Cardiology Flashcards

Question

Coronary Artery Anatomy

Answer 1

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

Answer 2

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.

Answer 3

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.

Answer 4

ST-segment elevation New left bundle branch block

Answer 5

ST segment depression T wave inversion

Answer 6

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

Answer 7

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

Answer 8

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

Answer 9

STEMI is diagnosed when the ECG shows either: ST elevation New left bundle branch block

Answer 10

NSTEMI is diagnosed when there is a raised troponin, with either: A normal ECG Other ECG changes (ST depression or T wave inversion)

Answer 11

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)

Answer 12

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).

Answer 13

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.

Answer 14

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).

Answer 15

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).

Answer 16

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

Answer 17

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.

Answer 18

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

Answer 19

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.

Answer 20

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

Answer 21

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.

Answer 22

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)

Answer 23

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).

Answer 24

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.

Answer 25

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.

Answer 26

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.

Answer 27

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.

Answer 28

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.

Answer 29

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.

Answer 30

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.

Answer 31

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.

Answer 32

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

Answer 33

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

Answer 34

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

Answer 35

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.

Answer 36

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)

Answer 37

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)

Answer 38

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.

Answer 39

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.

Answer 40

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.

Answer 41

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.

Answer 42

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

Answer 43

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).

Answer 44

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

Answer 45

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

Answer 46

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

Answer 47

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.

Answer 48

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

Answer 49

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

Answer 50

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)

Answer 51

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

Answer 52

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.

Answer 53

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.

Answer 54

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.

Answer 55

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.

Answer 56

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.

Answer 57

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

Answer 58

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.

Answer 59

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.

Answer 60

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.

Answer 61

Age Systolic Target Diastolic Target Under 80 years < 140 < 90 Over 80 years < 150 < 90

Answer 62

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.

Answer 63

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.

Answer 64

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.

Answer 65

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.

Answer 66

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

Answer 67

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?

Answer 68

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

Answer 69

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

Answer 70

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

Answer 71

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

Answer 72

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

Answer 73

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.

Answer 74

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

Answer 75

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.

Answer 76

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.

Answer 77

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)

Answer 78

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

Answer 79

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

Answer 80

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

Answer 81

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

Answer 82

Pulmonary stenosis is usually congenital and may be associated with: Noonan syndrome Tetralogy of Fallot

Answer 83

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

Answer 84

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.

Answer 85

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).

Answer 86

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

Answer 87

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.

Answer 88

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

Answer 89

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.

Answer 90

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)

Answer 91

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

Answer 92

The presenting symptoms are non-specific for an infection: Fever Fatigue Night sweats Muscle aches Anorexia (loss of appetite)

Answer 93

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)

Answer 94

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

Answer 95

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)

Answer 96

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

Answer 97

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

Answer 98

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.

Answer 99

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.

Answer 100

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.

Answer 101

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

Answer 102

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.

Answer 103

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.

Answer 104

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

Answer 105

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).

Answer 106

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

Answer 107

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

Answer 108

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.

Answer 109

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.

Answer 110

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

Answer 111

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).

Answer 112

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.

Answer 113

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)

Answer 114

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.

Answer 115

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

Answer 116

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

Answer 117

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.

Answer 118

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.

Answer 119

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)

Answer 120

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

Answer 121

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.

Answer 122

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

Answer 123

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.

Answer 124

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.

Answer 125

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.

Answer 126

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)

Answer 127

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

Answer 128

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

Answer 129

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.

Answer 130

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.

Answer 131

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.

Answer 132

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).

Answer 133

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.

Answer 134

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.

Answer 135

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.

Answer 136

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

Answer 137

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.

Answer 138

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

Answer 139

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.

Answer 140

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.

Answer 141

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.

Answer 142

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.

Answer 143

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.

Answer 144

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.

Answer 145

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).

Answer 146

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.

Answer 147

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

Answer 148

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.

Answer 149

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

Answer 150

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

Answer 151

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)

Answer 152

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.

Answer 153

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.

Answer 154

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.

Answer 155

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.

Answer 156

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

Answer 157

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

Answer 158

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

Answer 159

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.

Answer 160

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

Answer 161

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).

Answer 162

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

Answer 163

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.

Answer 164

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.

Answer 165

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.

Answer 166

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

Answer 167

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.

Answer 168

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

Answer 169

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

Answer 170

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

Answer 171

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.

Answer 172

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).

Answer 173

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)

Answer 174

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.

Answer 175

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

Answer 176

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).

Answer 177

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

Answer 178

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.