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Preclineazy Presenters HEART FAILURE & VTEs PATHOPHYSIOLOGY OF HEART FAILURE FEATURES OF HEART FAILURE MANAGEMENT OF HEART FAILURE THROMBUS FORMATION & ANTI-CLOTTING DRUGS ~45 MINS HEART FAILURETHE PUMP IN ALL ITS GLORY • EACH CARDIAC CYCLE CONSISTS OF SYSTOLE & DIASTOLE • IN DIASTOLE, THE MYOCARDIUM IS AT REST AND THE VENTRICLES FILL WITH BLOOD • IN SYSTOLE, THE MYOCARDIUM CONTRACTS TO ACTIVELY EJECT THE BLOOD OUT OF THE HEART • If either of these processes are faulty, the body is initially able to compensate. However, eventually, it may lead to heart failure. HEART FAILURE SYSTOLIC DIASTOLIC LEFT-SIDED RIGHT-SIDED HEART FAILURE can be distinguished using ejection fraction SYSTOLIC DIASTOLIC (HFrEF) (HFpEF) 20ml 20ml 50mL 50mL 50mL 20mL FAILURE TO PUMP FAILURE TO FILL NORMAL EDV, ↓SV REDUCED EDV, ↓SV REDUCED EF < 40% PRESERVED EFETIOLOGY OF HEART F AILURE SYSTOLIC HEART FAILURE COMMON GENERAL DIASTOLIC HEART FAILURE CAUSES Coronary artery disease, Dilated cardiomyopathy myocardial infarction, Restrictive cardiomyopathy Cardiac arrhythmias Hypertension Hypertrophic cardiomyopathy Myocarditis Diabetes mellitus Pericardial tamponade Valvular heart disease Constrictive pericarditis Renal disease Infilitrative disease e.g. haemochromatosis, amyloidosis MYOCARDIAL STRUCTURAL CHANGES Cardiac myocytes adapt to increased workload by assembling new sarcomeres PRESSHYPERTENSION OR VALVULAR STENOSIS VOLUVALVULAR REGURGITATION OR SHUNTS • New sarcomeres added in parallel, adjacent to • New sarcomeres added in series with existing existing sarcomeres sarcomeres • Growing muscle fibre diameter results in concentric• Muscle fibre length increases hypertrophy • Ventricles tend to dilate and the resulting wall • Ventricular wall thickness increases without an thickness can be increased, normal or decreased increase in chamber size HEART FAILURE ↓STROKE VOLUME ↓PERFUSION OF TISSUES COMPENSATOR Y MECHANISMS ↑ Renal water reabsorption ↓ Parasympathetic outflow to heart ↑ Heart rate ADH secretion ↓ LV function ↓ baroreceptor loading ↑ sympathetic ↑ contractility outflow ↓ Stroke ↓ Blood Peripheral vasoconstriction + volume pressure venoconstriction ↓ renal blood flow Activation of renin- angiotensin system ↑ Salt and Peripheral water retention vasoconstrictionDECOMPENSA TED HEART FAILURE PERSISTENT RAAS INCREASED FILLING & EXCESSIVE FILLING ACTIVATION & ADH VENTRICULAR PRESSURES CAUSE RELEASE PRESSURES DILATATION OF FILLING PRESSURES BECOME CAUSE CONGESTION IN VENTRICULAR WALLS EXCESSIVE PULMONARY CIRCULATION AS THE VENTRICLES DISTEND, THE AFTERLOAD INCREASES EXCESSIVE STRETCH OF CARDIAC ALVEOLAR OEDEMA (due to LV MYOCYTES (STARLING LAW) backpressure) DILATATION CAN ALSO CAUSE DISRUPTION OF AV VALVE DECREASED STROKE VOLUME PERIPHERAL OEDEMA (due to RV ANNULUS, LEADING TO backpressure) VALVULAR REGURGITATION PERSISTENT OXYGEN PERSISTENTLY HIGH TACHYCARDIA REQUIREMENTS OF LEVELS OF REDUCES THE DURATION OF HYPERTROPHIC ANGIOTENSIN II, DIASTOLE AND THUS THE DURATION OF CORONARY MYOCARDIUM ARE ALDOSTERONE & BLOOD FLOW AMPLIFIED CATECHOLAMINES WITH THE INCREASE IN CONTRACTILITY, MYOCARDIAL OWING TO INCREASED LEADS TO LEFT VENTRICULAR OXYGEN DEMAND IS INCREASED MYOCARDIAL CELL MASS. RIN CARDIAC METABOLISM,ES WHILE OXYGEN DELIVERY IS MYOCARDIAL THINNING AND REDUCED MYOCARDIUM BECOMES FIBROSIS VULNERABLE TO ISCHAEMIC INJURY HOWEXERCISE-RELATED FROM HYPERTROPHY?SYMPTOMS LEFT-SIDED HEART FAILURE • Dyspnoea GENERAL SYMPTOMS: • Orthopnoea FATIGUE • Paroxysmal nocturnal dyspnoea PALPITATIONS EXERCISE INTOLERANCE • Wheeze DIZZINESS • Dyspnoea • Ankle swelling DIAGNOSTICS: • Anorexia, nausea, B-type natriuretic peptide (BNP) abdominal discomfort • Secreted by LV in response to strain Nocturia • High BNP helps corroborate diagnosis RIGHT-SIDED HEART FAILURE NYHA CLASSIFICATION OF HEART FAILURE NYHA CLASS I NYHA CLASS II Mild symptoms No symptoms Slight limitation of physical activity: No limitation: ordinary exercise comfortable at rest but ordinary doesn’t cause undue fatigue, activity results in fatigue, palpitations dyspnoea or palpitations or dyspnoea NYHA CLASS III NYHA CLASS IV Severe symptoms Moderate symptoms Unable to carry out any physical Marked limitation of physical activity: activity without discomfort: symptoms comfortable at rest, but less than of heart failure are present even at ordinary activity results in symptoms rest with increased discomfort with any physical activityTREATMENT FIRST LINE: ACEi or Beta-blockers HEART SECOND LINE: aldosterone antagonist FAILURE DRUGS THIRD LINE (specialist-initiated): Digoxin, ivabradine, sacubitril-valsartan FIRST LINE: ACEi or Beta-blockers ACEi e.g. Ramipril ARBs BETA BLOCKERS ANGIOTENSIN-CONVERTING e.g. Candesartan e.g. Bisoprolol ENZYME INHIBITORS ANGIOTENSION II RECEPTOR BLOCKERS BETA-1 ADRENORECEPTOR First line for managing systolic COMPETITIVE INHIBITORS IN dysfunction-associated hf Selective for AT1R, so that CARDIAC TISSUE Angiotensin II binds to AT2R Reduce vasoconstriction, instead Negative chronotropic & negative aldosterone& ADH secretion and inotropic effect ventricular remodelling AT2R receptors have opposing effects to those of AT1R Can cause dry cough due to accumulation of bradykinin Used for patients intolerant to ACEi but more expensiveSECOND LINE: aldosterone antagonist PHYSIOLOGY OF WATER REABSORPTION GLOMERULUS FILTRATION ALDOSTERONE NAHCO 3 Na, Cl- (5%) Na+ H+ K+ PCT DCT Na (70&) COLLECTING DUCT Na+, K+ ADH (25%) 2Cl- H2O (70%) H2O IMPERMEABLE TO WATER LOOP OF HENLE LOOP DIURETICS E.G. FUROSEMIDE GLOMERULUS FUROSEMIDE PCT DCT Na+ Na+ Na+ COLLECTING DUCT Na+, K+ Na+ (25%) 2Cl- Na+ Na+ H2O IMPERMEABLE TO WATER LOOP OF HENLE THIAZIDIE DIURETICS E.G. BENDROFLUMETHIAZIDE GLOMERULUS FILTRATION BENDROFLUMETHIAZIDE Na, Cl- (5%) PCT DCT COLLECTING DUCT Na+ Na+ Na+ Na+ IMPERMEABLE TO WATER LOOP OF HENLE HYPOKALEMIA Loop & thiazide diuretics GLOMERULUS MORE K+ LEAVING = HYPOKALEMIA MORE H+ LEAVING = METABOLIC ACIDOSIS FILTRATION NAHCO 3 ALDOSTERONE Na, Cl- (5%) Na+ PCT DCT H+ K+ Na COLLECTING DUCT (70&) Na+ Na+, K+ ADH (25%) 2Cl- Na+ Na+ Na+ H 2 (70%) H 2 IMPERMEABLE TO WATER LOOP OF HENLE K+-SPARING DIURETICS E.G. SPIRONOLACTONE SPIRONOLACTONE GLOMERULUS MORE K+ STAYING = HYPERKALEMIA ALDOSTERONE Na+ PCT DCT H+ K+ COLLECTING DUCT ADH H 2 (70%) IMPERMEABLE TO WATER THIRD LINE (specialist-initiated): Digoxin, ivabradine, sacubitril-valsartan DIGOXIN IVABRADINE HCN channel blocker BLOCKS NA+K+ ATPase enzyme in cardiomyocytes, End result is increased concentration of Ca2+ in cell SACUBITRIL- VALSARTAN Positive inotrope Sacubitril: neprilysin inhibitor Valsartan: angiotensin receptor Useful in elderly, sedentary people blocker DIGOXIN TOXICITY: delayed after depolarizations, cerebral impairment, diarrhoea, dizziness, vision disorders, oesinophillia THROMBUS FORMA TION & ASSOCIATED DRUGS THE VIRCHOW TRIAD The 3 main pathophysiological components of thrombus formation HYPERCOAGULABILITY Increased platelet adhesion, thrombophilia, oral contraceptives, pregnancy, cancer ENDOTHELIAL VENOUS STASIS DAMAGE Varicosis, external pressure Inflammatory or traumatic on extremities, vessel injuries can lead to immobilization activation of clotting factors THE VIRCHOW TRIAD The 3 main pathophysiological components of thrombus formation HE’ s Virchow HYPERCOAGULABILITY Increased platelet adhesion, thrombophilia, oral contraceptives,percoagulability pregnancy, cancer Endothelial damage Venous stasis ENDOTHELIAL VENOUS STASIS DAMAGE Varicosis, external pressure Inflammatory or traumatic on extremities, vessel injuries can lead to immobilization activation of clotting factors Travel H ypercoagulable/ HRT Recreational drugs THROMBOEMBOLISM O ld (>60) M alignancy RISK FACTORS Blood disorders O besity/obstetrics Surgery/smoking Immobilization Sicknes(CHF/MI, IBD, nephrotic syndrome, vasculitis)THROMBOEMBOLISM RISK HASBLED SCORE ASSESSMENT ANTICOAGULANTS WARFARIN HEPARIN ANTIPLATELETS IV HEPARIN SC LMWH ASPIRIN CLOPIDOGREL /PRASUGREL/ TICAGRELOR DOACs FIBRINOLYTIC ALTEPLASE ANTI-THROMBOTIC DRUGS SUMMAR Y: MO A, indications, ADRs, contraindications Q U E S T I O N 1 Simon is a 58 year old male who has a 10 year history of hypertension. He also suffered a heart attack 3 A CLASS I years ago. He has come to his GP after he described feeling B CLASS II breathless when walking. He says he can no longer walk as far as he used to be during his daily dog walks. This breathlessness is sometimes accompanied by C CLASS III chest pain. This has had a significant impact on the exercise he is able to do, mainly due to the swelling he describes. D CLASS IV However, he is comfortable at rest. Where does Simon score on the New York Heart E CLASS V Association Classification? ANSWER ON THE ZOOM POLL Q U E S T I O N 1 Simon is a 58 year old male who has a 10 year history of hypertension. He also suffered a heart attack 3 A CLASS I years ago. He has come to his GP after he described feeling B CLASS II breathless when walking. He says he can no longer walk as far as he used to be during his daily dog walks. This breathlessness is sometimes accompanied by C CLASS III chest pain. This has had a significant impact on the exercise he is able to do, mainly due to the swelling he describes. D CLASS IV However, he is comfortable at rest. Where does Simon score on the New York Heart E CLASS V Association Classification? ANSWER ON THE ZOOM POLL Q U E S T I O N 2 John is a 76 year old man who was recently admitted to hospital following a pulmonary A Binds to factor IIa embolism. He tells his nurse that he hasn't been taking his prescribed Apixaban as B Binds to factor Xa instructed. John's CHADSVASc score is calculated to be 4, indicating that he does need anticoagulation therapy.. C Fibrinolysis Which of the following explains how John's D Stimulates anti-thrombin production medication works? E Vitamin K antagonist ANSWER ON THE ZOOM POLL Q U E S T I O N 2 John is a 76 year old man who was recently admitted to hospital following a pulmonary A Binds to factor IIa embolism. He tells his nurse that he hasn't been taking his prescribed Apixaban as B Binds to factor Xa instructed. John's CHADSVASc score is calculated to be 4, indicating that he does need anticoagulation therapy.. C Fibrinolysis Which of the following explains how John's D Stimulates anti-thrombin production medication works? E Vitamin K antagonist ANSWER ON THE ZOOM POLL Q U E S T I O N 3 Shirley comes into the GP for a medication review. She is currently being treated with A Bendroflumethiazide Ramipril and furosemide for hypertension but says that she has been troubled by a B Losartan persistent dry cough. The GP explains that this is a side effect of C Nifedipine the Ramipril and decides to change the Ramipril to a different drug. D Perindopril Which medication is most appropriate? E Digoxin ANSWER ON THE ZOOM POLL Q U E S T I O N 3 Shirley comes into the GP for a medication review. She is currently being treated with A Bendroflumethiazide Ramipril and furosemide for hypertension but says that she has been troubled by a B Losartan persistent dry cough. The GP explains that this is a side effect of C Nifedipine the Ramipril and decides to change the Ramipril to a different drug. D Perindopril Which medication is most appropriate? E Digoxin ANSWER ON THE ZOOM POLL Q U E S T I O N 4 Jenny is diagnosed with right sided heart A A wave failure. On examination she had a raised JVP . Which letter on the waveform below B C wave represents the bulging of the tricuspid valve into the right atrium, during ventricular systole? C X descent D V wave E Y descent ANSWER ON THE ZOOM POLL Q U E S T I O N 4 Jenny is diagnosed with right sided heart A A wave failure. On examination she had a raised JVP . Which letter on the waveform below B C wave represents the bulging of the tricuspid valve into the right atrium, during ventricular systole? C X descent D V wave E Y descent ANSWER ON THE ZOOM POLL PLEASE FILL OUT THE FEEDBACK FORM PLEASE TUNE IN TO OUR REMAINING SESSIONS THIS WEEK! @OSCEazyOfficial @osceazyofficial OSCEazy Osceazy@gmail.com