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Cardiology Part 1: Finals2Foundation DR MUHAMMAD IBRAHIM DR RAEES ZAEEMContents Part 1 ▪ ACS – Angina, N/STEMI ▪ Infective endocarditis ▪ Myocarditis ▪ Pericardial disease Part 2 ▪ ECG interpretation ▪ Tachyarrhythmias ▪ BradyarrhythmiasDebra, 60F, presented complaining of difficulty doing ADLs •On further questioning she reports a sensation in the centre of her chest whenever she starts working around the house •It has been going on for 3-4 weeks, but she didn’t think much about it as it would stop when she sat down. •She does not report any instances when sat down but is worried future episodes may not subside with rest. •She smokes 10/day and has done since she was in her early 20s •A glass of wine with meals on weekends and no recreational drug use •Her BMI is 30 Stable Angina • Syndrome of chest pain on exertion secondary • Clinical features: to myocardial ischaemia • Different to unstable angina, which is classified • Chest pain on exertion – squeezing, pressure, heaviness under ACS • Subsides with rest or after GTN in around 5 mins – key component for • Aetiology: stable angina • Atherosclerosis – primary cause • Radiation of pain – classical • Other compounding factors: coronary artery vasospasm, aortic stenosis, radiation to neck, jaw, left arm • If you have all 3 components = significant anaemia etc typical angina • RF – age, smoking, dyslipidaemia, • Other Sx: hypertension, DM, obesity etc. • Fatigue, SOB, nausea, sweating • DON’T FORGET – atypical Sx • Pathophysiology: such as SOB, weakness, • Complex, but underpinning idea - reduced fatigue, abdominal discomfort perfusion of myocardium • O/E - • Caused by atherosclerosis, unstable • Often normal if at rest, plaques rupturing, lining of blood vessels losing tone etc. depending on severity • Can have signs of underlying • Atypically can be caused through CVD coronary vasospasm - ? Cocaine use Stable Angina • Investigations: • Management: • Split into physical exam/ bedside tests, bloods and • Immediate sx relief scans ▪ Sublingual GTN ▪ Remember SE of dropping BP when • Physical exam – HS, HF signs, BP, BMI giving GTN • ECG (normal doesn’t rule out) • Long term sx relief ▪ Beta blocker/ CCB or combination • Bloods – FBC, U+E, LFT, Lipid profile, HbA1C, Troponin, • Use verapamil/ diltiazem for CCB BNP, CK monotherapy • If using a combo of beta blocker • CXR and CCB then use amlodipine • 1st line – CT coronary angiography or modified-release nifedipine as • 2nd line – non-invasive functional testing (stress tests) the CCB • 3rd line – Invasive coronary angiography • Don’t prescribe beta blocker and verapamil together ▪ Specialist can consider other additional meds such as ivabradine etc. • Secondary prevention ▪ Aspirin ▪ Atorvastatin • Surgery: ▪ PCI or CABGQuestion ▪ A 72-year-old man presents to his GP complaining of intermittent, exertional chest pain. He was diagnosed with stable angina a year ago. He still experiences chest discomfort when active. A recent ECG was normal. He is already on a maximum dose of bisoprolol and is wondering if there is anything further that we can do to help him. ▪ What is the most appropriate course of action for the GP to take? A: Prescribe amlodipine B: Prescribe ivabradine C: Discontinue bisoprolol and start isosorbide mononitrate D: Call ambulance and send to ED urgently E: Refer to cardiologists for an invasive coronary angiographyQuestion ▪ Which angina medication can patients often develop tolerance to? A: Amlodipine B: Modified release isosorbide mononitrate C: Nicorandil D: Ranolazine E: Standard release isosorbide mononitrate ACS - Unstable Angina • Classified as ACS • Syndrome of chest pain at rest or on minimal • Clinical features: exertion due to transient myocardial ischaemia • Chest pain at rest – squeezing, pressure, • Ischaemia without infarction heaviness • Typically, more than 20 minutes • Aetiology: • Radiation of pain – classical • Atherosclerosis – primary cause radiation to neck, jaw, left arm • Disruption of this plaque in a coronary artery -> partial or transient vessel • Other Sx: occlusion • Fatigue, SOB, nausea, sweating • Other compounding factors like stable • DON’T FORGET – atypical Sx such angina: coronary artery vasospasm, as SOB, weakness, fatigue, aortic stenosis, significant anaemia etc abdominal discomfort • O/E - • RF – age, smoking, dyslipidaemia, • Often normal but during episodes hypertension, DM, obesity etc. of angina: • S4 sound • Pathophysiology: • Hypotension • Same as stable angina - reduced • MR perfusion of myocardium • Signs of CCF – elevated JVP, • Caused by atherosclerosis, unstable peripheral oedema plaques rupturing, lining of blood vessels losing tone etc. ACS - Unstable Angina • Investigations - • Management - • The same as stable angina. Think about • Nitroglycerin – immediate chest pain that same process of splitting into sx sections • Aspirin 300 mg – continue indefintiely • Additional notes: unless CI ▪ Troponin should be tested • Second antiplatelet – typically immediately and then 3 hours after fondaparinux unless high bleeding risk sx onset. ▪ Risk stratification – GRACE score or or immediate angiography TIMII risk score (UA/ NSTEMI) • Long term Mx -•After 2 years, Debra, now 65F , presents to the ED with sudden onset chest pain while she was watching TV •Started 2 hours ago, suddenly with shortness of breath shortly after onset •Her son called the ambulance as she was in too much pain to stand and whilst waiting, she asked him to bring her GTN, which she used twice with no effect •Her angina has been worsening over the past 6 months, with frequent episodes at rest, but usually subside after 10-15 minutes or with GTN •When you walk into the resus bay, she looks pale and clammy and is clearly still in pain. There is a sick bowel on the side table ACS: N/STEMI • Classified as ACS • Clinical features - • Rupture of an atherosclerotic plaque AND partial or o Chest pain complete thrombosis of the infarct-related artery ▪ Classically left sided ▪ Pressure/tightness/crushing • Aetiology - ▪ Radiation to L. arm or neck o Age, male gender, FHx, Smoking, hypertension, o Dyspnoea DM etc. ▪ Can be the only sx on occasion o Sweating • Pathophysiology - o N+V o Develops in pt's that have ischaemic heart disease o Palpitations o This describes a build-up of fatty plaques within • Atypical sx - coronary arteries o Epigastric pain o This is caused by endothelial dysfunction, which is o Fatigue triggered by all the risk factors mentioned above o Syncope/ presyncope o The narrowing of the arteries will mean less blood • DON’T FORGET CAN PRESENT SILENTLY IN DIABETICS OR FEMALES reaches myocardium – angina o Sudden plaque rupture causing infarction – • O/E - STEMI/ NSTEMI o Anxious, restless, diaphoretic o Hypotensive o Tachy/ brady o Tachypnoea o Hypoxia -> cyanosisCoronary Territories ACS: NSTEMI • Investigations: • Management – • Split into physical exam/ bedside tests, bloods and o Think MONA scans ▪ Morphine – only severe pain ▪ O2 if sats <94 • Physical exam – as stated ▪ Nitrates – cautious of hypotension • ECG changes ▪ Aspirin 300mg – continue indefinitely unless CI o Second antiplatelet – typically fondaparinux unless high bleeding • Bloods – risk or immediate angiography ▪ Troponin – not required to diagnose a STEMI o Same treatment pathway as unstable angina ▪ At baseline and then repeat in ~ 3 hours ▪ FBC, U+E, LFT, Lipid profile, HbA1C, BNP, CK • CXR • Echocardiogram - mainly looking LV function • Cardiac rehabilitation and secondary prevention ACS: STEMI • Investigations: • Management – • Split into physical exam/ bedside tests, bloods and o Think MONA scans ▪ Morphine – only severe pain ▪ O2 if sats <94 • Physical exam – as stated ▪ Nitrates – cautious of hypotension in inferior STEMI • ECG changes ▪ Aspirin 300mg – continue indefinitely unless CI o Then assess for eligibility of reperfusion therapy • Bloods – ▪ Troponin – not required to diagnose a STEMI ▪ At baseline and then repeat in ~ 3 hours • If presented within 12 hrs of sx • If presented within 12 hrs of sx ▪ FBC, U+E, LFT, Lipid profile, HbA1C, BNP, CK onset AND PCI can be done within onset AND PCI can't be done 120 mins within 120 mins • CXR • ANGIOGRAPHY with follow on • FIBRINOLYSIS • Echocardiogram - mainly looking LV function primary PCI • Antithrombin at the same time • Dual antiplatelet therapy: aspirin + • ECG 60-90 mins later prasugrel/ clopidogrel • Dual antiplatelet therapy: aspirin + • Antithrombin drug prasugrel/ clopidogrel • Drug eluting stents • Cardiac rehabilitation and secondary prevention Question ▪ Avomiting. The shortness of breath is now improving, but still feels nauseas.arted 4 hours ago, associated with some nausea and ▪ Her obs were taken: o HR: 148 bpm o RR: 18/min o BP: 132/89 mmHg ▪ Atroponin levels are normal. What is the most likely diagnosis? T waves in V2-3 and 0.5mm ST depression in the same leads. The A: Ruptured AAA B: Community acquired pneumonia C: STEMI D: NSTEMI E: Unstable angina Question ▪ A 72-year-old man presents to ED. He has a history of crushing chest pain, scored 8 out of 10, which started one hour ago. He is a smoker. ▪ After an ECG and troponin testing, he is diagnosed with non-ST segment elevation myocardial infarction (NSTEMI). as being low. The nearest primary percutaneous intervention unit is more than two hours away.leeding is assessed How should this patient be managed? A: Aspirin B: PCI C: Fibrinolysis D: Aspirin, fondaparinux and ticagrelor E: Aspirin, clopidogrel• John, a 40M, presents to his GP , to seek advice • He has been advised to have teeth removed by his Dentist. Following the appointment, he began searching about the procedure and found a tweet advising that people having teeth removed should have antibiotics to reduce risk of infection to his heart. • He was concerned by this advice as he was not told this by his dentist, and he has a family history of heart problems. • He booked the appointment to ask why he needs antibiotics and if the GP can prescribe them to him. Infective Endocarditis • Infection of the endothelium of the Heart • Modified Dukes criteria • Dx if…… • Classically affects the valves • Pathological criteria • 2 Major A • Aetiology: • IVDU – classically tricuspid valve is • 1 Major + 3 minor affected • 5 minor • Pathological – Biopsy, Autopsy, Surgery • Staph Aureus – common part of resulting inpositive microbiology orhistology skin flora • Major • 2 +ve Blood cultures for typical • Prosthetic Heart valves and Indwelling organisms lines • Persistent bacteraemia forless typical organism • Staph Epidermis most common • if native valves affected, classically • Positive serology or molecular Assay mitral valve • ECHO findings – Abscess, New Regurg, Vegetations (A) • Rheumatic heart disease • Minor • Predisposing condition or IVDU • Non-major criteria microbiology B • Poor dental hygiene • Fever >38 degrees • Strep Mitis and Sanguinis • Vascularphenomenon – Splinter • HACEK organisms – Haemophilus, Actinobacillus, Cardiobacterium, haemorrhage, Janeway lesions (B), • Immune phenomenon – Osler’s nodes Eikenella, Kingella (C), Roth spots C Infective Endocarditis • Management: • Prolonged IV ABx course • Penicillin (Vancomycin if • The Following conditions do not need allergic) + Gentamicin – prophylaxis for Infective endocarditis usual course depending on (according to NICE guidelines) specific organism + • Dental procedures sensitivities • Tooth extractions • If prosthetic valve, then • UGIT and LGIT procedures generally add rifampicin into • Gastroscopy, colonoscopy etc. the mix • Genitourinary procedures • Urological - Cystoscopy • Surgical indications • Gynaecological • Haemodynamic instability • Obstetric procedures • Severe heart failure • Routine childbirth • Failed medical therapy • Upper and Lower Respiratory tract • Recurrent emboli procedures • Infected prosthetic valve • Bronchoscopy • Aortic root abscess• Sarah, a 30F, has presented to SDEC with complaints of feeling generally unwell, lethargic and some intermittent chest pains for the past week • She has no risk factors for ACS and is usually very fit and well, volunteering as a netball coach in her spare time • When you read her notes, you notice multiple prescriptions for nasal decongestants over the past few months, and when questioned she reports that she has suffered from sinusitis and had been trying to get antibiotics from the GP . • When you examine her, you notice she is Diaphoretic and Feverish (which she reports has started 2 days ago), and looks generally unwell • When questioned further she reports the chest pains are sharp and worsen with breathing Pericarditis • Inflammation of the pericardium - membrane • Investigations - surrounding the heart • Diagnosis needs ¾: • Acute - < 4-6 weeks • Classical Sx – sharp central pain, positional, infective Hx • Aetiology: • Pericardial friction rub – V.difficult to • Viral infections (Coxsackie) hear • TB A • Autoimmune • Classical ECG changes (A) • Post-MI (inc. Dressler's syndrome) • ST elevation – saddle shape • Malignancy • PR depression • Spodick sign – TP downsloping • ECHO results – Pericardial effusion • Pathophysiology: • Inflammatory response with cell infiltration • Other • Irritation of pericardiumandformationof • Inflammatory bloods – FBC, CRP, ESR pericardial effusion • CXR – assess cardiac contour and lungs • Clinical features: • U+Es – uraemic pericarditis • Retrosternal chest pain – sharp, central, pleuritic, worse when lying downandbetter • Management - when sitting forward, worse with deep • Colchicine and NSAIDS breaths • Steroids – if underlying inflammatory disease • Coryzal symptoms • Treat underlying chronic disease – e.g. CKD • Dyspnoea • Non-productive cough • Pericardiocentesis if concerns about size of pericardial effusion and tamponadeQuestion ▪ A 65-year-oldman presents with a 2-week history of dyspnoea. He also mentions that it has become more difficult for him to walk over this same time. On examination, he has a raised JVP that doesn't fall with inspiration. His lung bases are clear and a pericardial knock is heard on auscultation. When palpating his abdomen you also feel that his liver is enlarged. His only past medical history is angina for which he was recently investigated with a coronary angiogram. Given this presentation, which of the following is the most likely cause of his presentation? A: Myocarditis B: Acute pericarditis C: Acute heart failure D: Constrictive pericarditis E: Cardiac tamponade Myocarditis • Inflammation of the myocardium – middle portion • Investigation • Bloods of the cardiac wall • Inflammatory markers raised • Aetiology • Cardiac enzymes raised • Viral – coxsackievirus, HIV, EBV • BNPraised • Bacterial and Fungal – less common • ECG – can truly mimic MI so care needs to be taken • Diphtheria, Clostridia • STE + TWI +/- reciprocal changes • Lyme • Nodal block • Chagas, toxoplasmosis • Can coexist with pericarditis • Drugs – Cyclophosphamide, Doxorubicin • Metals – Copper, Iron, Lead, Lithium • ECHO • Cardiac MRI • Inflammatory and Autoimmune – GPA, SLE • Management • Treat underlying cause • Acute and HD stability • Supportive care • ACE-i/ARB for LV dysfunction • Acute and HD unstable • Vasodilators andcardiac support • End-stage – Dilated cardiomyopathy • Cardiac transplant • LV assist devices▪ NICE guidance - https://www.nice.org.uk/guidance/ng185 ▪ Passmedicine - https://www.passmedicine.com/menu.php?revise=all ▪ Zero to finals - https://zerotofinals.com/medicine/cardiology/ ▪ Life in the fast lane - https://litfl.com/acute-coronary-syndromes/Cardiology Part 2: Finals2Foundation DR MUHAMMAD IBRAHIM DR SYDNEY KUDAContents Part 1 ▪ ACS – Angina, N/STEMI ▪ Infective endocarditis ▪ Myocarditis ▪ Pericardial disease Part 2 ▪ ECG interpretation ▪ Tachyarrhythmias ▪ Bradyarrhythmias ECG Interpretation • Name, Age, D.o.B, Location of patient (1) ▪ Demographics + Settings • Time ECG was taken and context (Both Generally why the ECG was done, but also what the clinical status of the patient was at the time of the ECG ▪ Rate • ECG machine settings – Normally 25mm/second paper speed and 10mm/mV gain (3) ▪ Rhythm 1 ▪ Axis ▪ Intervals ▪ P wave ▪ QRS ▪ ST segment and T wave 3 ECG Interpretation ▪ Demographics + Settings ▪ Rate ▪ Rhythm ▪ Axis ▪ Intervals ▪ P wave ▪ QRS ▪ ST segment and T wave ECG Interpretation • Is the rhythm?: ▪ Demographics + Settings 1. Regularly Regular – repeating units with regular pattern and even spacing e.g. ▪ Rate Normal Sinus Rhythm (1) 2. Irregularly irregular – No obvious patterns with uneven spacing e.g. AF (2) 3. Regularly irregular – Group beating visible, repeating units but with visible gaps and ▪ Rhythm clear pattern e.g. Heart block (3) ▪ Axis 1 2 ▪ Intervals ▪ P wave ▪ QRS ▪ ST segment and T wave 3 ECG Interpretation ▪ Demographics + Settings • Axis can be used to refer to the average direction of transmission of electrical activity of any component of the ECG but is usually used to describe the QRS • Can be used to estimate the location of the Atrial/ventricular pacemaker ▪ Rate ▪ Rhythm ▪ Axis ▪ Intervals ▪ P wave ▪ QRS ** only truly LAD if lead II is ▪ ST segment and T wave negative (the same direction as aVF ECG Interpretation • Left Axis deviation – Causes include ▪ Demographics + Settings • LVH ▪ Rate • LBBB • Left Anterior Fascicular/Hemi Block • Right sided accessory pathways / WPW Type B ▪ Rhythm • Ostium Primum ASD due to AV valve involvement • Obesity ▪ Axis ▪ Intervals • Right Axis deviation – Causes include • RVH • Cor-Pulmonale ▪ P wave • PE ▪ QRS • Left Posterior Fascicular/Hemi Block • Left sided accessory pathways / WPW type A • Ostium Secundum ASD ▪ ST segment and T wave • Normal in young children usually < 1 years age • Tall people ECG Interpretation • PR Interval ▪ Demographics + Settings • Normal range – 120-200 m/s – 3-5 small squares ▪ Rate • Measured from start of P wave to start of QRS • Long PR – normal in younger people and athletes, AV Blocks • Short PR – accessory pathways / WPW, atypical Atrial pacemaker/s, Junctional ▪ Rhythm rhythms ▪ Axis • QT interval ▪ Intervals • Inversely proportional to Heart rate and so quantified using QTc ▪ P wave • Normal range – 350 - 440(m)/460(F) • QT is measured from start of QRS ▪ QRS • Long QTc - Hypo-K/Mg/Ca/thermia, raised ICP, Congenital Long QT syndrome, Myocardial ischaemia • Short QTc – Hypercalcaemia, digoxin, Congenital Short ▪ ST segment and T wave QT syndrome ECG Interpretation • Signifies Atrial depolarisation and contraction – starting in the SA node and depolarising the right ▪ Demographics + Settings atrium in an infero-antero-lateral direction, crossing into the left atrium via Bachman’s bundle and the depolarising in a largely posterior direction. ▪ Rate • Normal pacemaker site (SA node) and conduction direction can be approximated: • Upright P waves in lead I – right to left conduction ▪ Rhythm • Upright in inferior leads (II, III, aVF) – top-down conduction • Biphasic in V1 – back to front in right atrium, and front to back in left atrium • The right side of the P wave correlates with the right atrium and left side correlates with the left ▪ Axis atrium (A) – as seen in lead II • Enlargement of either atria causes the corresponding aspect of the P wave to enlargen ▪ Intervals Causes of Left atrial enlargement: • Mitral stenosis/regurgitation ▪ P wave • Hypertrophic cardiomyopathy Causes of Right atrial enlargement ▪ QRS A • Cor-pulmonale • Pulmonary hypertension ▪ ST segment and T wave • Tricuspid stenosis/regurgitation ECG Interpretation ▪ Demographics + Settings • QRS complex signifies ventricular depolarisation and contraction • 3 components can be viewed, but not always present in every lead • Q wave – initial negative deflection not following an R wave ▪ Rate • R wave – any positive deflection, if following S wave, then considered R’ • S wave – any negative deflection following an R wave • Normal QRS – 80-120ms (2-3 squares) ▪ Rhythm • widening could be due to Bundle Branch block, Pacemaker rhythm, Ventricular ectopic focus ▪ Axis ▪ Intervals ▪ P wave ▪ QRS ▪ ST segment and T wave ECG Interpretation RBBB ▪ Demographics + Settings • Block of the Right bundle leads to depolarisation fromleft to right • QRS length>120ms (3 small squares) • Textbook presentation can be remembered with MarroW (A) ▪ Rate • V1 – RSR’ with invertedT wave • V6 – QRS with wide (slurred) S wave A • Causes: ▪ Rhythm • Right Ventricularstrain – Cor-Pulmonale, PE, • Congenital - Atrial septal defects ▪ Axis • Ischaemia – new RBBB can be a sign of MI • Left Ventricularpacing ▪ Intervals LBBB B • Block of the Left bundle leads to depolarisation from right to left • QRS length>120ms (3 small squares) ▪ P wave • Textbook presentation can be remembered with WilliaM(B) • V1 – QS with upright T wave • V6 – R wave withnotching (looks like anM) ▪ QRS – Bundle Branch Block • Causes: • Ischaemia – New LBBB can be a sign of MI • Aortic stenosis ▪ ST segment and T wave • Left VentricularHypertrophy • Right Ventricularpacing ECG Interpretation • The ST segment is measured between the endof the S wave (called the J point) and the start of the T wave (not ▪ Demographics + Settings always super obvious) • ST segment deviation (Elevation or Depression) is commonin many conditions but most commonly associated withmyocardial ischaemia ▪ Rate • Many causes of ST segment deviation: • Myocardial ischaemia – STE in leads associated with area of injury andSTD in reciprocal leads ▪ Rhythm • Pericarditis – STEwidespread withsaddleback morphology, STD usually only present inaVR/V1 • BenignEarly Repolarisation – STEin various leads, often minimal compared with QRS amplitude and can have J point notching – Fish-hook (A) ▪ Axis • LBBB – STE and STD normally minimal and inopposite direction to the rest of the QRS (discordance) • Left ventricular Hypertrophy • Brugada syndrome – STEin V1-2 with Coved Brugada sign (B) ▪ Intervals B A ▪ P wave ▪ QRS ▪ ST segment and T wave ECG Interpretation A • The T wave represents Ventricular repolarisation following depolarisation. ▪ Demographics + Settings • Normal T wave presentation – upright in all leads except aVR and V1 • Can become abnormal for various reasons (examples below) • Hyperkalaemia – Tall, peaked with a sharp-ish point (A) ▪ Rate • Hypokalaemia – Flatter and wide, withU wave present • Myocardial ischaemia – ▪ Rhythm • Hyperacute T waves – Wide, symmetrical androunded T waves, look very big inrelation to associated QRS (B) • Inverted T waves – usually areciprocal change in active MI, can represent reperfusion of MI ▪ Axis • Raised ICP – Deep, and verywide T wave inversion (resulting in long QTc) usually inV1-6 • Juvenile T waves – T wave inversion across V1-3 • PE – T wave inversion in V1 (+V2 and V3) andlead III (C) ▪ Intervals B C ▪ P wave ▪ QRS ▪ ST segment and T waveBreak ANY QUESTIONS WELCOME Tachyarrhythmias - AF • Very common Arrhythmia, can be both acute • Other investigations and chronic • Bloods – FBC, CRP, TFTs, U+Es, Mg, Bone Profile, Cultures (context of Sepsis) • ECHO – dilated atria, Mitral Valve disease, visible Atrial Fibrillation, LV • Aetiology • Sepsis dysfunction • Valvular disease – usually mitral • Polysomnography/sleep study– Assess for sleep apnoea • Ischaemic Heart Disease • Thyrotoxicosis • ECG • Normal, Brady or Tachy – although Normal/Tachy is what is most tested for • Hypertension Medical school • Lifestyle factors – alcohol, smoking, • Irregularly Irregular – no common pattern to the rhythm caffeine • Lack of organised Atrial activity – messy baseline, fibrillation waves • QRS usually narrow, but can be wide with coexisting LBBB/RBBB • Presentation of Atrial fibrillation • Asymptomatic! • Chest pain • Palpitations • Dyspnoea • Anxiety • Secondary disease symptoms – Stroke, sepsis, Thyrotoxicosis Tachyarrhythmias - AF • Management • Acute • Haemodynamic instability = • If stable, then consider duration • <48 hours – rate or rhythmcontrol • >48 hours – rate control (oranticoagulated for 3 weeks) • Treat underlying issues – fluid resus insepsis can reverse AF caused by Sepsis • Rate vs Rhythm question • Generally, Rate control preferred • Rhythm control better for – younger pts, HF secondary to AF, neweronset • Rate control • BBs, CCBs, Digoxin(second line) • Rhythm control (Pharmacological cardioversion) • Amiodarone, flecainide (if not structural disease) • Cardioversion • Electrical orchemical • If AF onset >48 hours, then3 weeks of anticoagulation neededor…. • TOEto rule out Left atrial appendage thrombus Tachyarrhythmias - AF • Anticoagulation • AF represents a true ischaemic stroke risk due to turbulent blood flow • CHADSVASC is the key • 0 – No treatment required • 1 – Males – consider Anticoagulation, Females – No treatment required • 2 – Anticoagulation required • To Assess bleeding risk - use ORBIT • Choice of anticoagulant • Classically Warfarin – now second line • DOACs – first line – no regular monitoring needed unlike warfarin • Remember using –XABAN suffix • Following CVA • If TIA – start anticoagulant once bleed r/o – CT usually • If stroke – start anticoagulant after 2 weeks with bridging antiplatelet therapy Tachyarrhythmias - Atrial Flutter • Atrial Flutter represent an SVT with veryfast regular atrial activity in the form of flutter waves • Can appear like a Sawtooth pattern(A) whichis usually best seen in leads II andV1 • The speed of atrial activity is too fast for the AV node to conduct so an element of block occurs with regular pattern of flutter waves (saw teeth) to QRS complexes – this is usually represented as a ratio e.g. 2:1 or 4:1 • Keyto recognition is the rate of atrial activity (usually between 250- 350 bpm • Andthe Ventricular rate will be a factor of this atrial rate e.g. A VR of 75bpm when 4:1 block present • Can be variable block where the ratio is not fixed the whole time • management • Very similar to AF and the same drugs canbe used • Susceptible to radiofrequencyablationof the source of re- entrycircuits – oftenthe tricuspid valve isthmus Tachyarrhythmias – AVNRT/AVRT D These are Re-entry related SVTs in a similar way to Atrial A flutter • AVNRT (A) – re-entry based around the AV node • AVRT (B) – re-entry based around an accessory pathway Presentation: • Usually, younger patients with… • New onset SoB, palpitations, chest pain,syncope ECG basics: • Fast rhythm • Normally Narrow complex QRS – except Antidromic AVRT (C) • Lack of clear P waves – atrial activity is usually in the form of retrograde conduction, and can happen during or after the QRS – (usually best seen as a pseudo-R’ in V1 [D] or S wave in II) Management • 1st line – Vagal Manoeuvre’s – e.g.modified C Vandalva, Carotid Sinus massage B • 2 line – Adenosine (6/12/18mg) in a large bore cannula • DC cardioversion Long term management • Rate control measures • Ablation of re-entry circuits/accessory pathways Tachyarrhythmias - VT A • Arrhythmia originating in the ventricles of the heart, ratherthan the atria orAV node. • Can be either Monomorphic (one source of stimulus) or Polymorphic (alternating) – Torsades de Pointes is a type of PmVT • Presentation • Cardiac arrest – one of the shockable rhythms • Chest pain - coronary hypoperfusion • Syncope – cerebral hypoperfusion C • Dyspnoea, diaphoresis, confusion B • Asymptomatic • Investigations • A-E assessment • ECG – including assessment of recent ECGs if possible • Bloods – troponin, electrolytes, infectionmarkers D • Drug chart analysis • ECHO – structural heart disease such as HOCM ECG: • Wide complexes - >120ms due to originating in the ventricles and not usually following the • Management • Presence of fusion (B) or capture beats (C) from co-existing and competing supraventricular • If unstable or medical Mxfails– urgent DC cardioversion rhythm • Drug therapy – amiodarone normally, Lidocaine, procainamide • PmVT – alternating axis of the rhythm i.e. alternates between pointing up and down (D) – looks • For TdP – MgSO4 like a spiral to some people (or an Arctic Monkeys album cover) • ICD – particularly if heart failure inassociation Tachyarrhythmias - VF • Disorganised rhythm originating fromthe ventricles • Incompatible with propercardiac output • Results in cardiac arrest • Aetiology • ACS – ischaemic myocardium acts as focus • Electrolyte issues – long QT -> PmVT -> VF • Hypoxia • Congenital issues • Drugs • ECG • Very messy baseline • Very messy complexes • No visible supraventricular activity • Management: • BLS -> ALS – cardiac arrest algorithms • CPR • Defibrillation • Drugs – Amiodarone/Lidocaine • Correct underlying issues • ICD insertion – prevent further episodes of cardiac arrestQuestion A 46-year-old woman presents to the emergency department with 30 minutes of an acute, severe headache with nausea and vomiting. She describes the headache as unbearable, reaching maximum intensity within 5 minutes of its onset. She has neck stiffness and photophobia, but is afebrile, with no rashes or focal neurological deficits. Her pupils are equal and reactive, and she has had no seizures. During the assessment, she develops palpitations and dizziness and an ECG is performed. Her ventricular rate is 180 bpmand irregular. Which finding is most likely to be seen on the ECG? A. Atrial Fibrillation B. Sinus tachycardia C. SVT D. Tosardes de Pointes E. VFQuestion A 62-year-oldwoman presents to her GP describing occasional episodes of 'afluttering heartbeat'. These occur between once a week and once a month and are not associatedwith any other symptoms. Onexamination, the patient's heart rate is 60 beats per minute andregular. Her bloodpressure is 115/80mmHg. The patient has no past medical history, takes no medications and has no allergies. The results of some investigations are shown below: What is the most appropriate management? A. The patient does not require anticoagulation as her AF is not permanent B. The patient does not require anticoagulation as overall stroke risk is low C. Start warfarin D. Start apixaban E. Start aspirin Bradyarrhythmias Bradyarrhythmias are abnormal heart rhythms with a heart rate of <60 beats per minute (bpm) AETIOLOGY - Physiological causes: due to increase in vagal tone SYMPTOMS • Diving reflex - Confusion,dizziness, light-headedness, brain fog/memory • Athlete’s heart • Vagal manoeuvres,Valsalva manoeuvre deficit, chest pain/tightness, syncope, fatigue, dyspnoea • Respiratory-induced sinus arrhythmia (expiration phase) SIGNS - Pathological causes: usually due to abnormalities with impulse generation or signal - Raised JVP and cannon-a waves in the JVP conduction - Peripheralcyanosis/pallor • Cardiac causes- usually due to abnormalities with impulse generation or signal - Thyroid mass/goitre conduction ➢ SAN causes: sinus pause/arrest, SA exit block, sick sinus syndrome - Hypothermia nd rd - Features of raised ICP ➢ AVN causes: 2 degree AV block- Mobitz II & II,3 degree AV block, Junctional rhythm INVESTIGATIONS ➢ Other: idioventricular rhythm, cardiac ischaemia, Myocarditis, idiopathic - 12 lead ECG fibrosis/sclerosis ➢ Cardiac surgery - Bloods:routine, TFT, Troponin, Mg, glucose, tox screen, drug • Non cardiac causes levels if suspected (e.g. digoxin) - 24 hr Holter monitor ➢ Autoimmune: SLE - Echocardiogram ➢ Drugs: beta-blockers, CCBs(verapamil,diltiazem), negative inotropes, - CXR ivabradine - CT head ➢ Hypoglycaemia, hypo/hyperkalaemia,hypothermia, hypoxia ➢ Infection: myocarditis, Lyme disease, salmonella typhi, legionnaires' disease, Chagas disease ➢ Trauma: raised ICP (Cushing's reflex) Bradyarrhythmias – 1 Degree AV Block st Consistent prolongation of the PR Interval (> 0.20s). ECG findings - Rhythm: regular - P wave: every pwave present and followed by a QRS complex - QRS complex: normal morphology and duration (<0.12s) Management: Usually asymptomatic - Stop any AV blocking drugs - No intervention if asymptomatic - Consider pacemaker if symptomatic Complications - May progress to higher grade AV blocks - Increased risk of AF Bradyarrhythmias – 2 Degree AV Block (Mobitz nd Type 1) Progressive prolongationof the PRInterval until a QRS complex is dropped. AV nodal conduction then resumes with the next beat and the sequence repeats itself. ECG findings - Rhythm: irregular - P wave: every pwave present but not all are followed by a QRS complex - QRS complex: normal morphology and duration (<0.12s), but are occasionally dropped Management: Usually asymptomatic but although rare, can cause haemodynamic compromise - Stop any AV blocking drugs - No intervention if asymptomatic - Consider pacemaker if symptomatic - Followresus guidelines if haemodynamically unstable Complications - Can cause haemodynamic compromise Bradyarrhythmias – 2 Degree AV Block (Mobitz nd Type 2) Consistent PR Interval duration with intermittently droppedQRS complexes. The intermittent dropping of the QRS complex repeating cycle of every 3 (3:1 block) or 4 (4:1 block) P wave. ECG findings - Rhythm: irregular(may be regularly irregular in 3:1 or 4:1 block) - P wave: P waves present but not always followedby a QRS complex - QRS complex: could be normal (<0.12s) orbroad (>0.12s) Management: - Prompt cardiac monitoring due to risk of progression to complete AV block - Atropine 500mcg IV (repeated to a max of 3mg), Isoprenaline 5mcg/minIV, adrenaline 2-10mcg/min IV OR transcutaneous pacing - Permanent pacemakerusually inserted if no reversible causes identified Complications - Progression to complete AV block - Risk of asystole Bradyarrhythmias – 3 Degree AV Block rd Occurs due to complete conduction failure between atria and ventricles. There is therefore no association between atrialand ventricular electrical activity. Cardiac function is maintained by a junctional or ventricular pacemaker. ECG findings - Rhythm: variable - P wave: P waves present but not related to the QRS complexes - QRS complex: o Normal (<0.12s) in narrow complex escape rhythms originating above the bifurcation on the bundle of his. Typical HR >40bpm o Broad (>0.12s) in broad complex escape rhythms originating below the bifurcation of the bundle of his. These are usually slower leading to worse clinicalfeatures (e.g. heart failure, syncope etc) Management: - Prompt cardiac monitoring - Atropine 500mcg IV (repeated to a max of 3mg) [broad complex escape rhythms unlikely to respond], Isoprenaline 5mcg/min IV, adrenaline 2-10mcg/min IV OR transcutaneous pacing - Permanent pacemaker usually required Complications: - Risk of asystole or sudden cardiac death due to ventricular arrhythmias or ventricular standstillQuestion A 56-year-oldmanisbrought tothe Emergency Department. He works as a window cleaner. Hiscolleague describes him suddenly falling from the ladder without warning. On admission he isconscious witha bradycardiaofaround36/min.His bloodpressure is 110/62 mmHg andhe is wellperfusedwith no signs of heart failure.An ECG is takenonaccount ofhis bradycardia: A previousECG taken four monthsagowas completely normal. Whatisthe most likely diagnosis? B. Stokes-Adams attack with associatedcomplete heart block C. Mobitz type I D. Mobitz type II E. MI withnew LBBBQuestion A 75-year-old man presents to the emergency department following an episode of syncope with acute fatigue and shortness of breath. He has a past medical history of ischaemic heart disease. His pulse is 43 bpm, his blood pressure is 84/43 mmHg, his respiratory rate is 25 /min, and his temperature is 37.1ºC. The patient appears unwell and is sweating, with cold and clammy extremities. A 500 microgram IV bolus of atropine is given, however, the patient remains unwell. This is repeated 5 more times and despite this, he remains unwell. What is the most appropriate next step in his management? A. IV adenosine B. IV atropine infusion C. Immediate DC cardioversion D. Immediate Transcutaneous pacing E. Refer for transvenous pacingBRADYCARDIA RESUS GUIDELINES THANK YOU QUESTIONS? References: - Zero to Finals - Almost a Doctor - NICE guidelines - Pulsenotes - Life in the Fast Lane - Resuscitation Council UK - Mind The Bleep - Geeky medics - Life in the fastlane