CV PBL ILO’s Flashcards

Question

Causes of atrial fibrillation:

Answer 1

• Idiopathic • Ischaemic heart disease • Heart failure • Valve disease: mitral stenosis, mitral regurgitation • Hypertension • Hyperthyroidism • Alcohol induced Familial

Answer 2

Signs: • AF is the most common cardiac arrhythmia in adults. The prevalence of AF increases with age, particularly over 65 years, such that 10% of over 85-year-olds have atrial fibrillation. • The resulting chaotic electrical activity is intermittently conducted through the AVN which gives rise to the characteristic irregularly irregular ventricular rate seen in AF. • In AF, the ventricular rate is very variable and depends on the speed of AVN conduction. Young patients with slick AV nodes are often very symptomatic and tachycardic. • The presence of chaotic electrical activity within the atria also results in ineffective atrial contraction. The consequence of this is blood stasis within the atria which increases the chance of thrombosis (Virchow’s triad) and subsequently embolic complications including transient ischaemic attacks (TIA), stroke and systemic embolisation. • It is most commonly associated with hypertension, obesity and alcohol. • Irregularly irregular pulse when palpating radial/carotid arteries or auscultating at the apex Radial-apical deficit: this is important to assess because each ventricular contraction may not be sufficiently strong enough to transmit a pulse to the radial artery and palpating only the radial artery can miss tachycardia.

Answer 3

• Can be asymptomatic • Common presenting symptoms include breathlessness, chest discomfort, palpitations, dizziness, syncope, dyspnoea and reduced exercise tolerance • Transient ischaemic attack or stroke can be the presenting feature of AF. Essential that patients presenting with symptoms or signs of a TIA or stroke are also asked about the features of AF. Common ECG finding include irregular RR intervals and absent p-waves

Answer 4

• Stroke and thromboembolism = MAIN COMPLICATIONS --> dependent of the presence of stroke risk factors though --> stroke severity greater when stroke is associated with AF --> Peripheral thromboembolism can also occur • Heart failure --> due to disorganised electrical conduction in atria which results in ineffective ventricular filling • Tachycardia-induced cardiomyopathy and critical cardiac ischaemia as a result of persistently elevated ventricular rate seen in uncontrolled AF Sudden death

Answer 5

○ Rate Control is first line: ▪ Beta blocker – first line (e.g. atenolol 50-100mg once daily) ▪ Rate limiting CCB – diltiazem hydrochloride / verapamil hydrochloride (not preferable in heart failure) ▪ Digoxin – only as primary treatment in predominantly sedentary / if other rate limiting drugs are unsuitable ○ Used as monotherapies first but if it fails to control rate then use as combination If combination fails use rhythm control

Answer 6

○ Rhythm Control Drugs – pharmacalogical cardioversion ▪ Flecainide ▪ Amiodarone (drug of choice if patient has structural heart disease) ○ Long term rhythm control drugs: ▪ Beta blockers – 1st line ▪ Dronedarone – 2nd line, maintain normal rhythm when they’ve had successful cardioversion ▪ Amiodarone – in patients with heart failure or left ventricular dysfunction

Answer 7

Adenosine initial 6mg, then 12mg, then further 12mg if no improvement

Answer 8

Slows ventricular response in cases of atrial fibrillation and atrial flutter

Answer 9

Verapamil Hydrochloride

Answer 10

IV Beta blockers e.g. esmolol hydrochloride / propranolol hydrochloride

Answer 11

A sinus rhythm is any cardiac rhythm in which depolarisation of the cardiac muscle begins at the sinus node. It is characterised by the presence of correctly oriented P waves on the electrocardiogram

Answer 12

Sinus arrhythmia is a commonly encountered variation of normal sinus rhythm. Sinus arrhythmia characteristically presents with an irregular rate in which the variation in the R-R interval vary by more than 0.12 seconds

Answer 13

Ventricular tachycardia Ventricular fibrillation

Answer 14

AV Heart Block Asystole

Answer 15

Atrial Fibrillation: Irregularly irregular Abnormal P Waves R to R uneven Atrial Fluter: P waves = saw tooth Normal QRS R to R can be even or uneven Typically 2 or more P waves for every QRS

Answer 16

AVNRT Originates above the level of the bundle of His Commonest cause of heart palpitations in patients with no structural abnormality Slow Fast (Common) P waves often hidden being embedded in QRS complex Fast Slow (Uncommon) P waves are visible between the QRS and T wave AVRT: Rate usually 200-300bpm Orthodromic: Retrograde P waves are usually visible with a long RP Interval Antidromic: (Rare) Wide QRS complexes due to abnormal ventricular depolarisation

Answer 17

Ventricular tachycardia Ventricular fibrillation

Answer 18

Originates from the ventricles Several different forms - most common monomorphic VT ECG Features: Regular broad QRS Complexes

Answer 19

Most important shockable cardiac arrest rhythmFatal unless life support is rapidly used ECG: Chaotic irregular deflections or varying amplitude No identifiable P waves, QRS complex, or T waves Rate 150 to 500 bpm

Answer 20

AV Heart Block- First Degree Heart Block, Second Degree heart Block type 1 and 2, Third degree heart block Asystole

Answer 21

Arrhythmia where signal delayed or blocked in the conduction system due to damage or fibrosis

Answer 22

PR Interval > 200ms five small squares There is delay without interruption in conduction from atria to ventricles

Answer 23

Type 1 - Mobitz 1 block (Wenckeback Phenomenon) Progressive prolongation of the PR Interval Type 2 - Mobitz 2 (Hay Block) A form of 2nd degree AV Block in which there is intermittent non- conducted p waves without progressive prolongation of the PR Interval

Answer 24

Single blocked completely Not shockable in cardiac arrest Symptoms : syncope, confusion, dyspnea, severe chest pain Risk of dying ECG: Severe bradycardia due to absence of AV conduction AV Dissociation with independent atrial and ventricular rates

Answer 25

Flatline Represents the cessation of electrical and mechanical activity of the heart Not a shockable rhythm

Answer 26

• The cause is unknown BUT: • Any condition that leads to inflammation, stress, damage, or ischemia affecting the anatomy of the heart can result in the development of atrial fibrillation. • Electrically active foci within the pulmonary veins. • Electrical remodeling in the cardiac myocytes causing dilated cardiomyopathy • Failure of initiation of pharmacological intervention or failure of cardioversion. • Unresponsive rhythm

Answer 27

Palpitations are most commonly caused by: Atrial or ventricular extrasystoles (PACs or PVCs) - additional heartbeats that occur outside the physiological heart rhythm). Narrow QRS complex tachycardia (heart rate more than 100 beats per minute, QRS duration of less than 120 milliseconds). Atrioventricular nodal reentry tachycardia (AVNRT) is the most common type of supraventricular tachycardia (SVT). Wolff-Parkinson-White (WPW) syndrome is a condition that makes the heart suddenly beat abnormally fast, in an abnormal heart rhythm called SVTs - short PR intervals. Atrial fibrillation or flutter. Also caused by non cardiac related problems: psychiatric disorders and miscellaneous (i.e. Hyperthyroidism, alcohol)

Answer 28

Assessment of a person who currently has palpitations involves: Checking for symptoms suggestive of a serious cause or complication, such as breathlessness, chest pain, syncope or near syncope (fainting). Checking for a history of ischaemic heart disease, heart failure, cardiomyopathy, or valve disease, which could predispose to a serious arrhythmia. Asking about sudden cardiac death of a relative younger than 40 years of age. Examining the person’s heart rate and rhythm, blood pressure, and identifying any heart murmurs or lung crepitations - ensure haemodynamic stability. ○ Duration of palpitations -instant vs minutes ○ HR and rhythm regularity – describe the rate + regularity to me - tap it out. Taking an ECG immediately. Lab tests - thyroid function test

Answer 29

Cardiac causes: • Underlying structural heart disease (cardiomyopathy - disease of the heart muscle) • Identifiable conduction abnormality (long QT syndrome - heart signalling disorder) • Tachyarrhythmias, bradyarrhythmias, ectopic beats • Valvular heart disease (mitral valve prolapse - valve flaps of the mitral valve don't close smoothly or evenly) • Pacemaker syndrome (AV dyssynchrony due to single chamber pacing) • Atrial myxoma (nonca)ncerous tumor in the atria) High output cardiac states (resting cardiac output greater than 8 L/min

Answer 30

Supraventricular tachycardia - SVT Atrioventricular nodal reentry tachycardia - AVNRT Atrioventricular reentrant tachycardia - AVRT SINCE CHILDHOOD Paroxysmal supraventricular tachycardia - pSVT Atrial tachycardia Atrial fibrillation - AF OLDER PATIENTS Premature ventricular contractions - PVCs Complete heart block Ventricular tachycardia - VT POUNDING IN NECK Atrial fibrillation - AF Supraventricular arrhythmia FLUTTERING Supraventricular tachycardia - SVT Atrial fibrillation - AF Flutter PRESYNCOPE/SYNCOPE Supraventricular tachycardia - SVT Ventricular tachycardia - VT ABRUPT ONSET AND TERMINATION Atrioventricular nodal reentry tachycardia - AVNRT MORE AWAR OF PALPITATIONS ONCE STANDING AFTER SITTING

Answer 31

Rate Control medications: Reduce heart rate to less than 90bpm when resting Eg Beta Blockers (atenolol, bisoprolol) Calcium. Channel Blockers (Verapamil, diltiazem) Digoxin may be prescribed if other drugs are unsuitable Side effects: • beta blockers – tiredness, cold hands and feet, low blood pressure, nightmares and impotence • verapamil – constipation, low blood pressure, ankle swelling and heart failure Digoxin – arrythmias, cardiac conduction disorder, cerebral impairment, diarrhoea, dizziness, eosinophillia, nausea, skin reactions, vision disorders, vomiting

Answer 32

Rhythm control medications: Restore normal heart rhythm Flecainide, beta blockers (particularly sotalol) Side effects: beta blockers – tiredness, cold hands and feet, low blood pressure, nightmares and impotence flecainide – feeling sick, being sick and heart rhythm disorders

Answer 33

Reduce the chance of blood clots forming and casing a stroke

Answer 34

Rationale for anticoagulation choice in atrial fibrillation: • Pregnancy – warfarin can affect the unborn baby, apixaban, dabigatran, edoxaban and rivaroxaban are also not recommended during pregnancy. Heparin injections can be given while pregnant • Breastfedding – warfarin is usually ok while breastfeeding, heparin is safe while breastfeeding. Apixaban, dabigatran, edoxaban and rivaroxaban aren't recommended if you're breastfeeding because it's not clear if they're safe for the baby. • Sports/avoiding injury – anticoagulant medicines can make you more prone to bleeding if you are injured • Interactions with other medicines and remedies – prescription medicines, over the counter medicines and herbal remedies (St Johns Wort) Food and drink – important to have a healthy, balanced diet if taking anticoagulants and you should avoid making frequent changes to the amount of green vegetables/foods high in vitamin K you eat if you are taking warfarin. Warfarin is affected by alcohol but the restrictions don't usually apply if taking apixaban, dabigatran, edoxaban or riaroxaban

Answer 35

Cardioversion may be recommended for some people with atrial fibrillation. It involves giving the heart a controlled electric shock to try to restore a normal rhythm. Cardioversion is usually carried out in hospital so the heart can be carefully monitored. If you have had atrial fibrillation for more than 2 days, cardioversion can increase the risk of a clot forming. In this case, you'll be given an anticoagulant for 3 to 4 weeks before cardioversion, and for at least 4 weeks afterwards to minimise the chance of having a stroke. In an emergency, pictures of the heart can be taken to check for blood clots, and cardioversion can be carried out without going on medicine first. Anticoagulation may be stopped if cardioversion is successful. But you may need to continue taking anticoagulation after cardioversion if the risk of atrial fibrillation returning is high and you have an increased risk of having a stroke.

Answer 36

Catheter ablation is a procedure that very carefully destroys the diseased area of your heart and interrupts abnormal electrical circuits. It's an option if medicine has not been effective or tolerated. Catheters (thin, soft wires) are guided through one of your veins into your heart, where they record electrical activity. When the source of the abnormality is found, an energy source, such as high-frequency radio waves that generate heat, is transmitted through one of the catheters to destroy the tissue.

Answer 37

A pacemaker is a small battery-operated device that's usually implanted in your chest, just below your collarbone. It's usually used to stop your heart beating too slowly, but in atrial fibrillation it may be used to help your heart beat regularly. Having a pacemaker fitted is usually a minor surgical procedure carried out under a local anaesthetic (the area being operated on is numbed and you're conscious during the procedure). This treatment may be used when medicines are not effective or are unsuitable. This tends to be in people aged 80 or over.

Answer 38

NICE GUIDELINES Personalised package of care and information 1.4.1 Offer people with atrial fibrillation a personalised package of care. Ensure that the package of care is documented and delivered, and that it covers: • stroke awareness and measures to prevent stroke • rate control • assessment of symptoms for rhythm control • who to contact for advice if needed • psychological support if needed • up-to-date and comprehensive education and information on: - cause, effects and possible complications of atrial fibrillation - management of rate and rhythm control - anticoagulation - practical advice on anticoagulation in line with the recommendations on information and support for people having anticoagulation treatment in NICE's guideline on venous thromboembolic diseases 1.4 - support networks (for example, cardiovascular charities). [2014] 1.4.2 Follow the recommendations in NICE's guideline on shared decision making. [2014]

Answer 39

Cardioversion Followed by Amiodarone

Answer 40

Perform a transeosophageal to check for atrial thrombus or start a course of anticoagulation egheparin to ensure thrombolysis Once patient is no longer at a stroke risk, proceed to antiarrythmic drugs for mono therapy. If patient doesn’t respond consider a combination of 2 antiarrythmic drugs

Answer 41

Supraventricular Tachycardias 1. Valsalva maneouvre – ask patient to blow hard + fast against resistance 2. Carotid sinus massage – massage carotid on ONE SIDE gently 3. Adenosine 4. Verapamil (CCB) 5. Electrical cardioversion (if above treatment fails) • Long term management ○ Medication = beta blockers, CCB, or amiodarone Radiofrequency ablation

Answer 42

1. Unstable Angina - symptoms come on randomly whilst at rest ○ Insufficient oxygen delivery to the heart muscle leading to ischaemia 2. ST Elevation Myocardial Infarction (STEMI) -ST elevation or new left bundle branch block (occurs when something blocks or disrupts the electrical impulse that causes your heart to beat) ○ A STEMI is the most serious type of heart attack where there is a long interruption to the blood supply. 3. Non-ST Elevation Myocardial Infarction (NSTEMI) - no ST elevation, raised troponin levels and other ECG changes (ST depression or deep T wave inversion or pathological Q waves) A NSTEMI is a type of involving partial blockage of one of the coronary arteries, causing reduced flow of oxygen-rich blood to the heart muscle.

Answer 43

Patients with STEMI presenting within 12 hours of onset should be discussed urgently with local cardiac centre for either: • Initial drug therapy ○ Offer people with acute STEMI a single loading dose of 300-mg aspirin as soon as possible unless there is clear evidence that they are allergic to it. • Primary PCI (if available within 2 hours of presentation) ○ Percutaneous Coronary Intervention (PCI) involves putting a catheter into the patient’s brachial or femoral artery, feeding that up to the coronary arteries under xray guidance and injecting contrast to identify the area of blockage. This can then be treated using balloons to widen the gap or devices to remove or aspirate the blockage. Usually a stent is put in to keep the artery open. • Thrombolysis (if PCI not available within 2 hours) Thrombolysis involves injecting a fibrinolytic medication (they break down fibrin) that rapidly dissolves clots

Answer 44

B – Beta-blockers unless contraindicated A – Aspirin 300mg stat dose T – Ticagrelor 180mg stat dose (clopidogrel 300mg is an alternative if higher bleeding risk) M – Morphine titrated to control pain A – Anticoagulant: Fondaparinux (unless high bleeding risk) N – Nitrates (e.g. GTN) to relieve coronary artery spasm

Answer 45

Secondary Prevention Medical Management for STEMI and nSTEMI 6 A’s A – Aspirin A - Another antiplatelet (ticagrelor or clopidogrel) A – Atorvastatin A – ACE inhibitors A - Atenolol (beta-blocker) A – Aldosterone antagonist (clinical heart failure)

Answer 46

Fatty material that builds up inside your arteries. Made of cholesterol, protein and other substances.

Answer 47

Occurs when blood clots block veins/arteries, preventing the correct flow of blood.

Answer 48

Atherosclerosis • Atherosclerosis is a combination of atheromas (fatty deposit in the artery walls) and sclerosis (process of hardening or stiffening of blood vessel walls) • Affect medium and large arteries • Caused by chronic inflammation and activation of the immune system in the artery wall • The lipid deposits and inflammatory reaction to atherosclerosis by macrophages causes the development of atheromatous plaques • These plaques causes: ○ Stiffening of artery walls → leading to hypertension ○ Stenosis (narrowing) → leading to a reduced blood flow (e.g. in angina) Plaque rupture can give of a thrombus that blocks a distal vessel → may lead to ischaemia

Answer 49

• Thrombosis is the formation of a blood clot (partial or complete blockage) within blood vessels. • Arterial thrombosis typically initiates by the accumulation of lipid plaques in the arterial wall, provoking chronic inflammatory cell and platelet activation. ○ Platelets play a significant role in development of arterial thrombosis → explains why antiplatelet agents form cornerstone of prevention/treatment • Initial lipid plaques evolve into fibrous plaques. Fibrous plaque could rupture and erosion of the surfaces of some of these plaques could lead to release of additional pro-coagulating factors → atherosclerosis Atherosclerosis allows activation of platelets, causing adhesion ad aggregation, leading to formation of clot. • Thrombosis occurs when the plaque rupture gives off a thrombus which travels down the artery to a distal vessel and causes a blockage in either one of the arteries of veins. Thrombosis is a main cause of myocardial infarction as the blockage can reduce blood supply to the heart. Myocardial infarction in this case can be secondary to ischaemia as the blockage decreases blood flow and thus oxygen to the heart muscle.

Answer 50

Count the number of large squares present within one R to R interval and divide 300 by the number

Answer 51

o Count the number of complexes on the rhythm strip (each rhythm strip is typically 10 seconds long) Multiply the number of complexes by 6 (giving you the average number of complexes in 1 minute)

Answer 52

o P wave: depolarisation of atria (small amplitude) o P-R interval: time for conduction through AV node, bundle of His, Purkinje fibres (time from onset of atrial depolarisation to onset of ventricular depolarisation) o QRS complex: ventricular depolarisation (usually represent left ventricle) § Q wave: any initial negative deflection § R wave: any positive deflection § S wave: any negative deflection after R o ST segment: end of ventricular depolarisation to beginning of repolarisation o QT interval: total time for depolarisation and repolarisation of the ventricles T wave: ventricular repolarisation

Answer 53

A narrowing of the coronary arteries reduces blood flow to the myocardium (heart muscle). During times of high demand such as exercise there is insufficient supply of blood to meet demand. This causes symptoms the symptoms of angina, typically constricting chest pain with or without radiation to jaw or arms. • Angina is “stable” when symptoms are always relieved by rest or glyceryl trinitrate (GTN). • It is “unstable” when the symptoms come on randomly whilst at rest, and this is considered as an Acute Coronary Syndrome

Answer 54

The pathophysiology of angina • Angina is caused by reduced blood flow to the heart muscle. • Blood carries oxygen, which the heart muscle needs to survive. When the heart muscle isn't getting enough oxygen, it causes ischemia. Angina often results from ischemic episodes that excite chemo sensitive and mechanoreceptive receptors in the heart. • Ischemic episodes release chemicals such as adenosine and bradykinin, that excites the receptors of the sympathetic and vagal afferent pathways. • Sympathetic afferent fibers from the heart enter the upper thoracic spinal cord and synapse on cells of origin of ascending pathways. • Excitation of spinothalamic tract cells in the upper thoracic and lower cervical segments, except C7 and C8 segments, contributes to the anginal pain experienced in the chest and arm. Cardiac vagal afferent fibers synapse in the medulla and then descend to excite upper cervical spinothalamic tract cells. This innervation contributes to the anginal pain experienced in the neck and jaw.

Answer 55

Ischemia is a condition in which blood flow (and thus oxygen) is restricted or reduced in a part of the body. Cardiac ischemia is decreased blood flow and oxygen to the heart muscle.

Answer 56

Pain received in a region other than the site of the painful stimulus

Answer 57

Cardiac failure is when the cardiac output is not sufficient to meet the body’s metabolic demands. Pump Failure (systolic failure - can’t pump enough blood despite normal filling of he heart) Excessive preload Excessive afterload

Answer 58

Ejection fraction is the proportion of blood present at the end of diastole that is ejected from the ventricle during contraction. EF = EDV – ESV EDV Normal is considered as >0.5 (50-60%)

Answer 59

CARDIAC PRELOAD : when the cardiac muscle is stretched (more blood enters the ventricle) the muscle contracts with greater force so that the heart can pump extra blood out. Another name for this is left ventricular end-diastolic pressure. Thus cardiac pre load directly influences stroke volume. Excessive preload increases stroke volume to a certain point but after this it leads to increased hydrostatic pressure in the pulmonary capillaries and contributes to pulmonary oedema. Additionally excessive preload causes ventricular remodelling (dilation) which can reduce the ventricles elasticity as they become thin and weak thus impacting myocardial function, leading to a reduction in stroke volume ejected from the LV into the aorta. This is the primary cause of systolic heart failure.

Answer 60

CARDIAC AFTERLOAD -> the pressure exerted against the heart which it must overcome to be able to contract to eject blood from the ventricle Also known as systemic vascular resistance (SVR) Excessive afterload leads to ventricular remodelling (hypertrophy), the thickening of the ventricular walls to withstand the pressure which overtime results in diastolic dysfunction and congestive heart failure. This is diastolic heart failure.

Answer 61

Definition: dysfunction of the left ventricle, resulting insufficient delivery of blood to vital organs.

Answer 62

LVF causes a backlog of blood (like too many buses waiting to pick up people at a bus stop) that increases the amount of blood stuck in the left atrium, pulmonary veins and lungs. As the vessels in these areas are engorged with blood due to the increased volume and pressure they leak fluid and are unable to reabsorb fluid from the surrounding tissues. This causes pulmonary oedema, which is where the lung tissues and alveoli become full of interstitial fluid. This interferes with the normal gas exchange in the lungs, causing shortness of breath, oxygen desaturation and the other signs and symptoms.

Answer 63

There are two types of left ventricular heart failure: 1) Heart failure with reduced ejection fraction (HFrEF) - the left ventricle loses its ability to contract normally 2) Heart failure with preserved ejection fraction (HFpEF) - the left ventricle loses its ability to relax normally

Answer 64

Chronic heart failure is essentially the chronic version of acute heart failure. It is caused by either impaired left ventricular contraction (“systolic heart failure”) or left ventricular relaxation (“diastolic heart failure”). This impaired left ventricular function results in a chronic back-pressure of blood trying to flow into and through the left side of the heart.

Answer 65

Definition: a condition that causes the right side of the heart to fail. Cor pulmonale is right sided heart failure caused by respiratory disease. The increased pressure and resistance in the pulmonary arteries (pulmonary hypertension) results in the right ventricle being unable to effectively pump blood out of the ventricle and into the pulmonary arteries. This leads to back pressure of blood in the right atrium, the vena cava and the systemic venous system. Right ventricular heart failure usually occurs as a result of left-sided failure.

Answer 66

Definition: a combination of left-sided and right-sided heart failure. It involves both sides of the heart, and can cause a mix of both types of symptoms.

Answer 67

Classification of heart failure is by severity. The most commonly used classification is the New York Heart Association functional classification (https://www.heart.org/en/health-topics/heart-failure/what-is-heart-failure/classes-of-heart-failure).

Answer 68

Offer diuretic for congestive symptoms and fluid retention. To relieve symptoms of fluid overload: · Prescribe diuretic e.g. furosemide · Titrate the dose up/down according to symptoms · Review the dose and adjust as necessary after introducing other drug treatments for heart failure · Monitor renal function and serum electrolytes (before starting treatment, 1-2 weeks after starting treatment, after each dose increase) **U+Es need to be monitored closely** To reduce morbidity and mortality prescribe: · ACE inhibitor AND a beta blocker · AIIRA considered in patient develops intolerable side effects to ACE inhibitor *ACE avoided in those with valvular heart disease until indicated by specialist First line medical treatment - ABAL · ACE inhibitor (e.g. ramipril titrated as tolerated up to 10mg once daily) · Beta Blocker (e.g. bisoprolol titrated as tolerated up to 10mg once daily) · Aldosterone antagonist when symptoms not controlled with A and B (spironolactone or eplerenone) (and there is a reduced ejection fraction) – MRA drugs · Loop diuretics improves symptoms (e.g. furosemide 40mg once daily

Answer 69

ACE inhibitors (ACEi) E.g. Ramipril, lisinopril - Decrease symptoms, slow disease progression, and prolong life in heart failure - Most appropriate vasodilators – lower BOTH arterial and venous resistance Angiotensin II receptor antagonist (A2RA) E.g. Candesartan, losartan - Can be given if ACE inhibitors not tolerated

Answer 70

Aldosterone antagonists (MRA) E.g. spironolactone, eplerenone - Block activity of aldosterone, an adrenal cortex hormone that causes sodium retention - Recommended in patients with NYHA class II to IV heart failure and those with LVEF of 35% or less unless contraindicated - Can cause hyperkalaemia

Answer 71

Beta blockers E.g. bisoprolol, carvedilol and nebivolol (licenced for heart failure in the UK) - Long term – improve survival of stable patients with heart failure by blocking damaging effects of overactive sympathetic activity - Patients with heart failure with reduced ejection fraction should be offered this

Answer 72

(Loop) Diuretics E.g. furosemide, bumetanide, torasemide - Reduce preload to reduce ventricular filling - Improve pulmonary vascular congestion by decreasing filling pressures - Inhibit sodium-potassium-chloride cotransporter - Leads to diuresis and natriuresis - Can be given as IV or Oral

Answer 73

(Thiazide diuretics) E.g. Bendroflumethiazide, indapamide, metolazone, chlorthalidone - Added in addition to loop diuretics to potentiate their action - Inhibit sodium-chloride transporter in distal tube - Oral only

Answer 74

- Increases force of heartbeat and decreases heart rate - Induces an increase in intracellular sodium that will drive an influx of calcium in the heart, increase in contractility - When added to ACEi, beta blockers, and diuretics – reduce symptoms, prevent hospitalisation, control rhythm, and enhance exercise

Answer 75

Isosorbide dinitrate & hydralazine - Can be used as an alternative vasodilator, where ACEi and A2RA not tolerated

Answer 76

Ivabradine *Recommended in the UK in those with symptomatic heart failure with reduced ejection fraction (class II to IV) - Slows heart rate – look for bradycardia

Answer 77

Used for patients with HF Entresto – Sacubitril / Valsartan - Valsartan reduces blood vessel tightening and build-up of sodium and fluid - Sacubitril – only found in Entresto, relax blood vessel, and decrease sodium and fluid in the body

Answer 78

Inotropes Used in HF patients - Increase cardiac contractility, improving cardiac output

Answer 79

Dapagliflozin and Empagliflozin *Diabetic medications used for heart failure - Used as an ‘add-on’ to ACE, ARBs, MRAs - Helps to remove fluid from body

Answer 80

ECG findings associated with heart failure include: • Tachycardia • Atrial fibrillation (due to enlarged atria) • Left-axis deviation (due to left ventricular hypertrophy) • P wave abnormalities (e.g. P.mitrale/P.pulmonale due to atrial enlargement) • Prolonged PR interval (due to AV block) • Wide QRS complexes (due to ventricular dyssynchrony)

Answer 81

Echocardiography All patients with suspected chronic heart failure should undergo transthoracic echocardiography, with the urgency determined by their NT-proBNP level. An echocardiography is an ultrasound of the heart. It gives an accurate picture of the valves and chambers of the heart, and also gives an idea of the velocity of blood flow in certain areas thus helping you to determine if there is backflow / reduced flow in valve defects. Each valve is independently assessed, and noted whether there is any regurgitation or stenosis. If present, these are usually given a rating of mild, moderate or severe.

Answer 82

NT-proBNP N-terminal pro-B-type natriuretic peptide (NT-proBNP) should be measured in all patients presenting with symptoms and clinical signs of heart failure to inform the type and urgency of further investigations such as echocardiography: · NT-proBNP level >2000 ng/L – refer urgently for specialist assessment and transthoracic echocardiography within 2 weeks · NT-proBNP level 400-2000ng/L – refer routinely for specialist assessment and transthoracic echocardiography within 6 weeks · NT-proBNP level <400 ng/L – heart failure unlikely

Answer 83

Cardiac MRI is the gold standard investigation for assessing ventricular mass, volume and wall motion. It can also be used with contrast to identify infiltration (e.g. amyloidosis), inflammation (e.g. myocarditis) or scarring (e.g. myocardial infarction). It is typically used when echocardiography has provided inadequate views.

Answer 84

Typical chest X-ray findings associated with CHF include: ABCDE • Alveolar oedema (perihilar/bat-wing opacification) • Kerley B lines (interstitial oedema) • Cardiomegaly (cardiothoracic ratio >50%) • Dilated upper lobe vessels • Effusions (e.g. pleural effusions – blunted costophrenic angles)

Answer 85

The mitral valve is the valve separating the left atrium from the right atrium (sometimes known as the bicuspid valve).

Answer 86

Mitral valve disease is split into mitral regurgitation and mitral stenosis: Mitral Regurgitation- Mitral Valve doesn’t close completely therefore causing blood to re enter the left atrium Mitral Stenosis- During diastole the valve doesn’t open completely meaning blood can’t flow from the atrium to the ventricles efficiently

Answer 87

Mitral Stenosis (happens during diastole): The valve becomes fibrotic or calcified causing the flow from the left atrium to left ventricle to be hindered. Causes: Most often caused by rheumatic heart disease - auto antibodies are produced which attack and inflate the mitral valve. (Rheumatic heart disease can also result in mitral regurgitation, aortic stenosis and regurgitation) Calcium deposition in the Elderly End stage renal disease due to increase Calcium Carcinoid syndrome (more likely in tricuspid but can occur in mitral)

Answer 88

Mitral Valve Regurgitation (happens during systole): Causes: Most common cause is mitral valve prolapse: This is when the valve leaflets and papillary muscles and chordae tendinae are weakened (myxomatous degeneration) causing the valve to not fully shut during systole creating a back flow of blood from left ventricle to atrium. Why this happens is not fully understood but often connected with connective tissue disorders such as Marfan Syndrome and Ehlers Danilo’s syndrome. Infective endocarditis- bacteria destroys the valves Rheumatic heart disease Previous Myocardial Infarction (can cause destruction of papillary muscles) Secondary causes (not due to the valve leaflet, chordae tendinae or papillary muscles): Atrial regurgitation Systolic heart failure Hypertrophic obstructive cardiomyopathy Acute mitral regurgitation is a haemodynamic emergency and can be caused by: Infective endocarditis Papillary rupture -Others are most likely to be chronic

Answer 89

Mitral Stenosis: Listening: On the Left 5th Intercostal Space mid clavicle listen for a diastolic heart murmur ECG: ECG but only visible if they have left atrial enlargement (large P wave shaped as an M on V2) They are high risk of AF so check for AF on ECG High risk of right ventricular hypertrophy (R wave greater than S wave in V1-V3) - due to increased pulmonary pressure CXR: Blood backing up in the lungs - pulmonary oedema Left atrial enlargement causing left bronchus to lift superiorly Echo: Most Important Actually diagnoses Mitral Stenosis as well as severity -The larger the left atrial diameter, the worse the mitral stenosis -Look for left atrial thrombus -Able to measure the mitral valve area (normal is 4-6cm2, moderate <2cm2, severe <1cm2). The smaller the mitral valve area, the higher the pressure would be in the left atrium (mean pressure gradient- also measurable >10mmHg is bad)

Answer 90

Mitral Regurgitation: Listening: On the Left 5th Intercostal Space mid clavicle listen for a pansystolic murmur- these murmurs will increase during expiration or any instance of increase venous return (squatting/ leg raises) ECG: Same as mitral stenosis CXR: Same as mitral stenosis Echo: Most important -Regurgitation fraction (>50% = pretty bad) -Regurgitation jet wave (area) (>0.7cm = pretty bad) -Left ventricular end systolic diameter (>40mm = pretty bad) -Ejection Fraction ( < 60% = pretty bad as leading to HF)

Answer 91

Mitral Valve Disease: If it has lead to Heart Failure treat this first: Fluid + Sodium restriction Diuretics ACE Inhibitors Beta Blockers If patient has atrial fibrillation also treat this first: Anticoagulants- warfarin Rate and Rhythm Control drugs Mitral Stenosis: P.M.B.C - a balloon which opens up the valve (preferred treatment) Asymptomatic + Severe MVA <1cm2 Symptomatic + Moderate MVA <1.5cm2 ContraIndications of PMBC - large amount of calcification on the valve If this doesn’t work or large amount of calcification do a Valve replacement: Mechanical Valve (need anticoagulants forever - so will have to have low bleeding risk) Bioprosthetic Valve (only lasts about 10 years- give to older/high bleeding risk patients) Mitral Regurgitation: Acute Mitral Regurgitation - CV EMERGENCY Treat severe pulmonary oedema first: BIPAP Diuretics Treat hypOtension as may cause cardiogenic shock: Inotropes (to increase SV) Afterload reducers to drop the pressure in the aorta to increase CO and blood pressure Intraaortic balloon pump Once this is stabilised get straight to surgery and replace valve ASAP. Chronic Mitral Regurgitation: Regular check ups to measure: LVESD > 40mm If they have secondary mitral Regurgiation and have failed medical therapy (HF treatment) If LVEF is less than 60% Will often get a valve replacement

Answer 92

Pathophysiology • Inability of the heart to maintain adequate cardiac output • Preload = influenced by venous return and filling time • Afterload = influenced by vascular resistance and valvular disease • Contractility = influenced by myocardial strength and the autonomic nervous system 1. When the heart is failing there is an increase in end-systolic volume (amount of blood left in the heart after contraction) this results in a decreased ejection fraction 2. Increased ESV -> increased stretch 3. In a failing heart this causes a reduction in CO (due to the Frank-Starling principle) 4. Body compensates for decreasing CO by: a. Increasing preload b. Increasing heart rate c. Activation of RAAS Activation of sympathetic nervous system

Answer 93

• Causes: Ischaemic heart disease Valvular heart disease (commonly aortic stenosis) Hypertension Arrhythmias (commonly AF)

Answer 94

Signs + Symptoms Symptoms • Breathlessness (worsened by exertion) • Cough - this may produce frothy white/pink sputum • Orthopnoea • Paroxysmal nocturnal dyspnoea ○ Sudden waking in the night with severe shortness of breath + cough ○ Caused by: § Fluid settling across large area of lung as they're supine § Respiratory centre of brain is less responsive .: resp rate and effort doesn’t increase in response to decreased O2 levels § Less adrenalin circulating in sleep .: myocardium is more relaxed .: worsens CO • Peripheral oedema (ankles, pulmonary, sacrum) Signs • Raised JVP ○ Due to increased CVP • Displaced apex • Crackles ○ Due to pulmonary oedema • Ankle swelling • Heart sounds S3/S4 • Pulsus alternans • Hepatomegaly ○ Backup of blood in the liver due to increased preload • Ascites ○ Swelling in the abdomen, such as GI tract and liver

Answer 95

Pathophysiology • Develops 1-5 weeks after initial infection with group A beta-haemolytic streptococci, AKA Streptococcus pyogenes, a gram-positive organism • Initial Streptococcus pyogenes infection typically manifest a pharyngitis (strep throat) but may present in skin infection (i.e. cellulitis) • Rheumatic fever develops in susceptible hosts due to a hypersensitivity reaction against the bacteria. This type 2 sensitivity reaction causes the immune system to attack cells throughout the body.

Answer 96

To establish diagnosis there must be: • Evidence of recent group A Streptococcus infection: ○ Positive throat swab ○ Positive rapid streptococcal antigen test ○ Raised streptococcal antibody titre (ASO or DNAse B titres) ○ Recent episode of scarlet fever • Plus either: ○ Two major criteria ○ Or one major criterion and two minor criteria Major criteria: • Polyarthritis ○ Multiple joints affected. Become red, hot and swollen ○ Described as 'flitting' arthritis because it migrates to other joints within 1-2 months • Carditis ○ Every heart layer (endo, myo, pericardium) can be affected → pancarditis ○ Endocarditis can cause valvular dysfunction. Clinically significant murmurs ○ Myocarditis may result in heart failure and conduction defects ○ Pericarditis → may present clinically with a failry benign pericardial rub or may lead to more serious complications such as pericardial effusions or cardiac tamponade ○ Most common valve affected in rheumatic fever → mitral valve ○ In a rheumatic fever attack, valve incompetence (i.e. regurgitation) more likely to develop than valve stenosis. Stenosis tends to develop as feature of chronic disease many years later • Sydenham's chorea ○ Involuntary, semi-purposeful movements of the body which may be unilateral or bilateral • Erythema marginatum ○ Rash found in rheumatic fever which may present early on in the disease. Pink macular rash. Minor criteria • Polyarthralgia ○ Pain present in multiple joints • Prolonged PR interval on ECG • History of rheumatic fever • Fever • Raised inflammatory markers Including CRP, ESR, and leukocytes

Answer 97

Acute management Conservative management • Bed rest recommended as first line ○ Even more important in cases of suspected active myocarditis (indicated by abnormalities seen on the echocardiogram and a raised ESR). Exercise limitation is strongly advised ○ Best rest recommended until CRP has returned to normal range. Medical management • Penicillin antibiotic of choice ○ Single stat dose of intravenous benzylpenicillin initially, followed by oral penicillin V for at least 10 days ○ Patients allergic to penicillin → erythromycin or azithromycin give for 10 days ○ To limit inflammatory response → high-dose aspirin should be given with careful monitoring ○ If inflammation and fever do not improve, or child has evidence of moderate to severe carditis → corticosteroids ○ Acute heart failure → involves combination of ACE inhibitors and diuretics

Answer 98

Complications Valvular disease • Acute episodes may lead to leaky or regurgitant, valves. • However, long term, valves may become scarred, hardened and stenosed • Mitral regurgitation is the most common valve lesion in rheumatic fever ○ Mitral stenosis is the most common long-term cardiac complication accounting for approximate 70% of chronic rheumatic valve disease

Answer 99

Stenosis (narrowing or restriction of passage): Obstruction of the LV outflow resulting in decreased cardiac output. Can be characterised as mild to moderate, and is usually asymptomatic. Aortic Valve can be auscultated in the right 2nd intercostal space next to the sternum. Aortic valves in normal hearts should have 3 cusps. During cardiac cycle, when the aortic valve is open, so is the pulmonary valve When both of these are open, the tricuspid and the mitral valve are closed. When the aortic valve is stenosed the heart cannot pump blood effectively. Stenosis results in decreased blood flow, with decreased blood flow comes decreased cardiac output.

Answer 100

Dizziness on exertion Dyspnoea on exertion Angina on Exertion

Answer 101

When performing a CVS exam, you can feel signs of aortic stenosis in the carotid pulse, usually this pulse would be fast, but with stenosis it's abnormally slow and weak. If you auscultate a stenosed aortic valve on a CVS exam, you should hear a reduced intensity of the 2nd heart sound (S2). The 2nd heart sound is the sound made when both aortic and pulmonary valves snap closed during the cardiac cycle.

Answer 102

Aortic Murmur explained • Normally between 1st sound (S1) and 2nd sound (S2) , blood would be flowing normally out of the ventricles and up the aorta. When the aortic valve is stenosed, blood is squeezed through a tighter aperture, so you can hear turbulence of blood passing through the aorta during systole. • The sound aortic stenosis makes is called "systolic click crescendo decrescendo murmur or Ejection Systolic Murmur) • Murmur can radiate to the carotids.

Answer 103

• Congenital abnormal valves (having 2 cusps instead of 3) 2% of the population • Calcification of the aortic valve (a result of atherosclerotic processes, coming with the usual risk factors) • Rheumatic valvular heart disease (less common in the west in the modern era but still occurs especially in those who come from non-western countries or those who may have previously been exposed to tropical diseases)

Answer 104

Investigations performed: • ECG • Cardiac catheterisation and angiography TOE (Transoesophageal Echo) - gold standard for diagnosing valvular heart disease.

Answer 105

Management • Valve replacement or repair is best if the patient is a good candidate for surgery. Mechanical or bioprosthetic valves can be used. Mechanical valve replacement often used for younger patients as it lasts longer. Use of long term anticoagulants and antibiotics will usually be needed following surgery, potentially for the rest of life. • For patients who cannot have a mechanical valve replacement, they can have balloon valvuloplasty which is where a balloon is used to dilate the valve via cardiac catheterisation.

Answer 106

• Sclerosis will progress and be defined as stenosis once aortic valve cusps are clearly restricted upon echocardiogram, as well as an observable increase in "transaortic peak velocity".

Answer 107

Backflow into LV occurring during diastole. This results in a diastolic murmur. Increased preload causes left ventricular hypertrophy. Aorta is very elastic, and thus when high pressure blood passes through it expands, and then snaps back into place, acting as a pump in itself to help force blood against TPR. In aortic regurgitation however, this pump action doesn’t force blood forward, but pushes it back through the impaired aortic valve and into the left ventricle. Results in an increased LVEDV. More blood in the LV at the start of systole means higher systolic blood pressure or an "increased pulse pressure". This means the difference between systolic bp and diastolic bp is very wide.

Answer 108

Symptoms and clinical features • Syncope • Lvh • Angina - caused by impaired diastolic blood pressure. Diastole is when the coronary arteries are filled, with reduced pressure here, they cannot fill as adequately. This poor supply, in conjunction with an increased demand on the heart due to backflow and high LVEDV causes anginal pain. • Tachycardia is well tolerated (strangely) • High pitched murmur at the left sternal border, doing the accentuation manoeuvre of leaning forward • Austin flint murmur - the murmur occurring when blood flows back through the aortic valve, which interferes with the opening of the mitral valve. Collapsing water hammer pulse.

Answer 109

Causes Aortic rood dilation secondary to connective tissue disorder (ehlers danlos, marfans, lupus) Congenital valve abnormality Inflammatory or rheumatic disease and infective endocarditis (usually younger px)

Answer 110

Investigations Echocardiogram Chest x ray - LVH on x ray and pulmonary

Answer 111

Treatment • Loop diuretics to reduce volume and thus preload. • Reduce afterload via GTN • Valve replacement

Answer 112

Suspected acute Heart Failure/Cardiogenic Shock and Pulmonary Oedema…. WHAT SHOULD I DO? Patient is showing signs of acute heart failure/cardiogenic shock…… You have 30 minutes to save their life…….. Stabilise your patient by: • Giving patient inotropes, such as dopamine, nitrates and vasopressors. • If signs and symptoms persist you may need to refer potential patients for mechanical ventilation or heart transplant

Answer 113

Patient is showing signs of pulmonary oedema….. You have 30 minutes to save their life…. Stabilise your patient by: • Offering diuretics intravenously (thiazide, furosemide etc) to get rid of excess fluid in the lungs. • Monitor intake and output, kidney functions, urine and electrolytes etc.

Answer 114

Back flow of blood from right ventricles to right atrium during systole

Answer 115

Primary is less common causes include • carcinoid tumours • Blunt chest trauma • Drugs • Epstein anomaly - congenital abnormality of the tricuspid. • Pacemaker leads • Infective endocarditis • Rheumatic fever • Marfans

Answer 116

Secondary is more common and is a functional issue caused by: • pulmonary hypertension which results in changes in the heart and a dilatation of the right atrium and ventricle. • Anything that causes pulmonary hypertension i.e. Left sided heart failure, Mitral regurgitation, • Primary pulmonary diseases i.e. PE, COPD. • Atrial and ventricular septal defects • Pulmonary valve stenosis • Hyperthyroidism

Answer 117

On examination: • Shortness of breath • Peripheral cyanosis • Raised JVP • A pulsatile jugular vein • Right ventricular heave due to dilated right ventricle • Hollow systolic murmur at lower left sternal border. (will be louder during inspiration) • Hepatomegaly • Peripheral oedema • Ascites

Answer 118

Investigations • ECG - may reveal right ventricular hypertrophy, right axis deviation, atrial fibrillation due to increased pressure in right atrium. • Chest x ray - may reveal cardiomegaly and pleural effusion • Echocardiogram • Cardiac MRI • Cardiac catheterisation

Answer 119

Treatment and management • Treat underlying cause • Treating heart failure - i.e. loop diuretics and aldosterone • Valve replacement and anticoagulation • Cardiac catheterisation procedures.

Answer 120

Pulmonary Valve Stenosis • Narrowing of the pulmonary valve. • In adults it's usually due to a complication of another issue, • In children it's most often caused by a congenital abnormality. • Ranges from mild to severe.

Answer 121

Signs and Symptoms • Exertional fatigue • Profound Cyanosis • Exertional Dyspnoea • Exertional Anxiety • Syncope and collapse • Heart Murmur (mid systolic murmur preceded by an ejection click) • Chest Pain • Failure to thrive (in neonates)

Answer 122

Causes and risk factors • Rheumatic Fever • Noonan Syndrome • Alagille Syndrome • Williams Syndrome • Black ethnicity • Infectious endocarditis Myocardial tumours

Answer 123

Diuretics By reducing salt and water reabsorption from the glomerular filtrate in the kidney, diuretic drugs increase the excretion of Na+, which is followed by water to maintain osmolarity. • The result is a reduction of the plasma volume and a drop in cardiac output. Three types of diuretic are introduced: loop diuretics, thiazide diuretics and aldosterone antagonists. • All of these drugs lower blood pressure, but only the thiazides are used as mainstream anti-hypertensive drugs. Diuretics interfere with the reabsorption process, resulting in an increased loss of salt and water. Diuretics work at two main sites, the loop of Henle and the distal convoluted tubule.

Answer 124

Reserved for patients with pulmonary oedema, heart failure, renal insufficiency or resistant hypertension. Reduce oedema Usually administered as a low dose daily oral tablet, but intravenous infusion gives a rapid effect.

Answer 125

Until a few years ago, thiazides were the first-line treatment for hypertension. Now usually given as an add on, if other drugs are not sufficiently effective on their own. Thiazides potentiate the effects of other antihypertensive drugs. Administered as a daily oral tablet only.

Answer 126

Used in the treatment of: • heart failure • hyperaldosteronism • resistant hypertension, especially with low renin Prevents hypokalaemia when given with a loop or thiazide diuretic Given as a daily oral tablet.

Answer 127

Excessive loss of Na+ and water, resulting in hypovolaemia and hypotension. Decreased cardiac output. Potassium loss, resulting in hypokalaemia. Metabolic alkalosis

Answer 128

Safe drugs with few side effects, including: • more frequent urination • hypokalaemia erectile dysfunction (mechanism not known but could relate to vasodilator action

Answer 129

Potentially fatal hyperkalaemia Gastrointestinal upset Gynaecomastia, menstrual disorders and testicular atrophy due to actions at other steroid receptors

Answer 130

Thiazides Thiazides and related compounds are moderately potent diuretics; they inhibit sodium reabsorption at the beginning of the distal convoluted tubule through inhibiting the sodium-chloride transported. They act within 1 to 2 hours of oral administration and most have a duration of action of 6 to 24 hours; they are usually administered early in the day so that the diuresis does not interfere with sleep. In the management of hypertension a low dose of a thiazide produces a maximal or near-maximal blood pressure lowering effect, with very little biochemical disturbance. Higher doses cause more marked changes in plasma potassium, sodium, uric acid, glucose, and lipids, with little advantage in blood pressure control. • Chlortalidone and indapamide are the preferred diuretics in the management of hypertension. • Chlortalidone may be given on alternate days to control oedema. • Bendroflumethiazide can be used for mild or moderate heart failure.

Answer 131

Loop diuretics Loop diuretics are used in pulmonary oedema due to left ventricular failure; intravenous administration produces relief of breathlessness, by improving pulmonary vascular congestion by decreasing filling pressure, and reduces pre-load, thus reduces ventricular filling. Loop diuretics act in the loop of Henle and inhibit the reabsorption of sodium and water. When excess water and sodium are eliminated, less water remains in the bloodstream. They relieve symptoms such as oedema and breathlessness caused by the congestion of fluid. Loop diuretics are also used in patients with chronic heart failure. Diuretic-resistant oedema can be treated with a loop diuretic combined with a thiazide or related diuretic (e.g. bendroflumethiazide or metolazone). Furosemide and bumetanide are similar in activity; both act within 1 hour of oral administration and diuresis is complete within 6 hours so that, if necessary, they can be given twice in one day without interfering with sleep.

Answer 132

Mineralocorticoid receptor antagonists (aldosterone antagonists) Aldosterone receptor antagonists block the effects of aldosterone. This causes reabsorption of sodium by the kidneys and other glands, which encourages water loss, and a subsequent decrease in blood pressure and reduction in fluid around the heart. Potassium-sparing diuretics are not usually necessary in the routine treatment of hypertension, unless hypokalaemia develops. Spironolactone potentiates thiazide or loop diuretics by antagonising aldosterone; it is a potassium-sparing diuretic. K Spironolactone is of value in the treatment of oedema and ascites caused by cirrhosis of the liver; furosemide can be used as an adjunct. Low doses of spironolactone are beneficial in moderate to severe heart failure and when used in resistant hypertension [unlicensed indication]. Spironolactone is also used in primary hyperaldosteronism (Conn’s syndrome). It is given before surgery or if surgery is not appropriate, in the lowest effective dose for maintenance. Eplerenone is licensed for use as an adjunct in left ventricular dysfunction with evidence of heart failure after a myocardial infarction; it is also licensed as an adjunct in chronic mild heart failure with left ventricular systolic dysfunction. Potassium supplements must not be given with mineralocorticoid receptor antagonists.