Cardiology Conditions Flashcards

Question

How common is angina

Answer 1

An estimated 2 million people in England have, or have experienced, angina.

Answer 2

Smokers Obese / DM / hypertensive patients Those with a FHx of premature CAD

Answer 3

Atherosclerosis is an inflammatory process which predisposes individuals to angina and ACS. Involves lipids, macrophages and smooth muscle. Leads to the formation of an atheroma, which may contain plaque on its surface. The presence of atherosclerosis within coronary vessels is termed coronary artery disease (CAD) or ischaemic heart disease (IHD) and it may be obstructive (i.e. >50% of the vessel lumen) or non-obstructive (<50% of the vessel lumen).

Answer 4

``` Modifiable risk factors: • High cholesterol • Hypertension • Smoking • Diabetes • Obesity ``` ``` Non-modifiable risk factors: • Age • Family history • Male sex • Premature menopause ```

Answer 5

The three classic features of angina include: - Constricting pain experienced in the chest +/- typical radiation to the arm/neck/jaw - Precipitated by physical exertion. - Relieved by rest or GTN within 5 minutes Based on these classical features, angina can be differentiated into three types: Typical: all three of the above features Atypical: two of the above features Non-anginal: ≤1 of the above features Concerning chest pain Chest pain lasts > 10 minutes Chest pain not relived by two doses of GTN taken 5 minutes apart Significant worsening/ deterioration in angina (e.g. increased frequency, severity or occurring at rest) The above features may be suggestive of ACS and patients need immediate medical attention. Cardiovascular examination - Heart sounds - Signs of heart failure Dyspnoea Palpitations -Angina may be precipitated by tachyarrhythmias (e.g., AF). These increase the oxygen supply/demand mismatch and reduce filling time of the coronary vessels during diastole. Syncope: -May be suggestive of dangerous valvular or cardiac muscle disease causing angina, particularly if it occurs on exertion.

Answer 6

* Myocarditis * Pericarditis * Pleuritis * PE * Aortic dissection * CHF * MI * GORD

Answer 7

``` Cardiovascular complications of angina, caused by coronary artery disease, include: -Stroke. -Myocardial infarction. -Unstable angina. Sudden cardiac death. Other complications include: -Anxiety, and depression. -Reduced quality of life. ```

Answer 8

The prognosis of stable angina is variable. Important indicators of long-term prognosis are the extent and severity of coronary artery disease, left ventricular function, exercise duration or effort tolerance, and comorbidities. The prognosis depends on the time point at which the person is seen. For example, new-onset angina has a worse prognosis than established angina which has remained stable for some time.

Answer 9

Hypertension is the term used to describe high blood pressure, meaning a clinical bp measurement of 140/90 or an ambulatory/home reading of 135/85 Essential hypertension is also known as primary hypertension Essentially means that the hypertension has developed on its own and does not have a secondary cause

Answer 10

Essential hypertension accounts for 95% of hypertension

Answer 11

Essential hypertension develops on ots own and does not have a secondary cause Secondary causes of hypertension can be remembered by mneumonic ROPE: R-enal disease O-besity P-regnancy induced hypertension/ pre-eclampsia E-ndocrine (most endocrine conditions can cause hypertension but primarily hyperaldosteronism)

Answer 12

``` Obesity Aerobic exercise <3 times per week Moderate to high alcohol intake Metabolic syndrome Diabetes Black ancestry Age >60 years old Family history of hypertension or coronary artery disease Sleep apnoea Poor diet (high sodium, low fruit and veg) Dyslipidaemia ```

Answer 13

``` Signs and symptoms: Often asymptomatic and detected through routine checks Retinopathy BP ≥140/90 mmHg Headache Visual changes Dyspnoea Chest pain Sensory or motor deficit ```

Answer 14

Measure Blood pressure every 5 years to screen for hypertension but more often in those on the borderline for diagnosis and every year in pts with type 2 diabetes Pts with clinic blood pressure readings between 140/90 and 180/120 should have a 24 hour ambulatory blood pressure or home readings to confirm diagnosis due to white coat syndrome potentially causing higher readings

Answer 15

``` Essential hypertension Renal artery stenosis Chronic kidney disease Obstructive uropathy Obstructive sleep apnoea Coarctation of aorta Pre-eclampsia Glomerulonephritis Nephrotic syndrome Polycystic kidney disease Phaeochromocytoma Hyperaldosteronism Cushing's syndrome/disease Hyperthyroidism Hypothyroidism Chronic alcohol excess Medication Illicit drug use White coat hypertension ```

Answer 16

``` Extra strain put on blood vessels Sinister events may result: Heart attacks Heart disease Heart failure Strokes Peripheral arterial disease Abdominal aortic aneurysms Kidney disease Vascular dementia Reducing blood pressure, can reduce the risk of these events occurring Important not to place blame on the patient as there is then a risk of alienation, and instead work cohesively to understand their struggles in controlling the modifiable risk factors. ```

Answer 17

Initial management: - Establish a diagnosis - Investigate for possible causes and end organ damage - Advise on lifestyle (healthy diet, smoking cessation, reducing alcohol, caffeine and salt intake, taking regular exercise Medical management: - Offered to all with stage 2 - All under 80y/o with stage 1 and a q-risk score of 10% or more, diabetes, renal disease, CV disease or end organ damage ``` Medications: A- ACE inhibitor (rampipril) B- Beta blocker (bisoprolol) C- Calcium channel bllocker (amlodipine) D- Thiazide like diuretic (imdopamide) ARB- Angiotensin II respetor blocker (candesartan) ``` There are slightly different guidelines for younger patients and those aged over 55 or black: Step 1: Aged less than 55 and non-black use A. Aged over 55 or black of African or African-Caribbean descent use C. Step 2: A + C. Alternatively A + D or C + D. If black then use an ARB instead of A. Step 3: A + C + D Step 4: A + C + D + additional (see below) For step 4, if the serum potassium is less than or equal to 4.5 mmol/l consider a potassium sparing diuretic such as spironolactone. If the serum potassium is more than 4.5 mmol/l consider an alpha blocker (e.g. doxazosin) or a beta blocker (e.g. atenolol). Seek specialist advice if the blood pressure remains uncontrolled despite treatment at step 4.

Answer 18

``` Complications: Ischaemic heart disease Cerebrovascualr event (stroke or haemorrhage Hypertensive retinopathy Hypertensive nephropathy Heart failure ```

Answer 19

Stage 1: >140/90 (clinical) >135/85 (home) Stage 2: >160/100 (clinical) >150/95 (home) Stage 3: >180/120 (clinical)

Answer 20

The development of a blod clot in a major deep vein in the leg, thigh, pelvis, or abdomen, which may result in impaired venous blood flow and consequent leg swelling and pain Venous thrombosis may also occur in the upper extremities or in more unusual sites, such as the portal, mesenteric, ovarian and retinal veins, as well as the veins and venous sinuses of the brain. Superficial vein thrombosis, thrombosis affecting veins superficial to the musculature, also commonly occurs Venous thromboembolism is the broad term that inclused DVT and pulmonary embolism

Answer 21

Yearly incidence of VTE is ~ 1 in every 1000 adults and ~ 2/3 of all cases are DVT Estimated that 300,000 deaths per year are due to VTE

Answer 22

Usually occurs secondary to stagnation of blood and hyper-coagulable states

Answer 23

``` Immobility Recent surgery Long haul flights Pregnancy Hormone therapy with oestrogen (combine oral contraceptive pill and hormone replacement therapy) Malignancy Polycythaemia Systemic lupus erythematous Thrombophilia (conditions that predispose patients to develop blood clots): - Antiphospholipid syndrome - Antithrombin deficiency - Protein C or S deficiency - Factor V leiden - Hyperhomocysteinaemia - Prothombin gene variant - Activated protein C resistence ```

Answer 24

``` Almost always unilateral Bilateral DVT is rare and bilateral symptoms are more likely due to an alternative diagnosis such as chronic venous insufficiency or heart failure DVTs can present with: -Calf or leg swelling -Dilated superficial veins -Tenderness to the calf (particularly over the site of the deep veins) -Oedema -Colour changes to the leg ```

Answer 25

To examine for leg swelling measure the circumference of the calf 10cm below the tibial tuberosity More than 3cm difference between calves is significant Always examin with the suspicion of a potential pulmonary embolism as well Wells score: Predicts the risk of a pt presenting with symptoms having a DVT or PE Takes in to account risk factors such as recent surgery and clincial findings such as unilateral calf swelling 3cm greater than the other leg

Answer 26

Cellulitis Calf muscle tear/ Achilles' tendon tear Calf muscle haematoma Large or ruptures popliteal cyst (Baker's cyst) Pelvic/ thigh mass/ tumour compressing venous outflow from the leg

Answer 27

D-dimer is a sensitive (95%) but not specific blood test for VTE This makes it useful for exluding VTE where there is a low suspicion Almost always raised if there is a DVT, however other conditions can also cause a raised d-dimer: -Pneumonia -Malignancy -Heart failure -Surgery -Pregnancy Ultrasound doppler of the leg is required to diagnose DVT NICE recommend repeating negative ultrasound scans after 6-8 days if there is a positive D-dimer and the Wells score suggest a DVT is likely PE can be diagnosed with a CT pulmonary angiogram or VQ scan Investigating unprovoked DVT: - Recommended to investigate for possible cancer - - History and examination - - Chest X-ray - - Bloods (FBC, calcium, LFTs) - - Urine dipstick - - CT abdomen and pelvis in patients over 40 - - Mammogram in women over 40 - Also test for antiphospholipid syndrome by checking for antiphospholipid antibodies - Those with an unprovoked VTE with a family history of VTE, recommended to test for hereditary thrombophilias: - - Factor V Leiden - - Prothrombin G20210A - - Protein C - - Protein S - - Antithrombin

Answer 28

Initial management - Treatment dose low molecular weight heparin - Start immediately before confirming the diagnosis in pts where DVT or PE is suspected and there is a delay in getting the scan - Examples are enoxaparin and dalteparin Switching to long term anticogulation: -Warfarin, NOAC, DOAC or LMWH -Target INR for warfarin is 2-3. When switching to warfarin, continue LMWH for 5 days or the INR is 203 for 24 hours on warfarin (whichever is longer) -NOAC or DOAC are oral anticoagulants that are not warfarin. They are an alternative option for anticoagulation that does not require monitoring. Originally they were called novel oral anticoagulants but this has been changed to non-vitamin K oral anticoagulants because they are no longer novel This is changing to DOACs, standing for direct acting oral anticoagulants Main three options are apixaban, dabigatran and rivaroxaban -LMWH long term is first-line treatment in pregnancy or cancer Continue anticoagulation for: - 3 months if there is an obvious reversible cause (then review) - Beyond 3 months if the cuase is unclear, there is recurrent VTE or there is an irreversible underlying cause, such as thrombophilia, often 6 months in practice - 6 months in active cancer (then review) Inferior Vena Cava Filter: - Devices inserted into the IVC - Designed to filter the blood and catch any blood clots travelling from the venous system towards the heart and lungs - Act like a sieve, allowing blood to flow through whilst stopping larger blood clots - They are used in unusual cases of patients with recurrent PEs or those that are unsuitable for anticoagulation to prevent emboli traveling to the lungs

Answer 29

``` A blood clot develops in the hepatic vein, blocking the outflow of blood Associated with hyper-coagulable states Causes an acute hepatitis Presents with a classic triad of: -Abdominal pain -Hepatomegaly -Ascites ```

Answer 30

Occurs when the left ventricle is unable to adequately move blood through the left side of the heart and out into the body. This causes a backlog of blood 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 31

The amount of blood pumped out of the heart from each contraction

Answer 32

The amount of blood pumped out of the heart in one minute | Equivalent to Heart Rate x Stroke Volume

Answer 33

Stretching of cardiomyocytes at the end of diastole

Answer 34

Pressure or load against which the ventricles must contract

Answer 35

Refers to myocardial contractility (ie. the force of muscular contraction)

Answer 36

Most common type of heart failure

Answer 37

More common in elderly patient

Answer 38

The most common aetiologies of left heart failure are coronary artery disease and hypertension. The latter can cause left heart failure through left ventricular hypertrophy and also serves as a risk factor for coronary artery disease. Iatrogenic (e.g., aggressive IV fluids in frail elderly patient with impaired left ventricular function) which causes a low-output HF due to excessive preload. This can cause ventricular dilation and exacerbates pump failure. Sepsis Myocardial infarction Arrhythmias Mitral regurgitation (causes excessive preload) Aortic stenosis / HTN (causes excessive afterload leading to myocardial hypertrophy which then leads to stiff walls & diastolic dysfunction)

Answer 39

``` Old age Obesity Male sex Diabetes Sedentary lifestyle ```

Answer 40

``` Dyspnoea Looking and feeling unwell Poor exercise tolerance Fatigue Orthopnoea Paroxysmal nocturnal dyspnoea Nocturnal cough (+ frothy white/pink sputum) Displaced apex (if LV is dilated) ``` Some patients with advanced disease might experience weight loss, referred to as “cardiac cachexia”.

Answer 41

O/E Increased respiratory rate Reduced oxygen saturation Tachycardia 3rd heart sound (S3 gallop – indicative of elevated ventricular end-diastolic pressure) Bilateral basal crackles on auscultation Rales on lung auscultation suggestive of pleural effusion Hypotension in severe cases (cardiogenic shock) Increased abdominal girth due ascites. Reduced kidney perfusion o Pre-renal azotaemia / RAAS activation Irritability, restlessness, stupor and coma (Advanced cardiac failure can lead to cerebral hypoxia causing these signs/Sx) Signs related to underlying cause: Chest pain in ACS Fever in sepsis Palpitations in arrhythmias If they also have right sided heart failure as a result you could find: Raised Jugular Venous Pressure (JVP) Peripheral oedema (ankles, legs, sacrum).

Answer 42

Dyspnoea – primary pulmonary HTN, COPD, interstitial lung disease, anaemia Oedema – venous insufficiency, cirrhosis, nephrotic syndrome, lymphoedema, DVT

Answer 43

ECG May indicate cause – look for ischaemia, arrhythmias, MI and ventricular hypertrophy. Chest Xray -Cardiomegaly on a CXR is defined as a cardiothoracic ratio of more than 0.5. This is when the diameter of the widest part of the heart (the wides part of the cardiac silhouette) is more than half the diameter of the widest part of the lung fields. -Upper lobe venous diversion. Usually when standing erect the lower lobe veins contain more blood and the upper lobe veins remain relatively small. In LVF there is such a back-pressure that the upper lobe veins also fill with blood and become engorged (referred to as upper lobe diversion). This is visible as increased prominence and diameter of the upper lobe vessels on a chest xray. -Fluid leaking from oedematous lung tissue causes additional xray findings of: o Bilateral pleural effusions o Fluid in interlobar fissures o Fluid in the septal lines (Kerley lines) Echocardiography -Useful in assessing the function of the left ventricle and any structural abnormalities in the heart. -The main measure of the left ventricular function is the ejection fraction. o This is the percentage of the blood in the left ventricle is squeezed out with each ventricular contraction. o An ejection fraction above 50% is considered normal. -TTE can differentiate HF into three groups: o Heart failure with reduced ejection fraction (HFrEF): LVEF <40%  Causes: ID, MI, cardiomyopathy  Systolic failure o Heart failure with minimally reduced ejection fraction (HFmrEF): LVEF 40-49% o Heart failure with preserved ejection fraction (HFpEF): LVEF ≥50%  Ventricular hypertrophy, constrictive pericarditis, tamponade, restrictive cardiomyopathy, obesity.  Diastolic failure Bloods •FBC’s – for signs of infection •U&Es – for kidney function – low sodium indicates advanced disease. •LFTs – detect liver injury dur to volume overload •BNP o B-type Natriuretic Peptide is a hormone release from the heart ventricles when the myocardium is stretched beyond the normal range. o High result indicated the heart is overloaded beyond its normal capacity to pump effectively. o Action of BNP is to relax the smooth muscle in blood vessels. o BNP also acts on the kidneys as a diuretic. •Troponin – if suspecting MI •ABG Coronary angiography •Indicated in patients with anginal symptoms.

Answer 44

``` Pour Sod P-pour away (stop) their IV fluids S-sit up O-oxygen D-diuretics (furosemide 40mg stat) - SE: ↓K+ - if refractory oedema consider adding metolazone (5-20mg/24hrs PO) ``` Education -Patients should receive education on the importance of lifestyle modification o Avoidance of alcohol, nicotine and recreational drugs o Reasonable salt consumption Treating the underlying cause - Some heart failure conditions may be reversible when the precipitating factors are addressed, like cardiomyopathies induced by alcohol, tachycardia or ischemia. Tight control of blood pressure will also help prevent further deterioration. Beside treatment - Loop diuretics for volume overload Medication Pharmacological treatments differ between HFrEF and HFpEF •HFrEF o ACEi (e.g., Ramipril) OR ARBs (e.g., Candesartan)  If cough is a problem ARB may be substituted. o + Beta blocker (e.g., bisoprolol, carvedilol, metoprolol)  ↓mortality in patients •HFpEF o Control of BP o Revascularisation (if ischameic cardiomyopathy) o Management of arrhythmias o Minneralcorticoid receptor antagonist may be beneficial in these patients. (e.g., Spironolactone 25mg/24hrs PO) Digoxin (125mcg/24hrs PO) can help with symptoms Vasodilators - Hydralazine (SE: drug-induced lupus) and isosorbide dinitrate should be used if intolerant to ACE-I and ARBs as it reduced mortality. It also reduced mortality when added to standard therapy (including ACE-i) in black patients with HF. Other options to consider in severe acute pulmonary oedema or cardiogenic shock (not routinely used) include: •Intravenous opiates (opiates such as morphine act as vasodilators but are not routinely recommended). •Non-Invasive Ventilation (NIV). Continuous Positive Airway Pressure (CPAP) involves using a tight fitting mask to forcefully blow air into their lungs. This helps to open the airways and alveoli to improve gas exchange. If NIV does not work they may need full intubation and ventilation. •“Inotropes”, for example an infusion of noradrenalin. Inotropes strengthen the force of heart contractions and improve heart failure, however they need close titration and monitoring, so by this point you would need to send the patient to the local coronary care unit / high dependency unit / intensive care unit.

Answer 45

Right Ventricular Failure -When LVF and RVF occur together it is known as congestive heart failure. ``` Cardiogenic shock CVA Acute coronary syndrome PE Arrhythmias Anasarca (extreme generalised oedema) ```

Answer 46

The mortality rate in heart failure in 2008 was 18.2 per 100,000 for males and 15.8 per 100,000 for females. Worse outcome in heart failure: male gender, advancing age, low ejection fraction, high NYHA functional class, low haematocrit, and sodium levels, high brain natriuretic peptide, low peak exercise oxygen uptake, wide QRS, renal failure, low blood pressure, elevated heart rate, and volume overload refractory to medical treatment.

Answer 47

Heart failure with preserved ejection fraction (HFpEF) with ejection fraction over 50 percent. Heart failure with reduced ejection fraction (HFrEF) with ejection fraction less than 40 percent. Heart failure with mid-range ejection fraction, with ejection fraction between 41 and 49 percent

Answer 48

Is a condition in which the heart is unable to generate a cardiac output sufficient to meet the demands of the body without increasing diastolic pressure. It can result from any cardiac disease that compromises ventricular systolic or diastolic function or both.

Answer 49

Is the term used to described patients with breathlessness and abnormal sodium and water retention resulting in oedema. It is a result of a failure of both the right and left side of the heart.

Answer 50

Reduced left ventricular ejection fraction (LVEF) - the heart is pumping out a reduced proportion of the blood that fills its ventricles during diastole. Results in ventricular dilatation and characteristic eccentric remodelling

Answer 51

Impaired ventricular relaxation or filling. Contraction is unaffected and as such the LVEF is preserved. Diastolic heart failure may be called 'heart failure with preserved LVEF'. Ventricular hypertrophy tends to develop and characteristic concentric remodelling may occur.

Answer 52

Rapid onset of worsening symptoms and/or signs of heart failure Life-threatening condition that requires urgent evaluation and treatment May occur acutely (e.g. cardiogenic shock) or as a consequence of acute decompensation of chronic heart failure Most common causes of acute heart failure include acute myocardial dysfunction (ischaemic, inflammatory), acute valvular disease, pericardial tamponade.

Answer 53

Progressive cardiac dysfunction due to structural and/or functional cardiac abnormalities Results in reduced cardiac output and/or elevated intracardiac pressures at rest or on stress Precipitated by conditions that affect the muscles (e.g. cardiomyopathy), vessels (e.g. ischaemic heart disease), valves (e.g. aortic stenosis), or conduction (e.g. atrial fibrillation) Patients develop chronic, progressive symptoms but may present with acute decompensation.

Answer 54

The prevalence of CHF in the western world has been estimated at 1% to 2%, and the incidence is thought to approach 5 to 10 per 1000 people per year.

Answer 55

Prevalence increases with age

Answer 56

``` Coronary artery disease Hypertension - results in excess preload of atrium. Permanent dilation of ventricles and loss of elastic tissue Valvular disease (commonly aortic stenosis) Myocarditis. Ischaemic heart disease Arrhythmias (commonly AF) Cardiomyopathy (dilated/ hypertrophic) Congenital heart disease Beta blockers ```

Answer 57

``` MI DM Dyslipidaemia Old age Male HTN Cocaine abuse FHx High alcohol intake ```

Answer 58

``` Dyspnoea Orthopnoea Paroxysmal nocturnal dyspnoea (PND) Wheeze Fatigue Weight loss Fluid retention - Ankle swelling / bloated feeling Night cough Syncope / light-headedness ```

Answer 59

``` S3 gallop Cardiomegaly – displaced apex Hepatojugular reflux Raised JVP / HTN Neck vein distention Hepatomegaly (due to engorement) Ascites Bibasal crackles on auscultation of lung bases Peripheral oedema / pitting oedema Tachycardia (HR >120BPM) Cyanosis Narrow pulse pressure ```

Answer 60

``` COPD/pulmonary fibrosis Pneumonia PE Cirrhosis Venous stasis Post-partum cardiomyopathy ```

Answer 61

BNP blood test (specifically “N-terminal pro-B-type natriuretic peptide” – NT‑proBNP) •Protein released by cardiomyocytes in response to excessive stretching. •Used to assess likelihood of heart failure. •Other conditions that may raise BNP: - Diabetes - Sepsis - Old age - Hypoxaemia (PE, COPD) - Kidney disease - Liver cirrhosis. Transthoracic Echocardiogram (TTE) •Main investigation for the confirmation of heart failure. •Allows for the accurate determination of biventricular systolic and diastolic function. •Systolic heart failure: echo usually demonstrates a dilated left and/or right ventricle with low ejection fraction. •Pure diastolic heart failure: left ventricular ejection fraction (LVEF) is normal but there is evidence of left ventricular hypertrophy (LVH) and of abnormal diastolic filling patterns on Doppler evaluation. ECG •Evidence of underlying coronary artery disease, left ventricular hypertrophy, or atrial enlargement; may be conduction abnormalities and abnormal QRS duration CXR •Cardiomegaly (Cardiothoracic ratio > 50% on PA film) •Pleural effusion Cardiac MRI •May be used when transthoracic echo is non-diagnostic •May be used to determine the aetiology of heart failure (e.g. ischaemic versus non-ischaemic in dilated cardiomyopathy) Bloods •FBC – exclude anaemia, infective cause. •U&Es – exclude renal failure as a cause of oedema •LFT – exclude liver failure as a cause of oedema. •TFTs – exclude thyroid disease •Cholesterol and HbA1c – cardiovascular risk stratification •BNP Special tests: •Coronary angiogram: used for diagnostic and therapeutic purposes to diagnose/treat coronary artery disease •Right heart catheterisation: reserved for the investigation of right-sided heart failure •24 hr ECG: if an arrhythmia is suspected •Lung function tests: to exclude alternative pathology impacting on symptoms (e.g. breathlessness) Framingham Criteria

Answer 62

Management •Refer to specialist (NT-proBNP > 2,000 ng/litre warrants urgent referral) •Careful discussion and explanation of the condition •Medical management (see below) •Surgical treatment in severe aortic stenosis or mitral regurgitation •Heart failure specialist nurse input for advice and support ``` Additional management: •Yearly flu and pneumococcal vaccine. •Stop smoking & drinking alcohol. •Optimise treatment of co-morbidities. •Exercise at tolerated level. •Reduce sodium intake + fluid restriction + weight monitoring. ``` First Line Medical Treatment (ABAL) A-CE inhibitor (e.g. ramipril titrated as tolerated up to 10mg once daily) B-eta Blocker (e.g. bisoprolol titrated as tolerated up to 10mg once daily) A-ldosterone antagonist when symptoms not controlled with A and B (spironolactone or eplerenone) L-oop diuretics improves symptoms (e.g. furosemide 40mg once daily) Extra detail on medical treatment •An Angiotensin Receptor Blocker (ARB) can be used instead of an ACE inhibitor if ACE inhibitors are not tolerated (for example candesartan titrated up to 32mg once daily). •Avoid ACE inhibitors in patients with valvular heart disease until indicated 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 monitored closely whilst on diuretics, ACE inhibitors and aldosterone antagonists as all three medications can cause electrolyte disturbances.

Answer 63

* Pleural effusion * Chronic renal insufficiency * Anaemia * Acute decompensation of chronic heart failure * Acute renal failure * Sudden cardiac death

Answer 64

* Despite standard medical therapy the survival for patients with end-stage heart failure is poor. * Only 65% of patients in NYHA class 4 are alive at a mean follow-up of 17 months. * ~25-50% of patients die within 5yrs of diagnosis.

Answer 65

Cardiac: - Angina - Acute coronary syndrome - Aortic dissection - Pericarditis Respiratory: - PE - Pneumothorax - Pneumonia Gastrointestinal: - Oesophagitis - Oesophageal spasm - Peptic ulcer disease Other - Costochondritis - Rib fracture - Herpes zoster - Depression/ anxiety

Answer 66

Initial assessment •ABCDE (if acutely unwell) followed by brief history & examination. •ECG: urgent ECG to look for ST elevation or left bundle branch block (LBBB). If absent, look for other features of ischaemia (e.g. ST depression, T wave inversion) •Cardiac enzymes: troponin is the only recognises biomarker for the diagnosis of myocardial necrosis. Other investigations : Perform all the investigations you would normally arrange for stable angina: •Physical Examination (heart sounds, signs of heart failure, BMI) •ECG •FBC (check for anaemia) •U&Es (prior to ACEi and other meds) •LFTs (prior to statins) •Lipid profile •Thyroid function tests (check for hypo / hyper thyroid) •HbA1C and fasting glucose (for diabetes) Plus: •Chest xray to investigate for other causes of chest pain and pulmonary oedema •Echocardiogram after the event to assess the functional damage •CT coronary angiogram to assess for coronary artery disease Making a diagnosis •When a patient presents with possible ACS symptoms (i.e. chest pain) perform an ECG. •If there is ST elevation or new LBBB the diagnosis is STEMI. •If there is no ST elevation then perform troponin blood tests. -If there are raised troponin levels and/or other ECG changes (ST depression or T wave inversion or pathological Q waves) the diagnosis is NSTEMI. -If troponin levels are normal and the ECG does not show pathological changes the diagnosis is either unstable angina or another cause such as musculoskeletal chest pain.

Answer 67

``` ACS immediate management = MONA (IV) Morphine (+ antiemetic) Oxygen Nitrates (e.g., GTN) Aspirin (300mg) ``` Acute STEMI Treatment (always check local protocol) Patients with STEMI presenting within 12 hours of onset should be discussed urgently with local cardiac centre for either: •Primary PCI (if available within 2 hours of presentation) •Thrombolysis (if PCI not available within 2 hours) -- Examples: Streptokinase, Alteplase, Tenecteplase -- Significant bleeding risk can make this dangerous •The local cardiac centre will advise about further management (such as further loading with aspirin and ticagrelor). Acute NSTEMI treatment: BATMAN B – Beta blockers unless contraindicated A – Aspirin 300mg stat dose T – Ticagrelor 180mg stat dose (clopidogrel 300mg is an alternative) M – Morphine titrated to control pain A – Anticoagulant: Low Molecular Weight Heparin (LMWH) at treatment dose (e.g. enoxaparin 1mg/kg twice daily for 2-8 days) N – Nitrates (e.g. GTN) to relieve coronary artery spasm Give oxygen only if their oxygen saturations are dropping (i.e. <95%). GRACE Score to assess for PCI in NSTEMI: This scoring system gives a 6-month risk of death or repeat MI after having an NSTEMI: •<5% Low Risk •5-10% Medium Risk •>10% High Risk If they are medium or high risk they are considered for early PCI (within 4 days of admission) to treat underlying coronary artery disease. Secondary Prevention Lifestyle: •Stop smoking •Reduce alcohol consumption •Mediterranean diet •Cardiac rehabilitation (a specific exercise regime for patients post MI) •Opimise treatment of other medical conditions (e.g. diabetes and hypertension)

Answer 68

DREAD ``` D-death R-rupture E-edema (heart failure) A-arrhythmia D-dressler's syndrome ```

Answer 69

This is also called post-myocardial infarction syndrome. It usually occurs around 2-3 weeks after an MI. It is caused by a localised immune response and causes pericarditis (inflammation of the pericardium around the heart). It is less common as the management of ACS becomes more advanced. It presents with pleuritic chest pain, low grade fever and a pericardial rub on auscultation. It can cause a pericardial effusion and rarely a pericardial tamponade (where the fluid constricts the heart and prevents 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 (aspirin / ibuprofen) and in more severe cases steroids (prednisolone). They may need pericardiocentesis to remove fluid from around the heart.

Answer 70

The rate of sudden death in patients who have had a myocardial infarction is 4 to 6 times the rate in the general population. Statins and revascularisation, has decreased morbidity and mortality by reducing the likelihood of cardiogenic shock, recurrent myocardial infarction, and death. However, these benefits are offset by the mortality associated with trends of older age in patients who present with acute coronary syndrome.