The ions found in higher concentrations intracellularly than outside the cells are:

ATP
AMP
Potassium
Phosphate, and
Magnesium Adenosine diphosphate (ADP)

Sodium is a primarily extracellular ion.

The oxygen consumption rate (VO2) at rest is 3.5 ml/kg/minute (one metabolic equivalent or 1 MET).
3.86 ml/kg/minute thyrotoxicosis

Young children consume a lot of oxygen: around 7 ml/kg/min when they are born. The metabolic cost of breathing is higher in children than in adults, and it can account for up to 15% of total oxygen consumption. Similarly, an infant’s metabolic rate is nearly twice that of an adult, resulting in a larger alveolar minute volume and a lower FRC.

At term, oxygen consumption at rest can increase by as much as 40% (5 ml/kg/minute) and can rise to 60% during labour.

When compared to normal basal metabolism, sepsis syndrome increases VO2 and resting metabolic rate by 30% (4.55 ml/kg/minute). In septicaemic shock, VO2 decreases.

Dobutamine hydrochloride was infused into 12 healthy male volunteers at a rate of 2 micrograms per minute per kilogramme, gradually increasing to 4 and 6 micrograms per minute per kilogramme. Dobutamine was infused for 20 minutes for each dose. VO2 increased by 10% to 15%. (3.85-4.0 ml/kg/min).

The blood brain barrier (BBB) consists of the ultrafiltration barrier in the choroid plexus and the barrier around cerebral capillaries. The barrier is made by endothelial cells which line the interior of all blood vessels. In the capillaries that form the blood–brain barrier, endothelial cells are wedged extremely close to each other, forming so-called tight junctions.

Outside of the BBB lies the hypothalamus, third and fourth ventricles and the chemoreceptor trigger zone (CTZ).

Water, oxygen and carbon dioxide cross the BBB freely but glucose is controlled. The ability of chemicals to cross the barrier is proportional to their lipid solubility, not their water solubility. It’s ability to cross is inversely proportional to their molecular size and charge.

In neonates, the BBB is less effective than in adults. This is why there is increased passage of opioids and bile salts (kernicterus) into the neonatal brain.

In meningitis, the effectiveness and permeability of the BBB is affected, and as a result, this effect helps the passage of antibiotics which would otherwise not normally be able to cross.

The following is the Advanced Trauma Life Support (ATLS) classification of haemorrhagic shock:

Class I haemorrhage:
It has blood loss up to 15%. There is very less tachycardia, and no changes in blood pressure, RR or pulse pressure. Usually, fluid replacement is not required.

Class II haemorrhage:
It has 15-30% blood loss, equivalent to 750 – 1500 ml. There is tachycardia, tachypnoea and a decrease in pulse pressure. Patient may be frightened, hostile and anxious. It can be stabilised by crystalloid and blood transfusion.

Class III haemorrhage:
There is 30-40% blood loss. It portrays inadequate perfusion, marked tachycardia, tachypnoea, altered mental state and fall in systolic pressure. It requires blood transfusion.

Class IV haemorrhage:
There is > 40% blood volume loss. It is a preterminal event, and the patient will die in minutes. It portrays tachycardia, significant depression in systolic pressure and pulse pressure, altered mental state, and cold clammy skin. There is need for rapid transfusion and surgical intervention.

After the carotid body, the thyroid gland is the second most richly vascular organ in the body.

The global blood flow to the thyroid gland can be measured using:
1. Colour ultrasound sonography
2. Quantitative perfusion maps using MRI of the thyroid gland using an arterial spin labelling (ASL) method.

This table shows the blood flow to various organs of the body at rest:
Organ Blood Flow(ml/minute/100g)
Hepatoportal 58
Kidney 420
Brain 54
Skin 13
Skeletal muscle 2.7
Heart 87
Carotid body 2000
Thyroid gland 560

While the brain only weighs 3% of the body weight, 15% of the cardiac output goes towards the brain.

Between mean arterial pressures (MAP) of 60-130 mmHg, autoregulation of cerebral blood flow (CBF) occurs. Exceeding this, the CBF is maintained at a constant level. This is controlled mainly by the PaCO2 level, and the autonomic nervous system has minimal role.

Beyond these limits, the CBF is directly proportional to the MAP, not the systolic blood pressure.

Total body water (TBW) is about 50% to 70% in adults depending on how much fat is present. ECF is relatively contracted in an obese person.

The simple rule is 60-40-20. (60% of weight = total body water, 40% of body weight is ICF and 20% is ECF)

For this woman, the total body water is 36 litres (0.6 × 60). ECF is 12 litres (1/3 of TBW) and 24 litres (2/3 of TBW) is intracellular fluid .

Sodium concentration is approximately 135-145 mmol/L in the ECF.

The ECF is made up of both intravascular and extravascular fluid and plasma proteins is found in both.

When drugs are bound to proteins, drugs cannot cross membranes and exert their effect. Only the free (unbound) drug can be absorbed, distributed, metabolized, excreted and exert pharmacologic effect. Thus, when amide local anaesthetics are bound to ?1-glycoproteins, their duration of action are reduced.

The potency of local anaesthetics are affected by lipid solubility. Solubility influences the concentration of the drug in the extracellular fluid surrounding blood vessels. The brain, which is high in lipid content, will dissolve high concentration of lipid soluble drugs. When drugs are non-ionized and non-polarized, they are more lipid-soluble and undergo more extensive distribution. Hence allowing these drugs to penetrate the membrane of the target cells and exert their effect.

Tissue pKa and pH will determine the degree of ionization.

Changes in the osmolality of body fluids (changes as minor as 1% are sufficient) play the most important role in regulating AVP secretion. The receptors that monitor changes in osmolality of body fluids (termed osmoreceptors) are distinct from the cells that synthesize and secrete AVP, and are located in the organum vasculosum of the lamina terminalis (OVLT) of the hypothalamus. The osmoreceptors sense changes in body osmolality by either shrinking or swelling. When the effective osmolality of the plasma increases, the osmoreceptors send signals to the AVP synthesizing/secreting cells located in the supraoptic and paraventricular nuclei of the hypothalamus, and AVP synthesis and secretion are stimulated. Conversely, when the effective osmolality of the plasma is reduced, secretion is inhibited. Because AVP is rapidly degraded in the plasma, circulating levels can be reduced to zero within minutes after secretion is inhibited.

In this scenario, the osmolality of the plasma will decrease to an estimate of 2.5%, hence inhibition of AVP.

Stimulation of atrial stretch receptors is incorrect because the increase in plasma volume is still below the threshold for its activation.

Osmotic diuresis is incorrect because 5% dextrose is isotonic, hence osmotic diuresis is not probable.

Renin is inhibited when an excess of NaCl in the tubular fluid is sensed by the macula densa.

The pH of CSF is 7.31 which is lower than plasma.

Compared to plasma, it has a lower concentration of potassium, calcium, and protein and a higher concentration of sodium, chloride, bicarbonate and magnesium.

CSF usually has no cells present but if white cells are present, there should be no more than 4/ml.

The pressure of CSF should be less than 20 cm of water.

The concentration of glucose is approximately two-thirds of that of plasma, and it has a concentration of approximately 3.3-4 mmol/L.

The diaphragm has three opening through which different structures pass from the thoracic cavity to the abdominal cavity:

Inferior vena cava passes at the level of T8.

Oesophagus, oesophageal vessels and vagi at T10.

Aorta, thoracic duct and azygous vein through T12.

Sympathetic trunk and pulmonary branches of vagus nerve form a posterior pulmonary plexus at the root of the lung. Fibres continue posteriorly from superficial cardiac plexus to form Anterior pulmonary plexus. It contains vagi nerves and superficial cardiac plexus. These fibres then follow the blood vessel and bronchi into the lungs.

The lower border of the pleura is at the level of:

8th rib in the midclavicular line

10th rib in the lower level of midaxillary line

T12 at its termination.

Both lungs have oblique fissure while right lung has transverse fissure too.

The trachea expands from the lower edge of the cricoid cartilage (at the level of the 6th cervical vertebra) to the carina.

Crystalloids recommended for fluid resuscitation include 0.9% N saline and Hartmann’s solution(a physiological solution). 0.9% N. saline is not a physiological solution for the following reasons:

Compared with the normal range of 98-102 mmol/L, its chloride concentration is high (154 mmol/L)
It lacks calcium, magnesium, glucose and potassium
It does not have bicarbonate or bicarbonate precursor buffer necessary to maintain plasma pH within normal limits

There is a difference in the activity (concentration) of strong ions at a physiological pH. This imbalance can explain abnormalities of acid base balance. A normal strong ion difference (SID) is in the order of 40.

SID = ([Na+] + [K+] + [Ca2+] + [Mg2+]) – ([Cl-] + [lactate] + [SO42-])

This imbalance is made up with the weaker anions to maintain electrical neutrality.
Administration of a large volume of 0.9% normal saline during resuscitation results in excessive chloride administration and this impairs renal bicarbonate reabsorption. The SID of 0.9% normal saline is 0 (Na+ = 154mmol/L and Cl- = 154mmol/L = 154 – 154 = 0). A large volume of NS will decrease the plasma SID causing an acidosis.

Other causes of a hyperchloremic acidosis are:

Diabetic ketoacidosis
Total Parenteral Nutrition
Overdose of ammonium chloride and hydrochloric acid
Gastrointestinal losses of bicarbonate like in diarrhoea and pancreatic fistula
Proximal renal tubular acidosis with failure of bicarbonate reabsorption

An elevated arterial blood lactate level and an increase anion gap ([Na + K] – [Cl + HCO3]) of >20mmol gives rise to lactic acidosis. It can also be a result of overproduction and/or reduced metabolism of lactic acid.

The liver and kidney are the main sites of lactate metabolism, not skeletal muscle.

The two types of lactic acidosis that are known are:

Type A – due to tissue hypoxia, inadequate tissue perfusion and anaerobic glycolysis. These may be seen in cardiac arrest, shock, hypoxaemia and anaemia. The management of type A lactic acidosis involves reversing the underlying cause of the tissue hypoxia.

Type B – occurs in the absence of tissue hypoxia. Some of the causes of this include hepatic failure, renal failure, diabetes mellitus, pancreatitis and infection. Some drugs can also cause this lie aspirin, ethanol, methanol, biguanides and intravenous fructose.

The mainstay of treatment involves:
1. Optimising tissue oxygen delivery
2. Correcting the cause
3. Intravenous sodium bicarbonate

In resistant cases, peritoneal dialysis can be performed.

Sodium concentration for different fluids
3% N saline 513 mmol/L
5% N saline 856 mmol/L
0.9% N saline 154 mmol/L
Hartmann’s solution 131 mmol/L
0.45% N saline with 5% glucose 77 mmol/L

This means that:

500 mL 5% N saline contains 428 mmol of sodium
1000 mL 3% N saline contains 513 mmol of sodium
3500 mL 0.9% N saline contains 539 mmol of sodium
4000 mL Hartmann’s contains 524 mmol of sodium
6000 mL 0.45% N saline with 5% glucose contains 462 mmol of sodium.

These clinical signs suggest that 15-30% of circulating blood volume has been lost.

Pelvic fractures are associated with significant haemorrhage (>2000 ml) that can be concealed. This may require aggressive fluid resuscitation which is initially with crystalloids and then blood. What is also important is including stabilisation of the fracture(s) and pain relief.

The Advanced Trauma Life Support (ATLS) classification of haemorrhagic shock is as follows:

Class I haemorrhage (blood loss up to 15%):
<750 ml of blood loss
Minimal tachycardia
No changes in blood pressure, RR or pulse pressure
Patients do not normally not require fluid replacement as will be restored in 24 hours, but in trauma, this needs to be correct.

Class II haemorrhage (15-30% blood volume loss):
Uncomplicated haemorrhage requiring crystalloid resuscitation
Represents about 750 – 1500 ml of blood loss
Tachycardia, tachypnoea and a decrease in pulse pressure (due to a rise in diastolic component due action of catecholamines).
There are minimal systolic pressure changes.
There may be associated anxiety, fright or hostility

Class III haemorrhage (30-40% blood volume loss):
Complicated haemorrhagic state – crystalloid and probably blood replacement are required
There are classical signs of inadequate perfusion, marked tachycardia, tachypnoea, significant changes in mental state and measurable fall in systolic pressure.
Almost always require blood transfusion, but decision based on patient initial response to fluid resuscitation.

Class IV haemorrhage (> 40% blood volume loss):
Preterminal event patient will die in minutes
Marked tachycardia, significant depression in systolic pressure and very narrow pulse pressure (or unobtainable diastolic pressure)
Mental state is markedly depressed
Skin cold and pale.
Needs rapid transfusion and immediate surgical intervention.

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

Fluid resuscitation following trauma is a controversial area.

This clinical scenario points to a 15-30% blood loss. However, further crystalloid and blood replacement may be required after assessing the clinical situation. There is increasing evidence to suggest that transfusion of large volumes of crystalloid in the hospital setting are likely to be deleterious to the patient and hypotensive resuscitation and judicious blood and blood product resuscitation is a more appropriate option. A ratio of 1 unit of plasma to 1 unit of red blood cells is used to replace fluid volume in adults.

This patient does not require immediate transfusion of O negative blood and there is time for a formal crossmatch. The argument about colloids versus crystalloids has existed for decades. However, while they have a role in fluid resuscitation, they are not first line.

There is a risk of anaphylaxis, Hypernatraemia, and acute renal injury with colloidal solutions.

For this patient, his forced expiratory volume in 1 second (FEV1) will decrease at the same rate as a non-smoker.

There is a notable, but slow, decline in FEV1 when an individual reaches the age of 26. An average reduction of 30 mls every year in non-smokers, while a more significant reduction of 50-70 mls is observed in approximately 20% of smokers.

Considering the age of the patient, individuals who begin smoking cessation by the age of 60 are far less likely to achieve normal FEV1 levels, even in the next five years. It is expected that their FEV1 will be approximately 14% less than their peers of the same age.

The derived unit of energy, work or amount of heat is joule (J). It is defined as the amount of energy expended if a force of one newton (N) is applied through a distance of one metre (N·m)

J = 1 kg·m/s2·m = 1 kg·m2/s2 or 1 kg·m2·s-2

Kinetic energy (KE) = ½ MV2

An object with a mass of 1500 kg moving at 30 m/s correlates to 675 kJ:

KE = ½ (1500) × (30)2 = 750 × 900 = 675 kJ

Total energy released when 1 kg fat is metabolised to CO2 and water is 37 MJ. 1 g fat produces 37 kJ/g, therefore 1 kg fat produces 37,000 × 1000 = 37 MJ.

Raising the temperature of 1 kg water from 0°C to 100°C correlates to 420 kJ. The amount of energy needed to change the temperature of 1 kg of the substance by 1°C is the specific heat capacity. We have 1 kg water therefore:

4,200 J × 100 = 420,000 J = 420 kJ

In order to calculate the energy involved in raising a 100 kg mass to a height of 1 km against gravity, we need to calculate the potential energy (PE) of the mass:

PE = mass × height attained × acceleration due to gravity
PE = 100 kg × 1000 m × 10 m/s2 = 1 MJ

The heat generated when a direct current of 10 amps flows through a heating element for 10 seconds when the potential difference across the element is 1000 volts can be calculated by applying Joule’s law of heating:

Work done (WD) = V (potential difference) × I (current) × t (time)
WD = 10 × 10 × 1000 = 100 kJ

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

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

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

Glycolysis occurs in the cytoplasm of the cell. It converts 1 glucose molecule (6-carbon) to pyruvate (two 3-carbon molecules) and produces 4 ATP molecules and 2NADH but uses 2 ATP in the process with an overall net energy production of 2 ATP.

Pyruvate is then oxidised to acetyl coenzyme A (generating 2 NADH per pyruvate molecule). This takes place in the mitochondria and then enters the Krebs cycle (citric acid cycle). It produces 2 ATP, 8 NADH and 2 FADH2 per glucose molecule.

Electron transport phosphorylation takes place in the mitochondria. The aim of this process is to break down NADH and FADH2 and also to pump H+ into the outer compartment of the mitochondria. It produces 32 ATP with an overall net production of 36ATP.

In anaerobic respiration which occurs in the cytoplasm, pyruvate is reduced to NAD producing 2 ATP.

Osmolarity refers to the osmotic pressure generated by the dissolved solute molecules in 1 L of solvent. Measurements of osmolarity are temperature dependent because the volume of the solvent varies with temperature. The higher the osmolarity of a solution, the more it attracts water from an opposite compartment.

Osmolarity can be computed using the following formulas:

Osmolarity = Concentration x number of dissociable particles; OR
Plasma osmolarity (Posm) = 2([Na+]) + (glucose in mmol/L) + (BUN in mmol/L)

Posm = 2 (144) + 3.5 + 9.5 = 301 mOsm/L

Suppose there is electrical neutrality, the formula will double the cation activity to account for the anions.

Plasma osmolarity (Posm) = 2([Na+] + [K+]) + (glucose in mmol/L) + (BUN in mmol/L)

Posm = 2 (144 + 6) + 3.5 + 9.5 = 313 mOsm/L

In the neonatal stage, the tongue is usually large and comes to the normal size at the age of 1 year. The vocal cords lie inverse C4 and as it reaches the grown-up position inverse C5/6 by the age of 4 (not 1 year).

Due to the immature cricoid cartilage, the larynx lies more anterior in newborn children. That’s why the cricoid ring is the narrowest part of the paediatric respiratory tract, while in the adults the tightest portion of the respiratory route is vocal cords. The epiglottis is generally expansive and slants at a point of 45 degrees to the laryngeal opening.

The carina is the ridge of the cartilage in the trachea at the level of T2 in newborn (T4 in adults), that separates the openings of right and left main bronchi.

Neonates have a comparatively low number of alveoli and then this number gradually increases to a most extreme by the age of 8 (not 3 years).

Neonates are obligatory nose breathers and any hindrance can cause respiratory issues (e.g., choanal atresia).

The basal metabolic rate (BMR) is the amount of energy required to maintain basic bodily functions in the resting state. The unit is Watt (Joule/second) or calories per unit time.

Indirect calorimetry measures O2 consumption and CO2 production where gases are collected in a canopy which is the gold standard, Douglas bag, face-mask dilution technique or interfaced with a ventilator.

The BMR can be calculated using the Weir formula:

Metabolic rate (kcal per day) = 1.44 (3.94 VO2 + 1.11 VCO2)

The BMR should be measured while lying down and at rest with the following conditions met:

It should follow a 12 -hour fast
No stimulants ingested within a 12-hour period
It should be done in a neutral thermal environment (between 20°C-25°C)

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

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

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

Carbonic anhydrase is an enzyme which contains zinc and can be found in:
1. Erythrocytes
2. Pulmonary endothelium
3. The intestine
4. Pancreas
5. Cardiac muscle and skeletal muscle.

To date, there have been seven isoenzymes identified. Of note, isoenzyme IV is found in the brush border of the proximal convoluted tubule and isoenzyme II is found within the luminal cells.

Acetazolamides a carbonic anhydrase inhibitor and is used as prophylaxis against mountain sickness and in glaucoma management.

Spironolactone is a potassium diuretic and is an aldosterone antagonist.

In situations of poisoning or drug overdose with acid dugs like salicylates and barbiturates, forced alkaline diuresis may be used.

With regards to overdose with alkaline drugs, forced acid diuresis is used.

By changing the pH of the urine, the ionised portion of the drug stays in the urine, and this prevents its diffusion back into the blood. Charged molecules do not readily cross biological membranes.

The process involves the infusion of specific fluids at a rate of about 500ml per hour. This requires monitoring of the central venous pressure, urine output, plasma electrolytes, especially potassium, and blood gas analysis.

The fluid regimen recommended is:
500ml of 1.26% sodium bicarbonate (not 200ml of 8.4%)
500ml of 5% dextrose and
500ml of 0.9% sodium chloride.

The patient in the case has a fluid volume requirement of 30 mL/kg/day. His basic electrolyte requirement per day is:

Sodium at 2 mmol/kg/day x 110 = 220 mmol/day
Potassium at 1 mmol/kg/day x 110 = 110 mmol/day

His energy requirement per day is:

35 kcal/kg/day x 110 kg = 3850 kcal/day

One gram of glucose in fluid can provide approximately 4 kilocalories.

The following are the electrolyte components of the different intravenous fluids:

Fluid Na (mmol/L) K (mmol/L)
0.9% Normal saline (NSS) 154 0
0.45% NSS + 5% dextrose 77 0
0.18% NSS + 4% dextrose 30 0
Hartmann’s 131 5
5% dextrose 0 0

1000 mL of 5% dextrose has 50 g of glucose

Option B is inadequate for his sodium and caloric requirements (30 mmol of Na+ and 560 kcal). It is adequate for his K+ requirement (120 mmol of K+).

Option C is in excess of his Na+ requirement (462 mmol of Na+). Moreover, it does not provide any K+ replacement.

Option D is inadequate for his caloric requirement (600 kcal) and K+ requirement (60 mmol of K+). Moreover it does not provide any Na+ replacement.

Option E is in excess of his Na+ requirement (393 mmol of Na+), and is inadequate for his potassium requirement (15 mmol of K+)

Option A has adequate amounts for his Na+ (231 mmol of Na+) and K+ (120 mmol of K+) requirements. It is inadequate for his caloric requirement (600 kcal).

Body fluid compartments in a 70kg male:
Total volume=42L (60% body weight)
Intracellular fluid compartment (ICF) =28L
Extracellular fluid compartment (ECF) = 14L

ECF comprises:
Intravascular fluid (plasma) = 3L
Extravascular fluid = 11L

Extravascular fluids comprises:
Interstitial fluid = 10.5L
Transcellular fluid = 0.5L

Heme a exists in cytochrome a and heme c in cytochrome c; they are both involved in the process of oxidative phosphorylation. 5′-Aminolevulinic acid synthase (ALA-S) is the regulated enzyme for heme synthesis in the liver and erythroid cells.

There are two forms of ALA Synthase, ALAS1, and ALAS2.

Phosphate is the principal anion of the intracellular fluid, most of which is bound to either lipids or proteins. They dissociate or associate with different compounds, depending on the enzymatic reaction, thus forming a constantly shifting pool.

Calcium and magnesium are also present intracellularly, however in lesser amounts than phosphate.

Sodium is the most abundant extracellular cation, and Chloride and is the most abundant extracellular anion.

This scenario describes rebreathing management.

Changes is exhaustion of the soda lime and a progressive rise in circuit deadspace is the most likely explanation for the capnograph.

It is important that the soda lime canister is inspected for a change in colour of the granules. Initially fresh gas flow should be increased and then if necessary, replace the soda lime granules. Other strategies include changing to another circuit or bypassing the soda lime canister after the fresh gas flow is increased.

Any other causes of increased equipment deadspace should be excluded.

Intraoperative hypercarbia can be caused by:

1. Hypoventilation – Breathing spontaneously; drugs which include anaesthetic agents, opioids, residual neuromuscular blockade, pre-existing respiratory or neuromuscular disease and cerebrovascular accident.
2. Controlled ventilation- circuit leaks, disconnection, miscalculation of patient’s minute volume.
3. Rebreathing – Soda lime exhaustion with circle, inadequate fresh gas flow into Mapleson circuits, increased breathing system deadspace.
4. Endogenous source – Tourniquet release, hypermetabolic states (MH or thyroid storm) and release of vascular clamps.
5. Exogenous source – Absorption of CO2 absorption from the pneumoperitoneum.

CBF is defined as the blood volume that flows per unit mass per unit time in brain tissue and is typically expressed in units of ml blood/100 g tissue/minute. The normal average CBF in adults human is about 50 ml/100 g/min, with lower values in the white matter (,20 ml/100 g/min) and greater values in the gray matter (,80 ml/100 g/min).

Low CBF levels between 30-40 ml/100 g/min may begin to show poor prognostic EEG. EEG findings consistently associated with a poor outcome are isoelectric EEG, low voltage EEG, and burst suppression (specifically burst suppression with identical bursts), as well as the absence of EEG reactivity.

A major source of caloric expenditure and oxygen consumption in the body is work of breathing (WOB) and 70% of this is to overcome elastic forces. The remaining 30% is for flow-resistive work

In a normal patient breathing normally, the total area of hysteresis pressure volume curve represents the flow-resistive WOB.

The area of the expiratory resistive work increases during an asthma attack making the compliance curve larger in area. The larger the area the greater the work required to breathe.

The minimal alveolar concentration (MAC) is the concentration of an inhalation anaesthetic agent in the lung alveoli required to stop a response to the surgical stimulus in 50% of the patient.

Following factors don’t affect the MAC of the inhaled anaesthetic agents:

Gender, acidosis, alkalosis, hypothyroidism, hyperthyroidism, body weight, serum potassium level, and the duration of the anaesthesia.

MAC increase in children, elevated temperature, high metabolic rate, sympathetic increase and chronic alcoholism.

MAC decrease in low temperature, low oxygen level, old age, hypotension (<40 mmHg), depressant drugs e.g. opioids and low level of catecholamines; alpha methyl dopa. Carbon dioxide O2 at the pressure > 120mmHg is being used in anesthetic-Hinkman as an additive effect to decrease MAC, however, increase concentration of CO2 activates the sympathetic system resulting the MAC increases.

A decrease in the functional residual capacity (FRC) is the most important physiologic change to consider for such patients.

FRC is the sum of the expiratory reserve volume and the residual volume. It is the resting volume of the lung, and is an important marker for lung function. During this time, the alveolar pressure is equal to the atmospheric pressure. When morbidly obese individuals lie supine, the FRC decreases by as much as 40% because the abdominal contents push the diaphragm into the thoracic cavity.

Chest wall compliance is expected to reduce because of fat deposition surrounding adjacent structures.

Inspiratory reserve volume (IRV) is expected to increase, and peak expiratory flow is expected to decrease, however the decrease in FRC is more important to consider because of the risk of hypoxia secondary to premature airway closure and ventilation-perfusion mismatch.

1% solution contains 1 g of substance per 100 mL.

A solution of 10% glucose is 10 g/100mL. Therefore 1000 mL of this glucose solution will contain 100 g.

1 g of glucose yields about 4 kcal of energy. One litre of 10% glucose will therefore release approximately 4x100g = 400 kcal of energy.

A solution of 20% fat is 20 g/100mL. Therefore 1000 mL of this fat solution will have 200 g and 500 mL will contain 100 g.

1 g of fat yields approximately 9 kcal. 500 mL of 20% fat therefore has the potential to yield 900 kcal of energy.

The total energy input over this 24 hour period is approximately 400kcal + 900kcal = 1300 kcal.

The following table shows the compartments and their relative oxygen reserve:
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

Oxygen reserves in the body, with room air and after oxygenation.

FAO2-alveolar fraction of oxygen rises to 95% after administration of 100% oxygen (CO2 = 5%)
FRC- Functional residual capacity – (the most important store of oxygen in the body) – 2,500-3,000 mL in medium sized adults
PaO2-partial pressure of oxygen dissolved in arterial blood (80 mmHg breathing room air and 500 mmHg breathing 100% oxygen)
DF -dissolved form (0.3%)
PV-plasma volume (3L)
TG-total globular volume (5L)
Hb-haemoglobin concentration
SaO2-arterial oxygen concentration (98% breathing air and 100% when preoxygenated)

During glycolysis, 2,3-diphosphoglycerate (2,3-DPG) is
created in erythrocytes by the Rapoport-Luebering shunt.

The production of 2,3-DPG increases for several conditions
in the presence of decreased peripheral tissue O2 availability.
Some of these conditions include hypoxaemia, chronic lung
disease anaemia, and congestive heart failure. Thus,
2,3-DPG production is likely an important adaptive mechanism.

High levels of 2,3-DPG cause a shift of the curve to the right.
Low levels of 2,3-DPG cause a shift of the curve to the left,
as seen in states such as septic shock and hypophosphatemia.

Krebs’ cycle (tricarboxylic acid cycle or citric acid cycle) is a sequence of reactions in which acetyl coenzyme A (acetyl-CoA) is metabolised and this results in carbon dioxide and hydrogen atoms production.

This series of reactions occur in the mitochondria of eukaryotic cells, not the cytoplasm. The cycle requires oxygen and so, cannot function under anaerobic conditions.

It is the common pathway for carbohydrate, fat and some amino acids oxidation and is required for high energy phosphate bond formation in adenosine triphosphate (ATP).

When pyruvate enters the mitochondria, it is converted into acetyl-CoA. This represents the formation of a 2 carbon molecule from a 3 carbon molecule. There is loss of one CO2 but formation of one NADH molecule. Acetyl-CoA is condensed with oxaloacetate, the anion of a 4 carbon acid, to form citrate which is a 6 carbon molecule.

Citrate is then converted into isocitrate, alpha-ketoglutarate, succinyl-CoA, succinate, fumarate, malate and finally oxaloacetate.

The only 5 carbon molecule in the cycle is alpha-ketoglutarate.