Section 6 Flashcards

1
Q

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.

A

○ 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

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2
Q

Describe the ecG.

A

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

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3
Q

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

A

• 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

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4
Q

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

A

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)

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5
Q

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

A

○ 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

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6
Q

What is aortic stenosis?

A

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

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7
Q

How can you classify aortic
stenosis?

A
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8
Q

What are the symptoms and
signs of aortic stenosis?

A

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

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9
Q

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

A

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.

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10
Q

What are the causes of aortic
stenosis?

A

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

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11
Q

Describe the pathophysiology
of aortic stenosis. see
Figure 6.3

A
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12
Q

What other conditions are associated with congenital bicuspid valve?

A

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

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13
Q

What is the concern in coA?

A

○ 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.

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14
Q

What are the symptoms and csigns of coA?

A

• 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

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15
Q

What are the findings of coA on chest radiograph?

A

• 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

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16
Q

What are the cardiac
conditions where pregnancy is
contraindicated?

A

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

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17
Q

How can you risk stratify pregnant patients with cardiac diseases?

A

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

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18
Q

How would you manage this
patient?

A

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

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19
Q

Anaesthetic management

A

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

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20
Q

What medical management can
you offer this patient?

A

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.

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21
Q

What are the surgical
interventions in severe aortic
stenosis?

A

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.

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22
Q

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

A

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

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23
Q

How could her anticoagulation
be managed during pregnancy?

A

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.

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24
Q

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?

A

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

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25
What is the nerve supply of the larynx?
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
26
What are the effects of laryngeal nerve damage?
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.
27
What are the issues anaesthetising this patient?
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
28
What special investigations would you like this patient to have?
• 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.
29
What are the airway options in this case?
Standard intravenous induction with insertion of a micro laryngoscopy tube (MLT) or jet ventilation
30
What are the features of a micro laryngoscopy tube?
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
31
What can this lesion be?
• Laryngeal carcinoma (more likely) • Vocal cord nodules, polyps, or cysts • Laryngeal papilloma • Granuloma
32
What are the risks of laser surgery?
• 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.
33
What precautions are suggested in laser surgery?
• 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)
34
What are the pros and cons of jet ventilation?
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
35
What types of jet ventilation are available?
• Low-frequency jet ventilation delivered via Sanders or Manujet • High-frequency jet ventilation (HFJV)
36
What are the basic settings on a jet ventilator?
• 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).
37
What is the mechanism of gas exchange in HFJV?
• 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
38
Discuss the prevalence of head injury and its main causes.
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.
39
How will you manage this patient?
• 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
40
can you tell me the criteria for a ct scan in adult trauma patient?
• 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
41
How will you rule out cervical spine injury in trauma patient?
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%.
42
What are the indications for intubation in a head injury patient?
• 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
43
this patient has sustained an extradural haematoma and needs urgent transfer to a neurosurgical centre. How will you manage this transfer?
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
44
How will you manage a sudden rise of icP if it occurs during transfer?
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.
45
can you tell me the role of hypothermia in a head injury patient?
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.
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?
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
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How do you diagnose coPD?
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.
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What are the complications in untreated coPD patients?
• 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.
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How do you manage coPD?
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
50
How will you manage this patient?
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
51
What symptoms would a patient have with a blocked left coronary artery?
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
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
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.
53
What are the structures supplied by the left and right coronary arteries?
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What is the importance of knowing the coronary blood supply?
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)
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What can you tell me about the venous drainage?
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.
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How does the coronary blood supply relate to cardiac cycle in right and left ventricles?
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.
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What are the ecG changes associated with myocardial infarction in increasing chronology?
• 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
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What are the determinants of coronary circulation?
• 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
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What are the differences between systemic and coronary circulation?
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.
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What is the myocardial oxygen consumption and oxygen extraction ratio?
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.
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What is meant by the terms DPti and tti?
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.
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How would end stage hepatic disease present to anaesthetists?
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
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What is the pathophysiology of liver injury in alcoholic liver disease?
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.
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List the common clinical findings in patients with alcoholic liver disease.
• 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
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What is hepatorenal syndrome?
• 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.
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What is hepatic encephalopathy?
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
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How would you assess the prognosis of liver disease and how is this assessment tool useful?
• 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.
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What are the anaesthetic implications for anaesthetising patients with end-stage liver failure (for nonhepatic surgery)?
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
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What is secondary prevention post myocardial infarction (Mi)?
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
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What drugs are used as secondary prevention after an Mi?
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.
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is calcium channel blocker routinely offered?
No, It is offered only if beta blockers are contraindicated or need to be discontinued. Commonly used drugs are diltiazem or verapamil.
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What is Ace-i?
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
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can you give some examples of Ace-i?
Ramipril Lisinopril Captopril Enalapril
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What clinical situations require use of Ace-i?
• 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
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What are the common side effects of Ace-i?
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
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What are the sources of pollution in the operating theatre complex?
• 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
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What are the concerns?
• 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
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What are the effects of nitrous oxide?
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
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How may anaesthetic gas pollution be reduced or prevented?
• 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
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What are the current recommendations for theatre pollution levels?
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.
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What are the features of a scavenging system?
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
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What are the disadvantages of an active system?
• Excessive positive pressure may lead to barotrauma. • Excessive negative pressure can deflate reservoir bag of breathing system, leading to rebreathing
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What other systems are available to ensure efficient ventilation?
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.
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What other factors need to be taken into consideration when designing a theatre?
• Temperature control • Humidity