Cardiovascular TBL Сycle

Cardiovascular TBL cycle 6PY011Introduction/contextualisation Dr Mohamed Aboudounya and Fatimah Abbas 27 Oct 2025 Objectives for today • Summarise 5 cardiovascular conditions and briefly their symptoms (HTN, hypercholesterolaemia, stable angina, ACS, HF). • More detailed in hypertension and heart failure including drug therapies. • Mainly focussing on the drug treatments and NICE guidelines for the remaining conditions. • Do a case on heart failure. Hypertension • Sustained increase in systemic arterial blood pressure (BP). • Definition: Hypertension is defined by blood pressure readings above 140/90 mmHg, indicating chronic elevated pressure. • Types: a) Essential/Primary: multifactorial aetiology e.g. family history, Obesity, and an unhealthy diet, b) Secondary, c) Resistant Hypertension. • Key Mechanisms Involved: Activation of RAAS, sympathetic overactivity, sodium retention, endothelial damage, arterial stiffness (worsens hypertension over time) and organ strain. • Consequences of Hypertension: increased heart workload, CHD, atherosclerosis, stroke, vascular dementia, Heart failure etc. BP = Cardiac Output (CO) x Total Peripheral Resistance (TPR) (SV x HR) Symptoms of hypertension • Silent killer. Regular screening important. • Could include: headache, dizziness, fatigue/confusion; pounding in chest, neck or ears; Chest pain; irregular heart beat; difficulty breathing; vision problems; blood in urine. ➢Hypertensive Emergency (BP >180/120 mmHg) vs Hypertensive Urgency (>180/110 mmHg): Target organ damage ? Not clear cut. ➢Symptoms: severe headaches/vomiting, severe anxiety, shortness of breath, nosebleeds, retinal haemorrhage. Need A& E referral. Diagnostic Tests • BP • Fluctuations or White coat hypertension→ ABPM • ECG. • Proteinuria • Albumin: Creatinine ratio • Blood tests: HbA1c, electrolytes, FBC • Fundi (eye examination) Drugs used • ACEIs/ ARBs • CCBs • Diuretics • Alpha-blockers • Beta-blockers • Renin inhibitors See NICE NG136 for guidelines RAAS Pre-eclampsia • High BP (>140/90) in pregnant women • Usually in 3rd trimester, is a medical emergency • Symptoms may include: severe headache, vision problems, vomiting, severe pain below ribs, swelling of hands, face or feet • See NICE NG133 for treatment guidelines • “Use labetalol, nifedipine or methyldopa. Base the choice on any preexisting treatment, side effect profiles, risks (including fetal effects) and the woman’s preference”. Lifestyle Advice Diet and Salt Reduction Reducing salt intake and maintaining a balanced diet rich in fruits, vegetables, and whole grains help manage hypertension effectively. Physical Activity and Weight Management Regular physical exercise and maintaining a healthy weight significantly lower blood pressure and improve cardiovascular health. Avoiding Alcohol and Smoking Limiting alcohol consumption and quitting smoking are crucial lifestyle changes that reduce cardiovascular risk. Monitoring and Support Regular blood pressure monitoring at home and continuous lifestyle support ensures adherence and effective hypertension management. Hypercholesterolaemia Hypercholesterolaemia Role of Cholesterol in Body Cholesterol is vital for synthesising bile acids, steroid hormones, and fat-soluble vitamins A, D, E, and K. Cholesterol and Atherosclerosis Excess cholesterol (Elevated LDL cholesterol) deposits on artery walls forming plaques that narrow arteries and restrict blood flow. Cardiovascular Risks Plaque buildup increases risks of coronary artery disease, stroke, and peripheral vascular disease. Plaque rupture can cause blood clots leading to heart attacks or strokes. Importance of Screening Hypercholesterolaemia is often asymptomatic, so routine screening is essential for prevention. Signs and Risk Factors Clinical Signs of Hypercholesterolaemia Signs include angina, xanthomas, xanthelasmas, and corneal arcus indicating high cholesterol levels. Major Risk Factors Risk factors include obesity, diabetes, hypertension, family history, and familial hypercholesterolaemia genetic disorder. Additional Risk Factors Certain medications and conditions like thyroid and kidney diseases increase hypercholesterolaemia risk. Hypercholesterolaemia Genetic and Lifestyle Factors Familial hypercholesterolemia causes early cardiovascular issues; lifestyle factors like diet also raise risks. Early Management Importance Early identification and treatment are key to reducing cardiovascular morbidity and mortality, per guidelines. Normal Blood levels: TC < 5mmol/L LDL < 3mmol/L HDL > 1 mmol/L TG < 1.7mmol/L Diagnosis and Management Lipid Profile Testing Diagnosis relies on fasting lipid profile tests including total cholesterol, LDL, HDL, and triglycerides levels. Risk Assessment NICE recommends QRISK3 scoring combined with fasting blood tests for cardiovascular risk evaluation. Tools like QRISK3 help estimate 10-year cardiovascular risk to guide treatment decisions. Additional Diagnostic Tests Thyroid function tests are used to exclude secondary causes of elevated cholesterol. Lifestyle Modifications Management includes dietary changes, increased physical activity, and smoking cessation to reduce cholesterol levels. Pharmacological Treatment and Monitoring Statins like atorvastatin (which inhibit cholesterol synthesis), or ezetimibe are used, with lipid profile monitoring after 3 months and yearly. Drugs used in hypercholesterolaemia • • • • • • Statins Ezetimibe (Cholesterol absorption inhibitor) Bile acid sequestrants e.g. cholestyramine Fibrates Nicotinic acid Bempedoic acid: Bempedoic acid is an adenosine triphosphate citrate lyase (ACL) inhibitor which inhibits cholesterol synthesis in the liver, thereby lowering LDL-cholesterol. • Omega-3 fatty acid compounds- Icosapent ethyl available in restricted circumstances • Monoclonal antibodies: alirocumab and evolocumab Statins • Best taken at night. • Main side effects to look out for are: -muscle symptoms: myalgia,myopathy, myositis, muscle breakdown, rhabomyolysis in severe cases etc. -liver toxicity: elevated liver enzymes, jaundice…. Common side effects listed in BNF monograph under statins: arthralgia; asthenia; constipation; diarrhoea; dizziness; flatulence; gastrointestinal discomfort; headache; muscle complaints; nausea; sleep disorders. Also under atorvastatin: epistaxis, hyperglycaemia. • Important safety information. For all statins MHRA/CHM advice: Statins: very infrequent reports of myasthenia gravis (September 2023) Bempedoic acid: Nilemdo® 180mg Indications from BNF: • Primary hypercholesterolaemia or mixed dyslipidaemia in patients who have not responded adequately to other appropriate measures [in combination with a statin, or with a statin and other lipid-lowering therapies, or with other lipidlowering therapies or alone if a statin contra-indicated or not tolerated], • Established or at high-risk of atherosclerotic cardiovascular disease [in combination with the maximum tolerated dose of a statin with or without ezetimibe, or with ezetimibe or alone if a statin contra-indicated or not tolerated] Bempedoic acid witn ezetimibe Nustendi®180/10 • Bempedoic acid with ezetimibe is recommended as an option for treating primary hypercholesterolaemia (heterozygous familial and non-familial) or mixed dyslipidaemia as an adjunct to diet in adults. It is recommended only if: • statins are contraindicated or not tolerated • ezetimibe alone does not control low-density lipoprotein cholesterol well enough and • the company provides bempedoic acid and bempedoic acid with ezetimibe according to the commercial arrangement. Bempedoic acid with ezetimibe can be used as separate tablets or a fixed-dose combination. • Reference: Bempedoic acid with ezetimibe for treating primary hypercholesterolaemia or mixed dyslipidaemia Technology appraisal guidance Reference number:TA694. Published: 28 April 2021 NICE guidelines • See NICE CG238 on lipid modification. Also see NICE CG71 on familial hypercholesteroleamia • NHS England have produced a visual summary PDF document based on NICE guidance CG238 and CG71 (see next page) • Also, Health Innovation Yorkshire and Humber have produced this interactive link based on the NICE guidelines, Please see this link: https://www.healthinnovationyh.org.uk/lipid-management-tool/ • Lifestyle and Pharmacological Management Lifestyle Modifications Adopt a low saturated fat diet, exercise regularly, maintain healthy weight, limit alcohol, and avoid tobacco. Statin Therapy Statins like atorvastatin inhibit cholesterol synthesis and are first-line treatment for hypercholesterolaemia. Alternative Pharmacological Treatments Ezetimibe, bile acid sequestrants, fibrates, and monoclonal antibodies offer options for statin intolerance or familial cases. Cholesterol Targets Recommended cholesterol targets vary with cardiovascular risk, with stricter goals for high-risk patients. Monitoring and Education Regular lipid and liver function tests and patient education are vital for effective management and risk reduction. TAKE TIME TO LEARN THIS DIAGRAM! Stable angina Definition and Symptoms Stable angina causes chest pain due to reduced blood flow during exertion or stress, relieved by rest or GTN. Cause and Pathophysiology It results from fixed coronary artery narrowing by plaques, causing oxygen supplydemand mismatch in the heart muscle. Diagnosis Methods Diagnosis is clinical and supported by history, examination, ECG, exercise testing, and imaging to assess severity. Symptoms of Stable Angina Typical Chest Pain Stable angina causes retrosternal tight, gripping pain often radiating to arms, neck, jaw, or back. Associated Autonomic Symptoms Symptoms include breathlessness, sweating, pallor, and rapid heartbeat during angina episodes. Triggers and Relief Symptoms are triggered by exertion, stress, or cold and relieved by rest or GTN medication. Diagnostic Features Predictable, reproducible chest pain pattern and positive GTN response support diagnosis of stable angina. Pathophysiology of chronic angina Coronary Artery Obstruction Atherosclerotic plaque narrows coronary arteries by over 70%, reducing blood flow and leading to ischemia during exertion. Oxygen Supply-Demand Mismatch Increased heart rate and stroke volume during activity raise myocardial oxygen demand exceeding supply, causing ischemic pain. Symptom Relief by Vasodilation GTN dilates coronary arteries, enhances blood flow, and relieves ischemic chest pain by improving oxygen supply. Management and Control Controlling heart rate, blood pressure, and physical activity helps balance oxygen demand and reduce stable angina symptoms. NICE-Based Drug Treatment Immediate Relief Treatments Glyceryl trinitrate (GTN) provides rapid relief by dilating coronary arteries during angina attacks. Symptom Frequency Reduction Beta-blockers and calcium channel blockers reduce angina attack frequency and symptom severity effectively. Secondary Prevention Drugs Antiplatelets, high-intensity statins, and ACE inhibitors lower risk of heart attacks and improve outcomes. Lifestyle Modifications Smoking cessation, healthy diet, and exercise are vital for comprehensive angina management. Summary of Stable Angina Management Condition Overview Stable angina results from fixed coronary artery narrowing causing exertion-related chest pain relieved by rest or GTN. Pharmacological Management Treatment includes GTN for immediate relief, beta-blockers, calcium channel blockers, and drugs for cardiovascular risk reduction. SEE NICE CG 126. Patient Education and Lifestyle Education and lifestyle modifications improve outcomes and prevent progression to acute coronary syndromes. Follow-up and Monitoring Regular check-ups ensure treatment efficacy, adherence, and ongoing management of stable angina. Drugs used in stable angina • Glyceryl trinitrate (sublingual spray). • Calcium channel blockers (dihydropyridine types and diltiazem) • Beta-blockers • Long-acting nitrates (e.g. Isosorbide mononitrate)- note counsel patient on issues with tolerance. • Potassium channel activators • Ivabradine • Ranolazine • NICE CG126: Stable angina: management (2016). • NICE guideline CG126 provides a summary of managing stable angina by prioritizing optimal drug therapy with beta-blockers or calcium channel blockers as the first step. If drug therapy isn't enough, it recommends revascularisation (PCI or CABG). The summary also includes a focus on providing comprehensive information and support, lifestyle advice, and psychological support, while also outlining when to consider specialist care. • 1. Initial drug treatment • Start with anti-anginal drugs: • Offer optimal drug treatment with one or two anti-anginal drugs plus medications for secondary prevention of cardiovascular disease. • First-line therapy: • Beta-blockers or calcium channel blockers are usually the first-line treatments. If symptoms are not improved or are problematic, your doctor may adjust the dose, try a different drug, or a combination of two drugs. • Avoid combinations: • Non-DHP calcium channel blockers should not be combined with beta-blockers. NICE CG126 extracts Under Principles • 1.4.5 Review the person's response to treatment, including any side effects, 2 to 4 weeks after starting or changing drug treatment. • 1.4.6 Titrate the drug dosage against the person's symptoms up to the maximum tolerable dosage. • Drugs for treating stable angina • 1.4.7 Offer either a beta blocker or a calcium channel blocker as first-line treatment for stable angina. Decide which drug to use based on comorbidities, contraindications and the person's preference. • 1.4.8 If the person cannot tolerate the beta blocker or calcium channel blocker, consider switching to the other option (calcium channel blocker or beta blocker). • 1.4.9 If the person's symptoms are not satisfactorily controlled on a beta blocker or a calcium channel blocker, consider either switching to the other option or using a combination of the two. When combining a calcium channel blocker with a beta blocker, use a dihydropyridine calcium channel blocker, for example, slow release nifedipine, amlodipine or felodipine. • 1.4.10 Do not routinely offer anti-anginal drugs other than beta blockers or calcium channel blockers as first-line treatment for stable angina. NICE CG126 extracts continued • 1.4.11: If the person cannot tolerate beta blockers and calcium channel blockers or both are contraindicated, consider monotherapy with one of the following drugs: • a long-acting nitrate or • ivabradine or • nicorandil or • ranolazine. Decide which drug to use based on comorbidities, contraindications, the person's preference and drug costs……………… Since this guidance was produced, the Medicines and Healthcare products Regulatory Agency (MHRA) have published new advice about safety concerns related to ivabradine (June 2014 and December 2014) and nicorandil (January 2016). NICE CG126 extracts continued • 1.4.12 For people on beta blocker or calcium channel blocker monotherapy whose symptoms are not controlled and the other option (calcium channel blocker or beta blocker) is contraindicated or not tolerated, consider one of the following as an additional drug: • a long-acting nitrate or • ivabradine or • nicorandil or • ranolazine. Decide which drug to use based on comorbidities, contraindications, the person's preference and drug costs. Acute Coronary syndromes (ACS) Blood clot Overview of ACS Definition of ACS ACS includes conditions caused by sudden reduced blood flow to heart muscles from plaque rupture and clots. STEMI Characteristics STEMI is caused by complete artery blockage, leading to full-thickness heart muscle damage. NSTEMI Features NSTEMI results from partial artery blockage causing subendocardial, or partial thickness, necrosis. Unstable Angina Overview Unstable angina causes unpredictable chest pain without muscle damage but risks heart attack progression. Pathophysiology of ACS Plaque Rupture and Thrombus Formation Rupture of atheromatous plaque exposes lipid core, triggering platelet aggregation and thrombus formation in coronary arteries. STEMI and Myocardial Necrosis STEMI involves complete artery occlusion causing full-thickness, irreversible myocardial necrosis rapidly. NSTEMI and Subendocardial Damage NSTEMI features partial or intermittent occlusion leading to subendocardial myocardial damage. Unstable Angina Characteristics Unstable angina manifests as transient or partial occlusion without myocardial necrosis but high progression risk. ECG Changes in STEMI and NSTEMI ACS TYPE ECG CHANGES STEMI ST elevation, T wave inversion, Q wave formation NSTEMI ST depression, T wave inversion Unstable Angina Transient ST changes or normal ECG Clinical Presentation of ACS Chest Pain Characteristics ACS patients often experience central chest pain that may radiate to arms, jaw, neck, or back and feels crushing or tight. STEMI Symptoms STEMI presents with severe, sudden, prolonged chest pain over 30 minutes not relieved by rest or GTN. NSTEMI and Unstable Angina NSTEMI symptoms develop gradually and are less intense; unstable angina occurs at rest or worsens newly. Autonomic Symptoms Autonomic signs include pallor, clamminess, tachycardia, breathlessness, sweating, nausea, and anxiety. Cardiac Markers in ACS Role of Troponin Biomarkers Troponin I and T are critical for diagnosing myocardial infarction due to their high sensitivity and specificity. Troponin Levels in ACS Types STEMI shows high troponin elevation; NSTEMI moderate elevation; unstable angina usually normal levels. Timing and Measurement Troponin should be measured at presentation and 10–12 hours later to capture peak levels accurately. Clinical Importance Elevated troponin levels indicate increased risk and guide aggressive management in acute coronary syndrome. NICE-Based Management of STEMI Rapid Reperfusion Therapy Immediate PCI within 120 minutes is preferred for STEMI patients with ST-segment elevation. Thrombolytic Therapy Alternative When PCI is unavailable, thrombolytic agents like alteplase or tenecteplase are administered promptly. Initial Supportive Care Supportive treatments include oxygen, nitrates, and opioids to relieve pain and improve oxygenation. Antiplatelet and Anticoagulant Therapy Aspirin, clopidogrel or ticagrelor, along with heparin or fondaparinux, prevent further clot formation and reocclusion. NICE-Based Management of NSTEMI and Unstable Angina Risk Stratification Tools NICE recommends using GRACE or TIMI scores to stratify patient risk and guide treatment decisions. Initial Pharmacological Therapy Dual antiplatelet therapy and anticoagulants are used initially to prevent clot progression and reduce mortality. Additional Cardiac Medications Beta-blockers, statins, and ACE inhibitors stabilize plaques and support heart function in vulnerable patients. Invasive and Long-Term Management High-risk patients may receive early angiography and PCI; long-term care includes lifestyle changes and monitoring. Issues/Drugs to consider in Management of ACS • • • • • • • • • • • • • Check NICE guidelines NG185 for management of STEMI and NSTEMI/Unstable and compare the two. Visual summaries available. Initial management vs long term management. Also, oxygen and morphine usually given in acute attack/infarction. Thrombolysis vs. PCI Antiplatelet Antithrombotic drugs Nitrates Beta-blockers ACEI insulin Eplerenone statin The overall aims for STEMI management and the drugs principally used to address them can be summarised as follows: • 1. Provide initial supportive care/pain relief (oxygen, nitrates, strong opioids) • 2. Promote reperfusion/reduce mortality (aspirin, PCI, thrombolytic drugs) • 3. Reduce re-occlusion and systemic embolization (anticoagulants) • 4. Reduce mortality further (aspirin, beta-blocker, ACEI, statin) HEART FAILURE A quick summary HEART FAILURE (with a focus on Chronic Left sided with reduced EF) • Heart becomes too weak to pump efficiently, thus it cannot meet the metabolic demands of the body. • Could be due to previous MI, hypertension, heart valve abnormalities, cardiomyopathy or other causes. • Elevated serum levels of NT-proBNP (above 400 ng/litre)- biomarker released when ventricle expands following excessive pressure. • The BNP tells your blood vessels to open wider and your kidneys to get rid of water and salt through urine. This helps reduce the workload on the heart by lowering blood pressure and reducing the preload/amount of blood your heart has to pump. • Echocardiogram- helps exclude valve disease, assess systolic vs diastolic function of left ventricle & gives insight into the ejection fraction (EF) and any back flow that is occurring. • Heart Failure with reduced EF is when EF <40% (normal EF is between 50-70%). Heart Failure (with a focus on Chronic Left sided with reduced EF) • CO = HR x SV • SV proportional to Contractility x End diastolic volume Peripheral resistance • • • • End diastolic volume: preload Peripheral resistance: afterload CO is reduced in HF, RAAS is activated spiralling decline occurs. HF can be chronic or acute (e.g. acute exacerbation of chronic HF). Signs and Symptoms of HF • Pulmonary congestion/oedema: dyspnoea, gasping, orthopnoea, PND (a sensation of shortness of breath that awakens the patient, often after 1 or 2 hours of sleep, and is usually relieved in the upright position), nagging (persistent) cough, basal crackles……. • Peripheral congestion/oedema: pitting ankle oedema, raised JVP, ascites, weight gain…. • Reduced perfusion: fatigue, pallor, confusion/ slowness of thought, renal failure, cold extremities. • Tachycardia • Weakness • Cardiomegaly, 3rd and 4th heart sounds and other cardiac signs See NICE NG 106: Chronic heart failure in adults: diagnosis and management NYHA Classification • Class I: No limitation during normal physical activity. • Class II: Slight limitation of physical activity/on moderate exercise, e.g. walking/climbing stairs. Comfortable at rest but ordinary physical activity results in undue breathlessness, fatigue, or palpitations. • Class III: Marked limitation of physical activity. Symptoms occur on minimal exertion, e.g. walking in the flat. Comfortable at rest but less than ordinary physical activity results in undue breathlessness, fatigue, or palpitations. • Class IV: Breathlessness at rest— unable to carry out any physical activity without discomfort. Symptoms at rest can be present. If any physical activity is undertaken discomfort is increased. See NICE NG 106 According to the recent NICE guidelines (Sept 2025). Note: neprilysin is a circulating enzyme that degrades natriuretic peptides Drugs acting on RAAS and neprilysin inhibition • Image from Lang, C., Struthers, A. Targeting the renin–angiotensin–aldosterone system in heart failure. Nat Rev Cardiol 10, 125–134 (2013). https://doi.org/10.1038/nrcardio.2012.196 SGLT-2 inhibitors • Dapagliflozin and Empagliflozin • They have recently been recommended as options for treating symptomatic chronic heart failure with reduced ejection fraction in adults. • Their effects include improved cardiac metabolism, reduced inflammation, reduced cardiovascular death and reduced hospitalisations due to heart failure. Ivabradine • Ivabradine is also licensed for use in patients as an additional option for symptomatic patients <35% (or as an alternative to betablockers where contraindicated) who have a pulse of => 75 bpm. Sinus rhythm. • It should be initiated under specialist supervision in patients who have been stable on optimised standard therapy for at least 4 weeks. Sacubitril Valsartan • Sacubitril valsartan (brand name: Entresto®) has also been approved by NICE as a specialist option for patients with symptomatic chronic heart failure with reduced ejection fraction (NYHA classes II-IV; EF <= 35%) who are taking a stable dose of an ACE inhibitor or ARB. Drugs used in HF • ACEI/ARB • ARNI (Sacubitril/Valsartan) • Beta-blockers e.g. nebivolol • MRA: spironolactone or eplerenone • SGLT2-inhibitor: e.g. Dapagliflozin • Diuretic e.g. Furosemide • Digoxin (or dobutamine) • Ivabradine if EF <35% and sinus rhythm HR >75. • Nitrates or hydralazine if intolerant to ACEI/ARB/ARNI. Examples of Drugs to avoid in HF X Rate limiting calcium-channel blockers e.g. Diltiazem and verapamil– their negative inotropic actions, mean they can worsen heart failure as they’ll decrease myocardial contractility and heart rate. X NSAIDs- risk of hypervolaemia (due to sodium & water retention) which can worsen HF. X Antacids with high sodium content X effervescent tablets generally. Thank you ! Heart failure Case Case • Mr. AM; 81 year old male; Caucasian; BMI 21 • • PMH: HTN (10 years); OA (8 years); 1o open angle glaucoma (recently diagnosed) • SH: Widower; lives alone in a two-storey house; independently mobile; Drinks 4-6 units/month of beer • FH: Nil of note • PC: Has been experiencing progressive difficulty in mobilising over the last few weeks due to SOBOE- Now having difficulty climbing the stairs. Over the last week the neighbours are now shopping for him as he now can’t even walk on the flat without getting out of breath. His ankles have also begun to swell – the GP prescribed bendroflumethiazide 2.5mg om last week. The breathlessness is now occurring at night-time and he is having to open the windows to get fresh air. Frequently wakes up coughing at night – his neighbour brought him back a “cough bottle” from the chemist for his “frothy phlegm.” Propping himself up helps the cough most but he’s not getting much sleep and is tired enough as it is lately. • Drug Hx on admission: • Atenolol 100mg od • Diltiazem XL 180mg od • Bendroflumethiazide 2.5mg om • Naproxen 500mg tds • Co-codamol 8/500 ii prn • G. Timolol 0.5% • Benylin Mucus Cough Menthol; NKDA • • • • • • • • • • • • • • • • • Results: OE: Pale; bilateral pitting oedema; Weight 65Kg BP: 158/85 HR: 110 reg (60-100) T 36.7 TC 5.3mmol/L Random blood glucose 6.5mmol/L U&Es: Cr 221 micromol/L; Urea 9.2mmol/L (2.5-6.5); K+ 4.5mmol/L (3.5-5.3); Na+ 148mmol/L (133-149) LFTs: NAD TFTs: NAD Bloods: NAD ECG: NAD JVP  HS: S1 + S2 + 0 CXR : Bat’s wing shadowing; bilateral Kerley B lines Echo: LVEF = 34% NT-pro BNP: 3010 pg/ml (9-86) 1. Using the patient’s signs, symptoms and investigations explain the SPECIFIC diagnosis (including specific type and/or classification if appropriate) and the underlying pathophysiology. Provide a definition for this overall condition. 2. Comment on the possible aetiology of this condition in Mr AM The aims of management of chronic heart failure include the following: •Reduce mortality •Delay disease progression/reduce exacerbations •Control symptoms •Improve quality of life/exercise tolerance…………. 3. Propose a treatment plan for the patient including medication you would discontinue and add. Also consider titration, monitoring and counselling 4. Explain the pharmacological actions of your chosen drugs and the rationales for using them Case continued.. • The patient was started on medication as per the recent NICE guidelines for chronic heart failure. Later on, he complains of a bit of excessive thirst and sometimes dizziness and reckons it is one of the new drugs that he has been initiated on. He also complains that he is sometimes having to go to the toilet more often at night. He asks you which one it is. 5. Provide an interpretation of this adverse effect and what should be done. • Some months later, the patient was admitted to hospital with an acute exacerbation with significant oedema. While being an inpatient, the following 2 new drugs were initiated. • Furosemide 40mg tablets, 1 tablet o.m. • Digoxin 62.5 mg tablets, 1 tablet o.d. • 4 days later, you are the Pharmacist doing your ward round and you notice that the HR measured by the nurse one hour ago has gone down to 50 bpm. 6. Provide an explanation of this HR and what should be done.