7.AF

Sri Lestari FFaizal Reza PMuh Wildan HShochibul KahfiEMERGENCY DEPARTMENTRSSA FKUB2014CASE REPORTAtrial Fibrillation

Supervisor (dr. Ali Haedar Sp.EM)

INTRODUCTION

DefinitionAF is defined as a cardiac arrhythmia with the following characteristics:The surface ECG shows absolutely irregular RR intervals (AF is therefore sometimes known as arrhythmia absoluta), i.e. RR intervals that do not follow a repetitive pattern.There are no distinct P waves on the surface ECG. Some apparently regular atrial electrical activity may be seen in some ECG leads, most often in lead V1.The atrial cycle length (when visible), i.e. the interval between two atrial activations, is usually variable and ,200 ms (.300 bpm).

RASKaukasian >> negro

GENDERMale >> Female

Agein United State60 years 3,8%>80 years 10%

Atrial Fibrilation increase with age

Predisposing Factor

Classification

Atrial FactorsAny kind of structural heart disease may trigger a slow but progressive process of structural remodelling in both the ventricles and the atria.Structural remodelling results in electrical dissociation between muscle bundles and local conduction heterogeneities facilitating the initiation and perpetuation of AF.

Electophysiological mechanismFocal mechanismsFocal mechanisms potentially contributing to the initiation and perpetuationof AF have attracted much attention. Cellular mechanisms of focal activity might involve both triggered activity and re-entry. Because of shorter refractory periods as well as abrupt changes in myocyte fibre orientation, the pulmonary veins (PVs) have a stronger potential to initiate and perpetuate atrial tachyarrhythmias.

The multiple wavelet hypothesisAccording to the multiple wavelet hypothesis, AF is perpetuated by continuous conduction of several independent wavelets propagating through the atrial musculature in a seemingly chaotic manner.Fibrillation wavefronts continuously undergo wavefrontwaveback interactions, resulting in wavebreak and the generation of new wavefronts, while block, collision, and fusion of wavefronts tend to reduce their number.As long as the number of wavefronts does not decline below a critical level, the multiple wavelets will sustain the arrhythmia.

CTGF, connective tissue growth factor; ERP, effective refractory period; PV, pulmonary vein;RAAS, renin-angiotensin-aldosterone system; TGF- B, transforming growth factor .

Hemodynamic Effect

Thromboembolism

Clinical Manifestation

Acute ManagementA patient with atrial fibrillation discovered for the first time should be evaluated for a precipitating cause, such as thyrotoxicosis, mitral stenosis, pulmonary emboli, or pericarditissudden onset of atrial fibrillation with a rapid ventricular rate results in acute cardiovascular decompensation, electrical cardioversion is the initial treatment of choice

For patients who do not require emergent cardioversion, chemical cardioversion with IV antiarrhythmic drugs is effective in 35 to 75 percent of patientsIn the absence of decompensation, the patient can be treated with drugs such as digitalis, beta blockers, or calcium antagonists to maintain a resting apical rate of 60 to 80 beats/min

Long term ManagementFor the rate control strategy, digitalis, calcium channel blockers (diltiazem and verapamil) and beta blockers can be used alone or in combinationAs a general rule, for patients without structural heart disease, IC agents (propafenone and flecainide) are well-tolerated and reasonable first-line agents for maintenance of sinus rhythm.For patients with structural heart disease, amiodarone, dofetilide, or sotalol may be reasonable first-line therapies to maintain sinus rhythm

Risk factor-based point-based scoring system - CHA2DS2-VASc *Prior myocardial infarction, peripheral artery disease, aortic plaque. Actual rates of stroke in contemporary cohorts may vary from these estimates.

Adjusted stroke rate according to CHA2DS2-VASc score

The HAS-BLED bleeding risk score*Hypertension is defined as systolic blood pressure > 160 mmHg.INR = international normalized ratio.

extracardiaccardiacleading to the progressive decline of contractility, conductivity disorders, mechanical factorsall cases accompanied by hypoxia

Causes of circulation arrestCardiacExtracardiacIschemic heart disease (myocardial infarction, stenocardia)Arrhythmias of different origin and characterElectrolytic disordersValvular diseaseCardiac tamponadePulmonary artery thromboembolismRuptured aneurysm of aortaairway obstructionacute respiratory failureshockreflector cardiac arrestembolisms of different origindrug overdosepoisoning

INDICATIONS DC ShockDefibrillation (Non-Synchronized DC Shock):VFPulseless VTRecommended joule: 360 J

*

INDICATIONSSynchronized DC Shock (Only with unstable hemodynamic):

AFAtrial FlutterSVT

VT with pulse(despite ofmedication)*start with 50 Jstart with 100 JInfant and Children: 2 J/kg

DO NOT SHOCK!!!AsystolePulseless Electrical ActivityBradicardiaHeart BlockStable hemodynamic with AF, Atrial Flutter, SVT, & VT with pulse*

Supraventricular Tachyarrhytmia2005 : The recommended initial monophasic energy dose for cardioversion of AF is 100 to 200 J2010 : recommended initial biphasic energy dose for cardioversion of AF is 120-200 J, And monophasic is 200 J

Organized Post Cardiac Arrest CareOptimizing cardiopulmonary function and vital organ perfusion after ROSCTransportation to an appropriate hospital or critical care unit with comprehensive post cardiac arrest treatment system of careIdentification and intervention for acute coronary syndrome (ACS)Temperature control to optimize neurological recoveryAnticipation, treatment, and prevention of multiple organ dysfunction

General management of atrial fibrillation should focus on control of the rapid ventricular rate (rate control), conversion of hemodynamically unstable atrial fibrillation to sinus rhythm (rhythm control), or both.Patients with an atrial fibrillation duration of 48 hours are at increased risk for cardioembolic events, although shorter durations of atrial fibrillation do not exclude the possibility of such events

Patients who are hemodynamically unstable should receive prompt electric cardioversionMore stable patients require ventricular rate control as directed by patient symptoms and hemodynamicsIV b-blockers and nondihydropyridine calcium channel blockers such as diltiazem are the drugs of choice for acute rate control in most individuals with atrial fibrillation and rapid ventricular responseDigoxin and amiodarone may be used for rate control in patients with congestiv heart failure;

CASE REPORT

Patients Identity

Name: Mrs.SMAge: 49 y.oAddress: Blimbing, MalangMarital Status : MarriedRegister: 1059xxxxOccupation: HousewifeReligion : MoslemAdmission Time: 18th October 2014

Estimated Body Weight: 45kg

Admission time 18th October 2014 at 06.45

PRIMARY SURVEY

A:PatentB: RR 40 tpm, regular, symmetrical chest expansion, normal depthC:PR 156 bpm, irregular, thready pulse, BP 90/73 mmHg, warm and dry acral, Tax 37,60C, CRT < 2 secondsD: Alert (AVPU)

Patient then placed at P1

INITIAL MANAGEMENT

A:-B: Semifowler positionO2 support NRBM 10 lpm O2 CPAP 5-7 cmH2OC:IVFD NaCl 0,9% loading 200 ccD:-

Mrs.SM/ 49 yoChief complaint: shorthness of breathPatient came to ER RSSA with chief complaint of SOB since 1 week ago and worsened since 2 days ago. Previous she often suffered shortness of breath even when she took a rest. She slept with 2 pillows and intermitenly woke up in the midnight due to shortness of breath.She also complained fever and cough with bloody mucous. The patient has had the same shorthness of breath since seven year ago. History of dyspneu on effort +, paroxysmal nocturnal dyspneu +, orthopneu +, leg swelling +.

Mrs.SM/ 49 yo

Medical history : No history of diabetes. Patient had hypertension since 7 years ago. Patient has been examined by cardiologist and diagnosed with heart failure. Patient routinely control to cardiologist and receive digoksin, concor, and furosemideMedication history : Patient has not routinely taken medication for her heart problem. Family history : HT(-), DM(-), heart failure (-), allergy (-)

General Appearance looks severe illGCS 456Nutritional status: normoweight (BW 45 kg, height 155cm)BP= 90/73mmHgPR = 156 bpmRR = 40 tpm Sat.O2 (99%) CPAPTax : 37,6 0CHeadAnemic conjunctiva (+/+)Icteric sclera (-/-) NeckJVP R + 3cm H2O, 300 Thorax Cor Ictus invisible & palpable at ICS V I 1 cm lateral MCL S, Heave (+), thrill (+)RHM ~SL D, LHM ~ ictus; S1 S2 irregularPulmoSymmetricStem fremitus D=SSonor + +v vRh + +Wh - - + +v v + + - - + +v v + + - - AbdomenFlat , BS + N, soeflExtremitiesPretibialAnemic - - Warm acral + +Diaphoresis (-) edema -/- - - + +

ADDITIONAL EXAMINATION

Serial ECGLab. BGA, SE, GDAThorax Ro

Asinus, HR 151 bpmFrontal Axis: Left deviationHorizontal Axis: Clock wise rotationPR interval : cant to be evaluatedQRS complex: 0.10QT interval: 0.28ST changes: no ST elevation

Kesimpulan: Atrial Fibrillation, RVR

LabvalueNormal valueLabValueNormal valuepH 7,417,35-7,45Na 131mmol/L136-145pCO228mmHg35-45K3,17mmol/L3,5-5pO2217,6mmHg80-100Cl103mmol/L98-105Bicarbonate18mmol/L21-28GDA87mg/dl< 200BE-6,8mmol/L(-3)-(+3)Sat. O299,8%> 95Hb13,3g/dlSuhu37C

AP position, symmetrical, enough KV, enough inspirationTrachea in the middleBone and soft tissue within normal limitAorta in the middlePhrenico costalis angle D/S sharpHemidiaphragma D/S dome shapeLung : increase of vascular patternCor : enlargement of all chamber, apex rounded, straight weist heart with delta shape appearanceCTR 93%

Conclusion : Cardiomegaly all chamber enlargement dd efusi pericard

WORKING/PROVISIONAL DIAGNOSIS

1.SOB dt ALO cardiogenic2.AF RVR

MANAGEMENT

Bed rest semi fowler positionO2 NRBM 8-10 lpmCatheter insertion (+)IVFD NS 0,9% 500 cc/dayIntake peroral 1000 cc/dayInj. Ranitidine 50 mgInj. Metoclorpramide 10 mgInj.Furosemide 40 mg-0-0 (postpone)Inj. Digoxin 0,5 mg ECG/4 hrSpironolakton 0-25 mg-0 (PO)Warfarin 4 mgLaxadin 1x/dayDivisi Kardiologi

Review of the patientFemale 49 yoCame to ER with the problem in :Breathing : RR 40 tpmCirculation : PR 156 bpm, irregular, thready pulse, BP 97/73 mmHgShe had chief complaint SOBShe had medical history of Heart FailureECG : AF RVRChest X-Ray : Cardiomegaly all chamber

THEORY CaseEpidemiology:Male > FemaleIncreasing with ageRisk Factor:ACSHypertrofik cardiomyopathy Valvular heart diseaseArrythmiaPericarditisHipertensiDiabetes melitusHypertiroidismeCOPDHypertention pulmonalEmboli pulmonalICHGeriatricHeart failureFemale, 49 yoHeart failureHypertention

THEORY CaseClinical manifestationThe clinical manifestations of AF range from no symptoms at all to profound hemodynamic deterioration with cardiogenic shock or even cardiac arrest in some patients with WPW syndromeThe patient has no symptom

THEORY CaseAF is defined as a cardiac arrhythmia with the following characteristics:The surface ECG shows absolutely irregular RR intervals (AF is therefore sometimes known as arrhythmia absoluta), i.e. RR intervals that do not follow a repetitive pattern.There are no distinct P waves on the surface ECG. Some apparently regular atrial electrical activity may be seen in some ECG leads, most often in lead V1.The atrial cycle length (when visible), i.e. the interval between two atrial activations, is usually variable and ,200 ms (.300 bpm).

Asinus, HR 151 bpmFrontal Axis: Left deviationHorizontal Axis: Clock wise rotationPR interval : cant to be evaluatedQRS complex: 0.10QT interval: 0.28ST changes: no ST elevationConclusion : Atrial Fibrillation, RVR

THEORY CasePatients who are hemodynamically unstable should receive prompt electric cardioversionMore stable patients require ventricular rate control as directed by patient symptoms and hemodynamicsIV b-blockers and nondihydropyridine calcium channel blockers such as diltiazem are the drugs of choice for acute rate control in most individuals with atrial fibrillation and rapid ventricular responseDigoxin and amiodarone may be used for rate control in patients with congestiv heart failure;MANAGEMENT

Bed rest semi fowler positionO2 NRBM 8-10 lpmIVFD NS 0,9% 500 cc/dayIntake peroral 1000 cc/dayInj. Ranitidine 50 mgInj. Metoclorpramide 10 mgInj.Furosemide 40 mg-0-0 (postpone)Inj. Digoxin 0,5 mg ECG/4 hr

Cardiologic Dept : Spironolakton 0-25 mg-0 (PO)Warfarin 4 mgLaxadin 1x/day

Risk factor-based point-based scoring system - CHA2DS2-VASc *Prior myocardial infarction, peripheral artery disease, aortic plaque. Actual rates of stroke in contemporary cohorts may vary from these estimates.

ConclusionAF is cardiac arrythmia in atrium, narrow irregular RR, no distinct P waveA patient with atrial fibrillation discovered for the first time should be evaluated for a precipitating causePatients with heart failure often do worse when in AF, and it is difficult to know whether this is caused by loss of atrial contraction, too fast a ventricular rate, irregularity of rhythm, or a combination of factorsGeneral management of atrial fibrillation should focus on control of the rapid ventricular rate (rate control), conversion of hemodynamically unstable atrial fibrillation to sinus rhythm (rhythm control), or both.

Lesson learntSuspected AF patient due to any disease immediately perform ECG to evaluate for AFEKG interpretation : AFTherapy purpose : quick identification whether the patient need to get cardioversion or not , and prevent its mechanical complication.

Thank You

*******Tachycardia Algorithm.*Kebutuhan cairan dewasa 50 cc/kg/24 jam = 60x50 = 3000 cc dalam 24 jam = 120 cc perjam = 1,9 cc/menit = 20-30 tpm***Definition of a pathologic Q waveAny Q-wave in leads V2V3 0.02 s or QS complex in leads V2 and V3Q-wave 0.03 s and > 0.1 mV deep or QS complex in leads I, II, aVL, aVF, or V4V6 in any two leads of a contiguous lead grouping (I, aVL,V6; V4V6; II, III, and aVF)R-wave 0.04 s in V1V2 and R/S 1 with a concordant positive T-wave in the absence of a conduction defect

Lead III often shows Q waves, which are not pathologic as long as Q waves are absent in leads II and aVF (the contiguous leads)

*HeparinsHeparin is an indirect inhibitor of thrombin that has been widely used in ACS as adjunctive therapy for fibrinolysis and in combination with aspirin and other platelet inhibitors for the treatment of non-ST-segment elevation ACS. UFH has several disadvantages, including (1) the need for IV administration; (2) the requirement for frequent monitoring of the activated partial thromboplastin time (aPTT); (3) an unpredictable anticoagulant response in individualpatients; and (4) heparin can also stimulate platelet activation, causing thrombocytopenia. Because of the limitations of heparin, newer preparations of LMWH have been developed.*****Tachycardia Algorithm.Definition of a pathologic Q waveAny Q-wave in leads V2V3 0.02 s or QS complex in leads V2 and V3Q-wave 0.03 s and > 0.1 mV deep or QS complex in leads I, II, aVL, aVF, or V4V6 in any two leads of a contiguous lead grouping (I, aVL,V6; V4V6; II, III, and aVF)R-wave 0.04 s in V1V2 and R/S 1 with a concordant positive T-wave in the absence of a conduction defect


*Definition of a pathologic Q waveAny Q-wave in leads V2V3 0.02 s or QS complex in leads V2 and V3Q-wave 0.03 s and > 0.1 mV deep or QS complex in leads I, II, aVL, aVF, or V4V6 in any two leads of a contiguous lead grouping (I, aVL,V6; V4V6; II, III, and aVF)R-wave 0.04 s in V1V2 and R/S 1 with a concordant positive T-wave in the absence of a conduction defect


*Definition of a pathologic Q waveAny Q-wave in leads V2V3 0.02 s or QS complex in leads V2 and V3Q-wave 0.03 s and > 0.1 mV deep or QS complex in leads I, II, aVL, aVF, or V4V6 in any two leads of a contiguous lead grouping (I, aVL,V6; V4V6; II, III, and aVF)R-wave 0.04 s in V1V2 and R/S 1 with a concordant positive T-wave in the absence of a conduction defect


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7.AF

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