The most important determinant of preoxygenation adequacy is expired fraction of oxygen. Denitrogenating of the functional residual capacity is the purpose of preoxygenation. This is dependent on three vital factors: (1) respiratory rate; (2) inspired volume, and; (3) inspired oxygen concentration (FiO2).

Arterial oxygen saturation does not efficiently determine adequacy of preoxygenation because of its inability to measure tissue reserves. Arterial partial pressure of oxygen is also unsuitable for determining preoxygenation adequacy. Moreover, the absence of central cyanosis is a very crude sign of low tissue oxygenation.

Pupil size is reduced by the pupillary light reflex and during accommodation for near vision. In the pupillary light reflex, light that strikes the retina is processed by retinal circuits that excite W-type retinal ganglion cells. These cells respond to diffuse illumination. The axons of some of the W-type cells project through the optic nerve and tract to the pretectal area, where they synapse in the olivary pretectal nucleus. This nucleus contains neurons that also respond to diffuse illumination. Activity of neurons of the olivary pretectal nucleus causes pupillary constriction by means of bilateral connections with parasympathetic preganglionic neurons in the Edinger-Westphal nuclei. The reflex results in contraction of the pupillary sphincter muscles in both eyes, even when light is shone into only one eye.

The pituitary gland plays a crucial role in the neuro-endocrine axis. It is located at the base of the skull in the sella turcica of the sphenoid bone. It is connected superiorly to the hypothalamus, third ventricle, and visual pathways, and laterally to the cavernous sinuses, internal carotid arteries, and cranial nerves III, IV, V, and VI.

Pituitary tumours make up about 10-15% of all intracranial tumours. The majority of adenomas are benign. Over-secretion of pituitary hormones (most commonly prolactin, growth hormone, or ACTH), under-secretion of hormones, or localised or generalised pressure effects can all cause symptoms.

Compression of the optic chiasm can result in visual field defects, the most common of which is bitemporal hemianopia. This is caused by compression of the nasal retinal fibres, which carry visual impulses from temporal vision across the optic chiasm to the contralateral sides before continuing to the optic tracts.

The interruption of the visual pathways distal to the optic chiasm causes a homonymous visual field defect. The loss of the right or left halves of each eye’s visual field is referred to as homonymous hemianopia. It’s usually caused by a middle or posterior cerebral artery territory stroke that affects the occipital lobe’s optic radiation or visual cortex.

Binasal hemianopia is a condition in which vision is lost in the inner half of both eyes (nasal or medial). It’s caused by compression of the temporal visual pathways, which don’t cross at the optic chiasm and instead continue to the ipsilateral optic tracts. Binasal hemianopia is a rare complication caused by the internal carotid artery impinging on the temporal (lateral) visual fibres.

A monocular visual loss (that is, loss of vision in only one eye) can be caused by a variety of factors, but if caused by nerve damage, the damage would be proximal to the optic chiasm on the ipsilateral side.

A central scotoma is another name for central visual field loss. Every normal mammalian eye has a scotoma, also known as a blind spot, in its field of vision. The optic disc is a region of the retina that lacks photoreceptor cells and is where the retinal ganglion cell axons that make up the optic nerve exit the retina. When both eyes are open, visual signals that are absent in one eye’s blind spot are provided for the other eye by the opposite visual cortex, even if the other eye is closed.

Scotomata can be caused by a variety of factors, including demyelinating disease such as multiple sclerosis, damage to nerve fibre layer in the retina, methyl alcohol, ethambutol, quinine, nutritional deficiencies, and vascular blockages either in the retina or in the optic nerve.

Bilateral scotoma can occur when a pituitary tumour compresses the optic chiasm, causing a bitemporal paracentral scotoma, which then spreads out to the periphery, causing bitemporal hemianopsia. A central scotoma in a pregnant woman could be a sign of severe pre-eclampsia.

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

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

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

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

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

The axillary nerve arises from spinal roots C5-C6. It has both sensory and motor functions:

Sensory: Provides innervation to the skin over the lower deltoid area

Motor: Provides innervation to the teres minor (responsible for stabilisation of glenohumeral joint and external rotation of shoulder joint) and deltoid muscles (responsible for abduction of arms glenohumeral joint).

Injury to the axillary nerve will result in the patient being unable to abduct the arm beyond 15 degrees and a loss of sensory feeling over lower deltoid area.

These symptoms could also be a result of over-abduction of the arm (>90°) which would cause the head of the humerus to become dislocated.

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.

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 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.

Acute pulmonary embolism occurs when a blood clot becomes embedded in a pulmonary artery and restricts lung blood flow.

Thrombolysis is recommended in patients with extremely compromised circulation rather than reduced oxygen in the blood. It is effective when administered via a peripheral vein or a pulmonary artery catheter.

Anticoagulant therapy (heparin use) decreases the risk of further embolic evens and decreases constriction of pulmonary vessels.

An ECG may be normal in patients with an acute pulmonary embolism.

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.

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.

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%.

The blood alcohol concentration depends on:

-The rate of alcohol absorption from the gastrointestinal tract
-The volume of distribution of alcohol in the body, and
-The rate of elimination of alcohol from the body.

Total body water is approximately 50% in a female as compared to 60% in a typical male. This means that the volume of distribution of alcohol is lower in female compared with men. This is the principal reason for higher peak in alcohol levels.

About 4% of ingested alcohol is metabolised by the liver accounting for first pass metabolism and 0.4% is metabolised by gastric alcohol dehydrogenase (ADH). The absorbed alcohol is NOT distributed to fat cells but it is distributed throughout the water compartments (plasma, interstitial and intracellular) of the body. Women have very little gastric ADH, which further influences this exaggerated rise.

85-98% of the alcohol is oxidised by the liver to acetaldehyde and then to acetate. The metabolic pathway initially observes first order kinetics and then saturation or zero order kinetics leading to peaks in alcohol levels.

Clearance of ethanol per unit lean body mass is lower in male. The calculated alcohol elimination rate and liver volume per kilogram of lean body mass were 33% and 38% higher in women than in men, respectively.

Available evidence in the literature about the relationship of alcohol metabolism to the phases of the menstrual cycle is conflicting.

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.

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

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.

Bilirubin is formed by metabolizing heme, mostly from haemoglobin in red blood cells.

Bilirubin is conjugated to glucuronic acid in the hepatocytes by the glucuronyl transferase enzyme in order to enable it to become soluble and allow for its secretion across the canalicular membrane and into bile.

The conjugation process is increased by rifampicin and decreased by valproate.

Gilbert’s syndrome is caused by a decrease in glucuronyl transferase in the hepatic system, decreasing the transport of bilirubin into the hepatocyte, causing unconjugated bilirubinaemia.

Crigler-Najjer syndrome is caused by mutations in the genes responsible for hepatic glucuronyl transferase, decreasing the activity of the enzyme, meaning bilirubin cannot be conjugated, causing unconjugated bilirubinaemia.

Dubin-Johnson syndrome does not cause an impairment in the conjugation of bilirubin, but it blocks the transport of bilirubin out of the hepatocyte resulting in conjugated bilirubinaemia.

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.

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.

T3 is produced by peripheral de-iodination of T4. It is more active than T4.

TBG, like most binding proteins, is increased in pregnancy. Because of this, measurement of free thyroid hormone concentration is more important than total.

T4 and T3 concentrations are decreased in Illness and starvation.

L-T4 that is the active molecule while D-T4 is inactive.

Platelets are fragments of megakaryocytes and they are encapsulated by membrane.

They have no nucleus but are metabolically active and are able to express membrane receptors and release stored substances when triggered. adenosine diphosphate and serotonin are 2 of its content.

Because they have no nucleus, they are not able to produce new proteins. This is why aspirin and other drugs affect function for their entire lifespan after exposure. Its lifespan is approximately 9-10 days in normal individuals.

Platelets does NOT PRODUCE prostacyclin but are able to produce nitric oxide, prostaglandins and thromboxane.

Decreased platelet concentrations with eclampsia were described as early as 1922 by Stancke. The platelet count is routinely measured in women with any form of gestational hypertension. The frequency and intensity of thrombocytopenia vary and are dependent on the severity and duration of the preeclampsia syndrome and the frequency with which platelet counts are performed.

Overt thrombocytopenia defined by a platelet count < 100,000/microliter - indicates severe disease. In general, the lower the platelet count, the higher the rates of maternal and fetal morbidity and mortality. In most cases, delivery is advisable because thrombocytopenia usually continues to worsen. After delivery, the platelet count may continue to decline for the first day or so. It then usually increases progressively to reach a normal level within 3-5 days. In some instances with HELLP syndrome, the platelet count continues to fall after delivery. If these do not reach a nadir until 48 to 72 hours, then preeclampsia syndrome may be incorrectly attributed to one of the thrombotic microangiopathies. The following are other severe features associated with preeclampsia: Proteinuria: >/= 300 mg/24 hours; or urine protein: creatinine ratio >/= 0.3; or dipstick 1+

Renal insufficiency: serum creatinine > 1.1 mg/dL or doubling of creatinine in the absence of other renal disease

Impaired liver function: two times elevated AST/ALT or unexplained right upper quadrant pain or epigastric pain unresponsive to medications

Pulmonary oedema

Cerebral or visual symptoms: headache, visual disturbances

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.

An acetylcholinesterase inhibitor or anticholinesterase is a chemical that inhibits the cholinesterase enzyme from breaking down acetylcholine (ACh) therefore increasing the level and duration of action of the neurotransmitter acetylcholine(ACh).

ACh stimulates postganglionic receptors to produce the following effects:

Salivation
Lacrimation
Defecation
Micturition
Sweating
Miosis
Bradycardia, and
Bronchospasm.

Since these effects are produced by muscarine, they are referred to as muscarinic effects, and the postganglionic receptors are called muscarine receptors.

SLUD (Salivation, Lacrimation, Urination, Defecation – and emesis) is usually encountered only in cases of drug overdose or exposure to nerve gases. It is a syndrome of pathological effects indicating massive discharge of the parasympathetic nervous system.

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.

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 hypothalamus is primarily responsible for the regulation of the basal metabolic rate. It releases thyrotropin releasing hormones (TRH) in response to low levels of triiodothyronine (T3) and thyroxine (T4). The TRH acts on the pituitary gland to release thyroid stimulating hormone, which will stimulate the thyroid gland to synthesize more T3 and T4.

Basal metabolic rate refers to the energy expended by an individual in a resting, post-absorptive state. It represents the energy required to carry out normal body functions, such as respiration.

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.

Aldosterone is produced in the zona glomerulosa of the adrenal cortex and acts to increase sodium reabsorption via intracellular mineralocorticoid receptors in the distal tubules and collecting ducts of the nephron.

Its release is stimulated by hypovolaemia, blood loss ,and low plasma sodium and is inhibited by hypertension and increased sodium. It is regulated by the renin-angiotensin system.

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 .

A significant early feature of the metabolic response to trauma and surgery is hyperglycaemia. It is due to an increased glucose production and decreased glucose utilisation bought on by neuroendocrine stimulation. Catecholamines, Growth hormone, ACTH and cortisol, and Glucagon are all increased.

There is also a decreased insulin sensitivity peripherally and an inhibition of insulin production from the beta cells of the pancreas. These changes lead to hyperglycaemia.

The stress response to endoscopic surgery will only be prevented with use of high dose opioids or central neuraxial block at anaesthesia.
To reduce the risk of inducing hyperchloremic acidosis, Ringer’s lactate/acetate or Hartmann’s solution is preferred to 0.9% sodium chloride as routine maintenance fluids.

Though it has been suggested that administration of Hartmann’s solution to patients with type 2 diabetes leads to hyperglycaemia, one Litre of Hartmann’s solution would yield a maximum of 14.5 mmol of glucose. A rapid infusion of this volume would increase the plasma glucose by no more than 1 mmol/L..

Dexamethasone, a glucocorticoid, produces hyperglycaemia by stimulating gluconeogenesis . Glucocorticoids are agonists of intracellular glucocorticoid receptors. Their effects are mainly mediated via altered protein synthesis via gene transcription and so the onset of action is slow. The onset of action of dexamethasone is about one to four hours and therefore would NOT contribute to the hyperglycaemia in this patient in the time given.

0.9% Normal saline with or without adrenaline is the usual irrigation fluid. With this type of surgery, systemic absorption is unlikely to occur.

Fentanyl is not likely the primary cause of hyperglycaemia in this patient. In high doses (50 mcg/Kg) it has been shown to reduce the hyperglycaemic responses to surgery.

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.

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

Epinephrine is used for the treatment of cardiac arrest because it causes vasoconstriction via the alpha-adrenergic (?1) receptor. This vasoconstriction increases cerebral and coronary blood flow by increasing mean arterial, aortic diastolic, and cerebral pressures. Furthermore, epinephrine is also a?1 and ?2 adrenoreceptor agonist which shows inotrope, chronotrope, and bronchodilator effects.
– Adrenaline is also used to prolong the duration of action and decrease the systemic toxicity of local anaesthetics.
– Preferred route of adrenaline in patients with cardiac arrest is i.v. followed by intra-osseous and endotracheal

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.

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).

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.

Central cord syndrome is the most commonly occurring type of partial spinal cord lesion. It is more likely to occur in older patients with cervical spondylosis and a hyperextension injury. The injury to the spinal cord occurs in the grey matter causing the following symptoms:

Disproportionally higher motor function weakness in the upper limbs than in lower limbs
Dysfunction of the bladder
Degrees of sensory loss below the level of the lesion

An anterior spinal artery infarction will interrupt the corticospinal tract resulting in paralysis of motor function, loss of pain and temperature sensation, all occurring below the level of the injury.

Brown-Sequard syndrome occurs as a result of the hemisection of the spinal cord. Its symptoms include ipsilateral upper motor neurone paralysis and loss of proprioception, with contralateral loss of pain and temperature sensation.

Spinal cord infarctions rarely occur in the posterior spinal artery.

Cauda equina syndrome occurs as a result of compression of the lumbosacral spinal nerve roots below the level of the conus medullaris. Injury to these nerves will cause partial or complete loss of movement and sensation in this distribution.

This sudden change in pulse rate is due to the oculocardiac reflex. It is a >20% reduction in pulse rate as a result of placing pressure directly on the eyeball. The reflex arc has an afferent and efferent arm:

The afferent (sensory) arm: The trigeminal nerve (CN V)

The efferent arm: The vagus nerve (CN X)

The most appropriate action is to ask the surgeon to stop retraction of the extraocular muscles, Assess for hypoxia, and give 100% oxygen if indicated.

Atropine of glycopyrrolate can be administered to counteract the reflex, and also prevent any further vagal reflexes.

Administration of fentanyl may increase patient’s risk of bradycardia and sinus arrest in this case.

Adrenaline is not indicated here as other treatment options will provide sufficient relief from arrhythmia.

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.

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 common peroneal (fibular) nerve is a peripheral nerve in the lower limb. It arises of the L4-S2 nerve roots and has sensory and motor innervations:

Sensory: Provides innervation of the lateral leg and foot dorsum.

Motor: Provides innervation of the short head of the biceps femoris, as well as muscles of the anterior and lateral leg compartments.

It is the most commonly damaged nerve in the lower extremity, as it is easily compressed by a plaster cast or injured when the fibula is fractured.

Damage to the common peroneal nerve will result in loss of dorsiflexion at ankle (footdrop, as feet are permanently plantarflexed), with the accompanying high stepping gait.

The saphenous and sural nerve only provide sensory innervation.

The tibial nerve arises from the sciatic nerve (like the common peroneal), but it provides motor innervation to the posterior leg compartments and intrinsic foot muscles. Injury to the tibial nerve will cause loss of plantar flexion, toe flexion and weakened foot inversion.

Extreme hip flexion into the lithotomy or Lloyd-Davies position can result in stretch damage to the neurones (sciatic and obturator nerves) or by applying direct pressure (femoral nerve compression).

Patients who have sustained thermal injuries are at high risk of becoming hypercatabolic with larger cardiac outputs and oxygen consumptions.

The hypermetabolic states increase with an increase in the burn severity and surface area of the skin affected. A patient with thermal injuries affecting 60% of the total surface area of the body will have twice the normal metabolic rate.

The optimal temperature for nursing patients with burn injuries is 30°C to conserve the energy usage. The areas affected by the burn injuries should be covered to reduce loss of fluid via evaporation. Resetting hypothalamic thermoregulation will cause a 1-2°C increase in core temperature.

Burn injuries will have an immediate effect on the intestine, destroying the barrier function and allowing for the movement of bacteria and endotoxins within hours.

Enteral nutrition allows for the delivery of nutrients directly to the stomach or intestine. It has correlation with a dampened hypermetabolic response to a thermal and injury, especially when initiated early as it helps to protect the integrity of the mucosal lining and prevents the movement of bacteria into circulation.

Diet changes have been linked to reduced mortality due to burn injuries. Diets high in protein especially (calorie: nitrogen ratio of 100: 1), have the highest correlation with improved survival rates.

Parenteral feeds may be required alongside enteral nutrition, even with the increased risks of infection.

The functional residual capacity (FRC) is the volume in the lungs at the end of passive expiration. It is determined by opposing forces of the expanding chest wall and the elastic recoil of the lung. A normal FRC = 1.7 to 3.5 L. It a marker for lung function, and, during this time, the alveolar pressure is equal to the atmospheric pressure.

FRC cannot be measured by spirometry because it contains the residual volume.

Tidal volume, inspiratory reserve volume, forced expiratory volume in 1 second, and vital capacity can be measured directly.

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.

Monosynaptic reflexes is a type of reflex arc providing direct communication between motor and sensory innervation in a muscle. It occurs very quickly as it arises and ends in the same muscle. Examples include: biceps reflex, brachioradialis reflex, extensor digitorum reflex, triceps reflex, Achilles reflex and patellar reflex.

Polysynaptic reflexes facilitates contraction and inhibition in muscle by providing communication between multiple muscles.

Immunoglobulin E (IgE) are an antibody subtype produced by the immune system. They are the least abundant type and function in parasitic infections and allergy responses.

The most predominant type of immunoglobulin is IgG. It is able to be transmitted across the placenta to provide immunity to the foetus.

IgE is involved in the type I hypersensitivity reaction as it stimulates mast cells to release histamine. It has no role in type 2 hypersensitivity.

Its concentration in the serum is normally the least abundant, however certain reactions cause a rise in its concentration, such as atopy, but not in acute asthma.

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 of ECF is plasma, and three-quarters is interstitial fluid (ISF).
The volume receptors have a 7-10% blood volume change threshold. The osmoreceptors are sensitive to changes in osmolality of 1-2 percent.
Prior to the transfusion, the plasma osmolality is normal (between 287 and 290 mOsm/kg).
[Na+] in 0.9 percent N. saline is 154 mmol/L, which is similar to that of extracellular fluid. When given intravenously, this limits its distribution within the extracellular space, resulting in a plasma compartment:ISF volume ratio of 1:3.
In this time frame, one litre of 0.9 percent N. saline will increase plasma volume by about 250 mL, which could be the threshold for activation of the volume receptors in the atria, resulting in the release of atrial natriuretic peptide (ANP).

Because 0.9 percent N. saline is isosmotic, after a 1 L infusion, plasma osmolality will not change. No changes in antidiuretic hormone secretion will be detected by the hypothalamic osmoreceptors.

Because normal saline is protein-free, the oncotic pressure in the blood is slightly reduced after the saline infusion. As a result, fluid movement into the ISF is favoured (Starling’s hypothesis), and the lower oncotic pressure causes an immediate increase in the glomerular filtration rate (GFR) and a reduction in water reabsorption in the proximal tubule.

The flow of urine increases. There is no hormonal intermediary in this effect, so it is strictly local. Urine flow immediately increases. The fluid returns to the intravascular compartment, and urine flow continues until all of the transfused fluid has been excreted.

Blood pressure changes associated with a 1 L fluid infusion are unlikely to affect high-pressure baroreceptors in the carotid sinus.

The juxta-glomerular cells of the afferent arteriole are adjacent to the specialised cells (macula densa) of distal tubules. The sodium and chloride ions in the tubular fluid are detected by the macula densa. Renin release is inhibited when the tubular fluid contains too much sodium chloride. Hormonal changes take longer to manifest than physical changes that control glomerulotubular balance.
Hypertonic saline, not 0.9 percent N saline, is an osmotic diuretic.

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.