2. Cardiothoracic Flashcards
a) List the indications for endoscopic thoracic sympathectomy (ETS). (25%)
> Palmar, axillary or craniofacial hyperhidrosis.
Chronic regional pain syndromes.
Facial blushing.
Chronic angina pectoris, unmanageable by pharmacological or cardiac
intervention (very unusual indication now).
b) Outline the general (30%) and airway (15%) implications of managing a patient for ETS under general
anaesthesia.
General:
> Patients are predominantly young and fit, but may be older with
comorbidities especially if the indication is for refractory angina pectoris:
consider need for additional assessment and investigation preoperatively.
> Complications are rare but can be catastrophic: ensure the patient has
full understanding of risks versus benefits.
> Occasionally, conversion from laparoscopic to open surgery is necessary:
prep and drape ready for thoracotomy.
> Risk of major haemorrhage: ensure large-bore intravenous access and
two group and save samples for rapid blood issue.
> Periods of hypoxia common: shunt due to one-lung ventilation,
atelectasis and failure to fully inflate the first lung before proceeding with
surgery on the second side.
> Periods of hypotension due to capnothorax likely: consider invasive blood
pressure monitoring or more frequent noninvasive monitoring.
> Consider the complications of positioning:
• Usually supine, reverse Trendelenberg, arms abducted, with risk of
brachial plexus injury.
• Sometimes prone, with risk of facial or eye damage, dislodgement of
airway, difficulty with ventilation, nerve traction and injury.
• Sometimes lateral positioning with potential difficulty with ventilation,
dislodgement of injury, damage to pressure points such as common
peroneal nerve.
Airway:
Need to achieve collapse of one lung followed by the other for bilateral
surgery. Options include the following:
> One-lung ventilation via double lumen tube.
> One-lung ventilation via endotracheal tube with bronchial blocker.
> Endotracheal tube with intrathoracic carbon dioxide insufflation.
> Laryngeal mask airway with intrathoracic carbon dioxide insufflation
c) What are the most likely problems to be encountered in the intraoperative (15%) and postoperative
(15%) period?
Intraoperative:
Airway:
> Malposition of double lumen tube or bronchial blocker may cause
hypoxia.
Respiratory:
> One-lung ventilation causes shunt and, therefore, hypoxia. Efforts to improve
this may actually worsen hypoxia (oxygen insufflation or CPAP to the deflated
lung may reduce hypoxic pulmonary vasoconstriction; PEEP to the ventilated
lung may increase resistance to blood flow to the ventilated side)
> With bilateral surgery, atelectasis of the reinflated lung may cause
significant hypoxia when operating on the second side. Consider
reinflation under direct vision.
Cardiovascular:
> Hypotension due to capnothorax, rarely cardiac arrest due to rapid
insufflation.
> Cardiac arrhythmia induced by intrathoracic diathermy.
> Rarely, bleeding due to inadvertent damage to blood vessels on port
insertion. May be catastrophic.
Postoperative:
> Ongoing hypoxia due to atelectasis and residual pneumothorax.
> Risk of acute lung injury in the days following operation if protective one-
lung ventilation not used.
> Chest pain during the immediate postoperative period requiring
intravenous morphine – may necessitate overnight stay
a) What are the theoretical
advantages of ‘off-pump’
coronary artery bypass grafting
(OPCAB) compared to ‘on bypass’
technique? (35%)
> Avoidance of complications of CPB:
• Platelet dysfunction.
• Consumption of clotting factors.
• Accelerated fibrinolysis.
• Blood transfusion due to coagulation defects.
• Renal dysfunction.
• SIRS.
• Air emboli.
• Neurological dysfunction.
• Fluid overload/depletion.
• Electrolyte disturbance.
Earlier extubation, shorter/no ICU stay, reduced cost.
Overall reduced morbidity and mortality.
b) What causes haemodynamic
instability during OPCAB? (20%)
> Ischaemia due to vessel anastomosis (shunts are used to minimise this).
Manipulation of the heart for access to lateral and posterior aspects:
lifting of heart vertically out of pericardial sac, ventricular filling must then
happen vertically upwards, mitral and tricuspid annulus deformation
resulting in reflux.
Impaired filling due to immobilisation device.
Arrhythmias induced by ischaemia, manipulation, reperfusion.
Bleeding
c) Which strategies help to
minimise this haemodynamic
instability? (25%)
> Good communication between the anaesthetist and the surgeon.
Minimise manipulation, stop if major instability.
Periods of ischaemia minimised, including through the use of shunts.
Keep heart rate low/normal: minimises oxygen requirement, reduces
effect of periods of ischaemia.
Monitor and treat electrolyte disturbances: keep potassium over
4.5 mmol/l; give magnesium routinely.
Ensure that patient is adequately filled, guided by cardiac output
monitoring.
d) Outline the measures that
help to minimise perioperative
hypothermia during OPCAB. (20%)
Comply with NICE guidance on avoidance of perioperative hypothermia:
> Preoperative: check patient temperature, use extra bedding or forced air
warming if necessary.
> Intraoperatively: monitor temperature; minimise periods of leaving patient
uncovered; use warmed fluids, forced air warming blanket, under-body
warming mattress, heat conserving hat and ambient theatre temperature
at a minimum of 21°C.
> Postoperatively: continue to monitor temperature; use extra bedding and
forced air warming as necessary.
a) What are the indications for
‘one-lung ventilation’ (OLV)? (30%)
> Isolation of lung to prevent cross-contamination, e.g. empyema, massive
haemorrhage.
To control distribution of ventilation, e.g. for bronchopleural fistula.
To facilitate surgery, e.g. thoracoscopic surgery, oesophagectomy,
pneumonectomy, lobectomy, scoliosis surgery.
Unilateral lung lavage for treatment of alveolar proteinosis
b) How can the risks associated
with lung resection be quantified
preoperatively? (30%)
> Measure forced expiratory volume in 1 second (FEV1) and diffusing
capacity for carbon monoxide (DLCO).
Calculate the predicted postoperative (PPO) FEV1 and DLCO based on
anatomic calculation, ventilation/perfusion scans or CT evaluation.
If PPO FEV1 and DLCO are greater than 60%, the patient is low risk.
If PPO FEV1 or DLCO is less than 60% but both are greater than 30%,
proceed to stair climb or shuttle walk assessment. If good performance,
the patient is low risk; if poor performance, proceed to cardiopulmonary
exercise testing.
If PPO FEV1 or DLCO is less than 30%, poor performance on stair climb
or shuttle walk assessment or high risk according to cardiac evaluation
(including thoracic revised cardiac risk index score), then proceed to
cardiopulmonary exercise testing. If VO2max is greater than 10 ml/kg/
min, the patient is moderate risk; if less than 10, the patient is high risk
c) How would you manage the
development of hypoxaemia
during OLV? (40%)
Hypoxaemia during any anaesthetic is an emergency situation. Alert
the theatre team, request help, conduct simultaneous assessment and
management of the patient following an ABC approach.
A:
> 100% oxygen, take over manual ventilation of patient.
> Check for obvious equipment failure such as disconnection.
> Check for double lumen tube or bronchial blocker dislodgement.
> Check for secretions or blood that may have occluded the tube.
> Use bronchoscope to assess and clear secretions if necessary.
B:
> Assess for compliance, capnography waveform, oxygen saturations.
> Auscultate the chest (if feasible whilst patient is draped) and consider
bronchospasm, pneumothorax of ventilated lung, inadequate paralysis.
C:
> Assess for cardiovascular stability; check for sources of bleeding.
If assessment is otherwise normal, the likely cause is the abnormal lung
physiology caused by one-lung ventilation. Options to manage hypoxia
include the following:
> CPAP or high-frequency oscillatory ventilation to the non-ventilated lung
to reduce the shunt effect caused by ongoing perfusion to the non-
ventilated lung
> Intermittent two-lung ventilation.
> High-frequency jet ventilation to both lungs. Not an option if
need complete lung collapse or if there are concerns about
cross-contamination.
> If the surgery is for pneumonectomy, early clamping of pulmonary artery
will resolve shunt issues.
> Increase PEEP to the ventilated, dependent lung to counteract the
effect of mediastinal weight on functional residual capacity in the lateral
decubitus position.
> Decrease PEEP to reduce possible compression of pulmonary capillaries
by excessive intra-alveolar pressure.
> Increased airway pressure to ventilated lung to ensure adequate tidal
volume (however, excessive airway pressures risk impairing perfusion).
> Optimise CO and haemoglobin to ensure oxygen delivery. Does not
improve hypoxia but mitigates its effects.
a) Which clinical signs suggest
the development of acute cardiac
tamponade? (40%
> Classically, Beck’s triad: hypotension, raised jugular venous pressure,
muffled heart sounds.
Shock (hypotension, tachycardia, clammy, cool peripheries, poor capillary
refill, reduced cerebration, cardiac arrest) resistant to fluids and inotropes.
Pericardial rub.
Pulsus paradoxus: abnormally large reduction in systolic pressure during
inspiration.*
Kussmaul’s sign: rise/lack of fall of JVP with inspiration.**
* During spontaneous inspiration, the full right heart encroaches on the left
and blood pools in the pulmonary vasculature, both of which reduce left
heart filling, thus causing a decrease in systolic pressure. In tamponade, the
effect is exacerbated and the difference in pressure between the right and
left heart is lost. Positive pressure ventilation results in a reversal of timings.
**Due to failure of the constricted right heart to accommodate the increase
in venous return that occurs with the drop in intrathoracic pressure that
accompanies spontaneous inspiration.
b) List the investigations and their
associated derangements that
could confirm the diagnosis of
acute cardiac tamponade. (15%)
Transoesophageal or transthoracic echo:
> Pericardial separation of more than 1 cm (however, pericardial collections
may be atypical in appearance following cardiac surgery yet still cause
significant haemodynamic compromise).
> Sequentially, with worsening tamponade, right atrial free wall collapse in
systole, right ventricular free wall collapse in diastole, left atrial free wall
collapse in systole.
> Exaggerated respiratory variation in trans-tricuspid and trans-mitral flow.
> Left shift of the interventricular septum.
> Inferior vena cava dilatation without respiratory variation in size.
> ‘Swinging heart.’
> Chest radiograph: enlarged cardiac silhouette (‘flask shaped’).
> ECG: small complexes, electrical alternans.*
* Varying waveform size due to movement of the heart within the pericardial
sac from beat-to-beat.
Other diagnostic investigations are unlikely to be useful given the
time frame of acute tamponade:
> Ultrasound-guided pericardiocentesis: aspiration of free-flowing blood –
relatively contraindicated in patients with ongoing anticoagulation.
Neither cardiac catheter studies (equalisation of chamber pressures) nor CT
scan (presence of blood or clot in pericardial space) should be considered in
an acute, decompensated setting
c) What is the management of
acute cardiac tamponade in this
patient? (45%)
> Cardiac tamponade following cardiac surgery is likely to be due to failed
haemostasis and, therefore, rapidly progressive with risk of cardiac
arrest and high mortality. I would plan for decompressive sternotomy on
the intensive care unit as no time permitted for transfer to the operating
theatre. Opening the sternum usually reverses the life-threatening
haemodynamic compromise. I would follow an ABC approach, assessing
and managing the patient simultaneously.
Fast-bleep team and call for resternotomy trolley:
• The surgical team should be ready before induction.
• Anaesthetic and ODP support should be requested but may need to
proceed without their assistance if the patient is rapidly deteriorating.
• Perfusionist to be contacted – may need to go back on bypass.
• Major haemorrhage protocol to be activated.
Patient management:
• A: 100% oxygen reduces cardiac workload.
• B: Intubate (if not still intubated from earlier surgery). Positive pressure
ventilation will have deleterious effect on cardiac filling, and PEEP
and high airway pressures should be avoided. Do not induce until
surgeons are poised ready to go. Maintain oxygenation with minimal
ventilation.
• C: Large-bore intravenous access should be secured (if not already
present from theatre). Intravenous filling to attempt to maximise
effective venous return. Use of vasopressor if necessary.
• D: If the patient is sufficiently stable for induction drugs to be
used, consider use of opiates, ketamine, benzodiazepines. Avoid
causing myocardial depression. If the patient is periarrest, it may be
inappropriate to use any induction drugs.
• H: Massive haemorrhage protocol should be activated. However,
tamponade is not always associated with large blood loss. The
patient may already be coagulopathic from recent bypass surgery
or may develop coagulopathy with blood loss. Haemoglobin and
coagulation should be monitored with near patient testing, with blood
administration, reversal of heparin and administration of other clotting
products as indicated. Alternatively, management of anticoagulation to
go back on bypass may be needed
A 71-year-old patient requires a rigid bronchoscopy for biopsy and possible laser resection of an
endobronchial tumour.
a) Outline the options available to maintain anaesthesia (20%) and manage gas exchange. (30%)
Maintenance of anaesthesia: determined primarily by method of
management of gas exchange.
> Volatile: use of volatile not possible with jet ventilation, and awareness
more likely if volatile used with intermittent ventilation technique.
> Total intravenous anaesthesia: can be used with any option for gas
exchange management.
> Immobility should be assured for resection with muscle relaxant or
remifentanil infusion, and short-acting opioids are useful due to the highly
stimulating nature of rigid bronchoscopy.
Management of gas exchange: depends on the specific bronchoscope used
as not all options are compatible with all bronchoscopes.
> Intermittent ventilation with or without oxygen insufflation via side-port.
This may be sufficient for the diagnostic aspect of the procedure but
does not offer sufficiently reliable ventilation for resection.
> Controlled ventilation via the side port of a ventilating bronchoscope.
> Manual low-frequency jet ventilation, e.g. with Sanders manual jet
ventilator.
> Automated high-frequency jet ventilation.
b) How will use of the laser change
the management of anaesthesia?
(15%)
Use of laser changes the way a case is managed in theatre and, more
specifically, how anaesthesia is managed. Due to the difficulty in deciding on
a definitive difference between the two, I have included all of the changes.
Patient safety:
> Maintain inspired oxygen concentration as low as possible, certainly less
than 0.4 – therefore, use with jet or conventional ventilation.
> Saline-soaked gauze over mouth, teeth.
> Goggles for patient.
> Ensure that all equipment that will be used to instrument the airway is
laser-compatible.
General theatre safety:
> Goggles for staff.
> Signage on doors.
> Lock theatre doors.
> Blinds down.
> Presence of laser-trained staff member.
> Assurance of equipment maintenance.
Readiness for airway fire:
> Alertness.
> Syringes of saline ready for flooding airway.
> Airway equipment prepared in case surgery needs to be abandoned and
the patient needs to be intubated and ventilated on 100% oxygen
c) What are the possible
complications of rigid
bronchoscopy? (35%)
Anaesthetic complications:
> Barotrauma associated with jet ventilation: pneumothorax,
pneumomediastinum, pneumopericardium, pneumoperitoneum,
subcutaneous emphysema.
> Awareness: secondary to intermittent anaesthesia delivery.
> Inadequate gas exchange: hypercapnia, hypoxia. Patient with existing
lung pathology at higher risk.
> Laryngospasm, bronchospasm.
> Impaired venous return: high intrathoracic pressures associated with gas
trapping, resulting in cardiovascular instability.
> Dysrhythmia and associated cardiovascular instability associated with jet
ventilation.
> Airway contamination: ventilation without airway protection.
Surgical:
> Soft tissue trauma: lips, tongue, vocal cords, trachea, bronchi. Airway
oedema may cause airway compromise or obstruction post-procedure.
> Dental damage.
> Haemorrhage: associated with soft tissue damage or resection of lesion.
> Pneumothorax: due to resection or biopsy.
> Cervical spine damage: assess range of movement preoperatively.
Consider radiological assessment if the patient has a risk factor such as
rheumatoid arthritis
a) What are the purposes
(3 marks), typical composition
(4 marks) and physiological
actions of cardioplegia solutions?
(5 marks)
Purposes:
> Myocardial protection:
• Cardiac arrest in diastole and manipulation of the extracellular
environment to minimise ongoing metabolic activity and its deleterious
consequences during a period of suboptimal perfusion.
• Cooling of the heart.
> Facilitation of surgery:
• Still, relaxed heart.
• Bloodless field.
b) By which routes can solutions
of cardioplegia be administered?
(2 marks)
> Anterograde: cannula into ascending aorta or coronary ostia (dependent
on adequate root pressure, good coronary perfusion and competent
aortic valve to reach all of the myocardium).
Retrograde: cannula into the coronary sinus.
c) What are the possible
complications of cardioplegia
solution administration? (6 marks)
> Direct damage associated with the cannulae.
Failure to attain widespread cardiac perfusion with the cardioplegia,
leaving areas of myocardium warm and active whilst ischaemic.
Fluid overload.
Myocardial oedema, haemorrhage and injury resulting from high infusing
pressures.
Postoperative electrolyte derangement with consequent risk of
arrhythmia.
Air bubbles in the cardioplegia solution can cause air emboli in the
coronary arteries – bubble trap used
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)
> Check patient’s baseline activated clotting time (ACT) via arterial sample.
Give 300–400 iu/kg via a central venous cannula (CVC) (check line
patency first).
Take another arterial sample after three to five minutes.
Ensure ACT is 3× baseline or greater than 480 before initiating CPB.
Recheck every 30 minutes during CPB.
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
> Activated partial thromboplastin time (APTT), lab test:
Cheap test.
Slow turnaround time, which may result in less-well-directed
management.
Anti-Xa Assay, lab test:
Not widely used for this purpose, poor inter-laboratory correlation.
ACT, point-of-care (POC):
Rapid information, cheap, familiar.
Thrombocytopenia, antiplatelet agents, hypothermia,
haemodilution, aprotinin may all prolong ACT.
ACT has poor correlation with clinical anti-Xa activity.
Heparin concentration monitoring, POC:
Measuring of heparin concentration once haemodilution has
occurred with CPB may be more appropriate to direct heparin
administration than ACT, which is prolonged by commencing
CPB. Higher doses of heparin will therefore be required when
using heparin concentration measurement.
Expensive, not widely available.
c) What are the causes of
inadequate anticoagulation in
a patient whom it is believed
has already received heparin?
(5 marks)
Error:
> Wrong drug administered.
> Drug not given.
> CVC not patent.
> CVC not flushed after dose given.
Pharmacokinetic factors:
Heparin is highly protein bound, so an increase in the presence of certain
proteins reduces free and therefore active amount:
> Acutely ill patients.
> Malignancy.
> Peri- or post-partum.
Lack of antithrombin III:
> Drug induced: recent heparin use.
> Accelerated consumption: DIC, sepsis.
> Dilution: CPB.
> Decreased synthesis: liver cirrhosis.
> Increased excretion: protein-losing states.
> Familial: 1/2,000–20,000.
d) Describe the possible adverse
reactions to protamine. (3 marks)
> Arterial hypotension.
Reduced CO.
Pulmonary vasoconstriction.
Anaphylaxis.
Unbound protamine inhibits platelet reactivity, adhesion and aggregation.
An excessive dose therefore promotes bleeding.
a) What are the central and
peripheral neurological
complications of coronary artery
bypass surgery? (7 marks)
Central:
> Postoperative cognitive dysfunction – short- and long-term.
> Stroke: ischaemic, embolic (from existing patient thrombus/vessel lesions
or as a result of CPB) or haemorrhagic.
> Transient ischaemic attack.
> Gas emboli.
> Subtle behavioural or personality changes.
> Ischaemic spinal cord injury.
> Delirium.
Peripheral:
> Brachial plexus injury: central line insertion, positioning, sternal retraction
(rotation of first rib, pushes clavicles into retroclavicular space putting
traction on plexus) and internal mammary artery (IMA) harvesting (wider
retraction necessary).
> Ulnar nerve injury: positioning associated with artery harvesting.
> Phrenic nerve injury (left phrenic nerve passes between lung and
mediastinal pleura so at greater risk) with IMA harvesting.
> Recurrent laryngeal nerve injury: intubation (prolonged), surgical
dissection, especially of IMA.
> Saphenous nerve injury: damage occurring during saphenous vein
harvesting due to close proximity at ankle.
> Intercostal nerve damage: minimally invasive direct coronary artery
bypass (MIDCAB), where the incision is between the ribs rather than
sternotomy
b) What are the risk factors
for central neurological
complications? (6 marks)
Patient factors (these are most significant):
> Age.
> Hypertension.
> Hypercholesterolaemia.
> History of stroke.
> Diabetes mellitus.
> Carotid stenosis.
> Preoperative cognitive dysfunction, including that due to Alzheimer’s,
Parkinson’s and cerebral vascular disease.
> Poor left ventricular function.
Surgical factors:
> Duration of surgery (possibly relating to stress response, disruption of the
blood–brain barrier and altered autoregulation).
> Microemboli from diseased aorta when clamped, cannulated or handled.
> Microemboli from cardiopulmonary bypass (CPB) circuit.
> Rapid rewarming after hypothermia can cause loss of autoregulation,
resulting in cerebral oedema.
> Failure to maintain adequate brain perfusion pressure during CPB.
Anaesthetic factors (least significant):
> Low mean arterial pressure and so cerebral perfusion pressure.
> Prolonged deep hypnotic time
c) How can the incidence of
central neurological complications
be reduced? (7 marks)
Preoperative:
> Patient assessment, identification of high-risk patients and consider
whether appropriate to proceed.
Intraoperative:
> Minimally invasive techniques to reduce overall stress response.
> Adequate priming of CPB circuit, if used, and use of bubble traps and
embolus filters.
> Surgical care to avoid disrupting aortic plaques on clamping and
cannulation.
> Maintenance of haemodynamic stability to ensure adequate cerebral and
cord perfusion pressure.
> Careful anticoagulation monitoring and management.
> Careful neck positioning, especially if there are risk factors that may
already compromise blood supply to cervical cord.
> Optimal blood glucose management.
> Possibly avoiding excessive periods of excessively deep anaesthesia with
the use of depth of anaesthesia monitoring.
> Monitoring and management of acid–base balance to avoid deleterious
effects on brain autoregulation.
> If hypothermia induced, avoidance of fast rewarming which predisposes
to cerebral oedema.
> Cerebral regional oximetry monitoring with appropriate management in
response to decreases.
Postoperative:
> Avoidance of hypoxia.
> Management of modifiable cerebrovascular disease risk factors such as
blood glucose, blood pressure, cholesterol.
a) What is the pathophysiology
of worsening aortic stenosis?
(8 marks)
Latent phase:
> Left ventricular outflow obstruction due to abnormal valve (rheumatic
fever, congenital bicuspid valve, age-related calcification).
Compensatory phase:
> Left ventricle hypertrophies to overcome outflow obstruction, maintaining
ejection fraction.
> Consequent increased oxygen demand but poorer supply and diastolic
dysfunction.
Decompensation:
> Subendocardial ischaemia due to poor oxygen delivery to hypertrophied
myocardium.
> Increased left ventricular end-diastolic volume and pressure result in
increased pulmonary capillary pressure with pulmonary oedema, mitral
regurgitation.
> Ejection fraction starts to fall as hypertrophy increases in the face of
worsening outflow obstruction.
Symptomatic phase:
> As blood passes through the narrowed valve, it accelerates, gaining
kinetic energy. By the law of conservation of energy, it therefore loses
pressure, resulting in reduced perfusion pressure of the coronary arteries,
thus reducing oxygen delivery to an already embarrassed myocardium.
The consequences are angina, breathlessness, syncope, sudden death.
b) Which specific cardiac
investigations may be used in
assessing the severity of this
woman’s disease? (3 marks)
Echocardiography (transoesophageal or transthoracic):
> Assess valve: Doppler assessment of peak flow velocity, mean pressure
gradient, effective orifice area, presence of regurgitation.
> Assess consequences of its stenosis: left ventricular dimensions and
function; mitral valve competence, left atrium, pulmonary artery pressure,
right ventricular function, post-stenotic ascending aortic dilatation.
Left heart catheter study:
> Retrograde catheterisation of aortic valve to assess pressure gradient.
MRI:
> To assess the consequences of stenosis.
ECG:
> Will demonstrate the consequences of stenosis: left ventricular
hypertrophy, ischaemia, arrhythmias.
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)
Peak aortic flow velocity: greater than 4 m/s.
Mean pressure gradient: greater than 40 mm Hg.
Valve area: less than 1 cm2.
d) What would be your
haemodynamic goals for the
perioperative management of this
patient? (6 marks)
> Maintain myocardial oxygen delivery with adequate systolic and diastolic
blood pressure within 20% of normal values (as monitored by invasive BP
monitoring).
Maintain contractility (balanced anaesthetic technique, adequate filling as
guided by cardiac output (CO) monitoring, may need inotropic support if
left ventricle is poorly functioning).
Optimise pre-load with filling (guided by CO monitoring).
Maintain sinus rhythm at a rate of 60–80 bpm (5-lead ECG, avoidance of
tachycardia by managing pain, use of beta-blockers, possible need for
pacing post-bypass due to surgical interruption of conduction pathway).
Maintain afterload. Coronary artery filling is dependent on aortic root
pressure (avoid excessive doses of intravenous induction agents
or inhalational agents, may need alpha agonist, as guided by CO
monitoring).
a) What clinical features might
suggest the development of
cardiac tamponade? (9 marks)
Symptoms:
> Shortness of breath.
> Sharp chest pain radiating to the shoulder, neck, back, abdomen; may
be pleuritic.
> Anxiety, restlessness, dizziness, drowsiness.
Monitoring:
> Increasing CVP.
> Progressive hypotension or increasing dose of vasopressor required to
maintain blood pressure.
> Reduction or sudden loss of chest drain output.
> Equalisation of atrial and LVEDP if in pulmonary artery catheter in situ.
> Oliguria – although rapid timeframe may mean that this is not observed
before the patient is periarrest.
a) What is meant by counter
pulsation in the context of an
intra-aortic balloon pump (IABP)?
(1 mark)
b) Briefly explain the effect of
counter pulsation from an IABP on
coronary blood flow and the left
ventricle. (4 marks)
Inflation of the balloon in diastole and deflation in early systole.
b) Briefly explain the effect of
counter pulsation from an IABP on
coronary blood flow and the left
ventricle. (4 marks)
Inflation:
> Forces blood proximally, increasing the pressure within the proximal
aorta compared to the left ventricle, thus improving perfusion of coronary
arteries, increasing oxygen delivery.
> Forces blood distally, thus augmenting the apparent output from the left
ventricle.
> Augments Windkessel effect.
Deflation:
> Decrease in afterload reduces myocardial wall stress during systole, thus
reducing myocardial oxygen demand.
c) What are the indications for
(6 marks) and contraindications to
(3 marks) the use of an IABP in an
adult?
Indications:
> Cardiogenic shock due to myocardial infarction if revascularisation
planned.
> Acute mitral regurgitation or ventricular septal defect due to acute
myocardial infarction.
> Refractory ventricular arrhythmias whilst awaiting definitive treatment.
> Refractory unstable angina if treatment option available.
> Refractory left ventricular failure if destination treatment planned.
> Perioperative support for high-risk coronary artery bypass surgery.
> Perioperative support for high-risk non-cardiac surgery.
Contraindications:
Absolute
> Aortic regurgitation, dissection or stent.
> Chronic end-stage heart disease with no further possible intervention.
Relative
> Uncontrolled sepsis.
> Abdominal aortic aneurysm, severe peripheral vascular disease or arterial
reconstruction surgery.
> Uncontrolled bleeding disorder.
> Tachyarrhythmias.
d) List the possible complications
of an IABP. (6 marks)
> Haemodynamic compromise due to poor timing of counterpulsation or
malposition.
Limb, spinal cord or visceral (especially renal) ischaemia.
Compartment syndrome.
Aortic dissection.
Vascular injury causing bleeding, haematoma, false aneurysm,
arteriovenous fistula.
Cardiac tamponade.
Thromboembolism.
Thrombocytopaenia and haemolysis.
Infection.
Balloon rupture resulting in gas embolus.
How is the diagnosis of lung cancer made?
○ The initial presenting symptoms in patients with lung cancer are
constitutional and nonspecific, mainly related to metastatic disease. ○ Nonproductive cough, dyspnea, hemoptysis, and chest pain, along with an unresolved lung infiltrate on chestradiography, should suggest carcinoma.
○ In the attempt to make an early diagnosis, the American Cancer Society has issued preliminary guidelines for screening high-risk patients using low-dose computed tomography (LDCT) imaging.
○ Recommended candidates include subjects aged between 55 and
77 years with a smoking history of at least 30 packs per year, who are current smokers or quit within the past 15 years.
○ The main limitation of this test is the 23.3% incidence of false-positive results, which may lead to further testing includingvsurgical biopsy. ○ Biomarkers from large airway epithelial cells or buccal mucosal biopsies are being investigated and may represent early diagnostic options in the future.
○ Currently, the initial diagnosis and staging are done in the operating room and
include flexible bronchoscopy with airway washings and brush
biopsy, possibly followed by ultrasound-guided transbronchial
biopsy (endobronchial ultrasound [EBUS]) for mediastinal
lymph node biopsy. Additional areas for biopsy include palpable
lymph nodes in the neck or axilla, needle aspiration biopsy,
cervical mediastinoscopy, and possibly exploratory
thoracoscopy or thoracotomy. An extensive evaluation must be
performed to exclude metastases that would contraindicate
major surgery.
What is your prediction for the most likely type of malignancy? Lung ca
Cancers of the lung account for 12% of all malignancies and
nearly 18% of cancer-related deaths worldwide. Bronchogenic
carcinomas are the most common tumors requiring surgical
resection and can be classified into four major types: small cell,
large cell, squamous cell, and adenocarcinoma. For surgical
purposes, lung tumors are classified as non–small cell or small
cell. The former is amenable to surgical resection, whereas the
latter tends to be nonresectable and is medically treated.
Further subclassification of lung tumors involves the TNM
classification in which T designates tumor site, size, and local
extent; N the presence and location of regional lymph node
involvement; and M the presence of distal metastases beyond the
ipsilateral hemithorax. This system is used for staging
bronchogenic carcinomas and helps predict the response to
therapy. In general, small cell carcinomas that have spread
beyond possible resection by the time of presentation are
primarily managed with chemotherapy, with or without
radiation, and are associated with a 5-year survival of
approximately 20%. In contrast, non–small cell cancers found to
be localized at the time of presentation should be considered for
primary resection. The 5-year survival can be as high as 85% for
small tumors without regional lymph node involvement or
metastases (stage I). Approximately 45% of patients present with circumscribed extrapulmonary disease or lymphatic spread
to the ipsilateral mediastinal or subcarinal lymph nodes (stage
IIIa). Their 5-year postresection survival is less than 20%.
What are the less common manifestations of bronchogenic carcinoma?
○ Other manifestations of lung tumors are primarily related to
mass effects or altered metabolism. ○ In addition to bronchial obstruction (evident in this patient) occasionally leading to postobstructive pneumonia, mass effects include invasion into
the chest wall and pleura, compression of great vessels (e.g.,
superior vena cava syndrome) and heart, tracheobronchial
displacement, and/or paresis of the recurrent laryngeal or phrenic nerves and the sympathetic chain.
○ Pancoast syndrome can present with pain and upper extremity weakness secondary to invasion of the brachial plexus as well as the first and second thoracic and eighth cervical nerve roots.
○ Recognized metabolic manifestations of small cell lung tumors include symptoms resembling those of Cushing syndrome (from ectopic
adrenocorticotropic hormone production), carcinoid syndrome,
hypercalcemia and hypophosphatemia (resulting from ectopic parathyroid hormone or parathyroid hormone–related peptides), hypokalemia (caused by ectopic adrenocorticotropic hormone secretion), and hyponatremia (from inappropriate secretion of antidiuretic hormone and possibly atrial natriuretic factor).
○ Neurologic paraneoplastic syndromes include Eaton-Lambert
myasthenic syndrome, peripheral motor and sensory neuritis, cerebellar degeneration, retinopathy, limbic encephalopathy, and
autonomic neuropathy.
○ An autoimmune process has been
suggested for these findings, and it seems to be more common in
patients with limited disease.
○ Extrathoracic spread of the tumor can affect the bones, liver, adrenal glands, intra-abdominal and subcutaneous lymph nodes,
brain, and spinal cord, contributing to the nonspecific presentation of the cancer.
The patient has a long history of cigarette smoking.
What is the significance of this finding?
Cigarette smoking remains the leading cause of lung cancer in
the United States. Tobacco exposure is linked to chronic
obstructive pulmonary disease (COPD), which includes chronic
bronchitis and emphysema, and is strongly associated with an
increased incidence of stroke, myocardial infarction, and cancer
(lung, oral cavity, larynx, and esophagus). Pulmonary
hypertension from chronic hypoxemia and subsequent cor
pulmonale may also occur
Eight percent to 17% of patients with lung cancer who are
scheduled for surgical resection are still smoking at the time of
surgery. Current tobacco use increases the risk of postoperative
respiratory failure, pneumonia, aspiration, air leak, and
atelectasis as well as 1-year mortality. Preoperative smoking
cessation is strongly recommended, but it is unclear how long is
needed before surgery to see a significant reduction in
postoperative complications. Carboxyhemoglobin
concentrations decline substantially within 12 hours of smoking
cessation. Four weeks of abstinence decrease the incidence of
postoperative respiratory complications, probably because of an
improved mucociliary function. However, because continuous
local tumor growth and metastatic spread may preclude
resectability, a prolonged period of preoperative abstinence may
not be practical. Nonetheless, smoking cessation at any time
prior to surgery is still strongly recommended. A combined
approach including counseling and polypharmacology has been
shown to increase the success rate and decrease relapses after
hospital discharge.
