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![CHA2 DS2-VASc Score Recommended Therapy
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Atrial Fibrillations
- 1. Atrial Fibrillations Dr NabeyaViktor Kasi Medical Doctor 1
- 2. Outlines • Introduction • Epidemiology •Etiology • Clinical presentation • Investigation • Management • AF related outcomes and complications • Differential Diagnosis • References 2
- 3. Introduction • Atrial fibrillation(AF) poses significant burden to patients, physicians, and healthcare systems globally • The complexity of AF requires a multifaceted, holistic, and multidisciplinary approach to the management of AF patients 3
- 4. Definition • A supraventriculartachyarrhythmia with uncoordinated atrial electrical activation and consequently ineffective atrial contraction. Electrocardiographic characteristics of AF include Irregularly irregular R-R intervals (when atrioventricular conduction is not impaired) Absence of distinct repeating P waves, and Irregular atrial activations 4
- 5.
- 6. Epidemiology • Most frequentlyencountered cardiac arrythmia • Incidence - increases with age • The lifetime risk of Afib among individuals > 40 years is 1 in 4. • >95% of individuals with Afib are ≥ 60 years • Prevalence - 1% of US population 6
- 7. Mechanism • SA nodeis a dominant pacemaker of the heart which sends impulses to the atrium causing atrial contraction • From the SA nose, the impulse arrives at the AV node. • From the AV node, the impulses travels rapidly along the bundle of HIS – bundle branches and purkinje fibers where the impulse causes ventricular contraction 7
- 8. • Afib isas a result of an initial trigger thought to be from Ectopic foci firing rapidly from the pulmonary vein or Single localized reentry circuit in the atrial myocardium 8
- 9.
- 10. • Intrinsic CardiacDisorder Coronary artery disease Valvular heart disease(esp mitral valve disease) Congestive Heart Failure Preexcitation tachycardia eg WPW syndrome Sick Sinus syndrome (tachycardia-bradycardia syndrome) Cardiomyopathies Pericarditis 10
- 11. • Non cardiacdisorders Pulmonary disease- COPD, pulmonary embolism, pneumonia Hyperthyroidism Catecholamine release and/or increased sympathetic activity Electrolyte imbalances Drugs 11
- 12. Holiday heart syndrome Chronickidney disease • Genetic • Neurological disorder • Idiopathic 12
- 13. Classification • Hemodynamic Stability UnstableAfib Stable afib • Ventricular Rate Afib with rapid ventricular response Afib with slow ventricular response 13
- 14. Classification by onset Atrialfibrillation is referred to as recurrent when a patient has two or more episodes. The patterns of atrial fibrillation include: First diagnosed/new onset AF - AF not diagnosed before, irrespective of its duration or the presence/severity of AF-related symptoms. • Paroxysmal AF - If recurrent AF reverts spontaneously within seven days • Persistent AF - recurrent AF persisting needing either pharmacological or electrical cardioversion and it last more than seven days 14
- 15. • Long-standing persistentAF: AF that has been present for more than 12 months, either due to the failure of initiation of pharmacological intervention or failure of cardioversion • Permanent AF: It is the type where a decision has been made to abort all therapies because the rhythm is unresponsive 15
- 16. • Method ofdetection Clinical afib Subclinical afib • Mitral valve involvement Valvular afib Nonvalvular afib 16
- 17. Triggers of AtrialFibrillation • Several triggers excites focus in the atrial most commonly around the pulmonary veins and allows for an unsynchronized firing of electrical impulses leading to fibrillations. These are; Atrial ischemia Inflammation Alcohol or illicit drug use Hemodynamic stress 17
- 18.
- 19. Clinical Presentation 19 • Asymptomatic Hemodynamicallystable • Symptomatic Palpitations Dyspnea Fatigue Chest tightness/pain, poor effort tolerance, dizziness, syncope, disordered sleep
- 20. • Hemodynamically unstable Syncope Symptomatichypotension Acute HF, pulmonary edema Ongoing myocardia ischemia Cardiogenic shock 20
- 21. Symptoms and qualityof life • As symptoms related to AF may range from none to disabling, and rhythm control treatment decisions (including catheter ablation) are influenced by symptom severity, symptom status should be characterized using the European Heart Rhythm Association (EHRA) symptom scale 21
- 22.
- 23. Investigations • FBC • Basicmetabolic panel Serum elctrolytes Serum glucose BUECR • Thyroid function test • LFT • Troponin levels 23
- 24. • BNP orNT-proBNP • D-dimer • Serum toxicology and/or urine toxicology • Chest xray, CT scan(CTA or Head CT) • ECG • Echo 24
- 25. • ECG findingof atrial Fibrillation typical narrow complex "irregularly irregular" pattern No distinguishable p wave Typically narrow QRS complex (<0.12 seconds) ventricular rate usually ranges between 80 and 180/min Left ventricular hypertrophy 25
- 26.
- 27. • Transthoracic echocardiography(TTE)is helpful for the following To evaluate for valvular heart disease To evaluate atrial and ventricular chamber and wall dimension To estimate ventricular function and evaluate for ventricular thrombi To estimate pulmonary systolic pressure 27
- 28. • Transesophageal echocardiography(TEE) is helpful for the following To evaluate for atrial thrombus To guide cardioversion 28
- 29. • Holter Monitor Establisha diagnosis in cases of paroxysmal AF which are not evident on presentation Evaluate rate control 29
- 30. Management • It startswith the history and physical examination • Initial history and physical examination should include the following Documentation of clinical type of AF Assessment of type, duration, frequency of symptoms Assessment of precipitating factors 30
- 31. Assessment of modesof termination Documentation of prior use of antiarrhythmics and rate controlling agents Assessment of presence of underlying heart disease Documentation of any previous surgical or percutaneous AF ablation procedure ABC Vital signs(HR, BP, RR, oxygen saturation) 31
- 32. Approach • Unstable patients:emergent electrical cardioversion • Stable patients: The goal is to control heart rate and/or rhythm. Acute management Long-term management: • The choice of rate control versus rhythm control depends on institutional preferences and individual patient risk factors 32
- 33. • All patients •Consider referral to cardiology. • Correct reversible causes and/or treatable conditions, e.g. hyperthyroidism, electrolyte imbalances • Prevention of thromboembolic complications: Consider indications for anticoagulation • Encourage lifestyle modifications that reduce the risk of recurrence and decrease the likelihood of complications, e.g. weight loss, exercise, and reducing alcohol consumption 33
- 34. Acute • Hemodynamically unstable •Immediate synchronized cardioversion • Urgent cardiology consult • ICU/CCU transfer • Identify and treat the underlying cause • Continuous cardiac telemetry 34
- 35. • Hemodynamically stable •Afib with normal heart rate, consider indications for nonemergency cardioversion (e.g., first episode). • Refer to cardiology for long-term management with either rhythm or rate control • Afib with RVR < 48 hours duration: Consider rate or rhythm control > 48 hours: rate control • ICU/CCU consult and transfer if the patient has a refractory rapid ventricular rate 35
- 36. Rate control • Thegoal is to normalize the ventricular heart rate to reduce symptoms. • Target resting heart rate < 110/minute: for patients who remain asymptomatic or have normal LV systolic function < 80/minute: for patients who continue to be symptomatic with a lenient rate • Consider rate control strategy especially in elderly patients • Contraindication: Afib due to preexcitation syndromes 36
- 37. Pharmacological options 37 • Firstline Beta blockers (eg metoprolol, atenolol, propranolol) Preferred when afib is due to hyperthyroidism and in pregnant patients Avoid in patients with COPD • Nondihyropyridine calcium channel blockers (eg diltiazem, verapamil) Avoid in patients with decompensated heart failure (LV systolic dysfunction/low ejection fraction) Can be safely used in heart failure with preserved normal LV systolic function
- 38. • Second-line: digoxinpreferred initial therapy for patients with ADHF • Third-line: amiodarone typically reserved for patients in whom all other options have failed 38
- 39. Rhythm control • Goal Terminationof atrial fibrillation Restoration and maintenance of sinus rhythm Symptom improvement Prevention of atrial remodeling 39
- 40. Electrical Cardioverison • Patientswho are hemodynamically unstable, who have severe dyspnea or chest pain with AF, or who have preexcited AF should undergo urgent cardioversion. • Direct current (DC) cardioversion is the delivery of electrical current that is synchronized to the QRS complexes; it can be delivered in monophasic or biphasic waveforms. 40
- 41. Pharmacological cardioversion • Pharmacologicalcardioversion agents for Afib • The following are inpatient regimens of IV or oral antiarrhythmics; Flecainide Dofetilide Propafenone Amiodarone 41
- 42. Pill in pocketapproach • A single, self-administered dose of an anti-arrhythmic (e.g., flecainide , sotalol) used outside of the hospital to terminate atrial fibrillation • Typically given in conjunction with a beta blocker or ndHP CCB • May be used in patients with recent onset of Afib with infrequent episodes and no history of structural or ischemic heart disease • Patients should be monitored on the regimen in the hospital environment before they can self-administer. 42
- 43. Surgical options • AVnodal ablation and implantation of a permanent ventricular pacemaker Irreversible procedure Eliminates the need for rate-controlling medications but leads to lifelong dependence on a pacemaker 43
- 44.
- 45. Risk management assessment •The CHA2DS2-Vasc score uses a point system to determine yearly thromboembolic risk. Two points are assigned for a history of stroke or TIA, thromboembolism, or age of 75 years or older, and one point is given for age 65-74 years or a history of hypertension, diabetes, heart failure, arterial disease (coronary artery disease, peripheral arterial disease, or aortic plaque), or female sex 45
- 46.
- 47. CHA2 DS2-VASc ScoreRecommended Therapy 0 No therapy 1 No therapy, or aspirin 81-325 mg daily, or anticoagulation therapy (eg, warfarin [international normalized ratio (INR) goal 2-3], dabigatran, rivaroxaban, apixaban, edoxaban) ≥2 Anticoagulation therapy (eg, warfarin [INR goal 2-3], dabigatran, rivaroxaban, apixaban, edoxaban) 47
- 48. • The majoradverse effect of anticoagulation therapy with warfarin is bleeding. Factors that increase this risk include the following: • History of bleeding • Age older than 75 years • Liver or renal disease • Malignancy • Thrombocytopenia or aspirin use 48
- 49. • Diabetes mellitus •Hypertension • Anemia • Prior stroke • Genetic predisposition • Supratherapeutic INR 49
- 50. • Several riskmodels have been introduced. The risk model called HEMORR2HAGES assigns points to risk factors, as follows : • History of bleeding (2 points) • Hepatic or renal disease (1 point) • Alcohol abuse (1 point) • Malignancy (1 point) • Older age (>75 years) (1 point) 50
- 51. • Reduced plateletcount or function, including aspirin therapy (1 point) • Hypertension (1 point) • Anemia (1 point) • Genetic predisposition (1 point) • Excessive fall risk (1 point) • Stroke (1 point) 51
- 52.
- 53. Newer oral anticoagulantsversus warfarin • There are several advantages of using the noac over warfarin which are: • Predictable pharmacologic profiles with fewer drug–drug interactions, and dietary effects • Lower risk of intracranial bleeding • Rapid onset and offset of action, with no need for bridging with parenteral anticoagulant therapy during initiation or after interruption • No need for periodic INR testing • Superiority to warfarin for reducing the risk of thromboembolic events with dabigatran 150 mg BID and apixaban 53
- 54. Disadvantages of thenewer oral anticoagulants include the following • Requires strict compliance, because missing even a single dose could result in a period without anticoagulation • No FDA-approved reversal agents for rivaroxaban, apixaban, and edoxaban (currently under clinical trials) • Limited safety profile data for patients with severe kidney failure • No data for their use in the presence of mechanical heart valves (dabigatran was associated with increased risk of thromboembolic complications in patients with mechanical heart valves in the RE- ALIGN trial) or valvular AF, due to hemodynamically significant mitral stenosis • No data for their use in pregnant or lactating women, in children, or in patients with a recent stroke (≤7-14 days), reversible causes of AF, severe increase in blood pressure, and significant liver disease • Lack of reliable blood tests to ascertain therapeutic effect or toxicity 54
- 55.
- 56. 56 AF related outcomes Frequency inAF Mechanism(s) Death 1.5 – 3.5 fold increase Excess mortality related to HF, comorbidities Stroke Stroke 20 – 30% of all ischemic strokes, 10% of cryptogenic strokes Cardioembolic or relayed to comorbid vascular atheroma LV dysfunction/ Heart Failure In 20 – 30% of AF patients Excessive ventricular rate, Irregular ventricular contractions, A primary underlying cause of AF Cognitive decline/ vascular dementia 1.4/1.6 (irrespective of stroke history) Brain white matter lesions, inflammation, Hypoperfusion, Micro-embolism Depression Depression in 16 – 20% (even suicidal ideation) Severe symptoms and decreased quality of life, Drug side effects Impaired quality of life >60% of patients Related to AF burden, comorbidities Hospitalization 10 – 40% annual hospitalization rate AF management related to HF, MI or AF related symptoms, Treatment associated complications
- 57. Complications • Systemic thromboembolism CVAor TIA Pulmonary Embolism Splenic Infarct • Tachycardia induced cardiomyopathy • Cardiogenic shock 57
- 58. Differential Diagnosis • AtrialFlutter • Atrial Tachycardia • Multifocal Atrial Tachycardia • Wolf-Parkinson-White syndrome • Atrioventricular nodal reentry tachycardia. 58
- 59. Atrial Flutter • Itis a cardiac arrythmia characterized by atrial rates of 240 to 400bpm usually with some degree of atrioventricular block • ECG Sawtooth flutter(f) waves often visualized in leads II, III, avF or V1 Regularly irregular rhythm 59
- 60. Atrial Tachycardia • Isa type of supraventricular tachycardia that does not require the atrioventricular junction, accessory pathways or ventricular tissue for its initiation and maintenance • ECG Rate of 150bpm Negative waves in leads III and avF Persist despite the atrioventricular block 60
- 61. Multifocal atrial tachycardia •Irregular supraventricular tachycardia characterized by three distinct p wave morphologies and or pattern of atrial activation at different rate • The rhythm is always irregular 61
- 62. Wolff-Parkinson-White syndrome • Congenitalcondition involving abnormal conductive tissue between the atrial and the ventricles that provides a pathway for a reentrant tachycardia circuit in association with supraventricular tachycardia • Chest findings are mostly normal • Features associated with wpw syndrome includes; Hypertrophic Cardiomyopathy(AMPK mutation) Ebstein anomaly 62
- 63. • ECG Shortened PRinterval A slow rise of the initial upstroke of the QRS complex – delta wave Widened QRS complex (total duration > 0.12 secs) ST segment – T wave changes 63
- 64. • Echo To evaluateleft ventricular function To evaluate septal thickness To evaluate for wall motion abnormalities Stress testing and electrophysiologic studies could be done 64
- 65.
- 66. References • Nesheiwat, Z.,Goyal, A. and Jagtap, M., Continuing Education Activity. • Ralston, S.H., Penman, I.D., Strachan, M.W. and Hobson, R. eds., 2018. Davidson's Principles and Practice of Medicine E-Book. Elsevier Health Sciences. • Rosenthal, L., McManus, D.D. and Sardana, M., 2018. Atrial fibrillation treatment & management. 66
- 67.
Editor's Notes
- #8 Atrial contraction is represented by P wave on ecg The AV node acts as a gate keeper to the ventricles Ventricular contraction is represented by QRS complex on ecg
- #9 Ectopic foci are pacemaker cells which initiates an impulse from another location in a normal conduction system. It most often occurs from the left atrium in the muscular sleeves of the pulmonary vein. The ectopic foci will fire rapid impulses to the AV node and other part of the atria cancelling out the normal impulses that are generated. The AV node will pick up impulses irregularly resulting in an unsynchronized rhythm and a rapid ventricular rate Nb – reentry circuit can form as a result of ischemic heart disease, age, hypertension which changes the atrial morphology, the reentry circuit originates in the atrial myocardium which have now have varying conductivity and excitability Re-entry is more likely to occur in atria that are enlarged, or in which conduction is slow (as is the case in many forms of heart disease)
- #10 AF is strong age dependent affecting 4% of individuals older than 60 years and 8% of person older than 80 Hypertension – systemic or pulmonary
- #11 Haemodynamic stress(increased intra atrial pressure results in atrial electrical and structural remodeling and predisposes to afib) – mitral or tricuspid valve disease, left ventricular dysfunction, pulmonary embolism Inflammation – myocarditis and pericarditis which may be idiopathic or occur in association with collagen vascular disease
- #12 Catecholamine release and/or increased sympathetic activity Stress – sepsis, hypovolemia, post surgical state(esp following cardiac surgery), hypothermia Pheochromocytoma Cocaine, amphetamine Electrolyte imbalances such as hypomagnesemia, hypokalemia Drugs such as adenosine, digoxin etc
- #13 Holiday heart syndrome - irregular heartbeat classically triggered by mod - excessive alcohol consumption, stress, dehydration or lack of sleep Neurological – subarachnoid hemorrhage or stroke Idiopathic – lone atrial fibrillation alcohol related cardiomyopathy
- #14 Unstable afib – afib manifesting with signs of hemodynamic instability (eg chest pain, altered mental status, acute pulmonary edema, hypotension or cardiogenic shock) Afib with rapid ventricular response – Afib with a ventricular rate > 100–110/minute (tachycardic Afib) Afib with slow ventricular response - Afib with a ventricular rate < 60/minute (bradycardic Afib or slow Afib) - The causes of slow Afib include SA node dysfunction (tachy-brady syndrome) and hypothermia. Ventricular rate may also be slow in patients being treated with AV node depressants, such as beta blockers, ndHP(non dihyropyridine calcium channel blocker) CCBs, and/or digoxin.
- #15 Paroxysmal AF - In younger patients, paroxysmal AF has been commonly found to be secondary to electrically active foci within the pulmonary veins. Elimination of these foci is found to be effective in treating this type of AF since it eliminates the trigger for such episodes Persistent AF- if it is associated with a rapid and uncontrolled ventricular rate, it may lead to electrical remodeling in the cardiac myocytes causing dilated cardiomyopathy. This type of AF may present as the first episode or as a result of recurrent episodes of paroxysmal AF.
- #16 About 50% of all patients with paroxysmal AF and 20% of patients with persistent or permanent AF have structurally normal hearts; this is known as ‘lone atrial fibrillation’.
- #17 Clinical afib - An episode of Afib lasting ≥ 30 seconds that is documented on a surface ECG, may be symptomatic or asymptomatic Subclinical afib - Asymptomatic Afib not previously detected on a surface ECG that is discovered on implanted cardiac devices and confirmed on intracardiac electrograms Valvular afib - Afib in patients with moderate to severe mitral valve stenosis or an artificial (mechanical) heart valve Nonvalvular afib - Afib in patients without moderate to severe mitral valve stenosis or a mechanical heart valve
- #19 Genetic factors involving chromosome 10(10q22-q24) – long arm of chromosome 10 deletion that consist of a mutation in the gene, alpha subunit of cardiac IK5 which is responsible for pore formation. It is a gain of function mutation allowing for more pores thereby increasing the activity within the ion channels of the heart and thus affecting the stability of the membrane and reducing its refractory time
- #20 AF is often completely asymptomatic, in which case it is usually discovered as a result of a routine examination or ECG In patients with poor ventricular function or valve disease, it may precipitate or aggravate cardiac failure because of loss of atrial function and heart rate control
- #21 A fall in BP may cause lightheadedness, and chest pain may occur with underlying coronary disease.
- #24 Fbc for anaemia and signs of infections, bmp for electrolytes imbalance(na, k, mg, ca), serum glucose to assess for hyperglycemia, buecr to assess for kidney disease, tft for hyperthyroidism, lft to assess for liver, Troponin levels: to assess for myocardial injury or infarction
- #25 Brain-natriuretic peptide(A peptide hormone released from myocytes in response to increased stretch (e.g., due to fluid overload). Ventricular or brain natriuretic peptide (BNP) is released from ventricular myocytes, while atrial natriuretic peptide (ANP) is released by atrial myocytes. Leads to systemic vasodilation and increased diuresis.) (BNP) or NT-proBNP(created from the cleaving of the prohormone proBNP into BNP and NT-proBNP, elevated levels particularly if >1000pg/mL are suggestive of heart failure - To assess for underlying heart failure, Can be elevated in persistent and paroxysmal Afib D-dimer levels: if patients have risk factors (e.g., DVT) or clinical features of pulmonary embolism Serum toxicology (e.g., ethanol level, digoxin level) and/or urine toxicology (e.g., cocaine, amphetamines) Xray - to evaluate for pulmonary disease or heart failure Findings - Signs of heart failure e.g., cardiomegaly and signs of pulmonary edema, Signs of an underlying etiology, such as pulmonary embolism, pneumonia or COPD
- #26 12 lead ECG is critical in making the diagnosis of atrial fibrillation, THE VENTRICLES ARE ACTIVATED AT A RATE DETERMINED BY CONDUCTION THROUGH The AV NODE THUS PRODUCING THE XTERITIC Iregularly irregular, Rarely may be regular if there is complete AV dissociation(A condition in which atrial and ventricular contractions occur independently. Occurs if a ventricular pacemaker is faster than the sinus node pacemaker (e.g., ventricular tachycardia or sinus bradycardia with a junctional rhythm) or if there is disruption of electrical transmission through the atrioventricular (AV) node (e.g., third-degree AV block). Electrocardiogram shows no relationship between P waves and QRS complexes (i.e., P-R dissociation). P waves are replaced by irregular chaotic f waves at a frequency of 300–600/minute Broad complexes may be seen in some situations: Aberrant conduction e.g., bundle branch block or preexcitation (as seen in Afib with WPW) Complete AV block with a ventricular escape rhythm Ashman phenomenon: intermittent aberrant ventricular conduction which results in an isolated or short runs of wide QRS complexes
- #28 Another investigation is an echo – it could be a transthoracic or tranesophageal echo Estimate for pulmonary systolic pressure - (pulmonary hypertension) TTE –can also evaluate for pericardial disease
- #29 Point one - (particularly in the left atrial appendages) Point two - ( if thrombus is seen, cardioversion should be delayed)
- #30 Cardiac stress test: if underlying ischemic heart disease is suspected or to assess the adequacy of rate control Electrophysiological study - suspected preexcitation (delta wave on ECG), if there is suspicion for an underlying SVT triggering Afib, or to distinguish between ventricular tachycardia and Afib with aberrant conduction Sleep study: if obstructive sleep apnea is suspected
- #32 Mode of termination - (eg, vagal maneuvers)
- #33 When AF complicates an acute illness (e.g. chest infection, pulmonary embolism), effective treatment of the primary disorder will often restore sinus rhythm. Otherwise, the main objectives are to restore sinus rhythm as soon as possible, prevent recurrent episodes of AF, optimize the heart rate during periods of AF, minimize the risk of thromboembolism and treat any underlying disease.
- #35 ICU – INTENSIVE CARE UNIT CCU – CARDIAC CARE UNIT CARDIAC TELEMENTRY – MONITORING OF THE HEART (HEARTBEAT)
- #36 RVR(RAPID VENTRICULAR RESPONSE) – can cause palpitations, dyspnea, ffatigue, chest discomfort, dizziness
- #39 ADHF – ACUTE DECOMPENSATED HEART FAILURE
- #41 In stable patients with symptomatic new-onset AF, the rate-control strategy may be considered first to control the ventricular rate. If rate-control treatment does not elicit a response or if echocardiography does not reveal any valvular or functional abnormality of the heart, cardioversion is indicated The required energy for cardioversion is usually 100-200 J (sometimes higher energy is required) for monophasic waveforms and less for biphasic waveforms. The patient should be sedated. In patients with AF of relatively short duration in whom the left atrium is not significantly large, the success rate of cardioversion exceeds 75% (ie, the size of the left atrium and the duration of AF inversely correlate with the success rate of cardioversion).
- #42 Consider in situations in which procedural sedation may be harmful or if the patient prefers pharmacological cardioversion. Most likely to be effective for arrhythmias of < 7 days duration Consultation with a specialist (e.g., cardiologist, electrophysiologist) is strongly recommended. More effective for atrial flutter than Afib, but there is a risk of conversion to 1:1 conduction with propafenone and flecainide
- #43 Paroxysmal AF ‘pill in the pocket’ (eg sotalol or flecainide PRN) may be tried if: infrequent AF, BP >100mmHg systolic, no past LV dysfunction
- #44 Av nodal ablation - A cardiac catheterization procedure in which the atrioventricular node is ablated using high-frequency radio waves to cause a state of permanent AV block. Patients who undergo AV nodal ablation requires life-long cardiac pacing using a pacemaker. AV node ablation is typically used to treat atrial fibrillation that is not responsive to therapy with antiarrhythmics or negative chronotropic drugs Indications includes – recurrent afib Afib refractory to medical rate control Patients who do not tolerate the pharmacological options for afib management
- #46 One of the major management decisions in atrial fibrillation (AF) is determining the risk of stroke and appropriate anticoagulation regimen for low, intermediate, and high-risk patients CHA2DS2-VASc = Congestive heart failure, Hypertension, Age ≥75 years, Diabetes mellitus, Stroke, Vascular disease, Age 65 − 74 years, Sex category (female);
- #49 History of bleeding - (the strongest predictive risk factor)
- #51 HEPATIC OR RENAL DISEASE, ETHANOL ABUSE, MALIGNANCY, OLDER(AGED GREATER OR EQUAL TO 75), REDUCED PLATELET COUNT OR FUNCTIONAL REBLEEDING RISK, HYPERTENSION(UNCONTROLLED), ANAEMIA, GENETIC FACTORS(CYP2C9 SINGLE NUCLEOTIDE POYMORPHISM), EXCESSIVE FALL RISK, STROKE
- #52 When the bleeding risk outweighs the benefit, avoidance of anticoagulation therapy in AF should be considered. In addition, because of its teratogenic effects, anticoagulation with warfarin is contraindicated in pregnant women, especially in the first trimester
- #53 Interpretation 0 points: low risk 1–2 points: moderate risk ≥ 3: high risk TTR(TIME IN THERAPEUTIC RANGE <60% IN PATIENTS RECEIVING VIT K ANTAGONIST)
- #57 Atrial Fibrillation related outcomes
- #58 Tachycardia induced cardiomyopathy is a reversible left ventricular dysfunction which can be induced by any tachyarrhythmia and early recognition of T-CMO with appropriate treatment of the arrhythmia culprit will lead to recovery of LV function
- #59 atrial fibrillation has a distinctive irregularly irregular rhythm with absent P-waves, whereas atrial flutter has a regularly irregular rhythm with absent P-waves
- #60 Then flutter waves are typically inverted(negative) in leads II, III, avF, V6 and generally positive in V1 because of counter clockwise reentrant pathways. Flutter waves can deform the ST complex and may mimic an ischemic injury pattern
- #61 In addition to individuals with heart disease such as congestive heart disease, atrial tachycardia may also occur in parsons with structurally normal heart
- #63 There may be crackles heard as a result of pulmonary vascular congestion during or following a supraventricular tachycardia