6PY011 CVS Study Final 2023_24 PDF

6PY011 TBL: Cardiovascular System Cardiovascular system 2023-2024 The diagnosis and clinical management of common/important conditions of the cardiovascular system Facilitators Required References Prof Patrick Ball Before reading this study-pack re-familiarize yourself with the 5PY022 ([email protected]) Cardiovascular System TBL pack which is available in the CVS folder on Alan Hindle CANVAS™ ([email protected]) o British National Formulary online via Medicines Complete Simren Kachala o Clinical Pharmacy and Therapeutics, 6th edition, Churchill Livingston 2018, ([email protected]) edited by C. Whittlesea and K. Hodson Alison Stephen o Community Pharmacy: Symptoms, Diagnosis and Treatment, 4th Edition, ([email protected]) Churchill Livingstone 2017, Edited by P. Rutter Prof Angel Armesilla o Clinical Medicine, 9th edition, Churchill Livingston 2016, edited by Kumar ([email protected]) and Clark o Relevant Guidelines and Links referred to throughout the pack Learning Outcomes discussed within this pack: Understand the diagnosis, therapeutic and non-drug management (including preventative strategies) of cardiovascular conditions Identify the key signs, symptoms and investigations (diagnostic and physiological) pertaining to diagnosis including differential diagnosis of CV diseases Discuss the appropriate clinical management of patients based on patient factors and the application of the evidence base Discuss the evidence-based treatment selection of CV treatments Emergency treatments involving the cardiovascular system You should pay particular attention to: the anatomical recaps the various definitions that are clarified the common terminology that is used From that point it will then be useful to cross refer back to disease states covered in year 2 as and when you encounter them in this year 3 pack. A significant emphasis of the year 2 pack was how the pathophysiology of each condition was initially described in order to cement your understanding of how the pharmacological actions correct that adverse pathology. In this pack prior understanding of the pathophysiological processes involved, as well as risk factors and epidemiology, is essential to appreciating how a diagnosis is made. Furthermore, your baseline knowledge of the actions and adverse actions of cardiovascular drugs and the formulations that are commonly encountered are highly significant if you are to make decisions about the most appropriate therapy for a patient. 1 6PY011 TBL: Cardiovascular System Table of Contents Presenting signs/symptoms of hypertension................................................................................................................... 4 Drugs that cause hypertension......................................................................................................................................... 4 Diagnosing hypertension.................................................................................................................................................. 6 Using a Sphygmomanometer............................................................................................................................................ 9 Method for using a Sphygmomanometer......................................................................................................................... 9 Presenting signs/symptoms............................................................................................................................................ 15 Diagnosing hypercholesterolemia.................................................................................................................................. 16 Interpreting blood results............................................................................................................................................... 16 Ischaemic/Coronary Heart Disease................................................................................................................................. 22 Angina Pectoris............................................................................................................................................................... 24 Stable angina................................................................................................................................................................... 24 Acute coronary syndromes............................................................................................................................................. 28 Clinical Presentation....................................................................................................................................................... 30 Cardiac enzymes............................................................................................................................................................. 32 Sub-classifications of ACS................................................................................................................................................ 32 Management of ACS....................................................................................................................................................... 33 Myocardial Infarction with ST-segment elevation.......................................................................................................... 33 PCI................................................................................................................................................................................... 33 Thrombolysis (or fibrinolysis).......................................................................................................................................... 34 Unstable Angina and NSTEMI (early management)........................................................................................................ 36 Heart Failure................................................................................................................................................................... 39 Signs, symptoms and classification................................................................................................................................. 40 Differential diagnoses..................................................................................................................................................... 41 Management of chronic heart failure............................................................................................................................. 42 Non-pharmacological management............................................................................................................................... 42 Pharmacological management....................................................................................................................................... 42 Arrhythmias.................................................................................................................................................................... 45 Diagnosis......................................................................................................................................................................... 45 Non-pharmacological Treatment.................................................................................................................................... 45 Electrical Therapies – Direct Current Cardioversion....................................................................................................... 45 Pacing Strategies – Pacemakers...................................................................................................................................... 46 Pacing Strategies - ICDs................................................................................................................................................... 46 Ablation Strategies – Radiofrequency Ablation.............................................................................................................. 46 2 6PY011 TBL: Cardiovascular System Pharmacological Treatment............................................................................................................................................ 46 Atrial Fibrillation (AF)...................................................................................................................................................... 47 Rate Control.................................................................................................................................................................... 47 Rhythm Control............................................................................................................................................................... 48 ‘Pill in the pocket’ Strategy............................................................................................................................................. 49 Assessment of Stroke Risk.............................................................................................................................................. 49 Choice of Anticoagulation............................................................................................................................................... 51 Pharmacists’ Roles in Arrhythmia Management............................................................................................................ 52 Venous Thromboembolism (VTE)................................................................................................................................... 52 Prevention of VTE........................................................................................................................................................... 52 Non-pharmacological VTE prophylaxis........................................................................................................................... 53 Pharmacological VTE prophylaxis................................................................................................................................... 54 Diagnosis of VTE.............................................................................................................................................................. 54 Diagnosis of DVT............................................................................................................................................................. 55 Diagnosis of PE................................................................................................................................................................ 56 Pharmacological Treatment for DVT and PE................................................................................................................... 57 Duration of Anticoagulant Treatment............................................................................................................................ 57 Patient Counselling......................................................................................................................................................... 58 Stroke.............................................................................................................................................................................. 59 Risk Factors and Epidemiology....................................................................................................................................... 60 Ischaemic Stroke............................................................................................................................................................. 60 Transient Ischaemic Attack............................................................................................................................................. 61 Haemorrhagic Stroke...................................................................................................................................................... 61 Treatment of Stroke........................................................................................................................................................ 61 TIA Treatment................................................................................................................................................................. 62 Haemorrhagic Stoke Treatment...................................................................................................................................... 63 Treatment for all Stroke Patients.................................................................................................................................... 63 Emergency Resuscitation................................................................................................................................................ 64 3 6PY011 TBL: Cardiovascular System Hypertension https://www.nice.org.uk/guidance/ng136 Presenting signs/symptoms Hypertension is a condition characterized by abnormally high blood pressure which puts extra strain on the blood vessels, heart, brain, kidneys and eyes. Persistent high blood pressure increases the risk of developing coronary artery disease due to the added force against the artery walls. Over time, this extra pressure can damage the arteries, making them more vulnerable to the narrowing and plaque build-up associated with atherosclerosis and increases the risk of a number of serious and potentially life-threatening conditions, such as heart disease, stroke and vascular dementia. Often blood pressure presents with no symptoms and is picked up during a routine check-up. However, at very extremely high blood pressures, symptoms can include: o Fatigue or confusion o Vision problems o Chest pain o Difficulty breathing o Irregular heartbeat o Blood in the urine o Pounding in the chest, neck or ears It is important to be able to differentiate hypertension from other conditions which may be causing blood pressure to increase up such as anxiety, white coat syndrome, sleep apnoea, thyroid issues etc. This is done by carrying out relevant investigations to exclude other pathologies such as ambulatory blood pressure monitoring (ABPM), thyroid function tests etc. and if found to be positive treated appropriately. Drugs that cause hypertension It can become easy to think of hypertension as a disease that can be treated by drugs, but what about when drugs cause blood pressure to become raised? As pharmacists you will see prescriptions every day and need to make clinical decisions on the suitability of the prescribed medicines taking into consideration patient factors such as whether the patient is elderly, pregnant, of child bearing age, etc. When a particular medicine is not suitable or there is a clinical interaction, you will need to prioritize the patient’s treatment and advise on suitable alternatives. Activity On the page below is a table with a list of drug classes which may cause high blood pressure, some of which are available to buy OTC. Add drug names that fit into the class and explain how each drug/class of drug can cause blood pressure to become raised and whether it is available to purchase OTC. What could you do if one of your patients who was hypertensive was about to start taking any of the following drugs?. 4 6PY011 TBL: Cardiovascular System HINT: Use a combination of the BNF sections covering the relevant drug classes and a pharmacology textbook such as Rang and Dale’s ‘Pharmacology’ to identify drug examples and summarise their mechanisms of action in raising BP; and clinical pharmacy textbooks such as Whittlesea and Hodson’s ‘Clinical Pharmacy and Therapeutics’ and Rutter’s ‘Community Pharmacy: Symptoms, Diagnosis and Treatment’ to check for alternative treatment options. Drug groups and example(s) Mechanism of raising BP Classification Alternative options/plan NSAIDs: NSAIDs cause fluid retention and decrease renal OTC Recommend alternative analgesia such as Ibuprofen… function causing BP to become raised and putting paracetamol or recommend the lowest dose greater stress on the heart and kidneys. NSAIDs can possible of NSAID also increase the risks of heart attack or stroke, especially in higher doses. Recreational drugs: N/A Amphetamine, ecstasy, cocaine… Nasal decongestants: Pseudoephedrine… Migraine medication: … Oestrogen containing preparations: Oral contraceptive pills… Antidepressants… Corticosteroids… Cyclosporine 5 6PY011 TBL: Cardiovascular System Diagnosing hypertension Diastolic blood pressure and systolic blood pressure are both measured in millimetres of mercury (mmHg). The ideal blood pressure is considered to be between 90/60mmHg and 120/80mmHg. Targets vary but high blood pressure is considered to be 140/90mmHg or higher. Low blood pressure is considered to be 90/60mmHg or lower. A blood pressure reading between 120/80mmHg and 140/90mmHg could mean the patient is at risk of developing high blood pressure if they don't take steps to keep their blood pressure under control. If a patient presents with a blood pressure reading of greater than 140/90mmHg they should be recommended for ambulatory blood pressure monitoring (ABPM). ABPM is when your blood pressure is measured as you move around, living your normal daily life. It is measured for up to 24 hours. A small digital blood pressure monitor is attached to a belt around your waist and connected to a cuff around your upper arm. This gives a more accurate picture of how your blood pressure changes throughout the day. It avoids the problems of ‘white coat’ syndrome (where your blood pressure rises because you are feeling anxious about being tested by a healthcare professional). All adults over 40 are advised to have their blood pressure checked at least every five years and more often if there blood pressure is close to 140/90mmHg. Investigations to complete for people with hypertension: o Test for the presence of proteinuria by sending a urine sample for estimation of the albumin: creatinine ratio and test for haematuria using a reagent strip. (These tests are important in detecting renal disease). o Take a blood sample to measure glycated haemoglobin (HbA1C), electrolytes, creatinine, eGFR, serum total cholesterol and HDL cholesterol o Examine the fundi (interior lining of eyeball) for the presence of hypertensive retinopathy o Arrange for a 12-lead electrocardiograph to be performed. 6 6PY011 TBL: Cardiovascular System 7 6PY011 TBL: Cardiovascular System Activity There are different types of blood pressure. Research each one and makes notes on how they are different to each other in both their presentation and their treatments. Essential/primary hypertension Secondary hypertension Resistant hypertension 8 6PY011 TBL: Cardiovascular System Using a Sphygmomanometer Automated blood pressure machines are in wide-spread use however they may not be suitable for all patients, particularly those with arrhythmias, pre-eclampsia, atrial fibrillation and certain vascular diseases. If the pulse is irregular, an automated blood pressure device can give inaccurate readings due to beat-to-beat variation, A healthcare professional can check for this by palpating the radial or brachial pulse before checking the blood pressure. If the pulse is irregular blood pressure should be measured manually with auscultation over the brachial artery. Patients with an irregular or rapid pulse should be referred to their doctor. Method for using a Sphygmomanometer https://www.youtube.com/watch?v=f6HtqolhKqo 1. To begin blood pressure measurement, use a properly sized blood pressure cuff. 2. Wrap the cuff around the upper arm with the cuff's lower edge one inch above the elbow pit 3. Lightly press the stethoscope head (diaphragm/bell) over the brachial artery just below the cuff's edge 4. Rapidly inflate the cuff to 180mmHg, occluding the artery. 5. Release air from the cuff at a moderate rate (3mm/sec) 6. Listen with the stethoscope and simultaneously observe the dial or mercury gauge 7. As cuff pressure is lowered the blood will flow only when systolic pressure is above cuff pressure producing sounds of Korotkoff. The first knocking sound (Korotkoff) is the patient’s systolic pressure 8. These sounds will be heard until the cuff pressure is equal to the diastolic pressure causing the sounds to disappear. When the knocking sound disappears, that is the diastolic pressure 9. Record the pressure in both arms and note the difference; also record the subject's position (supine), which arm was used, and the cuff size (small, standard or large) 10. If the subject's pressure is elevated, measure blood pressure two additional times, waiting a few minutes between measurements Activity Using your BNF, read the chapter on cardiovascular, particularly the drug class sections, and use the information to fill in the following table on drugs used to treat hypertension: HINT: Use a pharmacology textbook such as Rang and Dale’s ‘Pharmacology’ to help you if you need to find more detail on the mechanism of action. Clinical pharmacy textbooks such as Whittlesea and Hodson’s ‘Clinical Pharmacy and Therapeutics’ and Rutter’s ‘Community Pharmacy: Symptoms, Diagnosis and Treatment’ often provide information on the MOST IMPORTANT side-effects, counselling and monitoring points that you need to know. 9 6PY011 TBL: Cardiovascular System Group Examples Mechanism of action Side effects Counselling points Monitoring points ACE inhibitors Enalapril ACEi produce vasodilation by Dry cough, Ramipril can cause dry cough, if Blood pressure (ACEi) Lisinopril inhibiting the formation of hyperkalaemia, affected can change to ARB. Renal function (patients Perindopril angiotensin II. Reduced angiodema, Take first few doses at night may have renal artery Ramipril angiotensin II formation and dizziness, time due to first dose stenosis) inhibition of bradykinin GI disturbance, skin hypotension Potassium levels breakdown lead to reactions Specialist supervision required vasodilatation. Reduced when initiating with diuretics aldosterone production and/or in heart failure reduced sodium and water Be mindful that it can cause retention dizziness/light headedness when newly started/at dose titration. Angiotensin-2 Receptor Blockers (ARB/AII antagonist) Calcium Channel Blockers (CCB) Diuretics Furosemide… Amiloride and spironolactone Renin inhibitors Beta-blockers Alpha-blockers 10 6PY011 TBL: Cardiovascular System Activity: NICE guidance states that hypertension should be treated in a step by step approach. It also emphasises the importance of patient education. Read through the guidance using the link below and make notes on each step: https://www.nice.org.uk/guidance/ng136 Step 1 Step 2 Step 3 Step 4 11 6PY011 TBL: Cardiovascular System 12 6PY011 TBL: Cardiovascular System Hypertensive Emergency A hypertensive emergency (also known as hypertensive crisis) is considered if a patient presents with BP with a reading of 180/120mmHg or over. Symptoms that may also present with severely raised BP are: o Severe headaches/vomiting o Severe anxiety o Shortness of breath o Nosebleeds o Retinal haemorrhage In any of the above situations urgent medical assistance should be sought. According to NICE/BNF, anything above 180/110mmHg is ‘severe hypertension’. However, if the BP is above 180/110mmHg and there is no acute target- organ damage (damage of target organs, such as heart, kidney, and brain) then this is considered a ‘hypertensive urgency’ case, not a hypertensive emergency. For it be considered a hypertensive emergency, the key difference is that there must be acute target organ damage and this usually occurs when the diastolic BP is greater than 120, hence why a hypertensive emergency is often referred to as a BP reading above 180/120mmHg. The important thing to remember is that there is no absolute value of BP that separates the two syndromes (urgency and emergency). Instead, the most important distinction is whether there is evidence of impending or progressive target-organ damage. Pre-eclampsia https://www.nice.org.uk/guidance/ng133 Pre-eclampsia is a condition that can occur in pregnant women and is characterised by high blood pressure (greater than 140/90mmHg) and a large amount of protein in the urine. It usually occurs in the third trimester and is a medical emergency. Signs and symptoms that may present in the pharmacy by a pregnant woman that would warrant an urgent referral include: Severe headache Problems with vision, such as blurring or flashing before the eyes Severe pain just below the ribs Vomiting Sudden swelling of the face, hands or feet. Activity See the table on the next page. There are many causes of high blood pressure such as taking oral contraceptive pills, having a thyroid disease, having arterial disease, etc. The following table lists a few but can you think of any more? Discuss why each is a risk factor. List the non-pharmacological interventions that you can use to counsel patients with hypertension. 13 6PY011 TBL: Cardiovascular System HINT: Use a clinical pharmacy textbook such as Whittlesea and Hodson’s ‘Clinical Pharmacy and Therapeutics’ or relevant NICE Clinical Knowledge Summaries to help you find information on management options and addressing risk factors. Hypertension risk factor Explain Non-pharmacological interventions Salt excess High salt intake means there is Advise patient to reduce salt intake more sodium in the blood stream therefore less water is removed from the kidneys Weight Family history Lack of exercise African/Caribbean descent Smoking Coffee/alcohol Lack of exercise Disturbed sleep or not getting enough sleep 14 6PY011 TBL: Cardiovascular System Hypercholesterolemia https://www.nice.org.uk/guidance/cg181 Presenting signs/symptoms Cholesterol is a waxy substance that may deposit as plaques on artery walls causing narrowing of arteries therefore restricting blood flow to organs such as the heart and brain. Additionally these plaques may rupture and cause dangerous blood clots. High cholesterol can cause atherosclerosis and increase the risk of complications such as myocardial infarction, coronary artery disease and stroke. Cholesterol plays a pivotal role in synthesising bile acids, steroid hormones, and fat soluble vitamins (Vitamin A, D, E, and K). Although cholesterol is essential for the body functioning, a high cholesterol level indicates the impending risk of heart disease. On average, the UK has one of the highest cholesterol levels in the world. Despite this, high cholesterol doesn't usually produce any obvious symptoms. Here are some signs and manifestations that you may come across in the pharmacy: 15 6PY011 TBL: Cardiovascular System Angina Xanthomas, which are fatty skin deposits on the elbows, buttocks, knees, and tendons. Cholesterol deposits around the eyelids, which are also known as xanthelasmas. Cholesterol deposits around the corneas, also known as corneal arcus. Familial hypercholesterolaemia (FH) https://www.nice.org.uk/guidance/cg71 FH is an inherited condition that results in high levels of total cholesterol and low-density lipoprotein (LDL) cholesterol. FH is a result of a mutated gene on chromosome 19 and is a genetic disorder. Unlike recessive genetic disorders that require both sides of the family to have the condition, FH is autosomal dominant, meaning that a child may have the condition even if only one parent has the mutated gene. Children who inherit the mutated gene from both parents are at greater risk for heart attack and death before age 30. Men with FH tend to have heart attacks when they’re in their 40s or 50s. Eighty-five percent of men with this condition have a heart attack by the time they reach 60. Women with this condition tend to have heart attacks in their 50s or 60s. More on the identification and management of this rare but serious condition can be found on the following link: Diagnosing hypercholesterolemia Usually, high cholesterol level is diagnosed with a simple blood test. To prepare for the test, the patient should have fasted (no food or drink except water) for 10-12 hours beforehand. This is called a fasting blood test and is usually done first thing in the morning between dinner the night before and a late breakfast. A syringe of blood may be taken or a finger prick test can be carried out. GPs will usually arrange cholesterol blood tests for people who are over 40 and those with other risk factors for high cholesterol such as: o Being overweight or obese o Having high blood pressure o Having diabetes o Having a family history of heart or cardiovascular problems o Having a family history of hypercholesterolaemia or inherited high cholesterol o Other medical conditions, age, sex and ethnic background can also make a difference Hypercholesterolemia is diagnosed by taking a sample of a patient’s blood and sending it to a laboratory for analysis. Results are returned as lipids and liver function tests. There are two types of lipid HDL and LDL and the blood results will give you a total cholesterol too. Often clinicians will also check a patient’s thyroid function, to ensure it isn't contributing towards the raised cholesterol. Interpreting blood results o Total cholesterol: This is a measure of LDL cholesterol, HDL cholesterol and other lipid components. Total cholesterol should be 5.0 millimoles per litre (mmol/L) or lower. The average in the UK is around 5.5 mmol/l for men and 5.6 mmol/l for women. o LDL (low density lipoprotein cholesterol): LDL cholesterol can build up on the walls of your arteries and increase the chances of getting heart disease. That is why LDL cholesterol is referred to as ‘bad’ cholesterol. The lower the LDL cholesterol number, the better it is for the patient’s health. LDL cholesterol should be 3mmol/L or lower. o HDL (high density lipoprotein cholesterol, also called "good" cholesterol) HDL cholesterol protects against heart disease by taking the "bad" cholesterol out of the blood and keeping it from building up in your arteries. A higher number for this cholesterol is a good sign. HDL level should be above 1 mmol/L. 16 6PY011 TBL: Cardiovascular System o Triglycerides (fats carried in the blood from the food we eat). Excess calories, alcohol or sugar in the body are converted into triglycerides and stored in fat cells throughout the body. Triglyceride level should be under 1.7 mmol/L. People with higher risks, such as heart disease or high blood pressure will be set lower targets: o Total cholesterol of 4mmol/L or lower o LDL of 2mmol/L or lower o The ratio of total cholesterol to HDL - total cholesterol divided by HDL - should be below 4. Clinicians will set individual cholesterol targets for patients based on their overall risk factors. Treatment may involve dietary changes to cut down on saturated fats, increasing exercise, or taking cholesterol lowering medication. Even if cholesterol is not high there may be occasions when lipid lowering therapy is still recommended, for example in patients at high risk of developing cardiovascular disease. NICE recommends offering atorvastatin 20 mg daily for primary prevention to people who have a 10% or greater 10-year risk of developing CVD (estimated using the QRISK3 assessment tool), including those with type 2 diabetes and CKD. QRISK3 is an algorithm for predicting cardiovascular risk. It estimates the risk of a person developing cardiovascular disease (CVD) over the next 10 years and can be applied to those aged between 35 and 74 years. Activity: There are many causes of high cholesterol levels, below is a list of some of them, can you think of any more? Discuss why each is a risk factor HINT: Use a clinical pharmacy textbook such as Whittlesea and Hodson’s ‘Clinical Pharmacy and Therapeutics’ or relevant NICE Clinical Knowledge Summaries to help you find information on management options and addressing risk factors. Gender- women tend to have higher cholesterol than men Pregnancy Diabetes Kidney disease 17 6PY011 TBL: Cardiovascular System Polycystic ovary syndrome Underactive thyroid gland Certain drugs, e.g. contraceptives, diuretics, beta-blockers, anti-depressants Any other risk factors: Drug choice The main choice of drug for treatment of hypercholesterolemia is a statin, however, sometimes, a non-statin lipid lowering drug can be offered such as ezetimibe or cholestyramine. The decision whether to start statin therapy should be made after an informed discussion between the clinician and the person about the risks and benefits of statin treatment, taking into account additional factors such as potential benefits from lifestyle modifications, informed patient preference, comorbidities, polypharmacy, general frailty and life expectancy. Before starting statin treatment baseline blood tests should be conducted and the person should be clinically assessed; comorbidities and secondary causes of dyslipidaemia should be treated. When a decision is made to prescribe a statin, the NICE guideline on lipid modification https://www.nice.org.uk/guidance/cg181) recommends using a statin of high intensity and low acquisition cost. Statins are grouped into 3 different intensity categories according to the percentage reduction in low-density lipoprotein cholesterol (LDL-C): The choice of treatment and dose will depend on the % reduction of LDL that is being aimed for. Low intensity Medium intensity High intensity (20–30% (31–40% (more than 40% LDL-C reduction) LDL-C reduction) LDL-C reduction) Fluvastatin 20–40 mg daily 80 mg daily - Pravastatin 10–40 mg daily - - Simvastatin 10 mg daily 20–40 mg daily 80 mg daily. Atorvastatin - 10 mg daily 20–80 mg daily Rosuvastatin - 5 mg daily 10–40 mg daily 18 6PY011 TBL: Cardiovascular System The only high-intensity statin specifically named in the NICE guidelines is atorvastatin 20–80 mg daily. Other possible high-intensity statins are rosuvastatin 10–40 mg daily and simvastatin 80 mg daily. The MHRA has advised that there is an increased risk of myopathy associated with simvastatin 80 mg daily, and that this dose should be considered only in people with severe hypercholesterolaemia and high risk of cardiovascular complications who have not achieved their treatment goals on lower doses, when the benefits are expected to outweigh the potential risk. Statins used in Primary Prevention Atorvastatin 20 mg daily should be offered for primary prevention to people who have a 10% or greater 10-year risk of developing CVD (estimated using the QRISK®3 assessment tool ( https://qrisk.org/three/ ), including those with type 2 diabetes and CKD. In people with type 1 diabetes treatment should be started with atorvastatin 20 mg daily. Primary prevention may be considered in type 1 diabetic patients with any of the following risk factors: adults who are older than 40 years those who have had diabetes for more than 10 years who have established nephropathy, or who have other CVD risk factors Statins used in Secondary Prevention Statin treatment for people with CVD (secondary prevention) should usually start with atorvastatin 80 mg daily. However, in people with CKD the initial dose should be 20 mg daily, and in other people a dose lower than 80 mg daily should be used if there are potential drug interactions with existing therapy, a high risk of adverse effects or the person prefers a lower dose. Monitoring with statins Total cholesterol, HDL cholesterol and non-HDL cholesterol should be measured in all patients who have been started on high-intensity statin treatment as above after 3 months of treatment, aiming for a greater than 40% reduction in non-HDL cholesterol. If this reduction in non-HDL cholesterol is not achieved; discuss adherence and the timing of the dose optimise adherence to diet and lifestyle measures consider increasing the dose if the person started on less than atorvastatin 80 mg daily and if they are judged to be at higher risk because of comorbidities, risk score or using clinical judgement. The dose of atorvastatin should be increased from 20 mg in people with CKD receiving it for primary or secondary prevention of CVD if a greater than 40% reduction in non-HDL cholesterol is not achieved and the person's eGFR is 30 ml/min/1.73 m2 or more. If their eGFR is less than this, any increase in dose should be discussed with a renal specialist. It is also advisable that healthcare professionals provide annual medication reviews for people taking statins; using these reviews to discuss medication adherence and lifestyle modification, address CVD risk factors and monitoring for adverse effects/intolerance of statins. If a person is not able to tolerate a high-intensity statin, the aim should be to treat with the maximum tolerated dose. Many people who stop treatment due to side effects or adverse effects, especially muscle pains, may be able to restart treatment on the same or a different statin. The patient should be advised that any statin at any dose reduces CVD risk. If someone reports adverse effects when taking high-intensity statins, the following strategies should be discussed with them; stopping the statin and trying again when the symptoms have resolved to check if the symptoms are related to the statin reducing the dose within the same intensity group changing the statin to a lower intensity group 19 6PY011 TBL: Cardiovascular System Ezetimibe People with primary hypercholesterolaemia should be considered for ezetimibe treatment in line with the licencing indication. Ezetimibe monotherapy is as an option for treating primary (heterozygous-familial or non-familial) hypercholesterolaemia in adults in 2 broad situations: As an alternative to a statin in people in whom statins are contraindicated or not tolerated; intolerance is defined as the presence of clinically significant adverse effects that represent an unacceptable risk to the patient or that may reduce compliance with therapy. In addition to initial statin therapy in people who have started statin treatment but whose serum total or LDL cholesterol concentration is not appropriately controlled either after appropriate dose titration or because dose titration is limited by intolerance to the initial statin therapy (defined as above) and consideration is being given to changing from initial statin therapy to an alternative statin. In the second of the situations above, in people with non-familial hypercholesterolaemia, adding ezetimibe to atorvastatin (the initial statin therapy recommended in the guideline) is an option if (and only if) a greater than 40% reduction in non-HDL cholesterol is not achieved: despite optimising adherence and timing of the dose of atorvastatin and optimising adherence to diet and lifestyle measures, and increasing the dose of atorvastatin (if started at less than 80 mg daily) is not effective or not tolerated or the person has to decrease the dose because of tolerability problems, and changing to a different statin is being considered. Bile acid sequestrants, fibrates and nicotinic acid Bile acid sequestrants (anion exchange resins) and nicotinic acid (niacin) should not be offered for primary or secondary prevention of CVD, alone or in combination with a statin, including in people with CKD or type 1 or type 2 diabetes. Additionally, fibrates should not be routinely offered for monotherapy for primary or secondary prevention of CVD including in people with CKD or type 1 or type 2 diabetes and should not be recommended in combination with a statin in these indications. See the NICE guideline on familial hypercholesterolaemia ( https://www.nice.org.uk/guidance/cg71 ) on the possible use of bile acid sequestrants, fibrates and nicotinic acid in people with this condition. Omega-3 fatty acid compounds People with or at high risk of CVD should be advised to consume at least 2 portions of fish per week, including a portion of oily fish. However, it is advised that omega-3 fatty acid compounds should not be offered for primary or secondary prevention of CVD, alone or in combination with a statin, including in people with CKD or type 1 or type 2 diabetes. Moreover, healthcare professionals should tell people that there is no evidence that omega‑3 fatty acid compounds help to prevent CVD. In addition, healthcare professionals should not offer or advise people who have had an MI to use omega‑3 fatty acid capsules or omega‑3 fatty acid supplemented foods to prevent another MI. Monoclonal antibodies For recommendations on managing primary heterozygous familial hypercholesterolaemia in people whose LDL C levels are not adequately controlled despite maximal tolerated lipid-lowering therapy, see the NICE technology appraisal guidance on alirocumab and evolocumab. 20 6PY011 TBL: Cardiovascular System Activity Using your BNF, read the chapter on lipid lowering therapy and use the information to fill in the following table on drugs used to treat hypercholesterolaemia: HINT: Use a combination of the BNF sections covering the relevant drug classes and a pharmacology textbook such as Rang and Dale’s ‘Pharmacology’ to identify drug examples and summarise their mechanisms of action; and clinical pharmacy textbooks such as Whittlesea and Hodson’s ‘Clinical Pharmacy and Therapeutics’ and Rutter’s ‘Community Pharmacy: Symptoms, Diagnosis and Treatment’ to help you find the MOST IMPORTANT cautions, contraindications, side effects, monitoring, interactions and counselling. Group Mechanism of Examples Side effects Counselling Monitoring action points/interactions Statin Competitively Simvastatin Rhabdomylosis Report any muscle Lipid profile; inhibit HMG Rosuvastatin aches/cramps, do LFTs CoA reductase, Atorvastatin not take with (transaminases an enzyme macrolides – upper limits involved I of normal); cholesterol Creatine synthesis, kinase; fasting especially in blood glucose the liver or HbA1c in patients at risk of DM Bile acid sequestrants Nicotinic acid Fibrates Gemfibrozil Cholesterol absorption inhibitor Monoclonal antibodies 21 6PY011 TBL: Cardiovascular System Non-pharmacological interventions Over half of the adults in the UK have high cholesterol (>5mmol/L); as pharmacists it is important that you offer patients education on ways in which they can help to prevent and reduce raised cholesterol levels. Furthermore, many people cannot tolerate the side effects associated with many lipid lowering therapies and or may want to reduce their dependence on multiple medications; as a healthcare professional you need to tailor advice on how this can be implemented: Exercise. Have cholesterol levels checked regularly and take medications if prescribed. Start and continue an exercise program with 30-60 minutes of vigorous activity at least 3 or 4 days a week. Maintain a healthy weight; lose weight if needed. Choose a wide variety of foods that are low in saturated fat, cholesterol and sodium and more unsaturated fats. Limit alcohol intake. Don't smoke and avoid "second hand" smoke. Have blood pressure checked regularly, and take steps to lower it if it's high. If patient has diabetes, follow doctor's recommendations for treatment. Read food labels. Advice patient to become an active participant in making treatment decisions and in solving problems relating to their health. Ischaemic/Coronary Heart Disease 22 6PY011 TBL: Cardiovascular System You should re-read the 5PY022 CVS pack sections on cardiovascular (CV) disease risk factors and the process of atherosclerosis, together with details of the epidemiology and impact of cardiovascular disease at the national level. Make notes below on the types of conditions that come under the umbrella term of cardiovascular disease (as opposed to heart disease). Hint: Not all cardiovascular diseases involve coronary arteries (arteries which supply the heart muscle tissue with oxygenated blood) but we are generally talking about atherosclerotic arterial disease when considering these conditions. Categorise the following risk factors for CV disease in to modifiable and non-modifiable: Increasing age; abdominal obesity; sex; hypertension; pre-existing CV disease; smoking; hyperlipidaemia; family history of CV disease; diabetes mellitus; South Asian descent; alcohol intake; diet; physical exercise Modifiable Non-modifiable Which of the above two categories is the most important and why? 23 6PY011 TBL: Cardiovascular System Angina Pectoris Using the year 2 CVS pack, re-familiarise yourself with the definitions and descriptions of stable angina, unstable angina, Prinzmetal’s variant angina, decubitus angina and nocturnal angina. For the purposes of this pack you will look specifically at stable angina and unstable angina, the latter being covered under Acute Coronary Syndromes. Stable angina https://www.nice.org.uk/guidance/cg126 This type of angina occurs in stable coronary artery disease where stable atheromatous plaques form in one or more major coronary arteries. Symptoms only tend to occur in patients that have significant stenosis (narrowing) of a coronary artery (> approximately 70%). This permanent restriction of blood flow causes a mismatch between the supply and the demand of oxygenated blood to the myocardium at times of stress or activity when cardiac output (CO) increases (remember CO is a function of heart rate and stroke volume; CO = HR x SV). Hence, patients are more likely to experience ischaemic pain when precipitated by exercise, stress or temperature change. For this reason symptoms in stable angina are very predictable and occur in a reproducible manner, hence pain can be relieved by either stopping the trigger e.g. by ceasing the activity or by using GTN (which dilates coronary arteries) prior to undertaking the causative activity. The symptoms of stable angina include: Retrosternal chest heaviness (constricting/gripping/tight/diffuse [not sharp]) Additional features: o Radiation to back/arms/neck/jaw o Associated breathlessness o Autonomic symptoms (such as tachycardia/sweating/pallor/clamminess) They are similar to those which can be experienced during a heart attack or in unstable angina and, while generally symptoms are less severe, the fundamental difference compared to acute coronary syndromes lies in the pattern of pain and in the response to glyceryl trinitrate. In other words, in stable angina, the symptoms are entirely predictable and stable. When making a diagnosis it is important to note that the fundamental features of stable angina include both the reversibility of the symptoms and the repetitiveness of the attacks over time (months to years). The pathophysiological mechanisms by which stable angina develops are eloquently described on the following video: https://www.youtube.com/watch?v=7PsDK2R95Sg(Note: that the UK pronunciation of angina, emphasises the ‘I’) A diagnosis of stable angina can be made clinically i.e. based upon physical examination, symptoms, history and risk factors but there are various investigations which may need to be performed when the diagnosis is uncertain. The outline of diagnosis can be seen in the following links: 24 6PY011 TBL: Cardiovascular System Activity Refer to the below links and make notes on the diagnosis of stable angina including categorisation between typical angina, atypical angina and non-anginal chest pain; and tests such as ECG, exercise ECG, CT Calcium scoring, non- invasive functional testing, invasive angiography and non-invasive CT angiography. NICE guideline CG95 Recent-onset chest pain of suspected cardiac origin found at https://www.nice.org.uk/guidance/cg95 NICE pathway (https://pathways.nice.org.uk/pathways/chest-pain/assessing-and-diagnosing-suspected-stable- angina#content=view-node%3Anodes-clinical-history-and-physical-examination ) NICE CKS 2018 ( https://cks.nice.org.uk/angina ) Stable Angina Non-stable Angina Non-anginal Chest Pain Diagnosis Tests Other Information 25 6PY011 TBL: Cardiovascular System Treatment of stable angina The pharmacological treatment of patients with stable angina should be considered with reference to three overarching aims: 1. Immediate resolution of angina attacks (or prevention of predictable attacks using sublingual GTN). 2. Decreasing the severity and/or frequency of angina attacks using anti-anginal drugs such as beta-blockers, calcium channel blockers, long-acting nitrates or potassium channel activators. 3. Providing secondary prevention treatment as the patient by definition has existing cardiovascular disease in the form of antiplatelet therapy, high intensity statins and ACE inhibitors (for patients with diabetes mellitus or another suitable indication for an ACE inhibitor) in accordance with other guidelines. Complete the following drugs table using the angina section and relevant sections in the BNF: HINT: Use a combination of the BNF sections covering the relevant drug classes to identify drug names and formulations; and clinical pharmacy textbooks such as Whittlesea and Hodson’s ‘Clinical Pharmacy and Therapeutics’ to help you find the MOST IMPORTANT cautions, contraindications, side effects, monitoring, interactions and counselling. Drug names Key cautions* and Key adverse Important Other notes and contraindications** effects AND interactions and counselling formulations monitoring Glyceryl trinitrate Calcium channel blockers (dihydropyridine types and diltiazem) Beta-blockers Long-acting nitrates Potassium channel activators Ivabradine Ranolazine 26 6PY011 TBL: Cardiovascular System Using BNF chapter 2.7 and the 2018 NICE Clinical Knowledge Summary (CKS) for Angina (new diagnosis) [http://cks.nice.org.uk/angina] complete the table below to summarise the first, second and third line strategies for reducing the severity and/or frequency of stable angina attacks. Consider the following anti-anginal drugs: calcium channel blockers, beta-blockers, long acting nitrates (e.g. isosorbide mononitrate), nicorandil, ivabradine and ranolazine; as well as revascularisation therapies in your summary. Strategies for reducing the severity and/or frequency of angina attacks for patients suffering attacks more than twice a week First line strategy Second line strategy Third line strategy Co-morbid conditions such as atrial fibrillation, chronic kidney disease, diabetes, chronic heart failure, hypertension, obesity, rheumatoid arthritis, and stroke and TIA should be optimally managed. Patients with any form of angina will also require advice on maintaining a healthy diet and lifestyle, smoking cessation (if applicable); and on implications for manual work, driving, flying and sexual activity. Using the NICE CKS make additional notes on the advice which should be given to newly diagnosed stable angina patients including those listed above. 27 6PY011 TBL: Cardiovascular System Acute coronary syndromes https://www.nice.org.uk/guidance/ng185 The 5PY022 CVS pack briefly mentions unstable angina and myocardial infarction (MI) and covers the pharmacology of the drugs used to treat them. Both of these conditions are, in fact, part of a spectrum of coronary events known as Acute Coronary Syndromes (ACS) Patients who have stable angina have atheromatous plaques in their coronary arteries which, while extending slowly, are stable in nature. As described above the extent of stenosis determines whether or not angina pain occurs (due to demand for oxygenated blood outstripping supply that is able to reach the myocardium). The following video provides an animated representation of how atheromatous plaques form in coronary arteries. It also shows what happens when plaques rupture and a resulting thrombus completely occludes a coronary artery causing a heart attack (myocardial infarction): https://www.youtube.com/watch?v=T_b9U5gn_Zk In ACS a plaque becomes unstable and ruptures exposing its lipid rich core. In itself this does not cause a problem except that circulating platelets become attracted to the exposed core and begin to aggregate which subsequently triggers thrombosis (clot formation). A thrombus can then either intermittently or partially occlude a coronary artery or it can completely block it. Thus, in ACS, three eventualities are possible: 1. Where total occlusion of a major coronary artery occurs no oxygenated blood can reach the part of the myocardium supplied by that artery and so death of heart muscle tissue will occur relatively quickly (over minutes or tens of minutes). Death (irreversible necrosis) occurs through the full thickness of the myocardium in the area of the myocardium perfused by that coronary artery. This is known as a full-blown MI (heart attack); ST elevation MI (STEMI or STE-ACS); or, sometimes, Q wave MI. 2. So-called intermittent occlusion occurs when a thrombus may break up or dislodge and move downstream to a smaller branch of a coronary artery which can become occluded. This will cause myocardial damage to a 28 6PY011 TBL: Cardiovascular System lesser extent which is still an MI and is referred to as a non-ST elevation MI (NSTEMI). There is a nevertheless danger that thrombosis will extend further and cause full blown STEMIs. 3. So-called partial occlusion occurs where a thrombus partially (but not completely) occludes a coronary artery. The plaque rupture and subsequent thrombus formation has made the situation unpredictable but no death of myocardial tissue occurs. These unpredictable angina symptoms are known as unstable angina (UA). Like 2 above there is a danger that thrombi will extend, break up or dislodge and cause full blown STEMIs. Both 2 and 3 above are grouped together as Non-ST Elevation Acute Coronary Syndromes (NSTEACS) since the treatment pathway for these is different to that taken in the very urgent full blown STEMI situation. Because of the unstable nature of the events which cause ACS all of these situations can occur in patients who have no previous awareness that they have any atherosclerotic damage in their coronary arteries. In other words a patient with less than 60 or 70% stenosis who has never suffered an angina attack can still have a plaque which ruptures and causes ACS. This is why patients can suffer heart attacks without any knowledge that there was previously anything wrong. 29 6PY011 TBL: Cardiovascular System The following video provides a more detailed description of the pathophysiology of coronary artery disease including stable angina and ACS. https://www.youtube.com/watch?v=EATkbpqlxvc Diagnosing ACS Acute coronary syndromes are differentially diagnosed (and from stable angina) on the basis of: Presentation: symptoms, examination and risk factors Electrocardiography (ECG) changes Cardiac markers Clinical Presentation STEMI Non-ST elevation MI (NSTEMI) Symptoms include crushing central chest pain/tightness Pain/location/radiation is the same as NSTE-ACS except or discomfort (pain may also occur in the arms, that it is usually (but not always) more sudden and shoulders, throat, jaw, teeth, back or upper abdomen) severe, lasts longer than 30 minutes and is not relieved and also breathlessness and sweating. by rest/GTN. The pattern of symptoms in ‘unstable angina’ is Other symptoms include dyspnoea, fear, pallor, sweating characterised by frequent attacks of angina for the first (clammy feeling), anxiety, vasoconstriction (peripheral) time OR sudden worsening of previously stable angina and shock. OR recurrent angina at rest OR sudden onset of severe chest pain at rest. The symptoms, in contrast to STEMI, may be more likely to develop over 24-72 or more hours. Therefore an attack of angina lasting longer than 20 minutes or that keeps recurring despite repeated use of GTN requires immediate hospital admission. Atypical ACS symptoms may include inframammary stabbing, back pain, abdominal pain, syncope or pain free dyspnoea. Pain need not be central and may also be completely absent (silent MI). While a positive response to sublingual GTN is indicative of stable angina it should not be used exclusively to make a diagnosis. Differential diagnoses include musculoskeletal pain, pleurisy, pulmonary embolism (PE), pericarditis and gastro oesophageal reflex disease (GORD). If the pain responds to GTN within 2-5 minutes this indicates that stable angina is the probable cause. NB. GORD can respond to GTN within 5-10 minutes. Dyspnoea and sweating can still be present in PE, although unlikely with the other differentials. Patients with chest pain within the previous 12 hours should also be referred for same day assessment. Electrocardiography (ECG) In suspected ACS a resting 12-lead ECG should be performed as soon as possible (often by paramedics). Regional ST segment elevation in the leads facing the infarcted area, or new left bundle branch block (LBBB), are suggestive of STEMI and local STEMI-based treatment protocols must be followed until the diagnosis is confirmed. The development of a STEMI is represented by the following illustrations 30 6PY011 TBL: Cardiovascular System Before Event R T P Q S STEMI ST Segment elevation occurs within After several hours the T wave inverts. Weeks afterwards the minutes of the occlusion occurring: The ST segment reverts to normal after patient is left with a several days and a Q-wave develops: persistent Q-wave which indicates full thickness myocardial damage: ST Elevation = showing STEMI NSTEMI ECG signs in unstable angina and NSTEMI include regional ST-segment depression and deep T wave inversion although there may be no ECG changes. 31 6PY011 TBL: Cardiovascular System Cardiac enzymes Cardiac troponin is released from the actin and myosin complex in damaged cardiac myocytes. It is more sensitive and specific for cardiac damage than the enzymes previously used to diagnose MI: Creatine kinase MB(CK-MB), Lactate dehydrogenase (LDH), Aspartate aminotransferase (AST) Troponin Troponin is the preferred biochemical marker for diagnosing acute MI. Cardiac troponin I or troponin T levels should be taken at initial assessment and then again 10-12 hours post onset of chest pain because troponin is released gradually towards its peak over that period (6-12 hours). Troponin I is detectable for 7-10 days post event whereas troponin T may be detected for 7-14 days. Normal levels (cTn I 3 TIMI risk factors. Conversely the GRACE score provides percentage rate figures for predicted 6-month mortality and can be readily applied to NICE guidelines. GRACE calculated risk status is attributed to the categories: lowest; low; intermediate; high and highest. The committee agreed that this should influence the choice between early invasive intervention (coronary angiography, with PCI if indicated) and conservative management (initial medical management, proceeding to coronary angiography and PCI if there is evidence of recurrent ischaemia). Please visit the following treatment summary: 36 6PY011 TBL: Cardiovascular System https://www.nice.org.uk/guidance/ng185/resources/visual-summary-unstable-angina-nstemi-pdf-8900622109 In addition to the above all patients with an MI should have their left ventricular function assessed since myocardial damage can precipitate this leading to acute heart failure. For people with unstable angina or NSTEMI who are having coronary angiography, offer: prasugrel or ticagrelor, as part of dual antiplatelet therapy with aspirin, if they have no separate indication for ongoing oral anticoagulation. clopidogrel, as part of dual antiplatelet therapy with aspirin, if they have a separate indication for ongoing oral anticoagulation. Management when PCI is not indicated Consider conservative management (initial medical management, proceeding to coronary angiography and PCI if there is evidence of recurrent ischaemia) without early coronary angiography for people with unstable angina or NSTEMI who have a low risk of adverse cardiovascular events (predicted 6-month mortality 3.0% or less). Offer ticagrelor, as part of dual antiplatelet therapy with aspirin, to people with unstable angina or NSTEMI when PCI is not indicated, unless they have a high bleeding risk. Consider clopidogrel, as part of dual antiplatelet therapy with aspirin, or aspirin alone, for people with unstable angina or NSTEMI when PCI is not indicated, if they have a high bleeding risk. Patients at intermediate, high or highest risk should receive a loading dose of clopidogrel in addition to aspirin. For these patients NICE also advises to: Offer unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor in combination with dual antiplatelet therapy to people with acute STEMI undergoing primary PCI with radial access. Consider bivalirudin with bailout glycoprotein IIb/IIIa inhibitor in combination with dual antiplatelet therapy for people with acute STEMI undergoing primary PCI when femoral access is needed. 37 6PY011 TBL: Cardiovascular System Compare the above with the recommendations given in BNF section 2.7.1 (Acute Coronary Syndromes: UA and NSTEMI - see https://bnf.nice.org.uk/treatment-summary/acute-coronary-syndromes.html and make notes in the box below. Hint: Consider also the use of oxygen; nitrates; opioids; antiemetics; and beta-blockers (or diltiazem/verapamil) and also the circumstances in which they are given. What do you consider to be the aims/rationales for using these additional treatments? Which drugs are used in long-term management and why? Hint: read the above recommended BNF section carefully in respect of UA/NSTEMI long-term management and ‘Prevention of Cardiovascular Events.’ 38 6PY011 TBL: Cardiovascular System Heart Failure IMPORTANT: revision from year 2 is required before studying this section. Using your year 2 CVS TBL pack, refresh your understanding of the gross anatomy of the cardiovascular system and the heart including: differences between right-sided and left-sided circulations. the roles of the arterial and venous circulations. the meaning of the terms cardiac output, stroke volume, venous return, inotropic, chronotropic, systole, diastole, blood pressure and resistance. You should also remind yourself of the effect that vessel diameter, blood viscosity and blood pressure has on arterial flow. Remember, in particular, the two equations: CO = HR x SV and SV ∝ Contractility x End Diastolic Volume Peripheral Resistance …where contractility equates to the force of contraction by the heart pump, end diastolic volume equates to the preload/venous return and peripheral resistance equates to the afterload. Next, go over last year’s pack’s section on Heart Failure, including definition; points of interest and terms; clinical syndromes of heart failure; aetiology; pathophysiology; and signs and symptoms. Follow this will a review of the subsequent sections on ACE inhibitors, β-adrenoceptor antagonists, diuretics, cardiac glycosides and dobutamine and the table which examines commonly used drugs used in heart failure. The section on ACE inhibitors and the renin angiotensin aldosterone system (RAAS) covered in the hypertension section is also particularly relevant. You will need to have a good understanding of all of the above before you can go on to consider how heart failure is diagnosed and how patients are managed. You may find the following video useful: https://www.youtube.com/watch?v=7uPuhWi7KiE (Bear in mind when watching the video that, as the RAAS is activated, angiotensin II has a vasoconstrictor action which has the effect of increasing the afterload that the heart has to pump against. In addition the increased levels of aldosterone cause sodium and then water retention which has the effect of increasing the preload. Increasing 39 6PY011 TBL: Cardiovascular System both preload and afterload, while addressing the problem of reduced CO in the short term, has the effect of exacerbating the spiralling decline that occurs in HF). Signs, symptoms and classification Symptoms and signs arise as a result of inadequate tissue perfusion, venous congestion (peripheral and pulmonary) and disturbances in water and electrolyte balance as follows: Pulmonary congestion: breathlessness, basal crackles, frothy sputum (?tinged red), PND, orthopnoea (pillows), gasping, seeks fresh air. Peripheral congestion: Pitting ankle oedema, raised JVP, hepatomegaly, ascites, bowel oedema, anorexia. Reduced perfusion: Fatigue, confusion/slowness of thought, pallor, renal failure, tachycardia, cold hands & feet. Also: 3rd/4th Heart sounds, displaced apex beat, murmurs, cardiomegaly. The New York Heart Association (NYHA) classifies HF based on symptoms and exercise tolerance and is frequently used in clinical trials which inform decisions on which patients will befit from specific treatments: Class I No limitation during normal physical activity. Class II Slight limitation on moderate exertion e.g. walking/climbing stairs. Class III Marked limitation. Symptoms occur on minimal exertion e.g. walking on the flat. Class IV Breathlessness at rest. NICE Pathways cover the diagnoses and management of both acute and chronic heart failure as follows: https://pathways.nice.org.uk/pathways/acute-heart-failure https://pathways.nice.org.uk/pathways/chronic-heart-failure This pack will focus on chronic heart failure with reduced ejection fraction and its management; which is also covered by relevant 2018 NICE Guidelines ( https://www.nice.org.uk/Guidance/NG106); and summarised in the 2019 NICE CKS for Chronic Heart Failure: Confirmed Heart Failure with Reduced Ejection Fraction (https://cks.nice.org.uk/heart-failure-chronic#!scenario) In order to make a diagnosis and to inform management various investigations may be performed: 40 6PY011 TBL: Cardiovascular System Systems review/physical examination and routine observations: including manifestations of peripheral or pulmonary oedema or poor perfusion including abdominal examination; heart sounds, JVP, pulse and BP measurement; exercise tests (for classification); spirometry/peak flow measurements to rule out respiratory diseases. Chest X-ray: Reveals pulmonary oedema, cardiomegaly and pleural effusion. Echocardiography: to ascertain the ejection fraction (EF) which will be impaired in a patient with diastolic dysfunction. EF

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