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In-patient management of A-FIB and A-Flutter

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Description

In this session we will cover the following:

aims

  • To understand the mechanisms of atrial flutter and atrial fibrillation
  • To describe the clinical history and examination of These patients
  • To understand the investigations required in the assessment.
  • To understand the treatment options available

Objectives

  • To describe the potential causes of AF
  • To present to you cases showing various clinical presentations of AF which will help you understand how to decide on anticoagulation for patients
  • To describe the current approaches to restoring sinus rhythm and controlling the ventricular rate in patients with AF.

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Computer generated transcript

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The following transcript was generated automatically from the content and has not been checked or corrected manually.

THE MANAGEMENT OF ATRIAL FLUTTER & FIBRILLATION DR. BRENDEN WALKER LOCUM REGISTRAR• AIMS • TO UNDERSTAND MECHANISMS OF ATRIAL FLUTTER AND ATRIAL FIBRILLATION • TO DESCRIBE THE CLINICAL HISTORY AND EXAMINATION OF THESE PATIENTS • TO UNDERSTAND THE INVESTIGATIONS REQUIRED IN ASSESSMENT • TO UNDERSTAND THE TREATMENT OPTIONS AVAILABLE • OBJECTIVES • TO DESCRIBE THE POTENTIAL CAUSES FOR AF • TO PRESENT TO YOU CASES SHOWING VARIOUS CLINICAL PRESENTATION OF AF WHICH WILL HELP UNDERSTAND HOW TO DECIDE ON ANTICOAGULATION FOR PATIENTS • TO DESCRIBE THE CURRENT APPROACHES TO RESTORING SINUS RHYTHM AND CONTROLLING THE VENTRICULAR RATE IN PATIENTS WITH AF. JANET 1ST ED ATTENDANCE • BIBA: PALPITATIONS AND DYSPNOEA, STRONG SMELL OF ALCOHOL. • NO PMH, NO REGULAR MEDICATIONS, NKDA • O/E HR 160BPM, NORMOTENSIVE, CRT. <2SEC • PALE AND SWEATY BUT WARM TO TOUCH • S/E WELL THROUGHOUT HER ANNIVERSARY PARTY, THEN DEVELOPED PALPITATIONS FOLLOWED BY LIGHTHEADEDNESS. NO OTHER SYMPTOMS • PHYSICAL EXAMINATION: NORMALLying BP 114/82 Standing bp 112/84 Bloods • Hb 141g/L, WCC 4.5, Plts 325 • Na 140mmol/L, K 4.6mmol/L, Urea 3.7mmol/L, Creatinine 64umol/L • INR 1.0, APTTr 1.0, Fib 2.3 • Troponin 2.3nmol/L, HbA1c 38mmol/mol, LDL 1.0mmol/L. • (TSH, Paracetamol and salicylate levels awaited)ECG shows an irregular narrow complex tachycardia. P waves are irregular and R-R intervals variable. You make a diagnosis of new onset atrial fibrillation. TREATMENT • WHAT SHOULD YOU CONSIDER NEXT? • VAGAL MANEUVRES, ADENOSINE • ANTICOAGULATION • RATE CONTROL, RHYTHM CONTROL • WHERE SHOULD SHE BE MANAGED? • ED RESUS, MAJORS, MINORS, AMBULATORY CARE, COMMUNITY SETTING • ADMISSION • CARDIAC MONITORING • IS SHE SAFE FOR DISCHARGE IS SHE SPONTANEOUSLY CARDIOVERTS? MARK RESUS 1 • BIBA: PROGRESSIVE DYSPNOEA, CHEST TIGHTNESS, PALPITATIONS, ORTHOPNOEA, PND. • PMH: HYPERTENSION, CABG • SOCIAL: ETOH EXCESS, EX-SMOKER, PREVIOUS RECREATIONAL DRUG USE • DH: AMLODIPINE, INDAPAMIDE, VALSARTAN, NKDA • ON ARRIVAL, CRITICALLY ILL, GCS 13/15 • O/E: RR 30, SPO2 74% ON 60% FIO2 VIA NON-REBREATHE MASK, PULSE 240 AND BP 65/40. CRT>5 SEC MARK CLINICAL ASSESSMENT • HIS PULSE IS WEAK AND THREADY, IRREGULAR AND IRREGULAR WITH A RATE OF 240BPM. • BILATERAL AUDIBLE CREPITATIONS WILL STONY DULL PERCUSSION AT THE BASES • JVP IS RAISED BY 4 CM. • PANSYSTOLIC MURMUR OF MITRAL REGURGITATION HEARD IN THE MITRAL AREA • HIS APEX IS DISPLACED TO THE LEFT INFERIORLY. • S3 GALLOP RHYTHM CAN BE HEARD. • MILD PERIPHERAL OEDEMA AND NO ASCITES. BROAD COMPLEX TACHYCARDIA SAW TOOTH APPEARANCE SAW TOOTH P WAVES APPEAR TO FALL IN A RATIO OF EITHER 1:1, 3:2 OR 2:1 WITH THE QRS COMPLEXES P WAVES ARE NEGATIVE IN LEADS II, III AND AVF TREATMENT • FOLLOW ALS PROTOCOL • CALL FOR HELP: CARDIAC ARREST OR MET CALL • ABC APPROACH • FOLLOW NARROW COMPLEX ALGORITM WHEN TREATING ATRIAL FLUTTER, THIS PARTICULAR RHYTHM IS NOT VT • CONSIDER TEP/DNAR STATUS • DC CARDIOVERSION WITH POST-ITU CARE ONGOING CARE • INVESTIGATIONS • THYROID FUNCTION • ECHO, CARDIAC ANGIOGRAM, CARDIAC MRI • RENAL/ADRENAL MRI AND CATECHOLAEMINE SCREEN IF RESISTANT HYPERTENSION • POST ITU CARE • 4 WEEKS ANTICOAGULATION FOLLOWING DCCV • CONSIDER LIFELONG ANTICOAGULATION • DECIDE ON STRATEGY TO MAINTAIN SINUS RHYTHM • DECIDE ON STRATEGY FOR RHYTHM CONTROL • CONSIDER HEART FAILURE MANAGEMENT ATRIAL FLUTTER PHYSIOLOGY • CAUSED BY A MACRO RE-ENTRANT CIRCUIT LOCATED IN THE RIGHT ATRIUM • 60% UNDELYING CORONARY ARTERY DISEASE OR HYPERTENSION • TYPICAL FLUTTER TRAVELS IN A COUNTER CLOCKWISE WAY- NEGATIVE P WAVES • REVERSE TYPICAL FLUTTER TRAVELS IN A CLOCKWISE WAY- POSITIVE P WAVES • ATYPICAL FLUTTER ORIGINATES OUTSIDE OF THE TRICUSPID ISTHMUS IN LEFT OR RIGHT ATRIUM JANET PRIVATE CONSULTATION • HOW DID SHE GET A FIB? • DOES SHE NEED TO BE CONTINUED ON ANTICOAGULATION? • WHAT ARE HER OPTIONS? • IS AF TRANSMISSIBLE TO OTHERS? • WHAT OPTIONS FOR RATE OR RHYTHM CONTROL OFFER THE BEST QUALITY OF LIFE AND LEAST IMPACT ON DAILY LIFE? ATRIAL FIBRILLATION PHYSIOLOGY • DEVELOPMENT OF ATRIAL FIBRILLATION IS BELIEVED TO BE DUE TO AN INITIATING FOCUS FOLLOWED BY CONTINUOUS ATRIAL REMODELING WHICH FURTHER CAUSES IT TO PERSIST. • THE OSTIUM OF THE PULMONARY VEINS IN THE LEFT ATRIUM IS A NOW RECOGNIZED ECTOPIC FOCUS • THE PRESENCE OF MULTIPLE FOCI MAKE IDENTIFYING SUITABLE ABLATION APPROACHES SOMETIMES MORE CHALLENGING JANET’S EMAILS ”DEAR DOCTOR, I HOPE MY EMAIL FINDS YOU WELL. I HAVE HAD PALPITATIONS WHILE READING THE SIDE EFFECT LIST OF BISOPROLOL SO I FEEL PREPARED TO CHOOSE DILTIAZEM. HOWEVER MY ACQUAINTANCE BARBARA FINDS USING FLECAINIDE AS A PILL IN THE POCKET USEFUL. I LIKE THIS IDEA, HAVING CONTROL OF MY A FIB. I SHALL CONTACT MY GP LATER TODAY FOR ADVICE” SENT FROM MY IPHONE “Dear colleague, I was surprised by my visit today from Janet as I understand that you have agreed to manage her atrial fibrillation. She has had more palpiatations and I am at my wits end as to how to treat these, I have considered Propranolol. She doesn’t mind taking Eliquis. I look forward to hearing how you get on with her investigstions.” CARDIAC CAUSES OF AF • Mitral valve disease • Tricuspid valve disease Raised atrial • Left ventricular dysfunction pressure • Pulmonary hypertension • Intra-cardiac tumours or thrombus Atrial • Severe ventricular ischaemia more commonly leads to raised intra-atrialAF pressure and AF ischaemia • Pericarditis Inflammation • Collagen vascular disease • Viral or bacterial infections • Cardiac, oesophageal or thoracic surgery POST ITU •and dapagliflozinfailure treatment with betablocker,entresto, eplerenone • Other antihypertensives stopped. Developed chest symptoms on Metoprolol Heart Team • CTPA confirmed infective COPD exacerbation, resolved pulmonary oedema • COPD diagnosed with lung function tests Respiratory • Treated with steroids, ipratropium nebs, Doxycycline andTazocin Team • Agreed to commence Nebivolol in hospital with monitoring • Medical therapy maximised so referred for CRT-D device • Atrial flutter not since recurred following DCCV • High risk AF so bridged from LMWH to Apixaban 5mgBD Heat team Non Cardiac Caused of AF Noncardiovascular Alcohol and drug use Endocrine disorders Neurological Disorders Familial Associations Age respiratory causes 1)Pulmonary embolism 1)Stimulants, 1)Hyperthyroidism 1)Subarachnoid Sodium channel 1)0.1% age less than methamphetamine haemorrhage disorders 55 1)Alcohol (Holiday or 1)Pneumonia Saturday night heart 1)Diabetes 1)Stroke 1)3.8% age over 60 causing alcohol related years cardiomyopathy) 1)Lung Cancer 1)Cocaine 1)Phaeochromocytoma 1)10% age over 80 years 1)Hypothermia TYPES OF AF Recurrent episodes Paroxysmal each lasting <7 days Persistent Any episode of AF lasting >7 days Longstanding Presence of AF >12 Persistent months Palpitations Chest pain KEY FEATURES Dyspnoea Syncope Oedema Irregular-irregular pulse Cardiac murmur Displacement of the cardiac apex Ischaemic heart disease & S3 sound Valvular heart disease Surgical scars Congential heart disease Palpable liver, ascites and peripheral oedema Heart failure Pulmonary hypertension Elevated jugular venous pulse, Cardiac surgery or interventions tricuspid insufficiency and loud P2 Pulmonary oedema, pleural effusion JANET DECIDES JANET RETURNS FOR RESULTS • THYROID FUNCTION NORMAL • ADRENAL FUNCTION NORMAL • ECHOCARDIOGRAM NORMAL • 7 DAY MONITOR SHOWS PAROXYSMAL AF, SOMETIMES ASYMPTOMATIC SHE AGREES TO COMMENCE DILTIAZEM 240MG MR AND WILL CONTINUE APIXABAN YOU OFFER AN OPEN APPOINTMENT MARK 2 YEARS ON • FOLLOWED UP BY COMMUNITY HEART FAILURE, RHYTHM DISTURBANCE AND DEVICES TEAMS • REQUIRED ORAL AND INTRAVENOUS DIURETICS • NYHA 2 BREATHLESSNESS • HOSPITALIZATIONS FOR ARRHYTHMIA AND DECOMPENSATED HEART FAILURE • RECURRENCE OF ATRIAL FLUTTER THEN FIBRILLATION • DC CARDIOVERSION • ATRIAL FLUTTER ABLATION • AFIB ABLATION • AV NODE ABLATION • CONSIDERING LAA APPENDAGE CLOSURE DEVICE JANET 3 YEARS ON • TRIALS OF DILTIAZEM, METOPROLOL AND BISOPROLOL NOT TOLERATED. • MANAGED TO GET AN ILR DEVICE (2 ND OPINION) • OPTED NOT TO TRY FLECAINIDE OR PROPAFENONE • NOT KEEN ON CHEMICAL CARDIOVERSION WITH IBUTILIDE, DOFETILIDE, VERNAKALANT, DRONEDARONE OR AMIODARONE DUE TO RISK PROFILES PRESENTED AND NEED FOR INPATIENT STAY • NOT KEEN ON DC CARDIOVERSION AS IT REQUIRES GENERAL ANAESTHETIC • OPTED FOR AF ABLATION UNDER LOCAL ANAESTHETIC BY PULMONARY VEIN ISOLATION, DISCHARGED AT 11AM • AFTER 6 MONTHS REMAINS IN SINUS RHYTHM SO OPTED TO HAVE ANTICOAGULATION AND RATE CONTROL STOPPED. • WILL MONITOR FOR RECURRENCE ON HER ILR.• THANK YOU FOR ATTENDING THIS SESSION • I WOULD LIKE TO INVITE YOU TO UTILIZE THE FOLLOWING RESOURCES FOR FURTHER READING • RESUSCITATION UK ADVANCED LIFE SUPPORT GUIDELINES • BRITISH HEART SOCIETY • EUROPEAN CARDIOLOGY SOCIETY • AMERICAN HEART ASSOCIATION