Detsky’s Modified cardiac risk classification system in patients undergoing non-cardiac surgery:

Age more than 70: 05 points

History of myocardial infarction:

Less than 6 months: 10 points
More than 6 months: 5 points

Angina Pectoris:

Angina with minimal exertion: 10 points

Angina at any level of exertion: 20 points

Pulmonary Oedema:

Within 7 days: 10 points
At any time: 5 points

Suspected aortic valve stenosis with valve area <0.6cm2: 20 points Arrhythmia: Any rhythm other than sinus or sinus with premature atrial complexes (PACs): 5 points More than 5 premature ventricular contractions: 5 points
Emergency Surgery: 10 points
Deficient general medical condition: 5 points

Risk classification:

Grade I: 0-15 points = low risk
Grade II: 15-30 points = moderate risk
Grade III: >30 points = high risk

Normally, at rest vagal influence is dominant producing the heart rate of 60-80 beats per minute even if the intrinsic automaticity of Sinoatrial Node is 100-110 beats per minute.

The transplanted heart has no autonomic nervous supply. So, it will respond to endogenous and exogenous catecholamine. This loss of parasympathetic innervation is responsible for the tachycardia in this patient.

Hypokalaemia can cause myocardial excitability and potential for ventricular ectopic and supraventricular arrhythmias. Hypothyroidism is also unlikely to cause tachycardia in this patient.

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.

When the eye is compressed or the extra-ocular muscles are tractioned, the oculocardiac reflex causes a decrease in heart rate.

The ophthalmic division of the trigeminal nerve provides the afferent limb. This synapses with the vagus nerve’s visceral motor nucleus in the brainstem. The efferent signal is carried by the vagus nerve to the heart, where increased parasympathetic tone reduces sinoatrial node output and slows heart rate.

The most common symptom is sinus bradycardia, but junctional rhythm and asystole can also occur.

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.

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.

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.

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.

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

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

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

There is increased renal calcium excretion with secretion of calcitonin.

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.

Continuous closure of the vocal cords resulting in partial or complete airway obstruction is called Laryngospasm. It is a reflex that helps protect against pulmonary aspiration.

Predisposing factors include: Hyperactive airway disease, Insufficient depth of anaesthesia, Inexperience of the anaesthetist, Airway irritation, Smoking, Shared airway surgery and Paediatric patients

Its primary treatment includes checking for blood or stomach aspirate in the pharynx, removing any triggering stimulation, relieving any possible supra-glottic component to airway obstruction and application of CPAP with 100% oxygen.

In this patient, all the above has been done and the next treatment of choice is the administration of a rapidly acting intravenous anaesthetic agent such as propofol (0.5 mg/kg) in increments as it has been reported to relieve laryngospasm in approximately 75% of cases. Administering suxamethonium to an awake patient would be inappropriate at this stage.

Magnesium and lidocaine are used for prevention rather than acute treatment of laryngospasm. Superior laryngeal nerve blocks have been reported to successfully treat recurrent laryngospasm but it is not the next logical step in index patient.

Trigeminal neuralgia is characterized by excruciating paroxysms of pain in the lips, gums, cheek, or chin and, very rarely, in the distribution of the fifth nerve. The pain seldom lasts more than a few seconds or a minute or two but may be so intense that the patient winces, hence the term tic. The paroxysms, experienced as single jabs or clusters, tend to recur frequently, both day and night, for several weeks at a time. They may occur spontaneously or with movements of affected areas evoked by speaking, chewing, or smiling. Another characteristic feature is the presence of trigger zones, typically on the face, lips, or tongue, that provoke attacks; patients may report that tactile stimuli – e.g., washing the face, brushing the teeth, or exposure to a draft of air – generate excruciating pain. An essential feature of trigeminal neuralgia is that objective signs of sensory loss cannot be demonstrated on examination.

Trigeminal neuralgia is relatively common, with an estimated annual incidence of 4–8 per 100,000 individuals. Middle-aged and elderly persons are affected primarily, and ,60% of cases occur in women. Onset is typically sudden, and bouts tend to persist for weeks or months before remitting spontaneously. Remissions may be long-lasting, but in most patients, the disorder ultimately recurs.

An ESR or CRP is indicated if temporal arteritis is suspected. In typical cases of trigeminal neuralgia, neuroimaging studies are usually unnecessary but may be valuable if MS is a consideration or in assessing overlying vascular lesions in order to plan for decompression surgery.

Approximately 70% of the heart’s ATP requirement is met by cardiac mitochondria through beta-oxidation of fatty acids at rest. The remaining 30% is supplied by glucose.

Amino acids and ketones, in the presence of ketoacidosis, may supply at most 10% of the ATP requirement. And, when in high levels, lactate may also contribute to the ATP requirement of the heart, particularly during moments of high muscular activity.

The ventilation/perfusion ratio varies in different areas of the lung. In an upright individual, although both ventilation and perfusion increase from the apex to the base of the lung, the increase in ventilation is less than the increase in blood flow. As a result, the normal V̇ /Q̇ ratio at the apex of the lung is much greater than 1 (ventilation exceeds perfusion), whereas the V̇ /Q̇ ratio at the base of the lung is much less than 1 (perfusion exceeds ventilation).

There is more volume in the alveoli found in the apices than in the bases of the lungs. This is due to the weight of the lung stretching the apical alveoli to the maximum size. Also, the weight of the lungs pull themselves away from the chest wall, creating a negative intrapleural pressure. These factors, however, do not directly affect the PAO2.

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.

BMR is lower in females than males.

It decreases with increasing age.

There is an increase in BMR with increased muscle (i.e. lean tissue)

BMR is increased in stress and illness. There is also an catabolic state in these conditions.

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

Codeine is easily absorbed from the gastrointestinal tract and converted to morphine and norcodeine in the liver via O- and N-demethylation. Morphine and norcodeine are excreted almost entirely by the kidney, primarily as conjugates with glucuronic acid.

By glucuronidation, phase II metabolism enzyme UDP-glucuronosyl transferase-2B7 converts morphine to morphine-3-glucuronide (M3G) and morphine-6-glucuronide (M6G) (UGT2B7).

Approximately 60% of morphine is converted to M3G, with the remaining 6-10% converted to M6G. M3G is inactive, but M6G is said to be 4 to 650 times more potent on the MOP receptor than morphine.

When codeine is consumed, cytochrome P450 2D6 in the liver converts it to morphine (CYP2D6).

Some people have DNA variations that increase the activity of this enzyme, causing codeine to be converted to morphine more quickly and completely than in others. After taking codeine, these ultra-rapid metabolisers are more likely to have higher than normal levels of morphine in their blood.

Respiratory depression/obstruction can be caused by high levels of morphine and M6G, especially in people who have a history of obstructive sleep apnoea. The estimated number of ultra-rapid metabolisers ranges from 1 to 7 per 100 people, but some ethnic groups may have as many as 28 per 100 people.

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.

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

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.

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.

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.

pH=7.36, PaCO2=8.5kPa, PaO2=7.5kPa, HCO3- = 43mmol/L is the correct answer.

Since the pH is the lower limit of normal, it is compensated despite a raised PaCO2. Retention of bicarbonate ions by the renal system suggests this process is chronic.

pH=7.24, PaCO2=3.5kPa, PaO2=8.5kPa, HCO3- =18mmol/L represents an acute uncompensated metabolic acidosis

The remaining stems are degrees of uncompensated respiratory acidosis and therefore incorrect.

Magnesium is a unique calcium antagonist as it can act on most types of calcium channels in vascular smooth muscle and as such would be expected to decrease intracellular calcium. One major effect of decreased intracellular calcium would be inactivation of calmodulin-dependent myosin light chain kinase activity and decreased contraction, causing arterial relaxation that may subsequently lower peripheral and cerebral vascular resistance, relieve vasospasm, and decrease arterial blood pressure.

The vasodilatory effect of MgSO4 has been investigated in a wide variety of vessels. For example, both in vivo and in vitro animal studies have shown that it is a vasodilator of large conduit arteries such as the aorta, as well as smaller resistance vessels including mesenteric, skeletal muscle, uterine, and cerebral arteries.

The theory of cerebrovascular vasospasm as the aetiology of eclampsia seemed to be reinforced by transcranial Doppler (TCD) studies which suggested that MgSO4 treatment caused dilation in the cerebral circulation as well as in animal studies that used large cerebral arteries.

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.

The ECG changes seen in hypomagnesaemia include:

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

These changes are almost the same as those of hypokalaemia.

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

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

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

A tall T wave is seen in hypermagnesemia.

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.

Pituitary tumours that compress the optic chiasma primarily affect the neurones that decussate at this location. Bitemporal hemianopia is caused by neurones that emerge from the nasal half of the retina and transmit the temporal half of the visual field.

The axons of ganglion cells in the retina form the optic nerve.

It exits the orbit through the optic foramen and projects to the thalamic lateral geniculate body. The optic chiasma forms above the sella turcica as the nasal fibres decussate along the way. The optic radiation travels from the lateral geniculate body to the occipital cortex.

Lesions at various points along this pathway cause the following visual field defects:

Scotoma implies partial retinal or optic nerve damage.
Monocular vision loss occurs when the optic nerve is completely damaged.
Pathology at the optic chiasma causes bitemporal hemianopia.
Cortical blindness with occipital cortex pathology and homonymous hemianopia with lesions compromising the optic radiation.

The most likely diagnosis is a spinal epidural haematoma, a neurological emergency. A full examination must be carried out to determine the nature of the neurological problem before conducting any investigations or imaging.

The effects of spinal anaesthesia should have worn off by this time point, and the severe back pain is a red flag.

The patient will also require an urgent neurological team referral as a spinal epidural haematoma requires immediate evacuation for spinal decompression. Analgesics may be prescribed for pain management.

Heparin would have been fully metabolised and so a reversal is unnecessary.

A spinal epidural haematoma is a pooling of blood in the epidural space, which can cause compression of the spinal cord. Its presenting symptoms are:

Usually begins with severe backpain and percussion tenderness
Cauda equina syndrome
Paralysis of the lower extremities.
If infected, a fever occurs in 66% of cases
Lower limb weakness developing after stopping an epidural infusion or weakness of the lower limbs which does not resolve within four hours of cessation of infusion of epidural local anaesthetic
Meningism.