Atrial fib & flutter
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This document provides an overview of atrial fibrillation (AF) and atrial flutter. It discusses the characteristics, mechanisms, ECG features, causes and clinical outcomes of AF. It also covers the classification, mechanisms, ECG patterns and examples of atrial flutter. Key points include that AF is characterized by disorganized atrial activation and irregular ventricular rhythm, while flutter involves a reentrant circuit in the right atrium causing a regular atrial rate of 300 bpm. Complications of AF include increased risk of stroke, heart failure and cardiac death.
Atrial fib & flutter
- 1. ECG PRESENTATION TOPIC -ATRIAL FIBRILLATION AND FLUTTER GUIDE - Dr. NEERAJ JAIN CANDIDATE -Dr. SUMEDH RAMTEKE
- 2. INTRODUCTION Atrial Fibrillation (AF) is the most common sustained arrhythmia. The incidence and prevalence of AF is increasing. Lifetime risk over the age of 40 years is ~25%. (1) Complications of AF include haemodynamic instability, cardiomyopathy, cardiac failure, and embolic events such as stroke. Characterised by disorganised atrial electrical activity and contraction.
- 3. Atrial Fibrillation is characterized by disorganised, rapid and irregular atrial activation with loss of atrial contraction and with an irregular ventricular rate that is determined by AV nodal conduction (1) • Paroxysmal AF AF that terminates spontaneously or with intervention within 7 d of onset. • Persistent AF Continuous AF that is sustained >7 d. • Long-standing persistent AF Continuous AF >12 mo in duration. • Permanent AF When the patient and clinician make a joint decision to stop further attempts to restore and/or maintain sinus rhythm.
- 4. MECHANISM • Focal activation – In which AF originates from an area of focal activity. This activity may be triggered, due to increased automaticity, or from micro re-entry. Often located in the pulmonary veins. (1) • Multiple wavelet mechanism – In which multiple small wandering wavelets are formed. The fibrillation is maintained by re-entry circuits formed by some of the wavelets. This process is potentiated in the presence of a dilated LA — the larger surface area facilitates continuous waveform propagation. (1)
- 5. The hallmark of AF is chaotic atrial impulses leading to irregularly irregular ventricular contraction, usually with incessant tachycardia
- 7. Causes of Atrial Fibrillation Hypertension Heart attacks/ CAD Valvular Heart Disease Congenital heart defects Hyperthyroid or other metabolic imbalance Exposure to stimulants such as medications, caffeine or tobacco, or to alcohol (holiday heart) Sick sinus syndrome — improper functioning of the heart's natural pacemaker Emphysema or other lung diseases CABG/ Previous heart surgery Viral infections /Pericarditis Stress due to pneumonia, surgery or other illnesses (Catecholamine) Pulmonary Embolus Pneumonia Sleep Apnea Pericarditis Lone A fib (younger people) Left ventricular Hypertrophy Cardiomyopathy CHF –Systolic or Diastolic Idiopathic – mostly in younger people – Lone Atrial Fib Familial Predisposition. Glucocorticoids Electrolyte abnormalities (especially Low Mg+2) Atrial fibrosis from Sarcoid, collegen vascular disease, infiltrating diseases
- 8. Clinical events (outcomes) affected by AF Outcome Parameter Relative change in AF patients 1.Death 2.Stroke 3.Hospitalisation 4.Quality of life and exercise capacity 5.LV function 1.Death rate is doubled 2.Stroke risk increases 5 times 3.More frequent 4.Can be markedly decreased 5.Tachycardiomyopathy/ heart failure
- 9. Risk factors & Biomarkers
- 10. Waldo et al divided AF into 4 types according atrial electrogram • Type – I --- ECG showed discrete complexes of variable morphology separated by a clear isoelectric baseline • Type – II --- ECG characterized by discrete atrial complexes with variable cycle lengths and morphology, the baseline is not isoelectric • Type – III --- ECGs were highly fragmented, showing no discrete complexes or isoelectric intervals • Type – IV --- Fibrillation was characterized by alterations between type III & other types Mechanisms
- 13. ECG FEATURES OF AF Irregularly irregular rhythm. No P waves. Absence of an isoelectric baseline. Variable ventricular rate. QRS complexes usually < 120 ms unless pre-existing bundle branch block, accessory pathway, or rate related aberrant conduction. Fibrillatory waves may be present and can be either fine (amplitude < 0.5mm) or coarse (amplitude >0.5mm). Fibrillatory waves may mimic P waves leading to misdiagnosis.
- 17. Example .1 Irregular ventricular response . Coarse fibrillatory waves are visible in V1. “Sagging” ST segment depression is visible in V6, II, III and aVF, suggestive of digoxin effect.
- 18. Example 2. Irregular ventricular response. Coarse fibrillatory waves are visible in V1.
- 19. Example 3. Irregular ventricular response. No evidence of organised atrial activity. Fine fibrillatory waves seen in V1.
- 20. Example 4. Irregular narrow-complex tachycardia at ~135 bpm. Coarse fibrillatory waves in V1.
- 21. Example 5. AF with slow ventricular response Irregular heart rate with no evidence of organised atrial activity. Fine fibrillatory waves in V1. ST depression / T wave inversion in the lateral leads could represent ischaemia or digoxin effect. The slow ventricular rate suggests that the patient is being treated with an AV- nodal blocking drug (e.g. beta-blocker, verapamil/diltiazem, digoxin). Another cause of slow AF is hypothermia.
- 22. Ashman’s Phenomenon – presences of aberrantly conducted beats, usually of RBBB morphology, due a long refractory period as determined by the preceding R-R interval. The ventricular response and thus ventricular rate in AF is dependent on several factors including vagal tone, other pacemaker foci, AV node function, refractory period, and medications. Commonly AF is associated with a ventricular rate ~ 110 – 160. AF is often described as having ‘rapid ventricular response’ once the ventricular rate is > 100 bpm. ‘Slow’AF is a term often used to describe AF with a ventricular rate < 60bpm. Causes of ‘slow’ AF include hypothermia, digoxin toxicity, medications and sinus node dysfunction.
- 23. Example 6. Ashman aberrancy Atrial fibrillation is diagnosed based on the irregular ventricular rate and presence of fibrillatory waves in V1. The third QRS complex is aberrantly conducted: it is broad with a different axis and morphology and occurs following a long RR / short RR cycle (= Ashman aberrancy).
- 24. Atrial Flutter type of supraventricular tachycardia caused by a reentry circuit within the right atrium. (2) The length of the re-entry circuit corresponds to the size of the RA, resulting in a fairly predictable atrial rate of around 300 bpm (range 200-400). (2) Ventricular rate is determined by the AV conduction ratio (“degree of AV block”). The commonest AV ratio is 2:1, resulting in a ventricular rate of ~150 bpm. Higher-degree AV blocks can occur — usually due to medications or underlying heart disease — resulting in lower rates of ventricular conduction, e.g. 3:1 or 4:1 block. Atrial flutter with 1:1 conduction can occur due to sympathetic stimulation or in the presence of an accessory pathway — especially if AV-nodal blocking agents are administered to a patient with WPW. Atrial flutter with 1:1 conduction is associated with severe haemodynamic instability and progression to ventricular fibrillation.
- 26. Classification A} Typical Atrial Flutter (Common, or Type I Atrial Flutter) Involves the IVC & tricuspid isthmus in the reentry circuit. Can be further classified based on the direction of the circuit: Anticlockwise Reentry. This is the commonest form of atrial flutter (90% of cases). Retrograde atrial conduction produces: Inverted flutter waves in leads II,III, aVF Positive flutter waves in V1 – may resemble upright P waves Clockwise Reentry. This uncommon variant produces the opposite pattern: Positive flutter waves in leads II, III, aVF Broad, inverted flutter waves in V1 B} Atypical Atrial flutter (Uncommon, or Type II Atrial Flutter) Does not fulfil criteria for typical atrial flutter. Often associated with higher atrial rates and rhythm instability. Less amenable to treatment with ablation.
- 27. ECG ATRIAL FLUTTER General Features Narrow complex tachycardia Regular atrial activity at ~300 bpm Flutter waves (“saw-tooth” pattern) best seen in leads II, III, aVF — may be more easily spotted by turning the ECG upside down! Flutter waves in V1 may resemble P waves Loss of the isoelectric baseline
- 28. Fixed AV blocks Ventricular rate is a fraction of the atrial rate, e.g. 2:1 block = 150 bpm 3:1 block = 100 bpm 4:1 block = 75 bpm Variable AV block The ventricular response is irregular and may mimic AF On closer inspection, there may be a pattern of alternating 2:1, 3:1 and 4:1 conduction ratios Atrial flutter with a 3:1 block
- 29. Handy tips for spotting flutter Rapid Recognition Narrow complex tachycardia at 150 bpm (range 130-170)? Yes -> Suspect flutter! Turn the ECG upside down and scrutinise the inferior leads (II, III + aVF) Vagal Manoeuvres + Adenosine Atrial flutter will not usually cardiovert with these techniques (unlike AVNRT), although typically there will be a transient period of increased AV block during which flutter waves may be unmasked.
- 30. Handy tips for spotting flutter RR intervals In atrial flutter with variable block the R-R intervals will be multiples of the P-P interval — e.g. assuming an atrial rate of 300bpm (P-P interval of 200 ms), the R-R interval would be 400 ms with 2:1 block, 600 ms with 3:1 block, and 800 ms with 4:1 block. Look for identical R-R intervals occurring sporadically along the rhythm strip; then look to see whether there is a mathematical relationship between the various R-R intervals on the ECG. In contrast, atrial fibrillation will be completely irregular, with no patterns to be discerned within the R-R intervals.
- 31. Example 7. Atrial Flutter with 2:1 Block There are inverted flutter waves in II, III + aVF at a rate of 300 bpm (one per big square) There are upright flutter waves in V1 simulating P waves There is a 2:1 AV block resulting in a ventricular rate of 150 bpm Note the occasional irregularity, with a 3:1 cycle seen in V1-3 This is the classic appearance of anticlockwise flutter.
- 32. Example 8. Atrial Flutter with Variable Block Inverted flutter waves in II, III + aVF with atrial rate ~ 300 bpm Positive flutter waves in V1 resembling P waves The degree of AV block varies from 2:1 to 4:1 The diagnosis of flutter with variable block could be inferred here from the R-R intervals alone (e.g. if flutter waves were indistinct) — note how the R-R intervals during periods of 4:1 block are approximately double the R-R intervals during 2:1 block.
- 33. Example 9. Atrial flutter with 4:1 block There are inverted flutter waves in II, III + aVF at a rate of 260 bpm. There are upright flutter waves in V1-2 (= anticlockwise circuit). There is 4:1 block, resulting in a ventricular rate of 65 bpm. The relatively slow ventricular response suggests treatment with an AV nodal blocking agent.
- 34. Example 10. Atrial Flutter with Variable Block The block varies between 2:1 and 4:1 The presence of positive flutter waves in lead II suggests a clockwise re-entry circuit (= uncommon variant).
- 35. Example 11. Atrial Flutter with High-Grade AV Block There is anticlockwise flutter with marked AV block (varying from 5:1 up to 8:1). The very low ventricular rate suggests treatment with AV nodal blocking drugs (e.g.digoxin, beta-blockers). Other possibilities could include intrinsic conducting system disease (true “AV block”) or electrolyte abnormality (e.g. hyperkalaemia). Tip: The combination of new-onset atrial flutter with high-grade AV block is very suspicious for digoxin toxicity.
- 36. Example 12. Atrial Flutter with 1:1 Block? There is a very rapid, regular narrow-complex tachycardia at 250-300 bpm. Flutter waves are not clearly seen, but there is an undulation to the baseline in the inferior leads suggestive of flutter with a 1:1 block. Alternatively, this may just be rapid SVT (AVNRT / AVRT) with rate-related ST depression. With ventricular rates as rapid as this, spending any further time evaluating the ECG is unwise! Resuscitation is the priority. This patient will almost certainly be haemodynamically unstable, requiring emergent DC cardioversion.
- 37. Example 13. Atrial Flutter with 2:1 Block There is a narrow complex tachycardia at 150 bpm. There are no visible P waves. There is a sawtooth baseline in V1 with flutter waves visible at 300 bpm. Elsewhere, flutter waves are concealed in the T waves and QRS complexes. The heart rate of 150 bpm makes this flutter with a 2:1 block. NB. Flutter waves are often very difficult to see when 2:1 block is present.
- 38. Exapmle 14. Atrial flutter with 3:1 Block Negative flutter waves at ~ 300bpm are best seen in the inferior leads II, III and aVF (= anticlockwise pattern). There is a 3:1 relationship between the flutter waves and the QRS complexes, resulting in a ventricular rate of 100 bpm.
- 39. Example 15. Suspect atrial flutter with 2:1 block whenever there is a regular narrow complex tachycardia at 150 bpm — particularly when the rate is extremely consistent. In contrast, the rate in sinus tachycardia typically varies slightly from beat to beat, while in AVNRT/AVRT the rate is usually faster (170-250 bpm). To tell the difference between these rhythms, try some vagal manoeuvres or give a test dose of adenosine — AVNRT/AVRT will often revert to sinus rhythm, whereas slowing of the ventricular rate will unmask the underlying atrial rhythm in sinus tachycardia or atrial flutter.
- 40. REFERENCES 1. HARRISON’S INTERNAL MEDICINE 19th EDITION 2. BRAUNWALD HEART DISEASE 10TH EDITION 3. www. LIFE IN FAST LANE 4. LEO SCHAMROTH, INTRODUCTION TO ECG 5. ACC/AHA GUIDELINES FOR ATRIAL FIBRILLATION
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