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Cardiovascular Medicine For Finals. Outline. ECG’s Arrhythmias Acute coronary syndromes Heart failure Infective Endocarditis Cardiomyopathies Valvular heart disease. ECG approach. Patient details Calibration Rate Rhythm Axis P waves QRS complex ST complex. ECG values. Values:
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Outline • ECG’s • Arrhythmias • Acute coronary syndromes • Heart failure • Infective Endocarditis • Cardiomyopathies • Valvular heart disease
ECG approach • Patient details • Calibration • Rate • Rhythm • Axis • P waves • QRS complex • ST complex
ECG values Values: • PR interval: 120-200ms (3-5 small squares of ECG paper) • QRS complex: less than 120ms (3 small squares) • QT interval (upper limit of normal is 450ms in men and 470ms in women)
Myocardial infarction: • ST elevation definition: • More than 2 mm’s of elevation in two congruent chest leads or more than 1mm ST elevation in two congruent limb leads • Myocardial infarction definition: - 2 of 3 from: Chest pain, ECG changes, Trop rise
Atrial fibrillation • Causes: • Ischaemic heart disease • Valvular disease • Hypertension • Hyperthyroidism • Electrolyte imbalances • Sepsis
Rhythm vs rate control Cardio-vert if: • Less than 65 • AF for less than 48 hours • Structurally normal heart Otherwise: • Rate control with a beta blocker • If contra-indications to beta blocker or LV impairment then use digoxin (as positively inotropic)
CHA2DS2VASC Latest ESC guidance: 0 = No treatment 1 = Consider oral anticoagulant (warfarin) 2 or more = warfarin No role for aspirin in the current guidance http://www.escardio.org/guidelines-surveys/esc-guidelines/GuidelinesDocuments/Guidelines_Focused_Update_Atrial_Fib_FT.pdf C = 1 for congestive heart failure (EF<35%) H = 1 for hypertension A = 2 if > 75 D = 1 if diabetic S = 2 if previous stroke, TIA or systemic emboli V = 1 if previous MI, PVD or aortic plaque A = 1 if age 65-74 S = 1 if female c
Anti-arrhythmic medications • Some Block Potassium Channels Class 1: Sodium channel blockers Class 2: Beta blockers Class 3: Potassium channel blockers Class 4: Calcium channel blockers Digoxin and Adenosine
Class I • 1A: Quinidine, procainamide, disopyramide Prolong action potential and are used for SVT’s and VT’s Side effects: N & V, anti-cholinergic, Hypotension, precipitate SLE • 1B: Lignocaine, tocainide Shorten the action potential and used in VT’s Side effects: Convulsions, N & V • 1C: Flecainide Slow conduction speed and used in SVT’s and VT’s Side effects: Arrhythmias & dizziness
Class II • Eg. Propanolol and atenolol block the increase in pacemaker activity that is produced by sympathetic stimulation of B-adrenoreceptors • Used for ectopic beats, AF and atrial tachycardia • Side effects: Tiredness and asthma NB. Sotalol ad bretylium have both class II and III actions
Class III • Eg. Amiodarone block K+ channels slowing repolarisation leading to a prolonged action potential and refactory period • Used in SVT’s and VT’s • Side effects: Photosensitivity, Blue/grey skin discolouration, Liver toxicity, Thyroid disorders, Neuropathy, Pulmonary alveolitis
Class IV • Eg. Verapamil block Calcium channels thereby decreasing spontaneous activity at both the SA and AV node • Used for SVT’s • Side effects: Precipitation of cardiac failure, AV block and constipation
Class V • Digoxin: Used for SVT’s especially AF Side effects: N & V, green-yellow vision, blurred vision, confusion, heart block, gynaecomastia NB. Potentiated by Hypokalaemia • Adenosine: Used to terminate SVT’s
Acute coronary syndromes • ST elevation myocardial infarction (ST elevation or new LBBB), non-ST elevation myocardial infarction, or unstable angina • Symptoms: Chest pain or tightness radiating to the jaw or left arm. May be associated with sweating, nausea and vomiting or shortness of breath
Treatment R = Reassurance O = Oxygen (15 litres non-rebreathe mask) M = Morphine A = Aspirin (300mg) N = Nitrates C = Clopidogrel (300mg – some centres 600 if for angioplasty) E = Enoxoparin (This trust clexane 2.5mg S/C)
STEMI and Non-STEMI • STEMI: once confirmed should be for PCI with the ACA recommending less than 90mins for door to PCI time. (If PCI not available: thrombolysis within 30 mins) • NSTEMI: ACS protocol of aspirin, clopidogrel and LMWH. 12 hour trop which if positive warrants urgent coronary angiography (ie. Next elective list)
TIMI Score - Age > 65 • Aspirin in last 7 days • At least 2 episodes of angina in last 24 hours • ST deviation (elevation or depression) of at least 0.5mm on ECG • Elevated Trop • Known CAD • At least 3 risk factors • Scores risk of MI and death and informs treatment
Heart Failure • Broadly divided in 2 categories: • Those that damage cardiac muscle (eg IHD and cardiomyopathies) • Those that demand extra work of the heart (eg systemic hypertension, valvular heart disease)
Pathophysiology • Decrease in contractility of the affected heart muscle • This shifts the Starling curve to the right reducing the force of contractility for a given filling pressure • Body attempts to increase filling pressure by: • Catecholamine release: Increasing rate and force • Vasoconstriction: Increases filling pressure • Renal retention of Na and water
Effect of this response • Effective for a while BUT: • Leads to dilatation: which can cause valvular disease • Increases oxygen demand: This predisposes the heart to ischaemia • Downregulation of B-adrenoreceptors: This stops the effect of increased sympathetic drive
Treatment • Heart failure can present as an acute exacerbation ie. Pulmonary oedema (predominantly left sided failure) or chronically with leg swelling (predominantly right sided) • Treatment can be acute ie. Offloading with diuretics and also prognostic
ACE inhibitors • Eg. Enalapril, Lisinopril, and Captopril: • Block production of angiotensin II and therefore aldosterone • Prevent the breakdown of bradykinin • Prolong life in heart failure Produce vasodilation thereby decreasing afterload and subsequent oedema
Beta blocker • The sympatholytic effects of beta-blockers have been shown to be beneficial in the long term management of heart failure • They act by slowing the heart rate and thereby increasing diastolic filling time NB. Not to be used in the treatment of acute heart failure
Spironolactone • Antagonise the effect of aldosterone or block Na channels at the distal tubule • Prevents Na reabsorption and K excretion • Shown to prolong life in heart failure • Main side effect is hyperkalaemia especially when used with ACE inhibitors
Digoxin • Cardiac glycosides inhibit the Na/K pump which leads to a rise in intracellular Ca which: • Increases the force of contraction • Reduces the hearts oxygen consumption • Slows heart rate through vagal effect • Side effects: Anorexia, N & V, Diarrhoea, Confusion, Arrhythmia in toxic doses
Non-drug treatment of heart failure • CRT: Patients with heart failure often have left bundle branch block – this leads to dys-synchrony in the ventricular contraction. Pacemakers that synchronise left and right ventricular function therefore increase cardiac output • ICD’s: Patients with heart failure are prone to malignant arrhythmias. ICD’s can prevent sudden cardiac death • Heart transplantation: With appropriate selection 1 year survival is 80% and 5 year 70%
Endocarditis • Infection of the endocardium usually involving the heart valves • Usually affects damaged valves and itself damages valves predisposing to future infections • Vegetations (consisting of fibrin, platelets and infecting organism) usually arise on the valves • Sequelae of infective endocarditis include: • Acute valve incompetence • Emboli to spleen, kidneys and brain • Glomerulonephritis and renal failure
Organisms: • Streptococcus viridans: subacute; common after dental procedures, tonsillectomy or bronchoscopy • Staph aureus: acute and common in IVDU’s and indwelling catheters • Enterococcus faecalis: common after pelvic surgery • Coxiella burnetti (Q fever): subacute • Staphylococcus epidermidis, aspergillus, candida, brucella, histoplasma: common in IVDU’s and prosthetic heart valves
Cardiomyopathies • 3 types: • Dilated (congestive) cardiomyopathy (85%) with dilated left ventricle and impaired systolic function • Hypertrophic (obstructive) cardiomyopathy (10%) hypertrophy of ventricles partciularly septum – reduced diastolic filling • Restrictive cardiomyopathy (5%): decreased ventricular compliance restricts ventricular filling
Dilated cardiomyopathy • Pathogenic factors include: • Genetic defect • Alcohol toxicity • Postviral myocarditis • Peripartum • Haemochromatosis • Systemic disease (eg. Sarcoid, SLE) • Drug therapy (eg. Cyclophosphamide) etc
Dilated cardiomyopathy • Morphology of cardiomyopathy is: • Cardiomegaly with dilated thin walls in all chambers • Irregular myocyte hypertrophy and fibrosis • Dilated cardiomyopathy can cause heart failure, arrhythmia and emboli • Mortality is 40% in 2 years
Hypertrophic cardiomyopathy • Hypertrophy of ventricles and septum which is often asymmetrical • Causes distorted contraction and an abnormal mitral valve movement • 50% of cases are inherited 9autosomal dominant • Can cause dyspnoea, angina, syncope, and sudden death NB. Death is normally due to ventricular arrhythmias rather than outflow obstruction
Restrictive cardiomyopathy • Restrictive cardiomyopathy is stiffening of the myocardium with restricted ventricular filling. • Often associated with: • Amyloidosis: most common in the West • Endomyocardial fibrosis: children and young adults in Africa • Loeffler’s endocarditis: temperate climates • Symptoms are similar to constrictive pericarditis
1) Mitral stenosis • Causes: • Rheumatic fever • Congenital eg. Lutembacher’s syndrome • Malignant (carcinoid) • SLE • Left atrial myxoma