Cardiology

Question 1

Components of Atherosclerosis

Answer 1

Atherosclerosis affects the medium and large arteries. It is caused by chronic inflammation and activation of the immune system in the artery wall. This causes the deposition of lipids in the artery wall, followed by the development of fibrous atheromatous plaques.

These plaques result in:

Stiffening
Stenosis
Plaque rupture

Stiffening of the artery walls leads to hypertension (raised blood pressure) and strain on the heart as it tries to pump blood against extra resistance.

Stenosis leads to reduced blood flow (e.g. in angina).

Plaque rupture creates a thrombus that can block a distal vessel and cause ischaemia. An example is acute coronary syndrome, where a coronary artery becomes blocked.

Question 2

Non-modifiable and modifiable risk factors of cardiovascular disease

Answer 2

Non-modifiable risk factors:

Older age
Family history
Male

Modifiable risk factors:

Raised cholesterol
Smoking
Alcohol consumption
Poor diet
Lack of exercise
Obesity
Poor sleep
Stress

Question 3

Medical Co-Morbidities of cardiovascular disease

Answer 3

Diabetes
Hypertension
Chronic kidney disease (CKD)
Inflammatory conditions, such as rheumatoid arthritis
Atypical antipsychotic medications

Question 4

Complications of atherosclerosis

Answer 4

Angina
Myocardial infarction
Transient ischaemic attacks
Strokes
Peripheral arterial disease
Chronic mesenteric ischaemia

Question 5

Primary Prevention of Cardiovascular Disease

Answer 5

Medication for primary prevention is based on the QRISK3 score.

The QRISK score estimates the percentage risk that a patient will have a stroke or myocardial infarction in the next 10 years. The NICE guidelines (updated February 2023) recommend when the result is above 10%, they should be offered a statin, initially atorvastatin 20mg at night.

Atorvastatin 20mg is offered as primary prevention to all patients with:

Chronic kidney disease (eGFR less than 60 ml/min/1.73 m2)
Type 1 diabetes for more than 10 years or are over 40 years

The draft NICE guidelines due for publication in mid-2023 advise that atorvastatin 20mg can be considered for primary prevention in patients with a QRISK3 score below 10%.

Question 6

Statins

Answer 6

Statins reduce cholesterol production in the liver by inhibiting HMG CoA reductase.

NICE recommend checking lipids 3 months after starting statins and increasing the dose to aim for a greater than 40% reduction in non-HDL cholesterol. Check adherence (are they taking the medications?) before increasing the dose.

NICE also recommend checking LFTs within 3 months of starting a statin and again at 12 months. Statins can cause a transient and mild rise in ALT and AST in the first few weeks of use. They usually do not need to be stopped if the rise is less than 3 times the upper limit of normal.

Question 7

Side effects of statins

Answer 7

Myopathy (causing muscle weakness and pain)
Rhabdomyolysis (muscle damage – check the creatine kinase in patients with muscle pain)
Type 2 diabetes
Haemorrhagic strokes (very rarely)

Usually, the benefits of statins far outweigh the risks, and newer statins (such as atorvastatin) are well tolerated.

TOM TIP: Several common medications interact with statins. One key interaction to remember is with macrolide antibiotics. Patients being prescribed clarithromycin or erythromycin should be advised to stop taking their statin whilst taking these antibiotics.

Question 8

Cholesterol Lowering Drugs

Answer 8

Ezetimibe works by inhibiting the absorption of cholesterol in the intestine. It can be used as an alternative when statins are not tolerated or in combination with a statin when statins alone are inadequate.

PCSK9 inhibitors (e.g., evolocumab and alirocumab) are monoclonal antibodies that lower cholesterol. They are highly specialist treatments, given as a subcutaneous injection every 2-4 weeks.

Question 9

Secondary Prevention of Cardiovascular Disease

Answer 9

A – Antiplatelet medications (e.g., aspirin, clopidogrel and ticagrelor)
A – Atorvastatin 80mg
A – Atenolol (or an alternative beta blocker – commonly bisoprolol) titrated to the maximum tolerated dose
A – ACE inhibitor (commonly ramipril) titrated to the maximum tolerated dose

Question 10

MI treatment

Answer 10

Aspirin 75mg daily (continued indefinitely)
Clopidogrel or ticagrelor (generally for 12 months before stopping)

Question 11

Ischaemic stroke

Answer 11

Clopidogrel is the antiplatelet of choice in peripheral arterial disease and following an ischaemic stroke.

Question 12

Familial Hypercholesterolaemia

Answer 12

Familial hypercholesterolaemia is an autosomal dominant genetic condition causing very high cholesterol levels. Several genes have the potential to cause the disorder.

Heterozygous means only one copy of the gene is abnormal. This occurs in about 1 in 250 people.

Homozygous means both copies of the gene are abnormal. This very rare condition causes extremely high cholesterol (over 13 mmol/L) and almost guaranteed early cardiovascular disease.

The Simon Broome criteria or the Dutch Lipid Clinic Network Criteria are used for making a clinical diagnosis. Three important features to remember are:

Family history of premature cardiovascular disease (e.g., myocardial infarction under 60 in a first-degree relative)
Very high cholesterol (e.g., above 7.5 mmol/L in an adult)
Tendon xanthomata (hard nodules in the tendons containing cholesterol, often on the back of the hand and Achilles)

Question 13

Treating familial hypercholesterolaemia

Answer 13

Management of familial hypercholesterolaemia involves:

Specialist referral for genetic testing and testing of family members
Statins

Question 14

What causes angina?

Answer 14

Angina is caused by atherosclerosis affecting the coronary arteries, narrowing the lumen (inside diameter) and reducing blood flow to the myocardium (heart muscle). During times of high demand, such as exercise, there is an insufficient supply of blood to meet the demand. This causes the symptoms of angina, typically constricting chest pain, with or without radiation to the jaw or arms.

Question 15

Define stable angina

Answer 15

Angina is “stable” when symptoms only come on with exertion and are always relieved by rest or glyceryl trinitrate (GTN).

Question 16

Define unstable angina

Answer 16

It is “unstable” when the symptoms appear randomly whilst at rest. Unstable angina is a type of acute coronary syndrome (ACS) and requires immediate management.

Question 17

Investigations for angina

Answer 17

All patients with angina should have the following baseline investigations:

Physical examination (e.g., heart sounds, signs of heart failure, blood pressure and BMI)
ECG (a normal ECG does not exclude stable angina)
FBC (anaemia)
U&Es (required before starting an ACE inhibitor and other medications)
LFTs (required before starting statins)
Lipid profile
Thyroid function tests (hypothyroidism or hyperthyroidism)
HbA1C and fasting glucose (diabetes)

Cardiac stress testing, dobutamine, ECG, echocardiogram, MRI or a myocardial perfusion scan (nuclear medicine scan).

CT coronary angiography involves injecting contrast and taking CT images timed with the heart contractions to give a detailed view of the coronary arteries, highlighting the specific locations of any narrowing.

Invasive coronary angiography involves an invasive procedure performed in a catheter laboratory (cath lab). A catheter is inserted into the patient’s brachial or femoral artery, directed through the arterial system to the aorta and the coronary arteries under x-ray guidance, where contrast is injected to visualise the coronary arteries and identify any areas of stenosis using x-ray images. This is considered the gold standard for determining coronary artery disease.

Question 18

Management of stable angina

Answer 18

R – Refer to cardiology
A – Advise them about the diagnosis, management and when to call an ambulance
M – Medical treatment
P – Procedural or surgical interventions
S – Secondary prevention

Referrals are usually sent to the rapid access chest pain clinic (RACPC).

Question 19

Medical management of stable angina

Answer 19

Immediate symptomatic relief during episodes of angina
Long-term symptomatic relief
Secondary prevention of cardiovascular disease

Question 20

Immediate symptomatic relief of stable angina

Answer 20

Sublingual glyceryl trinitrate (GTN) in the form of a spray or tablets. GTN causes vasodilation, improving blood flow to the heart muscle (myocardium). Patients are advised to:

Take the GTN when the symptoms start
Take a second dose after 5 minutes if the symptoms remain
Take a third dose after a further 5 minutes if the symptoms remain
Call an ambulance after a further 5 minutes if the symptoms remain

Key side effects of GTN are headaches and dizziness caused by vasodilation.

Question 21

Long-term symptomatic relief of stable angina

Answer 21

Beta blocker (e.g., bisoprolol)
Calcium-channel blocker (e.g., diltiazem or verapamil – both avoided in heart failure with reduced ejection fraction)

A specialist may consider other options for long-term symptomatic relief:

Long-acting nitrates (e.g., isosorbide mononitrate)
Ivabradine
Nicorandil
Ranolazine

Question 22

Surgical interventions for stable angina

Answer 22

Surgical procedures are generally offered to patients with more severe disease and where medical treatments do not control symptoms. There are two options:

Percutaneous coronary intervention (PCI)
Coronary artery bypass graft (CABG)

Percutaneous coronary intervention (PCI) involves inserting a catheter into the patient’s brachial or femoral artery. This is fed in, under x-ray guidance, through the arterial system to the coronary arteries. Then a contrast is injected to visualise the coronary arteries and identify areas of stenosis on the x-ray images. Areas of stenosis can be treated by dilating a balloon to widen the lumen (angioplasty) and inserting a stent to keep it open. This can be referred to as coronary angioplasty and stenting.

Coronary artery bypass graft (CABG) surgery may be offered to patients with severe stenosis. This involves opening the chest along the sternum, with a midline sternotomy incision. A graft vessel is attached to the affected coronary artery, bypassing the stenotic area. 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

Question 23

PCI versus CABG

Answer 23

PCI:
Faster recovery
Lower rate of strokes as a complication
Higher rate of requiring repeat revascularisation (further procedures)

TOM TIP: When examining a patient that you think may have coronary artery disease in your OSCEs, check for a midline sternotomy scar (previous CABG), scars around the brachial and femoral arteries (previous PCI) and along the inner calves (saphenous vein harvesting scar) to see what procedures they may have had done.

Question 24

Thrombus

Answer 24

When a thrombus forms in a fast-flowing artery, it is formed mainly of platelets. This is why antiplatelet medications such as aspirin, clopidogrel and ticagrelor are the mainstay of treatment.

Question 25

Coronary Artery Anatomy

Answer 25

Two coronary arteries branch from the root of the aorta:

Right coronary artery (RCA)
Left coronary artery (LCA)

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 left coronary artery becomes the:

Circumflex artery
Left anterior descending (LAD)

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 the septum

Question 26

Presentation of acute coronary syndrome

Answer 26

Acute coronary syndrome typically presents with central, constricting chest pain.

The chest pain is often associated with:

Pain radiating to the jaw or arms
Nausea and vomiting
Sweating and clamminess
A feeling of impending doom
Shortness of breath
Palpitations

Symptoms should continue at rest for more than 15 minutes.

Question 27

What is a silent MI?

Answer 27

A silent myocardial infarction is when someone does not experience typical chest pain during acute coronary syndrome. Patients with diabetes are particularly at risk of silent MIs.

Question 28

ECG change in a STEMI

Answer 28

ST-segment elevation
New left bundle branch block

Question 29

ECG changes in a NSTEMI

Answer 29

ST segment depression
T wave inversion

Question 30

Pathological Q waves

Answer 30

Pathological Q waves suggest a deep infarction involving the full thickness of the heart muscle (transmural) and typically appear 6 or more hours after the onset of symptoms.

Artery
Heart Area
ECG Leads

Left coronary artery
Anterolateral
I, aVL, V3-6

Left anterior descending
Anterior
V1-4

Circumflex
Lateral
I, aVL, V5-6

Right coronary artery
Inferior
II, III, aVF

Question 31

Troponin

Answer 31

Troponin is a protein in cardiac muscle (myocardium) and skeletal muscle. The specific type of troponin, normal range and diagnostic criteria vary based on different laboratories, so check the local policy. A rise in troponin is consistent with myocardial ischaemia, as they are released from the ischaemic muscle tissue.

Troponin results are used to diagnose an NSTEMI. They are not required to diagnose a STEMI, as this is diagnosed based on the clinical presentation and ECG findings.

Assessment may involve repeated troponin tests, depending on the local policy (e.g., at baseline and 3 hours after the onset of symptoms). A high troponin or a rising troponin on repeat tests, in the context of suspected acute coronary syndrome, indicates an NSTEMI.

Troponin is a non-specific marker, meaning that a raised troponin does not automatically imply acute coronary syndrome. The alternative causes of a raised troponin include:

Chronic kidney disease
Sepsis
Myocarditis
Aortic dissection
Pulmonary embolism

Question 32

Investigations for acute coronary syndrome

Answer 32

Baseline bloods, including FBC, U&E, LFT, lipids and glucose
Chest x-ray to investigate for pulmonary oedema and other causes of chest pain
Echocardiogram once stable to assess the functional damage to the heart, specifically the left ventricular function

Question 33

Diagnosing STEMI

Answer 33

STEMI is diagnosed when the ECG shows either:

ST elevation
New left bundle branch block

Question 34

Diagnosing NSTEMI

Answer 34

NSTEMI is diagnosed when there is a raised troponin, with either:

A normal ECG
Other ECG changes (ST depression or T wave inversion)

Question 35

Diagnosing unstable angina

Answer 35

Unstable angina is diagnosed when there are symptoms suggest ACS, the troponin is normal, and either:

A normal ECG
Other ECG changes (ST depression or T wave inversion)

Question 36

Initial management of acute coronary syndrome

Answer 36

C – Call an ambulance
P – Perform an ECG
A – Aspirin 300mg
I – Intravenous morphine for pain if required (with an antiemetic, e.g., metoclopramide)
N – Nitrate (GTN)

When the patient is pain-free, but the pain occurred within the past 72 hours, they need to be referred to the hospital for same-day assessment, usually to be seen by the medical team in the Ambulatory Care Unit (depending on local pathways). They may require emergency admission if there are ECG changes or complications (e.g., signs of heart failure).

Question 37

Management of a STEMI

Answer 37

Patients with STEMI presenting within 12 hours of onset should be discussed urgently with the local cardiac centre for either:

Percutaneous coronary intervention (PCI) (if available within 2 hours of presenting)
Thrombolysis (if PCI is not available within 2 hours)

The cardiac centre will advise about medications to be given in preparation for PCI, such as aspirin and prasugrel.

Thrombolysis involves injecting a fibrinolytic agent. Fibrinolytic agents work by breaking down fibrin in blood clots. There is a significant risk of bleeding, which can make thrombolysis dangerous. Some examples of thrombolytic agents are streptokinase, alteplase and tenecteplase.

Question 38

Management of a NSTEMI

Answer 38

B – Base the decision about angiography and PCI on the GRACE score
A – Aspirin 300mg stat dose
T – Ticagrelor 180mg stat dose (clopidogrel if high bleeding risk, or prasugrel if having angiography)
M – Morphine titrated to control pain
A – Antithrombin therapy with fondaparinux (unless high bleeding risk or immediate angiography)
N – Nitrate (GTN)

Give oxygen only if their saturation drops (less than 95% in someone without COPD).

Question 39

Angiography in NSTEMI

Answer 39

The GRACE score gives a 6-month probability of death after having an NSTEMI.

3% or less is considered low risk
Above 3% is considered medium to high risk

Patients at medium or high risk are considered for early angiography with PCI (within 72 hours).

Question 40

Ongoing management of acute coronary syndrome

Answer 40

Echocardiogram once stable to assess the functional damage to the heart, specifically the left ventricular function
Cardiac rehabilitation
Secondary prevention

Question 41

Medication for secondary prevention of acute coronary syndrome

Answer 41

Aspirin 75mg once daily indefinitely
Another Antiplatelet (e.g., ticagrelor or clopidogrel) for 12 months
Atorvastatin 80mg once daily
ACE inhibitors (e.g. ramipril) titrated as high as tolerated
Atenolol (or another beta blocker – usually bisoprolol) titrated as high as tolerated
Aldosterone antagonist for those with clinical heart failure (i.e. eplerenone titrated to 50mg once daily)

It is particularly essential to closely monitor the renal function in patients taking ACE inhibitors and aldosterone antagonists. Both can cause hyperkalaemia (raised potassium). The MHRA issued a safety update in 2016 that using spironolactone or eplerenone (aldosterone antagonists) plus an ACE inhibitor or angiotensin receptor blocker carries a risk of fatal hyperkalaemia.

Question 42

Complications of acute coronary syndrome

Answer 42

D – Death
R – Rupture of the heart septum or papillary muscles
E – “oEdema” (heart failure)
A – Arrhythmia and Aneurysm
D – Dressler’s Syndrome

Question 43

Dressler’s syndrome

Answer 43

Dressler’s syndrome is also called post-myocardial infarction syndrome. It usually occurs around 2 – 3 weeks after an acute myocardial infarction. It is caused by a localised immune response that results in inflammation of the pericardium, the membrane that surrounds the heart (pericarditis). It has become less common as the management of acute coronary syndrome has advanced.

It presents with pleuritic chest pain, low-grade fever and a pericardial rub on auscultation. A pericardial rub is a rubbing, scratching sound that occurs alongside the heart sounds. It can cause a pericardial effusion and rarely a pericardial tamponade (where the fluid constricts the heart and inhibits function).

A diagnosis can be made with an ECG (global ST elevation and T wave inversion), echocardiogram (pericardial effusion) and raised inflammatory markers (CRP and ESR).

Management is with NSAIDs (e.g., aspirin or ibuprofen) and, in more severe cases, steroids (e.g., prednisolone). Pericardiocentesis may be required to remove fluid from around the heart, if there is a significant pericardial effusion.

Question 44

First degree heart block

Answer 44

Jesus its bloody freezing = J waves, irregular rhythms, bradycardia, first degree heart block

Question 45

Pericarditis pathophysiology

Answer 45

The membrane that surrounds the heart is called the pericardium or pericardial sac. It 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.

There is a potential space between the two layers, called the pericardial cavity. The two layers usually touch each other, which is why it is only a potential space.

Question 46

Causes of pericarditis

Answer 46

Pericarditis refers to inflammation of the pericardium. There are many potential underlying causes for the inflammation:

Idiopathic (no underlying cause)
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)

Question 47

Pericardial effusion

Answer 47

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).

Question 48

Pericardial tamponade/ cardiac tamponade

Answer 48

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 reduces heart filling during diastole, decreasing cardiac output during systole. This is an emergency and requires prompt drainage of the pericardial effusion to relieve the pressure.

Question 49

Pericarditis presentation

Answer 49

Two key presenting features should make you think of pericarditis:

Chest pain
Low-grade fever

The chest pain is:

Sharp
Central/anterior
Worse with inspiration (pleuritic)
Worse on lying down
Better on sitting forward

Pericardial friction rub on auscultation is a key examination finding. A pericardial rub is a rubbing, scratching sound that occurs alongside the heart sounds.

Question 50

Pericarditis investigations

Answer 50

Blood tests show raised inflammatory markers (white blood cells, CRP and ESR).

ECG changes include:

Saddle-shaped ST-elevation
PR depression

Echocardiogram can be used to diagnose a pericardial effusion.

Question 51

Pericarditis management

Answer 51

Management involves:

Non-steroidal anti-inflammatory drugs (NSAIDs) are the mainstay of treatment (e.g., aspirin or ibuprofen)
Colchicine (taken longer-term, e.g., 3 months, to reduce the risk of recurrence)

Steroids may be used second-line, in recurrent cases or associated with inflammatory conditions (e.g., rheumatoid arthritis)

Underlying causes, such as tuberculosis and renal failure, should be treated appropriately.

Pericardiocentesis may be required to remove fluid from around the heart if there is a significant pericardial effusion or tamponade.

Most cases resolve within a month. It can be recurrent, returning after previously having resolved. Some cases may persist long-term, called chronic pericarditis.

Question 52

Acute left ventricular failure

Answer 52

Acute left ventricular failure occurs when an acute event results in the left ventricle being unable to move blood efficiently through the left side of the heart and into the systemic circulation.

Question 53

Cardiac output

Answer 53

Cardiac output is the volume of blood ejected by the heart per minute. Stroke volume is the volume of blood ejected during each beat. Cardiac output is the product of stroke volume x heart rate.

Question 54

Pulmonary oedema

Answer 54

Pulmonary oedema is where the lung tissue and alveoli are filled with interstitial fluid. This interferes with normal gas exchange in the lungs, causing shortness of breath and reduced oxygen saturation.

Question 55

Triggers of acute left ventricular failure

Answer 55

Acute left ventricular failure is often the result of decompensated chronic heart failure.

The potential triggers are:

Iatrogenic (e.g., aggressive IV fluids in a frail elderly patient with impaired left ventricular function)
Myocardial infarction
Arrhythmias
Sepsis
Hypertensive emergency (acute, severe increase in blood pressure)

TOM TIP: Acute left ventricular failure and pulmonary oedema are common in the acute hospital setting. When a nurse asks you to review a breathless and desaturating patient, ask yourself how much fluid that patient has been given and whether they will be able to cope with that amount. For example, an 85 year old patient with chronic kidney disease and aortic stenosis is prescribed 2 litres of fluid over 4 hours and then starts to drop her oxygen saturation. This is a common scenario, and a dose of IV furosemide can work like magic to clear the excess fluid and resolve the symptoms.

Question 56

Presentation of acute left ventricular failure

Answer 56

Acute LVF typically presents with acute shortness of breath. This is exacerbated by lying flat and improves on sitting up.

Acute LVF causes a type 1 respiratory failure (low oxygen without an increased carbon dioxide).

Symptoms include:

Shortness of breath
Looking and feeling unwell
Cough with frothy white or pink sputum

Signs on examination include:

Raised respiratory rate
Reduced oxygen saturations
Tachycardia (fast heart rate)
3rd heart sound
Bilateral basal crackles (sounding “wet”) on auscultation of the lungs
Hypotension in severe cases (cardiogenic shock)

There may also be signs and symptoms related to the underlying cause, for example:

Chest pain in acute coronary syndrome
Fever in sepsis
Palpitations with arrhythmias

If they also have right-sided heart failure, you could find:

Raised jugular venous pressure (JVP), caused by a backlog on the right side of the heart, leading to an engorged internal jugular vein in the neck
Peripheral oedema of the ankles, legs and sacrum

Question 57

Assessment of acute left ventricular failure

Answer 57

Assessment in patients with acute left ventricular failure includes:

Clinical assessment (history and examination, starting with an ABCDE approach in any acutely unwell patient)
ECG to look for ischaemia and arrhythmias
Bloods for anaemia, infection, kidney function, BNP, and consider troponin if suspecting myocardial infarction
Arterial blood gas (ABG)
Chest x-ray
Echocardiogram

Question 58

B-type Natriuretic Peptide

Answer 58

B-type natriuretic peptide (BNP) is a hormone released from the heart ventricles when the cardiac muscle (myocardium) is stretched beyond the normal range. A raised BNP blood result indicates the heart is overloaded beyond its normal capacity to pump effectively.

The action of BNP is to relax the smooth muscle in blood vessels. This reduces systemic vascular resistance, making it easier for the heart to pump blood through the system. BNP also acts on the kidneys as a diuretic to promote water excretion in the urine. This reduces the circulating volume, helping to improve the function of the heart in someone that is fluid-overloaded.

BNP is sensitive but not specific. This means that when the result is negative, it helps rule out heart failure, but it can be positive due to other causes. Other causes of a raised BNP include:

Tachycardia
Sepsis
Pulmonary embolism
Renal impairment
COPD

Question 59

Echocardiogram in acute left ventricular failure

Answer 59

Echocardiography is helpful in assessing the function of the left ventricle and any structural abnormalities in the heart. A key measure of the left ventricular function is the ejection fraction. This is the percentage of blood in the left ventricle that is squeezed out with each ventricular contraction. An ejection fraction above 50% is considered normal.

Question 60

Chest X-ray findings in acute left ventricular failure

Answer 60

Cardiomegaly on a chest x-ray is classified as a cardiothoracic ratio of more than 0.5. This is when the diameter of the widest part of the heart (the widest part of the cardiac silhouette) is more than half the diameter of the widest part of the lung fields.

Upper lobe venous diversion may also be seen. Usually, when standing erect, the lower lobe veins contain more blood, and the upper lobe veins remain relatively small. In acute LVF, there is such a back-pressure that the upper lobe veins also fill with blood and become engorged. This is referred to as upper lobe diversion. This is visible as increased prominence and diameter of the upper lobe vessels on a chest x-ray.

Fluid leaking from oedematous lung tissue causes additional x-ray findings of:

Bilateral pleural effusions
Fluid in interlobar fissures (between the lung lobes)
Fluid in the septal lines (Kerley lines)

Question 61

Management of acute left ventricular failure

Answer 61

Patients with acute left ventricular failure require hospital admission. Patients with severe pulmonary oedema or cardiogenic shock may require admission to the high dependency unit or intensive care unit. Get experienced seniors involved early.

The “sodium” mnemonic can be used for remembering the basic management of acute LVF:

S – Sit up
O – Oxygen
D – Diuretics
I – Intravenous fluids should be stopped
U – Underlying causes need to be identified and treated (e.g., myocardial infarction)
M – Monitor fluid balance

Sitting the patient up helps oxygenate the lungs. When lying flat, the fluid in the lungs spreads to a larger area. When upright, gravity takes it to the lung bases, leaving the middle and upper areas clear for better gas exchange.

Oxygen should be given for reduced oxygen saturation (below 95%). As always, be cautious with patients who have COPD, where the target saturations may be 88-92%. An arterial blood gas can help guide oxygen therapy when in doubt.

Diuretics (e.g., IV furosemide) increase the urine output of the kidneys, reducing the volume of fluid in the circulation. Reducing the circulating volume in a fluid-overloaded patient allows the heart to pump blood more effectively.

Fluid balance monitoring involves monitoring the fluid intake (oral and IV), urine output, U&Es and body weight.

Severe cases may require (guided by an experienced specialist):

Intravenous opiates, such as morphine, which act as vasodilators
Intravenous nitrates act as vasodilators, and may be considered in severe hypertension or acute coronary syndrome
Inotropes, such as dobutamine, to improve cardiac output
Vasopressors, such as noradrenalin, to improve blood pressure
Non‑invasive ventilation
Invasive ventilation (involving intubation and sedation)

Question 62

Inotropes

Answer 62

Inotropes are medications that alter the contractility of the heart. Positive inotropes act to increase the contractility of the heart. This increases cardiac output (CO) and mean arterial pressure (MAP). They are used in patients with a low cardiac output, for example, due to acute heart failure, recent myocardial infarction or following heart surgery.

Question 63

Vasopressors

Answer 63

Vasopressors are medications that cause vasoconstriction (narrowing of blood vessels). This increases the systemic vascular resistance and, consequently, mean arterial pressure (MAP). Vasopressors are commonly used by anaesthetists as a bolus dose or in ICU as an infusion to improve patient’s blood pressure and, therefore, tissue perfusion.

Question 64

Impaired left ventricular function

Answer 64

Impaired left ventricular function results in a chronic backlog of blood waiting to flow into and through the left side of the heart. The left atrium, pulmonary veins and lungs experience an increased volume and pressure of blood. They start to leak fluid and cannot reabsorb excess fluid from the surrounding tissues, resulting in pulmonary oedema.

Question 65

Ejection fraction

Answer 65

The ejection fraction is the percentage of blood in the left ventricle squeezed out with each ventricular contraction. An ejection fraction above 50% is considered normal.

Question 66

Heart failure with reduced ejection fraction

Answer 66

Heart failure with reduced ejection fraction is when the ejection fraction is less than 50%.

Question 67

Heart failure with preserved ejection fraction

Answer 67

Heart failure with preserved ejection fraction is when someone has the clinical features of heart failure but an ejection fraction greater than 50%. This is the result of diastolic dysfunction, where there is an issue with the left ventricle filling with blood during diastole (the ventricle relaxing).

Question 68

Causes of chronic heart failure

Answer 68

Ischaemic heart disease
Valvular heart disease (commonly aortic stenosis)
Hypertension
Arrhythmias (commonly atrial fibrillation)
Cardiomyopathy

Question 69

Presentation symptoms of chronic heart failure

Answer 69

Breathlessness, worsened by exertion
Cough, which may produce frothy white/pink sputum
Orthopnoea, which is breathlessness when lying flat, relieved by sitting or standing (ask how many pillows they use)
Paroxysmal nocturnal dyspnoea (more detail below)
Peripheral oedema
Fatigue

Question 70

Signs on examination, of chronic heart failure

Answer 70

Tachycardia (raised heart rate)
Tachypnoea (raised respiratory rate)
Hypertension
Murmurs on auscultation indicating valvular heart disease
3rd heart sound on auscultation
Bilateral basal crackles (sounding “wet”) on auscultation of the lungs, indicating pulmonary oedema
Raised jugular venous pressure (JVP), caused by a backlog on the right side of the heart, leading to an engorged internal jugular vein in the neck
Peripheral oedema of the ankles, legs and sacrum

Question 71

Paroxysmal nocturnal dyspnoea

Answer 71

Paroxysmal nocturnal dyspnoea (PND) describes the experience that patients have of suddenly waking at night with a severe attack of shortness of breath, cough and wheeze.

They may describe having to sit on the side of the bed or walk around the room, gasping for breath. They may feel suffocated and want to open a window to get fresh air. Symptoms improve over several minutes.

There are a few proposed mechanisms to explain paroxysmal nocturnal dyspnoea.

Firstly, fluid settles across a large surface area of the lungs as they lie flat to sleep, causing breathlessness. As they stand up, the fluid sinks to the lung bases, and the upper lung areas function more effectively.

Secondly, during sleep, the respiratory centre in the brain becomes less responsive, so the respiratory rate and effort do not increase in response to reduced oxygen saturation like they would when awake. This allows the person to develop more significant pulmonary congestion and hypoxia before they wake up feeling very unwell.

Thirdly, there is less adrenalin circulating during sleep. Less adrenalin means the myocardium is more relaxed, reducing cardiac output.

Question 72

Diagnosis of chronic heart failure

Answer 72

Clinical assessment (history and examination)
N-terminal pro-B-type natriuretic peptide (NT‑proBNP) blood test
ECG
Echocardiogram

Other investigations include:

Bloods for anaemia, renal function, thyroid function, liver function, lipids and diabetes
Chest x-ray and lung function tests to exclude lung pathology

Question 73

New York Heart Association Classification

Answer 73

Class I: No limitation on activity
Class II: Comfortable at rest but symptomatic with ordinary activities
Class III: Comfortable at rest but symptomatic with any activity
Class IV: Symptomatic at rest

Question 74

Management of chronic heart failure

Answer 74

R – Refer to cardiology
A – Advise them about the condition
M – Medical treatment
P – Procedural or surgical interventions
S – Specialist heart failure MDT input, such as the heart failure specialist nurses, for advice and support

The urgency of the referral and specialist assessment depends on the NT-proBNP result. According to the NICE guidelines:

From 400 – 2000 ng/litre should be seen and have an echocardiogram within 6 weeks
Above 2000 ng/litre should be seen and have an echocardiogram within 2 weeks

Additional management:

Flu, covid and pneumococcal vaccines
Stop smoking
Optimise treatment of co-morbidities
Written care plan
Cardiac rehabilitation (a personalised exercise programme)

Question 75

Medical treatment of chronic heart failure

Answer 75

A – ACE inhibitor (e.g., ramipril) titrated as high as tolerated
B – Beta blocker (e.g., bisoprolol) titrated as high as tolerated
A – Aldosterone antagonist when symptoms are not controlled with A and B (e.g., spironolactone or eplerenone)
L – Loop diuretics (e.g., furosemide or bumetanide)

An angiotensin receptor blocker (ARB) (e.g., candesartan) can be used instead of an ACE inhibitor if not tolerated. Avoid ACE inhibitors in patients with valvular heart disease until initiated by a specialist.

Aldosterone antagonists are used when there is a reduced ejection fraction and symptoms are not controlled with an ACEi and beta blocker.

Patients should have their U&Es closely monitored whilst taking diuretics, ACE inhibitors and aldosterone antagonists, as all three medications can cause electrolyte disturbances. It is particularly essential to closely monitor the renal function in patients taking ACE inhibitors and aldosterone antagonists. Both can cause hyperkalaemia (raised potassium), which is potentially fatal.

Additional specialist treatments in patients with heart failure are:

SGLT2 inhibitor (e.g., dapagliflozin)
Sacubitril with valsartan (brand name Entresto)
Ivabradine
Hydralazine with a nitrate
Digoxin

Question 76

Procedural and Surgical Interventions of chronic heart failure

Answer 76

Surgical procedures may be used to treat underlying valvular heart disease.

Implantable cardioverter defibrillators continually monitor the heart and apply a defibrillator shock to cardiovert the patient back into sinus rhythm if they identify a shockable arrhythmia. These are used in patients who previously had ventricular tachycardia or ventricular fibrillation.

Cardiac resynchronisation therapy (CRT) may be used in severe heart failure, with an ejection fraction of less than 35%. CRT involves biventricular (triple chamber) pacemakers, with leads in the right atrium, right ventricle and left ventricle. The objective is to synchronise the contractions in these chambers to optimise heart function.

A heart transplant may be considered in suitable patients with severe disease.

Question 77

Hypertension definition

Answer 77

The NICE guidelines on hypertension (updated 2022) suggest a diagnosis of hypertension with a blood pressure above 140/90 in the clinical setting, confirmed with ambulatory or home readings above 135/85.

Question 78

Causes of hypertension

Answer 78

Essential hypertension accounts for 90% of hypertension. This is also known as primary hypertension. It means a high blood pressure has developed on its own and does not have a secondary cause.

Secondary causes of hypertension can be remembered with the “ROPED” mnemonic:

R – Renal disease
O – Obesity
P – Pregnancy-induced hypertension or pre-eclampsia
E – Endocrine
D – Drugs (e.g., alcohol, steroids, NSAIDs, oestrogen and liquorice)

Renal disease is the most common cause of secondary hypertension. When the blood pressure is very high or does not respond to treatment, consider renal artery stenosis. Renal artery stenosis can be diagnosed with duplex ultrasound or an MR or CT angiogram.

Most endocrine conditions can cause hypertension. Hyperaldosteronism (Conn’s syndrome) is an important cause and may be present in 5-10% of patients with hypertension.

Specialist investigations should be considered in patients with a potential secondary cause for their hypertension or aged under 40 years.

Question 79

Complications of hypertension

Answer 79

High blood pressure increases the risk of:

Ischaemic heart disease (angina and acute coronary syndrome)
Cerebrovascular accident (stroke or intracranial haemorrhage)
Vascular disease (peripheral arterial disease, aortic dissection and aortic aneurysms)
Hypertensive retinopathy
Hypertensive nephropathy
Vascular dementia
Left ventricular hypertrophy
Heart failure

Patients with hypertension may develop left ventricular hypertrophy. The left ventricle is straining to pump blood against increased resistance in the arterial system, so the muscle becomes thicker. On examination, there may be a sustained and forceful apex beat. It can be seen on an ECG using voltage criteria and is best diagnosed with an echocardiogram.

Question 80

Diagnosing hypertension

Answer 80

NICE recommend measuring blood pressure every 5 years to screen for hypertension. It should be measured more often in borderline cases and every year in patients with type 2 diabetes.

Patients with a clinic blood pressure between 140/90 mmHg and 180/120 mmHg should have 24-hour ambulatory blood pressure or home readings to confirm the diagnosis. Having blood pressure taken by a doctor or nurse often results in a higher reading. This is commonly called “white coat syndrome”. The white coat effect involves more than a 20/10 mmHg difference in blood pressure between clinic and ambulatory or home readings.

NICE recommend measuring blood pressure in both arms, and if the difference is more than 15 mmHg, using the reading from the arm with the higher pressure.

Question 81

Stages of hypertension

Answer 81

Stage
Clinic Reading
Confirmed on Ambulatory or Home Readings

Stage 1 Hypertension
Above 140/90
Above 135/85

Stage 2 Hypertension
Above 160/100
Above 150/95

Stage 3 Hypertension
Above 180/120

Question 82

Checking for end organ damage in hypertensive patients

Answer 82

NICE recommend all patients with a new diagnosis should have:

Urine albumin:creatinine ratio for proteinuria and dipstick for microscopic haematuria to assess for kidney damage
Bloods for HbA1c, renal function and lipids
Fundus examination for hypertensive retinopathy
ECG for cardiac abnormalities, including left ventricular hypertrophy

NICE recommend calculating the QRISK score, which estimates the percentage risk that a patient will have a stroke or myocardial infarction in the next 10 years. When the result is above 10%, they should be offered a statin, initially atorvastatin 20mg at night.

Question 83

Management of hypertension

Answer 83

Lifestyle advice includes a healthy diet, stopping smoking, reducing alcohol, caffeine and salt intake and taking regular exercise.

Medications used in management are:

A – ACE inhibitor (e.g., ramipril)
B – Beta blocker (e.g., bisoprolol)
C – Calcium channel blocker (e.g., amlodipine)
D – Thiazide-like diuretic (e.g., indapamide)
ARB – Angiotensin II receptor blocker (e.g., candesartan)

Angiotensin receptor blockers (ARBs) are recommended by NICE instead of ACE inhibitors in patients of Black African or African-Caribbean family origin. In the steps below, you can replace A with ARB for these patients.

ARBs are an alternative if the person does not tolerate ACE inhibitors (commonly due to a dry cough). ACE inhibitors and ARBs are not used together.

Thiazide-like diuretics are used as an alternative if the patient does not tolerate calcium channel blockers (commonly due to ankle oedema).

The NICE recommendations vary for patients under 55 or over 55, type 2 diabetics and patients of Black African or African-Caribbean family origin:

Step 1: Aged under 55 or type 2 diabetic of any age or family origin, use A. Aged over 55 or Black African use C.
Step 2: A + C. Alternatively, A + D or C + D.
Step 3: A + C + D
Step 4: A + C + D + fourth agent (see below)

Step 4 depends on the serum potassium level:

Less than or equal to 4.5 mmol/L consider a potassium-sparing diuretic, such as spironolactone
More than 4.5 mmol/L consider an alpha blocker (e.g., doxazosin) or a beta blocker (e.g., atenolol)

Remember to check adherence. Specialist management is indicated for uncontrolled blood pressure at step 4.

Question 84

Potassium balance and hypertension

Answer 84

Spironolactone is a potassium-sparing diuretic. It works by blocking the action of aldosterone in the kidneys, resulting in sodium excretion and potassium reabsorption. It can be helpful when thiazide diuretics are causing hypokalaemia.

Using spironolactone increases the risk of hyperkalaemia. ACE inhibitors can also cause hyperkalaemia. Thiazide-like diuretics can also cause electrolyte disturbances. Therefore, it is essential to monitor U+Es regularly with these drugs.

Question 85

Treatment targets and hypertension

Answer 85

Age
Systolic Target
Diastolic Target

Under 80 years
< 140
< 90

Over 80 years
< 150
< 90

Question 86

Hypertensive emergency

Answer 86

Accelerated hypertension, also called malignant hypertension, refers to extremely high blood pressure, above 180/120, with retinal haemorrhages or papilloedema.

The NICE guidelines recommend a same-day referral for patients with accelerated hypertension. Therefore, patients with a blood pressure above 180/120 require a fundoscopy examination to look for these key findings. Additional complications also warrant same-day assessment, such as confusion, heart failure, suspected acute coronary syndrome or acute kidney injury.

Patients admitted with a hypertensive emergency are assessed for secondary causes and end-organ damage. Their blood pressure is closely monitored while medications bring it under control.

Intravenous options in a hypertensive emergency (guided by an experienced specialist) include:

Sodium nitroprusside
Labetalol
Glyceryl trinitrate
Nicardipine

How rapidly the blood pressure should be reduced depends on the individual patient. Elderly frail patients may be at risk of ischaemia if the blood pressure is reduced too quickly, as the higher pressure may be required to force blood through narrowed vessels.

Question 87

Normal heart sounds

Answer 87

The first heart sound (S1) is caused by the closing of the atrioventricular valves (the tricuspid and mitral valves) at the start of the systolic contraction of the ventricles.

The second heart sound (S2) is caused by the closing of the semilunar valves (the pulmonary and aortic valves) once the systolic contraction is complete.

Question 88

3rd heart sound

Answer 88

3rd Heart Sound

A third heart sound (S3) is heard roughly 0.1 seconds after the second heart sound. Think of it as rapid ventricular filling causing the chordae tendineae to pull to their full length and twang like a guitar string. The extra heart sound can result in what is described as a “gallop rhythm”.

S3 can be normal in young (15-40 years) healthy people because the heart functions so well that the ventricles allow rapid filling. In older patients, it can indicate heart failure, as the ventricles and chordae are stiff and weak and reach their limit much faster than usual. Think of this like tight hamstrings in an old de-conditioned patient sharply tightening as they bend forward.

Question 89

4th heart sound

Answer 89

A fourth heart sound (S4) is heard directly before S1. This is always abnormal and relatively rare to hear. It indicates a stiff or hypertrophic ventricle and is caused by turbulent flow from that atria contracting against a non-compliant ventricle.

Question 90

Valve areas

Answer 90

Listen over the 4 valve areas in turn for murmurs:

Pulmonary area – in the 2nd intercostal space, left sternal border
Aortic – 2nd intercostal space, right sternal border
Tricuspid – 5th intercostal space, left sternal border
Mitral – 5th intercostal space, mid clavicular line (apex area)

Listen to Erb’s point. This is in the third intercostal space on the left sternal border and is the best area for listening to heart sounds (S1 and S2).

Special manoeuvres can be used to emphasise certain murmurs:

Position the patient on their left side for mitral stenosis
Position the patient sat up, leaning forward and holding exhalation for aortic regurgitation

Question 91

Assessing a murmur

Answer 91

S – Site: where is the murmur loudest?
C – Character: soft/ blowing/ crescendo (getting louder)/ decrescendo (getting quieter)/ crescendo-decrescendo (louder then quieter)
R – Radiation: can you hear the murmur over the carotids (aortic stenosis) or left axilla (mitral regurgitation)?
I – Intensity: what grade is the murmur?
P – Pitch: is it high-pitched or low and rumbling? Pitch indicates velocity.
T – Timing: is it systolic or diastolic?

Question 92

Murmur grades

Answer 92

Grade I: Difficult to hear
Grade II: Quiet
Grade III: Easy to hear
Grade IV: Easy to hear with a palpable thrill
Grade V: Audible with stethoscope barely touching the chest
Grade VI: Audible with stethoscope off the chest

Question 93

Hypertrophy

Answer 93

When pushing against a stenotic valve, the muscle has to try harder, resulting in hypertrophy:

Mitral stenosis causes left atrial hypertrophy
Aortic stenosis causes left ventricular hypertrophy

Question 94

Dilation

Answer 94

When a leaky valve allows blood to flow back into a chamber, it stretches the muscle, resulting in dilatation:

Mitral regurgitation causes left atrial dilatation
Aortic regurgitation causes left ventricular dilatation

Question 95

Aortic stenosis

Answer 95

Aortic stenosis is the most common valvular heart disease and the most common indication for valve replacement surgery. It refers to narrowing of the aortic valve, restricting blood flow from the left ventricle to the aorta.

Aortic stenosis causes an ejection-systolic, high-pitched murmur due to the high blood flow velocity through the aortic valve. 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 start and end and fastest in the middle.

The murmur radiates to the carotids as the turbulence continues into the neck.

Other signs of aortic stenosis:

Thrill in the aortic area on palpation
Slow rising pulse
Narrow pulse pressure (the difference between systolic and diastolic blood pressure)
Exertional syncope (lightheadedness and fainting when exercising) due to difficulty maintaining a good flow of blood to the brain

Question 96

Causes of aortic stenosis

Answer 96

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

Question 97

Aortic regurgitation

Answer 97

Aortic regurgitation refers to an incompetent aortic valve, allowing blood to flow back from the aorta into the left ventricle.

Aortic regurgitation typically causes an early diastolic, soft murmur.

It can also cause an Austin-Flint murmur. This is heard at the apex as a diastolic “rumbling” murmur. This is caused by blood flowing back through the aortic valve and over the mitral valve, causing it to vibrate.

Other signs of aortic regurgitation:

Thrill in the aortic area on palpation
Collapsing pulse
Wide pulse pressure
Heart failure and pulmonary oedema

A collapsing pulse or water hammer pulse is a forcefully appearing and rapidly disappearing pulse. This is typically felt in the radial artery with the patient’s arm held straight upwards. It occurs as blood is forcefully pumped out of the left ventricle, then immediately flows backwards through the incompetent aortic valve.

Question 98

Causes of aortic regurgitation

Answer 98

Idiopathic age-related weakness
Bicuspid aortic valve
Connective tissue disorders, such as Ehlers-Danlos syndrome and Marfan syndrome

Question 99

Mitral stenosis

Answer 99

Mitral stenosis is a narrowed mitral valve restricting blood flow from the left atrium into the left ventricle.

Mitral stenosis causes a mid-diastolic, low-pitched “rumbling” murmur due to a low blood flow velocity. There will be a loud S1 due to thick valves requiring a large systolic force to shut, then shutting suddenly. There is an opening snap after S2, which triggers the onset of the murmur.

Other signs of mitral stenosis:

Tapping apex beat, which is a palpable, prominent S1
Malar flush
Atrial fibrillation (irregularly irregular pulse)

Malar flush refers to red discolouration of the skin over the upper cheeks and nose. It is due to the back pressure of blood into the pulmonary system, causing a rise in CO2 and vasodilation.

Atrial fibrillation is caused by the left atrium struggling to push blood through the stenotic valve causing strain, electrical disruption and resulting fibrillation.

Question 100

Causes of mitral stenosis

Answer 100

Rheumatic heart disease
Infective endocarditis

TOM TIP: When examining a patient with heart valve pathology, look for signs of the potential underlying cause. For example, look for signs of infective endocarditis in a patient with mitral stenosis, such as splinter haemorrhages, Janeway lesions, Osler’s nodes and splenomegaly, and offer fundoscopy for Roth spots. Look for signs of Marfan syndrome in a patient with aortic regurgitation, such as tall stature, long limbs, arachnodactyly (long slender fingers) and a high-arched palate. This will make you look very clever.

Question 101

Mitral regurgitation

Answer 101

Mitral regurgitation refers to an incompetent mitral valve, allowing blood to flow back from the left ventricle to the left atrium 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 is the second most common indication for valve replacement.

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.

Other signs of mitral regurgitation:

Thrill in the mitral area on palpation
Signs of heart failure and pulmonary oedema
Atrial fibrillation (irregularly irregular pulse)

Question 102

Causes of mitral regurgitation

Answer 102

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 103

Tricuspid regurgitation

Answer 103

Tricuspid regurgitation refers to an incompetent tricuspid valve, allowing blood to flow back from the right ventricle to the right atrium during systolic contraction of the right ventricle.

Tricuspid regurgitation causes a pan-systolic murmur. There is a split second heart sound due to the pulmonary valve closing earlier than the aortic valve, as the right ventricle empties faster than the left ventricle.

Other signs of tricuspid regurgitation:

Thrill in the tricuspid area on palpation
Raised JVP with giant C-V waves (Lancisi’s sign)
Pulsatile liver (due to regurgitation into the venous system)
Peripheral oedema
Ascites

Question 104

Causes of tricuspid regurgitation

Answer 104

Pressure due to left-sided heart failure or pulmonary hypertension (“functional”)
Infective endocarditis
Rheumatic heart disease
Carcinoid syndrome
Ebstein’s anomaly
Connective tissue disorders, such as Marfan syndrome

Question 105

Pulmonary stenosis

Answer 105

Pulmonary stenosis is a narrowed pulmonary valve, restricting blood flow from the right ventricle into the pulmonary arteries.

Pulmonary stenosis causes an ejection systolic murmur loudest in the pulmonary area with deep inspiration. There is a widely split second heart sound, as the left ventricle empties much faster than the right ventricle.

Other signs of pulmonary stenosis:

Thrill in the pulmonary area on palpation
Raised JVP with giant A waves (due to the right atrium contracting against a hypertrophic right ventricle)
Peripheral oedema
Ascites

Question 106

Causes of pulmonary stenosis

Answer 106

Pulmonary stenosis is usually congenital and may be associated with:

Noonan syndrome
Tetralogy of Fallot

Question 107

Components of Tetralogy of Fallot

Answer 107

Tetralogy of Fallot is a congenital condition where there are four coexisting pathologies:

Ventricular septal defect (VSD)
Overriding aorta
Pulmonary valve stenosis
Right ventricular hypertrophy

Question 108

Valve replacement scars

Answer 108

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 109

INR target range with mechanical valves

Answer 109

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 (higher than the 2 – 3 target for atrial fibrillation).

Question 110

Major complications of mechanical heart valves

Answer 110

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

Question 111

Transcatheter Aortic Valve Implantation

Answer 111

Transcatheter aortic valve implantation (TAVI) is a treatment for severe aortic stenosis, usually in patients 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, 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 still need to be clarified as it is a relatively new procedure. Therefore, open surgery is still the first-line option in younger, fitter patients.

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

Question 112

Infective endocarditis and mechanical heart valves

Answer 112

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

Staphylococcus
Streptococcus
Enterococcus

Question 113

Infective endocarditis definition

Answer 113

Infective endocarditis refers to infection of the endothelium (the inner surface) of the heart. Most commonly, it affects the heart valves. It can be acute, subacute or chronic, depending on how rapidly and acutely the symptoms present and the causative organism.

Question 114

Risk factors for infective endocarditis

Answer 114

The risk factors for infective endocarditis are:

Intravenous drug use
Structural heart pathology (see below)
Chronic kidney disease (particularly on dialysis)
Immunocompromised (e.g., cancer, HIV or immunosuppressive medications)
History of infective endocarditis

Structural pathology can increase the risk of endocarditis:

Valvular heart disease
Congenital heart disease
Hypertrophic cardiomyopathy
Prosthetic heart valves
Implantable cardiac devices (e.g., pacemakers)

Question 115

Causes of infective endocarditis

Answer 115

The most common cause is Staphylococcus aureus.

Other causes include:

Streptococcus (notably the viridans group of streptococci)
Enterococcus (e.g., Enterococcus faecalis)
Rarer causes include Pseudomonas, HACEK organisms and fungi

Question 116

Presentation of infective endocarditis

Answer 116

The presenting symptoms are non-specific for an infection:

Fever
Fatigue
Night sweats
Muscle aches
Anorexia (loss of appetite)

Question 117

Examination findings of infective endocarditis

Answer 117

New or “changing” heart murmur
Splinter haemorrhages (thin red-brown lines along the fingernails)
Petechiae (small non-blanching red/brown spots) on the trunk, limbs, oral mucosa or conjunctiva
Janeway lesions (painless red flat macules on the palms of the hands and soles of the feet)
Osler’s nodes (tender red/purple nodules on the pads of the fingers and toes)
Roth spots (haemorrhages on the retina seen during fundoscopy)
Splenomegaly (in longstanding disease)
Finger clubbing (in longstanding disease)

Question 118

Investigations of infective endocarditis

Answer 118

Blood cultures are essential before starting antibiotics. Three blood culture samples are recommended, usually separated by at least 6 hours and taken from different sites. The gap between repeated sets may have to be shorter if antibiotics are required more urgently (e.g., sepsis).

Echocardiography is the usual imaging investigation. Transoesophageal echocardiography (TOE) is more sensitive and specific than transthoracic echocardiography. Vegetations (an abnormal mass or collection) may be seen on the valves.

Special imaging investigations may be used in patients with prosthetic heart valves, where it can be more challenging to determine whether an infection is present in the prosthesis:

18F-FDG PET/CT
SPECT-CT

Question 119

Modified Duke Criteria

Answer 119

The Modified Duke criteria can be used to diagnose infective endocarditis. A diagnosis requires either:

One major plus three minor criteria
Five minor criteria

Major criteria are:

Persistently positive blood cultures (typical bacteria on multiple cultures)
Specific imaging findings (e.g., a vegetation seen on the echocardiogram)

Minor criteria are:

Predisposition (e.g., IV drug use or heart valve pathology)
Fever above 38°C
Vascular phenomena (e.g., splenic infarction, intracranial haemorrhage and Janeway lesions)
Immunological phenomena (e.g., Osler’s nodes, Roth spots and glomerulonephritis)
Microbiological phenomena (e.g., positive cultures not qualifying as a major criterion)

Question 120

Management of infective endocarditis

Answer 120

Patients require admission and are managed by the relevant specialist team (e.g., the infective endocarditis or infectious diseases team).

Intravenous broad-spectrum antibiotics (e.g., amoxicillin and optional gentamicin) are the mainstay of treatment. The choice of antibiotic may be more specific once the causative organism is identified on cultures. Antibiotics are typically continued for at least:

4 weeks for with native heart valves
6 weeks for patients with prosthetic heart valves

Surgery may be required for:

Heart failure relating to valve pathology
Large vegetations or abscesses
Infections not responding to antibiotics

Question 121

Complications of infective endocarditis

Answer 121

Infective endocarditis has a high mortality rate. Key complications include:

Heart valve damage, causing regurgitation
Heart failure
Infective and non-infective emboli (causing abscesses, strokes and splenic infarction)
Glomerulonephritis, causing renal impairment

Question 122

Hypertrophic obstructive cardiomyopathy definition

Answer 122

Hypertrophic obstructive cardiomyopathy (HOCM) is a condition where the left ventricle becomes hypertrophic, with thickening of the muscle. This tends to asymmetrically affect the septum of the heart, blocking the flow of blood out of the left ventricle. This is referred to as left ventricular outflow tract (LVOT) obstruction.

HOCM is associated with an increased risk of heart failure, myocardial infarction, arrhythmias and sudden cardiac death. Arrhythmias and sudden death often occur during exertion, when there is extra demand on the heart. It is a notable cause of sudden cardiac death in young people, including high-performing athletes.

Question 123

Genetic cause of HOCM

Answer 123

HOCM is an autosomal dominant genetic condition resulting from a defect in the genes for sarcomere proteins. It occurs in about 1 in 500 people.

Question 124

Presentation of hypertrophic obstructive cardiomyopathy

Answer 124

Most patients are asymptomatic.

Patients can present with non-specific symptoms. These may come on during exertion:

Shortness of breath
Fatigue
Dizziness
Syncope
Chest pain
Palpitations

Severe cases may present with symptoms of heart failure (e.g., cough, shortness of breath, orthopnoea, paroxysmal nocturnal dyspnoea and oedema).

Asking about a family history of heart disease and sudden death is important. It may occur in patients without a family history if a de novo (new) mutation occurs.

Question 125

Examination findings and signs in HOCM

Answer 125

Examination findings:

Ejection systolic murmur at the lower left sternal border (louder with the valsalva manoeuvre)
Fourth heart sound
Thrill at the lower left sternal border

If present, there may be signs of:

Atrial fibrillation (irregularly irregular pulse)
Mitral regurgitation (high-pitched, pan-systolic murmur)
Heart failure

Question 126

Investigating HCOM

Answer 126

An ECG may show left ventricular hypertrophy.

A chest x-ray is usually normal. It may show signs of pulmonary oedema if heart failure is present.

An echocardiogram or cardiac MRI is used to establish the diagnosis.

Genetic testing may be considered to establish the affected genes.

Question 127

Management of HCOM

Answer 127

Management depends on the severity and symptoms. Options include:

Beta blockers
Surgical myectomy (removing part of the heart muscle to relieve the obstruction)
Alcohol septal ablation (a catheter-based, minimally invasive procedure to shrink the obstructive tissue)
Implantable cardioverter defibrillator (for those at risk of sudden cardiac death or ventricular arrhythmias)
Heart transplant

Patients are advised to avoid intense exercise, heavy lifting and dehydration.

ACE inhibitors and nitrates are avoided as they can worsen the LVOT obstruction.

Patients are also offered genetic counselling, and relatives may be tested.

Question 128

Complications of HCOM

Answer 128

There is a spectrum of outcomes:

Minimal symptoms and a normal lifespan (most patients)
Arrhythmias (e.g., atrial fibrillation)
Mitral regurgitation
Heart failure
Sudden cardiac death

Question 129

Dilated cardiomyopathy

Answer 129

Dilated cardiomyopathy is a condition where the heart muscle becomes thin and dilated. It may be genetic or secondary to other conditions (e..g, myocarditis).

Question 130

Alcohol-induced cardiomyopathy

Answer 130

Alcohol-induced cardiomyopathy is a type of dilated cardiomyopathy caused by long-term alcohol use.

Question 131

Restricted cardiomyopathy

Answer 131

Restrictive cardiomyopathy is when the heart becomes rigid and stiff, causing impaired ventricular filling during diastole.

Question 132

Arrhythmogenic cardiomyopathy

Answer 132

Arrhythmogenic cardiomyopathy is a genetic condition where the heart muscle is progressively replaced with fibrofatty tissue. It becomes prone to ventricular arrhythmias. It is a notable cause of sudden cardiac death in young people, including high-performing athletes.

Question 133

Takotsubo cardiomyopathy

Answer 133

Takotsubo cardiomyopathy is a condition with a rapid onset of left ventricular dysfunction and weakness. This often follows severe emotional stress, for example, the death of a long-term partner. For this reason, it is known as broken heart syndrome. It tends to resolve spontaneously with time.

Question 134

Overall effects of atrial fibrillation

Answer 134

Irregularly irregular ventricular contractions
Tachycardia (fast heart rate)
Heart failure due to impaired filling of the ventricles during diastole
Increased risk of stroke

Question 135

Pathophysiology of atrial fibrillation

Answer 135

Normally, the sinoatrial node produces organised electrical activity that coordinates the contraction of the atria. Atrial fibrillation occurs when this electrical activity is disorganised, causing the contraction of the atria to become uncoordinated, rapid and irregular. This chaotic electrical activity overrides the regular, organised activity from the sinoatrial node. It passes through to the ventricles, resulting in irregularly irregular ventricular contraction.

Uncoordinated atrial activity means the blood can stagnate in the atria, forming a blood clot (thrombus). A thrombus formed in the left atrium may travel to the brain and block a cerebral artery, causing an ischaemic stroke. The risk of stroke is about 5 times higher than usual in patients with atrial fibrillation (depending on individual factors).

Question 136

Causes of AF

Answer 136

S – Sepsis
M – Mitral valve pathology (stenosis or regurgitation)
I – Ischaemic heart disease
T – Thyrotoxicosis
H – Hypertension

Alcohol and caffeine are lifestyle causes worth remembering.

Question 137

Presentation of AF

Answer 137

Patients are often asymptomatic, and atrial fibrillation is an incidental finding. It may be diagnosed after a stroke.

Patients may present with:

Palpitations
Shortness of breath
Dizziness or syncope (loss of consciousness)
Symptoms of associated conditions (e.g., stroke, sepsis or thyrotoxicosis)

Question 138

Examination findings of AF

Answer 138

The key examination finding is an irregularly irregular pulse. There are two differential diagnoses for an irregularly irregular pulse:

Atrial fibrillation
Ventricular ectopics

Ventricular ectopics disappear when the heart rate gets above a certain threshold. Therefore, a regular heart rate during exercise suggests a diagnosis of ventricular ectopics.

Question 139

Investigating AF

Answer 139

An ECG is required in all patients with an irregularly irregular pulse. The ECG findings in atrial fibrillation are:

Absent P waves
Narrow QRS complex tachycardia
Irregularly irregular ventricular rhythm

An echocardiogram may be required to investigate further in cases of:

Valvular heart disease
Heart failure
Planned cardioversion

Question 140

Paroxysmal AF

Answer 140

Paroxysmal atrial fibrillation refers to episodes of atrial fibrillation that reoccur and spontaneously resolve back to sinus rhythm. These episodes can last between 30 seconds and 48 hours.

Patients with a normal ECG and suspected paroxysmal atrial fibrillation can have further investigations with:

24-hour ambulatory ECG (Holter monitor)
Cardiac event recorder lasting 1-2 weeks

Question 141

Valvular AF

Answer 141

Valvular atrial fibrillation is AF with significant mitral stenosis or a mechanical heart valve. The assumption is that the valvular pathology has led to atrial fibrillation. Atrial fibrillation without valve pathology or with other valve pathologies, such as mitral regurgitation or aortic stenosis, is classed as non-valvular AF.

The NICE guidelines (2021) do not reference valvular atrial fibrillation. They recommend patients with valvular heart disease are referred to a cardiologist for further assessment and management.

Question 142

Management of AF

Answer 142

There are two principles to treating atrial fibrillation:

Rate or rhythm control
Anticoagulation to prevent strokes

TOM TIP: The following details on rate and rhythm control get quite detailed and complex. Most patients will end up on a beta blocker for rate control, often bisoprolol, plus a DOAC for anticoagulation. If you remember one thing about the treatment of atrial fibrillation, remember this combination.

Question 143

Rate control of AF

Answer 143

The function of the atria is to pump blood into the ventricles. In patients with atrial fibrillation, the atrial contractions are not coordinated, so the ventricles must fill by suction and gravity, which is considerably less efficient. The higher the heart rate, the less time is available for the ventricles to fill with blood, reducing the cardiac output. Rate control aims to get the heart rate below 100 and extend the time during diastole for the ventricles to fill with blood.

NICE guidelines (2021) suggest all patients with AF should have rate control as first-line, except with:

A reversible cause for their AF
New onset atrial fibrillation (within the last 48 hours)
Heart failure caused by atrial fibrillation
Symptoms despite being effectively rate controlled

Options for rate control:

Beta blocker first-line (e.g., atenolol or bisoprolol)
Calcium-channel blocker (e.g., diltiazem or verapamil) (not preferable in heart failure)
Digoxin (only in sedentary people with persistent atrial fibrillation, requires monitoring and has a risk of toxicity)

Question 144

Rhythm control of AF

Answer 144

Rhythm control may be offered to patients with:

A reversible cause for their AF
New onset atrial fibrillation (within the last 48 hours)
Heart failure caused by atrial fibrillation
Symptoms despite being effectively rate controlled

Rhythm control aims to return the patient to normal sinus rhythm. This can be achieved through:

Cardioversion
Long-term rhythm control using medications

Question 145

Cardioversion and AF

Answer 145

For cardioversion, there is a choice between:

Immediate cardioversion
Delayed cardioversion

Immediate cardioversion is used if the atrial fibrillation is either:

Present for less than 48 hours
Causing life-threatening haemodynamic instability

There are two options for immediate cardioversion:

Pharmacological cardioversion
Electrical cardioversion

For pharmacological cardioversion, the options are:

Flecainide
Amiodarone (the drug of choice in patients with structural heart disease)

Electrical cardioversion aims to shock the heart back into sinus rhythm. It involves using a cardiac defibrillator machine to deliver controlled shocks. This is usually done with sedation or general anaesthesia.

Delayed cardioversion is used if the atrial fibrillation has been present for more than 48 hours and they are stable. Electrical cardioversion is recommended. Transoesophageal echocardiography‑guided cardioversion is an option where available. Amiodarone may be considered before and after electrical cardioversion to prevent AF from recurring.

The patient should be anticoagulated for at least 3 weeks before delayed cardioversion. During the 48 hours before cardioversion, they may have developed a blood clot in the atria, and reverting them to sinus rhythm carries a high risk of mobilising that clot, causing a stroke. They are rate controlled whilst waiting for cardioversion.

Question 146

Long-term rhythm control and AF

Answer 146

Beta blockers first-line
Dronedarone second-line for maintaining normal rhythm where patients have had successful cardioversion
Amiodarone is useful in patients with heart failure or left ventricular dysfunction

Question 147

Management of Paroxysmal AF

Answer 147

Patients with paroxysmal atrial fibrillation may be appropriate for a “pill-in-the-pocket” approach. They take a pill to terminate their atrial fibrillation only when they feel the symptoms starting. To be suitable for a pill-in-the-pocket approach, they must have infrequent episodes without structural heart disease. They also need to be able to identify the signs of atrial fibrillation and understand when to take the treatment.

Flecainide is the usual treatment for a pill-in-the-pocket approach. There is a risk of flecainide converting the atrial fibrillation into atrial flutter, with 1:1 AV conduction to the ventricles, causing a very fast ventricular rate.

Patients with paroxysmal atrial fibrillation should still be anticoagulated based on their CHA2DS2-VASc score, similar to permanent atrial fibrillation.

Question 148

Ablation and AF

Answer 148

Where drug treatment for rate or rhythm control is not adequate or tolerated, there are two options for ablation:

Left atrial ablation
Atrioventricular node ablation and a permanent pacemaker

Left atrial ablation is performed in a catheter laboratory, often called a “cath lab”. It involves a general anaesthetic or sedation. A catheter is inserted into a femoral vein and fed through the venous system under x-ray guidance to the heart. The catheter punctures through the septum into the left atrium. Once in the left atrium, it is placed against different areas to test the electrical signals. The operator attempts to identify the location of any abnormal electrical pathways. Once identified, radiofrequency ablation (heat) is applied to burn the abnormal area of electrical activity. This leaves scar tissue that does not conduct electrical activity. The aim is to remove the source of the arrhythmia and restore normal sinus rhythm.

Atrioventricular node ablation involves destroying the connection between the atria and ventricles (the atrioventricular node). It is a catheter procedure. After the procedure, the irregular electrical activity in the atria cannot pass through to the ventricles. A permanent pacemaker is required to control ventricular contraction (the pacemaker is inserted before the ablation procedure). Anticoagulation is still needed to prevent strokes.

Question 149

Anticoagulation

Answer 149

Uncontrolled and unorganised activity in the atria leads to blood stagnating in the left atrium, particularly in the left atrial appendage. Eventually, this stagnated blood leads to a thrombus (clot). This thrombus then mobilises (becomes an embolus) and travels from the left atrium to the left ventricle, into the aorta and up in the carotid arteries to the brain. It can then lodge in a cerebral artery and cause an ischaemic stroke.

Anticoagulation treatment reduces coagulation (thrombus formation) by interfering with the clotting cascade. Without anticoagulation, patients with atrial fibrillation have around a 5% risk of stroke each year, depending on individual factors. With anticoagulation, patients with atrial fibrillation have around a 1-2% risk of stroke each year, depending on individual factors. Anticoagulation reduces the risk of stroke by about 2/3.

Anticoagulation treatment carries around a 2.5-8% risk of serious bleeding each year, depending on individual factors.

The NICE guidelines (2021) recommend for anticoagulation:

Direct-acting oral anticoagulants (DOACs) first-line
Warfarin second-line, if DOACs are contraindicated

TOM TIP: Every patient with a head injury whilst taking anticoagulation should have a CT head to assess for an intracranial bleed, according to the NICE guidelines on head injuries (updated 2019). Being asked to review a patient after a fall is very common, and it helps to remember that a head injury plus anticoagulation automatically qualifies them for a CT scan. Inform patients starting on anticoagulation that they will need medical attention (A&E) in the event of a head injury for this reason.

Question 150

Direct-Acting Oral Anticoagulants

Answer 150

Direct-acting oral anticoagulants (DOACs) are oral anticoagulants that do not require INR monitoring, unlike warfarin. They are suitable for most patients, including patients with cancer. They have a 6-14 hour half-life.

Apixaban, edoxaban and rivaroxaban are direct factor Xa inhibitors. Dabigatran is a direct thrombin inhibitor.

Apixaban and dabigatran are taken twice daily, and edoxaban and rivaroxaban are taken once daily.

Some of the DOACs have agents available to reverse the effects in uncontrolled or life-threatening bleeding:

Andexanet alfa (apixaban and rivaroxaban)
Idarucizumab (a monoclonal antibody against dabigatran)

Question 151

DOACs versus Warfarin

Answer 151

DOACs have several advantages compared with warfarin:

No monitoring is required
No issues with time in therapeutic range (provided they have good adherence)
No major interaction problems
Equal or slightly better than warfarin at preventing strokes in atrial fibrillation
Equal or slightly lower risk of bleeding than warfarin

Question 152

Common indications for DOACs

Answer 152

Stroke prevention in patients with atrial fibrillation
Treatment of deep vein thrombosis (DVT) and pulmonary embolism (PE)
Prophylaxis of venous thromboembolism (DVTs and PEs) after a hip or knee replacement

Question 153

Warfarin

Answer 153

Warfarin is a vitamin K antagonist. Vitamin K is essential for the functioning of several clotting factors. Warfarin blocks vitamin K. It prolongs the prothrombin time, which is the time it takes for blood to clot.

The INR (international normalised ratio) is used to assess how anticoagulated the patient is by warfarin. The INR calculates the patient’s prothrombin time compared with the prothrombin time of an average healthy adult. An INR of 1 indicates a normal prothrombin time. An INR of 2 means the patient has a prothrombin time twice that of an average healthy adult (it takes them twice as long to form a blood clot).

Warfarin requires close monitoring of the INR and frequent dose adjustments to keep the INR in range. It is given once daily, usually around 6 pm when in the hospital, so the INR is available before deciding the dose. The target INR for AF is 2 – 3.

Question 154

Time in therapeutic range (TTR)

Answer 154

Time in therapeutic range (TTR) refers to the percentage of time that the INR is in the target range. When the INR is too low, the patient is at increased risk of a stroke. When the INR is too high, the patient is at increased risk of bleeding.

Question 155

Metabolism of warfarin

Answer 155

The metabolism of warfarin involves the cytochrome P450 system in the liver. Therefore, the INR will be affected by other drugs that influence the activity of the P450 system, including many antibiotics. When starting new medications, the INR needs close monitoring, and the warfarin dose needs to be adjusted accordingly.

INR is also affected by many foods, particularly those that contain vitamin K, such as leafy green vegetables, and those that affect the P450 system, such as cranberry juice and alcohol. This means it is important to monitor the INR more closely when the patient changes their diet.

Vitamin K can reverse the effects of warfarin in the event of a very high INR or significant bleeding. Warfarin has a half-life of 1-3 days.

Question 156

CHA2DS2-VASc

Answer 156

CHA2DS2-VASc is a tool for assessing whether a patient with atrial fibrillation should start anticoagulation. It is a list of risk factors that increase the likelihood of a stroke. The higher the score, the higher the risk of developing a stroke or TIA.

CHA2DS2-VASc is a mnemonic for the factors that score a point:

C – Congestive heart failure
H – Hypertension
A2 – Age above 75 (scores 2)
D – Diabetes
S2 – Stroke or TIA previously (scores 2)
V – Vascular disease
A – Age 65 – 74
S – Sex (female)

NICE (2021) recommends, based on the CHA2DS2-VASc score:

0 – no anticoagulation
1 – consider anticoagulation in men (women automatically score 1)
2 or more – offer anticoagulation

Aspirin alone is not used for stroke prevention in atrial fibrillation (using aspirin was an option years ago).

Question 157

Bleeding risk

Answer 157

The NICE guidelines recommend using the ORBIT score for assessing the risk of major bleeding in patients with atrial fibrillation taking anticoagulation. The easiest way to calculate the ORBIT score is using an online calculator. The “ORBIT” mnemonic can be used to remember the 5 factors:

O – Older age (age 75 or above)
R – Renal impairment (GFR less than 60)
B – Bleeding previously (history of gastrointestinal or intracranial bleeding)
I – Iron (low haemoglobin or haematocrit)
T – Taking antiplatelet medication

For most patients with atrial fibrillation, the risk of stroke with no anticoagulation will outweigh the risk of bleeding on anticoagulation.

Question 158

Left atrial appendage occlusion

Answer 158

Left atrial appendage occlusion is an option for patients with contraindications to anticoagulation and a high stroke risk. The left atrial appendage is a small pouch in the wall of the left atrium. It is the most common site for a thrombus to form. Left atrial appendage occlusion involves inserting a catheter into the femoral vein, feeding that through the venous system to the right atrium and puncturing the septum between the atria to access the left atrium. Then, a plug is placed in the left atrial appendage, preventing blood from entering that area.

Question 159

Pathophysiology of supraventricular tachycardia

Answer 159

Normally, the electrical signals of the heart start in the sinoatrial node. The sinoatrial node is the heart’s natural pacemaker, dictating when the heart beats. It is located at the junction between the superior vena cava and the right atrium. The electrical signal travels through the right and left atrium, causing the atria to contract. Then it travels through the atrioventricular (AV) node, which is the pathway between the upper part (atria) and lower part (ventricles) of the heart, down to the ventricles, causing the ventricles to contract. The electrical signal in the heart can only go in one direction, from the atria to the ventricles. Normally, electrical activity cannot travel from the ventricles to the atria.

Supraventricular tachycardia is caused by the electrical signal re-entering the atria from the ventricles. The electrical signal finds a way from the ventricles back into the atria. Once the signal is back in the atria, it again travels through the atrioventricular node to the ventricles, causing another ventricular contraction. This causes a self-perpetuating electrical loop without an endpoint, resulting in narrow complex tachycardia. It is described as a “narrow complex”, as the QRS complex has a duration of less than 0.12 seconds.

Paroxysmal SVT describes a situation where SVT reoccurs and remits in the same patient over time.

Question 160

Narrow complex tachycardia

Answer 160

Narrow complex tachycardia is a fast heart rate with a QRS complex duration of less than 0.12 seconds. On a standard 25 mm/sec ECG, 0.12 seconds equals 3 small squares. Therefore, the QRS complex will fit within 3 small squares in SVT. On an ECG, SVT looks like a QRS complex followed immediately by a T wave, QRS complex, T wave and so on.

There are four main differentials of a narrow complex tachycardia. There are key ECG features that will help you differentiate these:

Sinus tachycardia
Supraventricular tachycardia
Atrial fibrillation
Atrial flutter

Question 161

Sinus tachycardia, a narrow complex tachycardia

Answer 161

Sinus tachycardia will take the normal P wave, QRS complex and T wave pattern. Sinus tachycardia is not an arrhythmia and is usually a response to an underlying cause, such as sepsis or pain.

Question 162

Atrial fibrillation, a narrow complex tachycardia

Answer 162

Absent P waves
Narrow QRS complex tachycardia
Irregularly irregular ventricular rhythm (as opposed to SVT, which causes a regular rhythm)

Question 163

Atrial flutter, a narrow complex tachycardia

Answer 163

In atrial flutter, the atrial rate is usually around 300 beats per minute and gives a saw-tooth pattern on the ECG. A QRS complex occurs at regular intervals depending on how often there is conduction from the atria. This often results in two atrial contractions for every one ventricular contraction, giving a ventricular rate of 150 beats per minute.

Question 164

Supraventricular tachycardia, a narrow complex tachycardia

Answer 164

Supraventricular tachycardia looks like a QRS complex followed immediately by a T wave, then a QRS complex, then a T wave, and so on. There are P waves, but they are often buried in the T waves, so you cannot see them. It can be distinguished from atrial fibrillation by the regular rhythm and atrial flutter by the absence of a saw-tooth pattern.

It can be tricky to distinguish SVT from sinus tachycardia. SVT has an abrupt onset and a very regular pattern without variability. Sinus tachycardia has a more gradual onset and more variability in the rate. The history is also important, where sinus tachycardia usually has an explanation (e.g., pain or fever), while SVT can appear at rest with no apparent cause.

TOM TIP: SVT can cause a broad complex tachycardia if the patient also has a bundle branch block. Therefore, consider this differential in patients with tachycardia and wide QRS complexes. The most important thing to remember is that SVT causes a narrow complex tachycardia.

Question 165

Types of supraventricular tachycardia

Answer 165

There are three main types of SVT, based on the source of the abnormal electrical signal.

Atrioventricular nodal re-entrant tachycardia is where the re-entry point is back through the atrioventricular node. This is the most common type of SVT.

Atrioventricular re-entrant tachycardia is where the re-entry point is an accessory pathway. An additional electrical pathway, somewhere between the atria and the ventricles, lets electricity back through from the ventricles to the atria. Having an extra electrical pathway connecting the atria and ventricles is called Wolff-Parkinson-White syndrome.

Atrial tachycardia is where the electrical signal originates in the atria somewhere other than the sinoatrial node. This is not caused by a signal re-entering from the ventricles but from abnormally generated electrical activity in the atria.

Question 166

Wolff-Parkinson-White Syndrome

Answer 166

Wolff-Parkinson-White syndrome (WPW) is caused by an extra electrical pathway connecting the atria and ventricles. It is also called pre-excitation syndrome. Normally, only the atrioventricular (AV) node connects the atria and ventricles. The extra pathway in Wolff-Parkinson-White syndrome may be called the Bundle of Kent. The additional pathway allows electrical activity to pass between the atria and ventricles, bypassing the atrioventricular node. This electrical pathway might not cause any symptoms, or it might cause episodes of SVT.

Question 167

ECG changes on WPW syndrome

Answer 167

Short PR interval, less than 0.12 seconds
Wide QRS complex, greater than 0.12 seconds
Delta wave

The delta wave appears as a slurred upstroke in the QRS complex. It is caused by the electricity prematurely entering the ventricles through the accessory pathway.

Question 168

Managing WPW syndrome

Answer 168

The definitive treatment for Wolff-Parkinson-White syndrome is radiofrequency ablation of the accessory pathway.

In someone with a combination of atrial fibrillation or atrial flutter and WPW, there is a risk that the chaotic atrial electrical activity can pass through the accessory pathway into the ventricles, causing a polymorphic wide complex tachycardia, which is a life-threatening medical emergency. The heart rate can get above 200, or even 300, beats per minute, and ventricular fibrillation and cardiac arrest can follow. Most anti-arrhythmic medications (e.g., beta blockers, calcium channel blockers, digoxin and adenosine) increase this risk by reducing conduction through the AV node and promoting conduction through the accessory pathway. Therefore, they are contra-indicated in patients with WPW that develop atrial fibrillation or flutter.

Question 169

Acute management of supraventricular tachycardia

Answer 169

The patient should have continuous ECG monitoring during management.

Management of supraventricular tachycardia in patients without life-threatening features involves a stepwise approach, trying each step to see whether it works before moving on.

Step 1: Vagal manoeuvres
Step 2: Adenosine
Step 3: Verapamil or a beta blocker
Step 4: Synchronised DC cardioversion

Patients with life-threatening features, such as loss of consciousness (syncope), heart muscle ischaemia (e.g., chest pain), shock or severe heart failure, are treated with synchronised DC cardioversion under sedation or general anaesthesia. Intravenous amiodarone is added if initial DC shocks are unsuccessful.

Patients with Wolff-Parkinson-White syndrome (pre-excitation syndrome) with possible atrial arrhythmias (e.g., atrial fibrillation or atrial flutter) should not have adenosine, verapamil or a beta blocker, as these block the atrioventricular node, promoting conduction of the atrial rhythm through the accessory pathway into the ventricles, causing potentially life-threatening ventricular rhythms. Sometimes it can be difficult to distinguish this from SVT, so the involvement of experienced seniors is essential. In this scenario, the usual management is procainamide (which does not block the AV node) or electrical cardioversion (if unstable).

Question 170

Vagal manoeuvres and supraventricular tachycardia

Answer 170

Vagal manoeuvres stimulate the vagus nerve, increasing the activity in the parasympathetic nervous system. This can slow the conduction of electrical activity in the heart, terminating an episode of supraventricular tachycardia.

Valsalva manoeuvres involve increasing the intrathoracic pressure. This can be achieved by having the patient blow hard against resistance, for example, blowing into a 10ml syringe for 10-15 seconds.

Carotid sinus massage involves stimulating the baroreceptors in the carotid sinus by massaging that area on one side of the neck (not both sides at the same time). Carotid sinus massage is avoided in patients with carotid artery stenosis (e.g., with a carotid bruit or previous TIA).

The diving reflex involves briefly submerging that patient’s face in cold water.

Question 171

Adenosine and supraventricular tachycardia

Answer 171

Adenosine works by slowing cardiac conduction, primarily through the AV node. It interrupts the AV node or accessory pathway during SVT and “resets” it to sinus rhythm. The half-life of adenosine is less than 10 seconds, meaning it is very quickly metabolised and stops having an effect. It needs to be given as a rapid bolus to ensure it reaches the heart with enough impact to interrupt the pathway for a short period. It will often cause a brief period of asystole or bradycardia that can be scary for the patient and doctor. However, it metabolises quickly, and sinus rhythm will return.

Adenosine is avoided in patients with:

Asthma
COPD
Heart failure
Heart block
Severe hypotension
Potential atrial arrhythmia with underlying pre-excitation

Adenosine must be given as a rapid IV bolus into a large proximal cannula (e.g., grey cannula in the antecubital fossa). The patient should be warned about the scary feeling of dying or impending doom when it is injected. This feeling quickly passes.

Three doses are attempted until sinus rhythm returns:

Initially 6mg
Then 12mg
Then 18mg

Question 172

Synchronised DC Cardioversion and supraventricular tachycardia

Answer 172

Synchronised DC (direct current) cardioversion involves an electric shock applied to the heart to restore normal sinus rhythm. A defibrillator machine monitors the electrical signal, particularly identifying the R waves. An electric shock is synchronised with a ventricular contraction, at the R wave on the ECG. If successful, the shock will be followed by sinus rhythm.

Synchronised cardioversion is used in patients with a pulse to avoid shocking the patient during a T wave. Delivering a shock during a T wave can result in ventricular fibrillation and, subsequently, cardiac arrest.

During a cardiac arrest scenario with pulseless ventricular tachycardia or ventricular fibrillation, where the patient does not have organised electrical activity or a pulse, there is no need for the shock to be synchronised.

Question 173

Managing paroxysmal supraventricular tachycardia

Answer 173

Patients with recurrent episodes of supraventricular tachycardia can be treated to prevent further episodes. The options are:

Long-term medication (e.g., beta blockers, calcium channel blockers or amiodarone)
Radiofrequency ablation

Question 174

Radiofrequency Ablation

Answer 174

Catheter ablation is performed in a catheter laboratory, often called a “cath lab”. It involves a general anaesthetic or sedation. A catheter is inserted into a femoral vein and fed through the venous system under x-ray guidance to the heart.

Once in the heart, the catheter tip is placed against different areas to test the electrical signals. The operator attempts to identify the location of any abnormal electrical pathways. Once identified, radiofrequency ablation (heat) is applied to burn the abnormal electrical pathway. This leaves scar tissue that does not conduct electrical activity. Destroying the abnormal electrical pathway aims to remove the source of the arrhythmia.

Radiofrequency ablation can permanently resolve certain arrhythmias caused by abnormal electrical pathways, including:

Atrial fibrillation
Atrial flutter
Supraventricular tachycardias
Wolff-Parkinson-White syndrome

Question 175

Cardiac arrest rhythms

Answer 175

These are the four possible rhythms in a pulseless patient. They are either shockable (meaning defibrillation may be effective) or non-shockable (meaning defibrillation will not be effective).

Shockable rhythms:

Ventricular tachycardia
Ventricular fibrillation

Non-shockable rhythms:

Pulseless electrical activity (all electrical activity except VF/VT, including sinus rhythm without a pulse)
Asystole (no significant electrical activity)

Question 176

Broad complex tachycardia

Answer 176

Broad complex tachycardia refers to a fast heart rate with a QRS complex duration of more than 0.12 seconds or 3 small squares on an ECG.

The resuscitation guidelines break down broad complex tachycardia into:

Ventricular tachycardia or unclear cause (treated with IV amiodarone)
Polymorphic ventricular tachycardia, such as torsades de pointes (treated with IV magnesium)
Atrial fibrillation with bundle branch block (treated as AF)
Supraventricular tachycardia with bundle branch block (treated as SVT)
Patients with life-threatening features, such as loss of consciousness (syncope), heart muscle ischaemia (e.g., chest pain), shock or severe heart failure, are treated with synchronised DC cardioversion under sedation or general anaesthesia. Intravenous amiodarone is added if initial DC shocks are unsuccessful.

Question 177

Atrial Flutter

Answer 177

Normally the electrical signal passes through the atria once, stimulating a contraction, then disappears through the atrioventricular node into the ventricles. Atrial flutter is caused by a re-entrant rhythm in either atrium. The electrical signal re-circulates in a self-perpetuating loop due to an extra electrical pathway in the atria. The signal goes round and round the atrium without interruption. The atrial rate is usually around 300 beats per minute.

The signal does not usually enter the ventricles on every lap due to the long refractory period of the atrioventricular node. This often results in two atrial contractions for every one ventricular contraction (2:1 conduction), giving a ventricular rate of 150 beats per minute. There may be 3:1, 4:1 or variable conduction ratios.

Atrial flutter gives a sawtooth appearance on the ECG, with repeated P wave occurring at around 300 per minute, with a narrow complex tachycardia.

Treatment is similar to atrial fibrillation, including anticoagulation based on the CHA2DS2-VASc score. Radiofrequency ablation of the re-entrant rhythm can be a permanent solution.

Question 178

Prolonged QT Interval

Answer 178

The QT interval is from the start of the QRS complex to the end of the T wave. The corrected QT interval (QTc) estimates the QT interval if the heart rate were 60 beats per minute. It is prolonged at:

More than 440 milliseconds in men
More than 460 milliseconds in women

A prolonged QT interval represents prolonged repolarisation of the heart muscle cells (myocytes) after a contraction. Depolarisation is the electrical process that leads to heart contraction. Repolarisation is a recovery period before the muscle cells are ready to depolarise again. Waiting a long time for repolarisation can result in spontaneous depolarisation in some muscle cells. These abnormal spontaneous depolarisations before repolarisation are known as afterdepolarisations. These afterdepolarisations spread throughout the ventricles, causing a contraction before proper repolarisation. When this leads to recurrent contractions without normal repolarisation, it is called torsades de pointes.

Question 179

Prolonged QT Interval, Torsades de pointes

Answer 179

Torsades de pointes is a type of polymorphic ventricular tachycardia. It translates from French as “twisting of the spikes”, describing the ECG characteristics. On an ECG, it looks like standard ventricular tachycardia but with the appearance that the QRS complex is twisting around the baseline. The height of the QRS complexes gets progressively smaller, then larger, then smaller, and so on.

Torsades de pointes will terminate spontaneously and revert to sinus rhythm or progress to ventricular tachycardia. Ventricular tachycardia can lead to cardiac arrest.

Question 180

Causes of prolonged QT

Answer 180

Long QT syndrome (an inherited condition)
Medications, such as antipsychotics, citalopram, flecainide, sotalol, amiodarone and macrolide antibiotics
Electrolyte imbalances, such as hypokalaemia, hypomagnesaemia and hypocalcaemia

Question 181

Managing a prolonged QT interval

Answer 181

Stopping and avoiding medications that prolong the QT interval
Correcting electrolyte disturbances
Beta blockers (not sotalol)
Pacemakers or implantable cardioverter defibrillators

Question 182

Acute management of torsades de pointes

Answer 182

Correcting the underlying cause (e.g., electrolyte disturbances or medications)
Magnesium infusion (even if they have normal serum magnesium)
Defibrillation if ventricular tachycardia occurs

Question 183

Ventricular ectopics

Answer 183

Ventricular ectopics are premature ventricular beats caused by random electrical discharges outside the atria. Patients often present complaining of random extra or missed beats. They are relatively common at all ages and in healthy patients. However, they are more common in patients with pre-existing heart conditions (e.g., ischaemic heart disease or heart failure).

Ventricular ectopics appear as isolated, random, abnormal, broad QRS complexes on an otherwise normal ECG.

Bigeminy refers to when every other beat is a ventricular ectopic. The ECG shows a normal beat (with a P wave, QRS complex and T wave), followed immediately by an ectopic beat, then a normal beat, then an ectopic, and so on.

Question 184

Management of ventricular ectopics

Answer 184

Reassurance and no treatment in otherwise healthy people with infrequent ectopics
Seeking specialist advice in patients with underlying heart disease, frequent or concerning symptoms (e.g., chest pain or syncope), or a family history of heart disease or sudden death
Beta blockers are sometimes used to manage symptoms

Question 185

First-degree heart block

Answer 185

First-degree heart block occurs where there is delayed conduction through the atrioventricular node. Despite this, every atrial impulse leads to a ventricular contraction, meaning every P wave is followed by a QRS complex. On an ECG, first-degree heart block presents as a PR interval greater than 0.2 seconds (5 small or 1 big square).

Question 186

Second-degree heart block

Answer 186

Second-degree heart block is where some atrial impulses do not make it through the atrioventricular node to the ventricles. There are instances where P waves are not followed by QRS complexes. There are two types of second-degree heart block:

Mobitz type 1 (Wenckebach phenomenon)
Mobitz type 2

Question 187

Mobitz type 1 (Wenckebach phenomenon)

Answer 187

Mobitz type 1 (Wenckebach phenomenon) is where the conduction through the atrioventricular node takes progressively longer until it finally fails, after which it resets, and the cycle restarts. On an ECG, there is an increasing PR interval until a P wave is not followed by a QRS complex. The PR interval then returns to normal, and the cycle repeats itself.

Question 188

Mobitz type 2

Answer 188

Mobitz type 2 is where there is intermittent failure of conduction through the atrioventricular node, with an absence of QRS complexes following P waves. There is usually a set ratio of P waves to QRS complexes, for example, three P waves for each QRS complex (3:1 block). The PR interval remains normal. There is a risk of asystole with Mobitz type 2.

A 2:1 block is where there are two P waves for each QRS complex. Every other P wave does not stimulate a QRS complex. It can be difficult to tell whether this is caused by Mobitz type 1 or Mobitz type 2.

Question 189

Third-degree heart block

Answer 189

Third-degree heart block is also called complete heart block. There is no observable relationship between the P waves and QRS complexes. There is a significant risk of asystole with third-degree heart block.

Question 190

Bradycardias

Answer 190

Bradycardia refers to a slow heart rate, typically less than 60 beats per minute. A heart rate under 60 can be normal in healthy fit patients without causing any symptoms. There is a long list of causes of bradycardia, including:

Medications (e.g., beta blockers)
Heart block
Sick sinus syndrome

Question 191

Sick sinus syndrome

Answer 191

Sick sinus syndrome encompasses many conditions that cause dysfunction in the sinoatrial node. It is often caused by idiopathic degenerative fibrosis of the sinoatrial node. It can result in sinus bradycardia, sinus arrhythmias and prolonged pauses.

Question 192

Asystole

Answer 192

Asystole refers to the absence of electrical activity in the heart (resulting in cardiac arrest). There is a risk of asystole in:

Mobitz type 2
Third-degree heart block (complete heart block)
Previous asystole
Ventricular pauses longer than 3 seconds

Question 193

Management of unstable patients and those at risk of asystole

Answer 193

Intravenous atropine (first line)
Inotropes (e.g., isoprenaline or adrenaline)
Temporary cardiac pacing
Permanent implantable pacemaker, when available

Question 194

Temporary cardiac pacing

Answer 194

Transcutaneous pacing, using pads on the patient’s chest
Transvenous pacing, using a catheter, fed through the venous system to stimulate the heart directly

Question 195

Atropine

Answer 195

Atropine is an antimuscarinic medication and works by inhibiting the parasympathetic nervous system. Inhibiting the parasympathetic nervous system leads to side effects of pupil dilation, dry mouth, urinary retention and constipation.

Question 196

Pacemakers

Answer 196

Pacemakers deliver controlled electrical impulses to specific areas of the heart to improve heart function. They consist of a pulse generator (the pacemaker box) and the pacing leads, which carry electrical impulses to the relevant part of the heart. The box is implanted under the skin (most commonly in the left anterior chest wall). The wires fed into the left subclavian vein and through the venous system to the relevant chambers of the heart.

Patients with a pacemaker are followed up regularly to download information from the pacemaker, check everything is working ok, and decide when the battery needs replacing. They are given an identity card and bracelet.

Pacemakers do not interact with most day-to-day electrical activities. However, they may be incompatible with MRI scans (due to powerful magnets), TENS machines (used for pain management) and diathermy (used during surgical procedures). Many modern pacemakers are MRI-compatible. Some smartphones may interact with pacemakers if held too close. Devices with strong magnets (e.g., handheld security scanners at airports) can affect the pacemaker function.

TOM TIP: Pacemakers must be removed before cremation in deceased patients. On the cremation form, one of the most critical tasks is to confirm whether the body has a pacemaker and whether it has been removed. You may hear stories about pacemakers “blowing up” crematoriums (this is a dramatic exaggeration, but they can explode, causing significant damage).

Question 197

Indications for a pacemaker

Answer 197

Symptomatic bradycardias (e.g., due to sick sinus syndrome)
Mobitz type 2 heart block
Third-degree heart block
Atrioventricular node ablation for atrial fibrillation
Severe heart failure (biventricular pacemakers)

Question 198

Single-chamber pacemakers

Answer 198

Single-chamber pacemakers have leads in a single chamber, either the right atrium or the right ventricle.

They are placed in the right atrium if the issue is with the sinoatrial node and conduction through the atrioventricular node is normal. This way, they stimulate depolarisation in the right atrium, and this electrical activity passes to the left atrium and ventricles.

They are placed in the right ventricle if conduction through the atrioventricular node is abnormal. They stimulate the ventricles directly.

Question 199

Dual-chamber pacemakers

Answer 199

Dual-chamber pacemakers have leads in both the right atrium and right ventricle. The pacemaker coordinates the contraction of the atria and ventricles.

Question 200

Biventricular (triple-chamber) pacemakers

Answer 200

Biventricular pacemakers have leads in the right atrium, right ventricle and left ventricle.

They are usually in patients with severe heart failure. They coordinate the contraction of these chambers to optimise heart function. This is referred to as cardiac resynchronisation therapy (CRT).

Question 201

Implantable cardioverter defibrillators

Answer 201

Implantable cardioverter defibrillators (ICDs) continually monitor the heart and apply a defibrillator shock if they identify ventricular tachycardia or ventricular fibrillation.

Implantable cardioverter defibrillators are used in patients at risk of ventricular tachycardia or fibrillation, for example:

Previous cardiac arrest
Hypertrophic obstructive cardiomyopathy
Long QT syndrome

Question 202

ECG changes and pacemakers

Answer 202

The pacemaker intervention can be seen as a sharp vertical line on all leads on the ECG trace. A line before each P wave indicates a lead in the atria. A line before each QRS complex indicates a lead in the ventricles. Therefore:

A line before either the P wave or QRS complex but not the other indicates a single-chamber pacemaker
A line before both the P wave and QRS complex indicates a dual-chamber pacemaker

TOM TIP: It is worth ensuring you can identify the type of pacemaker on an ECG, as this is common in exams.

Question 203

PAILS - Post, Ant, Inf, Lat, Septal
ST elevation in one will cause reciprocal ST depression in the leads of the next letter in the mnemonic. So posterior STEMI - reciprocal ST depression in anterior leads