to the right, decreasing haemoglobin’s affinity to oxygen to facilitate unloading of oxygen to the tissues.

After thyroid surgery, about 10-15% of patients experience a temporary subjective voice change of varying degrees. A frog in the throat or cracking of the voice, or a weak voice, are common descriptions. These modifications are only temporary, lasting a few days to a few weeks.

Swelling of the muscles in the area of the dissection, as well as inflammation and oedema of the larynx due to the dissection, or minor trauma from the tracheal tube, are all suspected causes.

On both sides of the thyroid gland, the superior laryngeal nerve (EBSLN) runs along the upper part. The muscles that fine-tune the vocal cords are innervated by these nerves. The quality of their voice is usually normal if they are injured, but making high-pitched sounds may be difficult. Injury to the EBSLN occurs in about 2% of the population.

Injuries to the recurrent laryngeal nerve (RLN) have been reported to occur in 1 percent to 14 percent of people. Except for the cricothyroid muscle, the RLN supplies all of the laryngeal intrinsic muscles.

This complication is usually unilateral and temporary, but it can also be bilateral and permanent, and it can be intentional or unintentional. The most common complication following thyroid surgery is a permanent lesion of damaged RLN, which manifests as an irreversible phonation dysfunction.

The crico-arytenoid joint dislocation is a relatively uncommon complication of tracheal intubation and blunt neck trauma. The probability is less than one in a thousand.

Vocal cord polyps affect 0.8 percent of people.

The cervical plexus is a complex network of nerves within the head and neck region, providing nerve innervation to regions within the head, neck and trunk.

It is comprised of nerves arising from the anterior primary rami of the C1-C4 nerve roots.

The cervical plexus gives off superficial and deep branches. The superficial branches penetrate through the deep fascia at the centre point of the posterior border of the sternocleidomastoid. It provides sensory innervation from the lower border of the mandible to the 2nd rib. The deep branches provide motor innervation to the neck and diaphragmatic muscles.

Cervical plexus block is surgically relevant as it is used to provide regional anaesthesia for procedures in the neck region. The anaesthesia should be injected into the centre point of the posterior border of the sternocleidomastoid. Complications arise when anaesthesia is instead injected into the wrong point, including into the vertebral artery, subarachnoid and epidural spaces, blockade of phrenic and recurrent laryngeal nerves, and the cervical sympathetic plexus.

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.

The respiratory quotient (RQ) is the proportion of CO2 produced by the body to O2 consumed per unit of time.

CO2 produced / O2 consumed = RQ

CO2 is produced at a rate of 200 mL per minute, while O2 is consumed at a rate of 250 mL per minute. An RQ of around 0.8 is typical for a mixed diet.

The RQ will change depending on the energy substrates consumed in the diet.

Granulated sugar is a refined carbohydrate that contains 99.999 percent carbohydrate and no lipids, proteins, minerals, or vitamins.

Glucose and other hexose sugars – RQ = 1
Fats – RQ = 0.7
Proteins – RQ is 0.9
Ethyl alcohol – RQ = 0.67

Selection of a chest drain will depend on the external circumference.

A cannula, whether intravenous or intra-arterial, are classified according to standard wire gauge, which refers to the number of wires that can fit into the same hole. If a cannula is labelled 22G, then 22 wires will fit into the standard size hole.

A more popular measurement than SWG nowadays is cross sectional area.

When the concern for selecting equipment is the rate of flow, then it is important to consider the diameter and the radius of a parallel sided tube. These, however, are not routinely considered when comparing sizes of a cannula.

ICP is significant because it influences cerebral perfusion pressure and cerebral blood flow. The normal ICP ranges from 5 to 13 mmHg.

The components within the skull include the brain (80%/1400 ml), blood (10%/150 ml), and cerebrospinal fluid (CSF) (10%/150 ml).

Because the skull is a rigid box, if one of the three components increases in volume, one or more of the remaining components must decrease in volume to compensate, or the ICP will rise (Monroe-Kellie hypothesis).

Primary brain injury occurs as a result of a head injury and is unavoidable unless precautions are taken to reduce the risk of head injury. A reduction in oxygen delivery due to hypoxemia (low arterial PaO2) or anaemia, a reduction in cerebral blood flow due to hypotension or reduced cardiac output, and factors that cause a raised ICP and reduced CPP are all causes of secondary brain injury. Secondary brain injury can be avoided with proper management.

The most important initial management task is to make certain that:

There is protection of the airway and the cervical spine
There is proper ventilation and oxygenation
Blood pressure and cerebral perfusion pressure are both adequate (CPP).

Following the implementation of these management principles, additional strategies to reduce ICP and preserve cerebral perfusion are required. The volume of one or more of the contents of the skull can be reduced using techniques that can be used to reduce ICP.

Reduce the volume of brain tissue
Blood volume should be reduced.
CSF volume should be reduced.

The following are some methods for reducing the volume of brain tissue:
Abscess removal or tumour resection
Steroids (especially dexamethasone) are used to treat oedema in the brain.
To reduce intracellular volume, use mannitol/furosemide or hypertonic saline.
To increase intracranial volume, a decompressive craniectomy is performed.

The following are some methods for reducing blood volume:

Haematomas must be evacuated.
Barbiturate coma reduces cerebral metabolic rate and oxygen consumption, lowering cerebral blood volume as a result.
Hypoxemia, hypercarbia, hyperthermia, vasodilator drugs, and hypotension should all be avoided in the arterial system.
PEEP/airway obstruction/CVP lines in neck: patient positioning with 30° head up, avoid neck compression with ties/excessive rotation, avoid PEEP/airway obstruction/CVP lines in neck

The following are some methods for reducing CSF volume:

To reduce CSF volume, an external ventricular drain or a ventriculoperitoneal shunt is inserted (although more a long term measure).

The gag reflex is a protective mechanism that prevents any foreign material to enter the aerodigestive tract.

This reflex has afferent (sensory) and effect (motor) components.
– Glossopharyngeal nerve form the afferent limb
– Vagus nerve form the efferent limb

The patient is rebreathing carbon dioxide that has been exhaled.

Exhaustion of the soda lime and failure of the expiratory valve are the two most likely causes. A leak in the inspiratory limb is a less likely cause. Increased inhaled and exhaled carbon dioxide levels may appear with a normal-looking capnogram if the expiratory valve is ineffective.

The patient will exhale into both the inspiratory and expiratory limbs if the inspiratory valve is inoperable. A slanted downstroke inspiratory phase (as the patient inhales carbon dioxide-containing gas from the inspiratory limb) and increased end-tidal carbon dioxide can be seen on the capnogram.

Even if the soda lime were exhausted, a high fresh gas flow would be enough to prevent rebreathing. The difference in oxygen concentrations in inspired and expired breaths would be less pronounced.

Hypercapnia is caused by respiratory obstruction and malignant hyperthermia, but not by rebreathing.