Neurological complications of CABG

a) What are the central and peripheral neurological complications of coronary artery bypass
surgery? (7
marks)
b) What are the risk factors for central neurological complications? (6 marks)
c) How can the incidence of central neurological complications be reduced? (7 marks)

Click for model answer by Dr Matt Devine

(a)

CENTRAL
Intraoperative stroke due to hypoperfusion and/or embolisation.
Postoperative stroke related to post op AF or pre-existing cardiac disease.
Intracranial haemorrhage secondary to haemorrhagic extension of ischaemic stroke.
Delirium
Seizures
Cognitive dysfunction due to global anoxic brain injury, stroke, intracranial haemorrhage
Ischaemic optic neuropathy

PERIPHERAL
Brachial plexus injury leading to upper limb neuropathy. This can occur due to traction,
compression during eternal retraction, hypothermia and haemodynamic changes.
Phrenic nerve palsy associated with the ice flush used to cool the heart.
Anterior intercostal nerve injury occurring during harvesting of internal thoracic artery

(b)
What are the risk factors for central neurological complications? (6 marks)
 PATIENT FACTORS
Advanced age
Male gender
LV systolic dysfunction
LV thrombus
Previous stroke
Carotid stenosis
Diabetes
AF
Renal failure

PROCEDURAL FACTORS
Long CPB time
Macro/micro embolus
Valve surgery
Hyperglycaemia
Poor temperature control
Cerebral hypoperfusion

(c)How can the incidence of central neurological complications be reduced? (7 marks)

Anticoagulation by heparinisation aiming for ACT level >400 sec

Use of hi quality arterial filters and membrane oxygenators to reduce microembolic load
Minimise CPB time, ideally less than 2 hours.
Utilising off pump techniques reducing risk of cerebral complications
Temperature control: mild hypothermia and avoiding hyperthermia on rewarming
Optimisation of co-morbidities including BP control and glycaemic control
Acid base control
Controlling the systemic inflammatory response to surgery

Anticoagulation and cardiac surgery

A 67 year-old patient is to undergo coronary artery surgery on cardiopulmonary bypass (CPB).

a) What dose of heparin is used to achieve full anticoagulation for CPB and how is it given? (2
marks)
b) Which laboratory and “point-of-care” tests determine the effectiveness of heparin
anticoagulation in
CPB patients? Give the advantages and/or disadvantages of each test. (10 marks)
c) What are the causes of inadequate anticoagulation in a patient whom it is believed has already
received
heparin? (5 marks)
d) Describe the possible adverse reactions to protamine. (3 marks)

Click for model answer by Dr Brian Og McAlary

a)
300-400 IU/kg
Intravenously
Post sternotomy and pre-insertion of aortic and atrial venous lines
 b)
Activated Clotting time
Advantages- familiar, cheap, easy to do, quick
Disadvantages- unreliable with hypothermia, haemodilution and antiplatelet agents

Activated Partial Thromboplastin time

Advantages- sensitive
Disadvantages- takes longer than other tests

High dose thrombin time

Advantages- less susceptible to artefact on CPB
Disadvantages- expensive, not as familiar

Heparin Management Test

Advantages- less susceptible to artefact on CPB, able to calculate individual doses of heparin and
protamine for each patient
Disadvantages- expensive, not as familiar

c)
Inherited
Anti thrombin III deficiency

Acquired
Previous heparin use
Reduced synthesis- liver cirrhosis
Increased consumption- DIC, sepsis
Dilutional- CPB
Increased excretion- Protein losing states

d)
Hypotension
Pulmonary hypertension
Anaphylaxis
Reduced cardiac output
Inhibiting platelet activity

Cardioplegia and hypothermic circulatory bypass

(a) What are the purposes, typical composition and physiological actions of cardioplegia
solutions?
(b) By which routes can solutions of cardioplegia be administered?
(c) What are the possible complications of cardioplegia solution administration?
(d) What are the advantages and disadvantages of hypothermic cardiopulmonary bypass?
(e) Describe the differences between the utilisation of alpha-stat and pH-stat?

Click for model answer by Dr Alison Blair

(a) What are the purposes, typical composition and physiological actions of cardioplegia
solutions?

a)Cardioplegia-
Creates a diastolic electro-mechanical arrest allowing the surgeon to work with a motionless,
bloodless heart.
Reduced the myocardial consumption of oxygen to allow the tissue to withstand a period of ischaemia

Cardioplegia is a hyperkalaemic solution which requires at least 20mmol per litre of KCL. The ideal
solution is still under research. It should be hyperosmotic to prevent oedema, alkalotic to attenuate
subsequent pH changes and low concentration of calcium. It may also contain aspartate and glutamine
to promote oxidative metabolism in energy-depleted hearts.

Esmolol may be an alternative as this may reduce myocardial oxygen consumption, or nicorandil as
this may cause arrest close the heart resting potential.

Cardioplegia can be in crystalloid or blood, warm or cold.

Blood cardioplegia is potassium in blood and offers the advantage of having increased oxygen carring
capacity with the presence of haemoglobin. Cold blood cardioplegia will move the oxygen
haemoglobin dissociation curve to the left.

It works by inactivating fast inward sodium channels preventing the upstroke of myocardial cell action
potentials, causing the myocardium to become unexcitable in diastolic arrest.

(b) By which routes can solutions of cardioplegia be administered?

- Antegrade- administered in the direction of blood flow into the aortic root or coronary ostium to
flow down the coronary arteries.
- Retrograde- through the right coronary sinus- this is used if there is occlusion of the coronary
circulation or aortic valve incompetence however this may not give adequate protection of the right
ventricle.

(c) What are the possible complications of cardioplegia solution administration?

- under dosage- avoided by using pre-made solutions or ampoules.
- complications include those that are involved with open heart surgery- MI, dysrhythmias, included
VF

(d) What are the advantages and disadvantages of hypothermic cardiopulmonary bypass?
Advantages
Reduces cerebral oxygen consumption so providing cerebral protection
Reduces the incidence of cerebral ischaemia by microemboli
Systemic oxygen requirements decrease including myocardial oxygen
consumption.
Decreases the rate of release of ecitatory amino acids and
neurotransmitters that are associated with axonal death
Reduces the inflammatory response
Reduces blood brain barrier permeability

Disadvantages
Increased blood viscosity so increased risk of embolism
Increased rate of infection
Decreased wound healing
 Peripheral Vasoconstriction
Moves oxygen-hb dissociation curve to the left so oxygen is not liberated as easily

(e) Describe the differences between the utilisation of alpha-stat and pH-stat?
- Alpha stat- blood gas levels are uncorrected for temperature and alkalosis is permitted during
cooling. This maintains cerebral autoregulation offering better control of cerebral blood flow and
reduces the chance of microemboli.

- pH stat- is corrected for temperature at 37 degrees Celsius and pH is kept constant. This allows pCO2
content during cooling that causes cerebral vessels to vasodilate. Cerebral blood flow looses it
autoregulation and becomes pressure dependent. This may improve cooling and oxygen delivery to
the brain.

Cardiac failure post cardiac surgery

(a) What are the causes of (i) hypotension (ii) hypertension following cardiac surgery?
(b) What are the causes of low cardiac output following cardiac surgery?
(c) What are the goals of inotrope and vasopressor use post-cardiac surgery?
(d) Describe the mechanism of action of milrinone and similar drugs
(e) What are the differences in cardiopulmonary resuscitation in post-cardiac surgery patients?

Click for model answer by Dr Alix Murphy

(a) What are the causes of (i) hypotension (ii) hypertension following cardiac
surgery?
i) Hypotension:
Cardiac –
MI
Kinking of bypass graft
Poor myocardial protection
Left ventricular dysfunction
Right ventricular dysfunction
Valvular failure – native or artificial
Arrhythmias
Cardiac tamponade
Circulatory –
Systemic inflammatory response
Ongoing vasoplegia
Hypovolaemia
Massive bleeding
Sepsis
Respiratory –
Tension pneumothorax
Pharmacological –
Excessive sedation
Excessive nitrates
Inotropes stopped inadvertently

ii) Hypertension
Inadequate sedation
Inadequate analgesia
Awareness with residual muscle relaxant onboard
Persistent hypothermia -> increased SVR
Hypoxia
Hypercarbia
Sympathetic vasoconstriction
LVH
Raised ICP (intracranial haemorrhage or infarct)
Inadvertent bolus of inotrope
Bladder distension

(b) What are the causes of low cardiac output following cardiac surgery?
Reduced preload –
Hypovolaemia
Cardiac tamponade
Increased intrathoracic pressure (High airway pressures, tension pneumothorax)
RV dysfunction (Pulmonary hypertension, RV infarction)
Decreased contractility –
Myocardial stunning
Pre-existing poor LV function
Graft kinking
Incomplete revascularisation
Acid/base disturbance
Arrhythmias
Increased afterload –
Vasoconstriction
LV outflow tract obstruction
Fluid overload -> ventricular distension
Diastolic dysfunction
Co-existing condition –
SIRS/Sepsis
Anaphylaxis
Adrenal insufficiency

(c) What are the goals of inotrope and vasopressor use post-cardiac
surgery?

Increased cardiac output

Improved myocardial contractility
Improved end-organ perfusion
Reduced ventricular diameter (in enlarged hearts)
Decreased myocardial oxygen demand
Decreased PVR -> Increased right heart output

(d) Describe the mechanism of action of milrinone and similar drugs

Milrinone is a Phosphodiesterase inhibitor –
 Competitive inhibition of phosphodiesterase isoenzymes (PDE)
Results in increased cAMP
Positive inotropy
Improved diastolic relaxation (lusitropy)
Also, potent vasodilator -> decreased preload, afterload and PVR
Sensitises myocardium to β-agonists
Inhibit platelet aggregation
Reduce post-ischaemic reperfusion injury
Dilate coronary arteries and grafts

(e) What are the differences in cardiopulmonary resuscitation in post-cardiac

surgery patients?
Immediately identifiable – highly monitored patient
For PEA –
Commence BLS
If no immediately reversible cause is identified -> resternotomy
For VF/VT –
3 shocks before BLS – external chest compressions can cause injury
If unsuccessful – BLS and emergency re-sternotomy
While waiting for re-sternotomy, follow standard ALS algorithm (30:2 compressions, shock every 2 mins,
Amiodarone 300mg after 3rd shock)
On re-sternotomy, commence internal cardiac massage and defibrillation
If unsuccessful – commence CPB
Severe Bradycardia/Asystole –
Immediate pacing (DDD 90-100bpm at max amplitude)
Atropine if epicardial pacing is unavailable or unsuccessful
Use vasopressors with caution

Off pump coronary artery bypass grafting

a) What are the theoretical advantages of off pump CABG (OPCAB) compared to on pump? (20%)
b) What are the disadvantages of OPCAB compared to on pump cardiac surgery? (10%)
c) What causes haemodynamic instability during OPCAB? (20%)
d) Which strategies help to minimise this haemodynamic instability? (20%)
e)What is ischaemic preconditioning? (10%)
f) What are the anaesthetic goals of management of OPCAB surgery? (20%)

Click for model answer by Dr Bronagh McKay

(a)
Reduced risk of CVA
Less disruption of normal coagulation system and reduced requirement for blood products
Lower heparin dosage can be used
Earlier extubation
Reduced length of stay
Reduced stress response
Isolated LAD grafting does not require a sternotomy- surgery can be performed through a small thoracotomy

(b)
More difficult operating conditions
Risk of myocardial ischaemia
 Mortality rate may be higher
Not suitable for all patients- contraindicated in small diameter vessels, diffuse disease, severe calcification and
intramyocardial vessels

(c)

Lifting of the heart out of the pericardial sac to work on the posterior and lateral sides of the heart causing compression on
the right side of the heart and reduced venous return
External compression from retractors
Verticalisation of the heart causing mitral and tricuspid regurgitation

(d)
Maintain high perfusion pressure- MAP >70 mmHg
Avoid tachycardias- keep myocardial oxygen consumption low
Treat bradycardias
Fluid
Vasopressors
Trendelenburg position
Conversion to on pump surgery if haemodynamic instability not corrected with the above

(e)
The ischaemia that results from occlusion of the coronary artey is better tolerated if the technique of ischaemic
preconditioning is used. This involves occlusion of the target vessel for 5 min, with subsequent reperfusion for 3 min
before occlusion for suturing. Preconditioning significantly preserves muscle adenosine triphosphate concentrations.

(f)
Safe induction and maintenance of anaesthesia with cardiac protection
Maintenance of haemodynamic stability
Early emergence and ambulation
Post operative analgesia

Aortic stenosis and transcatheter aortic valve implantation

(a) Describe the pathophysiology of aortic stenosis (20%)

(b) Classify aortic stenosis according to valve area and LV-aortic gradient (20%)
(c) What are the principles of anaesthesia for non-cardiac surgery in patients with AS? State the
haemodynamic goals. (30%)
(d) What are the different types of intervention possible for treating AS? (10%)
(e) What are the principles of anaesthesia for transcatheter aortic valve implantation (TAVI)? (20%)

Click for model answer by Dr Alison White

(a)
- Stenosed aortic valve results in fixed obstruction to ejection of blood from LV
- Increased LV systolic pressure due to overload of LV
- Compensatory LV hypertrophy – increased myocardial O2 demand, reduced myocardial O2 supply leading to
subendocardial ischaemia
- Diastolic dysfunction occurs – reduced compliance and increased reliance on atrial contraction for LV filling (preload and
sinus rhythm dependent), can lead to pulm congestion
- Systolic function is maintained
- LV dilatation with reduced EF occurs (end stage)

These changes can lead to symptoms of angina, breathlessness, syncope and sudden death.
(b)
Normal
3-4 Valve area (cm)
< 10 Peak gradient (mm Hg)
Mild
> 1.5 Valve area (cm)
< 40 Peak gradient (mm Hg)
Moderate
1.0 – 1.5 Valve area (cm)
40 – 65 Peak gradient (mm Hg)
Severe
< 1.0 Valve area (cm)
> 65 Peak gradient (mm Hg)

(c)
Preop
- Full preop assessment.
- Even if it means delaying non-urgent surgery, patients should have ECHO preop to assess stenosis severity and LV
function.
- If not possible, patients should be managed as if they have moderate AS.
- If required, consultation with primary surgical team, cardiologists and cardiac surgeons to determine if AVR required.
- If AVR not required before non-cardiac surgery, anaesthetist can assess risk from ECHO and discuss risks with patient,
family and surgical team as to whether to proceed.

Periop
- Careful haemodynamic monitoring including arterial line.
- Central venous access provides a route for vasoconstrictor therapy.
- Intra-op TOE may be appropriate to assess LV filling and contractility.
- Appropriate antibiotic prophylaxis should be given and strict aseptic precautions adhered to.
- Potential surgical causes of haemodynamic instability should be considered and modified wherever possible.
- Avoid systemic hypotension
* hypotension leads to myocardial ischemia and a downward spiral of reduced contractility causing further falls in BP and
coronary perfusion.
* aim to maintain BP at normal pre-anaesthetic values
* use neuroaxial techniques with caution
may require drugs to maintain systemic vascular tone
e.g. noradrenaline, phenylephrine, metaraminol
- Maintain SR
* atrial contraction important for LV filling
AF and nodal rhythms poorly tolerated
- Avoid tachycardia (ideal rate 60-80 beats/min)
* tachycardia reduces diastolic filling time
therefore reduced time for coronary perfusion
increases O2 demand
- Avoid bradycardia (ideal rate 60-80 beats/min)
* bradycardia results in a reduced CO as the stiff ventricle cannot increase the SV to compensate
* increase in ventricular filling due to longer diastole also increases ventricular wall tension further reducing coronary
perfusion
- Maintain high/normal preload
to enable adequate filling of LV

Postop
- Maintain appropriate iv filling and arterial BP.
- Minimise additional demands on the heart incurred with inadequate analgesia.
- Regional anaesthetic techniques have a potential role but require close monitoring.
- Vasocontrictor infusion may be required to offset any deleterious haemodynamic consequence of central neuraxial block.
 - Avoid NSAIDS – risk of postop renal dysfunction.

(d)
3 interventional options include:
1) surgical aortic valve replacement (AVR)
2) transcatheter aortic valve implantation (TAVI)
3) balloon valvuloplasty of the aortic valve (BAV)

(e)
TAVI will be performed under GA if using a transapical approach. However if a transvascular approach is used, local
anaesthesia with sedation may be possible.

- Preop visit:
Quantify patient’s perioperative risk, optimise co-existing morbidity and provide informed consent.
Give information on invasive monitoring, ECHO and postoperative care on ICU.
Careful premedication to reduce anxiety-induced sympathetic response.

- Monitoring, vascular access and haemodynamic principles:

When general anaesthesia is used tracheal intubation is routine – single lumen ETT for transapical TAVI.
Basic standard monitoring plus an arterial line before induction.
Large bore peripheral cannula, central venous catheter, urometer and temperature monitor is routine.
Use of pulmonary artery catheter is less common.

Haemodynamic goals include:

- maintaining myocardial O2 delivery via adequate systemic pressure and diastolic time
- maintenance of contractility
- optimise preload for a non-compliant left ventricle
- sinus rhythm with an ideal rate 60-80 beats/min.

- Opioid based technique may be favoured for induction/maintenance of anaesthesia to minimise vasodilation and
negative inotropy.
- Haemodynamic support with alpha-agonists and fluids and inotropic support may be required in a poorly functioning LV.
- Defibrillation pads essential.
- If TAVI is performed under GA, TOE should be used.
- If TAVI is performed without GA, TTE should be used.

- Postop
- Majority of patients extubated at end of procedure.
- PCA, intercostal blocks and paracetamol provide satisfactory analgesia after transapical TAVI.
- Most patients able to return to cardiac ward or HDU.
- Care must include identification and management of arrhythmias and pacing, chest drains, surgical incisions, and large
vascular access devices.

Anaesthesia for electrophysiological procedures

(a) What groups of patients may require anaesthesia for electrophysiological procedures? (10%)
(b) What are the principles of anaesthesia for electrophysiological procedures? (30%)
(c) What the minimum standards of monitoring which apply? (20%)
(d) What are the anaesthetic challenges of anaesthetising in the cardiac catheterisation laboratory?
(20%)
(e) What are the potential complications of catheter ablation procedures? (20%)

Click for model answer by Dr Caroline Martin

 (a)
- Patients requiring ablation of arrhythmogenic pathways
- Placement of pacemakers or implantable defibrillators
- Patients for diagnostic studies

(b)
- Range of anaesthesia from anxiolysis to GA with muscle relaxation.
- General principles of cardiac stability and maintenance of physiological parameters.
- Smooth emergence to prevent haematomas from access sites.
- Specifically, use of muscle relaxants may be required for accurate mapping of intracardiac structures; for ablation of re-
entrant tachycardia phrenic nerve stimulation is used and no relaxant is permitted. Volatiles may suppress this arrhythmia
so TIVA is often used.

(c)
- For sedation: at least pulse oximetry, usually ECG and NIBP. Propofol sedation requires capnography.
- For GA: pulse oximetry, ECG and NIBP; if inhalational agents are given, end tidal oxygen, CO2 and volatile agent
monitoring. Invasive BP often used but not required.

(d)
- Patient population – ranging from young, fit and healthy to elderly with multiple co-morbidities requiring invasive devices
such as intra-aortic balloon pump to maintain circulation.
- Environment – remote location, unfamiliar equipment, staff unused to unconscious patients, difficulty obtaining
advanced airway equipment / blood products, dim lighting.
- Limited access to patient head / arms (airway & IV)

(e)
- Vascular damage: bleeding / pseudoaneurysm
- Arrhythmias: any including bundle branch and complete heart block
- Oesophageal damage (thermal / fistula formation)
- Complications of trans-septal puncture: atrial / aortic perforation, pericardial effusion / tamponade
- Atrial stunning
- Embolic damage thrombus / air (TIA/stroke)
- Infection (endocarditis), burns (from skin electrodes)

Angina, dual antiplatelet therapy and troponin

(a) How may angina be categorised? (20%)

(b) What are the criteria necessary for the diagnosis of acute and established myocardial infarction
(MI)? (20%)
(c) List the mechanisms by which troponin may be raised in conditions other than myocardial
infarction. (20%)
(d) Describe the modes of action of aspirin and clopidogrel. For which groups of patients is dual
therapy with these agents recommended? (20%)
(e) What are the indications for prolonged or permanent dual antiplatelet therapy? (These are also
the risk factors for stent thrombosis) (20%)

Click for model answer by Dr Laura McNulty

(a)
- Angina is a commonly a dull, heavy retrosternal pain which commonly radiates to the neck, arm or jaw, which may be
exacerbated by exercise, stress or cold weather.

Categorised as follows;
- Chronic stable angina; usually caused by fixed stenosis, often with a significant stenosis of LAD or epicardial arteries.
Typical pattern of pain and triggers
- UNSTABLE ANGINA; new onset angina, increased severity or frequency or duration from previous stable symptoms, often
due to plaque rupture, part of spectrum of ACS
- NOCTURNAL ANGINA; most commonly at night, secondary to changes in respiratory patterns, eg OSA, which result in
hypoxia and myocardial ischaemia
- DECUBITUS ANGINA; occurs in supine position, increased filling pressures causes increased strain/tension on chamber
walls
- MICROVASCULAR ANGINA; triad of anginal pain, normal angiography but positive EST. Most commonly females and
diabetics
- VASOSPASTIC ANGINA/PRINZMETAL’S; at rest or on exertion, vasospasm of epicardial arteries, commonly associated with
illicit drug use, more common in males, and hyperinsulinaemia
- CHRONIC REFRACTORY ANGINA; not controlled by maximal medical therapy or interventions
- NON CARDIAC CHEST PAIN

- Also can be classified on severity, using the CANADIAN CARDIOVASCULAR SOCIETY CLASSIFICATION, which grades angina
based on symptoms from class I, no limitations, to class IV, debilitating disease

(b)
This has been derived from European Society of Cardiologists and American College Cardiologists

Acute MI;
Increase in troponin with gradual decline PLUS
Ischaemic symptoms
Pathological Q waves
Ischaemia on ECG
Coronary artery intervention eg PCI
OR… pathological findings of AMI

ESTABLISHED MI;
Development of pathological Q waves
OR… pathological findings of healing or healed MI

(c)
- Troponin is a regulatory protein, along with tropomyosin which is found on actin
- It is necessary for cardiac and skeletal muscle contraction and is released in myocardial necrosis
- However a number of conditions in which there is myocardial damage but not AMI/ACS, including

* DEMAND ISCHAEMIA; eg tachycardia, increased myocardial o2 demand but decreased diastolic time and therefore
myocardial perfusion time. Another example LV hypertrophy, increased mass of myocardium therefore endocardial
ischaemia more likely in high oxygen consumption

* ISCHAEMIA WITHOUT CORONARY ARTERY DISEASE; e.g vasospasm as discussed previously. Also CNS events such as
subarachnoid haemorrhage or CVA associated with troponin rise and ECG changes, thought to be secondary to increased
sympathetic outflow

* DIRECT CARDIAC INJURY;

May be MECHANICAL eg cardiac surgery, contusions, CPR; may be ELECTRICAL eg DC cardioversion; CHEMICAL eg
cardiotoxic chemotherapy; INFLAMMATORY eg pericarditis and myocarditis;
STRAIN; pathological stretching of myocardial units and chamber walls results in ischaemia, eg in CCF, RV strain in a large
PE
CKD; at risk of silent necrosis, but also a reduced clearance of plasma troponin

* INFLAMMATORY; inflammatory mediators causing direct injury eg in sepsis, septic emboli causing obstruction of
coronary arteries

(d)
Aspirin and Clopidogrel are both antiplatelet agent, they are similar in that they both cause irreversible platelet inhibit but
their mechanisms differ
 - ASPIRIN
* Irreversible COX 1 inhibitor. Therefore reduced conversion of arachidonic acid to Thromboxane A2, which promotes
platelet aggregation
* Favours production of prostaglandins which inhibit platelet aggregation
* Effects platelet for entire life span therefore takes 7-10 days for affected platelet to be destroyed for effects to diminish

- CLOPIDOGREL
* A thienopyridine, along with ticlopidine
* Selectively an irreversibly inhibits P2Y12 ADP receptor on the surface of the platelet; it has no effect on arachidonic acid
* It is a pro drug meaning that it must be metabolised by the liver in order for the drug to be active
* Similar to aspirin in that it takes 7-10 days for platelet turnover for effects to be reversed

Dual therapy recommended for certain patients as drugs synergistic, recommended in management of NSTEMI, in patients
with known CAD but at risk of MI, and in patients undergoing PCI

(e)
* Patients who have had a bare metal stent placed may only require dual therapy for 4 weeks after PCI
* This is increased from 3 – 12 months if a drug eluting stent is used, this is because the regrowth of epithelium around
stent is much delayed and this is the period of time when risk of thrombosis greates
Prolonged therapy recommended in patients who remain high risk for MI despite treatment
* Also indicated in patients with cerebrovascular disease who are at high risk of CVA, and in certain patients with PVD

Complications of cardiac surgery

(a) What are the potential cardiac complications immediately following cardiac surgery?
(b) What are the potential non-cardiac complications (excluding CNS) immediately following
cardiac surgery?
(c) What are the potential neurological complications immediately following cardiac surgery?
(d) What are the recent advances in CPB aimed at minimising complications to do with the CPB
circuit?

Click for model answer by Dr Najmiah Ahmad

(a)
Mechanical
- spasm or occlusion of a coronary artery graft
- prosthetic valve: paravalvular regurgitation
- cardiac tamponade, hematoma,
- and systolic anterior motion of the mitral valve with left ventricular outflow tract obstruction.

Physiological
- Myocardial stunning, low output state cardioplegia related, low inotropic state
- Inadequate preload, poor relaxation
- Vasoplegia /vasodilatory shock– low SVR
- Conduction abnormality –tachy brady arrhythmias, AF. Ventricular arrythmias
- Myocardial infarction

(b)
Pulmonary
Atelectasis, consolidation,pneumonia, decreased compliance, failure to wean, ALI, ARDS, pulmonary oedema, pulmonary
emboli
Pneumothorax
Pulmonary effusion (left), early blood, late serous fluid
Renal
 Acute kidney injury
Haematology
Bleeding
Transfusion related complications
Coagulopathy
Heparin Induced Thrombocytopaenia
Hypoperfusion/thromboembolic related liver and GIT complications
Other
Protamine related –bronchospasm, non cardiogenic pulmonary oedema anaphylaxis
Leg wound SVG harvest, bleeding, infection
Deranged acid base balance and electrolytes hyperkalaemia/hypocalcaemia

(c) What are the potential neurological complications immediately following cardiac
surgery?
Central
Stroke- haemorrhagic/embolic
Delirium
Neurocognitive impairment
Neuropsychiatric impairment
Seizure
Coma

Peripheral
Phrenic nerve palsy
Intercostal nerve damage
Upper limb- brachial plexus, ulnar nerve injury
Lower limb- common peroneal, tibial nerve injury

(d)
Centrifugal pump vs roller pump
Less damage to RBC, platelets, plasma proteins.
Non occlusive nature alters flow rate, prevents high pressure build up and prevents circuit rupture
Mini extracorporeal circulation – heparin bonded / phosphorycholine –reduce SIRS
Haemofiltration, reduces the prime volume and haemodilution
Continuous in line acid base and electrolytes monitoring
Leukocytes filter/ultrafiltration
Cell salvage

Cardiopulmonary bypass

(a) List the components of the cardiopulmonary bypass (CPB) circuit (30%)
(b) How may perfusion on CPB be assessed as adequate? (10%)
(c) What methods of myocardial protection are employed during cardiopulmonary bypass? (20%)
(d) Describe the process of weaning from cardiopulmonary bypass. (30%)
(e) What factors may indicate failure to wean from bypass? (10%)

Click for model answer by Dr Anna Laird

(a)
A circuit to direct blood from Right atrium/SVC/IVC to oxygenate it, remove CO2 and return it to aorta.

- Heparin/ phosphorylcholine coated tubing/components

- Venous line - large bore to drain under gravity
- Reservoir - Venous from venous line, surgical suction
- Cardiotomy - low volume cannula placed in left ventricle to prevent accumulation of blood
 - Filter - remove gas and particulate emboli, leukocyte depleters
- Oxygenator -
* Membrane - large surface area of fine capillary tubes allows gas flow. The FiO2 deterimines PaO2
* Bubble - not used as often due direct contact of blood with air surfaces which damage blood constituents
- Heat exchanger - allows manipulation of temperature
- Pump- roller/ centrifugal
- Arterial line - into aorta

- Separate circuit for cardioplegia suction solution to be enters back into circuit

(b)
Difficult to assess but aim to match blood flow with the organs oxygen demand.

- Factors related to
* CPB machine - blood flow per minute or prime viscosity
* Patient factors - vascular resistance, total body weight or temperature
MAP - aim 65mmHg
* Arterial blood gases can assess lactate and acid base balance
* Venous oxygen saturation
* Neurological physiologic monitoring such as EEG or evoked potential, near infrared spectroscopy (cerebral oximetry) and
transcranial Doppler are used to estimate cerebral blood flow.

(c)
- Monitoring - to assess if any electrical activity when on bypass
- Cardioplegia solution -anterograde and/or retrograde. Once the cross clamp is applied, cardioplegia can be given into the
aortic root or directly into the coronary ostia.
(St Thomas or harfield - k 20-80mmols, mg, ca, procaine, cl)
- Cooling with ice/slush to heart directly
- Cooling of patient - core temperature
- Myocardial ischaemic preconditioning

(d)
In order to make weaning possible a sequence of events must be perfectly balanced -
- T Temperature: Nasopharyngeal 36-37 C
- R Rate: Sinus rhythm and rate controlled by an epicardial pacing system
- A Air: Transoesophageal echocardiography used to confirm good intra-cardiac de-airing
- V Ventilation: Mechanical ventilation and alarm settings restarted. Visual observation.
- V Venting: Aortic root venting should be removed or reduced and matched by the arterial pump
- E Electrolytes: Normal physiological levels and Hb
- L Level: Operating table

(e)
- Low systemic BP- low SVR or poor CO
- Cardiac filling pressures - increased R atrial pressure signs of a failing Right or left ventricle
- Arrhythmias
- Anaemia,
- Acid- base disturbances,
- Hypovolaemia
- Air embolism
- Severe acidosis

Cardiac transplantation, anaesthesia and the transplanted heart

(a) What are the intraoperative anaesthetic principles governing heart transplantation? (50%)
(b) What are the complications of cardiac transplantation? (20%)
(c) What are the physiological differences of the transplanted heart? (20%)
(d) What is the pharmacological relevance of this to anaesthesia? (10%)

Click for model answer by Dr Neil McLoughlin

(a)
- Assess right ventricle function and pulmonary resistance
- Blood products should be made available
- Deactivate implantable cardioverter defibrillator
- External defibrillator pads are required if re-do surgery
- Transoesophageal echocardiography (TOE)
- Administration of immunosuppressants and prophylactic antibiotics, and meticulous attention to sterility
- Monitoring: multi-lead ECG, oxygen saturation, arterial blood pressure, central venous pressure, pulmonary artery
pressure
- Large bore venous access, central venous access, 8Fr central venous sheath, Foley catheter
- Balanced general anaesthetic with haemodynamic stability
- Antifibrinolytics (e.g. transexamic acid)
- TOE to provide information about donor heart function
- Left atrial pressure line can be sited intraoperatively for estimation of left ventricular end-diastolic pressure
- Inotropic support is nearly always used, agent varies by institution
- Reduction of pulmonary vascular resistance e.g. inhaled nitric oxide up to 20ppm or epoprostenol, sildenafil
- Pressure areas padded to avoid nerve compression
- Maintenance of normal body temperature following makes postoperative extubation feasible

(b)
- Donor coronary artery disease - commonest cause of death beyond the first year after transplantation
- Rejection - important clinical problem but infrequent in longer-term patients on stable immunosuppressive treatment
- Immunosuppression - usually achieved with triple therapy based on azathioprine, cyclosporin and prednisolone. Long
term treament with these drugs is accosiated with infection, increased incidence of malignancy, musculoskeletal problems
and chronic renal impairment
- Associated diseases - Patients may have required transplantation for a systemic disease, the complications of which may
have anaesthetic implications. For example:
- Ischaemic cardiomyopathy: generalised atherosclerosis.
- Diabetes secondary to steroid immunosuppression.
- Sarcoid and amyloid cardiomyopathy.
- Epilepsy is common post-cardaic transplantation.
- Hypertension is common after cardiac transplantation and may be related to cyclosporin therapy

(c)
- The transplanted heart has no autonomic innervation
- The resting heart rate is typically 90-100bpm due the loss of vagal tone.
- The normal reflex heart rate changes that occur in response to laryngoscopy, visceral traction or fluctuations in blood
pressure are lost.
- The lack of rapid homeostatic adjustments in heart rate to sudden drug-induced changes in vascular resistance can
produce wide swings in blood pressure which can be troublesome during anaesthesia, therefore an adequate preload must
be maintained.
- A blunted response to exercise is also seen with a gradual rise to a reduced maximal heart rate then a gradual decline
following cessation of exercise.
- Dependence on endogenous catecholamines in order to mount a chronotropic response rather than then normal
mechanism of vagal withdrawal together with an increase in cardiac sympathetic nerve activity.

(d)
- Denervation alters the pharmacological response to certain drugs.
- Cardiac vagolytic effect of drugs such as atropine and glycopyrrolate are lost and denervation supersensitivity to other
drugs is seen: Adenosine, Adrenaline, Noradrenaline.
- Digoxin controls the ventricular response rate in atrial fibrillation by increasing vagal tone and therefore cease to be
effective as an anti-arrhythmic in the transplanted heart.
Adult congenital heart disease

(a) How may grown-up congenital heart disease (CHD) be classified? (20%)
(b) What are the specific considerations in anaesthetising adult patients with CHD? (30%)
(c) What are the factors increasing and decreasing pulmonary vascular resistance? (10%)
(d) What factors make patients with CHD more prone to haemorrhage? (10%)
(e) Which groups of patients should receive antibiotic prophylaxis against infective endocarditis?
(10%)

Click for model answer by Dr Valerie Marshall

Paediatric congenital heart disease

(a) Describe the normal (or series) circulation physiology - contrast this with the parallel and single
ventricle or Fontan circulation pathophysiology of congenital heart disease. (30%)
(b) How may congenital heart disease in children be physiologically classified? (30%)
(c) How may children with heart disease undergoing non-cardiac surgery be stratified according to
risk? (10%)
(d) Describe the basic principles of management of a 3 month old with a large VSD presenting for
emergency surgery for scrotal swelling (10%)
(e) Describe the basic principles of management of a 6 year old with a repaired TOF presenting for
dental extraction (10%)
(f) Describe the basic principles of management of a 12 year old with Fontan circulation presenting
for emergency ORIF of fracture (10%)

Click for model answer by Dr Grainne Fitzpatrick

(a)
Normal (series) circulation: consists of a pulmonary and systemic circulation working together in series. Blood flows from
the right atrium to right ventricle, to the lungs where it is oxygenated and reaches the systemic circulation via the left
atrium and left ventricle. Some CHD conditions [Link] behaves as the normal series circulation but with mixing of
deoxygenated and oxygenated blood through one or more ‘holes’. The direction of blood flow through the lesion depends
on the pressure gradient across it. Accordingly the degree of shunt depends on the size of the defect and the relative
pressure gradients.
Balanced (parallel) circulation: Instead of the circulation being in series they are in parallel. Some CHD conditions involving
large intra/extra-cardiac communications meaning that blood flow to the systemic and pulmonary circulation varies
depending on the relative resistance in each circuit. Therefore blood flow to the lungs or the body depends on the balance
between pulmonary vascular resistance and systemic vascular resistence. Excessive pulmonary blood flow results in
pulmonary oedema and poor systemic perfusion. Conversely insufficient pulmonary blood flow causes profound cyanosis.
Children with large unrepaired AVSD’s or VSD’s lesions can exhibit a balanced circulation physiology.
Single ventricle circulation: Some forms of CHD are not amenable to full correction to a series circulation. Children with
these conditions will have palliation by creating a single ventricle circulation. This occurs as a staged process. The first
stage at 3-5months is known as a Glenn Shunt and involves the superior vena cava being connected directly to the right
pulmonary artery. The second stage connects the inferior vena cava to the right pulmonary artery, this separates the
systemic and pulmonary circulation and returns arterial oxygenation to normal. This stage occurs at around age 3-5. A
single ventricle pumps blood to the systemic circulation and the pulmonary circulation relies on blood flowing passively to
the lungs and down a pressure gradient from the pulmonary artery to the left atrium. The pressure gradient in the sole
determinant for pulmonary blood flow.

(b)
CHD can be classified in a number of ways. Firstly, as cyanotic and non-cyanotic.
Cyanotic heart disease incl:
Conditions were obstruction to pulmonary flow is present (eg. Tretralogy of Fallot, Pulmonary atresia)
Mixing in a common chamber (eg. trunctus ateriosus)
Separation of the pulmonary and systemic circulations (eg. transposition of the great arteries).

Non Cyanotic Heart incl:

1) Pressure overload conditions eg. Coarctation of the aorta and aortic stenosis.
2) Volume overload conditions eg. Ventricular and atrial septal defect, PDA and hypoplastic left heart syndrome.

Another physiological classification divides conditions depending on the direction of blood flow through the lesion.
1) Simple left to right shunts which cause an increase in pulmonary blood flow. This incl. ASD, VSD, AVSD and PDA.
2) Simple right to left shunts, which cause a reduction in PBF and cyanosis. Examples include Tretalogy of Fallot, pulmonary
atresia, tricuspid atresia and ebstein’s anomaly.
3) Complex shunts. These cause mixing of pulmonary blood flow and systemic blood flow. Amongst others these include:
Hypoplastic left heart syndrome, transposition of the great arteries and truncus ateriosus.

(c)
Generally, children with CHD undergoing non-cardiac surgery have an increased risk of morbidity, perioperative cardiac
arrest, and a higher 30 day mortality. However, the complexity of cardiac defects and the variety of non-cardiac surgery
means some are at an increased risk compared to others. Different studies identify a variety of factors associated with a
high risk of perioperative complications, such as disease complexity, physiological status, type of surgery, and young age.
The most important factors are the physiological status and complexity of heart disease.
High risk children for non-cardiac surgery include:
1) Physiologically poorly compensated and/or the presence of the following major complications
(a) Cardiac failure
(b) Pulmonary hypertension
(c) Arrhythmias
(d) Cyanosis
2) Complex lesions (single-ventricle or balanced circulation physiology, cardiomyopathy, aortic stenosis)
3) Major surgery (intraperitoneal, intrathoracic, anticipated major blood loss requiring transfusion)
4) Under 2 yr old
5) Emergency surgery
6) Preoperative hospital stay more than 10 days
7) ASA physical status IV or V

Intermediate risk includes:

1) Physiologically normal or well compensated
 2) Simple lesions
3) Major surgery (intraperitoneal, intrathoracic, anticipated major blood loss requiring transfusion)
4) Under 2 yr old
5) Emergency surgery
6) Preoperative hospital stay more than 10 days
7) ASA physical status IV or V

Low risk includes:

1) Physiologically normal or well compensated
2) Simple lesions
3) Minor (or body surface) surgery
4) Over 2 yr old
5) Elective surgery
6) Preoperative hospital stay less than 10 days
7) ASA physical status I – III

(d)
This depends on a number of factors. Firstly the anaesthetist needs to assess the severity of the CHD and if any symptoms
from it are present, for example poor weight gain, poor feeding, signs of cardiac failure, pulmonary oedema or
arrhythmias. If none if these signs are present and it is a simple VSD for which the child has compensated well, then he/she
can be classified as intermediate risk. If the operation is an emergency and the hospital in question is used to dealing with
children under the age of 2 then they can proceed with the operation, and if needed liaise with a specialist hospital for
advice. If however, the hospital does not preform paediatric surgery routinely, the child should be transferred to a
specialist hospital.
Induction of anaesthesia should be a slow cautious gas or intravenous induction, beware of the possibility of poor cardiac
reserve. Avoid high inspired oxygen concentrations in order to minimize left to right shunt and maximize systemic
perfusion. They may require higher ventilator pressures than expected because of pulmonary oedema. Avoid air bubbles in
venous lines because of the risk of paradoxical embolus. Endocarditis prophylaxis unnecessary

(e)
If the TOF is repaired then the lesion is likely to be small and well compensated for physiologically. Therefore the patient is
most likely low risk. The surgery could be performed in their local hospital without the need for specialist input. However if
there is evidence of VE’s on ECG then advice from cardiology is needed as this can sometime be an ominous sign.

(f)
As this is a single ventricle circulation, the patient has a very complex condition and would be deemed high risk. As this
facture may be an emergency there may not be time for transfer to a specialist hospital where this patient should ideally
be managed. If transfer is not possible then advice should be sought from the specialist centre.
Induction should be either a slow gas induction or slow IV induction. Spontaneous ventilation may be more beneficial as
this aids pulmonary blood flow but hypoxia, hypercarbia and basal collapse must be avoided, which will all increase
pulmonary vascular resistence and reduce blood flow. If using positive pressure ventilation, then high pressure, high PEEP
and long inspiratory times should be avoided as these too compromise PBF. Slight head up position aids venous return and
pulmonary blood flow, as does raising the legs.

Cardiomyopathies and ventricular assist devices

(a) What are the distinguishing pathological features between the different cardiomyopathies? How
do these affect anaesthetic management aims? (30%)
(b) What are the indications and contraindications for ventricular assist device (VAD) insertion?
(20%)
(c) What are the principles of anaesthesia for VAD insertion? (30%)
(d) What postoperative complications may be encountered? (20%)
Click for model answer by Dr Alexander Davey

(a)
Three types of cardiomyopathy

Dilated:
- An enlarged poorly contractile ventricle with impaired systolic function although diastolic dysfunction results in raised
LVEDP in extreme cases.
- Ensure medical therapy optimised and possible need for cardiac resynchronisation addressed electively.
- Aim for normal heart rate, rhythm, adequate preload and avoid negative inotropy or increases in afterload.
- Potassium and magnesium should be corrected.

Hypertrophic:
- Pressure overloaded left ventricle with normal or reduced chamber size.
- CPP is reduced secondary to increased LVEDP and the hypertrophied ventricle has a greater oxygen demand resulting in
high risk for ischaemia.
- Adequate volume loading also important with increased LVEDP.
- Significant interventricular septal hypertrophy - dynamic LVOT obstruction can occur. This can cause complete LVOT
obstruction if associated with systolic anterior motion of the anterior leaflet of the mitral valve.
- Aim for sinus rhythm (very important), high normal afterload and avoid inotropy and chronotropy.

Restrictive:
- Characterised by reduced ventricular compliance
(Idiopathic then amyloidosis, haemachromatosis and sarcoidosis).
- Anaesthesia can precipitate cardiac arrest due to reduced myocardial contractility, venous return (esp. if IPPV), and
reduced SVR.
- High filling pressures required and high normal SVR with maintenance of normal contractility and sinus rhythm.

(b)
- Acute heart failure as a bridge to recovery i.e. cardiogenic shock post MI or cardiotomy
- Chronic heart failure as a bridge to transplant i.e. secondary to IHD, HTN or other cardiomyopathy
- Destination (permanent) therapy when recovery is unlikely and transplant is contraindicated. Not a routine practice in the
UK.

(c)
- Preoperative: Multi-comorbidities are usual; cerebrovascular disease; COPD; renal impairment; hepatic congestion;
diabetes; anticoagulated; potential PVC / CVC sepsis. Premed can cause hypoventilation with disturbed PVR.

- Perioperative: Meticulous asepsis for new vascular catheters; IABP may be needed; attention to potential disturbance of
PVR with hypoxia or hypercarbia during induction using RSI. Minimal monitoring plus CVC, IABP, 5lead ECG,+/- PAC and
TOE. CPB may not be required.

- Postoperative: VAD in fixed mode for 24hours to avoid excess emptying & collapse; managed on CSICU; TOE left insitu to
monitor.

(d)
- Bleeding
- PFO: unmasked by left atrial decompression on VAD activation with consequent right to left shunt and hypoxia
- Right heart failure: from increased PVR or inadequate preload
- Hypotension: haemorrhage, aortic dissection; tamponade; septic; adrenal insufficiency and low VAD flows
- Arrhythmias: although VADs protect from lethal arrhythmia they will affect native function and reduce output
- CNS: from thromboembolic or haemorrhagic phenomena
- Infection: strict measures taken to avoid device / line infection
Coagulation issues in cardiac surgery

(a) Describe the normal process of haemostasis (30%)

(b) Describe the agents which may be employed for anticoagulation and reversal of anticoagulation
for cardiopulmonary bypass. (30%)
(c) Describe the monitoring of anticoagulation throughout the procedure. (20%)
(d) What is thromboelastography? Draw a normal TEG trace. (20%)

Click for model answer by Dr Ciara O'Donnell

(a)
The mechanism by which bleeding ceases following vascular disruption
3 key components:
- vascular endothelium disruption leading to vasoconstriction,
- platelet adhesion as exposed collagen and vWF bind to GPIa and GPIb platelet receptors respectively (primary
haemostasis) and
- activation of the coagulation cascade to produce thrombin and then fibrin from fibrinogen (secondary haemostasis)
Fibrin strengthens and stabilises the platelet plug

(b)
Heparin 4-5mg/kg (500IU/kg) is a negatively charged molecule that potentiates the action of antithrombin III
ABG for ACT after 3–5 min
Ensure ACT above 3–4 times of baseline ACT (>480 s) before initiating CPB
5000 IU unfractionated heparin in CPB prime solution
Monitor ACT at least every 30 min during CPB

In cases of HIT, alternative anticoagulants can be used e.g. bivalirudin , Low molecular weight heparin (LMWH) Danaparoid,
Lepirudin.

Reversal of heparinisation is by protamine 1mg per 100units of heparin administered.

(c)
Activated clotting time is monitored every 30min
Must be maintained >480sec
APTT and PT are lab tests only useful in the perioperative period
TEG measure whole blood viscoelastic changes and is a quick test taking around 10min

(d)
Thromboelastography (TEG) measures whole blood viscoelastic changes associated with fibrin polymerization.
information about coagulation factor activity and platelet function within 10–20 min
A pin, attached to a torsion wire, is suspended into a blood sample contained in an oscillating cuvette. Clot forms gradually
in the blood sample creating increasing displacement of the pin. This is translated into a graphical representation
Graph represents sheer elasticity vs time. The magnitude of the output represents the strength of the fibrin-plt bonds and
gives a wide TEG

Pacemakers and implantable defibrillators

(a) What are the indications for permanent pacing? (20%)

(b) What are the indications of placement of a permanent defibrillator? (20%)
(c) What key information should be obtained about the patient/device prior to anaesthesia and
surgery? (20%)
(d) What preoperative precautions should be taken with regard to a patient with a pacemaker/ICD?
(20%)
(e) Describe the considerations in a patient with a pacemaker that has not been switched off due to
emergent surgery. (20%)

Click for model answer by Dr Lisa Taylor

(a)
- Acquired 3rd degree heart block
- Symptomatic acquired 2nd degree heart block
- Chronic bifascicular and trifascicular block may be the indications if 3rd degree block or 2nd degree (type II) occurs
Post-MI infranodal AV block and associated BBB or persistent and symptomatic 2nd or 3rd degree block
- Sinus node dysfunction with symptomatic bradycardia and frequent sinus pauses or symptomatic chronotropic pauses
- Sustained VT
- Hypertensive carotid sinus syndrome
- Hypertrophic or dilated cardiomyopathy with sinus node dysfunction or AV block
- After cardiac transplantation, if symptomatic bradyarrhythmias
Chronic AF with associated bradycardia

(b)
- VF or SCD survivors
- VT causing syncope not related to acute MI or other correctable causes
- Minimally symptomatic VT with LVEF of <35%
- Patients with previous MI with LVEF <35%, asymptomatic spontaneous non-sustained VT with sustained VT/VF
- Long QT syndrome with recurrent syncope or family history of SCD
- Brugada syndrome presenting with VT/VF or syncope with inducible VT
- Arrhythmogenic right ventricular dysplasia with documented sustained VT/VF or those with a family history of SCD;
- HCOM with sustained VT/VF in the absence of reversible causes or with a family history of SCD

(c)
- Ask for the patient’s registration card for the device.
- Device manufacturer, model number, serial number, implanting and follow-up hospital
- Anatomical position
- Indication
- Date of insertion
- Details of recent check-up ( battery condition,
- Mode of action
- ? rate modulator function (should be de-activated prior to anaesthesia)
- ? any dizziness, syncope or heart failure
- ? any recent deterioration in underlying medical condition
- ECG – rhythm, pacemaker activity, electrical capture
- CXR – position of box leads electrode and cardiac failure
- Electrolytes – abnormalities effect capture
- Interrogation of the device

(d)
- Careful pre-op visit and review of notes
- ? rate modulator function (should be de-activated prior to - anaesthesia)
- Organise an interrogation or check-up of the device in the elective scenario
- Reprogramming of the device as is appropriate for the patient and the type of surgery (e.g. devices with minute
ventilation - sensors for rate modulation)
- Anti-tachycardia therapy should be disabled
- If high risk of EMI then precautions include the use of magnets if appropriate or temporary cardiac pacing
(transthoracic/transvenous)
- For ICD patients they should be connected to an external defrillator and continuously monitored
- Decide on method of diathermy and arrange for a telemetric programmer to be present if extensive close-proximity
 electrocautery is required
- Arrange post-operative reprogramming/ check-up
- Arrange post-operative care level e.g. may require HDU care

(e)
- Careful standard monitoring +/- invasive blood pressure monitoring and careful placement of any central venous access
(avoid vessels with leads)
- Diathermy – use bipolar if possible and if not position as far away from device as possible, at lowest amplitude and use in
short bursts
- Patient positioning, shivering, alteration in heart size and positive pressure ventilation may all cause lead displacement
which can result in loss of capture or increase in the pacing threshold
- Shivering and fasciculation can confuse rate modulators
- Peripheral nerve stimulators may interfere with function
- Defibrillation may cause damage
- Have facilities for CPR, emergency defibrillation and temporary pacing available
- Consider using a clinical magnet
- Check function as soon after surgery as possible

Ultrasound and transoesophageal echocardiography

(a) Describe the basic physics of ultrasound. What is the Doppler principle? (30%)
(b) What are the indications for transoesophageal echocardiography? (20%)
(c) What are the contraindications for TOE - relative and absolute? (10%)
(d) What are the complications of TOE? (20%)
(e) What haemodynamic variables can be measured or derived from TOE? (20%)

Click for model answer by Dr Mona Behravesh

(a)
- Ultrasound is defined as sound with a frequency greater than 20 kHz. Echocardiography machines typically emit
ultrasound at a frequency of 2e10 MHz. The speed of ultrasound is determined solely by the medium through which the
wave travels.
- The speed of sound in the heart is approximately 1540m/second.
Ultra sound waves produce by using piezoelectric effect in quartz crystals.

- Doppler: frequency of sound wave reflected from a moving object is different form the emitted frequency.

(b)
Specific indications for TOE:
1)Prolonged Imaging( Peri operative imaging)
2)Interest in posterior structures: LA,
3) High resolution required: Dx of Endocarditid especially in Obese or Emphysematous pt

American college of cardiology 2011

- Dx of Endocarditis
- To evaluate suspected aortic pathology: dissection
- To evaluate cardiac source of thrombus
- To evaluate for cardiac pathology when TTE is non diagnostic
- To facilitate clinical decision making: cardioversion, ablation of pt with AF, A flutter
- To assist with non coronary percutaneus cardiac interventions: percutaneous valve, placement of closure devices,
valvuloplasty.
- In ICU: to assess pt with
Severe hypotension
Blunt chest trauma
 Un explained hypoxia
Uncertain volume status
- To assess complications following MI i.e. valves, ventricular septal defect, free wall rupture with tamponade

(c)
- Relative:
Altered mental status
Oesophageal stricture or malignancy
Cervical spine arthritis with reduced movement
Severe thrombocytopaenia
Surgical interposion of oesophagus
Tenuous cvs status
Hx of odynophgia and dysphagia

- Absolute:
-Pt who is not fasted for 6 hrs
- pt refusal
- absence of oesophagus

(d)
Complications: 1-3% in clinical setting and up to 13% in emergency setting
- Sore throat
Airway device displacement
Airway obstruction
Oropharyngeal/ dental trauma
Gastric/ oesophageal trauma
Reflex stimulation (sympathetic): Arrhythmia, MI, ST segment changes
Aneurysmal rupture
Infection

(e)
- Measured:
*CO
*LV filling pressure
*Pulmonary artery pressures
*atrial interaction
*chamber preload

- Derived:
*Using flow signals of pulmonary artery, aortic and mitral and tricuspid valves *Can calculate Stroke volume, SVI

Postoperative cardiac output failure and the intra-aortic balloon pump

(a) What are the causes of low cardiac output post cardiac surgery? (20%)
(b) What is the mechanism of action (20%) and
(c) physiological effects of the intra-aortic balloon pump (IABP)? (20%)
(d) What are the indications and contraindications for the use of an IABP? (20%)
(e) What complications may be suffered as the result of use of the IABP? (20%)

Click for model answer by Dr Katie Megaw

(a)
Reduced preload:
Absolute hypovolaemia (bleeding)
Relative hypovolaemia (sedatives, rewarming, vasodilators)
Cardiac tamponade
Right ventricular dysfunction

Reduced contractility
Myocardial stunning
Preexisting poor left ventricular function
Acid-base abnormalities
Inadequate revascularisation

Increased afterload
Vasoconstriction
Fluid overload and left ventricular distension
Left ventricular outflow tract obstruction (post MVR)

Arrhythmias

Diastolic dysfunction

Co-existing pathologies
Sepsis, SIRS
Anaphylaxis
Adrenal insufficiency

(b)
Circulatory assist device
Consists of double lumen 8-9.5 French catheter with 25-50ml balloon attached at distal end and console with a pump to
drive balloon
Outer lumen used for gas delivery to balloon and inner lumen for monitoring systemic arterial pressure
Helium often used because of low density and easy absorption in case of balloon rupture
Inserted via femoral artery using Seldinger technique into descending aorta
Tip 2-3cm distal to origin left subclavian artery
Console detects trigger for balloon deflation. Commonly ECG waveform and systemic arterial pressure waveform
Counter pulsation - Inflates with helium during diastole (middle of t wave/dicrotic notch) and deflates during systole (peak
of r wave/just before upstroke on arterial pressure waveform)
Diastolic augmentation (see below)
Balloon inflation causes volume displacement within the aorta, both proximally and distally
Assistance every beat (1:1) or less often (1:2, 1:4, 1:8) depending on haemodynamic status


(c)
Haemodynamic effects:
Aorta: reduced systolic and increased diastolic pressure
Left ventricle: decreased systolic pressure/end-diastolic pressure/volume/wall tension
Heart: decreased afterload, decreased preload and increased cardiac output
Blood flow: increase or no effect on coronary blood flow
Overall decrease in myocardial oxygen demand and increased oxygen supply
Renal effects:
Blood flow can increase by 25% secondary to increased cardiac output
If positioned juxta-renal may decrease blood flow and urine output

Haematological effects:
Haemolysis of red blood cells causes reduction in haemoglobin and haematocrit by 5%
Thrombocytopenia through mechanical damage, heparin or both
 (d)
Indications for IABP:
Unstable angina refractory to medical treatment
Cardiogenic shock post myocardial infarction
Decompensated left ventricular failure
Mechanical complications of acute MI: mitral regurgitation and ventricular septal defect
Ischaemia related ventricular arrhythmias
Perioperative low cardiac output
Acute ischaemia associated with coronary angioplasty
Weaning from cardiopulmonary bypass
Bridge to cardiac surgery/transplantation
Paediatric complex cardiac anomalies
Contra-indications for IABP:
Absolute: aortic regurgitation, aortic dissection, chronic end stage heart disease with no anticipation of recovery, aortic
stents
Relative: Uncontrolled sepsis, abdominal aortic aneurysm, tachyarrhythmias, severe peripheral vascular disease, major
arterial reconstruction surger

(e)
Transient loss of peripheral pulse
Limb ischaemia
Thromboembolism
Compartment syndrome
Aortic dissection
Local vascular injury—false aneurysm, haematoma, bleeding from the wound
Infection
Balloon rupture (gas embolus)
Balloon entrapment
Haematological changes eg thrombocytopenia, haemolysis
Malpositioning causing cerebral or renal compromise
Cardiac tamponade

March 2016

A 70-year-old woman with aortic stenosis presents for an open aortic valve replacement (AVR).

 a) What is the pathophysiology of worsening aortic stenosis? (8 marks)

 b) Which specific cardiac investigations may be used in assessing the severity of this woman’s disease?
(3 marks)

 c) Give values for the peak aortic flow velocity, mean pressure gradient and valve area that would
indicate that this woman has severe aortic stenosis. (3 marks)

 d) What would be your haemodynamic goals for the perioperative management of this patient? (6 marks)
 SAQ
 Examiners' report
September 2015
 a) What are the central and peripheral neurological complications of coronary artery bypass surgery? (7
marks)

 b) What are the risk factors for central neurological complications? (6 marks)

 c) How can the incidence of central neurological complications be reduced? (7 marks)

 SAQ
 Examiners' report
March 2015

 A 67 year-old patient is to undergo coronary artery surgery on cardiopulmonary bypass (CPB).

 a) What dose of heparin is used to achieve full anticoagulation for CPB and how is it given? (2 marks)

 b) Which laboratory and “point-of-care” tests determine the effectiveness of heparin anticoagulation in
CPB patients? Give the advantages and/or disadvantages of each test. (10 marks)

 c) What are the causes of inadequate anticoagulation in a patient whom it is believed has already received
heparin? (5 marks)

 d) Describe the possible adverse reactions to protamine. (3 marks)

 SAQ
 Examiners' report
September 2014

 a) What are the purposes (3 marks), typical composition (4 marks) and physiological actions of cardioplegia solutions? (5
marks)

 b) By which routes can solutions of cardioplegia be administered? (2 marks)

 c) What are the possible complications of cardioplegia solution administration? (6 marks)

 SAQ
 Examiners' report
September 2013

You are asked to review a 65-year-old man on the Cardiac Intensive Care Unit who underwent coronary artery bypass surgery earlier in the
day.

a) Which clinical signs suggest the development of acute cardiac tamponade? (40%)

b) List the investigations and their associated derangements that could confirm the diagnosis of acute cardiac tamponade. (15%)

c) What is the management of acute cardiac tamponade in this patient? (45%)

 SAQ
 Examiners' report
September 2012

a) What are the theoretical advantages of “off pump” coronary artery bypass grafting (OPCAB)
compared to “on bypass” technique? (35%)

b) What causes haemodynamic instability during OPCAB? (20%)

c) Which strategies help to minimise this haemodynamic instability? (25%)

d) Outline the measures that help to minimise perioperative hypothermia during OPCAB. (20%)

 SAQ
 March 2011

a) What are the central and peripheral neurological complications of coronary artery bypass (CABG) surgery? (35%)

b) What are the risk factors for central neurological complications following CABG surgery? (30%)

c) How can the risk of central neurological complications of CABG surgery be reduced? (35%)

 SAQ
March 2010

a) Describe the principles of using an intra aortic balloon pump (IABP). (30%)

b) What are the indications (20%) and contraindications (15%) to use of an IABP?

c) List the main complications of using this device. (25%)

 SAQ
October 2004

A patient on the ICU, who had cardiac surgery completed 3 hours ago, is still intubated.
What clinical features might suggest the development of acute cardiac tamponade? (55%)
How might you confirm the diagnosis? (5%)
Outline your management of acute cardiac tamponade? (40%)

 SAQ
October 2003

What are the risks and benefits of thoracic epidural anaesthesia/analgesia for coronary artery surgery?

 SAQ
October 2002

What are the possible deleterious consequences of cardiopulmonary bypass when used in coronary artery surgery? How may
these be reduced?