Cardiothoracic Surgery

Question 1

Coronary artery bypass grafts

Answer 1

A coronary artery bypass graft (CABG) procedure involves using a graft blood vessel taken from elsewhere in the body (usually the saphenous vein) to bypass a blockage in a coronary artery. Depending on the affected areas, this may involve one, two, three or even four bypass grafts.

Question 2

Coronary anatomy

Answer 2

The left coronary artery (LCA) becomes the circumflex and left anterior descending (LAD) arteries.

The right coronary artery (RCA) curves around the right side and under the heart and supplies the:

Right atrium
Right ventricle
Inferior aspect of the left ventricle
Posterior septal area

The circumflex artery curves around the top, left and back of the heart and supplies the:

Left atrium
Posterior aspect of the left ventricle

The left anterior descending (LAD) travels down the middle of the heart and supplies the:

Anterior aspect of the left ventricle
Anterior aspect of septum

Question 3

Atherosclerosis

Answer 3

Athero- refers to soft or porridge-like and -sclerosis refers to hardening. Atherosclerosis is a combination of atheromas (fatty deposits in the artery walls) and sclerosis (the process of hardening or stiffening of the blood vessel walls). Atherosclerosis affects the medium and large arteries. It is caused by chronic inflammation and activation of the immune system in the artery wall. Lipids are deposited in the artery wall, followed by the development of fibrous atheromatous plaques.

These plaques cause:

Stiffening of the artery walls, leading to hypertension (raised blood pressure) and strain on the heart (whilst trying to pump blood against increased resistance)
Stenosis, leading to reduced blood flow (e.g., in angina)
Plaque rupture, resulting in a thrombus that can block a distal vessel and cause ischaemia (e.g., in acute coronary syndrome)

Question 4

Atherosclerosis risk factors

Answer 4

It is important to break these down into modifiable and non-modifiable risk factors. We cannot do anything about non-modifiable risk factors, but we can do something about modifiable ones.

Non-modifiable risk factors:

Older age
Family history
Male

Modifiable risk factors:

Smoking
Alcohol consumption
Poor diet (high in sugar and trans-fat and low in fruit, vegetables and omega 3s)
Low exercise / sedentary lifestyle
Obesity
Poor sleep
Stress

Question 5

Medical co-morbidities and atherosclerosis

Answer 5

Medical co-morbidities increase the risk of atherosclerosis and should be carefully managed to minimise the risk:

Diabetes
Hypertension
Chronic kidney disease
Inflammatory conditions such as rheumatoid arthritis
Atypical antipsychotic medications

TOM TIP: Think about risk factors when taking a history from someone with suspected atherosclerotic disease (such as someone presenting with intermittent claudication). Ask about their exercise, diet, past medical history, family history, occupation, smoking, alcohol intake and medications. This will help you perform well in exams and when presenting to seniors.

Question 6

Complications of atherosclerosis

Answer 6

Angina
Myocardial infarction
Transient ischaemic attack
Stroke
Peripheral arterial disease
Chronic mesenteric ischaemia

TOM TIP: Patients with one type of arterial disease are likely to have others. When a patient has symptoms of one type of arterial disease (e.g., intermittent claudication), consider the risk of others (e.g., coronary artery disease). Erectile dysfunction can often be the first indication of arterial disease and should prompt you to consider checking the lipid profile, blood pressure and Q-risk score (which is the percentage risk that a patient will have a stroke or myocardial infarction in the next 10 years).

Question 7

Coronary artery disease

Answer 7

Narrowing (stenosis) of the coronary arteries due to atherosclerosis may be asymptomatic, or present with:

Angina (stable or unstable)
Myocardial infarction

The options for management are:

Medical management (secondary prevention with statins, aspirin, beta-blockers and ACE inhibitors)
Percutaneous coronary intervention (PCI) with coronary angioplasty
Coronary artery bypass graft

Question 8

Cardiopulmonary bypass

Answer 8

The bypass machine takes blood from the vena cava or right atrium, pumps it through a machine that adds oxygen and removes carbon dioxide from the blood, then pumps it back into the ascending aorta. This way, blood bypasses the heart and lungs and is artificially oxygenated. Heparin is used to prevent blood clotting. The clinical perfusionist is responsible for operating and monitoring the cardiopulmonary bypass equipment.

Question 9

Cardioplegia

Answer 9

During a coronary artery bypass graft procedure, the heart needs to be still. Causing the heart to stop beating is called cardioplegia. The heart is only stopped after the cardiopulmonary bypass is up and running. A high potassium solution is delivered into the coronary circulation, causing the heart to stop. Once the surgery is complete, cardioplegia is stopped and the heart will spontaneously start beating. Cardioversion or temporary pacing may be used to treat arrhythmias that occur.

Question 10

Coronary artery bypass grafts

Answer 10

A separate blood vessel needs to be obtained to create a bypass. This blood vessel is called a graft. The three main options for graft vessels are:

Saphenous vein (harvested from the inner leg)
Internal thoracic artery, also known as the internal mammary artery
Radial artery

The internal thoracic artery is a branch of the subclavian artery. When the internal thoracic artery is used in a CABG, the proximal end may be left attached to the subclavian artery. The distal end is separated from any connections and then joined to the left anterior descending artery. As a result, blood flows from the subclavian artery, through the internal thoracic artery and into the left anterior descending artery. Leaving it proximally attached to the original site, whilst changing where it supplies, is described as a pedicled graft. The internal thoracic artery can also be used as a free graft if required.

A free graft refers to a section of blood vessel that is entirely separated from its original connections, before being reattached in a new site for the bypass. During a coronary artery bypass procedure, the graft vessel is attached directly to the ascending aorta, with the other end attached to the coronary artery, distal to the stenosis (bypassing the diseased portion of the artery). Blood flows from the ascending aorta, through the graft and into the coronary artery.

Vein grafts (i.e., from the saphenous vein) have a tendency to become stenosed (narrowed) over time in a process called intimal hyperplasia. The tunica intima layer in the vessel becomes thickened, mostly due to increased pressure. Arterial grafts (e.g., radial or internal thoracic) are less affected by this, so tend to make better grafts.

Question 11

Recovery after CABG

Answer 11

After cardiothoracic surgery, patients have careful monitoring and supportive care in the intensive care unit. They are usually discharged after about a week. There is a slow recovery period with a gradual increase in activity. In straightforward cases, patients make a full recovery and resume full normal activities after 3 months.

Question 12

Complications of CABG

Answer 12

The two most serious and notable complications are:

Death (2-3% in straightforward cases)
Stroke (1-5% in straightforward cases)

Other complications:

Infection
Acute kidney injury
Cognitive impairment
Myocardial infarction
Atrial fibrillation

Question 13

Valve replacement scars

Answer 13

Patients that have had a valve replacement will have a scar. Usually, this will be a midline sternotomy scar straight down the middle of the sternum indicating a mitral or aortic valve replacement or a coronary artery bypass graft (CABG). Less commonly a right-sided mini-thoracotomy incision can be used for minimally invasive mitral valve surgery.

Question 14

Aortic stenosis and signs

Answer 14

Severe aortic stenosis is the most common valvular heart disease you will encounter and the most common indication for valve replacement surgery.

Aortic stenosis causes an ejection-systolic, high-pitched murmur (high velocity of systole). This has a crescendo-decrescendo character due to the speed of blood flow across the value during the different periods of systole. Flow during systole is slowest at the very start and end, and is fastest in the middle.

Other signs:

The murmur radiates to the carotids as the turbulence continues up into the neck
Slow rising pulse and narrow pulse pressure
Patients may complain of exertional syncope (lightheadedness and fainting when exercising) due to difficulty maintaining a good flow of blood to the brain

Question 15

Causes of aortic stenosis

Answer 15

Idiopathic age-related calcification (by far the most common cause)
Rheumatic heart disease

Question 16

Mitral regurgitation and signs

Answer 16

Mitral regurgitation is the second most common indication for valve replacement.

Mitral regurgitation is when an incompetent mitral valve allows blood to leak back through during systolic contraction of the left ventricle.

The leaking valve causes a reduced ejection fraction and a backlog of blood waiting to be pumped through the left side of the heart, resulting in congestive cardiac failure.

Mitral regurgitation causes a pan-systolic, high pitched “whistling” murmur due to high-velocity blood flow through the leaky valve. The murmur radiates to the left axilla. You may hear a third heart sound.

Question 17

Causes of mitral regurgitation

Answer 17

Idiopathic weakening of the valve with age
Ischaemic heart disease
Infective endocarditis
Rheumatic heart disease
Connective tissue disorders, such as Ehlers Danlos syndrome or Marfan syndrome

Question 18

Bioprosthetic Versus Mechanical valves

Answer 18

Valves can be either replaced by a bioprosthetic or a metallic mechanical valve.

Bioprosthetic valves have a limited lifespan of around 10 years. “Porcine” bioprosthetic valves come from a pig.

Mechanical valves have a good lifespan (well over 20 years) but require lifelong anticoagulation with warfarin. The INR target range with mechanical valves is 2.5 – 3.5 (this is higher than the 2 – 3 target for atrial fibrillation).

Question 19

Mechanical heart valves and their complications

Answer 19

It is possible to hear a click when auscultating the heart sounds in a patient with a mechanical valve:

A click replaces S1 for metallic mitral valve
A click replaces S2 for metallic aortic valve

There are three major complications of mechanical heart valves:

Thrombus formation (blood stagnates and clots)
Infective endocarditis (infection in prosthesis)
Haemolysis causing anaemia (blood gets churned up in the valve)

Question 20

Transcatheter Aortic Valve Implantation

Answer 20

This is a treatment for severe aortic stenosis, usually in patients that are at high risk for an open valve replacement operation. It involves local or general anaesthetic, inserting a catheter into the femoral artery, feeding a wire under x-ray guidance to the location of the aortic valve, then inflating a balloon to stretch the stenosed aortic valve and implanting a bioprosthetic valve in the location of the aortic valve.

Long term outcomes for TAVI are still not clear as it is a relatively new procedure. Therefore, in younger, fitter patients, open surgery is still the first-line option.

Patients that have a TAVI do not typically require warfarin as the valve is bioprosthetic.

Question 21

Infective Endocarditis and valve replacement

Answer 21

This occurs in around 2.5% of patients having a surgical valve replacement. The rate is slightly lower for TAVI at around 1.5%. Infective endocarditis in a prosthetic valve has quite a high mortality of around 15%. This is usually caused by one of three gram-positive cocci organisms:

Staphylococcus
Streptococcus
Enterococcus

Question 22

Congenital cardiac conditions

Answer 22

Several congenital heart defects may present for the first time, or worsen, in adulthood. The conditions covered here are:

Atrial septal defects
Ventricular septal defects
Coarctation of the aorta

Other congenital heart conditions usually present and are managed in infancy or childhood. They require follow up and monitoring, but the defect is usually repaired by adulthood. These are discussed elsewhere in the paediatrics content:

Patent ductus arteriosus
Tetralogy of Fallot
Ebstein’s anomaly
Transposition of the great arteries

An echocardiogram is the initial investigation of choice for diagnosing congenital heart defects.

Question 23

Cyanotic heart disease

Answer 23

Congenital heart disease can be divided into two categories: cyanotic and acyanotic.

Cyanosis occurs when deoxygenated blood enters the systemic circulation. Cyanotic heart disease occurs when blood can bypass the pulmonary circulation and the lungs. This occurs across a right-to-left shunt. A right-to-left shunt describes any defect that allows blood to flow from the right side of the heart (the deoxygenated blood returning from the body) to the left side of the heart (the blood exiting the heart into the systemic circulation), without travelling through the lungs to get oxygenated.

Heart defects that can cause a right-to-left shunt, and therefore cyanotic heart disease, are:

Ventricular septal defect (VSD)
Atrial septal defect (ASD)
Patent ductus arteriosus (PDA)
Transposition of the great arteries

Patients with a VSD, ASD or PDA are usually not cyanotic. This is because the pressure in the left side of the heart is much greater than the right side, and blood will flow from the area of high pressure to the area of low pressure (left to right). This prevents a right-to-left shunt. If the pulmonary pressure increases beyond the systemic pressure, blood will start to flow from right to left across the defect, causing cyanosis. This is called Eisenmenger syndrome.

Question 24

Complications of congenital heart disease

Answer 24

Heart failure
Arrhythmias
Endocarditis
Stroke
Pulmonary hypertension
Eisenmenger Syndrome

Generally, the risks associated with congenital heart defects are much higher during pregnancy. Women with congenital heart defects need to be counselled by their specialist about the risks of pregnancy and require careful monitoring throughout pregnancy.

Question 25

Atrial septal defects

Answer 25

An atrial septal defect is a defect (a hole) in the septum (the wall) between the two atria. This connects the right and left atria allowing blood to flow between them.

The types of atrial septal defect, from most to least common, are:

Patent foramen ovale, where the foramen ovale fails to close (although this is not strictly classified as an ASD)
Ostium secondum, where the septum secondum fails to fully close, leaving a hole in the wall
Ostium primum, where the septum primum fails to fully close, leaving a hole in the wall (this tends to lead to a atrioventricular septal defect)

An atrial septal defect leads to a shunt, with blood moving between the two atria. Blood moves from the left atrium to the right atrium because the pressure in the left atrium is higher than the pressure in the right atrium. This means blood continues to flow to the pulmonary vessels and lungs to get oxygenated and the patient does not become cyanotic. However, the increased flow to the right side of the heart leads to right-sided overload and right heart strain. This right-sided overload can lead to right heart failure and pulmonary hypertension.

Eventually, pulmonary hypertension can lead to Eisenmenger syndrome. This occurs because the pulmonary pressure exceeds the systemic pressure, causing the shunt to reverse and become a right-to-left shunt across the ASD. This causes blood to bypass the lungs, resulting in the patient becoming cyanotic.

Question 26

Presentation of atrial septal defects

Answer 26

Atrial septal defects are often picked up on antenatal scans or newborn examinations. It may be asymptomatic in childhood and present in adulthood with:

Dyspnoea (shortness of breath) secondary to pulmonary hypertension and right-sided heart failure
Stroke in the context of venous thromboembolism (see below)
Atrial fibrillation or atrial flutter

TOM TIP: It is worth remembering atrial septal defects as a cause of stroke in patients with a DVT. Normally, when patients have a DVT and this becomes an embolus, the clot travels to the right side of the heart, enters the lungs and becomes a pulmonary embolism. In patients with an ASD the clot can travel from the right atrium to the left atrium across the ASD. This means the clot can travel to the left ventricle, aorta and up to the brain, causing a large stroke. An exam question may feature a patient with a DVT that develops a large stroke and the challenge is to identify that they have had a lifelong asymptomatic ASD.

Atrial septal defects cause a mid-systolic, crescendo-decrescendo murmur loudest at the upper left sternal border, with a fixed split second heart sound. Splitting of the second heart sound can be normal with inspiration. However, a “fixed split” second heart sound means the split does not change with inspiration and expiration. This occurs in an atrial septal defect because blood is flowing from the left atrium into the right atrium across the atrial septal defect, increasing the volume of blood that the right ventricle has to empty before the pulmonary valve can close. This doesn’t vary with respiration.

Interestingly, there is a possible link between migraine with aura and patent foramen ovale (PFO). However, patients with migraines are not routinely screened for PFO. This is because the surgical management of PFOs carry risks and it is not clear whether treatment for a PFO improves symptoms of recurrent migraines.

Question 27

Managing atrial septal defects

Answer 27

In cases where the ASD is small and asymptomatic, watching and waiting may be appropriate. ASDs can be corrected surgically using a percutaneous transvenous catheter closure (via the femoral vein) or open-heart surgery. Anticoagulants (such as aspirin, warfarin and DOACs) are used to reduce the risk of clots and stroke in adults.

Question 28

Ventricular septal defects

Answer 28

A ventricular septal defect (VSD) is a hole in the septum (wall) between the two ventricles. This can vary in size from tiny to the entire septum, forming one large ventricle.

Congenital VSDs can occur in isolation but there are often underlying genetic conditions associated with them (e.g., Down’s Syndrome and Turner’s Syndrome).

Ventricular septal defects can also develop after myocardial infarction, where there is damage to the ventricular septum due to ischaemia.

Similarly to atrial septal defects, VSDs usually feature a left-to-right shunt. Over time this causes right-sided overload, right heart failure and increased flow into the pulmonary vessels. Pulmonary hypertension may progress to a right-to-left shunt, resulting in cyanosis (Eisenmenger syndrome).

Question 29

Presentation of ventricular septal defects

Answer 29

Often VSDs are initially asymptomatic and patients can present as late as adulthood. They may be picked up on antenatal scans or when a murmur is heard during the newborn baby check.

Patients with a VSD typically have a pan-systolic murmur more prominently heard at the left lower sternal border in the third and fourth intercostal spaces. There may be a systolic thrill on palpation.

TOM TIP: When you hear a pan-systolic murmur it is worth giving your top differential but also mentioning the other causes of this type of murmur. The causes of a pan-systolic murmur are ventricular septal defect, mitral regurgitation and tricuspid regurgitation.

Question 30

Managing ventricular septal defects

Answer 30

VSDs can be corrected surgically using a transvenous catheter closure via the femoral vein or open-heart surgery.

There is an increased risk of infective endocarditis in patients with a VSD. Antibiotic prophylaxis should be considered during surgical procedures to reduce the risk of developing infective endocarditis.

Question 31

Coarctation of the aorta

Answer 31

Coarctation of the aorta is a congenital condition where there is a narrowing of the aortic arch, usually around the ductus arteriosus. The severity of the coarctation (or narrowing) can vary from mild to severe. It is often associated with an underlying genetic condition, particularly Turner’s syndrome.

Coarctation of the aorta can reoccur later after previously being treated in childhood.

Narrowing of the aorta reduces the pressure of blood flowing to the arteries that are distal to the narrowing. It increases the pressure in areas proximal to the narrowing, such as the heart and the three branches of the aorta arch (the brachiocephalic artery, the left common carotid and the left subclavian artery).

Question 32

Presentation of coarctation of the aorta

Answer 32

Coarctation may go undiagnosed until adulthood. Often the first sign in adulthood is hypertension.

There may be a systolic murmur heard below the left clavicle (left infraclavicular area) and below the left scapula.

Performing a four limb blood pressure will reveal high blood pressure in the limbs supplied from arteries that branch off the aorta before the narrowing and lower blood pressure in limbs that branch off the aorta after the narrowing.

Additional signs may develop over time:

Left ventricular heave due to left ventricular hypertrophy
Underdeveloped left arm where there is reduced flow to the left subclavian artery
Underdevelopment of the legs

CT angiography gives a detailed picture of the structure and narrowing in coarctation of the aorta.

Question 33

Managing coarctation of the aorta

Answer 33

The severity of the coarctation varies between patients. In mild cases, patients can live symptom-free until adulthood without requiring surgical input. In severe cases, patients will require emergency surgery shortly after birth.

In adulthood it can be treated with:

Percutaneous balloon angioplasty (stretching the stenosis), potentially with a stent inserted
Open surgical repair

Patients also need medical management of hypertension.

Question 34

Pericardial effusion

Answer 34

Pericardial effusion is where excess fluid collects within the pericardial sac. Pericardial effusion can be acute or chronic. They can fill the entire pericardial cavity or only a localised section.

The effusion can be made of:

Transudates (low protein content)
Exudates (associated with inflammation)
Blood
Pus
Gas (associated with bacterial infections)

Question 35

Pathophysiology of pericardial effusion

Answer 35

There is a membrane that surrounds the heart called the pericardium or pericardial sac. This has two layers with a small amount of fluid in between (less than 50mls), providing lubrication. These layers separate the heart from the rest of the contents of the mediastinum. Lubrication between the two layers allows the heart to beat without generating too much friction.

Between the two layers, there is a potential space, called the pericardial cavity. The two layers are usually touching each other, which is why it is only a potential space.

Pericardial effusion is when the potential space of the pericardial cavity fills with fluid. This creates an inward pressure on the heart, making it more difficult to expand during diastole (filling of the heart).

Pericardial tamponade (or cardiac tamponade) is where the pericardial effusion is large enough to raise the intra-pericardial pressure. This increased pressure squeezes the heart and affects its ability to function. It leads to reduced filling of the heart during diastole, resulting in decreased cardiac output during systole. This is an emergency requiring rapid drainage of the pericardial effusion to relieve the pressure.

Question 36

Causes of pericardial effusion

Answer 36

Increased venous pressure can reduce drainage from the pericardial cavity, resulting in a transudative effusion. This may occur in:

Congestive heart failure
Pulmonary hypertension

Exudative effusions may occur in any inflammatory process affecting the pericardium (pericarditis), such as in:

Infection (e.g., tuberculosis, HIV, coxsackievirus, Epstein–Barr virus and other viruses)
Autoimmune and inflammatory conditions (e.g., systemic lupus erythematosus and rheumatoid arthritis)
Injury to the pericardium (e.g., after myocardial infarction, open heart surgery or trauma)
Uraemia (raised urea) secondary to renal impairment
Cancer
Medications (e.g., methotrexate)

Rupture of the heart or aorta can cause bleeding into the pericardial cavity, resulting in a rapid-onset cardiac tamponade. Rupture may be the result of:

Myocardial infarction
Trauma
Aortic dissection (type A)

Question 37

Presentation of pericardial effusion

Answer 37

The speed of onset of symptoms relates to how quickly the effusion develops. A rapidly collecting effusion with cardiac tamponade can quickly cause haemodynamic compromise and collapse.

Slowly developing, chronic effusions, may initially be asymptomatic. As pressure rises, symptoms can develop, which may include:

Chest pain
Shortness of breath
A feeling of fullness in the chest
Orthopnoea (shortness of breath on lying flat)

The effusion may compress surrounding structures, causing additional symptoms:

Phrenic nerve compression can cause hiccups
Oesophageal compression may cause dysphagia (difficulty swallowing)
Recurrent laryngeal nerve compression may cause a hoarse voice

Signs on examination include:

Quiet heart sounds
Pulsus paradoxus (an abnormally large fall in blood pressure during inspiration, notably when palpating the pulse)
Hypotension
Raised JVP
Fever (with pericarditis)
Pericardial rub (with pericarditis)

Question 38

Diagnosing pericardial effusion

Answer 38

An echocardiogram is the investigation of choice. It can be used to:

Diagnose pericardial effusion
Assess the size of the effusion
Assess the effect on the heart function (haemodynamic effect)

Fluid analysis can be performed on the pericardial fluid to diagnose the underlying cause, including:

Protein content (to distinguish between transudative or exudative)
Bacterial culture
Viral PCR
Cytology and tumour markers (for cancer)

Question 39

Managing pericardial effusion

Answer 39

There are two components to treating a pericardial effusion:

Treatment of the underlying cause (e.g., infection)
Drainage of the effusion (where required)

Inflammatory causes (pericarditis) may be treated with:

Aspirin
NSAIDs
Colchicine
Steroids

There are two options for draining an effusion:

Needle pericardiocentesis (echocardiogram guided)
Surgical drainage

A pericardial window is a surgical procedure where a portion of the pericardium is removed, creating a “window” or fistula, that allows fluid to drain from the pericardial cavity into the pleural cavity or the peritoneal cavity.

Rarely, pericardiectomy (surgical removal of the pericardium) may be performed in recurrent cases.

Question 40

Thoracic aortic aneurysms

Answer 40

A thoracic aortic aneurysm refers to the dilation of the thoracic aorta. The most commonly affected area is the ascending aorta. The diameter of the thoracic aorta varies depending on several factors (e.g., age and body size), but is normally less than 4.5cm for the ascending and 3.5cm for the descending thoracic aorta.

The first time a patient may become aware of an aneurysm is when it ruptures, causing life-threatening bleeding into the mediastinum cavity. This has an extremely high mortality.

Question 41

False thoracic aortic aneurysms

Answer 41

There are three layers to the aorta: the intima, media and adventitia.

False aneurysms (or pseudoaneurysm) occur when the inner two layers (intima and media) rupture and there is dilation of the vessel, with the blood only being contained within the outer (adventitia) layer of the aorta. This typically occurs after trauma, such as a road traffic accident. It can also occur after surgery to the aorta or infection in the vessel.

True aneurysms are where the three layers of the aorta are intact but dilated. Aortic dissection is where the blood enters between the intima and media layers.

Question 42

Risk factors for thoracic aortic aneurysms

Answer 42

Men are affected significantly more often and at a younger age than women
Increased age
Smoking
Hypertension
Family history
Existing cardiovascular disease
Marfan syndrome and other connective tissue disorders

Question 43

Presentation of thoracic aortic aneurysms

Answer 43

Dilation of the thoracic aorta is often asymptomatic. It may be found incidentally on investigations for other reasons, for example on a chest x-ray, echocardiogram or CT scan.

An aneurysm may cause symptoms due to taking up space within the mediastinum:

Chest or back pain
Trachea or left bronchus compression may cause cough, shortness of breath and stridor
Phrenic nerve compression may cause hiccups
Oesophageal compression may cause dysphagia (difficulty swallowing food)
Recurrent laryngeal nerve compression may cause a hoarse voice

Question 44

Diagnosing and assessing thoracic aortic aneurysms

Answer 44

Echocardiogram
CT or MRI angiogram

Question 45

Managing thoracic aortic aneurysms

Answer 45

The risk of progression of a thoracic aortic aneurysm can be reduced by treating modifiable risk factors:

Stop smoking
Healthy diet and exercise
Optimising the management of hypertension, diabetes and hyperlipidaemia

Management options depend on individual patient factors and the size. The larger the size of the aneurysm, the higher the risk of rupture.

The options are:

Surveillance with regular imaging to monitor the size
Thoracic endovascular aortic repair (TEVAR), with a catheter inserted via the femoral artery inserting a stent graft into the affected section of the aorta
Open surgery (midline sternotomy) to remove the section of the aorta with the defect in the wall and replace it with a synthetic graft

Question 46

Complications of thoracic aortic aneurysms

Answer 46

Aortic dissection
Ruptured aneurysm
Aortic regurgitation (if the aortic valve is affected)

Question 47

Ruptured thoracic aortic aneurysms

Answer 47

The risk of rupture increases with the diameter of the aneurysm.

Rupture of a thoracic aortic aneurysm results in bleeding into the mediastinum. There may be bleeding into the:

Oesophagus, causing haematemesis (vomiting blood)
Airways or lungs, causing haemoptysis (coughing up blood)
Pericardial cavity, causing cardiac tamponade (compression of the heart)

A ruptured thoracic aortic aneurysm presents with:

Severe chest pain or back pain
Haemodynamic instability (hypotension and tachycardia)
Collapse
Death (often patients do not reach hospital)

Emergency open surgery is required, with replacement of the affected section of the aorta with a synthetic graft.

Question 48

Lung cancer

Answer 48

Lung cancer is the third most common cancer in the UK behind breast and prostate cancer. Smoking is the biggest cause. Around 80% of lung cancers are thought to be preventable.

Question 49

Anatomy of the lungs

Answer 49

Air enters the lung through the trachea, which splits into the left main bronchus and right main bronchus. These bronchi then split into lobar bronchi, segmental bronchi, bronchioles, then alveoli. Bronchi is pleural for bronchus.

The right lung has three lobes. The left lung has two lobes. The heart is on the left, leaving less room for an extra lobe. Both lungs have an oblique fissure separating the lobes. The right lung also has a horizontal fissure. Fluid may be seen in the fissures in acute heart failure and pulmonary oedema.

There is a membrane that surrounds the lungs called the pleura. There are two layers of this membrane, with a small amount of fluid between them (less than 20mls). These layers separate the lungs from the chest wall. Lubrication between the two layers allows the lungs to expand and move without creating friction with the chest wall.

Between the two layers, there is a potential space, called the pleural cavity. The two layers are usually touching each other, which is why it is only a potential space. There is negative pressure within the pleural cavity, pulling the two layers of the pleura together. As the chest wall expands, the negative pressure within the pleural cavity pulls the lungs outwards with the chest wall, causing them to expand.

A pleural effusion is when the potential space of the pleural cavity fills with excess fluid. This creates an inward pressure on the lungs, reducing the lung volume. A pneumothorax is when air gets into the pleural cavity.

Question 50

Histology of lung cancers

Answer 50

The histological types of lung cancer can be broadly divided into:

Small cell lung cancer (SCLC) (around 20%)
Non-small cell lung cancer (around 80%)

Non-small cell lung cancer can be further divided into:

Adenocarcinoma (around 40% of total lung cancers)
Squamous cell carcinoma (around 20% of total lung cancers)
Large-cell carcinoma (around 10% of total lung cancers)
Other types (around 10% of total lung cancers)

Small cell lung cancer cells contain neurosecretory granules that can release neuroendocrine hormones. This makes SCLC responsible for multiple paraneoplastic syndromes.

Question 51

Mesothelioma

Answer 51

Mesothelioma is a lung malignancy affecting the mesothelial cells of the pleura. It is strongly linked to asbestos inhalation. There is a huge latent period between exposure to asbestos and the development of mesothelioma of up to 45 years. The prognosis is very poor. Chemotherapy can improve survival, but it is essentially palliative.

Question 52

Presentation of lung cancer

Answer 52

Shortness of breath
Cough
Haemoptysis (coughing up blood)
Finger clubbing
Recurrent pneumonia
Weight loss
Lymphadenopathy – often supraclavicular nodes are the first to be found on examination

Question 53

Extrapulmonary manifestations in lung cancer

Answer 53

Lung cancer is associated with a lot of extrapulmonary manifestations and paraneoplastic syndromes. These are linked to different types and distributions of lung cancer. Exam questions commonly ask you to suggest the underlying cause of the paraneoplastic syndrome. Sometimes they can be the first evidence of lung cancer in an otherwise asymptomatic patient.

Recurrent laryngeal nerve palsy presents with a hoarse voice. It is caused by a tumour pressing on or affecting the recurrent laryngeal nerve as it passes through the mediastinum.

Phrenic nerve palsy, due to nerve compression, causes diaphragm weakness and presents with shortness of breath.

Superior vena cava obstruction is a complication of lung cancer. It is caused by direct compression of the tumour on the superior vena cava. It presents with facial swelling, difficulty breathing and distended veins in the neck and upper chest. “Pemberton’s sign” is where raising the hands over the head causes facial congestion and cyanosis. This is a medical emergency.

Horner’s syndrome is a triad of partial ptosis, anhidrosis and miosis. It can be caused by a Pancoast tumour (tumour in the pulmonary apex) pressing on the sympathetic ganglion.

Syndrome of inappropriate ADH (SIADH) can be caused by ectopic ADH secreted by a small cell lung cancer. It presents with hyponatraemia.

Cushing’s syndrome can be caused by ectopic ACTH secretion by a small cell lung cancer.

Hypercalcaemia can be caused by ectopic parathyroid hormone secreted by a squamous cell carcinoma.

Limbic encephalitis is a paraneoplastic syndrome where small cell lung cancer causes the immune system to make antibodies to tissues in the brain, specifically the limbic system, causing inflammation in these areas. This causes symptoms such as short term memory impairment, hallucinations, confusion and seizures. It is associated with anti-Hu antibodies.

Lambert-Eaton myasthenic syndrome can be caused by antibodies produced by the immune system against small cell lung cancer cells. These antibodies also target and damage voltage-gated calcium channels sited on the presynaptic terminals in motor neurones. This leads to weakness, particularly in the proximal muscles but can also affect intraocular muscles causing diplopia (double vision), levator muscles in the eyelid causing ptosis and pharyngeal muscles causing slurred speech and dysphagia (difficulty swallowing). Patients may also experience dry mouth, blurred vision, impotence and dizziness due to autonomic dysfunction.

Question 54

Referral criteria for possible lung cancer

Answer 54

The NICE guidelines on suspected cancer (updated January 2021) recommend offering a chest x-ray, carried out within 2 weeks, to patients over 40 with:

Clubbing
Lymphadenopathy (supraclavicular or persistent abnormal cervical nodes)
Recurrent or persistent chest infections
Raised platelet count (thrombocytosis)
Chest signs of lung cancer

TOM TIP: Remember two key examination findings that would automatically indicate an urgent chest x-ray: finger clubbing and supraclavicular lymphadenopathy. These are quick things to check for and spotting them could lead to an early diagnosis, potentially saving a patient’s life.

They also recommend considering a chest x-ray in patients over 40 years old who have:

Two or more unexplained symptoms in patients that have never smoked
One or more unexplained symptoms in patients that have ever smoked

The unexplained symptoms that the NICE guidelines list are:

Cough
Shortness of breath
Fatigue
Chest pain
Weight loss
Loss of appetite

TOM TIP: It is worth noting that this is quite a vague list. It is very common for patients to present with vague symptoms of fatigue or shortness of breath, and your first thought might not be of lung cancer. If a 60 year old ex-smoker presents feeling “tired all the time”, with no other symptoms, these guidelines suggest considering an urgent chest x-ray to exclude lung cancer. Doctors often do a general examination and get a set of blood tests in patients with this presentation, but don’t always consider getting a chest x-ray.

Question 55

Investigating lung cancer

Answer 55

Chest x-ray is the first-line investigation in suspected lung cancer. Findings suggesting cancer include:

Hilar enlargement
Peripheral opacity – a visible lesion in the lung field
Pleural effusion – usually unilateral in cancer
Collapse

Staging CT scan of chest, abdomen and pelvis is used to assess the stage, lymph node involvement and presence of metastases. This should be contrast-enhanced, using an injected contrast to give more detailed information about different tissues.

PET-CT (positron emission tomography) scans involve injecting a radioactive tracer (usually attached to glucose molecules) and taking images using a combination of a CT scanner and a gamma-ray detector to visualise how metabolically active various tissues are. They are useful in identifying areas that cancer has spread to by showing areas of increased metabolic activity.

Bronchoscopy with endobronchial ultrasound (EBUS) involves endoscopy with ultrasound equipment on the end of the scope. This allows detailed assessment of the tumour and ultrasound-guided biopsy.

Histological diagnosis requires a biopsy to check the type of cells in the tumour. This can be either by bronchoscopy or percutaneous biopsy (through the skin).

Question 56

Treatment options for lung cancer

Answer 56

All treatments are discussed at an MDT meeting involving various consultants and specialists, such as pathologists, surgeons, oncologists and radiologists. This is to make a joint decision about the most suitable options for the individual patient.

Surgery is offered first-line in non-small cell lung cancer to patients that have disease isolated to a single area. The intention is to remove the entire tumour and cure the cancer. See below for more detail on surgery.

Radiotherapy can also be curative in non-small cell lung cancer when diagnosed early enough.

Chemotherapy can be offered in addition to surgery or radiotherapy in certain patients to improve outcomes (“adjuvant chemotherapy”) or as palliative treatment to improve survival and quality of life in later stages of non-small cell lung cancer (“palliative chemotherapy“).

Treatment for small cell lung cancer is usually chemotherapy and radiotherapy. Prognosis is generally worse for small cell lung cancer compared with non-small cell lung cancer.

Endobronchial treatment with stents or debulking can be used as part of palliative treatment to relieve bronchial obstruction caused by lung cancer.

Question 57

Lung cancer surgery

Answer 57

There are several options for removing a lung tumour:

Segmentectomy or wedge resection involves taking a segment or wedge of lung (a portion of one lobe)
Lobectomy involves removing the entire lung lobe containing the tumour (the most common method)
Pneumonectomy involves removing an entire lung

The types of surgery that can be used are:

Thoracotomy – open surgery with an incision and separation of the rib to access the thoracic cavity
Video-assisted thoracoscopic surgery (VATS) – minimally invasive “keyhole” surgery
Robotic surgery

Minimally invasive surgery (i.e., VATS or robotic surgery) is generally preferred as it has a faster recovery and fewer complications.

There are three main thoracotomy incisions:

Anterolateral thoracotomy with an incision around the front and side
Axillary thoracotomy with an incision in the axilla (armpit)
Posterolateral thoracotomy with an incision around the back and side (the most common approach to the thorax)

TOM TIP: If you see a patient with a thoracotomy scar in your OSCEs, they are likely to have had a lobectomy, pneumonectomy or lung volume reduction surgery for COPD. If they have no breath sound on that side, this indicates a pneumonectomy rather than lobectomy. If they have absent breath sound in a specific area on the affected side (e.g., the upper zone), but breath sounds are present in other areas, this indicates a lobectomy. Lobectomies and pneumonectomies are usually used to treat lung cancer. In the past, they were often used to treat tuberculosis, so keep this in mind in older patients. If it is a cardiology examination and they have a right-sided mini-thoracotomy incision, this is more likely to indicate previous minimally invasive mitral valve surgery.

Question 58

Chest drains after thoracic surgery

Answer 58

A chest drain will be left in after thoracic surgery. The chest drain allows air and fluid to exit the thoracic cavity and the lungs to expand. A chest drain pump can be used to suck fluid and air out of the chest. They are removed when they are no longer required to drain air or fluid.

The external end of the drain is placed underwater, creating a seal to prevent air from flowing back through the drain, into the chest. Air can exit the chest cavity and bubble through the water, but the water prevents air from re-entering the drain and chest. During normal respiration, the water in the drain will rise and fall due to changes in pressure in the chest (described as “swinging”).

Question 59

Pneumothorax

Answer 59

Pneumothorax occurs when air gets into the pleural space, separating the lung from the chest wall. It can occur spontaneously, or secondary to trauma, medical interventions (“iatrogenic”) or lung pathology. The typical patient in exams is a tall, thin young man presenting with sudden breathlessness and pleuritic chest pain, possibly whilst playing sports.

Question 60

Causes of pneumothorax

Answer 60

Spontaneous
Trauma
Iatrogenic, for example, due to lung biopsy, mechanical ventilation or central line insertion
Lung pathologies such as infection, asthma or COPD

Question 61

Investigating pneumothorax

Answer 61

An erect chest x-ray is the investigation of choice for a simple pneumothorax.

It shows an area between the lung tissue and the chest wall where there are no lung markings. There will be a line demarcating the edge of the lung where the lung markings end and the pneumothorax begins.

Measuring the size of the pneumothorax on a chest x-ray can be done according to the BTS guidelines from 2010. This involves measuring horizontally from the lung edge to the inside of the chest wall at the level of the hilum.

CT thorax can detect a pneumothorax that is too small to see on a chest x-ray. It can also be used to accurately assess the size of the pneumothorax.

Question 62

Managing pneumothorax

Answer 62

The acute management here is based on the 2010 guidelines from the British Thoracic Society. Always check the latest local and national guidelines, and consult with seniors when managing patients.

No shortness of breath and less than a 2cm rim of air on the chest x-ray:

No treatment is required as it will spontaneously resolve
Follow up in 2 – 4 weeks is recommended

Shortness of breath and/or more than a 2cm rim of air on the chest x-ray:

Aspiration followed by reassessment
When aspiration fails twice, a chest drain is required

Unstable patients, bilateral or secondary pneumothoraces generally require a chest drain.

Question 63

Chest drain for pneumothorax

Answer 63

Chest drains can be inserted in the emergency department or on the ward. They are inserted in the “triangle of safety”. This triangle is formed by:

The 5th intercostal space (or the inferior nipple line)
The midaxillary line (or the lateral edge of the latissimus dorsi)
The anterior axillary line (or the lateral edge of the pectoralis major)

The needle is inserted just above the rib to avoid the neurovascular bundle that runs just below the rib. Once the chest drain is inserted, obtain a chest x-ray to check the positioning.

The external end of the drain is placed underwater, creating a seal to prevent air from flowing back through the drain, into the chest. Air can exit the chest cavity and bubble through the water, but the water prevents air from re-entering the drain and chest. During normal respiration, the water in the drain will rise and fall due to changes in pressure in the chest (described as “swinging”).

When the chest drain is successfully treating the pneumothorax, air will bubble through the fluid in the drain bottle. There will be swinging of the water with respiration. On a repeat chest x-ray there will be re-inflation of the lung. If these things do not occur, there may be a problem with the drain, such as:

Blocked or kinked tube
Incorrect position in the chest
Not properly connected to the bottle

Once the pneumothorax resolves, there should be no further bubbling in the drain bottle. The swinging of the water with respiration will also reduce.

Two key complications of chest drains are:

Air leaks around the drain site (indicated by persistent bubbling of fluid, particularly on coughing)
Surgical emphysema (also known as subcutaneous emphysema) is when air collects in the subcutaneous tissue

Question 64

Surgical management of pneumothorax

Answer 64

Patients may require surgical interventions when:

A chest drain fails to correct the pneumothorax
There is a persistent air leak in the drain
The pneumothorax reoccurs (recurrent pneumothorax)

Video-assisted thoracoscopic surgery (VATS) can be used to correct the pneumothorax.

The surgical options are:

Abrasive pleurodesis (using direct physical irritation of the pleura)
Chemical pleurodesis (using chemicals, such as talc powder, to irritate the pleura)
Pleurectomy (removal of the pleura)

Pleurodesis involves creating an inflammatory reaction in the pleural lining so that the pleura stick together and the pleural space becomes sealed. This prevents further pneumothoraces from developing.

Question 65

Tension pneumothorax

Answer 65

Tension pneumothorax is caused by trauma to the chest wall that creates a one-way valve that lets air in but not out of the pleural space. The one-way valve means that during inspiration air is drawn into the pleural space and during expiration, the air is trapped in the pleural space. Therefore, more air keeps getting drawn into the pleural space with each breath and cannot escape. This is dangerous as it creates pressure inside the thorax that will push the mediastinum across, kink the big vessels in the mediastinum and cause cardiorespiratory arrest.

Signs of Tension Pneumothorax

Tracheal deviation away from side of the pneumothorax
Reduced air entry on the affected side
Increased resonance to percussion on the affected side
Tachycardia
Hypotension

Question 66

Managing tension pneumothorax

Answer 66

The management sentence you need to learn and recite in your exams is: “Insert a large bore cannula into the second intercostal space in the midclavicular line.”

However, the Advanced Traumatic Life Support (ATLS) recommendations from 2018 recommend for adults, using the “fourth or fifth intercostal space, anterior to the midaxillary axillary line”. The reason for choosing this is this site is that the chest wall thickness may be smaller than in the second intercostal space.

If a tension pneumothorax is suspected, do not wait for any investigations. Once the pressure is relieved with a cannula then a chest drain is required for definitive management.

Question 67

Indications for heart transplant

Answer 67

The most common indiction for a heart transplant is congestive heart failure, which can be secondary to:

Ischaemic heart disease
Cardiomyopathy
Congenital heart disease

Question 68

Indications for lung transplant

Answer 68

The most common indications for a lung transplant are:

Chronic obstructive pulmonary disease (COPD)
Pulmonary fibrosis
Cystic fibrosis
Pulmonary hypertension

Question 69

Variations in heart and lung transplants

Answer 69

There are several ways heart and lungs can be transplanted:

Single lung transplant
Double lung transplant
Heart transplant
Heart-lung transplant

A double lung transplant can be performed as a bilateral single lung transplant (one lung, then the other), or an “en bloc” transplant where both lungs are implanted together. Bilateral single lung transplants are generally preferred.

Question 70

Incisions in heart and lung transplants

Answer 70

A lateral thoracotomy incision may be used for single lung transplants.

A midline sternotomy incision may be used for heart transplants.

A clamshell incision may be used for bilateral lung transplants.

Question 71

Heart and lung transplant procedure

Answer 71

The time between the death of the donor and the transplant needs to be as short as possible (under 6 hours). In the meantime, the organ is cooled to reduce the damage during transportation. This is referred to as the cold ischaemic time. Usually, the operation will begin before the donated organ has arrived, so that the transplant can take place immediately on arrival of the organ.

Heart or lung transplantation requires a cardiopulmonary bypass, to bypass the circulation in the organ(s) that will be removed and transplanted. The bypass machine takes blood from the vena cava or right atrium, pumps it through a machine that adds oxygen and removes carbon dioxide from the blood, then pumps it back into the ascending aorta. This way, blood bypasses the heart and lungs and is artificially oxygenated. Heparin is used to prevent blood clotting. The clinical perfusionist is responsible for operating and monitoring the cardiopulmonary bypass equipment.

After a donor heart is implanted, the heart is reperfused with blood and warmed. The treatment that prevents the heart from beating (cardioplegia) is stopped. The heart will then spontaneously start beating. Cardioversion or temporary pacing may be used to treat arrhythmias that occur.

Patients will be transferred to the intensive care unit after surgery.

Question 72

Post heart or lung transplant

Answer 72

Organ rejection is a major risk with any organ transplant. Patients will require life-long immunosuppression to reduce the risk of transplant rejection.

Immunosuppressants have a long list of complications, particularly:

Side effects of steroids (e.g., diabetes, osteoporosis and Cushing’s syndrome)
Severe or unusual infections
Skin cancer
Post-transplant lymphoproliferative disorder (a form of non-Hodgkins lymphoma)

A key complication after a heart transplant is cardiac allograft vasculopathy (CAV), which involves narrowing of the coronary arteries in the donor heart. The donor heart is not innervated, meaning the patient will experience symptoms of ischaemia in the heart tissue. This means they will not have any symptoms of angina or myocardial infarction. Patients have regular follow up coronary angiograms to monitor for this.

The key complications after a lung transplant are:

Primary graft dysfunction (PGD), which usually occurs within 3 days, with acute pulmonary oedema, alveolar damage and hypoxia
Bronchiolitis obliterans syndrome (BOS), which usually occurs within 1 year, with damage to the bronchioles
Dehiscence of the bronchial anastomosis, which causes air leakage into the mediastinum and is life-threatening

Survival is approximately:

85% at 1 year for heart or lung transplants
75% for heart transplants at 5 years
50% for lung transplants at 5 years