This cardiology teaching series part two will discuss Heart Blocks, AF (Fibrillation and Flutter), VF/VT, SVT, WPW, Bundle Branch Block. Our final year medical students, Michael Abu and Charlotte Moon, will be hosting this session and welcome any questions you may have. Don’t miss out on this great opportunity to advance your knowledge of these common, yet often complicated conditions.
NUCCS CARDIOLOGY TEACHING SERIES: PART 2 - HEART BLOCK, AF (FIBRILLATION AND FLUTTER), VF/VT, SVT, WPW, BUNDLE BRANCH BLOCK
Summary
Mobitz 1 slower until one completely Interval is not conducted
30 12/10/2023
Third degree
• Complete Block ,all atrial impulses are blocked & there’s
a complete disociation between atria and ventricles
31
Mx
• Pacemaker insertion:
If symptomatic
Cardiac structural abnormalities
High grade block & declining left
ventricular function or
complete AV block
Mobitz type 2
Underlying reversible cause
• Medication - requires caution
This on-demand teaching session on 12/10/2023 is a great opportunity for medical professionals to learn about a range of medical conditions related to the heart including Atrial Fibrillation, Atrial Flutter, Ventricular Tachycardia & Ventricular Fibrillation and Heart Block. The session will cover causes, symptoms, and management of these conditions, with particular
Description
Learning objectives
(Mobitz type 1) progressively longerpr pr interval until a beat is dropped once the pr interval becomes so long
that the next p wave
30 12/10/2023
drops the preceding QRS complex.
• Progression of pr interval
shortening until an RR cycle
is dropped
• Mobitz type 2 complete block
has a fixed pr interval for
all conducted beats.
31
Third degree
• Total block between atria and ventricles
• Atrial rate > ventricular rate
• Absence of any relation between P waves and QRS
complexes
• P waves visible, QRS complexes independent
32 12/10/2023
Learning objectives for the session on 12/10/2023:
- Describe the key characteristics of atrial fibrillation (AF), including symptoms, presentation, and management strategies.
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12/10/2023 1 Part A: AF/ Atrial Flutter , VT , VF , and Heart Block With Charlotte Moon 2 12/10/2023 Atrial Fibrillation 3 AF Key points • Uncoordinated contraction of the atria due to disorganized electrical activity • Causes irregularly irregular ventricular contractions • Absent P waves on ecg (reflects lack of coordinated electrical activity) and narrow QRS complex tachycardia • Stroke risk (use CHA2DS2-VASc) • Mx: control rhythm OR rate AND anticoagulate (Typical regime- bisoprolol for rate control and a DOAC eg apixaban for anti coagulation) 4 12/10/2023 •Irregular narrow-complex tachycardia at ~135 bpm 5 6 12/10/2023 Causes Presentation AF affects Mrs • Often asymptotic - AF found incidentally • S – Sepsis • M – Mitral valve pathology • Palpations (stenosis or regurgitation) or a • SoB mechanical valve • Syncope • I – Ischaemic heart disease • Symptoms from conditions eg • T – Thyrotoxicosis stroke, sepsis • H – Hypertension Alcohol and caffeine 7 Mx Rate – 1 line unless…. Rhythm 1. Beta blocker- bisoprolol, • Cardioversion atenolol Immediate-if AF <48 hrs or severely 2. Calcium Chanel blocker eg Reversible cause to AF haemodynamically unstable failiure) (not best in heart AF is new onset (within Delayed >48hrs +stable last 48 hours) Anticoag minimum 3 weeks with rate control 3. due to toxicity)s monitoring AF is causing HF • Pharmacological CV (1 line) Symptomatic despite effective rate control o Flecainide o Amiodarone (structural heart disease) • Electrical cardioversion Long term rhythm control • Beta blockers 1 line • Dronedarone, amiodarone 8 12/10/2023 Anticoagulation • 0-no anticoag • 1-consider if male, 2 –consider if female • >1 if male >2 if female- offer anticoag • DOAC eg apixaban are the usual choice, more expensive than warfarin but don’t require monitoring • W/o anticoag 5% risk of stroke each year • W/ anticoag the risk is reduced by about 2/3 9 • HAS-BLED or ORBIT gives us the anticoagulated patients bleed risk. • Generally bleeds are more reversible than strokes and have less long term consequences • In HAS-BLED a score of ≥3 indicates "high risk" and some caution and regular Bleed risk be anticoagulated.ent is needed, but does not necessarily mean patient can’t • OHigh. 8.1.s: Bleeds per 100 patient-years. 0-2. Low. 2.4. 3. Medium. 4.7. 4-7. 10 12/10/2023 Paroxysmal AF • Comes and goes , usually not more than 24hrs • Anticoagulate based on CHADSVASc • Pill in the pocket/Flecainide- may be appropriate if the episodes are infrequent and they do not have an underlying structural heart issue, or Atrial flutter. 11 Atrial Flutter 12 12/10/2023 Atrial flutter • Causes: age related, rare before 50, previous heart surgery, hpn, myocarditis, congenital heart disease. • “Saw-tooth”pattern of inverted flutter waves in leads II, III, aVF • a form of Supraventricular Tachycardia caused by a re-entry circuit within the right atrium. The length of the re-entry circuit corresponds to the size of the right atrium, resulting in a fairly predictableatrial rate of around300 bpm (range 200-400) • Usually presents with a block ratio eg 2 atrial beats per 1 ventricular contraction- 2:1 block 13 14 12/10/2023 Classification • Typical: involvesthe IVC & tricuspid isthmus in the reentry circuit and travels in an anti-clockwise manner(90%) • Atypical:atrial flutter arising in the left atrium or clockwise in the right atrium (10%), or around any site of previous surgery 15 16 12/10/2023 Mx • Rate/rhythm control- beta blockers or cardioversion • Treat underlying issue eg thyrotoxicosis,hpn • Radio frequency ablation • Anticoagulate based on CHADSVASC 17 Ventricular Tachycardia & Ventricular Fibrillation 18 12/10/2023 Ventricular tachycardia+Ventricular Fibrillation -ShockableRhythms • 4 possible rhythms in a pulse less unresponsive patient- VF+VT=shockable, pulseless electrical activityand asystole are not. • Mx is the same for both • Presentationsimilar: SoB, palpitations, syncope, nausea, chest pain. 19 VF •Typical rhythm strip of VF • activity renders the ventriclesical unable to contract in a synchronised manner, resulting in immediate loss of cardiac output •Appearance of fine VF • Prolonged ventricular fibrillation amplitude, from initial coarse VF to fine VF, ultimately degenerating into asystole due to progressive depletion of myocardial energy stores 20 12/10/2023 VT • Ventricular tachycardia (VT) is a wide complex tachycardia, defined as three or more consecutive beats at a rate of more than 100 per minute, arising from the ventricle • the most common is monomorphicVT, Monomorphic VT: Regular, broad complex tachycardia which originates from a single focus within the ventricles. • Cause: most often ischaemic heart disease.Also other cardiomyopathies, channelopathies, electrolyte imbalance, drugs such as drugs such as cocaine or methamphetamine, and digitalis toxicity. • Decreased cardiac output mayresult in decreased myocardial perfusion with degeneration into VF 21 22 12/10/2023 Mx for VF and VT 1. CPR and initially 3 synchronised shocks 2. After the 3 shock Resume CPR immediately and then give adrenaline 1 mg intravenously(IV) and amiodarone300 mg IV, while continuing CPR for a further 2 minutes.Withhold adrenaline if there are signs of return of spontaneous circulation (ROSC) during CPR. 3. Consider another Amiodarone dose 23 Torsade de pointes Mx • Correct cause(eg electrolyte disturbance or medications) Torsade de pointes is a form of • IV MagSulf ventricular tachycardia associated with • cardioversion a long QT syndrome • Implantable Defib ifreoccurence frequently recurrent and can cause impairment or loss of consciousness . If not controlled, the arrhythmia can progress to ventricular fibrillation and sometimes death. For TdP to be diagnosed, the patient must have evidence of both Causes: PVT and QT prolongation Long QT syndrome Meds: antipsych,citalopram,Flecainide,macroli de antibiotics, sotalol Electrolyte disturbances 24 12/10/2023 25 Heart Block 26 12/10/2023 Heart Block 27 st 1 degree • Delayed atrioventricular conduction through the AV node • PR Interval greater than 0.2 seconds (5 small or 1 big square) 28 12/10/2023 •Sinus bradycardia with 1st degree AV block •PR interval > 300 ms 29 Second degree- Mobitz 1 and 2 • Some atrial impulses don’t pass through the AV node so some p waves do not lead to QRS complexes Wenckebach Atrial inputs become Increasing pr interval until (Mobitz 1) weaker until one does not p wave does not produce a pass through the av node qrs. The cycle repeats to ventricles Mobitz 2 Intermittent failure or Missing qrs complexes Risk of Asystole interruption of av PR interval remains normal conduction Ratio block eg 2:1 The number of p waves for Can occur in both Mobitz 1 every qrs complex eg 2:1 and 2, can be hard to differentiate 30 12/10/2023 Mobitz 1 31 Mobitz 2- A form of 2nd degree AV block in which there is intermittent non-conducted P waves without progressive prolongation of the PR interval 32 12/10/2023 2:1 block 4:1 33 rd 3 degree-complete heart block • No relationship between p wavesand qrs • Severe Bradycardia • Significant risk of asystole 34 12/10/2023 Causes • Inferior myocardial infarction- right coronaryartery supplies inferior wall and AV node • AV-node blocking drugs (e.g. calcium-channel blockers, beta- blockers, digoxin) • Idiopathic degeneration of the conducting system (Lenegre’s or Lev’s disease), causing true trifascicular block 35 Mx • Temporary transvenous pacing – an electrode on the end of a wire that is fed into the right atrium to stimulate AV node • Atropine – antimuscarinic, inhibits parasympathetic nervous system • Damage may be permanent and require permanent pacemaker 36 12/10/2023 Benjamin is a 60-year-old man who has recently been diagnosed with atrial fibrillation after experiencing some palpitations. He has no other medical history and only takes atorvastatin for high cholesterol. He has no symptoms currently and his observations are stable with a heart rate of 75 beats per minute. His CHA DS -VA2c sc2re is 0. What is the next step in managing this patient? 1. Start him on rivaroxaban 2. start him on aspirin 3. Arrange for an echocardiogram 4. Start him on digoxin 5. Arrange for a chest X-ray 37 3. Arrange for an echocardiogram • In AF, if a CHA DS -VASc score suggests no need for anticoagulation do an echo to exclude valvular heart disease • The CHA D2 -V2Sc score is used to assess the risk of stroke in a patient with atrial fibrillation. and treatment should also be considered for males with a score of one or more. score of two or more, Rivaroxaban can be used as an anticoagulant in AF, however, in this scenario the patient does not meet the criteria for anticoagulation. Aspirin should not be used to prevent stroke risk in atrial fibrillation. It is advised that a transthoracic echo should be arranged in patients with AF, especially if it may change their management, or refine their risk of stroke and need for anticoagulation. control the rate of a patient who has a more sedentary lifestyle. Neither drug protects againstly used to stroke. 38 12/10/2023 A 32-year-old female presents to the emergency department after suffering from palpitations and excessive sweating for the past 2 and a half days. When questioned, she has no other symptoms, but admits to consuming a large quantity of alcohol and coffee 4 days previously. She has a past medical history of Wolff-Parkinson-White syndrome, which was diagnosed 13 years ago. Observations show the patient is afebrile, with a respiratory rate of 22 breaths/min, pulse of 73 beats/min, blood pressure of 122/83 mmHg and oxygen saturations of 95% on room air. A 12-lead ECG is performed, which shows atrial fibrillation (AF). Cardioversion is contraindicated in this patient for what reason? 1. Her oxygen saturations 2. Her past medical history 3. Her recent consumption of large volumes of alcohol 4. Her recent consumption of large volumes of caffeine 5. The duration of her symptoms 39 5. The duration of her symptoms • New onset AF is considered for electrical cardioversion if it presents within 48 hours of presentation • • The patient is presenting with of symptoms of palpitations and sweating, both of which are characteristic of AF. As symptoms initially occurred over 48 hours ago (her’s started 2 1/2 days ago), the cut-off for cardioversion without anticoagulation has already elapsed, meaning the procedure is currently contra- indicated. Please note, Wolff-Parkinson-White, which is a pre-excitation syndrome, and consumption of large quantities of alcohol and caffeine all predispose to AF. Pre-excitation refers to early activation of the ventricles, caused by impulses bypassing the AV node, due to an aberrant electrical pathway in the heart. Several types of pre-excitation syndromes have been described in addition to Wolff-Parkinson-White syndrome. One example is Lown-Ganong-Levine syndrome, which is caused by an aberrant connection between the atria and bundle of His. All of the other listed answers are wrong as they have no bearing on whether cardioversion may be given to a patient. • 40 12/10/2023 A 70-year-old man with a past medical history of osteoarthritis and asthma attends his annual health check-up. He does not complain of any ongoing symptoms, and examination is unremarkable apart from an irregularly irregular pulse. An ECG confirms your suspicion of atrial fibrillation (AF). After ruling out any underlying causes of his AF, you decide to commence this man on treatment. Which of the following drugs should be prescribed to achieve rate-control of this man's AF? 1. Amlodipine 2. Atenolol 3. Digoxin 4. Rivaroxaban 5. Verapamil 41 5-Verapamil • Beta-blockers are contraindicated in patients with asthma • Non-cardioselective beta-blockers may provoke bronchospasm in asthmatics. Atenolol is therefore verapamil, should be used instead.rol in this patient. A rate-limiting calcium channel blocker, like Amlodipine is not a rate-limiting calcium channel blocker, and therefore unsuitable for AF. Digoxin is not used first-line in AF. Rivaroxaban has no role in the rate-control of AF. It is however used to anticoagulate these patients. 42 12/10/2023 Part B: SVT, Wolff-Parkinson-White and Bundle Branch Block With Michael Abu 43 Supraventricular Tachycardia 44 12/10/2023 A 28-year-old female presents to A&E with chest palpitations. This is her first presentation, she has Presentation abnormalities are found on examination. Her ECG is shown below. 45 Definition: “Refers to any tachydysrhythmiaarising from above the level of the Bundle of His, and encompasses regular atrial, irregular atrial, and regular atrioventricular tachycardias” • SVT is caused by abnormal electrical impulses that start suddenly in the upper chambers of your heart (the atria). These rhythm.s override your heart's natural • Often used synonymously with AV nodal re- entry tachycardia (AVNRT), a form of SVT. • ECG will demonstratea narrow complex tachycardia. 46 12/10/2023 47 Signs & Symptoms • Usually feel your heart racing in your chest or throat and a very fast pulse (140-180beats per minute). • You may also feel: chest pain dizziness light-headedness fatigue (tiredness) breathlessness • On rare occasions,you may faint because of a drop in blood pressure. • Symptomsof SVT can last for seconds, minutes, hours, or (in rare cases) days. • They may occur regularly, several times a day, or very infrequently, once or twice a year 48 12/10/2023 Pathophysiology • Caused by the electrical signal re- entering the atria from the ventricles. • The electrical signal finds a way from the ventricles back into the atria. • Once the signal is back in the atria, it again travels through the atrioventricularnode to the ventricles, causing another ventricular contraction. • This causes a self-perpetuating electrical loopwithout an endpoint, resulting in narrowcomplex tachycardia.It is described as a “narrowcomplex”,as the QRS complex Normal vs. SVT has a duration of less than 0.12 seconds. 49 50 12/10/2023 DDXforNarrowComplexTachycardia There are four main complex tachycardia. There are key ECG features that will help you differentiatethese: • Sinus tachycardia • Supraventricular tachycardia • Atrial fibrillation • Atrial flutter 51 Types of SVT There are three main types of SVT, based on the source of the abnormal electrical signal: • Atrioventricular nodal re-entrant tachycardia AVNRT the re-entry point is back through the atrioventricular node. This is the most common type of SVT. • Atrioventricular re-entrant tachycardia AVRT the re-entry point is an accessory pathway. An additional electrical pathway, somewhere between the atria and the ventricles, lets electricity back through from the ventricles to the atria. • Atrial tachycardia is where the electrical signal originates in the atria re-entering from the ventricles but from abnormally generated electrical activity in the atria. 52 12/10/2023 53 Atrioventricularre-entrant tachycardiaAVRT Atrialtachycardia 54 12/10/2023 AcuteManagement of SVT 55 AcuteManagement of SVT Patientswith recurrent episodes of supraventricular tachycardia can be treated to prevent further episodes. The optionsare: • Long-term medication (e.g., beta blockers, calcium channel blockers or amiodarone) • Radiofrequencyablation RadiofrequencyAblation • Catheter ablation is performed in a catheter laboratory, often called a “cath lab”. • It involves a general anaesthetic or sedation.A catheter is inserted into a femoral vein and fed through the venous system under x-ray guidance to the heart. 56 12/10/2023 Supraventricular Tachycardia A 25-year-old male attended to A&E due to sudden onset of palpitationsin his chest. He described this as his heart was skipping a beat. On examination it was found that the patient had a SVT. Which of the following would be the most appropriate in the acute management of this patient to return to normal sinus rhythm? a) Valsalva manoeuvre b) Amiodarone c) Atropine d) DC cardioversion e) Adrenaline 57 Supraventricular Tachycardia A 25-year-old male attended to A&E due to sudden onset of palpitationsin his chest. He described this as his heart was skipping a beat. On examination it was found that the patient had a SVT. Which of the following would be the most appropriate in the acute management of this patient to return to normal sinus rhythm? a) Valsalva manoeuvre b) Amiodarone c) Atropine d) DC cardioversion e) Adrenaline 58 12/10/2023 Wolff-Parkinson- White Syndrome (WPW) 59 Definition: • Wolff-Parkinson-White syndrome (WPW) is connecting the atria and ventricles. • It is also called pre-excitation syndrome. • Nconnects the atria and ventricles. (AV) node • The extra pathway in Wolff-Parkinson-White syndrome maybe called the Bundle of Kent. • Tactivity to pass between the atria andl ventricles, bypassing the atrioventricular cause anysymptoms, or it mightcausenot episodes of SVT. 60 12/10/2023 • ECG changes in Wolff-Parkinson-White syndrome are: o Short PR interval, less than 0.12 seconds o Wide QRS complex, greater than 0.12 seconds o Delta wave • The delta wave appears as a slurred upstroke in the QRS complex. • It is caused by the electricity prematurely entering the ventricles through the accessory pathway. 61 Signs & Symptoms In general, signs and symptoms that may occur in people with WPW syndrome include: • A rapid, fluttering or pounding heartbeat (palpitations) • Chest pain • Difficulty breathing • Dizziness or lightheadedness • Fainting • Fatigue • Shortness of breath • Anxiety The most common arrhythmia seen with WPW syndrome is supraventricular tachycardia. 62 12/10/2023 Management for WPW • The definitive treatment for Wolff-Parkinson-White syndrome is radiofrequency ablation of the accessory pathway. Same as SVT Management • Vagal maneuvers. • Medications. If vagal maneuvers don't stop a fast heartbeat, you might need medications to control the may need to be given by IV.heart rhythm. Medications • Cardioversion. • Catheter ablation. 63 Bundle Branch Block 64 12/10/2023 Definition: • A condition in which there's a delay or blockage along the pathway that electrical impulses travel to make the heartbeat. • The delay or blockage can occur on the pathway that sends electrical impulses either to the left or the right side of the bottom chambers (ventricles) of the heart. • If one bundle is damaged, the ventricles rely signals from the right atrium. and respond to • beat very slowly, which can require at may pacemaker. 65 Signs & Symptoms • In most people, bundle branch block doesn't cause symptoms.Some people with the condition don't know they have bundle branch block. • Rarely, symptoms of bundle branch block may include fainting (syncope) or feeling as if you're going to faint (presyncope). • The main feature of bundle branch blocks is the broadening of QRS complexes. It is important to ensure other causes of broad complexes are excluded Risk Factors • Increasing age. Bundle branch block is more common in older adults than in younger people. • Underlying health problems. Having high blood pressure or heart disease increases the risk of having bundle branch block. 66 12/10/2023 LBBB is always RBBB can be either pathological. Left bundle physiological or the result branch block may be due of damage to the right to conduction system bundle branch. degeneration or myocardial pathologies Causes of damage include such as ischaemic heart disease, cardiomyopathy underlying lung pathology (COPD, pulmonary emboli, and valvular heart disease. cor pulmonale), primary heart muscle disease LBBB may also occur after (ARVC), congenital heart cardiac procedures, which disease (e.g. ASD), damage the left bundle ischaemic heart disease branch or His bundle. A and primary degeneration STEMI presenting as chest of the right bundle. pain with LBBB is exceedingly rare. 67 Left Bundle Branch Block The diagnosticcriteria for LBBB are: • Broad QRS complex: >120 ms (3 small squares) • Dominant S wave in V1 • Broad, monophasicR wave in lateral leads: I, aVL, V5-V6 • Absence of Q waves in lateral leads • Prolonged R wave >60ms in leads V5-V6 68 12/10/2023 Right Bundle Branch Block The diagnosticcriteria for RBBB are: • Broad QRS complex: >120 ms (3 small squares) • RSR’ pattern in V1-V3: an initial small upward deflection (R wave), a larger downward deflection (S wave), then another large upward deflection (a second R wave, which is indicated as R’) • Wide, slurred S wave in lateral leads: I, aVL, V5-V6 69 70 12/10/2023 A 76-year-old woman present to her GP with shortness of breath on exertion. She felt it has been graduallyworsening over the past 6- months. She denies any chest pain but says that she wakes up in the middle of the night gasping for breath. Her legs are oedematous on examination. Which of these investigations is first line for her diagnosis? a)CT Chest b) B-Natriuretic peptide c) Ankle brachial pressure index (ABPI) d)Echocardiogram e)ECG 71 A 76-year-old woman present to her GP with shortness of breath on exertion. She felt it has been graduallyworsening over the past 6- months. She denies any chest pain but says that she wakes up in the middle of the night gasping for breath. Her legs are oedematous on examination. Which of these investigations is first line for her diagnosis? a)CT Chest b) B-Natriuretic peptide c) Ankle brachial pressure index (ABPI) d)Echocardiogram e)ECG 72