Section 6

Question 1

You are on-call on labour ward and are alerted of a pregnant woman who had been admitted earlier that day with complaints of chest pain and breathlessness. She is 23-years-old in her first pregnancy at 32 weeks gestation. She had been seen by the senior Obstetric registrar and has had blood investigations, ECG, and an urgent ECHO. The consultant Obstetrician is on her way from home.
Past medical history She has a background of bicuspid aortic valve disease but had no cardiology follow-up due to social reasons. She gets breathless on moderate exertion
and does only minimal household work.
obstetric history She had seen the community midwife at 12 weeks and was then referred for a consultant-led obstetric clinic due to the ‘heart condition’. The patient
failed to attend further antenatal follow-ups for the fear of being told to terminate the pregnancy.
no significant past surgical history.
on examination:
Looks unsettled and anxious
Heart rate: 95/min
Respiratory rate: 34/min
Blood Pressure: 80/60 mmHg
Blood tests Hb 11.1 g/dL (13–16) Na 138 mmol/L (137–145)
WCC 3.0 × 109/L (4–11) K 4.8 mmol/L (3.6–5.0)
Platelets 242 × 109/L (140–400) Urea 2.5 mmol/L (1.7–8.3)
PCV 0.28 (0.38–0.56) Creat 42 umol/L (62–124)
summarise the case.

Answer 1

○ A high-risk primiparous pregnant woman in her third gestation, admitted with signs of decompensation with a background of underlying aortic valvular heart disease. The problems are:
• Congenital bicuspid aortic valve with severe aortic stenosis with a high gradient between the LV and aorta
• Signs of left ventricular hypertrophy with strain
• Pulmonary hypertension
• Poor social history and medical follow-up

Question 2

Describe the ecG.

Answer 2

LA: dilated
LV: hypertrophied
RA: Normal size and function
RV: Normal size and function
Aortic valve: Thickened, possibility of a bicuspid valve cannot be excluded;
no calcification
Valve area: 0.8 cm2
Peak gradient: 75 mmHg
Mitral valve: Minimal mitral regurgitation
Tricuspid Valve/Pulmonary Valve: Normal
Systolic pulmonary artery pressure: 35 mmHg
Interpretation:
• Voltage criteria for LVH
• Diffuse ST segment and T wave changes, indicating strain

Question 3

What findings can be diagnosed with a Doppler ecHo in a patient with valvular heart disease?

Answer 3

• Chambers—size and function, wall motion abnormalities, presence of thrombus
• Septum—thickening or thinning, motion abnormalities
• Valves—structural anatomy, thickening, number of cusps, calcification, stenosis, or regurgitation
• Measurements—pressures in chambers, aorta and pulmonary vasculature, peak velocity across valves and peak/mean gradients, ejection fraction

Question 4

How does a Doppler ecHo determine the valve area and the gradient?

Answer 4

Gradient:
○ Doppler echocardiography takes advantage of the acceleration of flow across a restrictive orifice based on Doppler shift.
○ Blood flow velocities can be converted to pressure gradients to yield mean and peak gradients according to the Bernoulli equation.
○ The gradient is the difference in pressure between the left ventricle and aorta in systole.
Valve area:
○ There are various ways to determine aortic valve area.
○ The most commonly used is the continuity equation.
○ By law of conservation of mass, flow in one area (i.e. left ventricular outflow
tract, LVoT) should be equal to the flow in the second area (i.e. valve orifice)
provided there are no shunts between the two areas.
○ Flow is derived from the cross-sectional area and the velocity of flow.
Applying the law of conservation of mass
Area of LVoT × Velocity in LVoT = Aortic Valve Area × Velocity at Valve
Aortic Valve Area (A2) = ALVoT (A1) × VLVoT (V1)
Vvalve (V2)

Question 5

is there any difference in the gradient values when measured using Doppler echocardiography and cardiac catheterisation techniques?

Answer 5

○ Doppler measurements overestimate the gradient, due to ‘pressure recovery’ based on fluid mechanics theory.
Explanation:
○ In fluid mechanics, flow equates to kinetic energy and pressure is potential energy.
○ According to the law of conservation of energy, the sum of kinetic and potential energy remains constant.
Kinetic energy (KE) + Potential energy (PE) = Constant
Proximal to stenosis: The blood flow in the left ventricle is such that there is a
higher pressure and lower flow.
Stenosis: As the blood passes through the valve, there is an increase in KE and a decrease in PE. This increased velocity of blood across the stenotic valve accounts for a reduced pressure.
Post stenosis: Distal to the orifice, the flow decelerates again. KE is reconverted into PE with a corresponding increase in static pressure. This increased pressure immediately distal to the orifice due to the reduction of KE is called pressure recovery.
Doppler measures the highest velocity across the stenosis; hence, the
Doppler gradients are markedly greater, whereas catheterisation measures a
more or less recovered pressure at some distance from stenosis.
This pressure recovery depends on:
• Aortic valve area
• Ascending aortic area
• Transvalvular velocity

Question 6

What is aortic stenosis?

Answer 6

Aortic stenosis is a fixed output state, where the narrowing of the aortic valve
impedes delivery of blood from the heart to the aorta.

Question 7

How can you classify aortic
stenosis?

Answer 7

Question 8

What are the symptoms and
signs of aortic stenosis?

Answer 8

The classic triad of symptoms are:
• Angina
• Heart failure: dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea
• Syncope
Also associated with palpitations, hypertension, and oedema
The signs are:
• Slow-rising pulse of decreased amplitude (pulsus parvus et tardus)
• Hypertension
• Absent S2 or paradoxical splitting of S2 due to late closure of aortic valve
• Prominent S4 due to forceful atrial contraction against a hypertrophied
ventricle
• Classic systolic murmur radiating to the carotids

Question 9

What does pregnancy do to maternal physiology that makes valvular diseases an important concern?

Answer 9

Pregnancy is associated with significant haemodynamic changes such as:
• 30%–50% increase in stroke volume and cardiac output
• Increase in heart rate
Normal pregnancy is a volume overloaded state where the valvular
heart diseases mainly severe stenotic lesions are not tolerated. Also, the
symptoms and signs that arise during the course of normal pregnancy are
similar to those reported by patients with cardiac disease; hence the difficulty
in diagnosing deterioration.

Question 10

What are the causes of aortic
stenosis?

Answer 10

• Congenital bicuspid aortic valve
• Rheumatic heart disease leading to mixed valve disease
• Degenerative calcific aortic stenosis

Question 11

Describe the pathophysiology
of aortic stenosis. see
Figure 6.3

Answer 11

Question 12

What other conditions are associated with congenital bicuspid valve?

Answer 12

can occur with other congenital heart diseases but mainly coarctation of aorta (CoA) and VSD

Question 13

What is the concern in coA?

Answer 13

○ Medial thickening and infolding of the intimal tissue of the descending aorta distal to the origin of the left subclavian artery (juxta-ductal position).
○ Also associated with VSD are berry aneurysms in brain and retina, Turner’s syndrome, and other congenital abnormalities.

Question 14

What are the symptoms and csigns of coA?

Answer 14

• Symptoms include headache, chest pain, fatigue and weak legs.
• Signs:
° Hypertension
° Prominent brachial and absent/weak femoral pulses
° Differential cyanosis
° Systolic or continuous murmur in the left infraclavicular and infrascapular areas

Question 15

What are the findings of coA on chest radiograph?

Answer 15

• Cardiomegaly due to LVH
• Signs of pulmonary oedema and failure
• ‘3’ sign (or inverted ‘3’ sign on barium studies)—coarctation with
pre- and post-stenotic dilatation
• Rib notching of the fourth through eighth ribs due to presence of
long-standing dilated intercostal collateral vessels

Question 16

What are the cardiac
conditions where pregnancy is
contraindicated?

Answer 16

Absolute
• Primary pulmonary hypertension
• Secondary pulmonary hypertension—Eisenmenger’s syndrome
• NYHA III/IV patients (New York Heart Association functional classification)
Relative
• Severe aortic and mitral stenosis
• Marfan’s syndrome with significant aortic root dilatation
• Prosthetic valves requiring anticoagulation
• Cyanotic heart diseases

Question 17

How can you risk stratify pregnant patients with cardiac diseases?

Answer 17

The WHo risk stratification seems an excellent model to predict pregnancy
outcome in patients with structural heart disease. With an increasing level
of risk score, more cardiac, obstetric, and neonatal complications were
encountered. A WHo score of 1 indicates low risk, while a WHo score
of 3 indicates a high risk and a WHo score of 4 is a contraindication for
pregnancy.
i: No detectable increased risk in maternal mortality (< 1%) and no/mild
increase in morbidity
• Uncomplicated PS, PDA, or mitral valve prolapse
• Successfully repaired simple lesions (ASD, VSD, TAPVD)
ii: Small increased risk of maternal mortality (5%–15%) and moderate
increase in morbidity
• Unoperated ASD or VSD
• Repaired TOF/COA
• Most arrhythmias
• Marfan’s syndrome without aortic dilatation
iii: Significantly increased risk of maternal mortality (25%–50%) or severe
morbidity
• Expert counseling required. If pregnancy is decided upon, intensive
specialist, cardiac, and obstetric monitoring needed throughout
pregnancy, childbirth, and puerperium.
° Mechanical valve
° Fontan circulation
° Unrepaired cyanotic heart disease
° other complex congenital heart diseases
° Marfan’s syndrome with aortic root dilatation 40–45 mm
iV: Extremely high risk of maternal mortality or severe morbidity
• Pregnancy contraindicated. If pregnancy occurs, termination should
be discussed.
° Pulmonary arterial hypertension of any cause
° Severe systemic ventricular dysfunction (LVEF < 30%, NYHA class
III–IV)
° Severe symptomatic MS and AS
° Marfan’s syndrome with aortic root dilation > 45 mm
° Native severe CoA

Question 18

How would you manage this
patient?

Answer 18

Preconception
• European Society of Cardiology guidelines on ‘Management of
Cardiovascular Disease During Pregnancy’ recommends that patients
with severe aortic stenosis should undergo intervention preconception if
they are symptomatic and have ventricular dysfunction (EF < 50%).
• Careful cardiac exam and assessment of functional capacity to determine
the likelihood of patients to tolerate the haemodynamic changes of
pregnancy.
• Serial echocardiographic assessment to see disease progression.
• Patient education and lifestyle changes.
• Other investigations as needed.
• Medical treatment to optimise functional capacity.
• Aortic valve replacement (AVR) is the definitive treatment, and ideally this
patient should have had an AVR preconception.
Antepartum
• Joint care with cardiology, obstetrics, and anaesthesia in a tertiary care
setup.
• Optimisation of medical therapy (discussed below).
intrapartum
• The timing and mode of delivery are discussed and are dictated by
medical and obstetric condition; vaginal delivery is indicated unless
obstetric indication for caesarean delivery.
• Position: Avoid supine and lithotomy position as they are poorly tolerated.
Nurse the patient in cardiac (legs lower than abdomen) or lateral position.
• Monitoring: Invasive arterial and central venous pressure monitoring
in severe cases. Pulmonary floatation catheter is used in patients with
severe and critical stenosis with symptoms of heart failure.
• Avoid pain and pushing: Sympathetic overactivity causes tachycardia,
and the increased venous return with pushing causes decompensation.
A short assisted second stage is recommended.
• Syntocinon is given as a diluted infusion.
• Auto transfusion is not tolerated; blood loss to some extent is beneficial
as long as venous return is maintained.
Postpartum
• Monitoring is continued until 24–48 hours postpartum.
• Cardiology follow-up for a definitive management

Question 19

Anaesthetic management

Answer 19

The goal is to maintain blood pressure and prevent maternal and foetal
distress, by maintaining preload, heart rate, and afterload.
BP = SV × HR × SVR
• Preload
° Maintain preload by optimal positioning, avoiding aortocaval
compression, and adequate fluid balance.
° Vasodilatation with regional and general anaesthesia can decrease the
venous return, jeopardising the situation.
• Contractility
° Maintain contractility: General anaesthesia causes myocardial
depression whereas regional techniques do not.
• Afterload
° Both general and regional anaesthesia decreases the afterload.
° As long as contractility is maintained, a decrease in SVR is beneficial
as this would aid forward flow. For this reason regional anaesthesia is
a good option as it does not have any effect on cardiac contractility.
• Heart rate
° Slow/normal heart rate is maintained and tachyarrhythmias are
avoided.
° Tachycardia reduces the coronary perfusion as diastolic time is
reduced, and also the preload is highly dependent on the ‘atrial kick’
and arrhythmias obviate this factor.
There is no absolute contraindication for any anaesthetic technique.
Understanding the pathophysiology aids management.
Traditionally GA was advocated for these patients. It should be borne in mind
that most anaesthetic agents cause vasodilatation and it is the conduct of
anaesthesia that is important rather than the specific technique. The safe
use of carefully titrated regional blocks using epidural and spinal catheters is
currently increasing.
Key goals
• Slow/normal heart rate
• Adequate preload
• Preserve contractility
• Maintain afterload
• Treat anaemia and careful fluid management
• Prevent triggers that increase pulmonary vascular resistance—
hypercarbia, hypoxia, acidosis, and pain
• Adequate invasive monitoring
• Transfer to tertiary care with progressive symptoms

Question 20

What medical management can
you offer this patient?

Answer 20

The treatment options are limited. There is no solid evidence that
pathological course of aortic stenosis is prevented with any medical therapy;
rather, it is symptomatic treatment that is considered to ‘buy time’. There
is equivocal evidence regarding the use of statins in preventing disease
progression.
Hypertension
• Vasodilators like ACE inhibitors and Angiotensin Receptor blockers
(ARBs) are well tolerated in mild/moderate aortic stenosis. They are used
in severe aortic stenosis with extreme caution to avoid critically reducing
preload or systemic arterial blood pressure. Be aware of the teratogenic
effects of these drugs.
• β blockers: Used with caution in pulmonary oedema, the prevention of
atrial fibrillation, and prevention of aortic root dilation.
Angina
• Bed rest, oxygen
• β blockers to decrease myocardial oxygen consumption
• Nitrates to dilate coronary vessels
• Prevent reduction of preload and blood pressure
syncope
• If syncope is due to brady/tachy arrhythmias, then pacemaker or
anti-arrhythmic drugs are used.
Pulmonary congestion
• Digoxin
• Diuretics—used with utmost care because they can precipitate
life-threatening haemodynamic compromise in patients who are
preload dependent
• Careful titration of ACE inhibitors and ARBs
This patient is symptomatic with signs of heart failure.
• Cautious use of diuretics and nitrates to treat pulmonary congestion
• Ideally dealt with in tertiary hospital with expert help
• Invasive monitoring—ideally pulmonary artery pressure monitoring
• Careful fluid management
Further deterioration despite optimal medical treatment warrants surgical
intervention.
In cases where patients remain severely symptomatic (in particular, if they
have signs of heart failure), aortic stenosis should be relieved before delivery.
This patient would benefit from a percutaneous balloon aortic valvuloplasty.

Question 21

What are the surgical
interventions in severe aortic
stenosis?

Answer 21

The surgical options are
• Percutaneous Balloon Aortic Valvuloplasty (PBAV)
• Aortic Valve Replacement (AVR)
• Transcatheter Aortic Valve Implantation (TAVI)
PBAV is ideal in this patient because it precludes the need for an open
bypass surgery in pregnancy and TAVI is done only in specialist centres.
This patient then comes in with a successful pregnancy 3 years later having
had a mechanical prosthetic valve after her first pregnancy.

Question 22

What is the risk of prosthetic
valve thrombosis in this patient?

Answer 22

Prosthetic valve thrombosis is a potentially devastating complication with an
incidence of 0.7%–6% per patient per year. The risk is higher in this patient
because of:
• Presence of mechanical, rather than biological, prosthetic valve
• Hypercoagulable state of pregnancy
• Chance of interruption of anticoagulation in pregnancy

Question 23

How could her anticoagulation
be managed during pregnancy?

Answer 23

Risk of valve thrombosis due to inadequate anticoagulation is weighed
against the risk of direct harm due to the teratogenic drugs on the fetus.
Warfarin
• Good for mother
• Bad for fetus as it crosses placenta and causes fetal embryopathy—nasal
cartilage hypoplasia, brachydactyly, IUGR—when administered between
6 and 12 weeks of gestation.
Heparin – unfractionated (UFH) or low molecular weight heparin
(LMWH)
• Good for foetus
• Bad for mother due to increase in the risk of valve thrombosis.
Three treatment choices according to the current recommendations are
suggested.
1. Treatment dose: subcutaneous UFH throughout pregnancy.
2. Treatment dose: subcutaneous LMWH throughout pregnancy.
3. UFH/LMWH until 13 weeks followed by warfarin. UFH/LMWH restarted at
36 weeks of gestation.
Monitoring anticoagulation with appropriate tests is important in pregnancy,
especially in high-risk patients with renal impairment.

Question 24

You are asked to see a 70-year-old man with a hoarse voice who is
booked for an elective micro laryngoscopy and excision of vocal cord lesion.
What are the causes of a hoarse
voice?

Answer 24

• Vocal cord pathology—paralysis, nodules, etc.
• Extrinsic airway compression
• Nerve lesions
• Functional dysphonia
• Laryngeal papilloma
• Reflux laryngitis
• Laryngeal carcinoma

Question 25

What is the nerve supply of the
larynx?

Answer 25

Motor and sensory supply is by branches of the Vagus nerve.
Motor
• Recurrent laryngeal nerve supplies all muscles except cricothyroid.
• External laryngeal nerve supplies cricothyroid muscle.
sensory
• Recurrent laryngeal nerve: sensation below vocal cords
• Internal laryngeal nerve: sensation above the vocal cords

Question 26

What are the effects of laryngeal
nerve damage?

Answer 26

Partial recurrent laryngeal nerve damage
The vocal cords are held in midline position as abductors are more affected
than adductors (Semon’s law).
• Unilateral lesion may lead to hoarseness.
• Bilateral lesions can lead to complete airway obstruction.
Complete recurrent laryngeal nerve damage
The vocal cords are held midway between the midline and abducted
position.
• Unilateral lesion can lead to stridor.
• Bilateral lesions result in loss of voice and aspiration.
Superior laryngeal nerve damage
• Leads to a weak voice because of slack vocal cords.

Question 27

What are the issues
anaesthetising this patient?

Answer 27

Patient factors
• Likely to be a smoker
• Cardiovascular and respiratory comorbidities
Anaesthetic factors
• Difficult airway risk
• Need for airway that allows surgery with possible use of jet ventilation and
lasers during surgery
surgical factors
• Shared airway
• Head end distant from anaesthetic machine

Question 28

What special investigations
would you like this patient to
have?

Answer 28

• Flexible nasendoscopy to know vocal cord movement
• CT scan of neck
• Pulmonary function tests if indicated
Your airway assessment on the patient does not show the presence of a
difficult airway.

Question 29

What are the airway options in
this case?

Answer 29

Standard intravenous induction with insertion of a micro laryngoscopy tube
(MLT) or jet ventilation

Question 30

What are the features of a micro
laryngoscopy tube?

Answer 30

It is longer than standard endotracheal tubes of this diameter (usually a small
diameter to aid surgery) with a high-volume, low-pressure cuff.
This is the micro laryngoscopy picture of the vocal cord lesion that the
surgeon decides to excise with laser.
See Figure 6.4. Published with permission from Department of Pathology,
University of Washington

Question 31

What can this lesion be?

Answer 31

• Laryngeal carcinoma (more likely)
• Vocal cord nodules, polyps, or cysts
• Laryngeal papilloma
• Granuloma

Question 32

What are the risks of laser
surgery?

Answer 32

• Ocular damage
The nondivergent beam of laser light, even when reflected, may be
focused on the fovea and cause irreversible blindness. Co2 lasers will not
penetrate farther than cornea. Staff should wear goggles to protect them
from specific wavelength that is being generated.
• Explosions and fires
Instruments should have a matte finish to minimise reflection. Special
hazard associated with laser surgery to upper airway. Surgical swabs and
packs can also ignite and thus must be kept moistened with saline.

Question 33

What precautions are suggested
in laser surgery?

Answer 33

• Flexible metallic or metallic coated tubes
• Cuff inflation with saline instead of air
• Use of nonexplosive mixture of gases
• Limitation of LASER power and duration of bursts
• Avoidance of tracheal intubation (e.g. HFJV)

Question 34

What are the pros and cons of
jet ventilation?

Answer 34

Advantages
• Improved surgical access
• Reduced peak airway pressure
• Reduced cardiovascular compromise
• Avoidance of endotracheal tube ignition if laser is used
Disadvantages
• Barotrauma—pneumothorax, pneumomediastinum, pneumopericardium,
pneumoperitoneum, subcutaneous emphysema
• Malposition—gastric distension, rupture
• Dysrhythmias
• Airway soiling during surgery
• Inhalational anaesthesia impossible
• Efficacy of gas exchange less predictable

Question 35

What types of jet ventilation
are available?

Answer 35

• Low-frequency jet ventilation delivered via Sanders or Manujet
• High-frequency jet ventilation (HFJV)

Question 36

What are the basic settings on a
jet ventilator?

Answer 36

• Driving pressure (DP)
The DP is the operating pressure for the jet ventilation that may range
from 103–405 kPa. ‘Start low, go slow’ is the appropriate approach
for initiating jet ventilation. In an adult, one can start with a DP of
150–200 kPa, apply a few manual breaths, watching chest movement,
airway pressure, and expiratory Co2.
• Frequency of breaths (respiratory rate)
Automatic jet ventilators are capable of delivering jets at 1–10 Hz.
An initial rate of 100–150 breaths/min is commonly chosen. It is then
adjusted depending on the limits of other interacting parameters and the
adequacy of ventilation.
• Inspiratory to Expiratory (I:E) Ratio
A longer expiratory time is normally chosen with a typical 1:E ratio of 1:3
for better emptying of the lungs.
• End Expiratory Pressure (EEP) Limit
Rate dependent gas trapping is due to inadequate time for full expiration
of gases and altered lung mechanics. The EEP is an indicator of alveolar
distension or the state of FRC. The value for EEP limit on the ventilator is
set at a similar level to the PEEP during IPPV (5–10 cm of H2o).

Question 37

What is the mechanism of gas
exchange in HFJV?

Answer 37

• Pendelluft occurs as a result of regional variation in airway resistance and
compliance causing some areas of the lung to fill or empty more rapidly
than others.
• Convective streaming/Taylor dispersion occurs as a result of the
asymmetrical velocity profile of the inspired gas front as it moves through
the bronchial tree. Molecules in the central zones where axial velocities
are higher diffuse to lateral zones with lower axial velocities.
• Cardiogenic mixing where beating heart enhances gas exchange through
agitation of surrounding lung tissue and molecular diffusion.
• Bulk flow—partial contribution

Question 38

Discuss the prevalence of head
injury and its main causes.

Answer 38

Prevalence and causes
• 70%–80% male.
• 10%–20% aged more than 65 yrs, 40%–50% children.
• Death due to head injury is 6–10 per 100 000 per annum.
Minor injury
• Falls (22%–43%) and assaults (30%–50%) are commonest cause of
minor head injury, followed by road traffic accident (25%).
Major injury
• Road traffic accident is the major cause of moderate to severe injury.

Question 39

How will you manage this
patient?

Answer 39

• Principal of management of head injury is to prevent secondary brain
injury due to hypoxia, hyper/hypocarbia, hypovolaemia, hypotension, and
increased ICP.
• Initial assessment and management as per ATLS guidelines.
• Primary survey and management of other life-threatening injury (tension
pneumothorax, cardiac tamponade, airway obstruction, etc.).
• Secondary survey

Question 40

can you tell me the criteria for
a ct scan in adult trauma
patient?

Answer 40

• GCS < 13 on presentation
• Suspected open or depressed skull fracture
• Signs of basal skull fracture (haemotympanum, CSF leak from ear or
nose, battle’s sign, panda eyes)
• Focal neurological signs
others
• More than one episode of vomiting following head injury
• History of loss of consciousness following injury or more than 30 minutes
of retrograde amnesia of events immediately prior to injury
• Mechanism of injury (e.g. cyclist or pedestrian struck by motor vehicle,
occupant ejected from a motor vehicle

Question 41

How will you rule out cervical
spine injury in trauma patient?

Answer 41

The cervical spine may be cleared clinically if the following preconditions
are met.
Alert and awake patient
• Fully orientated
• No head injury
• Not under influence of drugs or alcohol
• No neck pain
• No abnormal neurology
• No significant injury that may ‘distract’ the patient from complaining about
a possible spinal injury
Provided these preconditions are met, the neck may then be examined.
If there is no bruising or deformity, no tenderness and a pain-free range of
active movements, the cervical spine can be cleared. Radiographic studies
of the cervical spine are not indicated.
Unconscious, intubated patients
The standard radiological examinations of the cervical spine in the
unconscious, intubated patient are:
• Lateral cervical spine film.
• Antero-posterior cervical spine film.
• CT scan of occiput—C3.
• The open-mouth odontoid radiograph is inadequate in intubated patients
and will miss up to 17% of injuries to the upper cervical spine.
Axial CT scanning with sagittal and coronal reconstruction should be used to
evaluate abnormal, suspicious, or poorly visualised areas on plain radiology.
With technically adequate studies and experienced interpretation, the
combination of plain radiology and directed CT scanning provides a false
negative rate of less than 0.1%.

Question 42

What are the indications
for intubation in a head injury
patient?

Answer 42

• GCS < 8 in adult and < 9 in paediatric patients
• Seizure after trauma
• Airway obstruction, airway injury
• Severe facial injury (Le Fort fracture, mandible fracture)
• Inability to maintain oxygenation/ventilation (PaO2 < 9 kPa on air
or < 13 kPa with oxygen, PaCo2 < 4 kPa or > 6 kPa)
• To facilitate transfer of patient to tertiary centre
• Alcohol or other drug intoxication plus signs of head injury

Question 43

this patient has sustained an
extradural haematoma and
needs urgent transfer to a
neurosurgical centre. How will
you manage this transfer?

Answer 43

ensure
Patient
• Airway is secured and the patient is ventilated as indicated.
• Any life-threatening injury is dealt with and patient is optimally
resuscitated.
Personnel
• Fully trained doctor and assistant who are experienced in transferring
critically ill patient.
• Receiving team is aware and awaiting
equipment
• Monitoring equipment are all fully charged or replacement batteries taken.
Minimal monitor for transfer of patient with head injury are ECG, Spo2,
invasive arterial blood pressure, EtCo2, GCS, and pupillary reflex.
• Infusion pumps and ventilators are adequately charged and spare
batteries are taken for transfer.
• Oxygen cylinders are full and spares available.
• Cannulation and intubation kits.
Drugs
• For intubation
• Emergency drugs in case of decompensation
• Anti-seizure drugs
• Drugs that decrease ICP
• Fluids, blood, and blood products (if deemed necessary)
notes
• Patient notes and CT scan report plus hard copy in place
• All available blood results
Maintain
General
• 30–45 degree head up
• Neck is midline and free from any tight ties
• Cervical spine immobilisation
Ventilation
• Pao2 > 13 kPa and PaCo2 around 4.5 kPa
circulation
• MAP > 90 mmHg (to maintain CPP 60–70 mmHg, assuming that ICP is
20 mmHg)
• Use vasopressor to maintain MAP
others
• Treat hyperpyrexia
• Maintain blood glucose level

Question 44

How will you manage a sudden
rise of icP if it occurs during
transfer?

Answer 44

Steps to treat sudden increase in ICP (dilated pupil and direct absent
light reflex)
General
• Ensure that patient is 30 degree head up.
• Make sure that patient is adequately sedated and ventilated (bucking and
coughing increases ICP).
• ETT is in place and taped properly but not obstructing any venous
drainage.
numbers
• PaO2 > 13 kPa and PaCo2 around 4.5 kPa
• MAP > 90 mmHg
• Temperature and blood glucose are within normal limits
Drugs
• Phenytoin if convulsion is present.
• Mannitol: 0.25–0.5 gm/kg bolus over 5–10 minutes and repeated once
again if indicated, but always communicate with neurosurgeon before
second dose. Maximum 1 gm/kg, as above that it is not beneficial.
Hypertonic saline may also be used.
expert help
• Communicate with neurosurgeon in charge.

Question 45

can you tell me the role of
hypothermia in a head injury
patient?

Answer 45

Any hyperpyrexia increases cerebral metabolic rate of oxygen (CMRo2) and
should be aggressively treated.
Equally hypothermia reduces CMRo2, which can be beneficial for
neurological outcome but hypothermia below 35°C affects enzyme systems
and can cause clotting abnormality. This can result in further bleeding in
injured patient, which ultimately increases ICP; so, routinely there is no role of
active cooling of head injury patient.

Question 46

You take a telephone call from a concerned nurse regarding a
70-year-old female patient with COPD being admitted on the surgical ward.
The patient has a productive cough, respiratory rate of 32/min, and sats 88%
(on oxygen). The patient is awaiting an incisonal hernia repair.
can you define coPD?

Answer 46

CoPD is a chronic lung disease characterised by airflow limitation due to
progressive inflammatory disease, which is not fully reversible, and often
complicated by significant systemic manifestations and comorbidities.
Classic symptoms include productive cough, dyspnoea, wheeze, frequent
winter bronchitis, and exercise intolerance. The pathogenesis of CoPD
is thought to arise from the combined effects of inflammation, increased
oxidative stress, and an imbalance between proteinases and antiproteinases.
Historically there are two types: emphysema and chronic bronchitis.
Pathologic changes of CoPD are present throughout the lung.
• Large central airways: enlarged mucous glands, loss of cilia, and
decreased ciliary function, increased smooth muscle and connective
tissue deposition in the airway walls
• Small airways: collagen deposition and airway remodeling

Question 47

How do you diagnose coPD?

Answer 47

Spirometry is used to confirm the diagnosis and classify the severity of
CoPD but will be more robust when complemented with clinical status and
radiology investigations. Both the NICE and the GoLD offer guidelines for the
diagnosis and assessment of CoPD.
• Airflow obstruction [defined by a ratio of forced expired volume in one
second to forced vital capacity (FEV1/FVC) < 0.7] is used to diagnose
CoPD.
° If FEV1 is > 80% of the predicted value, then CoPD is diagnosed only
in presence of respiratory symptoms.
° Reversibility testing with corticosteroids or bronchodilators is
unnecessary for the diagnosis but they are used to differentiate CoPD
from asthma.

Question 48

What are the complications in
untreated coPD patients?

Answer 48

• Expiratory airflow limitation arises due to airway inflammation and
hyperplasia, mucus accumulation, fibrosis, and bronchospasm.
Expiratory flow is decreased and expiratory time prolonged with resultant
hyperinflation, which increases total lung capacity, functional residual
capacity, and residual volume, giving rise to exertional dyspnoea.
• V/Q mismatch due to increase in physiologic dead space and shunt.
• Chronic hypoxia leads to secondary polycythemia, pulmonary
hypertension, and eventually right ventricular dysfunction and cor
pulmonale.

Question 49

How do you manage coPD?

Answer 49

Preventive
• Smoking cessation is the only intervention that slows the progression.
• Yearly influenza vaccination has been shown to significantly reduce
morbidity and mortality and is recommended for all patients with CoPD.
Pharmacologic management
• Early-stage COPD: Short-acting inhaled bronchodilators
• Severe COPD:
° Long-acting inhaled bronchodilators (tiotropium) improve lung function
and relieve dyspnoea.
° Inhaled corticosteroids decrease frequency of exacerbations and slow
the rate of decline in FEV1.
° Combination therapy seems to show additive benefits.
treatment of acute exacerbations:
oxygen
• Domiciliary oxygen therapy for patients with hypoxia
Drugs
• Appropriate antibiotics if suspected infection
• Escalate bronchodilator therapy
• Systemic corticosteroids to shorten the recovery time
Ventilation
• Progressive hypercarbia and respiratory acidosis warrant noninvasive
mechanical ventilation to avoid the need for intubation.
• Patients with severe acidosis, refractory hypoxemia, or respiratory arrest
require intubation and mechanical ventilation.
treatment of end-stage disease
Treatment options for advanced CoPD are limited.
• Domiciliary oxygen therapy. Aim for sats > 90%
• Lung volume reduction surgery—high-risk palliative treatment, which is
performed especially for upper-lobe emphysema
• Lung transplantation

Question 50

How will you manage this patient?

Answer 50

Patients with CoPD have a two- to five-fold increase in risk of perioperative
pulmonary complications such as atelectasis, pneumonia, and respiratory
failure.
Preoperative management
• ABCD approach; optimise oxygen and drug therapy.
• Risk assessment—patient and surgical factors.
• Investigations—besides routine investigations, a bedside spirometry
and a chest radiograph is obtained to influence clinical management.
Consider echocardiography if ECG reveals right heart disease (right
ventricular hypertrophy or strain). A baseline ABG on room air with PaCo2
> 5.9 kPa and Pao2 < 7.9 kPa predict a worse outcome.
• Advice smoking cessation.
• Appropriate antibiotics for suspected bacterial infection, systemic
corticosteroid, and escalate bronchodilator therapy. If permissible, delay
surgery until after full recovery from an acute CoPD exacerbation.
intraoperative management
• Where possible, neuraxial analgesia and peripheral nerve blockade for
postoperative pain relief are offered.
• Airway manipulation can worsen the condition and may be treated with
short-acting bronchodilators such as β2 agonists or anticholinergics.
Bronchodilating volatile anaesthetics (isoflurane, sevoflurane, halothane,
enflurane) also may reverse acute bronchospasm.
• Titrated dose of neuromuscular blockers is crucial as is adequate reversal
at the end of operation.
• Ventilation strategy: Avoidance of dynamic hyperinflation by the use of a
slow respiratory rate, long expiratory time, and minimal tidal volume to
avoid excessive hypercapnia. Use extrinsic PEEP judiciously to replace
intrinsic PEEP.
• Fluid balance is crucial in patients with cor pulmonale where appropriate
right ventricular preload is essential to produce adequate cardiac output
when the right ventricular afterload is high.
Postoperative care
• HDU/ITU care
• Adequate pain control
• Lung expansion maneuvers such as deep breathing, chest physiotherapy,
and incentive spirometry
• Thromboprophylaxis and early ambulation to help restore baseline lung
volumes and to aid in clearing secretions
• Careful administration of oxygen to avoid suppressing ventilatory drives in
patients who are dependent on hypoxia

Question 51

What symptoms would a
patient have with a blocked left
coronary artery?

Answer 51

Acute coronary syndrome is the term used to describe the spectrum of
clinical presentation attributed to occlusion of coronary arteries.
The symptoms and signs depend on extent and duration of the
obstruction, volume of the affected myocardium and its complications.
They can be very varied and generally include
• Chest pain—squeezing or burning, often radiating to the left arm
or jaw
• Nausea, vomiting, and sweating due to vagal stimulation
• Dyspnoea, mainly because of cardiac failure
• Sense of impending doom
• Arrhythmias
• Hypo or hypertension
• Signs and symptoms of complications: ventricular aneurysm
and rupture of interventricular septum, papillary muscle or
ventricular wall leading to pulmonary oedema, and valvular incompetence

Question 52

Acute coronary syndrome is the term used to describe the spectrum of
clinical presentation attributed to occlusion of coronary arteries.
The symptoms and signs depend on extent and duration of the
obstruction, volume of the affected myocardium and its complications.
They can be very varied and generally include
• Chest pain—squeezing or burning, often radiating to the left arm
or jaw
• Nausea, vomiting, and sweating due to vagal stimulation
• Dyspnoea, mainly because of cardiac failure
• Sense of impending doom
• Arrhythmias
• Hypo or hypertension
• Signs and symptoms of complications: ventricular aneurysm
and rupture of interventricular septum, papillary muscle or
ventricular wall leading to pulmonary oedema, and valvular incompetence

Answer 52

The heart receives its blood supply from the right and left coronary arteries.
• The total coronary blood flow is about 250 mls/min, which equates to 5%
of the cardiac output. The blood flow increases by 5 times in strenuous
exercise.
Right coronary artery: arises from the right aortic sinus, runs between the
right atrium and the pulmonary trunk to descend in the right atrioventricular
groove. It winds around the inferior border to reach the diaphragmatic
surface of heart and runs backwards and left to reach posterior
interventricular groove. It terminates by anastomosing with left coronary
artery.
• Marginal branch
• Posterior interventricular artery (PIVA): This anastomoses with the AIVA
in the posterior interventricular groove. It is the PIVA that determines
the dominance of the arterial system. In this case the right coronary is
dominant.
Left coronary artery: After originating from the left aortic sinus, it passes
forwards and to the left and emerges between pulmonary trunk and the left
atrium and gives off two main branches.
• Anterior interventricular artery (AIVA), which runs downwards in anterior
interventricular groove and anastomose with the PIVA. This is the major
branch, as it supplies most of the muscle bulk.
• Circumflex branch, which runs to the left in the left atrioventricular sulcus,
winds around the left border of heart and terminates by anastomosing
with right coronary artery.

Question 53

What are the structures
supplied by the left and right
coronary arteries?

Answer 53

Question 54

What is the importance of
knowing the coronary blood
supply?

Answer 54

The ischaemic vessel can be identified from the clinical and ECG
presentation which would prevent delay in treatment. Also, ischaemia/
infarction of the ventricle can lead to abnormal conduction.
Example: Right coronary artery involvement leads to inferior MI and is also
associated with bradycardia and heart block.
Rt coronary artery infarct
• Inferior MI (ECG leads II, III, aVF)
• Posterior MI (prominent R in V1, V2)
Anterior interventricular artery infarct
• Anteroseptal MI (V1, V2)
• Anterior MI (V2–V4)
• Anterolateral MI (I, aVL, V4–V6)
circumflex artery infarct
• Lateral MI (I, aVL, V5, V6)

Question 55

What can you tell me about the
venous drainage?

Answer 55

Two thirds of the venous drainage is by veins that accompany the coronary
arteries and open into the coronary sinus in the right atrium. The remaining
one third drains the endocardium and inner myocardium directly into the
cardiac cavity.
The coronary sinus lies in the right atrium between the superior and inferior
vena caval openings. The main veins draining into the coronary sinus are:
• Great cardiac vein, which accompanies the AIVA
• Middle cardiac vein, which lies in the inferior interventricular groove near
the anastomosis of circumflex and right coronary arteries
• Small cardiac vein, which accompanies the marginal branch of the right
coronary artery
• Oblique vein, which drains the posterior half of left atrium.
The anterior cardiac vein drains most of the anterior surface of the heart and
opens into the right atrium directly.
The venae cordis minimae (Thebesian veins) drains the endocardium and
inner myocardium directly into the cardiac cavity and is an example of
physiological shunt as venous blood enters the left heart.

Question 56

How does the coronary blood
supply relate to cardiac cycle in
right and left ventricles?

Answer 56

Left ventricle
• During systole, intramuscular blood vessels are compressed and
twisted by the contracting heart muscle and blood flow is at its lowest
of only 10% to 30% of that during diastole. The force is greatest in
the subendocardial layers where it approximates to intramyocardial
pressure. It is important to note that the layers of the heart, excluding the
subendocardium, receive blood supply even in systole.
• In diastole, the heart musculature is relaxed and cardiac muscle effects
do not impede blood flow to the heart.
Right ventricle:
The compression effect of systole on blood flow is minimal as a result of the
lower pressures developed by that chamber.
The heart is perfused from the epicardial (outside) to the endocardial (inside)
surface. The mechanical compression of systole has a more negative effect on
the blood flow through the endocardial layers, where compressive forces are
higher and microvascular pressures are lower. Therefore, subendocardial layers
of the heart suffer more impairment and ischemia than do the epicardial layers.

Question 57

What are the ecG changes
associated with myocardial
infarction in increasing
chronology?

Answer 57

• Hyperacute changes (within minutes)
° Tall T waves and progressive ST elevation
• Acute changes (minutes to hours)
° ST elevation and gradual loss of R wave
• Early changes (hours to days)
° < 24 hours: inversion of T wave and the resolution of ST elevation
° Within days: pathological Q wave begins to form
• Indeterminate changes (days to weeks)
° Q waves and persistent T wave inversion
• Old changes (weeks to months)
° Persisting Q waves and normalised T waves

Question 58

What are the determinants of
coronary circulation?

Answer 58

• Factors inherent to the circulation
• Pressure or myogenic autoregulation
• Chemical/metabolic factors
• Neural factors
• Humoral factors
Factors inherent to the circulation
• Coronary perfusion pressure (CoPP) is the difference between aortic
diastolic pressure (ADP) and left ventricular end diastolic pressure
(LVEDP). Any factor that increases the ADP and decreases the LVEDP
would increase the CoPP.
• Heart rate—lower heart rate increases the diastole and thus the coronary
filling time.
• Cardiac output—directly proportional to the coronary blood flow.
• State of the cardiac cycle—coronary blood flow is the highest during the
isovolumetric relaxation phase.
Pressure or myogenic autoregulation
Coronary blood flow is autoregulated between a mean arterial pressure of
60–140 mmHg. This is by the myogenic constriction and dilatation of the
coronary vessels in response to changes in the blood flow and pressure.
chemical and metabolic
• O2, Co2, K+, H+, prostaglandins, endothelium-derived relaxing factor
(EDRF), nitric oxide, and adenosine
• Drugs that influence coronary blood flow include nitrates, aminophylline, etc
neural
Autonomic innervation has minimal influence on the vessel wall diameter but
can increase the blood flow by improving contractility and metabolism.
Hormonal
Angiotensin receptors present in the vessel wall can cause vasoconstriction,
thereby decreasing the coronary blood flow. T3/T4 increases cardiac muscle
metabolism, and thus coronary blood flow improves due to vasodilation

Question 59

What are the differences
between systemic and coronary
circulation?

Answer 59

Coronary circulation is a part of the systemic circulation that supplies the heart.
• Coronary blood flow changes with cardiac cycle and is minimum during
systole, whereas the converse is true for systemic circulation.
• The second major difference is the myocardial oxygen extraction ratio of
80% when compared to around 25% in the rest of the body.

Question 60

What is the myocardial oxygen
consumption and oxygen
extraction ratio?

Answer 60

Myocardial oxygen consumption is defined as the actual amount of oxygen
consumed by the heart muscle per minute. It is normally expressed as MVo2
and is about 30 mLs/min for a resting heart. owing to the obligatory aerobic
nature of myocardial metabolism, MV.
o2 serves as a measure of the total
energy utilisation of the heart.
The myocardial oxygen extraction ratio is about 70%–80%, which means
increased oxygen demand therefore has to be met by an increase in
coronary perfusion.

Question 61

What is meant by the terms
DPti and tti?

Answer 61

Diastolic pressure time (DPTI) and tension time (TTI) indices are measures
of myocardial supply and demand, respectively, collectively depicted as
endocardial viability.
Endocardial viability ratio (EVR) = DPTI
× HR T TI
EVR < 0.7 denotes a high likelihood of ischaemia. See Figure 6.6.

Question 62

How would end stage
hepatic disease present to
anaesthetists?

Answer 62

Acute decompensation secondary to
• Infection
• Hypovolemia
• Hypotension
• Diuretics
• Gastrointestinal haemorrhage
• Excess dietary protein
• Electrolyte imbalance
infection
• Flare-up of hepatitis (A, B, or C)
• Prone to acquiring fungal infections, TB
Portal hypertension
• Ascites—diaphragmatic splinting and respiratory distress
• Spontaneous bacterial peritonitis
• Varices—variceal bleeding
• Splenomegaly—thrombocytopenia
Bleeding
• Due to decreased production of clotting factors (II, VII, IX, X) and
splenomegaly-related thrombocytopenia
• Haematemesis
Hepatic encephalopathy

Question 63

What is the pathophysiology
of liver injury in alcoholic liver
disease?

Answer 63

Conventionally divided into three histological types, although may co-exist:
• Steatosis
° Metabolism of ethanol causes the accumulation of lipid in liver cells.
• Alcoholic hepatitis
° Ethanol metabolism generates reactive oxygen species and
neoantigens, which promote inflammation.
• Cirrhosis
° Prolonged hepatocellular damage generates myofibroblast-like cells
that produce collagen, resulting in fibrosis.
° As hepatocytes are destroyed and liver architecture changes, hepatic
function falls and increased resistance to portal blood flow produces
portal hypertension.

Question 64

List the common clinical findings
in patients with alcoholic liver
disease.

Answer 64

• Signs of acute hepatitis
° Jaundice
° Tender hepatomegaly
° Fever (< 38.5ºC, often sawtooth)
• Signs of chronic liver disease
° Leuconychia/palmar erythema/dupuytren’s contracture/spider naevi
° Telangactasia/bruising
° oedema (hypoalbuminaemia)
° Parotid swelling/hepatomegaly
° Gynaecomastia/testicular atrophy
° Encephalopathy
• Portal hypertension
° Ascites/splenomegaly/caput medusa
• Poor nutrition
° Muscle wasting/weight loss/cachexia/glossitis

Question 65

What is hepatorenal syndrome?

Answer 65

• Hepatorenal syndrome (HRS) is the reduced glomerular filtration rate
(GFR) and consequent decline in renal function caused by advanced liver
disease.
• Serum creatinine of > 133 µmol/litre in a patient with cirrhosis and
ascites that persists after all possible pathologies have been excluded or
treated.
• Due to generalised vasodilatation and altered hormone release (renin–
angiotensin, ADH, and sympathetic systems) subjecting the kidney to
hypotension, hypovolaemia, and local vasoconstriction.
hRS type 1: A rapid and severe progressive renal failure occurring in under
2 weeks.
• As a result of some precipitating factors, (e.g. Alcoholic hepatitis,
gastrointestinal bleeding, NSAIDs, aminoglycosides, or infection).
hRS type 2: A slowly progressive moderate deterioration in function.
Refractory ascites is the dominant clinical feature.

Question 66

What is hepatic encephalopathy?

Answer 66

occurrence of confusion, altered level of consciousness, and coma due to
liver failure
Grading:
I: Confused, altered mood
II: Inappropriate, drowsy
III: Stuporose, but rousable, very confused, agitated
IV: Coma, unresponsive to painful stimulus

Question 67

How would you assess the
prognosis of liver disease and
how is this assessment tool
useful?

Answer 67

• The Model for End-Stage Liver Disease (MELD) score uses bilirubin,
INR, and creatinine.
• The Child-Pugh score [Pugh’s modification (1972) of Child’s criteria
(1964)] is used to determine the prognosis, as well as the required
strength of treatment and the necessity of liver transplantation.

Question 68

What are the anaesthetic
implications for
anaesthetising patients with
end-stage liver failure
(for nonhepatic surgery)?

Answer 68

Preoperative
• Comprehensive assessment of suitability and work-up for procedure—
multidisciplinary approach
• Preoperative optimisation of fluid and nutritional status, as well as any
electrolyte disturbance or coagulopathy
• Consider preoperative abdominal paracentesis
• Delayed gastric emptying—antacid prophylaxis +/− rapid sequence
induction
intraoperative
• Drugs
° Altered drug handling
° Increased sensitivity to sedative agents
° Reduced metabolism of many drugs including opioids
° Increased volume of distribution and altered protein binding
° Short-acting drugs preferred (desflurane, remifentanil)
• Technique
° Extreme caution with epidural anaesthesia and other regional
procedures due to associated coagulopathy
• Monitoring
° Invasive monitoring for major surgery (oesophageal doppler
contraindicated in the presence of varices)
• Others
° Glycaemic control
° Thermoregulation
° Antibiotic prophylaxis and strict adherence to aseptic technique
Postoperative
Care on high-dependency unit or ITU

Question 69

What is secondary prevention
post myocardial infarction (Mi)?

Answer 69

Patients who have had a ST elevation myocardial infarction (STEMI) or non-
ST elevation myocardial infarction (NSTEMI) benefit from treatment to reduce
the risk of further MI or other manifestations of vascular disease. This is
known as secondary prevention.
NICE provides comprehensive guidelines to prevent further MI and
progression of vascular disease in patients who have had an MI either
recently or in the past (> 12 months ago

Question 70

What drugs are used as
secondary prevention after
an Mi?

Answer 70

Angiotensin-converting enzyme inhibitor (Ace-i)
• Offered to patients who present acutely with an MI as soon as they are
haemodynamically stable and continued indefinitely.
• Titrate dose upwards at short intervals (e.g. 12–24 hours before
discharge from hospital until maximum dose tolerated).
• If unable to titrate dose upwards during admission, this should be
completed within 4 to 6 weeks of hospital discharge.
• ACE-i is not to be combined with angiotensin II receptor blocker (ARB).
• Monitor renal function, serum electrolytes, and blood pressure.
Dual platelet therapy (aspirin plus second antiplatelet agent)
• Aspirin is offered to all patients after an MI and to continue indefinitely
unless aspirin intolerant or have indication for anticoagulation.
• Patients who have had an MI > 12 months ago should also be offered
aspirin.
• Ticagrelor in combination with low-dose aspirin is recommended for up to
12 months.
• Alternative is Clopidogrel for up to 12 months in patients who have had
NSTEMI or STEMI with bare metal or drug-eluting stents.
Beta blocker
• Offered as soon as possible after an MI, when patient is
haemodynamically stable.
• Continue for at least 12 months in patients with and without left
ventricular systolic dysfunction or heart failure.
• Continue indefinitely in patients with left ventricular systolic dysfunction.
statin
• Offered to all patients with clinical evidence of cardiovascular disease.

Question 71

is calcium channel blocker
routinely offered?

Answer 71

No, It is offered only if beta blockers are contraindicated or need to be
discontinued. Commonly used drugs are diltiazem or verapamil.

Question 72

What is Ace-i?

Answer 72

ACE-i inhibits the angiotensin-converting enzyme in the renin—angiotensin—
aldosterone system.
Angiotensinogen (from liver)
Renin (from juxtaglomerular apparatus in kidney)
Angiotensin i
ACE (from surface of pulmonary and renal endothelium)
Angiotensin ii
• Increase sympathetic activity.
• Increase tubular sodium and chloride reabsorption and water retention.
• Increase tubular potassium excretion.
• Increase aldosterone secretion in adrenal cortex.
• Arteriolar vasoconstriction—increase blood pressure.
• Increase antidiuretic hormone (ADH) in posterior pituitary to increase
water absorption in the collecting duct

Question 73

can you give some examples
of Ace-i?

Answer 73

Ramipril
Lisinopril
Captopril
Enalapril

Question 74

What clinical situations require
use of Ace-i?

Answer 74

• After an MI
• Hypertension– first-line treatment for patients < 55 years old or
non-Afro-Caribbean origin
• Heart failure
• Diabetic nephropathy—renal protective
• Chronic kidney disease—slows the progress of kidney disease

Question 75

What are the common side
effects of Ace-i?

Answer 75

Renal impairment
• Under normal circumstances, angiotensin II maintains renal perfusion by
altering the caliber of the efferent glomerular arterioles. ACE-i inhibits this
causing drop in renal perfusion pressure, which can lead to renal failure
in patients with pre-existing impaired renal circulation. ACE-i is therefore
contraindicated in patients with renal artery stenosis.
Dry cough
• Due to increased bradykinin, which is normally degraded by ACE
Hypotension
• First-dose hypotension—test dose should be given at night.
• Can cause refractory hypotension with anaesthesia. ACE-i is usually
omitted for 24 hours prior to surgery.
Angioedema
• Swelling of lips, eyes, and tongue
• More common in Afro-Caribbean patients

Question 76

What are the sources of
pollution in the operating
theatre complex?

Answer 76

• Gas induction
• Spillage
• Leaks from breathing circuit
• Facemasks
• Laryngeal masks
• T-piece or other open circuits
• Post-anaesthetic exhalation of vapour
• Failure to turn off vapour or gas flow after anaesthesia

Question 77

What are the concerns?

Answer 77

• Reports of increased spontaneous abortion rates in female staff
• Increased rates of malignancy
• Decreased fertility
• Mortality
• Staff particularly at risk: paediatric anaesthetists, bronchoscopists,
recovery staff
• Pollution and global warming

Question 78

What are the effects of nitrous
oxide?

Answer 78

Bone marrow toxicity and neurotoxicity
• Methionine synthetase inhibition can prevent production of methionine
and tetrahydrofolate.
• Methionine is a precursor of S-adenosyl methionine (SAM), which is
incorporated into myelin. Its absence can lead to subacute combined
degeneration of the spinal cord in chronic B12 deficiency and acutely to
dorsal column dysfunction and peripheral neuropathy.
• Tetrahydrofolate is required for nucleotide and DNA synthesis.
• Megaloblastic anaemia can occur in folate and B12 deficiency.
Teratogenicity
• Association is not strong.
Spontaneous miscarriage
• Reports suggesting an increased incidence of miscarriages in dental
practice nurses working with nitrous oxide.
Substance abuse

Question 79

How may anaesthetic gas
pollution be reduced or
prevented?

Answer 79

• Ensuring operating theatres are efficiently ventilated
(minimum 15 exchanges/hour)
• Use of closed circuits with soda lime
• Use of TIVA with oxygen/air
• Use of regional anaesthesia
• Consideration when using nitrous oxide and inhalational agents—
consider low flow
• Careful filling of vaporizers avoiding spillage and using keyed fillers
• Monitoring of theatre pollution levels
• Use of scavenging
• Use of low flow and ultra low flow breathing systems

Question 80

What are the current
recommendations for theatre
pollution levels?

Answer 80

Control of Substances Hazardous to Health (CoSHH) sets maximum
exposure limits to chemicals and other hazardous substances. Currently
the maximum anaesthetic pollutant levels (based on 8-hour time weighted
average, parts per million) are as follows:
Halothane 10 ppm
Enflurane 50 ppm
Isoflurane 50 ppm
Nitrous oxide 100 ppm
In the USA, the maximum exposure limit for all halogenated volatiles is
2 ppm.

Question 81

What are the features of a
scavenging system?

Answer 81

Scavenging systems can be classified into passive and active.
Passive:
• Patient dependent.
• No active positive or negative pressure.
• 30 mm connector used between patient and system.
• Gases are vented to atmosphere either by patient’s spontaneous
respiratory efforts or by mechanical ventilator.
• These are rarely used in modern theatres.
• Cardiff Aldasorber: canister containing charcoal particles that absorb
halogenated volatile agents. Absorption does not render agents inert.
Inhalational agents are released into atmosphere when canister is
disposed of by incineration. Device does not absorb nitrous oxide.
Active:
Collecting system: Collection of expired gases from breathing system or
ventilator via 30 mm connector so that misconnection is prevented.
Transfer system: Wide-bore 30 mm tubing.
Receiving system: Reservoir with visual flow indicator. Consists of two
springloaded valves guarding against excessive positive pressure (1000 Pa)
and negative pressure (–50 Pa) developing in the scavenging system.
Disposal system: Air pump or fan generates a vacuum. Connected to the
wall and vented outside. Able to cope with flows up to 120 L/min.
Exterior

Question 82

What are the disadvantages
of an active system?

Answer 82

• Excessive positive pressure may lead to barotrauma.
• Excessive negative pressure can deflate reservoir bag of breathing
system, leading to rebreathing

Question 83

What other systems are
available to ensure efficient
ventilation?

Answer 83

Laminar flow
• Can be used to create an ultra clean environment
• Recommended for prosthetic implant surgery
• Provides over 400 air changes per hour by recirculating air after passing
it through high-efficiency filters (0.5 μm)
All ventilation systems should provide a positive pressure across any
openings so that when doors are opened, there is less chance of bacterial
escape.
opening of doors can make system less efficient.

Question 84

What other factors need to be
taken into consideration when
designing a theatre?

Answer 84

• Temperature control
• Humidity