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.

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

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

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

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

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

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

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

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

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

Vocal cord polyps affect 0.8 percent of people.

The 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.

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.

When the convulsion lasts for five or more than five minutes, or if there are recurrent episodes of convulsions in a 5 minute period without returning to the baseline, it is termed as Status Epilepticus.
The first priority in the patient with seizures is maintaining the airway, breathing, and circulation.

Guideline for the management of Status Epilepticus in children by Advanced Life Support Group is as follow:

Step 1 (Five minutes after the start of seizures):

If intravascular access is available start treatment with lorazepam 0.1 mg/kg IV
If no intravascular access then give buccal midazolam 0.5 mg/kg or rectal diazepam 0.5 mg/kg.

Step 2 (Ten minutes after the start of seizure):

If the convulsions continue then a second dose of benzodiazepine should be given. Senior should be called on-site and phenytoin should be prepared.
No more than two doses or benzodiazepines should be given (including any doses given before arrival at the hospital)
If still no IV access then obtain intraosseous access (IO).

Step 3 (Ten minutes after step 2)

Senior help along with anaesthetic/ICU help should be sought
Phenytoin 20 mg/kg IV over 20 minutes
If the seizure stops before the full dose of phenytoin is given then the infusion should be completed as this provides up to 24 hours of anticonvulsant effect
In children already receiving phenytoin as treatment for epilepsy then an alternative is phenobarbitone 20 mg/kg IV over five minutes
Once the phenytoin is started, senior staff may wish to give rectal paraldehyde 0.4 mg/kg although this is no longer included in the routine algorithm recommended by APLS.

Step 4 (20 minutes after step 3)

If 20 minutes after starting phenytoin the child remains in status epilepticus then rapid sequence induction of anaesthesia with thiopentone and a short acting paralysing agent is needed and the child transferred to paediatric intensive care.

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

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).

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.

A person remaining at high altitudes for days, weeks, or years becomes more and more acclimatized to the low PO2, so it causes fewer deleterious effects on the body.

After acclimatization, it becomes possible for the person to work harder without hypoxic effects or to ascend to still higher altitudes. The principal means by which acclimatization comes about are (1) a great increase in pulmonary ventilation, (2) increased numbers of red blood cells, (3) diffusing capacity of the lungs, (4) increased vascularity of the peripheral tissues, and (5) increased ability of the tissue cells to use oxygen despite low PO2.

The cardiac output often increases as much as 30% immediately after a person ascends to high altitude but then decreases back toward normal over a period of weeks as the blood haematocrit increases, so the amount of oxygen transported to the peripheral body tissues remains about normal.

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.

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

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

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

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

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

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

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%.

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.

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

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

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

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

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

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

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

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

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

The following are some methods for reducing blood volume:

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

The following are some methods for reducing CSF volume:

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

Triiodothyronine (T3) is more potent than thyroxine (T4). It is able to bind to more receptors (90%) compared to T4 (10%), and the onset of action is more immediate (within 12 hours) than T4 (2 days).

Ninety-three percent of thyroid hormones synthesized is T4, and the remaining 7% is T3. The half-life of T3 is shorter (1 day), and its affinity for thyroxine-binding globulin is lower than T4.

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.

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.

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

Taste sensation from the anterior two-thirds of the tongue is carried by chorda tympani, a branch of the facial nerve.

The general somatic sensation of the anterior two-third of the tongue is supplied by the lingual nerve, a branch of the mandibular nerve.

Both general somatic sensation and taste from the posterior third of the tongue are carried by the glossopharyngeal nerve.

All the muscles of the tongue except palatoglossus are supplied by the hypoglossal nerve whereas palatoglossus is supplied by the vagus nerve. (This is because palatoglossus is the only tongue muscle derived from the fourth branchial arch)

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.

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

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

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

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

The umbilical vein closes once the umbilical cord is clamped following birth. This causes a rise in systemic vascular resistance, closing the ductus venosus.

Upon birth, the pulmonary vascular resistance is decreased as the lungs are aerated.

At birth, there is a rise in oxygen tension which causes the corresponding constriction of the ductus arteriosus. This prevents a left to right shunt as it stops aortic blood and blood from the pulmonary artery from mixing. The ventricles do no have an opening connecting them.

The foramen ovale closes soon after birth. It is the septum opening between the left and right atrium.

An adult’s cardiac output is expected to be 5 L/min

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.

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.

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

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

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

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

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

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

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

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

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

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

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

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

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.

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